PSY192 • Psychology Special #2

Table of Contents

PSY192 • Psychology Special #2

How to Receive Credit

NetCE 6 Hour Course #67264 • Ethics for Psychologists

67264 • Ethics for Psychologists

1. INTRODUCTION

2. GENERAL CONCEPTS

3. A HISTORY OF PSYCHOLOGY AND ETHICS IN THE UNITED STATES

4. ETHICAL STANDARDS

5. ETHICAL DECISION MAKING

6. COMPLAINTS AND CHARGES

7. CONCLUSION

8. APPENDIX

Works Cited

NetCE 4 Hour Course #66474 • Obsessive-Compulsive Disorder

66474 • Obsessive-Compulsive Disorder

1. INTRODUCTION

2. EPIDEMIOLOGY

3. NATURAL HISTORY

4. DIAGNOSTIC CRITERIA

5. PATHOPHYSIOLOGY

6. DIFFERENTIAL DIAGNOSIS

7. COMORBIDITIES

8. TREATMENT

9. CONCLUSION

10. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

NetCE 10 Hour Course #66564 • Alcohol and Alcohol Use Disorder

66564 • Alcohol and Alcohol Use Disorder

1. INTRODUCTION

2. HISTORY

3. CURRENT ESTIMATES OF ALCOHOL USE

4. BENEFITS

5. RISK AND PROTECTIVE FACTORS

6. ALCOHOL USE DISORDER

7. COMPLICATIONS

8. OTHER PSYCHIATRIC DISORDERS ASSOCIATED WITH ALCOHOL USE DISORDERS

9. DETECTING ALCOHOL USE DISORDERS

10. BRIEF INTERVENTION

11. TREATMENT

12. CONCLUSION

13. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

PSY192 • Psychology Special #2

Margaret Donohue, PhD

John J. Whyte, MD, MPH

www.netce.com

Copyright © 2025 NetCE, All rights reserved.

PSY192 • Psychology Special #2

Expiration Date: 06/30/2026

How to Receive Credit

To complete this Special Offer for continuing education credit please go to http://www.netce.com/specials in your browser.

For assistance with receiving continuing education credit, please contact us at help@netce.com.

67264 • Ethics for Psychologists

Margaret Donohue, PhD

www.netce.com

Copyright © 2023 NetCE, All rights reserved.

General ethical concepts applicable to all psychologists regardless of setting include competence, informed consent, privacy and confidentiality, and avoiding harm or exploitation. This course provides specific information regarding each of the areas and how they apply to psychologists in a variety of settings with a variety of professional relationships. Psychologists also must be able to understand and differentiate the complex relationships between the American Psychological Association's Ethical Principles of Psychologists and Code of Conduct, the ethics codes of various state psychological associations, regulations of state licensing boards, institutional policies and procedures, state and federal law, and community and local standards of practice. Common ethical issues and complaint procedures are also reviewed.

Table of Contents

67264 • Ethics for Psychologists

Course Overview

Audience

Accreditations & Approvals

Designations of Credit

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Director of Development and Academic Affairs

Director Disclosure Statement

About the Sponsor

Disclosure Statement

Implicit Bias in Health Care

1. INTRODUCTION

2. GENERAL CONCEPTS

3. A HISTORY OF PSYCHOLOGY AND ETHICS IN THE UNITED STATES

4. ETHICAL STANDARDS

COMPETENCE

INFORMED CONSENT

PRIVACY AND CONFIDENTIALITY

AVOIDING HARM AND EXPLOITATION

5. ETHICAL DECISION MAKING

6. COMPLAINTS AND CHARGES

7. CONCLUSION

8. APPENDIX

Works Cited

67264 • Ethics for Psychologists

Education Category. Ethics - Human Rights

Release Date. 07/01/2023

Expiration Date. 06/30/2026

Course Overview

General ethical concepts applicable to all psychologists regardless of setting include competence, informed consent, privacy and confidentiality, and avoiding harm or exploitation. This course provides specific information regarding each of the areas and how they apply to psychologists in a variety of settings with a variety of professional relationships. Psychologists also must be able to understand and differentiate the complex relationships between the American Psychological Association's Ethical Principles of Psychologists and Code of Conduct, the ethics codes of various state psychological associations, regulations of state licensing boards, institutional policies and procedures, state and federal law, and community and local standards of practice. Common ethical issues and complaint procedures are also reviewed.

Audience

This intermediate course is designed for all licensed psychologists in all practice settings.

Accreditations & Approvals

Continuing Education (CE) credits for psychologists are provided through the co-sponsorship of the American Psychological Association (APA) Office of Continuing Education in Psychology (CEP). The APA CEP Office maintains responsibility for the content of the programs. NetCE is accredited by the International Accreditors for Continuing Education and Training (IACET). NetCE complies with the ANSI/IACET Standard, which is recognized internationally as a standard of excellence in instructional practices. As a result of this accreditation, NetCE is authorized to issue the IACET CEU.

Designations of Credit

NetCE designates this continuing education activity for 6 credit(s). NetCE is authorized by IACET to offer 0.6 CEU(s) for this program.

Course Objective

The purpose of this course is to provide psychologists with an understanding of ethical issues common to their practices and tools necessary for effective ethical decision making.

Learning Objectives

Upon completion of this course, you should be able to:

1. Define general concepts at the core of an ethical psychology practice.

2. Outline the history of psychology and ethics in the United States.

3. Discuss the principle of competence and its significance in psychology.

4. Identify key aspects of informed consent.

5. Review the principles of privacy and confidentiality and the psychologist's responsibilities when protecting clients' privacy.

6. Describe the impact of technology and exploitation on the psychologist-client relationship

7. Outline components of ethical decision making and the process for complaints.

Faculty

Margaret Donohue, PhD, is a psychologist in Los Angeles, California. She received her doctorate from the California School of Professional Psychology in Los Angeles. Her clinical and forensic practice focuses on the areas of health and medical psychology especially complex psychological and neuropsychological assessments. She is licensed in both California and Nevada.
In addition to her private practice, Dr. Donohue currently teaches at The Chicago School of Professional Psychology in Los Angeles. She is actively involved with the California Psychological Association's Office of Professional Development as a Third Reviewer for courses for continuing education for psychologists. She is a member of the American Psychological Association, the Los Angeles County Psychological Association, and the National Register of Health Service Providers in Psychology.
Dr. Donohue has frequently provided ethical consultation to colleagues in the area of professional boundaries, ethics and psychological assessment, and ethics in professional practice. Her public speaking events have included being a panel presenter in the January 1987 Los Angeles conference on ethics and boundaries for lesbian therapists. She has also presented for the California Psychological Association on the personal impact of head injuries in neuropsychologists with Jonathan Greene, PhD, in 2006.
Dr. Donohue has published articles on Tarasoff notification and racism; quality evaluation in health care; benchmarking access to outpatient services in managed health organizations; treatment of anxiety in young children; and the development of assessment techniques in evaluations of young children and assessing organizational productivity and quality.

Faculty Disclosure

Contributing faculty, Margaret Donohue, PhD, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Director of Development and Academic Affairs

Sarah Campbell

Director Disclosure Statement

The Director of Development and Academic Affairs has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Implicit Bias in Health Care

The role of implicit biases on healthcare outcomes has become a concern, as there is some evidence that implicit biases contribute to health disparities, professionals' attitudes toward and interactions with patients, quality of care, diagnoses, and treatment decisions. This may produce differences in help-seeking, diagnoses, and ultimately treatments and interventions. Implicit biases may also unwittingly produce professional behaviors, attitudes, and interactions that reduce patients' trust and comfort with their provider, leading to earlier termination of visits and/or reduced adherence and follow-up. Disadvantaged groups are marginalized in the healthcare system and vulnerable on multiple levels; health professionals' implicit biases can further exacerbate these existing disadvantages.

Interventions or strategies designed to reduce implicit bias may be categorized as change-based or control-based. Change-based interventions focus on reducing or changing cognitive associations underlying implicit biases. These interventions might include challenging stereotypes. Conversely, control-based interventions involve reducing the effects of the implicit bias on the individual's behaviors. These strategies include increasing awareness of biased thoughts and responses. The two types of interventions are not mutually exclusive and may be used synergistically.

1. INTRODUCTION

General ethical concepts applicable to all psychologists regardless of setting include competence, informed consent, privacy and confidentiality, and avoiding harm or exploitation. This course provides specific information regarding each of the areas and how they apply to psychologists in a variety of settings with a variety of professional relationships. Psychologists also must be able to understand and differentiate the complex interactions between the American Psychological Association's (APA's) Ethical Principles of Psychologists and Code of Conduct, the ethical codes of various state psychological associations, regulations of state licensing boards, institutional policies and procedures, state and federal law, and community and local standards of practice. Common ethical issues and complaint procedures are also reviewed.

2. GENERAL CONCEPTS

As noted, there are four ethical standards applicable to all psychologists regardless of setting: competence, informed consent, privacy and confidentiality, and avoiding harm or exploitation [1]. Ethical rules and standards provide a frame of reference for guidance in decision making about the most appropriate action to take in a given situation. As experience and circumstances change, the ethical standards for psychologists evolve from a strict set of rules about behavior and conduct to becoming more aspirational in nature. The practice of being ethical changes to being more involved with thinking through the consequences of actions and more cognizant about the day-to-day impact of ethics on practice.

Ethics differs slightly from values, morals, and laws. Values are ways to determine what is more or less important in decision making [2,3]. Morals are specifically about motivations and actions and how those motivations and actions are good and bad. Morals have a social component and pertain to rules that govern life in a social structure. Morals are based in culture, history, and generally religious authority. They are usually agreed upon by the culture and serve to form the basis of the laws in the society. The laws are an external system of constraints on behavior that apply equally to everyone within the society. Ethics are a self-imposed system for constraining behavior based on values and morals [2,3]. It is also a system of moral values governing the conduct of a person or the members of a profession. Ethics form the basis of professional standards that are then codified into laws regulating the members of a profession.

Psychology has developed ethics and ethical decision making over several decades with multiple revisions to the APA Ethics Code. The APA Ethics Code has attempted to be scientifically based in principles that will allow for decision making and are generalizable to the profession as a whole. More recently, it has focused more on problem areas that serve as the basis of complaints against psychologists to licensing boards.

3. A HISTORY OF PSYCHOLOGY AND ETHICS IN THE UNITED STATES

The APA was founded in July 1892 at Clark University by a group of 26 men, many of whom accepted invitation to the group by mail. The first meeting involved the presentation of 6 research papers [4]. Its first president was G. Stanley Hall, and it began with 31 members [5]. It was the aspiration of the APA that the organization would provide guidance and assistance to members who were obtaining advanced degrees and becoming credentialed in new fields of expertise. There was a progressive movement in politics and a need for more professionals to assist in political demands.

Following the Civil War, the United States entered into a rapid growth phase. There was corruption in the building of the Transcontinental Railroad and there were Congressional scandals related to the misuse of governmental funds, bribery, and excess charges. In addition to corruption in the government, there was a high crime rate, a high poverty rate, concerns about the use of "greenbacks" (or Confederate money), and limitations in the monetary supply based on reliance on the gold standard. G. Stanley Hall had established Clark University as a research institution and founded the American Journal of Psychology. Psychology as a young field was moving into research, which was controversial, and away from work with healthy individuals and anthropology. The field was expanding to include work with animals, children, sick people, and the new practice of hypnosis [4,5]. Ideas of what was and was not appropriate for the field began to coalesce. After World War II, the APA began to expand and grow quickly. The need for an ethical code and ethical standards came out of the expanding profession and out of situations in which psychologists found themselves without clarity for decision making.

The first Committee for Ethical Standards for Psychologists formed in 1947. The Committee worked on developing a description of critical situations in which psychologists made decisions involving ethical considerations. More than 2,000 members contributed to formulating the first Ethics Code in 1953. Consisting of 171 pages, it was a lengthy document, reflecting the post-war concerns of conflicts of the academic freedom movement, McCarthyism, and requests to design tests to support racial segregation [6]. The next edition, published in 1959, consisted of 18 principles and a preamble.

Today, the APA has more than 146,000 members and 54 divisions in subfields of psychology [7]. The 2002 edition of the revised Ethics Code consists of an introduction and an applicability section and separates the ethical code and laws regarding the professional practice of psychology. The APA's Ethical Principles of Psychologists and Code of Conduct was amended in 2010 to deal with conflicts of psychologists providing services to the military and potentially violating human rights and again in 2016 to ensure that psychologists take reasonable steps to avoid harming those with whom they work and to assert that psychologists do not participate in, facilitate, assist, or otherwise engage in torture [8]. The current Ethics Code consists of an introduction, a preamble, five general principles, and specific ethical standards.

4. ETHICAL STANDARDS

General ethical principles of psychology stem from a value that psychologists "work to develop a valid and reliable body of scientific knowledge based on research" [9]. The current Ethics Code has a stated goal of ensuring "the welfare and protection of the individuals and groups with whom psychologists work and education of the members, students, and the general public regarding ethical standards of the discipline" [8].

COMPETENCE

Competence is a fundamental ethical principle in the healthcare professions. Medicine and psychology define competence as, "the habitual and judicious use of communication, knowledge, technical skills, clinical reasoning, emotions, values, and reflection in daily practice for the benefit of the individual and community being served" [1,10]. To be considered adequately or well qualified to practice psychology (i.e., competent) is a process of evaluation of a specific area. Both the individual psychologist and the profession as a whole strive to determine areas of competent practice and the basis on which to form those evaluations.

The profession has set forth educational standards for doctoral programs in psychology. This involves accreditation of schools and colleges at a regional level and setting forth standards for accreditation by the APA for graduate school. Internships and postdoctoral fellowships may also be accredited by the APA, the Association of Psychology Postdoctoral and Internship Centers, or both.

Following graduation and completion of internships and postdoctoral fellowships, licensing boards in states with licensure requirements for professional practice set additional minimum standards for competence. Some states require continuing education following licensure to remain current on the research and developments within the field. The psychology boards often work in conjunction with the Association of State and Provincial Psychology Boards to set standards for examination or certification and to facilitate mobility of licensure to other states, territories, or provinces.

Following licensure, recognition can be obtained from the National Register of Health Service Providers in Psychology, or certification from the Association of State and Provincial Psychology Board's Certificate of Professional Qualification in Psychology (CPQ). The American Board of Professional Psychology provides an additional examination to document competence in areas of expertise. Additionally, some types of training offer certification documenting training and skill in a particular technique or area.

Competence involves knowing all aspects about the services, treatment, evaluation, and decisions made in an area of expertise being provided. Clinical practice recommendations and evidence-based approaches provide guidelines regarding what constitutes effective practice. The purpose of the guidelines is to limit idiosyncratic, self-serving methodologies that may cause harm to an individual or to the profession.

The 2016 APA Ethics Code addresses competence in standard 2.0 [8]. The following sections are reprinted with permission:

2.01 Boundaries of Competence

(a) Psychologists provide services, teach, and conduct research with populations and in areas only within the boundaries of their competence, based on their education, training, supervised experience, consultation, study, or professional experience.

(b) Where scientific or professional knowledge in the discipline of psychology establishes that an understanding of factors associated with age, gender, gender identity, race, ethnicity, culture, national origin, religion, sexual orientation, disability, language, or socioeconomic status is essential for effective implementation of their services or research, psychologists have or obtain the training, experience, consultation, or supervision necessary to ensure the competence of their services, or they make appropriate referrals, except as provided in Standard 2.02, Providing Services in Emergencies.

(c) Psychologists planning to provide services, teach, or conduct research involving populations, areas, techniques, or technologies new to them undertake relevant education, training, supervised experience, consultation, or study.

(d) When psychologists are asked to provide services to individuals for whom appropriate mental health services are not available and for which psychologists have not obtained the competence necessary, psychologists with closely related prior training or experience may provide such services in order to ensure that services are not denied if they make a reasonable effort to obtain the competence required by using relevant research, training, consultation, or study.

(e) In those emerging areas in which generally recognized standards for preparatory training do not yet exist, psychologists nevertheless take reasonable steps to ensure the competence of their work and to protect clients/patients, students, supervisees, research participants, organizational clients, and others from harm.

(f) When assuming forensic roles, psychologists are or become reasonably familiar with the judicial or administrative rules governing their roles.

2.02 Providing Services in Emergencies

In emergencies, when psychologists provide services to individuals for whom other mental health services are not available and for which psychologists have not obtained the necessary training, psychologists may provide such services in order to ensure that services are not denied. The services are discontinued as soon as the emergency has ended or appropriate services are available.

2.03 Maintaining Competence

Psychologists undertake ongoing efforts to develop and maintain their competence.

2.04 Bases for Scientific and Professional Judgments

Psychologists' work is based upon established scientific and professional knowledge of the discipline. (See also Standards 2.01e, Boundaries of Competence, and 10.01b, Informed Consent to Therapy.)

2.05 Delegation of Work to Others

Psychologists who delegate work to employees, supervisees, or research or teaching assistants or who use the services of others, such as interpreters, take reasonable steps to (1) avoid delegating such work to persons who have a multiple relationship with those being served that would likely lead to exploitation or loss of objectivity; (2) authorize only those responsibilities that such persons can be expected to perform competently on the basis of their education, training, or experience, either independently or with the level of supervision being provided; and (3) see that such persons perform these services competently. (See also Standards 2.02, Providing Services in Emergencies; 3.05, Multiple Relationships; 4.01, Maintaining Confidentiality; 9.01, Bases for Assessments; 9.02, Use of Assessments; 9.03, Informed Consent in Assessments; and 9.07, Assessment by Unqualified Persons.)

2.06 Personal Problems and Conflicts

(a) Psychologists refrain from initiating an activity when they know or should know that there is a substantial likelihood that their personal problems will prevent them from performing their work-related activities in a competent manner.

(b) When psychologists become aware of personal problems that may interfere with their performing work-related duties adequately, they take appropriate measures, such as obtaining professional consultation or assistance and determine whether they should limit, suspend, or terminate their work-related duties. (See also Standard 10.10, Terminating Therapy.)

Psychologists generally do not attempt to perform services for which they feel incompetent; they attempt to perform services they believe they can effectively offer. As time goes on, they may be swayed by financial considerations, misdirected ideas about trying to be helpful, or beliefs regarding what is appropriate. Consider the following scenarios:

- A psychologist accepts a new position at a company offering to provide training in a new area of services for her. After she is scheduled to see patients, she finds that the "training" consists only of being given copies of outlines of reports to follow. She begins to see patients but is immediately overwhelmed. The company complains she is not meeting performance standards. She turns in her resignation but is told she is already scheduled with patients and to leave prematurely would harm patients who had already waited weeks to be scheduled. She leaves, and the company files an ethics complaint against her.

- A psychologist joins a group practice to provide production testing for a large company under contract. The psychologist has taken a few semesters of testing while in graduate school but has done no testing in at least a decade. Although the psychologist seeks supervision independently, the supervising psychologist suggests the services currently being provided are so far below the standard of practice as to appear unethical. The psychologist decides to pursue other employment.

When starting a new position, it is important to know exactly what will be required to determine whether or not the psychologist will be competent to perform the task. Positions that are described as "training" or "under supervision" should provide to the psychologist a clear delineation of the supervision, training expectations, methods of evaluation, and feedback or evaluation procedures. In recent years, more focus has been given to models of training and supervision, including competency-based supervision.

Competency-Based Supervision

Competency-based supervision has been defined as, "an approach that explicitly identifies the knowledge, skills, and values that are assembled to form a clinical competency and develops learning strategies and evaluation procedures to meet criterion-referenced standards in keeping with evidence-based practices and requirements of the local clinical setting" [11]. The focus on competency-based standards came following the 2002 revision of the APA Ethical Principals and Code of Conduct. There was a shift in education from assessment of curricula to educational outcomes and an emphasis on accountability to the public in education. Over time, the competency model moved into supervision and training programs as well as graduate school programs.

Quality assessment and evaluation came out of program evaluation in business, then it slowly migrated to general health care, to the professional schools of psychology, to professional organizations, and finally to ideas about outcomes of services. The idea of determining objectively whether or not what was desired by the client was achieved and the expected outcome produced was quite novel in psychology prior to 1990. Along with this came the idea of developing benchmarks for quality and guidelines for achievement to ensure that quality was maintained throughout an organization. Research designs examining outcomes and "best practices" were developed. In addition, organizations started asking clients about their needs, expectations, and ideas. This led to the concept of partnerships or collaboration between psychologists and patients in creating a treatment plan. It also led to surveys from patients and appraisals for teachers, employers, supervisors, and healthcare providers regarding whether or not expectations were being met. The concept of competency started to have, as a basis for evaluation, objective data on outcome and self-assessment, expected developmental progressions, and benchmarks for achievement of foundational skills and abilities at various points in time along a continuum of professional development. In addition to foundational skills (the knowledge basis one needs to be competent), functional skills (the abilities one must demonstrate to be considered competent) were proposed.

Finally, the idea of outcome assessment (how does one know if what they are doing is working) was built into the model as a feedback loop for refinement of competency assessment. In an educational setting, these concepts were superimposed on a developmental perspective applicable to teachers, mentors, and supervisors. Eventually, the concepts were incorporated into psychology professional schools and APA accreditation processes for education in psychology.

In 2007, the Assessment of Competency Benchmarks Workgroup published their document for the APA entitled The Assessment of Competency Benchmarks Workgroup: A Developmental Model for the Defining and Measuring of Competence in Professional Psychology [12]. They created a three-dimensional "Cube Model," with foundational competencies and functional competencies forming the 12 core competencies for clinical practice. These were placed in a developmental model to guide supervisors from practicum training through advanced practice to lifelong learning.

Within the Cube Model, the foundational competencies consist of reflective practice self-assessment, scientific knowledge and methods, relationships, ethical and legal standards policy, individual and cultural diversity, and interdisciplinary systems. The functional competencies consist of assessment/diagnosis/case conceptualization, intervention, consultation, research/evaluation, supervision/teaching, and management/administration [12,34].

The healthcare field in general began to look at models to assess value, the idea of the consumer of services being important to evaluate the services and outcomes of the services, and benchmarking quality for provision of health care. In the United States and Canada, psychology moved from a practice of completing hours and coursework and moved toward a focus on competency for accreditation standards as a benchmark for quality education. Competency-based education, training, and credentialing efforts in professional psychology included graduate, practicum, internship, and postdoctoral levels; licensure; post-licensure certifications; and board certification. General and specialty credentialing efforts in North America and internationally followed suit.

Cultural Competency

In addition, psychology became increasingly aware of cultural and community reactions to diverse groups feeling excluded, stigmatized, and alienated. Over a period of about 40 years, psychology evolved from a profession in which "even the rats were white" and a focus on pathology of differences, to a field in which diversity in all forms (cultural and ethnic differences; gender, racial, and sexual orientation; knowledge about different communities; sensitivity to disabilities, heritage, and individual strengths and weaknesses; and the value of diversity itself) became expectations of competence. Explore how cultural competence affects psychologists' practice in the following examples:

- A White psychologist is working with a group of predominantly African American and Hispanic clients on "anger issues" in a group practice. In talking with colleagues in the group practice, he discovers that his group on "anger management" consists of 75% African American men while the population of clients of the group practice is 85% White. In questioning the colleagues about their criteria for referring clients to the group, they feel that the expression of anger by their African American patients was "more of a problem" than the expression of anger by their White patients. A retrospective review of charts showed that the group on "anger" is capturing only about 15% of eligible clients. White clients are not being referred regardless of whether anger was a presenting problem.

- A psychologist seeks consultation regarding treatment of a gay male couple in family therapy. He indicates to the consultant that he is uncomfortable treating the couple now that they are legally married and are planning to adopt a child.

- A psychologist uses an interpreter to assist with the evaluation of a Spanish-speaking client. The psychologist asks the client, "Are you suicidal?" The interpreter translates, "You aren't suicidal, are you?"

- A psychologist is asked to provide interven-tion strategies to help a group home for developmentally disabled adults keep a male client and a female client from having a sexual relationship because it makes the staff uncomfortable.

Case Study

A psychologist decides to treat a family in therapy. The parents of two minor children decide at some point in treatment to get a divorce. Records are requested for a court hearing regarding custody of the children, and the therapist is asked to testify on behalf of the wife and to separately evaluate the children regarding custody.

There are a number of issues regarding competence in this scenario. The psychologist has been acting as a therapist, and attempting to transition to the role of impartial evaluator in a forensic setting requires expertise above what is routine for a treating therapist. The blurring of roles and boundaries suggests the family may not understand what is appropriate in the situation and how the role of a forensic evaluator in a custody case differs from the role of a treating family therapist. Records of the family may have been kept on each person individually or on the family as a whole, making the release of records, if indicated, problematic. Knowing how to keep records appropriately is an issue of competence. Finally, the therapist is being asked to testify on behalf of the wife in the divorce and custody proceeding. The relationship of the therapist at the start of the treatment clarifies to all parties the areas in which the therapist is competent. To enter into a separate relationship with just the wife will raise issues of boundaries and role clarification and may highlight areas that were not competently addressed at the outset of treatment.

INFORMED CONSENT

Informed consent in psychology has several aspects. The first part is that psychologists know what it is that they are anticipating in providing services and can provide that information clearly to the client. The second part is that the person receiving services is able to understand and make use of the information the psychologist is providing. The third part is that the person receiving the services has the legal ability to consent to the services to be provided. Fourth, the person receiving the services must have the intellectual and psychological capacity to consent to the services being provided. The fifth part is the client's ability to form rational decisions about the information being provided. Lastly, the documentation of the agreement to provide services and to consent to those services being provided is essential.

Informed consent is described as having two goals: to promote individual autonomy and to encourage rational decision making. This presumes that the individual entering into the relationship has done so voluntarily and is capable of understanding what the psychologist is disclosing.

Informed consent can be broken down into the following areas [13]:

- Information: What is disclosed, how, when, and by whom?

- Understanding: What did the client understand about what would happen? How did that understanding develop?

- Competency: Did the client have the cognitive and emotional capacity to understand what was being communicated? Did they actually understand?

- Voluntariness: Is the client free to choose or not? Are they subject to undue influence or coercion? Is someone else responsible for ensuring that the client will decide or is someone else deciding for the client?

- Decision: How are the decisions about treatment being made? What role does the disclosure play?

The 2016 APA Ethics Code documents the need for informed consent in psychology in Standard 3.10 [8]. The following section has been reprinted with permission:

3.10 Informed Consent

(a) When psychologists conduct research or provide assessment, therapy, counseling, or consulting services in person or via electronic transmission or other forms of communication, they obtain the informed consent of the individual or individuals using language that is reasonably understandable to that person or persons except when conducting such activities without consent is mandated by law or governmental regulation or as otherwise provided in this Ethics Code. (See also Standards 8.02, Informed Consent to Research; 9.03, Informed Consent in Assessments; and 10.01, Informed Consent to Therapy.)

(b) For persons who are legally incapable of giving informed consent, psychologists nevertheless (1) provide an appropriate explanation, (2) seek the individual's assent, (3) consider such persons' preferences and best interests, and (4) obtain appropriate permission from a legally authorized person, if such substitute consent is permitted or required by law. When consent by a legally authorized person is not permitted or required by law, psychologists take reasonable steps to protect the individual's rights and welfare.

(c) When psychological services are court ordered or otherwise mandated, psychologists inform the individual of the nature of the anticipated services, including whether the services are court ordered or mandated and any limits of confidentiality, before proceeding.

(d) Psychologists appropriately document written or oral consent, permission, and assent. (See also Standards 8.02, Informed Consent to Research; 9.03, Informed Consent in Assessments; and 10.01, Informed Consent to Therapy.)

As discussed, informed consent means providing information on the nature of the services being provided, the anticipated course of services, any anticipated benefits from the services, any anticipated risks in having the services or not, and alternatives to the proposed course of services being suggested, including what might occur with no treatment. These components are required both legally as well as ethically. The first legally recognized use of the term "informed consent" comes from the Salgo v. Leland Stanford etc. Bd. Trustees, 154 Cal. App. 2d 560 [Civ. No. 17045. First Dist., Div. One. Oct. 22, 1957.] case [14]. In this case Mr. Salgo was not told that an angiogram might result in complications such as paralysis. From this case came the outline of the requirements that an individual be fully informed about the nature of procedures, risks, benefits, and alternatives, and that the understanding be documented in the medical record.

Over time, informed consent has grown to also include agreeing to the policies and procedures of the facility in which the person is being seen. These include policies regarding:

- Scheduling: Frequency of meetings, time frames for scheduling, time frames for changing or cancelling appointments, and issues that would impact scheduling, such as availability of the psychologist due to other obligations

- Cancellation: The method of cancellation or rescheduling of services, charges for missed sessions, emergency notification procedures

- Payment for services: Cost of services, which services are covered, use of third-party payors (such as insurance), when payment is expected, whether credit cards or checks are acceptable, the expected time frames for payment for services, the procedure if an insurance company or other third-party payor declines to pay for services, and fees for other services such as evaluations, court testimony and depositions, reports, record review, and photocopying records to another party

- Record keeping: The manner in which records will be kept, how they are kept, length of record retention, information regarding protected health information, patient rights and access to records, legal access to records by the court or others (i.e., who has access to records besides the psychologist, how is security maintained, how and to whom records may be released), and whether the records will include any audio or video tapes, phone logs, or email correspondence

- Supervision: What information can be discussed with other professionals, including interns and postdoctoral fellows. If the psychologist is providing formal supervision, does the supervisee have an understanding of the exact expectations of the relationship and requirements for hours or completion of the program? Does the supervisee understand the role of the supervisor and has he or she communicated that role to the client? What evaluation methods will be used for the supervision? What is expected in case of a crisis for the client or supervisee?

- Collaboration with others: What will be discussed, which people or organizations have access to protected health information, how collaboration will occur, what roles others will have. Limitations regarding the people or organizations the psychologist is allowed to talk with and what information may be shared should be clarified.

- Rights and responsibilities: What is expected of the client, rights clients have regarding their treatment, what clients have a right to know prior to agreeing to a specific treatment, what clients should expect from the psychologist providing treatment, how treatment will proceed, what clients should do if they are not satisfied with treatment, what regulatory agencies are available to advocate on behalf of a client. Clients should also be advised of the limitations of any rights they are likely to believe they have, such as situations in which they are seen on behalf of the court and information will be provided back to the court.

- Children and adolescents: Consent for treatment, obligations to reveal records to parents or guardians on demand, limitations to confidentiality, obligations to reveal information legally for personal or community safety

- Availability: When, how, and where patients can interact with the psychologist, expectations of privacy and confidentiality, use of insurance or changes in insurance reimbursement, how to make contact in an emergency or between sessions, options available for dealing with emergencies

- Use of insurance or third-party payors: Information regarding Health Insurance Portability and Accountability Act (HIPAA). (Records are transmitted, accessed, and used electronically for providing services, to handle billing, for healthcare operations, and as required by law, and clients should be advised regarding the standardized formatting of information to be transmitted electronically, such as for insurance billing, and the use of reasonable state-of-the-art protective measures for computer security, such as limiting access by use of passwords or encryption, backing up stored information before moving hardware, and maintaining patient privacy.) Also discuss the use of insurance, collection of copayments, the insurance company's request for records and information, and the right to decline to use insurance for services.

Many of the difficulties psychologists have with reference to ethical complaints involve clients not fully understanding the nature of the services, including the policies and procedures of the office, the risks and benefits, and the alternatives available. A simple signature on a form can document what is expected and thought to be understood but is not sufficient for establishing informed consent. Informed consent is not a single process that takes place at the outset of treatment; it is involved in every step of the treatment process and often must be revisited as treatment progresses through different stages. Consider how informed consent may or may not have been attained in the following scenarios:

- Mr. X is contacted by his employer for an evaluation by Dr. J prior to returning to work after an injury. He signs paperwork at Dr. J's office and completes an initial intake form. He did not bring his reading glasses to the appointment, and the office clerk has to show him where to put his signature on the form and read questions to him so he can understand what is required. When Mr. X sees Dr. J, there is no mention from the clerk that his reading glasses are not available or the fact that he was unable to sign forms without assistance. Dr. J simply asks Mr. X if he had any questions prior to the evaluation. Mr. X says, "No." The evaluation is then completed, and the report is provided to Mr. X's employer. Mr. X is upset that information was not kept confidential and that he was not allowed to return to work. He did not understand the purpose of the evaluation or the fact that it was going to be used by his employer in determining whether he could return to work. Dr. J had a form signed by Mr. X that spelled out all of this information. The fact that Mr. X viewed the form as a formality and was not able to read it was not known to Dr. J.

- Dr. S decides that in vivo desensitization is the best form of treatment for Ms. Z's fear of spiders. Ms. Z consents to therapy. When Dr. S actually brings a spider into the office, however, Ms. Z runs from the room sobbing, indicating that she "had no idea" that actual spiders were to be used in her treatment.

- Miss C is 5 years of age and is afraid of anyone wearing a mask or costume. Her parents bring her into treatment for her fearfulness. Dr. D explains to Miss C directly the purpose of treatment and how treatment would progress. Dr. D outlines to Miss C and her parents that the patient will start by drawing masks and throwing them out and that at any part of drawing she can stop or just close her eyes. She would progress to using dolls and putting dolls in masks. Again, she could stop or close her eyes. She would then put dolls in costumes. Eventually, she would be expected to go on a field trip to see people dressed in animal costumes and is expected to do that without being scared or afraid. In addition to her parents understanding what is involved in treatment, Miss C is explained the treatment in detail.

It is possible to abdicate or waive the informed consent process. In these cases, the client must demonstrate an understanding of the right to have information about treatment and be involved in decisions about the treatment process. The client then may specifically indicate that he or she wants the psychologist to make those decisions on the client's behalf. This is often referred to as an "opt-out" procedure and involves research with minimal risk, in which full disclosure will be detrimental; emergency process and potentially life-saving techniques are being studied; or a substitute for the consent process is not readily available and failure to provide treatment would result in harm.

There are also cases in which the person is not competent to make decisions due to being a minor or having been found by the court to be incompetent. In these cases, assent or dissent to treatment will not authorize or constitute a valid refusal, and a substitute for informed consent would be required. This is contrasted with someone who may be psychotic, intoxicated, severely intellectually disabled, or unconscious and is unable to make rational decisions and understand the information that is being presented by the psychologist. When reviewing the following case examples, analyze how issues of incompetence might apply:

- Mr. I is an autistic adult being evaluated for a sheltered workshop program at the request of his parents. He has been recognized as incompetent by the court, and his parents are his legal guardians.

- Ms. P has taken a Minnesota Multiphasic Personality Inventory and wants to review the results. Her psychologist determines that such information may worsen her depression and increase her already present suicidal ideation and withholds the information based on therapeutic privilege.

- Ms. T is unconscious following a suspected overdose when brought to an emergency department for evaluation by a psychologist.

In each of these situations, the decision about treatment will be made by someone other than the patient. Family members or friends, the treating psychologist, a governmental authority, or hospital authority will provide third-party consent.

In general, psychiatric patients who are involuntarily hospitalized must be provided with informed consent to treatment. In California, the law also requires that voluntarily hospitalized patients be told specifically of their right not to be treated without their informed consent [15]. For individuals in California who are developmentally delayed and involuntarily hospitalized, the hospital is required to have a patient advocate available to provide informed consent on behalf of the patient and advocate on his or her behalf.

PRIVACY AND CONFIDENTIALITY

There are distinctions between privacy, confidentiality, and privileged communications. Privacy is an essential part of the professional psychologist's treating relationship with a patient, consultant, or supervisee. What is revealed in the treatment relationship must remain private so the treatment will be effective. The patient, consultant, or supervisee must feel free to readily disclose information to join into the treatment relationship.

Examples of privacy issues include:

- There is little soundproofing between offices, and discussions between a client and therapist can be overheard easily in the next room.

- A psychologist discusses a client on an online ListServ in ways that make the client identifiable.

- A psychologist recognizes a client at a social party, makes eye contact, then immediately leaves, making it obvious there is some relationship between the psychologist and client to others in attendance.

- A client contacts a psychologist on Facebook requesting to be "friends."

Confidentiality concerns information that is gathered by a psychologist. Federal and state laws govern which records must be kept, and the Ethics Code stipulates that psychologists are to keep records [8]. The nature and extent of the records will vary based on the purpose, setting, and context of the psychological services [16]. Records benefit both the client and the psychologist, allowing a delineated treatment plan, notation of services provided, monitoring of treatment, and assistance in legal or ethical proceedings or when transferring care to another provider. Guidelines for record keeping were set forth by the APA and were approved in February 2007. The guidelines expired in 2017. As of that date, users are encouraged to contact the APA Practice Directorate to determine whether the guidelines remain in effect [16]:

- Responsibility for records: Psychologists generally have responsibility for the maintenance and retention of their records.

- Content of records: A psychologist strives to maintain accurate, current, and pertinent records of professional services as appropriate to the circumstances and as may be required by the psychologist's jurisdiction. Records include information such as the nature, delivery, progress, and results of psychological services and related fees.

- Confidentiality of records: The psychologist takes reasonable steps to establish and maintain the confidentiality of information arising from service delivery.

- Disclosure of record-keeping procedures: When appropriate, psychologists inform clients of the nature and extent of record-keeping procedures (including a statement on the limitations of confidentiality of the records according to Ethics Code Standard 4.02).

- Maintenance of records: The psychologist strives to organize and maintain records to ensure their accuracy and to facilitate their use by the psychologist and others with legitimate access to them.

- Security: The psychologist takes appropriate steps to protect records from unauthorized access, damage, and destruction.

- Retention of records: The psychologist strives to be aware of applicable laws and regulations and to retain records for the period required by legal, regulatory, institutional, and ethical requirements.

- Preserving the context of records: The psychologist strives to be attentive to the situational context in which records are created and how that context may influence the content of those records.

- Electronic records: Electronic records, like paper records, should be created and maintained in a way that is designed to protect their security, integrity, confidentiality, and appropriate access, as well as their compliance with applicable legal and ethical requirements.

- Record keeping in organizational settings: Psychologists working in organizational settings (e.g., hospitals, schools, community agencies, prisons) strive to follow the record-keeping policies and procedures of the organization as well as the APA Ethics Code.

- Multiple-client records: The psychologist carefully considers documentation procedures when conducting couple, family, or group therapy in order to respect the privacy and confidentiality of all parties.

- Financial records: The psychologist strives to ensure accuracy of financial records.

- Disposition of records: The psychologist plans for transfer of records to ensure continuity of treatment and appropriate access to records when the psychologist is no longer in direct control, and in planning for record disposal, the psychologist endeavors to employ methods that preserve confidentiality and prevent recovery.

Confidentiality is a concern in each of the following cases:

- A client refers a friend or family member for treatment.

- Information regarding clinical treatment of a client is overheard.

- Patient records are stolen from a parked car.

- A family member requests information regarding a client's issues.

- A release of records is requested for one member of a couple being seen jointly, and the records contain information about the other member as well.

Privileged communication is defined as the legal right of an individual to keep confidential disclosures from any judicial proceeding or court of law. The legal definition may vary according to state statutes and laws. The California Evidence Code section 1014 notes [17]:

The patient, whether or not a party (to a legal proceeding), has a privilege to refuse to disclose, and to prevent from disclosing, a confidential communication between patient and psychotherapist if the privilege is claimed by:

(a) The holder of the privilege (e.g., the client).

(b) A person who is authorized to claim the privilege by the holder of the privilege (e.g., parent or legal guardian).

(c) The person who was the psychotherapist at the time of the confidential communication, but the person may not claim the privilege if there is no holder of the privilege in existence or if he or she is otherwise instructed by a person authorized to permit disclosure (e.g., the client, parent, or legal guardian).

Issues of privilege include:

- A client puts his or her mental health at issue in a workers' compensation case.

- A client is mandated for evaluation by federal or state law.

- A child seeks treatment independently from his or her family.

- A victim of crime seeks treatment.

- A psychologist seeks to limit information to a government agency regarding treatment following receipt of a subpoena.

- A psychologist seeks to obtain evaluation records of a patient undergoing a legally mandated evaluation and has authorization from the patient but not from the holder of privilege (the legally mandated referral agency).

The APA Ethics Code addresses standards of privacy and confidentiality in Standard 4: Privacy and Confidentiality. This standard is reprinted with permission in the following sections [8]:

4.01 Maintaining Confidentiality

Psychologists have a primary obligation and take reasonable precautions to protect confidential information obtained through or stored in any medium, recognizing that the extent and limits of confidentiality may be regulated by law or established by institutional rules or professional or scientific relationship. (See also Standard 2.05, Delegation of Work to Others.)

4.02 Discussing the Limits of Confidentiality

(a) Psychologists discuss with persons (including, to the extent feasible, persons who are legally incapable of giving informed consent and their legal representatives) and organizations with whom they establish a scientific or professional relationship (1) the relevant limits of confidentiality and (2) the foreseeable uses of the information generated through their psychological activities. (See also Standard 3.10, Informed Consent.)

(b) Unless it is not feasible or is contraindicated, the discussion of confidentiality occurs at the outset of the relationship and thereafter as new circumstances may warrant.

(c) Psychologists who offer services, products, or information via electronic transmission inform clients/patients of the risks to privacy and limits of confidentiality.

4.03 Recording

Before recording the voices or images of individuals to whom they provide services, psychologists obtain permission from all such persons or their legal representatives. (See also Standards 8.03, Informed Consent for Recording Voices and Images in Research; 8.05, Dispensing with Informed Consent for Research; and 8.07, Deception in Research.)

4.04 Minimizing Intrusions on Privacy

(a) Psychologists include in written and oral reports and consultations, only information germane to the purpose for which the communication is made.

(b) Psychologists discuss confidential information obtained in their work only for appropriate scientific or professional purposes and only with persons clearly concerned with such matters.

4.05 Disclosures

(a) Psychologists may disclose confidential information with the appropriate consent of the organizational client, the individual client/patient, or another legally authorized person on behalf of the client/patient unless prohibited by law.

(b) Psychologists disclose confidential information without the consent of the individual only as mandated by law, or where permitted by law for a valid purpose such as to (1) provide needed professional services; (2) obtain appropriate professional consultations; (3) protect the client/patient, psychologist, or others from harm; or (4) obtain payment for services from a client/patient, in which instance disclosure is limited to the minimum that is necessary to achieve the purpose. (See also Standard 6.04e, Fees and Financial Arrangements.)

4.06 Consultations

When consulting with colleagues, (1) psychologists do not disclose confidential information that reasonably could lead to the identification of a client/patient, research participant, or other person or organization with whom they have a confidential relationship unless they have obtained the prior consent of the person or organization or the disclosure cannot be avoided, and (2) they disclose information only to the extent necessary to achieve the purposes of the consultation. (See also Standard 4.01, Maintaining Confidentiality.)

4.07 Use of Confidential Information for Didactic or Other Purposes

Psychologists do not disclose in their writings, lectures, or other public media, confidential, personally identifiable information concerning their clients/patients, students, research participants, organizational clients, or other recipients of their services that they obtained during the course of their work, unless (1) they take reasonable steps to disguise the person or organization, (2) the person or organization has consented in writing, or (3) there is legal authorization for doing so.

Exceptions to Confidentiality

There are basic exceptions to confidentiality based on the ideas of doing no harm and providing a benevolent relationship to the community in which a psychologist works. Breaches of confidentiality can produce feelings of betrayal and loss of trust in the therapeutic relationship, and such breaches are made only when it is necessary to do so. One exception to confidentiality is to ensure the safety of the person in treatment or any others. If a person divulges intent to harm or kill him- or herself, then it is the duty of the therapist to assist the patient in maintaining his or her safety. This may include breaching confidentiality to law enforcement, family members, hospital personnel, or treating physicians to ensure that no harm comes to the patient. The APA Ethics Code notes, "Psychologists [should] take reasonable steps to avoid harming their clients/patients, students, supervisees, research participants, organizational clients, and others with whom they work, and to minimize harm where it is foreseeable and unavoidable" [8].

Suicide and Self-Harm

Out of the obligation of psychologists to minimize harm where it is foreseeable and unavoidable comes a duty to assist with civil commitment and involuntary hospitalization [18]. Suicide is a serious public health problem that affects people of all ages. For Americans, suicide is the 11th leading cause of death. It resulted in 48,183 lives lost in 2021 [19]. The top three methods used in suicides are firearm, suffocation, and poisoning [19].

More people survive suicide attempts than actually die. In 2020, 187,000 people received medical care for self-inflicted injuries at emergency departments across the United States [19]. Complicating evaluation and treatment is the issue of attempting to predict how likely persons expressing suicidal ideation are to actually harm themselves. Clinical assessment has relied almost exclusively on an individual's self-report [20]. According to the Harvard Medical School Guide to Suicide Assessment and Intervention, "There is no psychological test, clinical technique, or biological marker sufficiently sensitive and specific to support accurate short-term prediction of suicide in an individual person" [21]. Risk management strategies are used to lessen the risk of suicide and strengthen the ethical and legal documentation of that evaluation. Several guidelines have been established for psychologists working with suicidal patients [3]:

- Be familiar with the current literature regarding risk factors, epidemiology, and management of the suicidal patient. It is equally important for clinicians to be knowledgeable of the law of the jurisdiction and current developments in the field.

- Take a complete patient history that includes indicators of suicide risk based upon diagnostic criteria and known risk factors for suicide. Throughout treatment, when risk is elevated the clinician should ask specific, forensically significant questions about depression and suicidal feelings and thoughts.

- Obtain releases to consult with past therapists and secure the patient's medical and mental health records.

- Use the Diagnostic and Statistical Manual of Mental Disorders diagnostic criteria to accurately diagnose patients and guide treatment.

- Recognize limitations (e.g., time restraints, appointment availability), understand technical proficiencies (training, education, and experience), and be aware of emotional tolerance levels when working with suicidal patients.

- Good record keeping is paramount. The model risk-benefit progress note should include: (a) an assessment of suicide risk; (b) the information alerting the clinician to that risk; (c) which high-risk factors were present in that situation and in the patient's background; (d) what low-risk factors were present; (e) what information, namely the patient's history and the clinician's professional judgment, led to actions taken and rejected.

- Routinely seek consultations from professional colleagues who have expertise in treating suicidal patients.

- Consult with legal counsel to determine if the insurance carrier needs to be notified of a serious suicide attempt or completed suicide.

Harm of Others

The same types of issues arise with concerns that a patient will harm others. Following legal landmark cases (e.g., 1976 California Supreme Court decision on Tarasoff v. Regents of the University of California; 1983 Hedlund v. Superior Court; and 2004 Ewing v. Goldstein), states have enacted laws to require psychologists to warn those at risk and persons in close relationship to the object of the person's threat and to include information from family members, not just the patient directly. In the Ewing case, the APA dissented from the ruling, stating that "requiring a therapist to warn intended victims when notified by a family member would have a 'chilling effect' on patients" [1]. The facts of the case document some information that is often omitted from discussion regarding the ethical issues involved in the case. The following is from Ewing v. Goldstein, 15 Cal. Rptr. 3d 864 - Cal: Court of Appeals, 2nd Appellate Dist., 8th Div. 2004 [22]:

Respondent Dr. David Goldstein is a marriage and family therapist. Between 1997 and June 2001, Goldstein provided personal therapeutic services to Geno Colello, a former member of the Los Angeles Police Department. Goldstein treated Colello for work-related emotional problems and problems concerning his former girlfriend, Diana Williams.

Beginning in early 2001, Colello became increasingly depressed and despondent over the termination of his relationship with Williams. Colello's feelings of depression significantly increased in mid-June, after learning of her romantic involvement with another man.

Goldstein last met with Colello at his office on June 19, 2001. Goldstein spoke with Colello on the telephone on June 20 and again on June 21, when he asked Colello if he was feeling suicidal. Colello "was not blatantly suicidal, but did admit to thinking about it." Goldstein asked Colello to consider checking himself into a psychiatric hospital and also sought and obtained Colello's permission to speak with his father, Victor Colello.

Colello had dinner with his parents on June 21. He was extremely depressed. Colello talked to his father about how he had lost the desire to live and about his building resentment toward Williams' new boyfriend. He told his father "he couldn't handle the fact that [Williams] was going with someone else," and said he "was considering causing harm to the young man that [Williams] was seeing." Colello's father contacted Goldstein and told him what Colello had said. Goldstein urged Colello's father to take Colello to Northridge Hospital Medical Center, where Goldstein arranged for him to receive psychiatric care. Colello was voluntarily admitted the evening of June 21, under the care of Dr. Gary Levinson, a staff psychiatrist.

On June 22, Levinson told Colello's father he planned to discharge Colello. Concerned that his son was being released prematurely, Colello's father called Goldstein. Goldstein contacted Levinson, with whom he had not yet spoken and explained why Colello should remain hospitalized. Levinson told Goldstein that Colello was not suicidal and would be discharged. Goldstein urged Levinson to re-evaluate Colello and keep him hospitalized through the weekend. He did not do so.

Colello was discharged on June 22. Goldstein had no further contact with his patient. On June 23, Colello murdered Williams' new boyfriend, Keith Ewing, and then committed suicide.

Keith's parents, Cal and Janet Ewing, sued Goldstein for wrongful death based on professional negligence. The Ewings alleged Colello posed a foreseeable danger to their son and had directly or indirectly through third persons communicated to Goldstein his intention to kill or cause serious physical harm to him. They alleged Goldstein failed to discharge his duty to warn their son or a law enforcement agency of the risk of harm his patient posed to their son's safety.

What is often omitted in discussions about this case is the fact that Geno Colello was a police officer and had access to weapons and substantial knowledge and training in using them. Complicating the clinical treatment decision making was the fact that June 22, when Geno Colello was released from the hospital, was a Friday and Geno Colello was not scheduled to be seen by Dr. Goldstein until the next week. Dr. Goldstein appropriately questioned the validity of Dr. Levinson's assessment in light of contradictory information from the family but failed to do anything to make his own assessment of the patient and failed to notify law enforcement or the potential victim or family members of the potential threat. Had Dr. Goldstein gone to the hospital and independently evaluated Geno Colello and determined he was not a threat, then the Ewing family would not have reasonably been able to assert professional negligence.

The risks for notification of the victim of potential harm are not unsubstantial. In one case in which a patient made the assertion that he "could get a gun in exchange for a couple of tacos" and shoot his former employer, the patient was arrested by the police department after the former employer called them. While charges in the case were eventually dropped, the patient faced some time in jail as well as legal expenses [23]. In a similar case in Louisiana, a patient was arrested and charged with extortion after his threats were conveyed to the workers' compensation carrier for his employer [24].

When a patient reveals he or she has harmed a child or an elder, there are state laws that may require the notification of the police or some other legal authority [25]. The same may be true of a dependent adult [26]. If a child indicates he or she is a victim of a crime, the psychologist is required under child abuse laws to report the abuse [25].

Other Exceptions

Until November 1999, there was no patient-psychotherapist confidentiality for psychologists involved in treating or evaluating military personnel. There is now limited confidentiality (Appendix) [27]. Psychologists are also allowed to breach privacy when a patient seeks psychological services to enable him- or herself to commit a crime or avoid detection for having committed a crime[1].

Under some circumstances, the holder of privilege to release information is not the patient. This is true when the court has ordered an evaluation and the psychologist is court-appointed, when there are legal proceedings to establish sanity or competency, or when the patient has put his or her mental state at issue in a legal proceeding, such as a malpractice claim, a personal injury claim, or a claim for disability benefits due to a mental disorder. Confidentiality is also voided in cases when a patient sues a therapist for breach of duty or a therapist sues a patient for inappropriate behavior.

Patients are able to allow the release of their records by signing an authorization. The authorization must comply with state law, if any applies, and with any federal regulations, such as HIPAA. Two exceptions are if a patient requests to view his or her own clinical record and the therapist believes that such a release may harm the patient, or if a parent or guardian wishes to view the clinical record of his or her child and the psychologist believes that releasing the records would have a detrimental effect on treatment, the safety of the child, or the child's well-being [28]. When a patient dies, a psychologist may release records concerning the conveyance of a will or deed, but clinical records generally remain confidential even after the death of a patient.

Technology

The use of technology in psychotherapy impacts confidentiality, privacy, privilege, and even how therapy is conducted. It is now common for therapists to have websites, and the use of search engines enables patients and therapists alike to obtain information that previously was not generally available. Some psychologists have embraced the use of technology, setting up telehealth services and offering treatment via video-conferencing, e-mail, and cell phone, while others have incorporated policy statements on the use of Google, Facebook, and Twitter into their practices [29,30]. While the APA Ethics Code is not continually revised to reflect the rapid advances in technology, supplementary publications (e.g., the Guidelines for the Optimal Use of Social Media in Professional Psychological Practice and the Guidelines for the Practice of Telepsychology) are informed by the Ethics Code and legal regulatory requirements and are available to assist providers in maintaining compliance with HIPAA laws [30,32,35]. While point-to-point contacts with computers may be secure, remote access and the use of video conferencing (e.g., Skype) and other Internet-based phone services or the utilization of cloud computing, email, and social networking sites may limit privacy and confidentiality. In all of these instances, patients must be advised that others may have access to their information. Well-understood protocols for all individuals using technological systems (e.g., psychologists, billing agencies, patients, support staff) should be in place to limit the risk of others obtaining data they are not entitled to. The use of laptop and tablet computers increases the risk of data being stolen or lost; password encryption is required. Up-to-date virus protection is also required to limit dissemination of information or being immobilized. Clients should be informed of the risks of the use of technology prior to their use in therapy [30,32,35].

AVOIDING HARM AND EXPLOITATION

Ethics codes for psychologists have always been concerned with preventing the infliction of harm on others. Principal A of the APA Ethics Code deals with beneficence and nonmaleficence [8]:

Psychologists strive to benefit those with whom they work and take care to do no harm. In their professional actions, psychologists seek to safeguard the welfare and rights of those with whom they interact professionally and other affected persons, and the welfare of animal subjects of research. When conflicts occur among psychologists' obligations or concerns, they attempt to resolve these conflicts in a responsible fashion that avoids or minimizes harm. Because psychologists' scientific and professional judgments and actions may affect the lives of others, they are alert to and guard against personal, financial, social, organizational, or political factors that might lead to misuse of their influence. Psychologists strive to be aware of the possible effect of their own physical and mental health on their ability to help those with whom they work.

Harm may or may not be intentional; it may result from incompetence or lack of awareness. However, exploitation is more deliberate and consists of using someone unfairly or benefiting unjustly from someone. Some harmful relationships may not be exploitative, while other relationships are both harmful and exploitative. Incompetence that results in harm has been addressed earlier in this course. Harm from a lack of awareness may arise when the psychologist has issues that impact his or her mental or physical well-being, a lack of insight into his or her own perceptions and biases, and/or a lack of understanding of the foreseeable consequences of a course of action. Harmful and exploitative relationships generally involve boundary violations and role-confusion, such as sexual involvement with a patient, research subject, supervisee, or student. The involvement of third parties as payors, grant funders, or other types of relationships that include remuneration may create a conflict of interest situation. Conflicts of interest may also arise when the psychologist is acting in multiple roles, such as in providing an objective assessment in a forensic case as well as being a patient advocate in treatment.

5. ETHICAL DECISION MAKING

In many situations, psychologists need a framework for determining the most ethical course of action. The theoretical orientation of the psychologist may provide some guidance, such as in how much to disclose about one's personal life or whether or not nonsexual touch is permitted. For others, religious views dictate overriding concepts of morality and values and guide ethical decision making. Models have been proposed to assist with ethical decision making in forensic cases, general ethical decisions, and health care [33,36]. Nagy documents seven different models for ethical decision making [1,37,38,39,40,41,42,43,44]:

- Worst case scenarios

- Eight-step model

- 10-step process

- Nine questions for multiple role relationships

- Five-step model

- Three-factor model

- Four-factor model

Other possible frameworks include an 18-step model and the formulation of ethical issues from a feminist perspective [45,46]. Consultation with colleagues and/or legal counsel can assist a psychologist in formulating a decision when faced with an ethical dilemma.

6. COMPLAINTS AND CHARGES

When psychologists violate ethical standards or state or federal laws, people who believe they were harmed can file a complaint with the state licensing authority or can institute a lawsuit against the psychologist. If the psychologist is a member of the APA, a grievance can be filed through the APA Ethics Office. The psychologist has the option to withdraw membership when contacted to begin the preliminary investigation. The process of investigation is lengthy and can take more than a year. The psychologist may seek legal advice from an attorney in responding to the investigation. The Ethics Office ultimately will make a decision whether or not to impose sanctions on the psychologist. These sanctions can range from:

- Reprimand: There is a violation, but no harm came to an individual or to the profession of psychology.

- Censure: There is harm to someone, but it is not substantial.

- Expulsion: There are egregious acts resulting in harm to another or to the profession.

- Stipulated resignation: Serious violations have occurred whereby the psychologist is allowed to resign but may reapply when they comply with certain stipulations or directives. Because the APA is not a licensing authority, even if one resigns or is expelled, he or she is still allowed to practice unless the state licensing authority chooses to investigate and decides to suspend or revoke the license.

The APA Ethics Office can also issue directives in addition to these sanctions. These include:

- Cease and desist order: Requires the psychologist to stop the unethical conduct

- Corrective actions: Steps to ensure that the unethical conduct will not recur, including supervision, additional education, treatment, or probation and monitoring to ensure compliance

The state licensing board is part of a regulating agency designed to protect consumers. Complaints are reviewed by a state Ethics Committee. States vary in types of disciplinary actions they may take, and the procedures differ from those of the APA. In California, complaints are reviewed through an administrative law process. The process starts when a member of the public files a complaint. At that particular stage, the professional receives a Letter of Inquiry of a Complaint requiring a response in a very short period of time. If the case is not resolved at this level, the matter may lose its confidentiality and the licensing board may file an accusation, which is a public document somewhat like an indictment. There are very precise procedures following an accusation that the attorney must know in order to properly defend the client. Cases may go to trial before an administrative law judge following a set of rules called the Administrative Procedure Act, which is part of California Government Code Section 11340 [31]. Professionals facing a trial may call witnesses, cross-examine every witness called by the licensing board, call experts, and offer a variety of types of evidence. In trial, there tends to be relaxed rules of evidence, such as allowing hearsay as evidence in proceedings against a professional. After the trial, the judge issues a decision that goes back to the licensing board for adoption or nonadoption. States can issue a variety of penalties, including a letter of warning, probation, suspension, and revocation of licensure.

Psychologists can also face civil lawsuits and criminal charges for serious issues. Psychologists usually notify their malpractice insurance provider when faced with such charges and are assigned an attorney. The legal process is different than in administrative law and more formal rules of evidence and a higher burden of proof apply.

By understanding the APA Ethics Code and laws governing the practice of psychology, psychologists can reduce the likelihood of receiving an ethical complaint.

7. CONCLUSION

Ethical theory is complicated, and its application is challenging. Ethical decision making tackles many pressing issues facing psychologists. In order to chart a problem-solving course, all psychologists need specific tools to assist in this endeavor.

Familiarity with and adherence to the APA Ethics Code can offer a degree of protection from the various pitfalls of practicing psychology in contemporary American society, such as administrative sanctions and malpractice suits. Following federal, state, and local laws, along with any/all ethical codes or rules where practicing, offers further protection from legal or administrative action; however, ethical principles are primarily intended to benefit the client. It is the goal of ethics to instill clients and the public with trust in psychologists and a sense of autonomy while ensuring client safety.

Psychologists should update skills in law and ethics routinely. The psychologist with a good understanding of ethics is equipped to deal with questions regarding care plans and, when confronted with difficult choices or ethical dilemmas, is capable of consistently making ethically sound decisions and justifying those decisions. Furthermore, discussion of newer ethical issues advances the practice and scope of psychology.

8. APPENDIX

WHITE HOUSE, Washington, D.C.—Sec. 2. Part III of the Manual for Courts-Martial, United States, Military Commission Rules of Evidence, Rule 513. Psychotherapist-patient privilege [27].

1. General Rule. A patient has a privilege to refuse to disclose and to prevent any other person from disclosing a confidential communication made between the patient and a psychotherapist or an assistant to the psychotherapist, in a case arising under the Uniform Code of Military Justice, if such communication was made for the purpose of facilitating diagnosis or treatment of the patient's mental or emotional condition.

2. Definitions. As used in this rule of evidence:

1. A "patient" is a person who consults with or is examined or interviewed by a psychotherapist for purposes of advice, diagnosis, or treatment of a mental or emotional condition.

2. A "psychotherapist" is a psychiatrist, clinical psychologist, clinical social worker, or other mental health professional who is licensed in any State, territory, possession, the District of Columbia, or Puerto Rico to perform professional services as such, or who holds credentials to provide such services from any military healthcare facility, or is a person reasonably believed by the patient to have such license or credentials.

3. An "assistant to a psychotherapist" is a person directed by or assigned to assist a psychotherapist in providing professional services, or is reasonably believed by the patient to be such.

4. A communication is "confidential" if not intended to be disclosed to third persons other than those to whom disclosure is in furtherance of the rendition of professional services to the patient or those reasonably necessary for such transmission of the communication.

5. "Evidence of a patient's records or communications" is testimony of a psychotherapist, or assistant to the same, or patient records that pertain to communications by a patient to a psychotherapist, or assistant to the same, for the purposes of diagnosis or treatment of the patient's mental or emotional condition.

3. Who May Claim the Privilege. The privilege may be claimed by the patient or the guardian or conservator of the patient. A person who may claim the privilege may authorize trial counsel, defense counsel, or any counsel representing the patient to claim the privilege on his or her behalf. The psychotherapist or assistant to the psychotherapist who received the communication may claim the privilege on behalf of the patient. The authority of such a psychotherapist, assistant, guardian, or conservator to so assert the privilege is presumed in the absence of evidence to the contrary.

4. Exceptions. There is no privilege under this rule:

1. when the patient is dead;

2. when the communication is evidence of child abuse or neglect, or in a proceeding in which one spouse is charged with a crime against a child of either spouse;

3. when federal law, state law, or service regulation imposes a duty to report information contained in a communication;

4. when a psychotherapist or assistant to a psychotherapist believes that a patient's mental or emotional condition makes the patient a danger to any person, including the patient;

5. if the communication clearly contemplated the future commission of a fraud or crime or if the services of the psychotherapist are sought or obtained to enable or aid anyone to commit or plan to commit what the patient knew or reasonably should have known to be a crime or fraud;

6. when necessary to ensure the safety and security of military personnel, military dependents, military property, classified information, or the accomplishment of a military mission; or

7. when an accused offers statements or other evidence concerning his mental condition in defense, extenuation, or mitigation, under circumstances not covered by R.C.M. 706 or Mil. R. Evid. 302. In such situations, the military judge may, upon motion, order disclosure of any statement made by the accused to a psychotherapist as may be necessary in the interests of justice.

5. Procedure to Determine Admissibility of Patient Records or Communications.

1. In any case in which the production or admission of records or communications of a patient other than the accused is a matter in dispute, a party may seek an interlocutory ruling by the military judge. In order to obtain such a ruling, the party must:

1. file a written motion at least 5 days prior to entry of pleas specifically describing the evidence and stating the purpose for which it is sought or offered, or objected to, unless the military judge, for good cause shown, requires a different time for filing or permits filing during trial; and

2. serve the motion on the opposing party, the military judge and, if practical, notify the patient or the patient's guardian, conservator, or representative that the motion has been filed and that the patient has an opportunity to be heard as set forth in subparagraph (e)(2).

2. Before ordering the production or admission of evidence of a patient's records or communication, the military judge shall conduct a hearing, which shall be closed. At the hearing, the parties may call witnesses, including the patient, and offer other relevant evidence. The patient shall be afforded a reasonable opportunity to attend the hearing and be heard. However, the hearing may not be unduly delayed for this purpose. The right to be heard under this rule includes the right to be heard through counsel, including Special Victims' Counsel under section 1044e of title 10, United States Code. In a case before a court-martial composed of a military judge and members, the military judge must conduct the hearing outside the presence of the members.

3. The military judge may examine the evidence or a proffer thereof in camera, if such examination is necessary to rule on the production or admissibility of protected records or communications. Prior to conducting an in-camera review, the military judge must find by a preponderance of the evidence that the moving party showed:

1. a specific, credible factual basis demonstrating a reasonable likelihood that the records or communications would contain or lead to the discovery of evidence admissible under an exception to the privilege;

2. that the requested information meets one of the enumerated exceptions under subdivision (d) of this rule;

3. that the information sought is not merely cumulative of other information available; and

4. that the party made reasonable efforts to obtain the same or substantially similar information through non-privileged sources.

4. Any production or disclosure permitted by the military judge under this rule must be narrowly tailored to only the specific records or communications, or portions of such records or communications, that meet the requirements for one of the enumerated exceptions to the privilege under subdivision (d) of this Rule and are included in the stated purpose for which the records or communications are sought under subdivision (e)(1)(A) of this Rule.

5. To prevent unnecessary disclosure of evidence of a patient's records or communications, the military judge may issue protective orders or may admit only portions of the evidence.

6. The motion, related papers, and the record of the hearing must be sealed in accordance with R.C.M. 701(g)(2) or 1113 and must remain under seal unless the military judge, the Judge Advocate General, or an appellate court orders otherwise.

Works Cited

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2. Corey G, Corey MS, Corey C. Issues and Ethics in the Helping Professions. 10th ed. Independence, KY: Cengage Learning; 2018.

3. Gladding ST. Counseling: A Comprehensive Profession. 8th ed. Upper Saddle River, NJ: Merrill; 2017.

4. Fernberger SW. The American Psychological Association 1892–1942. Psychol Rev. 1943;50(3):33-60.

5. American Psychological Association. APA History and Archives. Available at https://www.apa.org/about/apa/archives. Last accessed May 25, 2023.

6. Fisher CB. Decoding the Ethics Code: A Practical Guide for Psychologists. 4th ed. Thousand Oaks, CA: Sage Publications; 2016.

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8. American Psychological Association. Ethical Principles of Psychologists and Code of Conduct: Including 2010 and 2016 Amendments. Available at https://www.apa.org/ethics/code/index. Last accessed May 25, 2023.

9. American Psychological Association. Ethical Principles of Psychologists and Code of Conduct. Available at https://www.apa.org/ethics/code/ethics-code-2017.pdf. Last accessed May 25, 2023.

10. Epstein RM, Hundert EM. Defining and assessing professional competence. JAMA. 2002;287(2):226-235.

11. Falendar CA, Shafranske EP. Competence in competency-based supervision practice: construct and application. Prof Psychol Res Pr. 2007;38(3):232-240.

12. American Psychological Association. Assessment of Competency Benchmarks Work Group: A Developmental Model for the Defining and Measuring of Competence in Professional Psychology. Available at https://www.ccptp.org/assets/2011-Conference-Resources/benchmark_competencies_document_-_feb_2007.pdf. Last accessed May 25, 2023.

13. Lidz CW, Meisel A, Zerubavel E, Carter M, Sestak RM, Roth LH. Informed Consent: A Study of Decisionmaking in Psychiatry. New York, NY: Guilford Press; 1984.

14. Justia US Law. Salgo v. Leland Stanford etc. Bd. Trustees. Available at https://law.justia.com/cases/california/court-of-appeal/2d/154/560.html. Last accessed May 25, 2023.

15. California Department of Healthcare Services. Rights for Individuals in Mental Healthcare Facilities. Available at https://www.dhcs.ca.gov/services/Documents/DHCS_Handbook_English.pdf. Last accessed May 25, 2023.

16. American Psychological Association. Record Keeping Guidelines. Available at https://www.apa.org/practice/guidelines/record-keeping. Last accessed May 25, 2023.

17. California Legislative Information. Evidence Code Section 1014. Available at http://leginfo.legislature.ca.gov/faces/codes_displaySection.xhtml?sectionNum=1014.&lawCode=EVID. Last accessed May 25, 2023.

18. Parry J, Gilliam FP. Handbook on Mental Disability Law. Washington, DC: American Bar Association; 2002.

19. Centers for Disease Control and Prevention. FastStats: Suicide and Self-Harm Injury. Available at https://www.cdc.gov/nchs/fastats/suicide.htm. Last accessed May 25, 2023.

20. Nock MK, Banaji MR. Prediction of suicide ideation and attempts among adolescents using a brief performance-based test. J Consult Clin Psychol. 2007;75(5):707-715.

21. Jacobs D, Brewer M, Klein-Benheim M. Suicide assessment: an overview and recommended protocol. In: Jacobs DG (ed). Harvard Medical School Guide to Suicide Assessment and Intervention. San Francisco, CA: Jossey-Bass; 1999: 3-39.

22. Ewing v. Goldstein (2004), Cal.App.4th. Available at https://caselaw.findlaw.com/ca-court-of-appeal/1010184.html. Last accessed May 25, 2023.

23. Applebaum GT. Racism, workers' compensation evaluations and Tarasoff laws. Am J Forensic Psychol. 1993;11(2):61-67.

24. United States of America, Plaintiff-Appellant, v. John C. Auster, Defendant-Appellee, United States Court of Appeals for the Fifth Circuit. Available at http://www.ca5.uscourts.gov/opinions/pub/07/07-30084-CV0.wpd.pdf. Last accessed May 25, 2023.

25. California Penal Code Section 11164-11174.3. Available at https://leginfo.legislature.ca.gov/faces/codes_displayText.xhtml?lawCode=PEN&division=&title=1.&part=4.&chapter=2.&article=2.5. Last accessed May 25, 2023.

26. California Welfare and Institutions Code Section 15630. Available at https://leginfo.legislature.ca.gov/faces/codes_displayText.xhtml?lawCode=WIC&division=9.&title=&part=3.&chapter=11.&article=3. Last accessed May 25, 2023.

27. Joint Service Committee on Military Justice. Manual for Courts-Martial, United States: 2019 Edition. Available at https://jsc.defense.gov/Portals/99/Documents/2019%20MCM%20(Final)%20(20190108).pdf. Last accessed May 25, 2023.

28. California Health and Safety Code Section 123115. Available at http://leginfo.legislature.ca.gov/faces/codes_displaySection.xhtml?lawCode=HSC&sectionNum=123115. Last accessed May 25, 2023.

29. Gavazzi J. Social Media and Ethics: Psychologists Self-Reflect When Engaging Through Technology. Available at https://www.ethicalpsychology.com/2016/04/social-media-ethics-psychologists-self.html. Last accessed May 25, 2023.

30. American Psychological Association. APA Guidelines for the Optimal Use of Social Media in Professional Psychological Practice. Available at https://www.apa.org/about/policy/guidelines-optimal-use-social-media.pdf. Last accessed May 25, 2023.

31. California State Legislature. Government Code Section 11340-11342.4. Available at https://leginfo.legislature.ca.gov/faces/codes_displayText.xhtml?lawCode=GOV&division=3.&title=2.&part=1.&chapter=3.5.&article=1. Last accessed May 25, 2023.

32. American Psychological Association. Guidelines for the Practice of Telepsychology. Available at https://www.apa.org/practice/guidelines/telepsychology. Last accessed May 25, 2023.

33. Bush SS, Connell MA, Denney RL. Ethical Practice in Forensic Psychology: A Guide for Mental Health Professionals. 2nd ed. Washington, DC: American Psychological Association; 2019.

34. Fouad NA, Grus CL, Hatcher RL, et al. Competency Benchmarks: A Model for Understanding and Measuring Competence in Professional Psychology Across Training Levels. Available at https://drjeffchang.webs.com/benchmarks.pdf. Last accessed May 25, 2023.

35. American Psychological Association. The HIPAA Final Rule: What You Need to Do Now. Available at https://www.apaservices.org/practice/update/2013/07-25/hipaa-final-rule.pdf. Last accessed May 25, 2023.

36. Hanson SL, Kerkhoff TR, Bush SS. Health Care Ethics for Psychologists: A Casebook. Washington, DC: American Psychological Association; 2005.

37. Sonne JL. Nonsexual Multiple Relationships: A Practical Decision-Making Model for Clinicians. Available at https://kspope.com/site/multiple-relationships.php. Last accessed May 25, 2023.

38. Bransford JD, Stein BS. The Ideal Problem Solver: A Guide to Improved Thinking, Learning, and Creativity. 2nd ed. New York, NY: Worth Publishers; 1993.

39. Gottlieb MC. Avoiding exploitative dual relationships: a decision-making model. Psychotherapy (Chic). 1993;30(1):41-48.

40. Härtel CEJ, Härtel GF. SHAPE-assisted intuitive decision making and problem solving: information-processing-based training for conditions of cognitive busyness. Group Dynamics. 1997;1(3):187-199.

41. Bell T. Death Threats, Interfering Daughters and Other Worst-Case Scenarios. Presented at the Cincinnati Children's Hospital Medical Center Conference on Medical Interpreting. August 21, 2010. Available at https://www.slideshare.net/terenabell/cincy-pres. Last accessed May 25, 2023.

42. Keith-Spiegel P, Koocher GP. Ethics in Psychology: Professional Standards and Cases. 2nd ed. New York, NY: Random House; 1998.

43. Canadian Psychological Association. Canadian Code of Ethics for Psychologists. Available at https://cpa.ca/aboutcpa/committees/ethics/codeofethics. Last accessed May 25, 2023.

44. Younggren JN, Gottlieb MC. Managing risk when contemplating multiple relationships. Prof Psychol Res Pr. 2004;35(3):255-260.

45. Brabeck MM (ed). Practicing Feminist Ethics in Psychology. Washington, DC: American Psychological Association; 2000.

46. Pope K. Ethical Standards and Practice Guidelines for Assessment, Therapy, Counseling, and Forensic Practice. Available at https://www.kspope.com/ethcodes/index.php. Last accessed May 25, 2023.

66474 • Obsessive-Compulsive Disorder

John J. Whyte, MD, MPH

www.netce.com

Copyright © 2024 NetCE, All rights reserved.

Obsessive-compulsive disorder (OCD) is a debilitating psychiatric illness affecting approximately 2.5% of the population. Characterized by recurrent thoughts or worries (obsessions) and a strong desire to perform certain actions or activities (compulsions), OCD has a significant effect on day-to-day functioning and on quality of life. Unfortunately, OCD often goes unrecognized. Patients may hesitate to disclose their symptoms, and healthcare professionals unfamiliar with this disorder may confuse its manifestations with other psychiatric illnesses. Common comorbidities can further cloud the diagnosis. This course will discuss the epidemiology, diagnostic criteria, pathophysiology, and differential diagnosis of OCD. Then, it will review the first-line treatments, recommended duration of therapy, and options for patients who do not respond to initial therapy. Finally, it will address roles of inpatient treatment and experimental options.

Table of Contents

66474 • Obsessive-Compulsive Disorder

Course Overview

Audience

Accreditations & Approvals

Designations of Credit

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Division Planner

Division Planner Disclosure

Director of Development and Academic Affairs

Director Disclosure Statement

About the Sponsor

Disclosure Statement

Implicit Bias in Health Care

1. INTRODUCTION

2. EPIDEMIOLOGY

SOCIOECONOMIC IMPACT

3. NATURAL HISTORY

4. DIAGNOSTIC CRITERIA

COMMON THEMES

INSIGHT

SUICIDE RISK

CHALLENGES TO DIAGNOSIS

OVERCOMING CHALLENGES TO DIAGNOSIS

LANGUAGE BARRIERS

5. PATHOPHYSIOLOGY

6. DIFFERENTIAL DIAGNOSIS

7. COMORBIDITIES

8. TREATMENT

TREATMENT GOALS

PHARMACOLOGIC THERAPY

PSYCHOLOGICAL THERAPY

ADDITIONAL TREATMENT OPTIONS

9. CONCLUSION

10. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

66474 • Obsessive-Compulsive Disorder

Education Category. Psychiatric / Mental Health

Release Date. 05/01/2024

Expiration Date. 04/30/2027

Course Overview

Obsessive-compulsive disorder (OCD) is a debilitating psychiatric illness affecting approximately 2.5% of the population. Characterized by recurrent thoughts or worries (obsessions) and a strong desire to perform certain actions or activities (compulsions), OCD has a significant effect on day-to-day functioning and on quality of life. Unfortunately, OCD often goes unrecognized. Patients may hesitate to disclose their symptoms, and healthcare professionals unfamiliar with this disorder may confuse its manifestations with other psychiatric illnesses. Common comorbidities can further cloud the diagnosis. This course will discuss the epidemiology, diagnostic criteria, pathophysiology, and differential diagnosis of OCD. Then, it will review the first-line treatments, recommended duration of therapy, and options for patients who do not respond to initial therapy. Finally, it will address roles of inpatient treatment and experimental options.

Audience

This introductory course is designed for psychologists working with adults or adolescent patients who exhibit symptoms of obsessive-compulsive disorder.

Accreditations & Approvals

Continuing Education (CE) credits for psychologists are provided through the co-sponsorship of the American Psychological Association (APA) Office of Continuing Education in Psychology (CEP). The APA CEP Office maintains responsibility for the content of the programs. NetCE is recognized by the New York State Education Department's State Board for Psychology as an approved provider of continuing education for licensed psychologists #PSY-0240. This course is considered self-study by the New York State Board for Psychology.

Designations of Credit

NetCE designates this continuing education activity for 4 credit(s).

Course Objective

The purpose of this course is to provide psychologists with a basic understanding of obsessive-compulsive disorder (OCD), its clinical manifestations, and basic treatment approaches in order to facilitate optimum patient care and outcomes.

Learning Objectives

Upon completion of this course, you should be able to:

1. Review the epidemiology of obsessive-compulsive disorder (OCD).

2. Outline the diagnostic criteria and pathophysiology of OCD and possible barriers to diagnosis.

3. Describe the differential diagnosis and common comorbidities associated with OCD.

4. Discuss the use of pharmacotherapy in the management of OCD, including selection of treatment, duration, and how to address partial response or non-response.

5. Describe the use of cognitive-behavioral therapy in OCD treatment, with a focus on exposure and response prevention.

6. Identify appropriate interventions for treatment refractory OCD and experimental therapies.

Faculty

John J. Whyte, MD, MPH, is currently the Chief Medical Officer at WebMD. In this role, he leads efforts to develop and expand strategic partnerships that create meaningful change around important and timely public health issues. Previously, Dr. Whyte was the Director of Professional Affairs and Stakeholder Engagement at the FDA’s Center for Drug Evaluation and Research and the Chief Medical Expert and Vice President, Health and Medical Education at Discovery Channel, part of the media conglomerate Discovery Communications.
Prior to this, Dr. Whyte was in the Immediate Office of the Director at the Agency for Healthcare Research Quality. He served as Medical Advisor/Director of the Council on Private Sector Initiatives to Improve the Safety, Security, and Quality of Healthcare. Prior to this assignment, Dr. Whyte was the Acting Director, Division of Medical Items and Devices in the Coverage and Analysis Group in the Centers for Medicare & Medicaid Services (CMS). CMS is the federal agency responsible for administering the Medicare and Medicaid programs. In his role at CMS, Dr.Whyte made recommendations as to whether or not the Medicare program should pay for certain procedures, equipment, or services. His division was responsible for durable medical equipment, orthotics/prosthetics, drugs/biologics/therapeutics, medical items, laboratory tests, and non-implantable devices. As Division Director as well as Medical Officer/Senior Advisor, Dr. Whyte was responsible for more national coverage decisions than any other CMS staff.
Dr. Whyte is a board-certified internist. He completed an internal medicine residency at Duke University Medical Center as well as earned a Master’s of Public Health (MPH) in Health Policy and Management at Harvard University School of Public Health. Prior to arriving in Washington, Dr. Whyte was a health services research fellow at Stanford and attending physician in the Department of Medicine. He has written extensively in the medical and lay press on health policy issues.

Faculty Disclosure

Contributing faculty, John J. Whyte, MD, MPH, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Margaret Donohue, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Director of Development and Academic Affairs

Sarah Campbell

Director Disclosure Statement

The Director of Development and Academic Affairs has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Implicit Bias in Health Care

The role of implicit biases on healthcare outcomes has become a concern, as there is some evidence that implicit biases contribute to health disparities, professionals' attitudes toward and interactions with patients, quality of care, diagnoses, and treatment decisions. This may produce differences in help-seeking, diagnoses, and ultimately treatments and interventions. Implicit biases may also unwittingly produce professional behaviors, attitudes, and interactions that reduce patients' trust and comfort with their provider, leading to earlier termination of visits and/or reduced adherence and follow-up. Disadvantaged groups are marginalized in the healthcare system and vulnerable on multiple levels; health professionals' implicit biases can further exacerbate these existing disadvantages.

Interventions or strategies designed to reduce implicit bias may be categorized as change-based or control-based. Change-based interventions focus on reducing or changing cognitive associations underlying implicit biases. These interventions might include challenging stereotypes. Conversely, control-based interventions involve reducing the effects of the implicit bias on the individual's behaviors. These strategies include increasing awareness of biased thoughts and responses. The two types of interventions are not mutually exclusive and may be used synergistically.

1. INTRODUCTION

Obsessive-compulsive disorder (OCD) is a debilitating psychiatric illness affecting up to 2.5% of the population [1]. More than half (50.6%) of these cases are classified as "severe" [2]. Characterized by recurrent thoughts or worries (obsessions) and a strong desire to perform certain actions or activities (compulsions), OCD has a significant effect on day-to-day functioning and on quality of life.

Unfortunately, OCD often goes unrecognized [3]. Patients may hesitate to disclose their symptoms, and healthcare professionals unfamiliar with this disorder may confuse its manifestations with other psychiatric illnesses. Common comorbidities can further cloud the diagnosis.

This course will cover the epidemiology, diagnostic criteria, pathophysiology, and differential diagnosis of OCD. It will go on to discuss the first-line treatments, recommended duration of therapy, and options for patients who do not respond to initial therapy. Finally, it will address the role of inpatient treatment and experimental options.

2. EPIDEMIOLOGY

The exact prevalence of OCD is unknown. The National Comorbidity Survey Replication (NCS-R), a nationally representative household survey designed to assess the prevalence, severity, and comorbidity of various psychiatric disorders in the United States, found that OCD affects roughly 2.2 million American adults, or about 1% of adults in any given year [2,4]. The NCS-R researchers used criteria from the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) to make the diagnosis, based on responses to a version of the World Health Organization's Composite International Diagnostic Interview (CIDI). The Epidemiologic Catchment Area Study, conducted in the 1980s, found an OCD lifetime prevalence of 1.94% to 3.29% across five study sites [5]. This study employed lay interviewers to administer the National Institute of Mental Health Diagnostic Interview Schedule (DIS). However, the reliability of the DIS-based diagnosis is open to question; at re-interview 12 months later, only 19.2% of patients who met OCD criteria on initial interview admitted to ever having had OCD-criteria symptoms. More recent nationally representative surveys confirm that OCD has a lifetime prevalence of 2% to 3% and that it is associated with substantial comorbidity and mortality [6]. OCD is estimated to make a significant contribution to the global burden of disease, with considerable uniformity of OCD symptoms across the globe [7,8]. The incidence of OCD is reported to be higher in dermatology and cosmetic surgery patients [9].

OCD affects men and women about equally, and the prevalence appears to be similar across races and ethnicities [6]. It is not uncommon for women to experience the onset of OCD during pregnancy [9]. The NCS-R found a median age of onset of 19 years, with about one-fifth of cases starting before 10 years of age [4]. Other studies suggest a mean age of onset between 22 and 35 years, with one-third beginning before 15 years of age [10]. Early onset often leads to a long duration of untreated illness (around seven years on average), which leads to late interventions and poor response to therapy, particularly pharmacologic therapy [11]. Younger age at onset appears to be associated with more severe symptoms and higher rates of specific comorbidities, including attention deficit hyperactivity disorder, tic disorders, and other anxiety disorders. These patients may be less responsive to first-line pharmacologic treatment as adults [10].

SOCIOECONOMIC IMPACT

OCD can have significant effects on functioning, including work and personal relationships. It can adversely affect marriage, sexual functioning, family life, religious expression, leisure activities, and friendships [12]. Patients may avoid social situations due to embarrassment or anxiety. Carrying out compulsions may consume too much time to allow attending social events or may interfere with punctuality and efficiency at work. Several studies have shown a link between severity of OCD and decreased quality of life [13,14,15,16].

In 2001, the World Health Organization rated OCD among the top 20 causes of disability for people 15 to 44 years of age worldwide [17]. Other studies indicate that OCD is among the top 10 most disabling of all disorders, accounting for 2.2% of all years lost to disability [18]. Studies of the costs of mental disorders are limited; however, in the mid-1990s it was estimated that lifetime indirect costs of OCD due to lost wages were $40 billion [19]. A 2008 estimate on the economic cost of OCD in the United States showed $10.6 billion in annual direct and indirect costs among those with a formal diagnosis who were in treatment [20]. This study noted that OCD had the lowest cost of all mental disorders, mainly due to the comparatively greater functionality of affected individuals and low frequency of the disorder.

3. NATURAL HISTORY

OCD tends to have a waxing and waning course. Most studies have followed patients for only a few months to years, making it difficult to draw conclusions about long-term outcomes.

Much of what is known about the course of OCD comes from a Swedish study that tracked more than 100 patients for a mean of 47 years, beginning in the mid-1950s [21]. Participants had been hospitalized for OCD between 1947 and 1953 and were examined for the study between 1954 and 1956, then again between 1989 and 1993. By the end of four decades, 83% had improved, with 20% recovering completely and 28% having minimal symptoms. Improvement was gradual in 65% and fast in only 9%; the rest had a course of improvement that was difficult to qualify. Among patients who had no symptoms at the first study examination, 37% had symptoms at the second. Conversely, among patients who did have symptoms at the first examination, only 58% had symptoms at the second.

4. DIAGNOSTIC CRITERIA

The first step in correctly diagnosing and treating OCD is understanding its definition. Although previously considered an anxiety disorder, OCD is classified as an obsessive-compulsive disorder in the revised fifth edition of the DSM (DSM-5-TR) along with other related conditions, including body dysmorphic disorder, hoarding disorder, trichotillomania, and excoriation disorder. Essentially, OCD involves obsessions and/or compulsions that cause distress or interfere with functioning. The obsessions are usually associated with anxiety, and compulsions often serve to ameliorate that anxiety. People with the disorder are usually aware, at least at some point in time, that their obsessions or compulsions are not reasonable.

The DSM-5-TR definition of OCD is based on four criteria [22]. The first criterion is the presence of either obsessions or compulsions. Obsessions are defined by [22]:

- Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted and cause marked anxiety or distress in most individuals.

- The person attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action.

Compulsions are defined by:

- Repetitive behaviors (e.g., handwashing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession or according to rules that must be applied rigidly.

- The behaviors or mental acts are aimed at preventing or reducing anxiety or distress or preventing some dreaded event or situations; however, these behaviors or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent or are clearly excessive. Note: Young children may not be able to articulate the aims of these behaviors or mental acts.

Secondly, diagnosis of OCD is dependent upon disruption of day-to-day life. The obsessions or compulsions are time consuming (take more than one hour per day) or significantly interfere with the person's normal routine, occupational (or academic) functioning, usual social activities or relationships, or other important areas of functioning.

The third diagnostic criterion is that the disturbance is not due to the direct physiologic effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition.

Disease-specific manifestations are the fourth criterion. In order for OCD to be diagnosed in patients with another Axis 1 disorder, the content of the obsessions or compulsions may not be restricted to the other disorder (e.g., preoccupation with food in the presence of an eating disorder; hair pulling in the presence of trichotillomania; concern with appearance in the presence of body dysmorphic disorder; preoccupation with having a serious illness in the presence of hypochondriasis; preoccupation with sexual urges or fantasies in the presence of a paraphilia; or guilty ruminations in the presence of major depressive disorder).

The diagnosis of OCD may specify insight. At some point during the course of the disorder, the person may recognize that the obsessions or compulsions are excessive or unreasonable; this would be diagnosed as OCD with good or fair insight. If, for most of the time during the current episode, the person does not recognize that the obsessions and compulsions are excessive or unreasonable, the diagnosis is OCD with poor insight. If an individual is completely convinced that obsessions and compulsions are true or necessary, OCD with absent insight/delusional beliefs would be diagnosed.

Identifying the age of symptom onset as well as the age of OCD diagnosis can help predict the patient's prognosis [23].

COMMON THEMES

The DSM-5-TR diagnostic criteria do not specify the content of obsessions or any specific form of compulsion. However, several themes are common in OCD. These include being contaminated or spreading contamination, contracting a disease, causing harm to others, making an important mistake, committing a religious or moral sin, the possibility of committing homosexual or pedophilic acts, and being thought homosexual [10]. Common compulsions include cleaning or washing hands, checking to be sure a task was done, counting, arranging objects, confessing to sins or errors, making lists, and hoarding. Compulsions may be physical or mental, such as repeating a silent prayer.

Patients may have multiple, concomitant symptoms fitting more than one theme, and different symptoms may appear at different times. In addition, the possibility of OCD should not be dismissed merely because a patient's thoughts or behaviors do not fit these themes. Many patients will have obsessions involving other topics and compulsions with different manifestations.

INSIGHT

Most patients with OCD will have some insight into the fact that their obsessions or compulsions are not logical or reasonable. However, as noted, there is a subpopulation of patients for whom insight is absent. Lack of insight may be a manifestation of a particular bout with OCD symptoms, for example if the patient's level of anxiety overrules what, at another time, he or she might recognize as common sense. Occasionally, patients will report that they have never interpreted the fears or compulsions as less than reasonable. The actual number of patients who lack insight is unknown. In a DSM-IV field trial involving 431 patients at seven outpatient sites, 8% of participants had no insight at the time of interview and 5% had never had insight [24]. Among the 250 subjects whose obsessions involved some feared consequence, only 13% felt certain that the consequence would not occur. Twenty-six percent were mostly certain that it would occur, and 4% were certain that it would occur. Poorer insight has been linked to poorer outcomes [22].

SUICIDE RISK

Evidence Based Practice Recommendation

According to the American Psychiatric Association (APA), clinicians should understand that individuals with OCD are not immune to co-occurring disorders that may increase the likelihood of suicidal or aggressive behavior. When such co-occurring conditions are present, it is important to arrange treatments that will enhance the safety of the patient and others.

https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/ocd.pdf

Last Accessed: April 19, 2024

Strength of Recommendation: I (Recommended with substantial clinical confidence)

The risk of suicide appears to be elevated in patients with OCD compared to the population as a whole [10]. OCD symptoms and comorbid depression may be contributing factors. The precise risk of suicide is not known; in the NCS-R, the odds ratio for suicidal ideation in patients with OCD, compared to the general population, was 6.9 [25]. In the intake sample for the Brown Longitudinal Obsessive Compulsive Study, an ongoing, non-random, prospective study of the course of OCD, 52% of patients had a history of suicidal ideation and 15% had at least one suicide attempt [3]. A report from the International College of Obsessive-Compulsive Spectrum Disorders found a history of suicide attempt in approximately 15% of patients with OCD, with higher rates of psychiatric and medical comorbidities and previous hospitalizations in patients with a previous suicide attempt [26]. In general, patients with OCD should be carefully evaluated for suicidal ideation and any history of suicide attempts [10].

CHALLENGES TO DIAGNOSIS

While the criteria for OCD are straightforward, research has demonstrated that the diagnosis is often missed. Among the population in the Brown Longitudinal Obsessive Compulsive Study intake, subjects first received treatment an average of more than 17 years after having their first obsessive-compulsive symptoms and 11 years after meeting the diagnostic criteria [3].

Challenges to diagnosis include patients' own reluctance to discuss symptoms. They may be embarrassed to admit to their obsessions or ashamed of the extent to which they pursue compulsions, and they may be unaware that treatment is available. The wide differential diagnosis and the fact that comorbidities are common may also serve to obscure the diagnosis.

Symptoms resembling those of OCD can appear in the absence of disease [10]. Up to 80% of healthy people have intrusive or unwanted thoughts, and about 50% may have ritualized behaviors. The same themes common in OCD can appear in these thoughts and behaviors. However, the thoughts and behaviors do not cause marked distress and do not interfere greatly with functioning.

OVERCOMING CHALLENGES TO DIAGNOSIS

Asking more than once about possible or suspected symptoms, perhaps at different visits, and making these questions part of routine history taking can help patients overcome embarrassment. Recalling that OCD can have widely varied themes, not merely the popularly recognized handwashing or counting, will help prevent missed diagnoses.

Most patients will have both obsessions and compulsions, but a small percentage will have only one or the other. In the DSM-IV field trial, about 2% of participants had mostly obsessions and 2% mostly compulsions [10]. Patients may be more troubled by obsessions, more concerned about compulsions, or equally disturbed by both.

When OCD is suspected, a thorough patient interview can both confirm the diagnosis and provide a baseline for evaluating treatment. The interview should include [10]:

- Current symptoms, including content of obsessions and manifestations of compulsions

- Effect of symptoms on functioning and quality of life

- Evaluation of safety of the patient and others

- Past psychiatric history, including any treatment

- Presence of other psychiatric symptoms

- General medical history and review of systems

- Family history, with attention to OCD and other psychiatric disorders

A physical exam is also important, both as an element of general medical care and to help establish that symptoms are not caused by an underlying neurologic problem. There are no distinctive physical signs of OCD, but an exam may reveal clues. Some patients will have chapped hands from handwashing or evidence of common comorbidities, such as skin picking or trichotillomania. However, most can be expected to have a normal physical exam.

The physical exam should include [10]:

- A mental status exam, with particular attention to thought process and content, illusions or hallucinations, suicide or homicide risk, insight, and judgment

- A neurologic exam, which may identify tics related to OCD

Neuropsychological assessment of patients with OCD suggests that there are deficits across a broad range of domains (e.g., poor performance on memory, visuospatial ability, and cognitive flexibility tests), with system/ordering behaviors more strongly related to poorer neuropsychological performance overall [27,28].

Screening tools are available to help evaluate the impact of OCD. One of the best-known is the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). The Y-BOCS includes two components: a symptom checklist and a severity scale. The Y-BOCS is widely used in research studies of OCD treatment, with reductions in severity used as markers of treatment success. The symptom checklist includes obsessions and both physical and mental compulsions. The severity scale is based on time spent on obsessions and compulsions, resistance to these symptoms, interference from symptoms, related distress, and level of control. Increasing numbers of points are assigned for increasing levels of impact. The scale is scored as follows [29]:

- Mild: 8–15 points

- Moderate: 16–23 points

- Severe: 24–31 points

- Extreme: 32–40 points

Other measurement tools are also available. The Obsessive-Compulsive Inventory-Revised is a brief, self-rated scale asking about specific symptoms and degrees of distress related to them [30]. A simple visual analog scale, with symptoms rated from "none" to "incapacitating," may also be used.

LANGUAGE BARRIERS

As a result of the evolving racial and immigration demographics in the United States, interaction with patients for whom English is not a native language is inevitable. Because patient history is such a vital aspect of the assessment of OCD, it is each practitioner's responsibility to ensure that information and instructions are explained in such a way that allows for patient understanding. When there is an obvious disconnect in the communication process between the practitioner and patient due to the patient's lack of proficiency in the English language, an interpreter is required.

In this multicultural landscape, interpreters are a valuable resource to help bridge the communication and cultural gap between clients/patients and practitioners. Interpreters are more than passive agents who translate and transmit information back and forth from party to party. When they are enlisted and treated as part of the interdisciplinary clinical team, they serve as cultural brokers, who ultimately enhance the clinical encounter. In any case in which information regarding diagnostic procedures, treatment options, and medication/treatment measures are being provided, the use of an interpreter should be considered.

5. PATHOPHYSIOLOGY

The pathophysiology of OCD is not fully understood. A genetic component is apparent, with higher incidence in first-degree relatives of affected patients. In a meta-analysis of five family studies involving adult probands, researchers found a four-fold increase of OCD incidence among first-degree relatives [31,32]. Twin studies consistently show higher concordance of OCD in monozygotic than in dizygotic twins [33]. Concordance ranges from 47% to 50% for dizygotic to 80% to 87% for monozygotic twins [10].

Evidence Based Practice Recommendation

Patients with OCD who are parents of young children may want advice regarding the genetic risk of OCD. The APA recommends that clinicians explain to such patients that the available data indicate an increased but modest risk of OCD in the children of affected individuals; patients wanting more information may be referred to a genetic counselor.

https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/ocd.pdf

Last Accessed: April 19, 2024

Strength of Recommendation: I (Recommended with substantial clinical confidence)

While the possibility of a specific genetic etiology has been considered, none has been identified with certainty, and research is limited. A 2017 study analyzing more than 600 genes thought to be associated with OCD among humans, dogs, and mice elicited the identification of four specific genes prominent in several of those with OCD [32]. These findings are consistent and provide evidence of the current common genetic theories of OCD [32].

One theory is that a defect in neural pathways, likely including orbitofrontal-striatal circuits, may be involved, but specific pathology has not been consistently shown [34,35]. The theory posits that hard-wired primal behaviors (e.g., checking, cleaning) are exacerbated due to a hyperstimulated thalamus [36]. Imaging studies of OCD brains have found increased metabolic activity in the caudate nucleus, cingulate gyrus, and orbital frontal cortex.

One study also showed defects in neural pathways, with a hyperactivation in the connections between the structures in the cortico-striato-thalamo-cortical (CSTC) circuit, which is primarily responsible for regulating complex behaviors [32,37]. In addition, the cell-adhesion gene CTTNBP2 was one of the commonly identified genes in those with OCD, supporting the potential that neural pathways play a significant role in OCD behaviors [32]. Another 2017 study showed results similar to previous studies, with inflammation occurring in the neurocircuitry in more than 30% of participants, especially in the orbitofrontal cortex and CSTC [38].

Another hypothesis regarding the underlying cause of OCD involves serotonin [36]. Research regarding a role for serotonin was spurred by studies of the effectiveness of antidepressants, such as clomipramine and desipramine, for OCD in non-depressed patients [34,39]. Clomipramine, which acts primarily as a serotonin reuptake inhibitor (SRI), has proved to be more effective than desipramine, which is thought to act primarily by inhibiting norepinephrine reuptake [40]. The ability of selective serotonin reuptake inhibitors (SSRIs) to reduce OCD symptoms further supports a role for serotonin abnormalities in the pathogenesis of OCD, a theory supported by the 2017 study in which a gene that includes a serotonin receptor, HTR2A, was found to be among the most commonly associated in those with OCD [32]. A specific mechanism, however, has not been elucidated, and studies involving measures of serotonergic function have been inconsistent.

An important challenge to the serotonin hypothesis is that SSRIs fail to bring significant improvement for a substantial number of patients with OCD. Other neurotransmitters, including dopamine and glutamate, are also being investigated for their influence in OCD [41]. The 2017 study supports this, showing that two of the four genes found to have a possible association with OCD, NRXN1 and REEP3, are involved in a process that may cause OCD behaviors by creating an imbalance of excitatory glutamate and inhibitory GABAergic neuron differentiation [32]. Some researchers have raised the question of whether OCD may be an immune-related disorder [42,43]. Exploration of this possibility began with the observation of an association between Sydenham chorea and OCD. Obsessive-compulsive symptoms have been observed in children following streptococcal infection, a condition termed pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS). Although the relationships between OCD and immune response remain unclear, available literature supports the role of immune processes in the pathophysiology of OCD, suggesting immunotherapeutic treatments may be useful in the treatment of OCD [43,44].

6. DIFFERENTIAL DIAGNOSIS

The differential diagnosis of OCD is broad and includes other anxiety disorders, such as generalized anxiety disorder and post-traumatic stress disorder, as well as schizophrenia, delusional disorder, depression, Tourette syndrome, and obsessive-compulsive personality disorder (OCPD).

OCPD is characterized by preoccupation with order, perfection, and control, but not by the presence of obsessions or compulsions [24]. It is often compared to a "perfectionist" personality. Unlike OCD, symptoms must appear by early adulthood for the diagnosis to be made; however, OCD and OCPD may occur in the same person. The frequency of both diagnoses occurring together is not known, but studies suggest that it is not uncommon [45]. Estimates from OCD study populations indicate a concomitant rate between 23% and 32%, although these samples were not designed to be representative of all patients with OCD [45,46]. For comparison, the prevalence of OCPD has been observed to be about 0.9% to 2% in community samples [45,46]. There is also some evidence that OCPD is more common in people with OCD than in patients with other psychiatric disorders.

Post-traumatic stress disorder is characterized by onset in the wake of an extreme traumatic stressor. Symptoms include avoidance of stimuli associated with the trauma and persistent thoughts about the event, which may seem to resemble behaviors and obsessions seen in OCD [22]. However, the obsessions and compulsions of OCD are not related to a specific, preceding traumatic event.

Generalized anxiety disorder involves excessive anxiety and worry about feared events. Unlike OCD, the diagnostic criteria also include the presence of additional symptoms, including restlessness, a tendency to be easily fatigued, difficulty concentrating, irritability, muscle tension, and sleep disturbance [22]. Further, the anxiety in generalized anxiety disorder tends to focus on more realistic forthcoming problems and concerns.

Delusional disorder features the presence of one or more nonbizarre delusions. The content of the delusions may resemble that of an obsession in OCD; for example, a delusion that one has contracted an infection may resemble anxiety about contamination in OCD. Classically, a patient with OCD would have insight into his or her illness while a patient with delusional disorder would not; however, when insight is lacking, OCD may closely resemble delusional disorder. OCD with delusional beliefs may also superficially resemble schizophrenia. However, the additional symptoms of schizophrenia will generally be lacking.

Depression may be accompanied by intrusive, unpleasant thoughts, as in OCD, but these thoughts do not generally lead to compulsions. Depression may occur in conjunction with OCD, but OCD itself is not characterized by depressed mood and anhedonia. However, these conditions frequently co-occur, and careful evaluation is necessary [47].

Tourette syndrome is characterized by tics, which first manifest during childhood in the majority of patients. Tics in Tourette syndrome tend to be preceded by a physical sense of "needing" to do the movement, but not by anxiety about a specific outcome or the desire to avert a feared event. However, the tics may be quite complex and may even resemble compulsions, leading to diagnostic confusion in some cases.

7. COMORBIDITIES

Most studies of comorbidities in OCD are based on case series or convenience samples, making it difficult to estimate the prevalence of comorbid conditions among patients with OCD overall. Available evidence does suggest that certain psychiatric illnesses are more common among people with OCD than among the general population. In one interview-based study of 334 patients with OCD, only 8% of participants had no psychiatric comorbidity [48]. In the Brown Longitudinal Obsessive Compulsive Study intake, 91% of subjects had at least one other Axis 1 disorder [3].

Comorbid disorders that begin prior to the onset of OCD symptoms may influence the occurrence of additional comorbidities over time [49]. In one study involving 1,001 patients with OCD, separation anxiety disorder preceded OCD in 17.5% of patients and was associated with a higher lifetime frequency of post-traumatic stress disorder. ADHD preceded OCD in 5.0% of patients and was associated with higher lifetime frequencies of substance abuse and dependence. Tic disorders preceded OCD in 4.4% of patients and were associated with higher lifetime frequencies of OCD spectrum disorders [50].

Depression is a particularly common comorbidity. A chart review of 120 patients with OCD in the Netherlands found depression in one-third, and a separate structured psychiatric interview found similar results (31%) for major depression [51,52]. The Epidemiologic Catchment Area Study in the United States found 67% of individuals identified as having OCD had at least one episode of major depression [47]. In addition, OCD has been shown to comorbidly occur with social phobia (11% to 24%), simple phobia (including body dysmorphic disorder) (7% to 14%), and panic disorder (6% to 14%, 35% lifetime incidence) [9]. Associations have also been observed between OCD and other conditions, including bipolar disorder, eating disorder, generalized anxiety disorder (20%), alcohol dependence/substance abuse, and Tourette syndrome (5% to 7%) [9,10,53]. Richter and colleagues looked at patients with OCD, social anxiety disorder, or panic disorder and found that trichotillomania, skin picking, body dysmorphic disorder, and tics were more strongly associated with OCD than with the other two anxiety disorders [54].

In addition to considering other psychiatric diagnoses in the setting of OCD, clinicians should be alert for OCD symptoms in patients who have already been diagnosed with a different psychiatric illness. For example, eating disorders are often accompanied by anxiety disorders, including OCD. One survey showed the comorbid rate of eating disorder and OCD to be roughly 8% [52]. OCD is also common in patients with Tourette syndrome. One large international registry found that 27% of people with Tourette syndrome also had OCD, and other studies have found percentages ranging from 28% to 62% [9,10,55,56,57]. A separate study showed that of patients with OCD, approximately 5% will have comorbid Tourette syndrome [52]. Childhood-onset OCD may have a higher rate of comorbidity with Tourette syndrome and ADHD [9].

8. TREATMENT

In the Practice Guideline for the Treatment of Patients with Obsessive-Compulsive Disorder, the American Psychiatric Association (APA) recommends two options for first-line therapy, either alone or in combination: SRIs and cognitive-behavioral therapy (CBT) [10].

Five SRIs are approved by the U.S. Food and Drug Administration (FDA) for OCD treatment, including four SSRIs and one serotonin-specific tricyclic antidepressant (TCA) [58]:

- Fluoxetine

- Fluvoxamine

- Paroxetine

- Sertraline

- Clomipramine

Two other SSRIs and one serotonin norepinephrine reuptake inhibitors (SNRIs) also appear to be effective, although they do not have an indication for OCD [59]:

- Citalopram (approved for depression)

- Escitalopram (approved for depression and generalized anxiety disorder in the United States; approved for OCD in Europe)

- Venlafaxine (approved for depression)

All of the SSRIs are recommended as options for first-line therapy by the APA. Pharmacologic therapy is also recommended for those patients whose symptoms may be exacerbated by CBT or when access to a mental healthcare professional is unavailable and severe symptoms are present [60]. Specific aspects of these medications, including efficacy and side effects, will be discussed further in this course.

The form of CBT most commonly studied in OCD involves exposure and response prevention [58]. Exposure and response prevention consists of talk therapy and specific exercises designed to reduce anxiety and dampen the need to perform compulsions. Unless otherwise specified, "CBT" will be used in this course to refer to forms of therapy that incorporate exposure and response prevention.

CBT should be initiated and monitored by a professional trained in this specific mode of treatment. The exercises often can and should be done by the patient at home, which requires a strong level of commitment. Patients who experience too much anxiety to do the exercises or are not willing to accept this form of participatory treatment may be better candidates for pharmacotherapy, at least as the first step.

Overall considerations for selecting pharmacotherapy or CBT include:

- Patient choice

- Failure of prior attempt with the other option

- Willingness to take medication

- Willingness to do the work of CBT

Another form of CBT commonly used is Internet-based self- or professional-guided therapy. This form of treatment may be beneficial for those in rural areas or whose behaviors make them resistant to seek traditional face-to-face treatment [60].

Whether SRIs, CBT, or their combination are more effective has not been widely studied. One meta-analysis suggested SRIs and CBT are equally effective, but the authors concluded that there was not enough evidence to draw a firm conclusion [61]. There also appears to be a benefit to combining SRI and CBT in some patients, although possibly not all. In addition, there is some limited evidence that CBT, alone or in combination with medication, may lead to lower symptom severity after treatment is discontinued [62,63]. The APA recommends combining treatments for patients who do not respond adequately to monotherapy, who wish to limit the duration of SRI use, who have comorbidities that will benefit from SRIs, or who have severe OCD [10].

In 2008, Simpson and colleagues conducted a randomized controlled trial to examine the effects of augmenting SRIs with exposure and ritual prevention [62]. Participants were 108 adult outpatients with OCD. All had been taking an SRI at a therapeutic dose for at least 12 weeks prior to entry but still had a Y-BOCS total score of 16 or greater. The patients were provided with 17 biweekly sessions of CBT, either an OCD-specific program of exposure and ritual prevention or a control setting of stress management training, while still continuing the SRI. After eight weeks, patients receiving the exposure and response prevention sessions were more likely to have at least a 25% decrease in severity on the Y-BOCS scale. They were also more likely to have achieved a Y-BOCS score of 12 or less.

In 2011, the Pediatric OCD Treatment Study II (POTS II) compared SRI therapy combined with 14 one-hour CBT sessions over 12 weeks to both medication alone and medication plus CBT instructions given at in-person medication management visits [64]. Each of the three study groups consisted of 42 patients, and the measure for success was 30% improvement in initial Y-BOCS score over the 12-week study period. The success rate of combination SRI and CBT (68.8%) was twice as high as either SRI plus instruction (34%) or medication alone (30%) [64].

A 2018 literature review assessed the efficacy of combining drug and psychological treatments for OCD [65]. The review included 10 controlled studies assessing the efficacy of using combination strategies from the start of treatment versus CBT alone; 6 assessing combination strategies from the start of treatment versus SSRIs alone; and 11 randomized controlled trials assessing treatments given sequentially [65]. The combination strategies administered from the start of treatment were not found to be superior to monotherapy alone, except for patients with severe depression. Sequential administration of CBT after medications was found useful in promoting remission in patients who partially responded to drugs and in promoting response in resistant patients [65].

TREATMENT GOALS

Evidence Based Practice Recommendation

Because the patient's beliefs about the nature of the illness and its treatments will influence adherence, the APA asserts that providing patient and family education may enhance adherence to treatment.

https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/ocd.pdf

Last Accessed: April 19, 2024

Strength of Recommendation: II (Recommended with moderate clinical confidence)

Unfortunately, OCD is a difficult disease to fully cure. Some patients will achieve full remission, but many will retain at least some obsessive or compulsive symptoms. In most cases, the goal is to allow the patient to return to normal or near-normal functioning, including the ability to work and to have healthy and satisfying social relationships. Elements of this process include decreasing the frequency and severity of symptoms and helping the patient to cope with residual disease. Discussing with patients the possibility that medication or CBT may not make OCD disappear entirely can help avoid disappointment and frustration.

Improvement in OCD often occurs slowly, requiring months-long medication trials and/or many weeks or months of CBT. Patients may also need extra time to consider their treatment options, especially if their symptoms include "doubting," as they may doubt their ability to make the right decision.

PHARMACOLOGIC THERAPY

When pharmacologic therapy is selected as first-line treatment, the APA recommends beginning with an SSRI instead of clomipramine, due to the better safety profile of the SSRIs [10]. Choice of SSRI should be individualized and should include consideration of [10]:

- Drug-specific side effects

- Drug-drug interactions

- Comorbidities

- Past response

Some have suggested that the response of first-degree relatives to a specific medication may indicate an increased chance for response. Additional research is necessary before a recommendation may be made. No data support the practice of combining two SSRIs [58].

Studies suggest that approximately 40% to 60% of patients will have a clinically useful response to SSRIs, with about a 20% to 40% decrease in symptoms [58,60,66]. Data on long-term improvement is limited. In a 3-year prospective follow-up study, researchers evaluated outcomes in 79 Italian patients with OCD treated with SSRIs [67]. Some patients also received augmented therapy with low doses of neuroleptics. They found a 65% probability of achieving at least partial remission and a 38% probability of achieving full remission. However, the rate of relapse was 60%. Worse outcomes were predicted by greater severity of illness, longer duration, and comorbid schizotypal personality disorder. In a systematic review of 17 studies involving 3,097 participants, researchers examined the efficacy and adverse effects of SSRIs versus placebo for the treatment of OCD [68]. They found that SSRIs were more effective than placebo in achieving clinical response at six and 13 weeks post-treatment. The pooled relative risk was similar between individual SSRI drugs. Nausea, headache, and insomnia were the most commonly reported adverse effects in each of the studies. The long-term efficacy and tolerability of SSRIs for OCD has yet to be established [68].

Clomipramine

Clomipramine is a TCA with multiple actions, including significant activity as a serotonin reuptake inhibitor. It was the first medication approved in the United States for treatment of OCD [69]. Some studies have suggested that clomipramine is more effective than the SSRIs, but others have found equal effectiveness or more improvement with an SSRI [69,70,71,72,73]. Direct, controlled comparison studies have found fluvoxamine, paroxetine, and sertraline equal in efficacy to clomipramine. Patients with OCD who have comorbid tics or schizotypal personality are unlikely to respond to clomipramine or an SSRI alone [74]. Due to serious adverse effects, a high daily dose of clomipramine is not advised unless SSRI monotherapy is not adequate to control OCD behaviors [70]. In addition, clomipramine may be used as combination therapy with an SSRI to receive the benefits of the TCA without the problematic side effects of higher doses of the drug [70]. Concurrent use of clomipramine and fluoxetine is not advised, as fluoxetine inhibits the metabolism of clomipramine in the liver, creating high serum levels of clomipramine [70].

Clomipramine does have a higher potential for adverse effects than the SSRIs, particularly if used in combination with an SSRI [75]. Anticholinergic side effects are common, and overdose can lead to cardiac arrhythmias, seizures, hypotension, and death [76]. Risks of arrhythmogenic effects, cardiotoxicity, and seizure are concerns at doses greater than the maximum dose of 250 mg/day, and electrocardiograph monitoring is recommended for continued high dosages [59,70].

SSRIs

The use of each SSRI in OCD is supported by placebo-controlled trials. Although available evidence suggests that efficacy is similar across this class of drugs, no trials have compared all the SSRIs under controlled conditions [69]. Thus, their actual relative efficacy is unknown. Further, different trials have used different definitions for response, making comparisons difficult.

Paroxetine

A multinational, double-blind, 12-week trial conducted by Zohar and colleagues compared flexible-dose paroxetine, 20–60 mg daily, to placebo [77]. Response was defined as a 25% decrease in the Y-BOCS score. Response rates were 55% for paroxetine and 35% for placebo.

Hollander and colleagues compared paroxetine 20 mg, 40 mg, or 60 mg per day to placebo in a 12-week, double-blind trial [78]. Response was considered to be a decrease of 25% in the Y-BOCS score or a decrease in Clinical Global Impression-Severity (CGI-S) score of two points or more. Response rates were 25% for the 40-mg dose, 29% for the 60-mg dose, and 13% for placebo. Improvement with the 20-mg dose was not statistically significant compared to placebo.

Another trial supports effectiveness in a Japanese population. In a 12-week, double-blind trial, Kamijima and colleagues compared flexible-dose paroxetine, starting at 20 mg and titrating to as high as 50 mg per day, to placebo [79]. Response rates were significantly higher for paroxetine.

Fluvoxamine

The largest study of fluvoxamine was conducted by Hollander and colleagues [80]. This double-blind, 12-week trial involved 253 subjects and identified two response levels: a 35% or 25% reduction in the Y-BOCS score. Response at both levels was significantly higher for the treatment group compared to the placebo group. Remission rates were also significantly higher: 44% versus 31% for a Y-BOCS score of 16 or less, and 18% versus 8% for a Y-BOCS score of 8 or less.

Two pivotal trials for fluvoxamine in OCD found that after 10 weeks of treatment, Y-BOCS scores decreased significantly more in the fluvoxamine group compared to the placebo group. Among patients who received one or more post-baseline ratings, the mean Y-BOCS score decreased by 21% in patients who received fluvoxamine and 7% in patients who received placebo [10].

Sertraline

A placebo-controlled trial of flexibly dosed sertraline for OCD was published by Kronig and colleagues in 1999 [81]. The trial involved 167 patients, with treatment for 12 weeks and doses ranging from 50–200 mg. The treatment group had significantly greater improvement on Y-BOCS scores, and significantly more sertraline patients showed a therapeutic response according to Clinical Global Impression-Improvement (CGI-I) scores (41% versus 23%).

An earlier trial, published by Greist and colleagues in 1995, compared different doses of sertraline in 325 patients [82]. Patients were randomized to 50 mg, 100 mg, or 200 mg per day for 12 weeks, and were assessed using the Y-BOCS, the National Institute of Mental Health Global Obsessive Compulsive Scale (NIMH-GOCS), CGI-S and CGI-I, and the Maudsley Obsessive Compulsive Inventory. Overall, patients using sertraline did better than those prescribed placebo on all measures. The 50-mg and 200-mg groups also did better than placebo on all of the investigator-related scales, although the 100-mg group was better only on the NIMH-GOCS.

Fluoxetine

The largest trials of fluoxetine for OCD were published in the mid-1990s. Montgomery and colleagues followed 214 patients over eight weeks of treatment with daily fluoxetine doses of 20 mg, 40 mg, or 60 mg, or placebo [83]. At the 40-mg and 60-mg doses, the response rates, defined as a decrease in the Y-BOCS total score of at least 25% and a CGI-I rating of "much improved" or "very much improved," were significantly higher with fluoxetine than with placebo. Response rate was 47% at the 60-mg dose, 48% at the 40-mg dose, and 26% with placebo.

Tollefson and colleagues studied 355 patients over 13 weeks, again comparing fluoxetine doses of 20 mg, 40 mg, 60 mg, or placebo [84]. At all doses, there was significant improvement on Y-BOCS scores compared to placebo.

A 2020 systematic review found that fluoxetine is well-tolerated and associated with significantly greater reduction in OCD severity in children and adolescents, as measured by the Children's Y-BOCS [85].

Citalopram

Citalopram is the most serotonin-selective of the SSRIs. Although it does not have an FDA-approved indication for OCD, it is included as an equivalent option to the other SSRIs in the APA guideline [10].

Montgomery and colleagues tested different doses of citalopram against placebo in 401 patients with OCD over 12 weeks, with "improvement" considered to be a 25% reduction in baseline Y-BOCS scores [86]. The percentage of patients who reached this endpoint was significantly higher in the treatment groups: 65% of subjects at 60 mg per day, 52% at 40 mg per day, and 57% for 20 mg per day, compared to 37% of subjects receiving placebo. The differences between the individual doses of citalopram were not statistically significant.

In 2011, the FDA issued a warning advising patients and prescribers that citalopram should no longer be used at a dosage greater than 40 mg due to risk of potentially fatal abnormal heart rhythms, including torsades de pointes and should not be used in patients with factors predisposing them to either of those conditions [87]. Additionally, doses of 60 mg per day have not been found to have reasonable benefit over doses of 40 mg per day [87,88]. In 2012, a revised warning was issued to clarify that citalopram is "not recommended" rather than "contraindicated" in those with congenital long QT interval syndrome, should not be used at doses greater than 20 mg per day in patients older than 60 years of age, and should be discontinued in patients with a QTc measurement greater than 500 ms [88]. Citalopram must be dispensed with an FDA-approved patient medication guide [59].

Escitalopram

Escitalopram, an enantiomer of citalopram, is also not FDA approved for OCD. Like citalopram, it is included with the other SSRIs as an option in the APA recommendations [10].

A 24-week, double-blind, randomized trial, conducted by Stein and colleagues, showed a benefit of escitalopram over placebo in OCD [89]. Escitalopram at both 10 mg and 20 mg per day was superior to placebo on multiple measures, including remission at 12 weeks, defined as a Y-BOCS score of 10 or less. At 24 weeks, remission was significantly greater than placebo for escitalopram 10 mg per day, although only numerically greater than placebo for the 20-mg dose.

SRIs in OCD

Although clomipramine and the SSRIs are also used to treat depression, their use in OCD has somewhat different parameters. Patients with OCD may require higher doses, and the onset of action may be slower. In depression, improvement may be expected as early as one week after initiating treatment. The APA guideline for the treatment of major depressive disorder recommends re-evaluating treatment if at least moderate improvement has not occurred after six to eight weeks [10]. In OCD, a full trial of SRI therapy takes 8 to 12 weeks, including 4 to 6 weeks on the highest tolerable dose [58,70].

Starting at a low dose of an SRI helps to avoid side effects, including nausea, diarrhea, drowsiness, and headache. Many pills can be split, and some SRIs are available in liquid formulations that allow for even more flexible titration schedules. Usual doses of SRIs in OCD are provided in the APA guideline and updated manufacturer labeling (Table 1).

Table 1: ADULT DOSING OF SSRIs FOR THE TREATMENT OF OCDa

SSRI

Starting and Incremental Dose

Usual Target Dose

Usual Maximum Dose

Occasionally Prescribed Maximum Dose

Citalopram

20 mg

40 mgb

40 mgb

40 mgb

Escitalopram

10 mg

10–20 mg

40 mg

60 mg

Fluoxetine

20 mg

40–60 mg

80 mg

120 mg

Fluvoxamine

50 mg

100–300 mg

300 mg

450 mg

Paroxetine

20 mg

20–60 mg

60 mg

100 mg

Sertraline

50 mg

200 mg

200 mg

400 mg

aDosages are for immediate-release formula, not controlled-release.

bMaximum dose: 40 mg

Source: [10,59]

Side Effects

Many patients will tolerate SSRIs well, but for some, side effects can be significant. Some side effects, including nausea, agitation, and sleep disturbances, commonly occur when the medication is first started and disappear over the first few weeks to months. Explaining this to patients can help to encourage them to continue the medication, with the understanding that other options are available should the side effects fail to subside.

In some cases, lowering the dose, changing the timing of doses, or changing to a different SRI will help to alleviate side effects; in others, adding an additional medication may be helpful [10]. Some side effects are particularly likely with certain SSRIs. For example, paroxetine is the most anticholinergic and appears to be more likely to cause weight gain than other SSRIs. Insomnia may be addressed by taking the SSRI in the morning instead of the evening or by the addition of a sleep-promoting agent. Modafinil may help with fatigue. Excessive diaphoresis may be improved by the addition of a low-dose anticholinergic.

Sexual symptoms, including decreased libido and difficulty with orgasm, may be difficult to overcome, but there are options that will work for some patients. In some cases, sexual symptoms will decrease over time. Some patients may be willing to wait until OCD symptoms have improved and weaning from the SSRI is appropriate. Some may benefit from a "drug holiday" up to once per week, stopping the SSRI for one day before a sexual encounter. In general, stopping an SSRI abruptly is not recommended due to the possibility of withdrawal effects, but with most of the SSRIs, missing one dose is not expected to affect outcomes adversely. The short half-life of paroxetine makes it a poor choice for this technique, and the half-life of fluoxetine may be too long for the one-day "holiday" to be useful.

SSRIs and clomipramine carry a warning from the FDA regarding a possible increased risk of suicidality in children, adolescents, and young adults [59]. Patients should be closely monitored for suicidality throughout therapy, particularly when beginning treatment or altering the dose.

Partial Response and Non-Response

As noted, the APA recommends a trial of at least 8 to 12 weeks with a given SRI, including at least four to six weeks at the highest tolerable dose [10]. For patients who fail to achieve a reduction in symptoms by the end of this time or who have only minimal response, there are several APA-recommended options [10]. One strategy is to offer a trial of a different SSRI. It may take multiple trials to find the right match for a given patient. Additional options include switching to clomipramine, switching to the serotonin-norepinephrine reuptake inhibitor venlafaxine, or adding a second-generation antipsychotic. Switching to mirtazapine is also offered as a strategy, although supporting evidence is limited. Switching to venlafaxine may be less effective than switching to a different SRI.

Some patients will be partial responders to SSRIs, with symptoms improving but still having a significant impact on functioning. For these patients, the APA recommends continuing the pharmacotherapy but augmenting it with either a second-generation antipsychotic or CBT. Antipsychotics alone have not proven useful in OCD. However, there is some evidence to support their use to augment SRI therapy, with response rates of about 40% to 55% [10]. Unfortunately, the details of best use, including dose, duration, and subsets of patients who may benefit most, have not yet been established.

Duration of Treatment

The best duration for pharmacotherapy in OCD has not been determined. A minimum of one to two years has been recommended before withdrawal should be considered [10,90]. Others recommend that pharmacotherapy should be continued indefinitely. Data suggest that patients' symptoms will return within one to two months after medications are stopped, even after two years of successful pharmacotherapy. Up to 20% of patients who discontinue a successful drug will not respond when the drug is restarted [74]. The presence of a comorbid diagnosis can interfere with clinical recovery and may guide the choice of interventions [58]. The decision to continue or to stop medication should be individualized and discussed with each patient.

As noted, neither SSRIs nor clomipramine should be stopped abruptly. Instead, these medications should be tapered slowly, decreasing by 10% to 25% every one to two months [10]. Sudden discontinuation can lead to a drug discontinuation syndrome, with symptoms that may include nausea and vomiting, headache, dizziness, insomnia, and agitation or lethargy. Patients may also experience paresthesias or myoclonic jerks.

PSYCHOLOGICAL THERAPY

Of all potential psychological therapies for OCD, CBT is supported by the best evidence. Most studies have used some form of exposure and response prevention as the mode of therapy, with variations in frequency, intensity, and guidance. These studies have generally been small, with at most a few dozen patients. One larger, multisite trial compared exposure and response prevention to clomipramine, placebo, or a combination of the two treatments [91]. This study involved intensive, daily exposure and response prevention for four weeks, followed by maintenance sessions for another eight weeks. Overall, 71% of the 122 randomized patients completed treatment. Response rates at week 12, measured as improvement on the Y-BOCS, CGI-S, and NIMH-GOCS, were all significantly better for exposure and response prevention than for clomipramine. Exposure and response prevention plus clomipramine was not significantly better than exposure and response prevention alone. Based on the CGI-I measure, an "excellent" response was seen more often in the exposure and response prevention group and in the combination group than in the clomipramine-alone group.

Another large trial, involving 218 patients, compared two different techniques for exposure and response prevention to a control group [92]. One group received weekly instruction by therapists on performing exposure and response prevention techniques at home. The second group used a workbook and a computer program. The controls received relaxation training. In an intent-to-treat analysis, both the therapist-guided and computer-guided exposure and response prevention sessions were significantly superior to the control therapy, and the therapist-guided therapy was significantly more effective than the computer sessions.

In 2007, a Cochrane review compared psychological treatment for OCD with "treatment as usual" [93]. Eight relevant studies, all randomized trials, were identified, and in each one, patients on a waiting list were used as the controls. In all but one of the studies, some patients also received pharmacologic treatment. Study treatment duration ranged from six to 20 weeks. Patients receiving any type of CBT were found to have significantly fewer symptoms following treatment, with overall effect being influenced by baseline severity. The authors recommended further study to identify the best forms of CBT, predictors of response, and cost-effectiveness.

Not all patients will be able to complete a course of CBT. For some, the commitment level is too high. For others, the anxiety induced by facing or thinking about the feared objects or events is simply too strong. An estimated 22% to 30% of patients can be expected to drop out or refuse to comply with exposure and response prevention therapy [58,94]. For these patients, Internet-based self- or professional-guided therapy may be a beneficial alternative [60].

Some patients who are willing and able to attempt CBT will be stymied by insurance constraints. For these patients, and with appropriate guidance, self-help in the form of workbooks and exercises to be done at home is an option [58]. However, as experienced in the POTS II trial, CBT instruction-only response rates are likely much lower than that of weekly CBT sessions [64]. CBT available as online video teletherapy and through self-help apps are areas of current research for treatment of OCD [95,96].

Techniques for CBT

Exposure and response prevention consists of a specific series of techniques. It may be offered as individual therapy or in a group setting. The APA recommends at least weekly sessions [10].

Exposure and response prevention is based on the idea that obsessions and compulsions serve to reinforce one another [97,98]. The obsessions are associated with great anxiety; because compulsions serve to reduce that anxiety, the performance of these behaviors is reinforced with each cycle. At the same time, the use of ritualized behaviors to combat anxiety prevents the development of other methods of coping with the anxious feelings. Thus, repeated exposure to a feared stimulus while avoiding the use of ritualized behavioral responses should, over time, lead to a dampening of the anxiety response and a lessening of the need to perform compulsions. Exercises generally start with exposure to a situation that causes a moderate level of anxiety and progress to exposures that are more intensely feared. Patients are encouraged to think about the feared consequences of not performing their rituals. At the same time, they are asked to abstain from these ritualistic behaviors and encouraged to develop alternative ways of tolerating and overcoming anxiety. When exposure and response prevention is successful, patients gradually become accustomed to the idea that feared outcomes are unlikely to happen even though rituals are not performed. The patient's family should be involved when possible. To be of most help to the patient, the family may need to be willing to change their responses to the patient (e.g., not provide requested reassurance to irrational doubts) [58]. Successful treatment depends in part on the family's willingness to reduce their accommodation of the patient's compulsive behaviors [99]. Additionally, a family history of OCD can significantly decrease the patient's response to CBT [100].

Recommended Duration of CBT

There is no strong evidence to support a given duration of CBT. However, the consensus, according to the APA guideline, is for an initial course of 13 to 20 weeks of weekly CBT or three weeks of daily sessions [10]. If treatment is successful, it may be tapered to monthly sessions for another three to six months. Some patients will benefit from occasional booster sessions as well. The APA recommends ongoing maintenance, although details are not specified [10]. The exact probability of relapse following CBT is unclear.

Patients who have not achieved benefit after an initial course of CBT should be re-evaluated. Lack of compliance with treatment may be a barrier to success, and reasons for noncompliance should be explored and, if possible, addressed. Some patients may require a longer duration of therapy. For partial responders, the APA recommends a trial of an SSRI to accompany CBT [10]. Other options include increasing the intensity of treatment or adding cognitive therapy to exposure and response prevention, although the effectiveness of these choices has not been established.

ADDITIONAL TREATMENT OPTIONS

Some patients will fail to respond to both standard pharmacologic options and to outpatient CBT. Others will achieve a partial response but remain unable to return to a satisfactory level of functioning. A subset of patients will be so disabled by symptoms that they are unable to participate in standard outpatient treatment. These patients should generally be referred to specialty psychiatric care, preferably to a physician with expertise in OCD.

One option for patients with severe OCD is inpatient therapy. Highly structured, intensive outpatient treatment may also be beneficial. Treatment-refractory patients may benefit from the use of other medications added to standard pharmacotherapy or from monotherapy with drugs other than SRIs. Limited evidence suggests that patients who are not helped by oral SRIs may benefit from oral morphine, IV clomipramine, IV citalopram, combinations of antidepressants, or other therapies; however, more research is needed to determine efficacy and identify appropriate use [40,101,102]. One randomized double-blind study tested the safety and efficacy of the central nervous system (CNS) stimulant methylphenidate extended-release (MPH-ER) as add-on therapy for SRI treatment-refractory OCD [103]. The study involved 44 adults (66% male) with SRI treatment-refractory OCD, receiving fluvoxamine pharmacotherapy, and with Y-BOCS scores higher than 20. Participants were randomized into two groups: group one received fluvoxamine (250 mg/day) plus MPH-ER (36 mg/day); group two received fluvoxamine (250 mg/day) plus identical placebo tablets. All participants were followed for eight weeks. Improvement in the Y-BOCS total score and Y-BOCS obsession subscale score was more prominent in the fluvoxamine plus MPH-ER group compared with those receiving placebo [103].

Psilocybin, cannabis, nicotine, and morphine for treatment of OCD were the subject of a systematic review of 16 observational and interventional studies. While the overall results were promising and showed a reduction in Y-BOCS scores, the authors concluded that further research and clinical trials are needed [104]. There is some evidence supporting augmentation with a second-generation antipsychotic (e.g., risperidone, paliperidone, aripiprazole); however, the use of these agents for OCD is off-label [59,105].

Several other experimental treatments have been investigated. Cingulotomy, anterior capsulotomy, subcaudate tractotomy, limbic leucotomy, and deep brain stimulation may have benefit for select patients with severe OCD who do not respond to less invasive treatment [36,106]. However, best practice for these procedures has not been established, and the risk of serious adverse effects, including seizures, apathy, and executive dysfunction, must be weighed carefully against the potential benefit. There is conflicting evidence for transcranial magnetic stimulation (TMS), with some trials showing improvement while others show no effect. A 2003 Cochrane review concluded that there was too little evidence to draw conclusions about the usefulness of this treatment [107]. More recent analyses confirm that additional research, using large controlled trials, is needed to determine the usefulness of TMS for the treatment of OCD [49,108,109,110].

9. CONCLUSION

OCD is a potentially debilitating illness that affects work, interpersonal relationships, and overall quality of life. In spite of straightforward criteria, evidence shows that the diagnosis is frequently missed. Varied presentations, comorbidities, and patients' own hesitation to discuss symptoms can cloud the diagnosis. Physicians must be familiar with the diagnostic criteria and with the variations in presentation in order to identify patients with OCD.

First-line therapies for OCD will relieve symptoms in some patients and provide partial improvement in others; however, some patients will prove to have illness that is refractory to established treatments. Changing or augmenting therapy, as according to recommendations in the APA guideline, can be helpful when initial therapy provides only partial improvement or no improvement at all. Patients with severe or treatment-refractory OCD should generally be referred to specialty care.

Although treating OCD can be challenging, recognition and appropriate care of this disorder can help a great many patients, reducing or even eliminating disability and improving their overall quality of life.

10. RESOURCES

American Psychiatric Association

https://www.psychiatry.org

Medical specialty society concerned with ensuring humane care and effective treatment for all persons with mental disorders.

American Psychological Association

https://www.apa.org

An association of professional psychologists actively involved in basic psychological research, applied research, and the treatment of psychological and mental disorders.

Anxiety and Depression Association of America

https://adaa.org

National nonprofit organization including clinicians, researchers, and consumers concerned with informing the public, healthcare professionals, and media about anxiety disorders.

Association for Behavioral and Cognitive Therapies

https://www.abct.org

An interdisciplinary organization for the scientific study of problems that may be treated by behavioral and/or cognitive therapies.

Behavioral Health Treatment Services Locator

https://findtreatment.gov

A service of the Substance Abuse and Mental Health Services Administration, part of the U.S. Department of Health and Human Services, that provides a listing of local mental health services throughout the United States and its territories.

National Institute of Mental Health

https://www.nimh.nih.gov

A division of the National Institutes of Health, a component of the U.S. Department of Health and Human Services, with the goal of improving the understanding and treatment of mental illnesses through basic and clinical research.

International OCD Foundation

https://iocdf.org

International not-for-profit organization offering education and support to people with OCD and supporting medical research and education about OCD and related disorders.

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79. Kamijima K, Murasaki M, Asai M, et al. Paroxetine in the treatment of obsessive-compulsive disorder: randomized, double-blind, placebo-controlled study in Japanese patients. Psychiatry Clin Neurosci. 2004;58(4):427-433.

80. Hollander E, Koran LM, Goodman WK, et al. A double-blind, placebo-controlled study of the efficacy and safety of controlled-release fluvoxamine in patients with obsessive-compulsive disorder. J Clin Psychiatry. 2003;64(6):640-647.

81. Kronig MH, Apter J, Asnis G, et al. Placebo-controlled, multicenter study of sertraline treatment for obsessive-compulsive disorder.J Clin Psychopharmacol. 1999;19(2):172-176.

82. Greist JH, Jefferson JW, Kobak KA, et al. A 1-year double-blind placebo-controlled fixed dose study of sertraline in the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol. 1995;10(2):57-65.

83. Montgomery SA, McIntyre A, Osterheider M, et al. A double-blind, placebo-controlled study of fluoxetine in patients with DSM-III-R obsessive-compulsive disorder. Eur Neuropsychopharmacol. 1993;3(2):143-152.

84. Tollefson GD, Rampey AH, Potvin JH, et al. A multicenter investigation of fixed-dose fluoxetine in the treatment of obsessive-compulsive disorder. Arch Gen Psychiatry. 1994;51(7):559-567.

85. Maneeton N, Maneeton B, Karawekpanyawong N, Woottiluk P, Putthisri S, Srisurapanon M. Fluoxetine in acute treatment of children and adolescents with obsessive-compulsive disorder: a systematic review and meta-analysis. Nord J Psychiatry. 2020;74(7):461-469.

86. Montgomery SA, Kasper S, Stein DJ, Hedegarrd KB, Lemming OM. Citalopram 20 mg, 40 mg, and 60 mg are all effective and well tolerated compared with placebo in obsessive-compulsive disorder. Int Clin Psychopharmacol. 2001;16(2):75-86.

87. US Food and Drug Administration. FDA Drug Safety Communication: Abnormal Heart Rhythms Associated With High Doses of Celexa (Citalopram Hydrobromide). Available at https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-abnormal-heart-rhythms-associated-high-doses-celexa-citalopram. Last accessed April 9, 2024.

88. U.S. Food and Drug Administration. FDA Drug Safety Communication: Revised Recommendation for Celexa (Citalopram Hydrobromide) Related to the Potential Risk of Abnormal Heart Rhythms with High Doses. Available at https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-revised-recommendations-celexa-citalopram-hydrobromide-related. Last accessed April 9, 2024.

89. Stein DJ, Andersen EW, Tonnoir B, Fineberg N. Escitalopram in obsessive-compulsive disorder: a randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study. Curr Med Res Opin. 2007;23(4):701-711.

90. Greist JH, Bandelow B, Hollander E, et al. WCA recommendations for the long-term treatment of obsessive-compulsive disorder in adults. CNS Spectr. 2003;8(S1):7-16.

91. Foa EB, Liebowitz MR, Kozak MJ, et al. Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry. 2005;162(1):151-161.

92. Greist JH, Marks IM, Baer L, et al. Behavior therapy for obsessive-compulsive disorder guided by a computer or by a clinician compared with relaxation as a control. J Clin Psychiatry. 2002;63(2):138-145.

93. Gava I, Barbui C, Aguglia E, et al. Psychological treatments versus treatment as usual for obsessive compulsive disorder (OCD). Cochrane Database Syst Rev. 2007;(2):CD005333.

94. Foster PS, Eisler RM. An integrative approach to the treatment of obsessive-compulsive disorder. Compr Psychiatry. 2001;42(1): 24-31.

95. Feusner JD, Farrell NR, Kreyling J, et al. Online video teletherapy treatment of obsessive-compulsive disorder using exposure and response prevention: clinical outcomes from a retrospective longitudinal observational study. J Med Internet Res. 2022;24(5):e36431.

96. Rezaee R, Parsa Z, Ahmadzadeh L, Ahmadian L, Avazzadeh S, Marzaleh MA. Self-help application for obsessive-compulsive disorder based on exposure and response prevention technique with prototype design and usability evaluation: a cross-sectional study.Health Sci Rep. 2023;6(9):e1577.

97. Conlan L, Heyman I. Helping patients to overcome obsessive compulsive disorder. Practitioner. 2007;251(1700):57, 59, 61.

98. Bolton D, Perrin S. Evaluation of exposure with response-prevention for obsessive compulsive disorder in childhood and adolescence.J Behav Ther Exp Psychiatry. 2008;39(1):11-22.

99. Gomes JB, Cordioli AV, Heldt E. Obsessive-compulsive disorder and family accommodation: a 3-year follow-up. Psychiatry Res. 2017;253:107-109.

100. Garcia AM, Sapyta JJ, Moore PS, Freeman JB, Franklin ME, March JS, Foa EB. Predictors and moderators of treatment outcome in the pediatric obsessive compulsive treatment study (POTS I). J Am Acad Child Adolesc Psychiatry. 2010;49:1024-1033.

101. Koran LM, Aboujaoude E, Bullock KD, Franz B, Gamel N, Elliott M. Double-blind treatment with oral morphine in treatment-resistant obsessive-compulsive disorder. J Clin Psychiatry. 2005;66(3):353-359.

102. Pallanti S, Quercioli L, Koran LM. Citalopram intravenous infusion in resistant obsessive-compulsive disorder: an open trial. J Clin Psychiatry. 2002;63(9):796-801.

103. Zheng H, Jia F, Han H, et al. Combined fluvoxamine and extended-release methylphenidate improved treatment response compared to fluvoxamine alone in patients with treatment-refractory obsessive-compulsive disorder: a randomized double-blind, placebo-controlled study. Eur Neuropsychopharmacol. 2019;29(3):397-404.

104. Khan I, Jaura TA, Tukruna A, et al. Use of selective alternative therapies for treatment of OCD. Neuropsychiatr Dis Treat. 2023;19:721-732.

105. Brakoulias V, Stockings E. A systematic review of the use of risperidone, paliperidone and aripiprazole as augmenting agents for obsessive-compulsive disorder. Expert Opin Pharmacother. 2019;20:47-53.

106. Lipsman N, Neimat JS, Lozano AM. Deep brain stimulation for treatment-refractory obsessive-compulsive disorder: the search for a valid target. Neurosurgery. 2007;61(1):1-11.

107. Martin JLR, Barbanoj MJ, Pérez V, Sacristán M. Transcranial magnetic stimulation for the treatment of obsessive-compulsive disorder. Cochrane Database Syst Rev. 2003;(3):CD003387.

108. Blom RM, Figee M, Vulink N, Denys D. Update on repetitive transcranial magnetic stimulation in obsessive-compulsive disorder: different targets. Curr Psychiatry Rep. 2011;13(4):289-294.

109. Jaafari N, Rachid F, Rotge JY, et al. Safety and efficacy of repetitive transcranial magnetic stimulation in the treatment of obsessive-compulsive disorder: a review. World J Biol Psychiatry. 2012;13(3):164-177.

110. Berlim MT, Neufeld NH, Van den Eynde F. Repetitive transcranial magnetic stimulation (rTMS) for obsessive-compulsive disorder (OCD): an exploratory meta-analysis of randomized and sham-controlled trials. J Psychiatr Res. 2013;47(8):999-1006.

Evidence-Based Practice Recommendations Citations

1. American Psychiatric Association. Practice Guideline for the Treatment of Patients with Obsessive-Compulsive Disorder. Arlington, VA: American Psychiatric Association; 2007. Available at https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/ocd.pdf. Last accessed April 19, 2024.

66564 • Alcohol and Alcohol Use Disorder

Mark S. Gold, MD, DFASAM, DLFAPA

www.netce.com

Copyright © 2024 NetCE, All rights reserved.

No substance, legal or illegal, has a more paradoxical mythology than alcohol. It is undeniably one of the most widely and safely used intoxicants in the world; however, it is also potent and dangerous, both from a psychologic and physiologic viewpoint. Alcohol is currently responsible for more deaths and personal destruction than any other known substance of abuse, with the exception of tobacco. All of this is known with scientific certainty. Alcohol is legal, easily obtained, and supported by a multi-billion-dollar worldwide industry. Alcohol consumption reduces social inhibitions and produces pleasure and a sense of well-being. It also can have some rather impressive positive medical effects, such as a reduced risk of cardiovascular disease. This course will include core competencies related to alcohol use and abuse as well as knowledge, assessment, and treatment-based competencies.

Table of Contents

66564 • Alcohol and Alcohol Use Disorder

Course Overview

Audience

Accreditations & Approvals

Designations of Credit

Course Objective

Learning Objectives

Faculty

Faculty Disclosure

Division Planner

Division Planner Disclosure

Director of Development and Academic Affairs

Director Disclosure Statement

About the Sponsor

Disclosure Statement

Implicit Bias in Health Care

1. INTRODUCTION

SUBSTANCE ABUSE AND ADDICTION

2. HISTORY

3. CURRENT ESTIMATES OF ALCOHOL USE

COSTS OF ALCOHOL USE DISORDERS

DEFINITIONS

4. BENEFITS

WHAT TO ADVISE PATIENTS ABOUT DRINKING ALCOHOL

5. RISK AND PROTECTIVE FACTORS

ALCOHOL AND GENETICS

PSYCHOLOGICAL AND SOCIOENVIRONMENTAL RISK FACTORS MODELS

KNOWN RISK FACTORS FOR ALCOHOL USE DISORDER

ABUSE AND ADVERSE CONDITIONS IN THE HOME

PROTECTIVE FACTORS

6. ALCOHOL USE DISORDER

WITHDRAWAL

INCREASED TOLERANCE

IMPAIRED CONTROL OF DRINKING

PREOCCUPATION WITH ALCOHOL

USE OF ALCOHOL DESPITE ADVERSE CONSEQUENCES

DENIAL AS A DEFENSE MECHANISM

RELAPSE

PHYSICAL CLUES THAT MAY SUGGEST ALCOHOL USE DISORDER

7. COMPLICATIONS

LIVER DISEASE

ALCOHOL/ACETAMINOPHEN INTERACTION

CARDIOVASCULAR DISORDERS

CANCER

GASTROINTESTINAL DISORDERS

CHRONIC PANCREATITIS

BODY WEIGHT

MALNUTRITION

INFECTIOUS DISEASES

SLEEP DISORDERS

NERVOUS SYSTEM DYSFUNCTION

COMPLICATIONS SPECIFIC TO WOMEN

EFFECTS ON FAMILIES

VIOLENCE

TRAFFIC ACCIDENTS

8. OTHER PSYCHIATRIC DISORDERS ASSOCIATED WITH ALCOHOL USE DISORDERS

DEPRESSIVE DISORDERS

BIPOLAR DISORDER

ANXIETY

PAIN

ABUSE/DEPENDENCE ON OTHER DRUGS

EATING DISORDERS

PATHOLOGIC GAMBLING

SEXUAL DYSFUNCTION

9. DETECTING ALCOHOL USE DISORDERS

RECOMMENDED STANDARDIZED QUESTIONS OR TESTS

ADDITIONAL STANDARDIZED QUESTIONS OR TESTS

SCREENING FOR ALCOHOL ABUSE IN NON-ENGLISH-PROFICIENT PATIENTS

LABORATORY TESTS

10. BRIEF INTERVENTION

COMMON ELEMENTS OF BRIEF INTERVENTION

EFFECTIVENESS OF BRIEF INTERVENTION

READINESS TO CHANGE

11. TREATMENT

PHASES OF TREATMENT

ALCOHOLICS ANONYMOUS AND OTHER 12-STEP PROGRAMS

COUNSELING

MEDICATIONS USED TO TREAT ALCOHOL USE DISORDER

TREATMENT OF ALCOHOL WITHDRAWAL

MANDATORY TREATMENT

12. CONCLUSION

13. RESOURCES

Works Cited

Evidence-Based Practice Recommendations Citations

66564 • Alcohol and Alcohol Use Disorder

Education Category. Psychiatric / Mental Health

Release Date. 06/01/2024

Expiration Date. 05/31/2027

Course Overview

No substance, legal or illegal, has a more paradoxical mythology than alcohol. It is undeniably one of the most widely and safely used intoxicants in the world; however, it is also potent and dangerous, both from a psychologic and physiologic viewpoint. Alcohol is currently responsible for more deaths and personal destruction than any other known substance of abuse, with the exception of tobacco. All of this is known with scientific certainty. Alcohol is legal, easily obtained, and supported by a multi-billion-dollar worldwide industry. Alcohol consumption reduces social inhibitions and produces pleasure and a sense of well-being. It also can have some rather impressive positive medical effects, such as a reduced risk of cardiovascular disease. This course will include core competencies related to alcohol use and abuse as well as knowledge, assessment, and treatment-based competencies.

Audience

This intermediate course is designed for psychologists involved in the treatment or care of patients who consume alcohol.

Accreditations & Approvals

Continuing Education (CE) credits for psychologists are provided through the co-sponsorship of the American Psychological Association (APA) Office of Continuing Education in Psychology (CEP). The APA CEP Office maintains responsibility for the content of the programs. NetCE is recognized by the New York State Education Department's State Board for Psychology as an approved provider of continuing education for licensed psychologists #PSY-0240. This course is considered self-study by the New York State Board for Psychology.

Designations of Credit

NetCE designates this continuing education activity for 10 credit(s).

Course Objective

The purpose of this course is to address the ongoing alcohol competency educational needs of practicing psychologists. The material will include core competencies as well as knowledge, assessment, and treatment-based competencies.

Learning Objectives

Upon completion of this course, you should be able to:

1. Review facts about the history, costs, and prevalence of alcohol use and abuse.

2. Define moderate drinking and take a history of alcohol use as defined by the standard drink equivalency.

3. Identify benefits reported in the literature for moderate alcohol consumption.

4. Distinguish between genetic and environmental risk and protective factors for developing alcohol problems.

5. Describe clinical characteristics of alcohol use disorder, intoxication, and withdrawal.

6. List complications associated with alcohol use disorders.

7. Recognize mental health diagnoses associated with alcohol use disorders.

8. Discuss screening instruments for detecting alcohol use disorders, including considerations for non-English-proficient patients.

9. Explain brief intervention efficacy and techniques.

10. Describe and evaluate treatment modalities.

Faculty

Mark S. Gold, MD, DFASAM, DLFAPA, is a teacher of the year, translational researcher, author, mentor, and inventor best known for his work on the brain systems underlying the effects of opiate drugs, cocaine, and food. Dr. Gold was a Professor, Eminent Scholar, Distinguished Professor, Distinguished Alumni Professor, Chairman, and Emeritus Eminent Scholar during his 25 years at the University of Florida. He was a Founding Director of the McKnight Brain Institute and a pioneering neuroscience-addiction researcher funded by the NIH-NIDA-Pharma, whose work helped to de-stigmatize addictions and mainstream addiction education and treatment. He also developed and taught courses and training programs at the University of Florida for undergraduates and medical students.

He is an author and inventor who has published more than 1,000 peer-reviewed scientific articles, 20 text books, popular-general audience books, and physician practice guidelines. Dr. Gold was co-inventor of the use of clonidine in opioid withdrawal and the dopamine hypothesis for cocaine addiction and anhedonia. Both revolutionized how neuroscientists and physicians thought about drugs of abuse, addiction, and the brain. He pioneered the use of clonidine and lofexidine, which became the first non-opioid medication-assisted therapies. His first academic appointment was at Yale University School of Medicine in 1978. Working with Dr. Herb Kleber, he advanced his noradrenergic hyperactivity theory of opioid withdrawal and the use of clonidine and lofexidine to ameliorate these signs and symptoms. During this time, Dr. Gold and Dr. Kleber also worked on rapid detoxification with naloxone and induction on to naltrexone.

Dr. Gold has been awarded many state and national awards for research and service over his long career. He has been awarded major national awards for his neuroscience research including the annual Foundations Fund Prize for the most important research in Psychiatry, the DEA 30 Years of Service Pin (2014), the American Foundation for Addiction Research’s Lifetime Achievement Award (2014), the McGovern Award for Lifetime Achievement (2015) for the most important contributions to the understanding and treatment of addiction, the National Leadership Award (NAATP) from addiction treatment providers for helping understand that addiction is a disease of the brain, the DARE Lifetime Achievement Award for volunteer and prevention efforts, the Silver Anvil from the PR Society of America for anti-drug prevention ads, the PRIDE and DARE awards for his career in research and prevention (2015), and the PATH Foundation’s Lifetime Achievement Award (2016) as one of the “fathers” of addiction medicine and MAT presented to him by President Obama’s White House Drug Czar Michael Botticelli. He was awarded Distinguished Alumni Awards at Yale University, the University of Florida, and Washington University and the Wall of Fame at the University of Florida College of Medicine. Gold was appointed by the University President to two terms as the University’s overall Distinguished Professor, allowing him to mentor students and faculty from every college and institute. The University of Florida College of Medicine’s White Coat Ceremony for new medical students is named in his honor.

Since his retirement as a full-time academic in 2014, Dr. Gold has continued his teaching, mentoring, research, and writing as an Adjunct Professor in the Department of Psychiatry at Washington University and an active member of the Clinical Council at the Washington University School of Medicine’s Public Health Institute. He regularly lectures at medical schools and grand rounds around the country and at international and national scientific meetings on his career and on bench-to-bedside science in eating disorders, psychiatry, obesity, and addictions. He continues on the Faculty at the University of Florida College of Medicine, Department of Psychiatry as an Emeritus Distinguished Professor. He has traveled extensively to help many states develop prevention, education, and treatment approaches to the opioid crisis.

Faculty Disclosure

Contributing faculty, Mark S. Gold, MD, DFASAM, DLFAPA, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Margaret Donohue, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Director of Development and Academic Affairs

Sarah Campbell

Director Disclosure Statement

The Director of Development and Academic Affairs has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Implicit Bias in Health Care

The role of implicit biases on healthcare outcomes has become a concern, as there is some evidence that implicit biases contribute to health disparities, professionals' attitudes toward and interactions with patients, quality of care, diagnoses, and treatment decisions. This may produce differences in help-seeking, diagnoses, and ultimately treatments and interventions. Implicit biases may also unwittingly produce professional behaviors, attitudes, and interactions that reduce patients' trust and comfort with their provider, leading to earlier termination of visits and/or reduced adherence and follow-up. Disadvantaged groups are marginalized in the healthcare system and vulnerable on multiple levels; health professionals' implicit biases can further exacerbate these existing disadvantages.

Interventions or strategies designed to reduce implicit bias may be categorized as change-based or control-based. Change-based interventions focus on reducing or changing cognitive associations underlying implicit biases. These interventions might include challenging stereotypes. Conversely, control-based interventions involve reducing the effects of the implicit bias on the individual's behaviors. These strategies include increasing awareness of biased thoughts and responses. The two types of interventions are not mutually exclusive and may be used synergistically.

1. INTRODUCTION

No substance, legal or illegal, has a more paradoxical mythology than alcohol. It is undeniably one of the most widely and safely used intoxicants in the world; however, it is also potent and dangerous, both from a psychological and a physiologic viewpoint. Alcohol is currently responsible for more deaths and personal destruction than any other known substance of abuse, with the exception of tobacco. All of this is known with scientific certainty. Alcohol is legal, easily obtained, and supported by a multi-billion-dollar worldwide industry. Alcohol consumption at reasonable doses reduces social inhibitions and produces pleasure and a sense of well-being. It also can have some rather impressive positive medical effects, such as a reduced risk of cardiovascular disease[1,2].

SUBSTANCE ABUSE AND ADDICTION

Alcohol is defined as a substance of abuse by self-administration in lab animals and man. All drugs of abuse affect the brain's reward pathways. The effects of alcohol appear to be related to complex multiple interactions with the dopamine, gamma-aminobutyric acid (GABA), serotonin, opioid, and N-methyl-D aspartate (NMDA) neurotransmitter systems [3,4]. Studies suggest that the reinforcing effect of alcohol is partially mediated through nicotinic receptors in the ventral tegmental area, which when combined with nicotine may be a factor in the high incidence of smoking among those with alcohol use disorder [5,6,7]. Alcohol, food, and other drugs of abuse have similar effects on dopamine receptors. The development of addiction, including to alcohol, is affected by genetic predisposition and influenced by alterations in the rewarding chemicals released per dose.

Substances of abuse are often put into categories based on their effects. Alcohol has effects similar to other depressants. Characteristics include:

- Decreased cognitive function while intoxicated

- Decreased inhibition and increased impulsivity

- Risk of overdose

- Development of depressive symptoms in heavy users

- Withdrawal symptoms similar to other depressants

- Symptoms of anxiety during withdrawal

- Substance-induced psychoses in some heavy users

The established criteria for the diagnosis of alcohol abuse and dependence will be discussed in detail later in this course.

2. HISTORY

From the earliest days of colonial settlement to the present, Americans have been drinking alcohol. The early American experience with alcohol provides a glimpse of patterns of use, as well as controversies involving alcohol. The argument could be made that alcohol, in one form or another, was used more in early revolutionary America than it is today. Drinking had almost religious support, with alcohol portrayed as a gift from God; a gift that could be abused by excessive drinking or drunkenness.

The story of alcohol in America begins with the Mayflower. The Mayflower dropped anchor in Plymouth, Massachusetts, in February 1621. The passengers were out of beer, and the crew was in no mood to share. Running out of beer or spirits was no laughing matter. So seriously did the crew take this lack of spirits that they quickly dropped the passengers off the Mayflower into very harsh conditions at Plymouth. This preference for beer was at least partly because it was a reliable source of nonpathogenic hydration, as bacteria and parasites are killed during the boiling stage of brewing.

In 1741, Benjamin Franklin, when listing the thirteen cardinal virtues, started with "Temperance: Drink not to elevation." Still, he noted that beer, applejack, and other alcohol-containing beverages of the day were safer to drink than the water in Boston or Philadelphia. Like Londoners, the colonists drank beer with breakfast after a sherry eye-opener, and drank beer at lunch and brandy if it was cold. They would have wine with dinner and punch or other liqueurs thereafter. Dr. Benjamin Rush, a signer of the Declaration of Independence who is also known as the father of American psychiatry, became alarmed by what he viewed as rampant health problems caused by alcohol and called for temperance. He described addiction and identified alcohol as an addictive substance. He argued that addiction was like a disease, and that the alcoholic victim was completely unable to control his consumption. Dr. Rush, a citizen of the Enlightenment Age, accurately described and anticipated the fifth revised edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) description of alcohol use disorder. However, he also suggested that alcoholism could be treated by whippings, bleeding, shame, emetics, oaths, and plunging the patient in cold water.

American attitudes about alcohol have flip-flopped from a free marketplace in the 18th and 19th centuries, to Prohibition in the 1920s, to the repeal of Prohibition in the 1930s, to lowering of the legal drinking age in most states during the late 1960s and early 1970s, and a return to the 21-years-of-age limit with the National Minimum Drinking Age Act of 1984. Alcohol consumption tends to be high during war years and was lowest during the Great Depression [8]. It was very high in the early 1980s, perhaps due to the lowered drinking age and poor economy. Like other consumer goods, alcohol consumption is generally inversely affected by changes in taxes and prices [9]. But interesting trends have been noted in the United States. While inflation-adjusted prices of alcohol declined between the late 1970s through the late 1990s, per capita alcohol consumption has also been declining since the mid-1980s [8,10]. One study revealed that changing demographics, such as a shift to an older population that consumes less alcohol, could have more of an impact on consumption levels than falling prices. Other sources cite increased health awareness, national drunk-driving campaigns, and a less tolerant public attitude toward heavy drinking and youth intoxication [8].

This roller coaster of historical attitudes toward alcohol use results from conflicting sociologic and psychological factors. For centuries, alcohol has been part of our social fabric and part of holidays and traditions. Simultaneously, our society has either shunned or punished those who succumbed to alcohol abuse, treating dependence as a legal issue or a moral failing rather than as a mental health problem. On one hand, alcohol is readily and cheaply accessible, safe for most people, moderately beneficial to health, and an important sector of our economy. However, we also understand that some individuals are at a high risk of losing control over alcohol.

3. CURRENT ESTIMATES OF ALCOHOL USE

As many as 90% of adults in the United States have had some experience with alcohol [11]. People drink alcohol for a variety of reasons:

- The pleasurable feeling that often accompanies drinking, including reduced tension and/or anxiety

- Enjoyment of the taste

- Social inclusion

- Self-medication

- Peer pressure

- Behavioral and physical addiction

Nearly one-half (47.4%) of all Americans older than 12 years of age reported being current consumers of alcohol in the 2022 National Survey on Drug Use and Health [12]. This translates to an estimated 137.5 million people, slightly less than the 2019 estimate of 139.7 million people [12]. An estimated 21.7% of Americans participated in binge drinking at least once in the 30 days prior to the survey. This represents approximately 61.1 million people. Heavy drinking was reported by 5.7% of the population 18 years of age and older (16.0 million people) [12]. The 2022 estimates for binge and heavy drinking are lower than the 2019 estimates [12].

There is some evidence that drinking and alcohol-related injuries increased during the COVID-19 pandemic [13]. National mortality data revealed a 25% increase in alcohol-related deaths from 2019 to 2020, outpacing the all-cause increase in mortality over the same period (16.6%).

Binge drinking among various races is 10.9% for Asian Americans, 21.3% for Black Americans, 26.5% for persons reporting two or more races, 22.2% for White Americans, and 23.1% for Hispanic Americans [12].

Use of alcohol is higher for college graduates compared to those with only a high school diploma (66.2% and 33.8%, respectively) [12]. However, binge and heavy use is slightly higher for young adults 18 years of age and older who have not completed college [12]. The pattern of higher rates of current alcohol use, binge alcohol use, and heavy alcohol use among full-time college students, compared with rates for others 18 to 22 years of age, has remained consistent since 2002 [14]. In a 2002 study of alcohol use on college campuses, researchers at Harvard University reported that of the more than 14,000 students surveyed, 31% met the criteria for alcohol abuse and an additional 6% met the criteria for diagnosis of alcohol dependence [15]. In the study, alcohol abuse was defined as a positive response to any one of the four abuse criteria and the absence of dependence. Alcohol dependence was defined as a positive response to any three or more of seven dependence criteria. Percentages of students meeting specific alcohol abuse and dependence criteria are presented in Figure 1[15]. Male students are at greater risk than female students. Almost 10% of male students and 5% of female college students younger than 24 years of age met the criteria for a 12-month diagnosis of alcohol dependence [15].

Figure 1: PERCENTAGE OF COLLEGE STUDENTS MEETING SPECIFIC ABUSE AND DEPENDENCE CRITERIA

Source: [15]

About 40% of people who drink have experienced an alcohol-related problem [11]. Between 3% and 8% of women and 10% to 15% of men will develop alcohol use disorder at some point in their lives. While alcohol use disorders can develop at any age, repeated intoxication at an early age increases the risk of developing an alcohol use disorder [11]. Usually, dependence develops in the mid-twenties through age forty.

COSTS OF ALCOHOL USE DISORDERS

The National Institute on Drug Abuse (NIDA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) estimated that the annual economic cost of alcohol and drug abuse was $365.4 billion in 1998 [9]. This estimate represents roughly $1,350 each year for every man, woman, and child living in the United States. Alcohol use disorders generated about half of the estimated costs ($184.6 billion). This figure rose to $249 billion in 2010, representing approximately $807 for every man, woman, and child living in the United States [16].

Nearly three-fourths (72%) of the costs of alcohol abuse are related to lost workplace productivity ($179 billion); 11% are related to healthcare expenses for treating problems caused by excessive drinking ($28 billion); 10% are law enforcement and other criminal justice expenses ($25 billion); and 5% are losses from motor vehicle crashes related to excessive alcohol use ($13 billion) [16]. Binge drinking is responsible for the majority of the cost at $191 billion [16]. Alcohol use disorder generally reduces the lifespan by 15 years [11]. Approximately $99.6 billion of the total costs of alcohol abuse is paid by federal, state, and local governments [16]. When both direct and indirect costs are included, the estimated annual cost of alcohol-related problems alone may be much greater [16].

DEFINITIONS

Tolerance: Either (1) a need for markedly increased amounts of the substance to achieve intoxication or desired effect; or (2) a markedly diminished effect with continued use of the same amount of the substance [17].

A Standard Drink: 1.5 ounces of 80-proof distilled spirits, 5 ounces of table wine, or 12 ounces of standard beer [18,19].

Alcohol Intoxication: Clinically significant problematic behavioral or psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment) that developed during, or shortly after, alcohol ingestion [17]. Changes include slurred speech, loss of coordination, unsteady walking or running, impairment of attention or memory, nystagmus, stupor, or coma.

Alcohol Withdrawal: The presence of certain symptoms after stopping or reducing heavy and prolonged alcohol use [17]. The symptoms of alcohol withdrawal may develop within a few hours to a few days after stopping or reducing use and symptoms cause significant physical and emotional distress in social, occupational, or other important areas of functioning. Symptoms include increased hand tremor, sweating, increased pulse rate, nausea, vomiting, insomnia, temporary hallucinations or illusions, anxiety, psychomotor agitation, and generalized tonic-clonic seizures. Fewer than 5% of persons who develop alcohol withdrawal experience severe symptoms such as seizures and death [20].

Blood Alcohol Concentration (BAC): The percentage of alcohol present in the bloodstream. The BAC is usually what is measured by police officers to determine legal intoxication. It can be measured directly from a blood sample or a breath sample collected by a "Breathalyzer." The national legal limit for intoxication is a BAC of 0.08.

Moderate Drinking: No more than one drink per day for women and no more than two drinks per day for men [19].

Current Use: At least one drink in the past 30 days [16].

Binge Drinking: Consuming five or more drinks on the same occasion in the past 30 days [16,19].

Heavy Drinking: Five or more drinks on the same occasion on each of 5 or more days in the past 30 days [16].

Fetal Alcohol Syndrome (FAS): A severe fetal alcohol spectrum disorder (FASD), FAS is a lifelong syndrome in children with confirmed prenatal exposure to alcohol. Signs include growth deficiencies, facial abnormalities, and neurocognitive deficits that may lead to problems with vision, hearing, attention, learning, memory, or any combination thereof [21]. There is no safe recommended level of alcohol use in pregnancy.

4. BENEFITS

Alcohol is consumed sensibly by the vast majority, but it can also be a cause of considerable damage and death when used excessively. Alcohol is part of many cultures, and most individuals learn from their bad experiences to moderate their drinking. Consequently, the majority of people do not have accidents or develop alcohol use disorder. Additionally, data suggests that moderate consumption of alcohol does have some health benefits.

The French consume large amounts of wine and high-cholesterol foods, yet they have a low incidence of heart disease. The Japanese drink large amounts of sake, but eat basically low-cholesterol foods and have a low incidence of heart disease. Other cultures traditionally drink whiskey and beer. Should we be drinking more, more regularly, or less on both counts?

Data for health benefits associated with low-to-moderate drinking appear to be common in many medical journals [22]. Light-to-moderate alcohol intake from beer, wine, or spirits is associated with a reduction in all-cause mortality, possibly due to its ability to decrease cardiovascular diseases, especially coronary heart disease (CHD). The relationship between alcohol intake and reduced risk of coronary disease is generally accepted as a U-shaped curve of low-dose protective effect and higher doses producing a loss of protective effects and increased all-cause deaths [23,24,25,26,27,28,29,30]. The World Health Organization (WHO) reported that there is convincing evidence that low-to-moderate alcohol intake decreases risk for heart disease [31].

Many researchers have replicated the finding that moderate alcohol consumption is associated with a reduced risk of coronary artery disease, peripheral artery disease, sudden death, and stroke and suggest that this effect is to a large extent mediated by increases in high-density lipoproteins (HDLs) [1]. A 2011 meta-analysis inclusive of 84 out of 4,235 studies on the benefits of alcohol concluded that the lowest risk of CHD mortality was conferred by one to two drinks per day and that the lowest stroke mortality risk was conferred by consuming one or fewer drinks per day [2]. Research suggests that the protective effect may be a result of an interaction between diet and genetics, specifically related to a genetic variation in alcohol dehydrogenase (ADH) [32]. Moderate drinkers who are homozygous for the slow-oxidizing ADH3 allele have higher HDL levels and a substantially decreased risk of myocardial infarction [32]. An acute protective effect of alcohol consumption was also found for regular drinkers who consumed one or two drinks in the 24 hours preceding the onset of cardiac symptoms. Risk of a major coronary event is lowest among men who report daily drinking and among women who report one or two drinks daily. Alcohol does have effects on several markers for coronary risk factors, such as blood pressure, HDL cholesterol, low-density-lipoprotein (LDL) cholesterol, fibrinogen, clotting factors, and insulin sensitivity.

Prescribing alcohol to patients is not recommended, but research should continue in an attempt to identify the beneficial effects of alcohol alone. The psychiatric and other medical costs associated with drinking should be considered. Epidemiologists and other researchers are weighing the benefits of moderate alcohol consumption against the risks of addiction and accidents.

Alcohol clearly causes detrimental effects on a number of critical organs and systems in the human body when taken in large doses over time. Excessive alcohol consumption increases cardiovascular risk factors and mortality. Alcohol abuse is often considered the second most common cause of preventable death in the United States [33]. However, light-to-moderate drinking may protect against ischemic stroke and abstaining from alcohol may increase the risk of stroke [2]. A prospective study of moderate alcohol consumption and risk of peripheral arterial disease in U.S. male physicians found that any alcohol consumption decreases the risk of peripheral artery disease [1]. No evidence exists for a reduction in cardiovascular mortality in anyone younger than 40 years of age. Because almost no one dies of coronary artery disease before age 40, the studies to see if drinking in individuals younger than 40 years of age is particularly protective in later life have yet to be done.

Cardiovascular protection occurs primarily through blood lipids such as HDL, especially HDL subfraction 2 [1]. Moderate alcohol consumption inhibits platelets, especially after a fatty meal, suggesting an aspirin-like effect for moderate alcohol consumption [34]. Alcohol's effects on clotting appear to be related to the findings that drinking reduces acute heart attack risk. Certain alcoholic beverages, namely red wine, may also have an additional positive antioxidant effect as it contains flavonoids, which possibly slow oxidation of unsaturated fatty acids [35]. Additionally, low amounts of drinking can also enhance insulin sensitivity, reduce fasting insulin, and may also reduce stress.

Risk-to-benefit analysis should take into account a person's age, sex, family history, likelihood of an adverse effect on blood pressure, cancer risk, medication interaction, accidents, and dependency. Light-to-moderate alcohol consumption reduces overall risk of ischemic stroke; however, greater alcohol consumption has no additional benefit and can be harmful [2].

It has been questioned whether the cardiac protective effects can be easily generalized to women, in whom the risk of breast cancer complicates alcohol risks. For example, the consumption of seven or more drinks per week is associated with a twofold increase in postmenopausal hormone-sensitive breast cancers; however, several studies have shown that moderate alcohol consumption reduces the mortality of breast cancer [36,37,38]. It should also not be forgotten that alcohol increases the risk of certain other cancers (e.g., liver, mouth, esophageal, laryngeal, pharyngeal) that affect both men and women. Multiple case-control studies and meta-analyses have reported on the relationship between alcohol and cardiovascular disease and mortality. Many of these studies reported that low-to-moderate alcohol consumption decreases the number of adverse cardiovascular events and deaths when compared with abstinence. Beginning in the early 2000s, the cardioprotective effects of low doses of alcohol were refuted by the results of large epidemiological studies. Since that time, alcohol use is consistently associated with cardiac arrhythmias, dilated cardiomyopathy, arterial hypertension, atherosclerotic vascular disease, and type 2 diabetes [39,40].

Moderate drinking is heart-healthy for diabetics in the same way it is for other people, easing concerns that alcohol may disrupt diabetics' blood-sugar balance. In a 12-year study, diabetics who had one or two drinks daily were up to 80% less likely to die of heart disease than diabetics who did not drink [41]. However, alcohol consumption is a marker for poorer adherence to diabetes self-care behaviors [42,43].

WHAT TO ADVISE PATIENTS ABOUT DRINKING ALCOHOL

Although alcohol appears to have some moderate health benefits, physicians need not alter the drinking habits of those who consume low-to-moderate amounts of alcohol. It is problematic to advise a patient who is abstinent or who drinks infrequently to begin or increase alcohol consumption. In addition, social and religious factors may already dictate the patient's drinking habits.

Vulnerability to alcohol use disorders, depression, and alcohol-related pathologies varies greatly among individuals and cannot always be predicted before a patient begins or escalates drinking. Some individuals may be genetically predisposed to acquiring problems with alcohol use disorder. Similarly, excessive consumption often escapes detection before the onset of related health consequences. The balance of risk to benefit appears to favor encouraging some patients in midlife who are very infrequent drinkers to increase slightly the frequency of drinking. Again, this is debatable and will vary with the individual patient. Consuming alcohol is not the only means to reduce the risk of cardiovascular disease. Exercising, not smoking, lowering fat intake and lipids, and other health-related lifestyle issues should also be addressed.

For those who already have heart disease, it is clear that heavy drinkers should reduce their consumption or abstain and that everyone should avoid heavy and binge drinking. Data does not support advising abstainers with a history of myocardial infarction or decreased left ventricular function to start drinking for their health [44]. In general, moderate drinkers with these conditions should be able to continue to drink alcohol in moderation [44].

Alcohol is not without risks. Alcohol abuse worsens the course of psychiatric disorders. In countries with high alcohol consumption, the suicide rate is also high. One should ask whether the promotion of moderate alcohol consumption, justified on the basis of a biomedical effect (e.g., a reduction in all-cause mortality), might change a patient's quality of life or cause them to take offense. However, existing public educational efforts that target reductions in hazardous and harmful drinking and at the same time encourage drinkers to consume alcohol at responsible levels are appropriate and ethical.

5. RISK AND PROTECTIVE FACTORS

ALCOHOL AND GENETICS

Research has shown that genetic factors play a strong role in whether a person develops alcohol use disorder, accounting for 40% to 60% of the risk [45,46]. In fact, family transmission of alcohol use disorder has been well established. Individuals who have relatives with alcohol use disorder are at three- to five-times greater risk of developing alcohol use disorder than the general population. The presence of alcohol use disorder in one or both biologic parents is more important than the presence of alcohol use disorder in one or both adoptive parents. The genetic risk of alcohol use disorder increases with the number of relatives with alcohol use disorder and the closeness of the genetic relationship [46]. However, most children of parents with alcohol use disorder do not become alcoholics themselves, and some children from families where alcohol is not a problem develop alcohol use disorders when they get older. Alcohol use disorder is seen in twins from alcoholic parents, even when they are raised in environments where there is little or no drinking. Identical twins adopted into households with an alcoholic stepfather do not show more alcohol use disorders than the general population. Children with close biologic relatives with alcohol use disorder, who are adopted into a never drinking, even religiously opposed family, can readily develop alcohol problems [47].

As mentioned previously, genetic factors are thought to account for 40% to 60% of the risk of developing alcohol use disorder [25,46]. Animal studies have shown that genetic factors may be responsible for enhanced brain reward produced by alcohol, decreased initial impairment, or even altered metabolism of alcohol [48,49,50,51,52,53,54].

Genetic factors appear to influence the level of response (LR) to alcohol, as measured by the intensity with which one reacts to a given quantity [55]. The level of response to alcohol varies from individual to individual depending on the tolerance. Low LR at an early age contributes to the risk of alcohol use disorder later in life [55,56].

Genetic differences in metabolic or other biologic processes may play a role in the development of alcohol use disorder in specific individuals. Studies using a self-rated scale have shown consistent results in sons of alcoholic fathers scoring themselves lower than sons of nonalcoholic fathers on feelings of drunkenness, dizziness, drug effect, and sleepiness following alcohol consumption [57]. This suggests that sons of alcoholic fathers have a less intense reaction to alcohol than sons of nonalcoholic fathers. Low reaction to alcohol suggests tolerance and impaired ability to recognize even modest levels of alcohol intoxication, indicators of tendency towards dependence [58,59]. High alcohol sensitivity in men is associated with substantially decreased risk of alcohol use disorder. Understanding reactions to alcohol could establish a better understanding of future risk of developing alcohol use disorder in these men.

Studies have found similar results of higher tolerance for alcohol among daughters of parents with alcohol use disorder. One study examined the drinking patterns of 38 daughters of alcoholics compared with 75 family-history-positive men from the same families and 68 men with no family history of alcohol use disorder [60]. Family-history-positive men and women both displayed low reaction to alcohol. This indicates that the degree of genetic influence on alcohol-related behavior is similar for both men and women with family history of alcohol use disorder. In a study of adolescent and young adult offspring from families where alcohol use disorders are prevalent, researchers found both neurophysiologic and neuroanatomical differences, such as reduced right amygdala volume, when comparing these offspring to controls [61]. Another study assessed the relationship between amygdala and orbitofrontal cortex volumes obtained in adolescence and substance use disorder outcomes in young adulthood among high-risk offspring and low-risk controls [62]. A total of 78 participants 8 to 19 years of age (40 high-risk, 38 low-risk) from a longitudinal family study underwent magnetic resonance imaging. Volumes were obtained with manual tracing. Outcomes were assessed at approximately one-year intervals. The ratio of orbitofrontal cortex volume to amygdala volume significantly predicted substance use disorder survival time across the sample. A reduction in survival time was seen in participants with smaller ratios; this was true for both high-risk and low-risk participants [62].

Native Americans and Alaskan Natives have a lower level of response and an increased risk of alcohol use disorder [46]. The alcohol metabolizing enzymes are another important genetic influence, especially for persons of Asian descent. About 50% of Japanese, Chinese, and Korean persons flush and have a more intense response to alcohol because they have a form of alcohol dehydrogenase (ADH) that causes high levels of acetaldehyde. Forms of ADH and aldehyde dehydrogenase (ALDH) (e.g., homozygous or heterozygous) contribute to a higher rate of alcohol metabolism, intensify the response to alcohol, and lower the risk of alcohol use disorder. High levels of impulsivity/sensations seeking/disinhibition are also genetically influenced and may impact alcohol use disorder risk [46].

An estimated 178,000 people (approximately 120,000 men and 59,000 women) die from alcohol-related causes annually. According to NIAAA, alcohol is a significant cause of death, disease, and disability, currently ranked as one of the leading preventable causes of death in the United States [63]. According to a 2022 SAMSHA survey reported by NSDUH, 29.5 million Americans 12 years of age and older (10.5% of this age group) have alcohol use disorder [63]. Almost 1 in 4 adults have had a heavy drinking event in the past year (defined as five or more drinks for men and four or more drinks for women). The NIH and the CDC report increasing alcohol problems, deaths, and alcohol use disorders. An analysis of death certificates from 2019 and 2020 showed that deaths involving alcohol rose from approximately 79,000 to more than 99,000, a 25.5% increase [64]. Increases in alcohol-related deaths are consistent with reports of increased alcohol sales, consumption, alcohol-involved emergency department visits, and hospitalizations. The most recent alcohol data provide more evidence of increasing heavy alcohol use and associated consequences during the COVID-19 pandemic [65]. A 2023 study demonstrated that only individuals with prepandemic history of alcohol use disorder reported greater increases in drunkenness frequency during the COVID-19 pandemic [66]. Increased alcohol use may also worsen medical and mental health problems. Among people who die by suicide, alcohol use disorder is the second most common mental disorder and involved in an estimated one in four deaths by suicide [64].

PSYCHOLOGICAL AND SOCIOENVIRONMENTAL RISK FACTORS MODELS

Researchers who study risk factors have developed models of how known risk factors may interact to create pathways in children that lead to alcohol use disorders.

Children with Conduct Problems

One model focuses on children who have temperaments that make it difficult for them to regulate their emotions and control their impulses. Clearly, these children are difficult to parent, and if one or both of their parents have alcohol use disorder, it is likely that they will be poorly socialized and have trouble getting along in school [67,68]. Poor academic performance and rejection by more mainstream peers at school may make it more likely for these children to join peer groups where drinking and other risky behaviors are encouraged. Parents with alcohol use disorders will likely not monitor their children closely and will lose control over them at an early age. These children will begin drinking early, often before 15 years of age [69]. If such a child is genetically predisposed to alcohol use disorders, these environmental factors may further increase the tendency [70].

Stress and Distress

Another model of risk factors leading to alcohol use disorder focuses on drinking to regulate inner distress [71]. Some children have temperaments that make them highly reactive to stress and disruption. This type of child may be born into a family with history of alcohol use disorder, where the stressors may be intense, or a nonalcoholic family, with everyday types of low-level stressors. Regardless of the child's family environment, he or she maintains higher levels of inner distress (anxious and depressed feelings) than other children. When they take their first drink, the inner distress dissipates for a while. This leads to more drinking and may lead to alcohol use disorder. However, for some individuals, at certain doses, alcohol may induce rather than reduce the stress response. Research demonstrates that alcohol actually induces the stress response by stimulating hormone release by the hypothalamus, pituitary, and adrenal glands [72]. Research also demonstrates a bidirectional relationship between alcohol and stress [73]. More research is required before the role of stress as a risk factor in alcohol use disorders is understood.

Sensitivity to Alcohol's Effects

A third risk factor model focuses on sensitivity to the effects of alcohol, both to its sedative properties and its stimulating qualities [74]. The stimulant-like (increased heart rate and blood pressure) and sedative properties (impaired vigilance and psychomotor performance) depend on the quantity of alcohol consumed, the time elapsed since consumption, and individual differences in response [75,76]. Researchers believe that this subjective response to alcohol may be an important endophenotype in understanding genetic influences on drinking behavior and alcohol use disorders. While subjective response predicts alcohol use and problems, the exact pattern of association remains unclear [77,78,79]. Two prominent models of subjective response have been discussed in the literature. The low level of response model suggests that high-risk individuals experience decreased sensitivity to the full range of the effects of alcohol. The differentiator model suggests that high risk for alcohol problems is associated with increased sensitivity to alcohol's positive effects but decreased sensitivity to its negative effects [77,78]. A literature review of studies that employed challenge paradigms to assess a range of the effects of alcohol (i.e., impairment, stimulation, sedation) found some support for both models [77]. Results of a quantitative review and meta-analysis suggest that the two models may describe two distinct sets of phenotypic risk with different etiologies and predictions for development of alcohol use disorder [78]. A total of 32 independent samples were combined to produce estimates of the effects of risk-group status (i.e., positive family history of alcohol use disorder or heavy alcohol consumption). Groups with positive family history for alcohol experienced reduced overall subjective response relative to groups with negative family history, as predicted by the low level of response model. In contrast, consistent with the differentiator model, heavy drinkers of both genders responded less on measures of sedation than did lighter drinkers, but more on measures of stimulation [78].

The effects of alcohol on the electroencephalogram (EEG) of subjects at risk for developing alcoholism are well known [80,81,82]. Researchers found that low EEG response to small amounts of alcohol may be associated with future development of alcohol use disorder. Additionally, differences in EEG response to alcohol may have ethnic variations [82]. Other studies have shown that heavy drinkers had less sedation and cortisol response after alcohol consumption than light drinkers. In addition, heavy drinkers were more sensitive to the positive stimulant-like properties as blood alcohol levels increased [74,83].

KNOWN RISK FACTORS FOR ALCOHOL USE DISORDER

With these three models in mind, a review of some of the research findings on genetic and psychosocial risk factors may provide a better understanding of the factors leading to alcohol use disorders [11,84]:

- Temperament: Moodiness, negativity, and provocative behavior may lead to a child being criticized by teachers and parents. These strained adult-child interactions may increase the chances that a child will drink.

- Hyperactivity: Hyperactivity in childhood is a risk factor for the development of adult alcohol use disorders. Children with attention deficit hyperactivity disorder (ADHD) and conduct disorders have increased risk of developing an alcohol use disorder. Childhood aggression also may predict adult alcohol abuse.

- Parents: The most compelling and largest body of research shows parents' use and attitudes toward use to be the most important factor in an adolescent's decision to drink.

- Gender: Among adults, heavy alcohol use is almost three times more common among men than women and also more common among boys in middle or high school than among girls. Men with ADHD and/or conduct disorders are more likely to use alcohol than men without these disorders, while women who experience more depression, anxiety, and social avoidance as children are more likely to begin using alcohol as teens than women who do not experience these negative states.

- Psychology: Bipolar disorder, schizophrenia, antisocial personality disorder, and panic disorder all also increase the risk of a future alcohol use disorder.

ABUSE AND ADVERSE CONDITIONS IN THE HOME

Childhood abuse is a significant risk factor for later alcohol and substance abuse [85]. Women who were physically abused are 1.5 to 2 times more likely to abuse alcohol than non-abused adults. Children from crowded, noisy, and disorderly homes without rules or religion are more likely to abuse alcohol as teens. Children who are quick to anger, who perceive themselves to be highly stressed, who are resentful of parents' absences, or who have repeated conflicts at home are more likely to abuse alcohol as teens.

PROTECTIVE FACTORS

An exciting area of research is focused on protective factors and poses the question, "What protects children from taking one of the risk pathways to alcohol use disorder?"

In 1997, some good news came from the National Longitudinal Study on Adolescent Health, a survey in which nearly 12,000 students in grades 7 through 12 were given lengthy interviews timed one year apart. The researchers were trying to determine what kept children, over the course of that year, from taking health risks in four areas: substance abuse (cigarettes, alcohol, and marijuana), sexuality, violence, and emotional health [86]. The researchers found two factors that protected these children in all four areas. They named the factors: parent-family connectedness and school connectedness.

Children identified as having parent-family connectedness said they felt close to their mother or father, felt that their mother or father cared about them, felt satisfied with their relationship with their mother or father, and felt loved by family members [86]. School connectedness was experienced as a feeling of being part of one's school and a belief that students were treated fairly by the teachers.

There is broad evidence of the protective role of parenting on adolescent health risks. Another well-established protective factor is adolescents' perceived disapproval of alcohol use by their parents [87,88,89,90,91]. In 2022, the National Survey on Drug Use and Health asked children 12 to 17 years of age about their perceptions of the level of parental disapproval of substance use initiation, including alcohol [12]. Most adolescents (88.9%) reported that their parents would strongly disapprove of them having one or two alcoholic drinks nearly every day. This percentage was similar to percentages in most years since 2002, with rates ranging from 88.5% to 91.2% [12]. The number of past-year initiates 12 years of age or older for alcohol also remained stable between 2002 and 2022 [12].

6. ALCOHOL USE DISORDER

Alcohol use disorder, also referred to as alcohol abuse and/or alcohol dependence, is defined in the DSM-5-TR as a problematic pattern of use with two or more of the following criteria over a one-year period [17]:

- Alcohol often taken in larger amounts or over a longer period than was intended

- A persistent desire or unsuccessful efforts to cut down or control alcohol use

- A great deal of time spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects

- Craving, or a strong desire or urge to use alcohol

- Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home

- Continued alcohol use despite having persistent or recurrent social or inter-personal problems caused or exacerbated by the effects of alcohol

- Important social, occupational, or recreational activities given up or reduced because of alcohol use

- Recurrent alcohol use in situations in which it is physically hazardous

- Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol

- Tolerance

- Withdrawal

Alcohol use disorder is extremely amenable to brief intervention. Brief intervention usually includes giving patients information about problems associated with excessive drinking and advising them to cut down on their drinking or abstain. Without intervention, 10% will likely progress to dependence and 50% to 60% will continue to experience problems over the next five years [92,93].

Alcohol use disorder is a primary and chronic disease that is progressive and often fatal; it is not a symptom of another physical or mental condition. It is a disease in itself, like cancer or heart disease, with a very recognizable set of symptoms that are shared by others with the same disorder. About 29.5 million people in the United States met DSM-5-TR criteria for alcohol use disorder in 2022, with an additional 5.3 million abusing or dependent on both alcohol and illicit drugs [12,94].

Like cancer and many other chronic diseases, alcohol use disorder progresses over time. People with alcohol use disorder experience physical, emotional, and other changes in their lives and relationships. These changes may worsen if drinking continues and if treatment specifically targeted to alcohol use disorder is not initiated. Left untreated, alcohol use disorders may lead to premature death through overdose or through damage to the brain, liver, heart, and many other organs. Excessive alcohol consumption is highly associated with suicide, motor vehicle accidents, violence, and other traumatic events [94]. People with untreated alcohol use disorders often lose their jobs, their families, their relationships, and other freedoms that were once important to them.

Evidence Based Practice Recommendation

The U.S. Preventive Services Task Force (USPSTF) recommends screening for unhealthy alcohol use in primary care settings in adults 18 years of age or older, including pregnant women, and providing persons engaged in risky or hazardous drinking with brief behavioral counseling interventions to reduce unhealthy alcohol use.

https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/unhealthy-alcohol-use-in-adolescents-and-adults-screening-and-behavioral-counseling-interventions

Last Accessed: May 20, 2024

Strength of Recommendation/Level of Evidence: B (The USPSTF recommends that clinicians provide this service to eligible patients based on at least fair evidence that the service improves important health outcomes and concludes that benefits outweigh harms.)

As noted, alcohol problems can often be prevented by early identification and brief intervention. A weak link in the early identification of problems is the lack of skill and competencies necessary to perform such an assessment and the experience to confidently move to more specific questions and suggestions for change.

Alcohol dependence is included in the DSM-5-TR umbrella definition of alcohol use disorder [17]. The symptoms of withdrawal and tolerance have been the hallmarks of more severe disease, though alone they are neither necessary for nor sufficient to make the diagnosis.

Healthcare professionals should understand the criteria and warning signs of alcohol use disorder. This enables confrontation and intervention earlier in the course of the illness rather than relying on toxic liver markers. Verifying the facts that show a person is at risk for alcohol use disorder and confronting the impaired individual with those facts is the definition of an office or brief intervention. Brief intervention is most effective before dependence is reached. Once diagnosable, the patient needs more comprehensive intervention.

WITHDRAWAL

Individuals with alcohol use disorder often experience a severe, potentially fatal withdrawal syndrome when they either abruptly discontinue or sharply reduce their alcohol consumption. The symptoms may include sweating, rapid heartbeat, hypertension, tremors, anorexia, insomnia, agitation, anxiety, nausea, and vomiting. Tremors of the hands are usually the earliest symptom of alcohol withdrawal. Hallucinosis, seizures, and delirium tremens (DTs) are the most severe form of alcohol withdrawal. Hallucinosis, when it occurs, occurs one to two days after decreasing or abstaining from alcohol. While the effects of DTs can be life threatening, all other symptoms, with or without treatment, usually resolve several hours or days after appearance. Alcohol withdrawal in tolerant individuals can occur before the BAC has dropped below the established legal limit for intoxication. Some persons with alcohol use disorder have symptoms of irritability, emotional lability, insomnia, and anxiety that persist for weeks to months after alcohol withdrawal. The symptoms may be due to the residual effects of alcohol toxicity on the central nervous system and can be post-acute withdrawal symptoms; members of Alcoholics Anonymous (AA) refer to this as being a "dry drunk." AA considers alcoholics who are only abstaining from alcohol but who are not working a recovery program and remaining in essentially the same emotional state as they were when they were drinking to be "dry drunks."

INCREASED TOLERANCE

Long-term heavy drinking and genetic predisposition can result in the development of tolerance, which is the body's adaptation to the presence of alcohol. As tolerance develops, the drinker requires increasing amounts of alcohol to feel the same effect. For this reason, the usual reported effects for various BAC levels do not apply to individuals with tolerance. In our society, people are often admired for their ability to "hold their drinks." But the fact is, tolerance may be an early warning sign that a physical dependence on alcohol is developing. During the late stages of alcohol use disorder, reverse-tolerance occurs, meaning the individual becomes intoxicated more quickly and with less alcohol.

IMPAIRED CONTROL OF DRINKING

Impaired control over drinking means that a person is consistently unable to limit the number of occasions when alcohol is used or the amount of alcohol ingested on those occasions. Often, because of the damage alcohol causes in their lives, people with alcohol use disorder will express a strong and persistent desire to cut down or stop drinking. Often they may be able to do so, sometimes for a matter of weeks, a month, or even longer. One does not need to be a daily drinker to meet criteria for alcohol use disorder, as even those who go weeks or months without a drink may binge and meet diagnostic criteria. However, because alcohol use disorder is a chronic progressive disease, once patients with alcohol use disorder resume drinking, even after years of sobriety, they typically return to the previous quantities of consumption, with worsening adverse consequences.

PREOCCUPATION WITH ALCOHOL

Individuals with alcohol use disorder may have a preoccupation with alcohol, defined as a noticeable shift in priorities, with a focus on obtaining and consuming an adequate supply of alcohol. Drinking alcohol becomes a central focus in their lives. Over time, the energies of individuals with alcohol use disorder are diverted from people, places, and things that were once important to them.

Another highly noticeable feature of the preoccupation with alcohol may be the large amount of time that drinking consumes. Thinking about alcohol, obtaining alcohol, drinking alcohol, and recovering from the effects of alcohol take more and more of the individual's time. Hobbies and other activities once enjoyed are abandoned one by one, and the only pleasure seems to come from drinking.

USE OF ALCOHOL DESPITE ADVERSE CONSEQUENCES

Continued drinking despite adverse consequences is characterized by the inability of individuals with alcohol use disorder to stop drinking even when they recognize that their family, interpersonal, spiritual, occupational, legal, and financial problems are the result of their drinking. Furthermore, alcohol may be causing serious health and psychological problems (e.g., anemia, gastritis, liver disease, neurologic disorders, depression) and still the dependent individual cannot stop.

DENIAL AS A DEFENSE MECHANISM

Denial is a common characteristic distortion in thinking that becomes profound in people with alcohol use disorder. For decades, those who have treated individuals with alcohol use disorder, and recovering alcoholics themselves, have puzzled over why these persons continue to drink when the link between alcohol and the losses they suffer is so clear. Denial is an integral part of the disease of alcohol use disorder and a major obstacle to recovery. Although the term denial is not specifically used in the wording of the diagnostic criteria, it underlies the primary criteria described as, "drinking despite adverse consequences."

RELAPSE

Because alcohol use disorder is a chronic disease, another symptom that is increasingly being recognized and treated is relapse. Although alcohol use disorder is a treatable, chronic disease, as yet, no cure has been found. This means that even if individuals with alcohol use disorder have been sober for a long time and have regained their health and reclaimed other important aspects of their lives, they may experience a relapse that will require further treatment in order to return to remission.

PHYSICAL CLUES THAT MAY SUGGEST ALCOHOL USE DISORDER

While a strong attachment to alcohol is the hallmark of early dependency, if the patient refuses to acknowledge a problem and no one from home or work helps to confirm the diagnosis, healthcare professionals are often left with nothing more than clinical intuition, resulting in a missed diagnosis. However, late in the course of alcohol use disorder, physical clues typically become increasingly apparent and suggestive of alcohol abuse and/or dependence. Alcohol abuse and dependence are often referred to as the "Great Masquerader" because many of the signs and symptoms are also commonly found in other conditions [95].

Elevated Laboratory Findings

- Serum glutamic oxaloacetic transaminase (SGOT)

- Lactic acid dehydrogenase (LDH)

- Cholesterol

- Gamma-glutamyltransferase (GGT)

- Mean corpuscular volume (MCV)

- Alkaline phosphatase

- Triglycerides

- Blood alcohol concentration (BAC)

- Urinary ethyl glucuronide (EtG) and ethyl sulfate (EtS)

- Whole blood phosphatidylethanol (PEth)

- Serum transferrin

- Uric acid

Gastrointestinal Signs/Symptoms

- Nausea

- Vomiting

- Reflux

- Diarrhea

- Gastritis

- Ulcers

- Esophagitis

Cardiopulmonary Signs/Symptoms

- Hypertension

- Palpitations

- Arrhythmias

- Recurrent respiratory infections

Central Nervous System (CNS) Signs/Symptoms

- Anxiety

- Insomnia

- Memory impairment

- Depression

- Irritability

- Panic

- Suicide attempt(s)

- Suicidal thinking

Behavioral Clues

- Loss of interest in previously favorite activities and people

- Marital and financial problems

- Positive family history

- Cigarette smoking

- Problems at home and work

- Anger when someone asks about drinking

- Legal difficulties

- Higher than normal scores on screening questionnaires, such as the Michigan Alcohol Screening Test (MAST) and CAGE

Miscellaneous Signs/Symptoms

- Gout

- Impotence

- Bloated face

- Parotid swelling

- Trauma injuries

- Aches and pains

- Unusual accidents

- Broken bones

- Driving accidents, multiple citations, and other problems

7. COMPLICATIONS

Alcohol use disorders are often associated with physical disorders and related problems.

LIVER DISEASE

The liver is a particularly vulnerable organ to alcohol consumption, in large part because it is where alcohol is metabolized prior to elimination from the body. As few as six drinks a day for men have been found to be associated with liver damage. The most common manifestation among persons with alcohol use disorder is called "fatty liver." Among heavy drinkers, the incidence of fatty liver is almost universal. For some, a fatty liver may precede the onset of alcoholic cirrhosis. Fatty deposits have been associated with men who have six or more drinks a day and women who have only one or two drinks daily.

Alcoholic hepatitis is a condition that, when severe, is characterized by jaundice, fever, anorexia, and right upper-quadrant pain. Between 10% and 35% of heavy drinkers (those drinking five or six standard drinks a day or more) develop alcoholic hepatitis and 10% to 20% develop cirrhosis [96,97]. More than 60% of persons who develop both alcoholic hepatitis and cirrhosis will die within four years. Drinking 12 beers a day for 20 years has been associated with a 50% incidence of cirrhosis. It is not known which individuals will develop cirrhosis. Studies have shown that women develop liver disease faster and at lower levels of alcohol consumption than men [97,98]. Women also have a higher incidence of alcoholic hepatitis and higher mortality rate from cirrhosis [99].

Alcohol use disorder is also a strong predictive factor for the development of hepatocellular cancer [100]. The presence of other hepatic risk factors, including hepatitis C, fatty liver disease, smoking, and obesity, further increases this risk.

Liver Transplantation

The leading indication for liver transplantation in the United States is chronic hepatitis C [101]. Cirrhosis due to alcoholic liver disease is the second most common cause for a person to require a liver transplantation [101]. Candidates for liver transplantation should be adequately screened for alcohol use disorders and receive appropriate treatment both perioperatively and as part of long-term follow-up. Patient survival after transplantation for both of these conditions is surprisingly good, with 72% of patients surviving after five years [101]. Short-term survival is similar; however, long-term survival for patients with hepatitis C now appears to be compromised by universal recurrence. When patients have both alcohol use disorder and chronic hepatitis C, they do worse than when both diseases occur independently. One study demonstrated that patients' short-term survival is the same for those who have alcohol use disorder, hepatitis C, or both diseases [102].

ALCOHOL/ACETAMINOPHEN INTERACTION

Chronic heavy drinking appears to activate the enzyme CYP2E1, which may be responsible for transforming the over-the-counter pain reliever acetaminophen into toxic metabolites that can cause liver damage [103]. Even when acetaminophen is taken in standard therapeutic doses, liver damage has been reported in this population [104,105]. A review of studies of liver damage resulting from acetaminophen-alcohol interaction reported that, in individuals with alcohol use disorder, these effects may occur with as little as 2.6 grams of acetaminophen (four to five "extra-strength" pills) taken over the course of the day by persons consuming varying amounts of alcohol [106]. The damage caused by alcohol-acetaminophen interaction is more likely to occur when acetaminophen is taken after, rather than before, the alcohol has been metabolized [107]. Moderate drinkers should also be made aware of this potential for interaction. There is now a warning label on the bottle that states, "If you consume three or more alcoholic drinks every day, ask your doctor whether you should take acetaminophen or other pain relievers/fever reducers." Further, in 2014 the U.S. Food and Drug Administration (FDA) issued a statement that combination prescription pain relievers containing more than 325 mg acetaminophen per dosage unit should no longer be prescribed due to reported severe liver injury with acetaminophen in patients who took more than the prescribed dose in a 24-hour period; took more than one acetaminophen-containing product at the same time; or drank alcohol while taking acetaminophen products [108].

CARDIOVASCULAR DISORDERS

Alcohol can have a detrimental effect on the heart, including a decrease in myocardial contractility, hypertension, atrial and ventricular arrhythmias, and secondary nonischemic dilated cardiomyopathy [109]. A common complication in alcohol use disorder is elevated pulse and blood pressure, often in the hypertension range. Younger people with alcohol use disorder and those without existing hypertension are less likely to have an elevation than those who are older and predisposed to some hypertension. When drinking stops, the blood pressure often returns to normal over a period of a few days. One study found that people who had six or more drinks a day were twice as likely to suffer from hypertension than moderate drinkers (two or fewer drinks per day) or nondrinkers. Increased serum GGT levels may be an indicator of an individual's susceptibility to the hypertensive effect of alcohol [110].

Aside from hypertension, chronic heavy drinking can adversely affect the heart primarily through direct toxicity to striated muscle, leading to a form of cardiomyopathy [109,111]. Alcoholic cardiomyopathy is probably more common than is currently thought because of underdiagnosis of alcohol use disorder in general. The reported prevalence of alcoholic cardiomyopathy has varied widely from 4% to 40% or more, depending on the characteristics of the study population and the threshold of alcohol consumption used to identify the disorder [112].

The association between heavy alcohol consumption and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people, is called "holiday heart syndrome" [111,113]. The syndrome was first described in persons with heavy alcohol consumption, who typically presented on weekends or after holidays, but it may also occur in patients who usually drink little or no alcohol [111,114]. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. The incidence of holiday heart syndrome depends on the drinking habits of the studied population, but it continues to be a prevalent occurrence in emergency department settings, with alcohol serving as a precipitating factor for atrial fibrillation in 35% to 62% of cases, particularly 12 to 36 hours post-binge drinking [115]. Additionally, the observed trend for increased binge alcohol use in younger adults may be associated with an increased incidence of atrial fibrillation in this population [116]. Holiday heart syndrome should be considered as a diagnosis particularly in patients without overt heart disease presenting with new onset atrial fibrillation. Though recurrences occur, the clinical course is benign and specific antiarrhythmic therapy is usually not warranted [111,113,114].

Vitamin Deficiency, Alcohol, and Cardiovascular Disease

Abnormally high plasma levels of the amino acid homocysteine have been shown in studies to increase the risk for cardiac and other vascular diseases [117]. Even small increases in homocysteine appear to increase the risk of heart disease. Vitamins like folate, B12, and B6 are required for homocysteine disposal within cells. The lower the concentration of these and other vitamins, the greater the concentration of homocysteine. A number of nutritional problems have been reported in people with alcohol use disorder. Malnourished persons with alcohol use disorder and liver diseases have been found to have B6 and folate deficiencies. In addition, average homocysteine levels are twice as high in patients with chronic alcohol use disorder when compared to nondrinking controls. Thus, homocysteine may contribute to the cardiovascular complications experienced by many with chronic alcohol use disorder. Lowering homocysteine with B vitamin supplementation may reduce cardiovascular risk [118,119]. Further research is necessary to determine whether abstinence and recovery reverses the risk of cardiovascular disease, and whether folate and vitamins B12 and B6 should be considered as appropriate nutritional supplements for patients with alcohol use disorder [120].

CANCER

Heavy drinking increases the risk of cancer of the upper gastrointestinal and respiratory tracts [121]. Almost 50% of cancers of the mouth, pharynx, and larynx and approximately 75% of esophageal cancers in the United States are associated with chronic, excessive alcohol consumption [122,123,124]. When alcohol consumption is combined with tobacco use, the risk of esophageal cancer increases markedly, as much as 130-fold in one study [125,126]. Alcohol increases production of estradiol, and increased levels of estradiol have been linked to an increased risk of breast cancer in women who drink [127].

GASTROINTESTINAL DISORDERS

Alcohol produces irritation and inflammation of the mucosal lining of the gastrointestinal tract and influences the motility in the esophagus, stomach, and small bowel [128]. Frank ulceration may occur with chronic excessive alcohol use. This well-known alcohol related "heartburn" is due to esophageal reflux with esophagitis that commonly occurs with irritation and inflammation of the gastroesophageal junction. Severe vomiting from alcohol gastritis may result in mucosal tears at the gastroesophageal junction, resulting in frank, usually transient pain in the upper gastrointestinal tract.

Short-term and long-term alcohol ingestion are associated with gastritis, erosive gastritis, gastric ulceration, atrophic gastritis, and gastric hemorrhage. Furthermore, duodenitis and duodenal ulcerations are a direct result of chronic excessive alcohol irritation and inflammation.

Patients who have undergone gastric bypass surgery for obesity have higher breath-alcohol levels after drinking the same amount as other people. Many bypass surgeries attach the jejunum directly to the stomach, allowing delivery of alcohol more rapidly to the jejunal site of primary absorption as well minimizing the effect of the stomach's alcohol dehydrogenase. Findings from a small study suggest that it takes much longer for their levels to return to zero [129].

CHRONIC PANCREATITIS

Alcohol consumption is the leading cause of chronic pancreatitis, accounting for approximately 70% of cases in the United States; however, fewer than 10% of heavy alcohol drinkers develop the disease [130,131,132,133,134]. While there are many theories regarding the pathophysiology of chronic pancreatitis, the most prevalent for alcohol-induced chronic pancreatitis involves the effect of toxic metabolites on the pancreas. This theory suggests that inflammation and fibrotic changes in the pancreas are the direct result of premature activation of enzymes due to ethanol's effect on the Golgi complex [132,134,135]. Another theory suggests that pancreatic hypoxia results from decreased blood flow to the pancreas. Alcohol-induced acinar injury may reduce capillary flow and result in edema and capillary compression [132]. Individuals with alcohol use disorder may develop diabetes mellitus or hyperglycemia as a result of chronic pancreatitis, when the islet cells in the pancreas are eventually destroyed. Once alcohol-induced chronic pancreatitis has developed, ingestion of even small amounts can result in severe flare-up requiring hospitalization.

BODY WEIGHT

Although alcohol has a relatively high caloric value, 7.1 calories per gram (1 gram of fat contains 9 calories), alcohol consumption does not necessarily result in increased body weight. Moderate, regular doses of alcohol added to the diets of lean men and women do not seem to lead to weight gain. However, in some studies obese patients have gained weight when alcohol is added to their diets.

An analysis of data collected from the first National Health and Nutrition Examination Survey (NHANES I) found that although drinkers had significantly higher intakes of total calories than nondrinkers, drinkers were not more obese than nondrinkers. In fact, women drinkers had significantly lower body weight than nondrinkers. As alcohol intake among men increased, their body weight decreased. An analysis of data from the second National Health and Nutrition Examination Survey (NHANES II) and other large U.S. studies found similar results for women [136]. When chronic heavy drinkers substitute alcohol for food in their diets, they typically lose weight and weigh less than their nondrinking counterparts [137].

Many older studies, such as those discussed, have focused on total volume of alcohol based on intake over time (e.g., number of drinks per week), an average that reveals little about the actual drinking habits of individuals. This has led to a very inconsistent array of data on the relationship of drinking and body mass index (BMI). One study sought a better understanding of the relationship between BMI and regular/moderate versus infrequent binge drinking [138]. Researchers found that although individuals of similar height might consume the same weekly average of alcohol (e.g., 14 drinks per week), individuals who consume two drinks each day of the week typically have low BMIs and individuals who consume seven drinks on each of two days of the week typically have high BMIs. A 2018 study examined the associations of alcoholic beverage consumption with dietary intake, waist circumference, and BMI [139]. A total of 7,436 men and 6,939 women 20 to 79 years of age were included in the study. By average daily drinking volume, the differences in waist circumference and BMI between former and moderate drinkers were +1.78 cm and +0.65, respectively, in men and +4.67 cm and +2.49, respectively, in women. Compared with moderate drinking, heavier drinking volume (three drinks/day or more in men, two drinks/day or more in women) was not associated with higher waist circumference or BMI, whereas drinking five or more drinks/day was associated with higher waist circumference and BMI in men. There were no significant differences in women who consumed four or more drinks/day compared with women who consumed one drink/day [139].

It is also important to note those individuals who have undergone bariatric surgery. According to a research study conducted at a substance abuse treatment facility, bariatric surgery patients were more likely to be diagnosed with alcohol withdrawal than those who had not had the surgery [140]. In another study of patients in active weight management being considered for bariatric surgery, an inverse relationship was found between BMI and alcohol consumption—the more overweight the patient, the less alcohol was consumed [141]. Past-year alcohol consumption actually decreased as BMI increased. Surgeons felt it rare to have a patient excluded for bariatric surgery due to excessive alcohol consumption. The authors concluded that it is likely that food and alcohol compete at brain reward sites.

MALNUTRITION

Excessive drinking may interfere with the absorption, digestion, metabolism, and utilization of nutrients, particularly vitamins. Individuals with alcohol use disorder often use alcohol as a source of calories to the exclusion of other food sources, which may also lead to a nutrient deficiency and malnutrition. In the late stage of the disease, patients may develop anorexia or severe loss of appetite, and refuse to eat. Persons with alcohol use disorder account for a significant proportion of patients hospitalized for malnutrition [137].

Direct toxic effects of alcohol on the small bowel causes a decrease in the absorption of water-soluble vitamins (e.g., thiamine, folate, B6). Studies have suggested that alcoholism is the most common cause of vitamin and trace-element deficiency in adults in the United States. Alcohol's effects are dose dependent and the result of malnutrition, malabsorption, and ethanol toxicity [142]. Vitamins A, C, D, E, K, and the B vitamins are deficient in some individuals with alcohol use disorder. All of these vitamins are involved in wound healing and cell maintenance. Because vitamin K is necessary for blood clotting, deficiencies can cause delayed clotting and result in excess bleeding. Vitamin A deficiency can be associated with night blindness, and vitamin D deficiency is associated with softening of the bones. Deficiencies of other vitamins involved in brain function can cause severe neurologic damage (e.g., deficiencies of folic acid, pyridoxine, thiamine, iron, zinc).

Thiamine deficiency from chronic heavy alcohol consumption can lead to devastating neurologic complications, including Wernicke-Korsakoff syndrome, cerebellar degeneration, dementia, and peripheral neuropathy [143]. Thiamine deficiency in patients with alcohol use disorder who are suffering from Wernicke-Korsakoff syndrome leads to lesions and increased microhemorrhages in the mammillary bodies, thalamus, and brainstem. This syndrome can also be associated with diseases of the gastrointestinal tract when there is inadequate thiamine absorption. All patients with alcohol use disorders should receive supplemental thiamine whenever entered into hospitalization or treatment to reduce this possibility.

INFECTIOUS DISEASES

Alcohol abuse is a major risk factor for many infectious diseases, especially pulmonary infections [144]. Studies have shown that alcohol abuse increases the risk for acute respiratory distress syndrome and chronic obstructive pulmonary disease [145,146,147,148]. Pneumonia, tuberculosis, and other pulmonary infections are frequent causes of illness and death among patients with alcohol use disorder [149]. Other infectious diseases that are over-represented among individuals with alcohol use disorder are bacterial meningitis, peritonitis, and ascending cholangitis. Less serious infections are chronic sinusitis, pharyngitis, and other minor infections.

Acute and chronic alcohol abuse also increase the risk for aspiration pneumonia. Alcohol use disorders are associated with increased risk of aspiration of gastric acid and/or oropharyngeal flora, decreased mucus-facilitated clearance of bacterial pathogens from the upper airway, and impaired pulmonary host defenses [150]. In addition, pathogenic colonization of the oropharynx is more common in patients with alcohol use disorder.

The consumption of alcohol alters T-lymphocyte functions, immunoglobulin production by B cells, NK cell function, and neutrophil and macrophage activities making patients with alcohol use disorder more susceptible to septic infection [151,152,153]. Studies have shown that animals given ethanol are unable to suppress infections that can ultimately result in progressive organ damage and death [154,155,156].

SLEEP DISORDERS

Although some people believe that alcohol helps them sleep, chronic excessive drinking can induce sleep disorders by disrupting the sequence and duration of sleep states and by altering total sleep time, as well as the time required to fall asleep [157,158]. Specifically, drinking within an hour of bedtime appears to disrupt the second half of the sleep period [159]. The person may sleep poorly during the second half of sleep, awakening from dreams and returning to sleep with difficulty, resulting in daytime fatigue and sleepiness [157,160].

Individuals with alcohol use disorder may be at increased risk for sleep apnea, a disorder in which the upper air passage narrows or closes during sleep [161,162,163,164]. The combination of alcohol, obstructive sleep apnea, and snoring increases a person's risk for heart attack, arrhythmia, stroke, and sudden death [165]. Obstructive sleep apnea significantly increases the risk of stroke or death from any cause, independent of other risk factors, including hypertension [166,167].

NERVOUS SYSTEM DYSFUNCTION

The most common neurologic abnormality among patients with alcohol use disorder is dementia syndrome, which manifests primarily as impairment in recent memory, and more subtle fluctuations in abstractions, calculations, and other aspects of cognitive functions. As previously stated, one specific neurologic complication resulting from thiamine deficiency is Wernicke-Korsakoff syndrome, which involves delirium, clouded sensorium, confusion, ophthalmoplegia, nystagmus, and ataxia [168]. Immediate administration of thiamine is usually successful in treating the symptoms, but in some cases permanent memory loss occurs [168]. Once delirium and confusion resolve, there is sometimes a profound loss in recent memory (out of proportion to the other cognitive deficits) and alcoholic peripheral neuropathy, which results in diminished sensitivity to touch, pinprick, and vibration (objectively, and paraesthesias subjectively).

The acute effects of alcohol on the nervous system are signs people commonly think of when they envision an intoxicated person, such as slurred speech, loss of coordination, unsteady gait, impairment of attention or memory, nystagmus, stupor, or coma. The degree to which the central nervous system is impaired is directly proportional to the BAC and degree of tolerance.

Alcohol and the Brain

Alcohol affects most neurochemical systems including NMDA, GABA, serotonin, dopamine (DA), and opioid systems.

Alcohol inhibits NMDA systems, which may contribute to feeling intoxicated. NMDA receptors change as tolerance develops. These receptor systems are overactive during withdrawal. Alcohol also enhances the action of the GABA system, producing some of the symptoms of acute intoxication. GABA receptors are especially sensitive to alcohol. The GABA system is underactive during withdrawal, and the genes that control these receptors may have an impact on the risk of alcohol use disorder [169,170].

Alcohol causes the release of 5-HT, or serotonin. Lower 5-HT levels in the brain are associated with increased alcohol intake in animals and humans, while higher 5-HT levels are associated with slightly reduced alcohol intake. Several 5-HT genes may be related to the genetic risk of alcohol use disorder [11,46].

Alcohol activates DA in the reward system in the ventral tegmental area of the brain. Alcohol also causes the release of DA. Several DA receptors may be related to the genetic risk of alcohol use disorder [11,46].

Finally, alcohol causes the release of endogenous opioids. Opioid receptors change with tolerance and withdrawal. Some receptors may affect genetic predisposition for alcohol use disorder, and opioid antagonists can decrease voluntary alcohol consumption. Alcohol may also affect acetylcholine, norepinephrine, and steroids.

Most people who drink do not develop brain damage. However, studies do indicate that impaired cognition and motor abilities occur in some individuals who are heavy drinkers. Older persons with alcohol use disorder exhibit more brain tissue loss than both older and younger persons without alcohol use disorder. These results suggest that aging may render a person more susceptible to the effects of chronic excessive alcohol. Most studies suggest that, following long-term abstinence, most brain changes resolve.

Magnetic resonance imaging has been used to measure changes in the brain structure and volume in persons with alcohol use disorder at three weeks after abstinence from alcohol [171]. The results indicated that the brain volume in men and women with alcohol use disorder was significantly reduced as compared with healthy men and women. The differences, however, were much more significant in women than in men [172]. These results indicate that alcohol inflicts greater neurotoxic effects in women with alcohol use disorder than men, but again, these brain changes may resolve with long-term abstinence. Results from a 2021 study found significant impacts of age, but not sex, on white matter microstructure in individuals with alcohol use disorder [173].

COMPLICATIONS SPECIFIC TO WOMEN

Although the literature on gender differences in addiction can appear at times to be inconsistent, as a whole men are more substance dependent than women for all substances except benzodiazepines and analgesics, on which women are equally or more frequently dependent [174]. However, on average, women show the effects of alcohol more immediately, more intensely, and for longer periods of time than men. They achieve higher concentrations of alcohol in the blood after drinking the same amounts of alcohol [175]. Women also produce a lower level of the enzymes required to break down alcohol. In addition, female hormones make women's bodies more susceptible to alcohol at certain times of the menstrual cycle. Women also tend to be shorter and weigh less than men. Because women generally have a higher percentage of body fat, they reserve alcohol in the body for longer periods of time. This is important because when a person drinks a large amount of alcohol, it is deposited in fatty tissues. Neurophysiology is more compromised in women with alcohol use disorder than men [176].

It may be because of these factors that women develop alcohol problems more quickly than men, and their progression to severe complications, such as liver disease, is more rapid. The death rate among women with alcohol use disorder is 50% to 100% greater than that of men because of their increased risk for suicide, alcohol-related accidents, cirrhosis, and hepatitis [177]. It is important to note, however, that women are more likely than men to obtain help, participate in treatment, and have long-term involvement in AA, and therefore are more likely to have better life outcomes [178].

International studies of gender differences indicate that the greater the societal gender equality in a country, the smaller the gender differences in drinking behavior. The gender gap in alcohol drinking is one of the few universal gender differences in human social behavior [179].

Fetal Alcohol Spectrum Disorders

Evidence Based Practice Recommendation

The World Health Organization recommends that healthcare providers should offer a brief intervention to all pregnant women using alcohol.

https://www.who.int/publications/i/item/9789241548731

Last Accessed: May 20, 2024

Strength of Recommendation/Level of Evidence: Strong/Low

The dangers of drinking while pregnant are well-documented. Pregnant women who drink risk the chance of their child developing FASD. Prenatal alcohol exposure is known to be toxic to the developing fetus and is one of the leading known preventable causes of intellectual disability. Excess fetal mortality secondary to drinking is most prevalent during the first trimester of pregnancy. Even drinking as little as one beer a day has been associated with decreased birth weights and spontaneous abortions. Although FASD has received a great deal of publicity, the majority of people may not understand it correctly. For example, one large study of adults 18 to 44 years of age found that the majority of respondents incorrectly assumed that FAS referred to infants born with an addiction to alcohol.

FASDs refer to the whole range of conditions that can affect the offspring of mothers who drank alcohol during pregnancy. These conditions can affect each person in different ways and can range from mild to severe. A person with an FASD might have [180]:

- Abnormal facial features, such as a smooth ridge between the nose and upper lip (the philtrum)

- Small head size

- Shorter-than-average height

- Low body weight

- Poor coordination

- Hyperactive behavior

- Difficulty with attention

- Poor memory

- Difficulty in school (especially with math)

- Learning disabilities

- Speech and language delays

- Intellectual disability or low IQ

- Poor reasoning and judgment skills

- Sleep and sucking problems as an infant

- Vision or hearing problems

- Problems with the heart, kidneys, or bones

There are a variety of conditions that are considered FASDs. Alcohol-related neurodevelopmental disorder (ARND) is associated with intellectual difficulties and problems with behavior and learning. Patients with ARND may do poorly in school, with particular issues with math, memory, attention, judgment, and impulse control [180]. Offspring of mothers who consumed alcohol, during pregnancy may also develop alcohol-related birth defects, including congenital malformations of the heart, kidneys, and/or bones or hearing problems.

The most commonly studied FASD is FAS. FAS is defined by the existence of certain physical characteristics of children whose mothers drank during pregnancy. These characteristics include [180]:

- Intellectual disability

- Growth deficiencies

- Central nervous system dysfunction

- Decreased brain size

- Low birth weight

- Distorted facial features

- Behavioral maladjustments

- Abnormal joints and limbs

Other less visible symptoms of FAS include [181,182,183,184,185,186,187,188,189,190]:

- Verbal learning and memory problems

- Visual-spatial learning problems

- Attention deficits and hyperactivity

- Increased reaction time/slow information processing

- Executive function problems

- Structural and functional changes in the brain

Alcohol apoptotic neurodegeneration has been shown to appear in the forebrain when rats are injected with alcohol. Seven-day-old rats were divided into a group receiving saline solution and another group receiving alcohol solution. The brains were examined after 24 hours of ingesting alcohol or saline. The alcohol group showed a very dense, widely distributed area of deterioration (cell death). When alcohol is administered, various neurons in the forebrain show sensitivity. Also, the brain weight of the alcohol-treated rats was much lower than the saline group. Exposure of the developing rat brain to alcohol for a certain period of time during a specific developmental stage induces destruction of brain cells that deletes large numbers of neurons from several areas of the brain. This period of time in humans is the last three months of gestation [191].

Alcohol is especially neurotoxic to the developing fetus. Vulnerability is highest at six months' gestation to several years after birth. During this period, alcohol exposure can kill millions of neurons in the developing brain. This helps to explain reduced brain size and behavior disturbances associated with FAS. The most disabling effects are hyperactivity and learning disabilities, depression, and psychosis. Depending on the time of exposure to alcohol, different neurons are depleted, which shows evidence of alcohol being an agent that can contribute to many mental disabilities.

The Centers for Disease Control and Prevention (CDC) reported in 2022 that nearly 14% (or 1 in 7) pregnant women 18 to 44 years of age used alcohol and 5.0% (1 in 20) were binge drinkers [192]. According to the CDC, the cost to the United States for FAS alone is more than $4 billion annually [192]. Additionally, an estimated 6 to 9 out of 1,000 U.S. school children may have FASDs [180]. Binge drinking among pregnant women increased from 4.7% in 2021 to 5.3% in 2022[12]. FASD is 100% preventable when pregnant women abstain from drinking alcohol [180,193].

EFFECTS ON FAMILIES

Living with a non-recovering family member with alcohol use disorder can contribute to stress for all members of the family. Children raised in these families have different life experiences than children raised in nonalcoholic families. For example, children living with a non-recovering alcoholic score lower on measures of family cohesion, intellectual cultural orientation, active recreational orientation, and independence. They also experience higher levels of conflict within the family. Many children of alcoholics experience other family members as distant and noncommunicative and may be hampered by their inability to grow in developmentally healthy ways. The level of dysfunction or resiliency of the nonalcoholic spouse is a key factor in the effects of problems impacting the children. Support groups, such as Children of Alcoholics, are available to help people deal with these issues.

Alcohol use disorder usually has strong negative effects on marital relationships. Separated and divorced men and women were three times as likely as married men and women to say they had been married to a person with alcohol use disorder or problem drinker. Almost two-thirds of separated and divorced women and almost one-half of separated or divorced men younger than 45 years of age have been exposed to alcohol use disorder in the family at some time. As of 2022, approximately 29.7 million Americans met the diagnostic criteria for alcohol use disorder; this number represents an increase from 18.1 million Americans in 2002 [12].

Child Abuse

The majority of studies suggest an increased prevalence of alcohol use disorder among parents who abuse children. Existing research suggests that alcoholism is more strongly related to child abuse than are other disorders, such as parental depression, but the most important factor is whether the abusive parent was abused themselves or witnessed a parent or sibling being abused. Although several studies report very high rates of alcoholism among the parents of incest victims, much additional research in this area is needed [194,195].

VIOLENCE

Among some individuals and subgroups, excess alcohol consumption is associated with the risk of violent behavior. Alcohol may encourage aggression or violence by disrupting normal brain function, especially in levels of serotonin [196]. There is considerable overlap among nerve cell pathways in the brain that regulate aspects of aggression, sexual behavior, and alcohol consumption. Alcohol may weaken brain mechanisms that normally restrain impulsive behaviors, including inappropriate aggression.

Drinking and violence may occur together by chance. Also, violent criminals who drink heavily are more likely to be caught and consequently are over-represented in samples of people arrested for violent behavior. Antisocial personality disorder (ASPD) and early-onset alcoholism are common traits in many criminals. A person who intends to engage in a violent act may drink to bolster his or her courage or in hopes of evading punishment or censure. The motive of drinking to avoid censure is encouraged by the popular view of intoxication as a "time-out," during which a person is not subject to the same rules of conduct as when sober. Such alcohol-violence interactions are not readily treated. However, ongoing research has identified medications that have the potential to reduce violent behavior in both alcoholic and nonalcoholic subjects.

Young men who exhibit violent and antisocial behaviors often "burn out" with age [197]. By the time they reach 40 years of age, serotonin concentrations are increasing and testosterone concentrations are decreasing, both of which help to restrain violent behavior [198].

Research suggests that increasing the unit price of alcohol by raising alcohol taxes is an effective strategy for reducing excessive alcohol consumption and related harms, including violent behavior [199]. An examination of the impact of the price of alcoholic beverages on violence and other delinquent behavior among college students found that an increase in the price of beer could reduce the overall number of students involved in some sort of violent behavior by 4% [200]. In a study that used data from the National Household Survey on Drug Abuse, higher taxes on beer led to significant reductions in crime (e.g., property damage, use of force), with the largest impact among individuals younger than 21 years of age [201]. Another study that examined the impact of tax increases and advertising bans on reducing the prevalence of underage drinking and subsequent alcohol-related harms found both interventions to be effective [202]. A literature review of studies of underage populations found that increased taxes were significantly associated with reduced consumption and alcohol-related harms [203]. Public policies that affect the price of alcohol appear to have significant effects on alcohol-related disease and injury rates. The results of one systematic review suggest that doubling the tax on alcoholic beverages could reduce alcohol-related violence by 2% and crime by 1.4% [204].

According to the National Council on Alcoholism and Drug Dependence, on college campuses each year an estimated 696,000 students 18 to 24 years of age are assaulted by another student who has been drinking, and 97,000 students report experiencing alcohol-related sexual assault or date rape [205]. Four out of every five juvenile and teen arrestees are under the influence of alcohol or drugs while committing their crimes, test positive for drugs, are arrested for committing an alcohol- or drug-related offense, admit having substance abuse problems, or share some combination of these characteristics [206].

TRAFFIC ACCIDENTS

In 2022, 10,317 people died in alcohol-related traffic fatalities, accounting for 32% of all traffic-related deaths in the United States [207]. Of the 1,090 traffic-related fatalities in 2020 among children 0 to 14 years of age, 229 (21%) involved an alcohol-impaired driver [208]. Of the estimated 127 million episodes of alcohol-impaired driving among U.S. adults, 1 million drivers were arrested for driving under the influence [208]. The CDC estimates that 32 people in the United States die in alcohol-related crashes every day [208]. In a study of persons who have been convicted of driving while impaired, 85% of women and 91% of men reported a lifetime alcohol use disorder [209]. Psychiatric comorbidity may be a key element distinguishing driving under the influence (DUI) offenders from others and in distinguishing repeat offenders from first-time offenders [210].

A study found that although marijuana's effects on driving performance were small or moderate when taken alone, the effects were severe when combined with even a low dose of alcohol. These findings are very serious considering the frequency with which these two substances are combined, especially in young inexperienced drivers [211,212,213,214,215]. One study conducted at seven trauma centers involving 4,243 drivers who were seriously injured in crashes found that 54% of these drivers tested positive for alcohol and/or drugs from September 2019 to July 2021. Of these, 22% of the drivers tested positive for alcohol, 25% tested positive for cannabis, 9% tested positive for opioids, 10% tested positive for stimulants, and 8% tested positive for sedatives [216].

8. OTHER PSYCHIATRIC DISORDERS ASSOCIATED WITH ALCOHOL USE DISORDERS

Persons with alcohol use disorder, like other addicts, generally have comorbid disorders, meaning they have alcohol problems as well as other illnesses or conditions [217]. These problems may include personality disorders (formerly Axis II disorders), other drug use (especially tobacco use disorders), or a number of psychiatric disorders, from major depression and bipolar illness to eating disorders and anxiety disorders. One study reported that 50% of women and 33% of males with a history of alcohol use disorders have at least one other psychiatric disorder [209]. Treatment of the comorbid disorder is absolutely essential in preventing relapses to drinking and in preventing other adverse consequences, such as suicide among patients with depression and alcohol use disorder.

DEPRESSIVE DISORDERS

Alcohol is both a stimulant and a depressant, depending on the levels and time after drinking. Patients with alcohol use disorder are often misdiagnosed with depression because of the many symptoms that mimic depression. Insomnia, reduced appetite, and decreased energy are just a few of the symptoms that can occur in both diseases. Alcohol can cause temporary depressive symptoms, even in persons who have no history of depression. In fact, as many as 80% of men and women with alcohol use disorder complain of depressive symptoms, and at least one-third meet the criteria for a major depressive disorder (excluding, of course, criterion D) [218]. Depression is often a comorbid disorder but can also be solely or partially due to alcohol. This carries important implications in the way depressive symptoms are evaluated and treated in patients with alcohol use disorders. Alcohol intoxication, especially binge drinking, can also cause mood swings that mimic the "highs" of people with manic depression/bipolar disorder. Thirty to fifty percent of persons with alcohol use disorder suffer from major depression at the same time [218,219]. Studies have found that many cases initially diagnosed as substance-induced depression were later reclassified as independent depression (i.e., not substance-induced) because the condition persisted after a period of abstinence [220].

How alcohol use disorder is related to depression is not clear. Some studies have suggested that both conditions may share common risk factors. For example, both problems may run in families. Co-occurrence is very common, but likely has independent though inter-related etiology.

Treatment professionals have found that after two to three weeks of abstinence from alcohol and with good nutrition, the temporary depressive effects of alcohol dissipate. However, there are subgroups of individuals with alcohol use disorder who have a co-occurring depression or manic depression, and it is critically important to diagnose and treat these illnesses during alcohol treatment. If true co-occurring depression is left untreated, many patients will drop out of treatment and relapse to drinking. Alcohol use disorders and depression are important risk factors for suicidal thinking or actions. Because alcohol can increase impulsivity and make depression worse, even intolerable, alcohol is often a factor in suicides.

Suicide

Suicide is the 2nd leading cause of death among persons 25 to 34 years of age and the 3rd leading cause of death among persons 15 to 24 years of age [221]. Most people who attempt suicide and 90% of suicide victims have a diagnosable psychiatric disorder [222]. Alcohol is the number one drug of abuse associated with suicide. In 2021, 48,183 people in the United States died by suicide and an estimated 1.7 million attempted suicide [221]. Among people who attempt suicide, alcohol use disorder is a common diagnosis. Major depression and alcohol use disorder, respectively, are the most commonly diagnosed psychiatric disorders in patients who die by suicide. They also are more common among planned suicide attempts than among impulsive attempts [223]. Next to age, alcohol and drug addictions are the second most important risk factors in suicide. As many as 85% of individuals who die by suicide suffer from depression or alcohol use disorder, and 70% of patients with comorbid alcohol use disorder and depression report that they have made a suicide attempt at some point in their lives [224]. The reported likelihood of suicide in diagnosed alcoholism is between 60 and 120 times that of persons without mental illness [225]. Suicide attempts among women with alcohol use disorder are more mental health-related, whereas suicide attempts among men are more related to the severity of alcohol use disorder [226].

Alcohol intoxication can exaggerate depression and increase the likelihood of an impulsive act like suicide or other forms of violence. Alcohol use is frequently detected in suicide methods involving firearms, driving a vehicle, or overdosing. Alcohol impairs judgment and lowers the threshold to attempt suicide, explaining its association with suicide methods that involve a high level of pain [227]. In a case-control study, researchers examined the relationship between near fatal suicide attempts and aspects of alcohol consumption, such as amount and frequency of drinking, alcoholism, binge drinking, and drinking within three hours of a suicide attempt, and found a J-shaped relationship between alcohol exposure and near lethal attempts for all measures [228].

In a comprehensive review of the subject, it is estimated that the lifetime suicide risk among individuals with alcohol use disorder is 10% to 15%, a figure 5 to 10 times greater than seen in the general population [227,229]. Between 15% and 20% of persons with alcohol use disorder will attempt suicide, and of those who have attempted in the past, 15% to 20% will attempt suicide again in the next five years [229]. Approximately 40% of all patients seeking treatment for alcohol use disorder report at least one suicide attempt at some point in their lives [227].

One study conducted in Japan showed that, among drinkers, the risk of suicide increased with the amount of alcohol consumed. An unusual finding of this study was a U-shaped relationship between alcohol and suicide. Abstainers also have a significantly increased risk, similar to heavy drinkers. Among middle-aged males, moderate drinkers had the lowest risk for suicide [230].

In order to be most effective at the prevention of suicide, healthcare providers should be adept at eliciting both a substance use history and a psychiatric history. Risk factors associated with completed suicide with alcohol use disorder include comorbid major depression, active drinking, serious medical illness, living alone, and interpersonal loss and conflict.

Treatment of Patients with Comorbid Depression and Alcohol Use Disorder

Male, alcoholic, and depressed are the most common descriptors for suicide attempters. Always evaluate persons with alcohol use disorder for depression, suicide, and appropriate referral to a psychiatrist or psychologist. Depression and alcohol use disorder are common problems in the United States. Both are at the top of the list of problems that commonly require psychiatric treatment. Unfortunately, both problems are difficult to diagnose by physicians due to patient fears and stigma and the realities of a busy medical office. Treating one problem but not the other is also very common. In order to successfully treat alcohol use disorder and depression it is important that healthcare providers diagnose and treat both problems.

Treatment of alcohol use disorder begins with evaluation, stabilization, and detoxification and the appropriate level of treatment, which may include a 12-step program. Adding an antidepressant and treating the depression requires a number of subtle changes in thinking. First, the physician must be convinced that the depression is not transient and related to alcohol or detoxification or so severe that the patient is unable to do treatment work. Next, the patient must be willing to accept and adhere to simultaneous, coordinated treatment.

The next issue is determining which antidepressant to use. Lithium and tricyclics used to treat depression alone may not be effective or could have serious adverse effects when used in patients with comorbid depression and alcohol use disorder. Another class of antidepressants, selective serotonin reuptake inhibitors (SSRIs), has been studied to treat depression after failing to treat alcohol use disorder. SSRIs generally cause less serious adverse effects than tricyclics, but some, like fluoxetine, work slowly and cause sexual performance side effects. SSRIs, such as fluoxetine, sertraline, and paroxetine, and herbal remedies such as St. John's wort have been tried in a variety of studies and are generally able to help alleviate depression, but do not appear to help with drinking outcomes. Results of a systematic review found only low-quality evidence to support the use of antidepressants for the treatment of co-occurring depression and alcohol use disorder [231]. A Japanese study observed lower response to antidepressant treatment in patients with comorbid depression and alcohol use disorder [232]. Venlafaxine and bupropion appear to be especially effective in treating patients with depression and alcohol use disorder. Venlafaxine is well suited to treat alcohol use disorder with depression and even depression with anxiety [233]. Venlafaxine is effective in mild and severe depression with anhedonia. Bupropion is effective as well, but it has seizure risks in this population [234]. One study that evaluated treatment outcomes in patients with comorbid alcohol use disorder and depression found venlafaxine and bupropion to be less effective than antidepressants [235]. Men with depression who are using alcohol appear very sensitive to the sexual side effects of the SSRIs and may discontinue their use and drop out of treatment. Both pharmacologic and behavioral treatments have demonstrated efficacy for patients with comorbid depression and alcohol use disorder; however, treatment response is modest, particularly for drinking outcomes [236]. Transcranial magnetic stimulation is now available for refractory depression, and studies are in progress for its use in treating substance use disorder [237].

BIPOLAR DISORDER

A 2000 study analyzed the substance/alcohol abuse patterns of 89 patients with a confirmed diagnosis of bipolar disorder (71 with bipolar I and 18 with bipolar II) [238]. The diagnosis was confirmed by a structured clinical interview for DSM-IV Axis I, an attending psychiatrist, a medical records review, and family members. The age of the patients ranged from 18 to 65 years. Among those with bipolar disorder I, 41 patients (57.8%) abused or were dependent on one or more substances (including alcohol), 28.2% abused or were dependent on two substances, and 11.3% abused or were dependent on three or more substances. Among those with bipolar disorder II, 39% of patients abused or were dependent on one or more substances, 17% were dependent on two or more substances, and 11% were dependent on three or more substances. The risk for substance or alcohol abuse was higher among patients with bipolar I disorder than with bipolar disorder II. Patients with both bipolar disorders I and II abused alcohol more often than any other substances [238]. One study sought to identify the demographic and clinical differences between patients with bipolar disorder both with and without alcohol use disorder [239]. Data from 238 patients with bipolar disorder included alcohol use, social demographics, longitudinal course of bipolar disorder, clinical features of depressive episodes, comorbid physical diseases, anxiety disorder, and other substance use disorder. Of the 238 patients with bipolar disorder, 74 had alcohol use disorder, with the best predictors of alcohol use disorder being male sex, younger age, and comorbidity with other unclassified substance dependence [239].

ANXIETY

Alcohol withdrawal causes many of the signs and symptoms of anxiety and can even mimic panic attacks. Alcohol works much like a benzodiazepine; many people who abuse and are dependent on alcohol have learned to drink to temporarily relieve anxious feelings.

Special problems exist for people who drink to self-medicate the symptoms of a true generalized anxiety disorder, social phobia, or panic disorder. Alcohol may provide temporary relief, but it is not a good treatment for shyness or an anxiety disorder. The price a person may pay for self-medication are two diseases: anxiety and alcohol use disorder. Social anxiety can be a major impediment to active participation and even attendance to group therapy and 12-step meetings.

PAIN

Pain is a subjective experience, and the perception of being in pain is an important factor of the alcohol use disorder. It is hypothesized, as well as established in some research, that individuals in pain will drink as a means to decrease their perception of pain or as a reaction to painful stimuli [240]. According to the National Institute on Alcohol Abuse and Alcoholism, an estimated one in four adults in chronic pain reports self-medicating with alcohol and 43% to 73% of people with alcohol use disorder report experiencing chronic pain [241].

ABUSE/DEPENDENCE ON OTHER DRUGS

All drugs of abuse, including alcohol, cause dopamine release in the mesolimbic system in the brain. This dopamine system, sometimes referred to as the neuroanatomy of pleasure or reinforcement, starts in the ventral tegmental area and projects to the nucleus accumbens. Alcohol- or drug-taking results in a dopamine reward that stimulates its taking. Pavlovian conditioning to environmental cues (e.g., sights, smells, and sounds of a bar) that precede use become associated with use of the drug. Notably, this sense of "reward," which confers evolutionary fitness, is more likely to be perceived as crucial than even that produced by natural, survival-oriented stimuli (e.g., food, sex). This conditioning is reflective of synaptic strengthening mediated by the glutamatergic system, with neuroplasticity changes in brain areas thought to mediate drug-taking behavior, including the amygdala (stress and anxiety), hippocampus (memory), and dorsal striatum (routine motor movements). Natural stimuli (e.g., food, sex, other previously pleasurable activities) become less enjoyable, resulting in a profound state of anhedonia. With time, alcohol use disorders become ingrained. Ultimately, this preference for alcohol compared to natural rewards is mediated through a process of "bad learning," or neuroplasticity changes in the extended amygdala, also referred to as the antireward system. The anti-reward system involves stress-response hormones, including corticotrophin-releasing hormone and dynorphin. Long- or short-term abstinence activates the antireward system, and with more abstinence, it becomes even more difficult to ignore with the attendant anxiety, dysphoria, craving, and anhedonia. Over time, with repeated administration, nucleus accumbens dopamine receptors desensitize, leading to a functional decrease in available dopamine, anhedonia, and decreased sense of pleasure. Real-world examples include an individual with alcohol dependence developing a sudden craving for a drink when watching a beer commercial, walking by a bar, or seeing a place where s/he drinks. This stage reveals one of the remarkable properties of addiction; the act of drug-taking transitions from being impulsive (i.e., pleasure-seeking without afterthought) to compulsive (i.e., undertaken to relieve stress, tension, or physical signs such as pain).

Alcohol use disorders are often associated with dependence on or abuse of other substances, such as marijuana, cocaine, opioids, amphetamines, anxiolytics, designer or "club drugs," and tobacco. Alcohol may be used to alleviate the unwanted effects of these other substances or to augment their effects or substitute for them when they are not available.

Cocaine

According to the most recent National Survey on Drug Use and Health, about 5.2 million Americans 12 years of age and older were past year cocaine users in 2019 [12]. Many cocaine addicts also use alcohol to enhance euphoria, to reduce the mania associated with intoxication, or to calm or reduce the impact of dysphoria caused by cocaine withdrawal. Use of cocaine impairs both mental and physical functions, including learning and memory, hearing and seeing, motor coordination, speed of information processing, and problem-solving ability. Alcohol use has its own set of impairments, but many overlap with cocaine use. The negative impact exerted by alcohol and cocaine on either mental or physical activities has been found to be greater than when either is used alone. This is due to the production of a compound called cocaethylene. Cocaethylene is a novel compound that is produced in the bodies of individuals using cocaine and alcohol. Cocaethylene has been linked to cardiotoxicity, neurotoxicity, overdose deaths, and acute functional impairment [242,243]. The combination of cocaine and alcohol may be associated with other neurologic changes, including poor memory and poorer judgment. Alcohol use can also be a trigger for cocaine relapse.

Nicotine Addiction

As many as 50% of persons with alcohol use disorder smoke, compared with about 18% of the general population [12,244]. In a cohort study of 845 persons who had been treated for alcohol use disorder, more than 25% of the sample had died within 12 years [245]. Approximately one-half of the deaths were related to tobacco use and one-third were related to alcohol. Smoking and excessive alcohol use are risk factors for cardiovascular and lung diseases and some forms of cancer. Compared to nonsmoking nondrinkers, the risk for developing mouth and throat cancer is seven times greater for those who use tobacco, six times greater for those who use alcohol, and 300 times greater for those who use both tobacco and alcohol [246].

Both nicotine and alcohol consumption cause the release of dopamine in the nucleus accumbens. Neurobiology may make the combination of the two substances more rewarding than if either substance was taken alone. Certain enzymes in the liver (i.e., microsomal enzymes) convert some of the ingredients found in tar from cigarette smoke into chemicals that can cause cancer [247]. Long-term excessive alcohol consumption may activate these enzymes as well as decrease the body's ability to respond to infections or abnormal states. Smoking and excessive alcohol use are significant risk factors for cancer of the mouth, throat, and esophagus [246].

A 2000 study revealed that people who smoke, drink alcohol (one or more drinks per day) and develop non-small cell lung cancer had more mutations in the p53 gene when compared to those who smoked only or did not smoke or drink [248]. Mutations in the p53 gene have been seen in smoking-associated tumors and were present more often in alcohol drinkers who smoked cigarettes, than in nondrinkers who smoked cigarettes or in nondrinkers who did not smoke. Seventy-six percent of patients who consumed one or more alcoholic drinks per day and smoked were found to have mutations in the p53 gene. In contrast, 42% of smokers who did not drink (consuming less than one drink per day) had gene mutations [248].

A 2006 study sought to determine how nicotine delivered by tobacco smoke influences alcohol intake. Findings suggest that smoking increases alcohol consumption in at least a subset of smokers [249]. Animal studies have found that chronic nicotine use leads to escalation of alcohol self-administration through a dysregulation in opioid signaling [250,251].

One of the major barriers to treating tobacco dependence in patients with a co-occurring alcohol use disorder is the notion that it is too difficult to quit both alcohol and tobacco and that attempts to quit tobacco might adversely affect the patient's recovery from alcoholism [252,253]. Treatment facilities often concentrate on the "primary" addiction to alcohol and treat tobacco use as a more benign addiction. Fewer than 1 in 10 treatment facilities ban tobacco use on their grounds and many treatment facilities do not screen for or treat tobacco dependence [254]. Moreover, many treatment facilities enable patient smoking by adjourning meetings for "smoke breaks" and allowing staff to smoke openly with patients [255]. In fact, studies show that quitting smoking does not cause abstinent alcoholics to relapse and may actually decrease the likelihood of relapse [256]. Further, quitting smoking has been found to facilitate drinking cessation among tobacco and alcohol co-users [257].

EATING DISORDERS

Alcohol use disorder and eating disorders are commonly comorbid conditions, with patterns of comorbidity differing by eating disorder subtype [258]. A community-based sample of women found that those with lifetime alcohol use disorder or nicotine dependence were at higher risk for eating disorders [259]. The process of alcohol detoxification and treatment is often accompanied by overeating with weight gain, and in some cases food becomes a replacement for alcohol [141,260].

PATHOLOGIC GAMBLING

As lotteries proliferate and states legalize casino gambling, pathologic or compulsive gambling is being recognized as a major public health problem. Alcohol use disorder is often a comorbid condition among compulsive gamblers. As with depression, each disorder can make the other more serious. Individuals with alcohol use disorder may bet more money and may be reluctant to quit chasing their losses. In one study, subjects received either three alcoholic drinks or an equal volume of a nonalcoholic beverage (placebo) [261]. The alcohol group persisted for twice as many gaming trials as the placebo group. One-half of the alcohol group lost their entire cash stake, compared with 15% of the placebo group [261].

Another study examined how alcohol affects judgment and decision-making during gambling, with a focus on sequential decision-making, including the gambler's fallacy (i.e., thinking that a certain event is more or less likely, given a previous series of events) [262]. Thirty-eight male participants completed a roulette-based gambling task 20 minutes after receiving either an alcoholic or placebo beverage. The task measured color choice decisions (red/black) and bet size, in response to varying lengths of color runs and winning/losing streaks. Color choice affected run length in line with the gambler's fallacy, which further varied by previous wins or losses. Bet size increased particularly for losing streaks. The alcohol group placed higher bets following losses than did the placebo group [262].

SEXUAL DYSFUNCTION

Alcohol metabolism alters the balance of reproductive hormones in men and women. In men, alcohol can impair the synthesis of testosterone and reduce sperm production. In women, chronic excessive alcohol use may cause a decreased interest in sex.

9. DETECTING ALCOHOL USE DISORDERS

Problem drinking described as severe is given the medical diagnosis of alcohol use disorder. An estimated 28.8 million adults 18 years of age and older in the United States have an AUD, including 17.1 million men and 11.7 million women. In addition, an estimated 753,000 adolescents 12 to 17 years of age had an alcohol use disorder [63].

AUD is a chronic relapsing addiction previously called alcoholism and characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences. To be diagnosed with alcohol use disorder, individuals must meet the specific DSM criteria. Using the DSM-5-TR, anyone meeting any 2 of the 11 criteria during the same 12-month period receives a diagnosis of alcohol use disorder. The severity of the disorder—mild, moderate, or severe—is assigned based on the number of criteria met.

RECOMMENDED STANDARDIZED QUESTIONS OR TESTS

A variety of screening instruments are available to detect unhealthy alcohol use in adults. After conducting a systematic evidence review of trials published between 1985 and 2011 on screening and behavioral counseling interventions for unhealthy alcohol use in adults, the U.S. Preventive Services Task Force (USPSTF) recommends that clinicians screen all patients 18 years of age or older for alcohol abuse using one of the following tools [263,264]:

- The abbreviated three-question AUDIT-Consumption (AUDIT-C)

- The NIAAA-recommended Single Alcohol Screening Question (SASQ)

Evidence Based Practice Recommendation

For patients in general medical and mental healthcare settings, Veterans Affairs recommends recommend screening for unhealthy alcohol use periodically using the three-item Alcohol Use Disorders Identification Test, Consumption (AUDIT-C) or Single Item Alcohol Screening Questionnaire (SASQ).

https://www.healthquality.va.gov/guidelines/mh/sud

Last Accessed: May 20, 2024

Strength of Recommendation: Strong for

The USPSTF concludes that there is insufficient evidence to determine the benefits and harms of screening for unhealthy alcohol use in adolescents 12 to 17 years of age [263].

The three questions on the Alcohol Use Disorders Identification Test-Concise (AUDIT-C) inquire about frequency of alcohol use, typical amount of alcohol use, and occasions of heavy use. The test takes one to two minutes to administer. Preliminary evidence suggests that the USAUDIT-C (based on U.S. standards) may be more valuable in identifying at-risk college drinkers [265]. In contrast, the SASQ inquires about past-year alcohol use and takes less than one minute to administer [263].

The CAGE questionnaire is the best known and most often studied screening tool used to detect alcohol problems. In an office setting, the four CAGE questions are often used to detect alcohol problems [266]. The first question, "Have you ever felt the need to cut down on your drinking?" is an easy question to ask. It is not threatening and at the same time suggests to the patient that you understand their pathologic attachment to alcohol [266]. A positive answer to the first and second questions strongly suggests further evaluation and brief intervention [263]. However, by itself, the CAGE questionnaire is not an adequate screening for alcohol use problems; it should trigger more intensive screening if positive [266,267].

CAGE Questionnaire

Ask current drinkers the CAGE questions:

1. Have you ever felt that you should cut down on your drinking?

2. Have people annoyed you by criticizing your drinking?

3. Have you ever felt bad or guilty about your drinking?

4. Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (eye opener)?

If there is a positive response to any of these questions:

- Ask if this occurred during the past year.

A patient may be at risk for alcohol-related problems if:

- Alcohol consumption is:
Men:

14 drinks per week or

4 drinks per occasion

Women:

7 drinks per week or

3 drinks per occasion

Or

- One or more positive responses to the CAGE that have occurred in the past year

When is screening for alcohol problems appropriate?

- As part of a routine health examination

- Before prescribing a medication that interacts with alcohol

- In response to presenting problems that may be alcohol related

One "yes" response to the CAGE questionnaire suggests an alcohol use problem. More than one "yes" is a strong indication that a problem exists [267,268].

AUDIT Questionnaire

If a patient is CAGE positive, or if clinical suspicion remains high, the AUDIT questionnaire may be administered and can be extremely useful in detecting alcohol problems [252]. The AUDIT was developed by the WHO to identify persons whose alcohol consumption has become problematic to their health [253]. Research has shown that the AUDIT may be especially useful when screening women and minorities and has shown promise when tested in adolescents and young adults [254]. The AUDIT consists of 10 screening questions with three questions about the frequency and amount of drinking, three about dependence, and four questions about problems caused by alcohol [246,249,255].

1. How often do you have a drink containing alcohol?
0 Never

1 Monthly or less

2 2 to 4 times a month

3 2 to 3 times a week

4 4 or more times a week

2. How many drinks containing alcohol do you have on a typical day when you are drinking?
0 1 or 2

1 3 or 4

2 5 or 6

3 7 or 8

4 10 or more

3. How often do you have 6 or more drinks on one occasion?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

4. How often during the past year have you found that you were not able to stop drinking once you had started?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

5. How often during the past year have you failed to do what was normally expected from you because of drinking?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

6. How often during the past year have you needed a first drink in the morning to get yourself going after a heavy drinking session?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

7. How often during the past year have you had a feeling of guilt or remorse after drinking?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

8. How often during the past year have you been unable to remember what happened the night before because you had been drinking?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

4 Daily or almost daily

9. Have you or someone else been injured as a result of your drinking?
0 No

2 Yes, but not in the past year

4 Yes, during the past year

10. Has a relative or friend or a doctor or other health worker been concerned about your drinking or suggested you cut down?
0 No

2 Yes, but not in the past year

4 Yes, during the past year

The minimum score is 0 and the maximum possible score is 40. A score of 8 or more indicates a strong likelihood of hazardous or harmful alcohol consumption [203].

AUDIT-C Questionnaire

The AUDIT-C is a 3-question screening tool that can help identify persons who are at-risk drinkers (who may not be alcohol dependent) or who have active alcohol use disorders, including alcohol abuse or dependence [256].

1. How often do you have a drink containing alcohol?
0 Never

1 Monthly or less

2 2 to 4 times a month

3 2 to 3 times a week

4 4 or more times a week

2. How many standard drinks containing alcohol do you have on a typical day?
0 1 or 2

1 3 or 4

2 5 or 6

3 7 or 8

4 10 or more

3. How often do you have six or more drinks on one occasion?
0 Never

1 Less than monthly

2 Monthly

3 Weekly

A score of 4 or more in men and 3 or more in women (when not all points are from question 1) is considered positive for hazardous drinking or alcohol use disorder [273].

Single Alcohol Screening Question (SASQ)

The SASQ consists of one question: "How many times in the past year have you had X or more drinks in a day?" [263]. The question is individualized based on sex, with X being five for men and four for women. A response of more than one is considered positive and requires additional assessment.

ADDITIONAL STANDARDIZED QUESTIONS OR TESTS

Michigan Alcohol Screening Test (MAST)

The Michigan Alcohol Screening Test (MAST) continues to be a good screening test for alcohol abuse and dependence, but for optimal results it should be used with a questionnaire that asks about the amount and frequency of alcohol consumption. The following questions are from the 13-item Short MAST (SMAST) regarding the respondent's involvement with alcohol during the past 12 months [249]:

1. Do you think you are a normal drinker? (By normal we mean you drink less than or as much as most other people.)
No = 1 Yes = 0

2. Does your wife, husband, a parent, or other near relative ever worry or complain about your drinking?
No = 0 Yes = 1

3. Do you feel guilty about your drinking?
No = 0 Yes = 1

4. Do friends or relatives think you are a normal drinker?
No = 1 Yes = 0

5. Are you able to stop drinking when you want to?
No = 1 Yes = 0

6. Have you ever attended a meeting of Alcoholics Anonymous?
No = 0 Yes = 1

7. Has drinking ever created problems between you and your wife, husband, a parent, or other near relative?
No = 0 Yes = 1

8. Have you ever gotten into trouble at work because of your drinking?
No = 0 Yes = 1

9. Have you ever neglected your obligations, your family, or your work for two or more days in a row because you were drinking?
No = 0 Yes = 1

10. Have you ever gone to anyone for help about your drinking?
No = 0 Yes = 1

11. Have you ever been in a hospital because of drinking?
No = 0 Yes = 1

12. Have you ever been arrested for drunken driving, driving while intoxicated, or driving under the influence of alcoholic beverages?
No = 0 Yes = 1

13. Have you ever been arrested, even for a few hours, because of drunken behavior?
No = 0 Yes = 1

Key: There are two definitions for this test.

Seltzer Definition:

0-1 points = Nonalcoholic

2 points = Possibly alcoholic

3 or "yes" to 6, 10, or 11 = Alcoholic

Ross Definition:

5 points = Alcohol abuse

Comorbidity-Alcohol Risk Evaluation Tool (CARET)

There are certain risks and comorbidities (e.g., psychiatric and medical conditions requiring pharmacologic treatment) that may modify the criteria of at-risk drinking, especially within the geriatric population [275]. It is important for healthcare providers to assess each patient's threshold for alcohol use, taking into account their level of risk and comorbidities. The Comorbidity-Alcohol Risk Evaluation Tool (CARET) may be helpful in this task, with comorbidity-specific measures to place patients in "at-risk" or "not-at-risk" groups [276].

SCREENING FOR ALCOHOL ABUSE IN NON-ENGLISH-PROFICIENT PATIENTS

Communication with patients regarding history and current alcohol use patterns is a necessary step in determining if alcohol use has become a problem. When there is an obvious disconnect in the communication process between the practitioner and patient due to the patient's lack of proficiency in the English language, an interpreter is required. Frequently, this may be easier said than done, as there may be institutional and/or patient barriers.

If an interpreter is required, the practitioner should acknowledge that an interpreter is more than a body serving as a vehicle to transmit information verbatim from one party to another. Instead, the interpreter should be regarded as part of a collaborative team, bringing to the table a specific set of skills and expertise [277]. Several important guidelines should be adhered to in order to foster a beneficial working relationship and a positive atmosphere.

When interpreters are enlisted and treated as part of the interdisciplinary clinical team, they serve as cultural brokers, who ultimately enhance the clinical encounter. When providing care for patients for whom English is a second language, the consideration of the use of an interpreter and/or patient education materials in their native language may improve patient understanding and outcomes.

In addition, several organizations provide information and toolkits in languages other than English. The National Hispanic Medical Association offers an alcohol screening kit in Spanish, including patient education sheets [278]. The National Institute on Alcohol Abuse and Alcoholism also provides patient education brochures and pamphlets in English and Spanish [279].

LABORATORY TESTS

The FDA has approved a test to detect alcohol use disorder and alcohol-related diseases. The test detects the level of carbohydrate-deficient transferrin (CDT) in the body, which is elevated in persons with alcohol use disorder and remains elevated even several weeks after drinking is stopped [280]. The advantages of the CDT test are reliability and the availability of automated test results within four hours [281,282]. The CDT is often used in combination with other screening tests, such as the gamma-glutamyl transferase (GGT) test. While both CDT and GGT are independently associated with alcohol abuse, combining tests may dramatically increase sensitivity [267,283]. CDT is less sensitive/specific in women than in men [267].

Tests for Recent Alcohol Use (Hours)

The relationship between alcohol and the liver serves as the basis for many of the tests that identify possible alcohol abusers. Alcohol markers for recent alcohol ingestion include urine/breath/blood, AlcoPatch, methanol, urinary ethyl glucuronide (EtG) and ethyl sulfate(ES), whole blood phosphatidylethanol, and the ratio of 5-hydroxytryptophol (5-HTOL) to 5-hydroxyindole-3-acetic acid (5-HIAA) [267,284].

Tests for Less Recent Alcohol Use (Weeks)

The CDT test is often used to assess prolonged ingestion of high amounts of alcohol (more than 50–80 g/day for two to three weeks) [267]. Another test examines hemoglobin or whole blood acetaldehyde adducts. In a study of almost 3,000 women and 4,000 men, the combination of CDT and GGT compared with either alone shows a higher diagnostic sensitivity and specificity and is correlated more strongly with alcohol consumption than either test alone (Table 1) [285,286,287].

Table 1: LABORATORY MARKERS FOR ALCOHOL USE

Markers

Sensitivity

Specificity

Men

CDT

73%

96%

GGT

65%

89%

CDT with GGT

90%

84%

Women

CDT

52%

94%

GGT

54%

97%

CDT with GGT

76%

91%

Source: [285]

Tests for Chronic Alcohol Use (Years)

Tests in this category look at the classic toxic markers that use of alcohol leaves on the body. They include [267]:

- Liver function tests

- GGT

- Aspartate aminotransferase (AST)

- Alanine aminotransferase (ALT)

- Red blood cell index

- Mean corpuscular volume (MCV)

10. BRIEF INTERVENTION

Despite the fact that alcohol abuse complications have caused grave illness and many deaths, physicians are not always good at detecting alcohol and other drug abuse in their patients. Even when physicians and other health professionals identify an individual with alcohol use disorder, they are sometimes unsure of how to proceed. At times, the physician will offer help but the patient refuses. Nevertheless, the addiction specialist or the primary care physician with a continuous, comprehensive, patient-centered approach to the medical, psychosocial, and family issues is the ideal person to offer intervention, treatment, and recovery support.

Evidence Based Practice Recommendation

For patients without documented alcohol use disorder who screen positive for unhealthy alcohol use, Veterans Affairs suggest providing a single initial brief intervention regarding alcohol-related risks and advising to abstain or drink within established limits for daily and weekly consumption.

https://www.healthquality.va.gov/guidelines/mh/sud

Last Accessed: May 20, 2024

Strength of Recommendation: Weak for

Almost 20% of patients treated in a primary care setting drink at levels that may place them at risk for developing alcohol-related problems [267,288]. Brief intervention, as part of primary healthcare, can help reduce this risk. Brief intervention is generally conducted over one to a few visits with each session lasting from just a few minutes up to one hour. The type of brief intervention varies depending on how severe the problem. Brief intervention is often used with patients who have not yet developed alcohol use disorder and the goal may be to reduce drinking rather than abstinence. For persons with alcohol use disorder, the goal of brief intervention is abstinence, and for these individuals, referral to a more comprehensive treatment may be necessary. The USPSTF recommends that clinicians provide patients who are engaged in risky or hazardous drinking with brief behavioral counseling interventions to reduce alcohol misuse [263].

COMMON ELEMENTS OF BRIEF INTERVENTION

Miller and Sanchez proposed six elements, summarized by the acronym FRAMES, to describe the key elements of brief intervention: feedback, responsibility, advice, menu of strategies, empathy, and self-efficacy [289]. How these elements enhance effectiveness has been supported in other reviews [290,291]. Goal setting, follow-up, and timing are also important in brief intervention [292,293].

- Feedback of Personal Risk: Health professionals use current drinking behaviors, lab test results, and actual or potential consequences of drinking to provide patients with feedback on the risk of developing a problem.

- Responsibility of the Patient: Brief intervention often includes encouraging the patient to recognize that it is his or her responsibility and choice to change the behavior. This gives patients a sense of personal control in the process of change.

- Advice to Change: Brief intervention may also include recommendations about moderate- or low-risk drinking and advice on cutting down or eliminating alcohol consumption.

- Menu of Ways to Reduce Drinking: Patients are advised about how to cut back or avoid alcohol consumption. Health professionals can help patients set limits, recognize reasons for drinking, and acquire skills to avoid high risk drinking. Often, self-help materials such as drinking diaries are given to patients to help monitor their progress.

- Empathetic Counseling Style: Confrontational methods of brief intervention are not as effective as when health professionals use a more empathetic counseling approach.

- Self-Efficacy or Optimism of the Patient: Patients should be encouraged during brief intervention to help themselves by creating a plan to change their behavior and to think positively about their ability to reduce or stop drinking. Health professionals often use motivation-enhancing techniques.

In addition to FRAMES, the following items are important:

- Establishing a drinking goal: Patients should be encouraged to set a drinking goal with help from their physician. In some cases it is helpful to put the goal in writing. The drinking goal may be abstinence.

- Follow-up: It is important that the healthcare provider follows the patient's progress by telephone calls, or repeat tests or visits.

Patients are more likely to change their behavior when they recognize they have a problem and when they are optimistic about prospects for change; therefore, evaluating readiness to change is an important part of brief intervention. Some patients are not ready to change at the start of brief intervention, but may be ready when they experience adverse consequences of alcohol use. One study found that 77% of patients who were very confident and motivated were able to reduce their alcohol consumption by using self-help instructions and drinking diaries [291]. Motivation techniques are more useful to the resistant patient than self-help instructions.

Motivational interviewing is a method of brief intervention that is used to help move individuals from the precontemplation, contemplation, or determination/preparation stage into the action stage of change related to their drinking. In addition to focusing on the patient's view of the problem and consequences of the behavior, the interview often includes a comprehensive assessment of drinking behaviors with personalized feedback. Motivational interviewing therapists emphasize personal responsibility and support their patients' feelings of self-efficacy for making a change in their drinking. This method has demonstrated empirical efficacy with problem drinkers [294].

EFFECTIVENESS OF BRIEF INTERVENTION

Many studies have documented that brief intervention can assist patients without clinical alcohol use disorder to reduce alcohol consumption [295,296,297,298,299]. Brief intervention can also help motivate the patient with alcohol use disorder to enter treatment. One study in an emergency care setting found that 65% of individuals with alcohol use disorder who received brief counseling kept a follow-up appointment for treatment, compared with only 5% percent of those who did not have counseling [295]. Some studies have found that brief intervention may be as effective as more specialized treatment for some patients with alcohol use disorder [296,300].

Researchers conducted a comprehensive meta-analysis of controlled studies of brief intervention in treatment and nontreatment settings [301]. In this meta-analysis, effect sizes were calculated for several outcome variables, including amount and timing of alcohol consumed, abstinence rates and duration, proportion and duration of non-problem drinking, frequency of intoxication, laboratory markers, ratings of drinking severity, ratings of improvements, dependence symptoms, and problems resulting from drinking [301]. Two types of investigations were examined. The first group of studies (N=34) compared brief intervention to control conditions in non-treatment-seeking patients and generally did not include persons with severe alcohol problems. The second group of investigations (N=20) included persons who had more severe alcohol problems in a treatment setting. The effect size for brief intervention on alcohol consumption was noted at between three to six months in studies that excluded more severe alcohol problems [301]. This meta-analysis provides further documentation of the effectiveness of brief intervention provided by healthcare professionals to patients with alcohol problems, especially during the first three to six months after intervention. Effectiveness may decrease over time, so progress should be monitored and referrals made if necessary. For those with more severe alcohol problems in a treatment setting, brief intervention may be appropriate as an initial treatment with nonresponders receiving more extensive/intensive treatment [301].

In summary, brief intervention can help patients without disordered alcohol consumption reduce or stop drinking, can help motivate patients with alcohol use disorder to enter treatment, and can be used to treat some patients with alcohol use disorder. One study reported that brief intervention is associated with decreased alcohol consumption and decreased healthcare utilization, motor vehicle events, and other related costs [302]. The study also reported that the cost-benefit analysis suggests that for every $10,000 invested in early intervention, there will be a $43,000 decrease in future healthcare costs [302]. A meta-analysis of brief alcohol interventions for adolescents and young adults found that the interventions yielded modest, but clinically significant positive effects on problematic alcohol use trajectories among youth [303].

READINESS TO CHANGE

Readiness to Change was Dimension 4 of the third edition of the American Society of Addiction Medicine's (ASAM's) Six Dimensions of Multidimensional Assessment (also known as the ASAM Criteria) that is the standard for placement, continued stay, transfer, or discharge of patients with substance use disorder and co-occurring conditions [304]. Readiness to Change is now considered within each of the six dimensions in the fourth edition of the ASAM Criteria. The six dimensions of the fourth edition include: intoxication, withdrawal, and addiction medications; biomedical conditions; psychiatric and cognitive conditions; substance use-related risks; recovery environment interactions; and person-centered considerations (new). This new sixth dimension considers barriers to care, patient preferences, and need for motivational enhancement [304]. Several factors influence a person's readiness and ability to change behaviors. It is useful to help patients to weigh the risks of continued alcohol consumption and benefits of decreasing or eliminating alcohol consumption. Physicians can help motivate the patient to become ready for treatment if the patient appears ready to change.

Is the patient ready to change? The role of motivation is an important part of changing behavior. Table 2 summarizes the "pros" and "cons" of changing [305].

Table 2: MOTIVATIONS FOR CHANGE

Patients are more likely to seek treatment if:

- There are few actual or perceived barriers to treatment.

- The expectation is that treatment will work and that it is a positive change.

- They think they need help

- They "hit bottom."

- They no longer feel in control.

- They cannot change on their own.

- They want to change their behavior.

- They perceive that treatment will suit their needs

- There is social pressure to stop drinking or get treatment.

- They experience notable or multiple problems (e.g., black-outs, DUI arrest, etc.).

Patients are less likely to seek treatment if:

- There are numerous real or perceived barriers to treatment.

- They fear being unable to cope without alcohol.

- There are negative perceptions of treatment or changing behavior.

- They think that treatment will not work.

- There is fear of withdrawal.

- They think they will be stigmatized.

- They believe that they will be unable to stop.

- They fear failure.

- They perceive continued use as positive.

Source: [305]

The Stages of Change Model is also useful in determining where a patient is in the process of change [306]. The stages of change include:

- Precontemplation

- Contemplation

- Preparation

- Action

- Maintenance

- Relapse

11. TREATMENT

Treatment works. People who make the decision to stop drinking will be able to find the treatment and support they need to quit, remain sober, and regain their lives. However, as with treatment for any other disease, it is important to have a good idea of the options available in order to make informed choices.

PHASES OF TREATMENT

To understand treatment and make the right treatment choices, it helps to have an overview. Treatment should be seen as having three phases.

- Phase 1: Assessment and evaluation of disease symptoms and accompanying life problems including co-occurring medical and psychiatric conditions utilizing ASAM Criteria, detoxification (withdrawal management), acute stabilization of comorbid conditions, making treatment choices, and developing a plan

- Phase 2: Residential treatment or therapeutic communities, intensive and regular outpatient treatment, medications to help with alcohol craving and to discourage alcohol use, medications to treat concurrent psychiatric illnesses, treatment of concurrent medical conditions, trauma and family therapy, 12-step programs, other self-help and mutual-help groups

- Phase 3: Maintaining sobriety and relapse prevention with ongoing outpatient treatment as needed, facilitated group meetings, contingency management, 12-step programs, other self-help and mutual-help groups

Drug testing frequently, randomly, and for-cause should be a mandatory component of all phases. Transition from one phase to the next should not be based on time but on individual symptoms and progress.

Getting Started

First, the individual with alcohol use disorder must overcome denial and distorted thinking and develop the willingness to begin treatment—what AA calls the desire to stop drinking. At this stage, it is important to obtain the help of someone knowledgeable about treatment and the options available.

When getting started, some people have lost control over alcohol to such an extent that they will only be able to make immediate decisions and set the most basic goal of quitting drinking. Development of a detailed treatment plan with goals and choices may have to wait until after detoxification. On the other hand, getting started is exactly the place where some people with alcohol problems get stuck. In being stuck, denial is always a problem, but complete denial is not universal: people have various levels of awareness of their alcohol use problems, which means they are in different stages of readiness to change their drinking behavior. Professionals have taken advantage of this insight about alcohol use disorder to develop treatment approaches that are matched to a person's readiness to change. Addiction specialists can best decide which treatment is best and which is the less restrictive at specific times during recovery.

Detoxification

Individuals with alcohol use disorder must stop using in order to be able to progress in treatment, which can be done on either an inpatient or outpatient basis. Medical evaluation and treatment are particularly important at this stage. A large proportion of persons with alcohol use disorder develop dangerous withdrawal symptoms that must be medically managed either in a hospital or on an outpatient basis.

Although detoxification is a critical step for many with alcohol use disorder, most treatment professionals are reluctant to call it treatment, and for good reason. Treatment is what helps a person develop a commitment to change, keep the motivation to change, create a realistic plan to change, and put the plan in action. Successful treatment means a person begins to experience the rewards of seeing the plan work. Just taking away the alcohol does not automatically produce any of these outcomes.

Withdrawal Symptoms and Medical Management

Abrupt discontinuation or even cutting down on the amount of drinking by persons who are physiologically dependent on alcohol produces a characteristic withdrawal syndrome with sweating, rapid heartbeat, hypertension, tremors, anorexia, insomnia, agitation, anxiety, nausea, and vomiting [307]. In some ways, alcohol withdrawal resembles withdrawal from opioids, but unlike opioid withdrawal, which is rarely life-threatening in and of itself, alcohol withdrawal can be fatal. As many as 15% of persons with alcoholism progress from the autonomic hyperactivity and agitation common to withdrawal from other drugs to seizures and, for some, even death. In some cases, DT may occur within the first 48 to 72 hours and can include disorientation, confusion, auditory or visual hallucinations, and psychomotor hyperactivity [307].

The Revised Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar) is a symptom-triggered, 10-item scale that quantifies the risk and severity of alcohol withdrawal [307]. However, in order to be most useful, it requires patient input, which may not be feasible in patients undergoing severe DTs. If the patient is able, the assessment takes only minutes and aids in identification of patients who may need immediate pharmacologic treatment to prevent further complications. Very mild withdrawal usually corresponds with a score of 9 or less, mild withdrawal with a score between 10 and 15, modest withdrawal with a score between 16 and 20, and scores greater than 20 indicate severe withdrawal [308]. Patients scoring less than 9 may not require pharmacologic intervention. However, reassessment of symptoms should be performed every one to two hours until withdrawal is resolved.

Pharmacologic management of acute alcohol withdrawal generally involves the use of benzodiazepines, which reduce related anxiety, restlessness, insomnia, tremors, DT, and withdrawal seizures [307]. While benzodiazepines may have abuse liability in some patients, they have been safely used for years [309,310,311]. These medications may be administered either on a fixed interval or symptom-triggered schedule. However, both short-acting and long-acting benzodiazepines have their problems. The long-acting benzodiazepines can decrease rebound symptoms and work for long periods of time, but intramuscular absorption can be very erratic. Short-acting benzodiazepines have less risk of oversedation, no active metabolites, and considerable utility in patients with liver problems or disease. Yet, breakthrough symptoms can and do occur, and risk of seizure is imminent.

Patients with withdrawal symptoms are generally treated with diazepam or chlordiazepoxide until withdrawal subsides [307,309,310]. These medications are preferred due to their long action, which decreases the risk of rebound symptoms. If intramuscular administration is necessary, lorazepam is the drug of choice. More severe withdrawal is generally treated in a hospital setting. In patients with severe hepatic dysfunction, benzodiazepines that are metabolized outside the liver (lorazepam and oxazepam) are preferred. Treatment-resistant withdrawal warrants the use of phenobarbital or propofol, both with demonstrated efficacy in management [311].

Other medications may be used in conjunction with benzodiazepines for the treatment of withdrawal. Anticonvulsants, especially carbamazepine, are used safely to treat withdrawal [309]. They do not have abuse liability and have anticonvulsant and antikindling effects. Nevertheless, they also have problems. They do not reduce delirium and can have liver toxicity. The anticonvulsant gabapentin has demonstrated efficacy for mild alcohol withdrawal and early abstinence, but there is concern about its potential for abuse [312]. Alpha-adrenergic agonists like clonidine can reverse many of the behavioral symptoms of withdrawal but do not prevent seizure and can cause hypotension. However, for those patients with coronary artery disease, use of an alpha-adrenergic agonist or beta blocker may be indicated. It is important to note that these agents do not prevent seizures and can mask some signs of worsening withdrawal. They should be used only in conjunction with benzodiazepines [313]. More research is necessary regarding the efficacy of calcium channel antagonists in the treatment of alcohol withdrawal [314]. Studies have shown that those who have withdrawal seizures may have a worse prognosis than those who do not [92,93].

In the earliest views of alcohol use disorder, relapse to alcohol use was primarily seen as the patient's failure to respond to withdrawal treatment. After all, if the addicted person's primary problem was the trap of withdrawal, it would be reasonable to expect that the newly freed prisoner would gratefully and persistently grasp onto alcohol-free status, never to return voluntarily to the prison of addiction. But many people returned repeatedly for detoxification.

The medical profession was remarkably slow to recognize the ineffectiveness of repeated detoxification. Rather than question the underlying assumption that medical diagnosis and treatment of withdrawal was the solution to the problem of dependence, physicians seemed content to recycle people through one emergency room or detoxification experience after another for what often proved to be an addiction-shortened lifetime. Detoxification is only the first step in the treatment process, and the beginning of a lifelong process.

As the detoxification process occurs, careful evaluation should be done to identify co-occurring medical and psychiatric conditions that require acute stabilization. This should be done before facilitating a smooth transition to phase 2.

It is crucial to decide if the patient requires acute hospitalization or inpatient detoxification. It has been established that hospitalization can be cost-effective, but this is not always a possibility. However, if a patient appears to have acute intoxication, exhibits or will exhibit withdrawal symptoms that will require medical management, has failed outpatient detoxification, appears to be depressed or suicidal, relapses shortly after previous detoxification, has an extremely unstable home situation, or has the possibility of family disruption or job loss, then inpatient hospitalization is likely indicated. If you are in doubt, call a physician who is a member of the ASAM or the American Academy of Addiction Psychiatry who specializes in these problems.

Active Treatment

The next step is what has been commonly known as "active treatment." Relapse to alcohol use disorder is most likely to occur in the first three to six months after a person stops drinking; a period characterized by physiologic abnormalities, mood changes, and complaints of anxiety, depression, insomnia, and hormone and sleep problems. Getting active help and support during the early months of sobriety is critical for treatment to succeed.

This is the stage in which a person gains the motivation necessary to maintain a commitment to sobriety, the knowledge and skills necessary to stay sober, and the support systems necessary to cope with all the problems of daily life (the problems that everyone has to face) without resorting to the old "solution" of drinking. This is when the assistance of a treatment professional is important. A professional can help patients better understand how alcohol has affected their lives, so they can set goals and develop a plan to stay sober. In addition, the treatment professional can assist the patient in choosing the treatment options that are right for them.

Some proven medications are available to help with alcohol craving and to discourage alcohol use and will be discussed in detail later in this course. The treatment professional will also need to choose medications and treatments for concurrent psychiatric illnesses, like depression or anxiety, if appropriate, or for a variety of health problems that often accompany alcohol use disorder.

Research has shown that the longer people stay in treatment, remain sober, and are actively committed to sobriety, the more likely it is that they will maintain sobriety. Some treatment professionals think of the phase of active treatment as lasting from 6 to 12 months. During the first critical months of treatment, people often need a variety of supports, especially drug testing and AA or other self-help groups, to achieve and maintain lasting sobriety.

Maintaining Sobriety and Relapse Prevention

It is often difficult to pinpoint when the active treatment phase ends and a person enters the maintenance phase of recovery. In phase 2, people learn what they need to do to stay sober and they develop the many skills they will use to avoid relapse. A person could be said to enter this maintenance and growth stage when he or she is comfortable with these skills and has had a chance to rely on them to stay sober when life throws them the inevitable curveballs, either as a crisis or an everyday problem. Many people in recovery attribute their ongoing sobriety to participation in a support group such as AA or Women for Sobriety.

A promising approach to maintain gains made in active treatment is a low-intensity, telephone-based approach. In a 2005 study, this program of follow-up care was compared with two more intensive face-to-face continuing care interventions. Patients with alcohol use disorder who had completed 4-week intensive outpatient programs were provided three 12-week continuing care treatments. Telephone-based continuing care was found to be an effective form of step-down treatment for most patients with alcohol use disorder who complete an initial stabilization treatment, compared with more intensive face-to-face interventions [315].

ALCOHOLICS ANONYMOUS AND OTHER 12-STEP PROGRAMS

The grandfather of successful alcohol treatment is Alcoholics Anonymous, a self-help organization founded in 1935 that changed the way professionals thought about alcohol use disorder and treatment. AA developed a very successful 12-step program that combines self-help with a spiritual foundation and is based on the fellowship of recovering alcoholics. Although there is a spiritual foundation in AA, one is not required to be religious. The organization is run entirely by recovering alcoholics and reaches into virtually every community with a specific program as well as around-the-clock assistance. Membership is available to anyone wishing to join, and there are no financial dues. AA has probably done more to promote the self-help concept than any other organization.

For many people with alcohol use disorder, attending an AA meeting is like brushing their teeth. Prevention of relapse is an active daily process. AA provides fellowship that can be exceptionally positive and counterbalance the feelings of loss, grief, and shame often associated with alcohol use disorder.

AA and other 12-step programs are effective treatment programs that facilitate long-term abstinence after treatment, especially for patients with low psychiatric severity [316]. AA provides important peer-led support for individuals with alcohol use disorder. AA also helps individuals with relapse and relapse prevention by prescribing that people keep it simple, take it one day at a time, and avoid the people, places, and things associated with their use. They also help recovering alcoholics to develop positive lifestyles and find new ways to solve old problems. The feeling of fellowship, the support, and guidance to sobriety makes recovery more likely. Reduction of shame and guilt and acceptance of powerlessness over drinking may be reported by individuals with alcohol use disorder after attending meetings every day. An AA meeting may take one of several forms, but at any meeting you will find alcoholics talking about what drinking did to their lives and personalities, what actions they took to help themselves, and how they are living their lives today.

Patients can find the listing for a nearby AA group in the telephone book or online. Typically, a person in recovery will answer the telephone. Websites provide printable lists of all local meetings with time, location, types of meeting, and often directions. One of AA's principles is the value of performing services that will help other alcoholics. Answering the telephone at the local AA office is one of these services, reserved for those who have been in recovery long enough to answer questions in a knowledgeable manner and provide a nonjudgmental ear.

A Cochrane review found that AA, the premier mutual aid peer-recovery program definitely helps people get sober [317]. In addition, AA has significantly higher rates of continuous sobriety compared with evidence-based professional mental health therapy, such as cognitive-behavioral therapy, alone. AA was often was found to be markedly better than other interventions or quitting cold turkey. One study found the program 60% more effective than alternatives [317].

The study by Harvard and Stanford addiction researchers of 10,565 subjects determined that AA was nearly always found to be more effective than psychotherapy in achieving abstinence [317].This review concluded that AA participation improved the duration of abstinence and the amount they reduced their drinking (if they continued drinking). AA had harm reduction features as well, reducing the medical consequences of drinking and related healthcare costs. While not a random assignment treatment comparison study, in this analysis, AA was never found less effective than other treatments. As such, AA could be a helpful addition to any treatment for alcohol use disorder. For example, adding AA to naltrexone would be expected to be better than pharmacotherapy alone. Recent studies and the preponderance of evidence supports the effectiveness of 12-step program involvement in sustaining abstinence [10]. Stable and long-term abstinence was associated with living longer, better mental health, better marriages, being more responsible parents, and being successful employees.

A brain imaging study by Yale researchers showed that those diagnosed with alcohol use disorder showed disruptions of activity between the ventromedial prefrontal cortex and striatum, a brain network linked to decision making [318]. Time is necessary for re-learning how to be sober but also for brain recovery. The more recent the last drink, the more severe the disruption, and the more likely the individual will relapse to drinking. The Yale researchers also found that the severity of disruption between these brain regions recovers very slowly, day after day, gradually over time. They conclude the longer subjects with alcohol use disorder abstain from alcohol, the better. The number of days of alcohol abstinence at treatment initiation significantly affected functional disruption of the prefrontal-striatal responses to alcohol cues in patients with alcohol use disorder and brain imaging abnormalities [318].

COUNSELING

Cognitive-behavioral therapies (CBTs) are among the most frequently evaluated approaches used to treat substance use disorders [319,320]. CBTs have been shown to be effective in several clinical trials of substance users [321]. Characteristics of CBTs include:

- Social learning and behavioral theories of drug abuse

- An approach summarized as "recognize, avoid, and cope"

- Organization built around a functional analysis of substance use (i.e., understanding substance use with respect to its antecedents and consequences)

- Skill training focused on strategies for coping with craving, fostering motivation to change, managing thoughts about drugs, developing problem-solving skills, planning for and managing high-risk situations, and cultivating drug refusal skills

Basic principles of CBTs are that [322,323]:

- Basic skills should be mastered before more complex ones are given.

- Material presented by the therapist should be matched to patient needs.

- Repetition fosters the development of skills.

- Practice is needed for mastery of skills.

- The patient is an active participant in treatment.

- Skills taught are general enough to be applied to a variety of problem areas.

Structured behavior therapy techniques can be effective components of alcohol use disorder treatment. Contingent incentive procedures are designed to enhance a patient's motivation to meet treatment goals by offering concrete rewards for specific performance outcomes.

Behavioral therapy techniques are often part of CBT. In this approach, substance use is believed to develop from changes in behavior and a reduction in opportunities for reinforcement of positive experience. The goal is to increase the person's engagement in positive or socially reinforcing activities. Techniques such as having patients complete a schedule of weekly activities, engaging in homework to learn new skills, role-playing, and behavior modification are used. Activity, exercise, and scheduling are major components of this approach based on the following:

- Drug abuse patients need motivation and skills to succeed in stopping drug use.

- Research has shown that drug abuse behavior can be reduced by offering contingent incentives for abstinence.

- The most striking successes have come from positive reinforcement programs that provide contingent incentives for abstinence using money-based vouchers as rewards.

- Research provides examples, but treatment providers may need to be creative in discovering reinforcers that can be used for contingency management in their own clinical settings.

Family therapy is a highly effective treatment for alcohol use disorder, especially in adolescents. While most treatments emphasize the individual as the target of intervention, the defining characteristic of family therapy is the transformation of family interactions. Repetitive patterns of family interactions are the focus of treatment. Changing these patterns results in diminished antisocial behavior including alcohol abuse. Family therapy can work with a broad range of family and social network populations. Family therapy approaches have developed specific interventions for engaging and keeping reluctant, unmotivated adolescents and family members in treatment.

MEDICATIONS USED TO TREAT ALCOHOL USE DISORDER

Alcohol drinking is an immensely complex human behavior, but it has been modeled in laboratory animals. Two similar strains of alcoholic rats, the alcohol-preferring (P) rats and the high-alcohol-drinking (HAD) rats, have been successfully used to study alcohol use disorders. Like patients with DSM-5-TR qualifying alcohol use disorders, these rats self-administer alcohol, show tolerance, lose control over alcohol, and spend a lot of time. They also have cravings and physical stigmata of withdrawal, providing psychopharmacologic researchers with excellent face validity with animal models. Models have helped us develop anti-withdrawal, anti-craving, and harm-reducing treatments.

Several medications are available to help treat alcohol use disorder [324,325]. Some are used for detoxification and others are used to prevent relapse. Research has shown that medications are most effective when used in conjunction with other therapies.

Disulfiram

Disulfiram, commonly known as Antabuse, was the first drug to be made available for the treatment of alcohol use disorder. It was approved for treatment of alcohol use disorder by the FDA in 1951 and has been used safely and effectively for more than half a century. It works by blocking an enzyme, aldehyde dehydrogenase, that helps metabolize alcohol. Taking even one drink while on disulfiram causes the alcohol at the acetaldehyde stage to accumulate in the blood. This produces nausea, vomiting, sweating, and even difficulty breathing. More alcohol in the patient's system produces more severe reactions (e.g., respiratory depression, cardiovascular collapse, unconsciousness, convulsions, death) [325,326]. Patients must also be mindful of consuming even minute amounts of alcohol in foods, over-the-counter medications, mouthwash, and even topical lotions. Disulfiram can be effective for people who have completed alcohol withdrawal, are committed to staying sober, and are willing to take the medication under the supervision of a family member or treatment program [325]. Due to more modern and improved medication modalities, many clinicians prescribe disulfiram as a last resort intervention. Although widely used, it is less clearly supported by clinical trial evidence [327,328,329].

The recommended dose for disulfiram is 250 mg/day, which can be increased to 500 mg based upon whether a patient experiences the disulfiram-ethanol reaction [330]. Doses may need to be reduced in patients older than 60 years of age [325]. Labeling for disulfiram includes several precautions regarding drug-drug interactions; therefore, caution should be used when prescribing it to older adults at risk for polypharmacy [325]. Due to the physiologic changes that occur with use, use of disulfiram is not recommended in patients with diabetes, cardiovascular or cerebrovascular disease, or kidney or liver failure. It also is contraindicated in the presence of psychoses and pregnancy and in those with high levels of impulsivity and suicidality [325].

Naltrexone

Naltrexone (ReVia) is an opioid antagonist that interferes with the rewarding or pleasurable effects of alcohol and reduces alcohol craving [331,332,333]. The exact mechanisms by which naltrexone induces the reduction in alcohol consumption observed in patients with alcohol use disorder is not entirely understood, but preclinical data suggest involvement of the endogenous opioid system [325]. Naltrexone has been shown to reduce alcohol relapses, decrease the likelihood that a slip becomes a relapse, and decrease the total amount of drinking [325]. The FDA approved the use of oral naltrexone in alcohol use disorder in December 1994 [325,333]. In 2006, the FDA approved an extended-release injectable formulation, which is indicated for use only in patients who can refrain from drinking for several days prior to beginning treatment [325]. In 2010, the FDA approved the injectable naltrexone for the prevention of relapse to opioid dependence following opioid detoxification [325]. Naltrexone, which has long been used to treat heroin addicts, was not known as a treatment that could reduce alcohol relapse until the 1980s. In 1980, researchers reported reductions in monkey ethanol self-administration when they were pretreated with naltrexone [334].

By 1992, researchers reported a six-week, double-blind placebo-controlled outpatient naltrexone trial with 70 individuals with alcohol use disorder. They found that the naltrexone-treated patients had a lower relapse rate, fewer drinking episodes, longer time to relapse, and reduced tendency for a slip to become a relapse [335]. These and other data suggested that endogenous opioids were important in alcohol reinforcement.

Also in 1992, researchers compared naltrexone with placebo and found that naltrexone-treated patients had lower rates of relapse to heavy drinking, consumed fewer drinks per drinking-day, and had lower dropout rates than placebo-treated patients with alcohol use disorder [336]. These results have since been supported by other studies [337]. Research suggests that naltrexone may be most effective for individuals with alcohol use disorder and a family history of alcohol use disorder [338]. However, one study found no significant effects for naltrexone in individuals with a family history of alcoholism on percentage of days abstinent, drinks per drinking day, and percentage of heavy drinking days [339].

Another study investigated pretreatment social network variables as potential moderators of naltrexone's treatment effects [340]. The study sample included 1,197 participants from the COMBINE study, the largest pharmacotherapy trial conducted for alcoholism in the United States. In treatment conditions involving combined CBT and medical management, the effects of naltrexone on heavy drinking were significantly greater for individuals with frequent drinkers in their social network and greater frequency of contact with those drinkers, indicating patterns of environmental exposure to alcohol [40,341]. In an attempt to replicate and extend the findings of the COMBINE study, researchers conducted a secondary analysis of a 12-week randomized clinical trial of daily or targeted naltrexone among problem drinkers, with a focus on those who received a daily dose of either naltrexone or placebo [342]. Four reward/relief phenotypes were identified: low reward/low relief; low reward/high relief; high reward/low relief; and high reward/high relief. When compared with the placebo group, individuals in the high reward/low relief phenotype who received daily naltrexone had significantly fewer drinks per drinking day and a lower proportion of heavy drinking days [342].

After a complete history, physical exam, and laboratory testing, most patients are started on 50 mg orally per day [234]. For most patients, this is the safe and effective dose of naltrexone. However, in a four-month study period, the COMBINE study demonstrated efficacy of naltrexone at a dose of 100 mg daily [343]. Some treatment providers give patients a naltrexone identification card or ask them to order a MedicAlert bracelet that clearly indicates that they are maintained on an opioid antagonist, so if they need an opiate drug or medication for pain relief, the dose of the pain medication can be adjusted higher. Meta-analyses have revealed that approximately 70% of previous clinical trials that measured reductions in "heavy or excessive drinking" demonstrated an advantage for prescribing naltrexone over placebo [344]. In another trial, naltrexone was determined to have the greatest impact on reducing daily drinking when craving for alcohol was highest [345]. The approved dose of the extended-release formulation is 380 mg IM once per month. Pretreatment with oral naltrexone is not required before induction onto extended-release injectable naltrexone [325].

The most common side effects of naltrexone are light-headedness, diarrhea, dizziness, and nausea. Pain or tenderness at the injection site is a side effect unique to the extended-release injectable formulation [325]. Most side effects tend to disappear quickly in most patients. Naltrexone is not recommended for patients with acute hepatitis or liver failure, for adolescents, or for pregnant or breastfeeding women [325,343]. Weight loss and increased interest in sex have been reported by some patients. In general, patients maintained on opioid antagonists should be treated with nonopioid cough, antidiarrheal, headache, and pain medications. The patient's family or physician should call the treating physician if questions arise about opioid blockade or analgesia. It is important to realize that naltrexone is not disulfiram; drinking while maintained on naltrexone does not produce side effects or symptoms.

Naltrexone works best when it is used in the context of a full spectrum of treatment services, possibly including traditional 12-step fellowship-based treatments. Studies show also that naltrexone is effective when coupled with CBT. Patients receiving medical management with naltrexone, CBT, or both fared better on drinking outcomes [343].

Acamprosate

Acamprosate (Campral) is a synthetic compound that has a chemical structure similar to that of the naturally occurring amino acid neurotransmitters taurine and GABA [234]. Because chronic alcohol use is associated with decreased GABA and glutamate activity, a hyperexcitable glutamate system is one possible alcohol withdrawal mechanism. Glutamate systems may become unstable for 12 months after a person stops drinking. In a review of published, double-blind, placebo-controlled clinical trials evaluating the safety and efficacy of acamprosate in the treatment of alcohol use disorder, Mason reported that acamprosate appeared to improve treatment completion rate, abstinence rate and/or cumulative abstinence during treatment, and time to first drink, than placebo [346]. The effect on abstinence, combined with an excellent safety profile, lend support to the use of acamprosate across a broad range of patients with alcohol use disorder. A dose of 2,000 mg/day is associated with the greatest efficacy regardless of body weight [347]. It is important to note that medication in combination with therapies can improve outcomes.

In July 2004, after many years of safe use in Europe and around the world, the FDA approved the use of acamprosate for the maintenance of alcohol abstinence [333]. As in the case of naltrexone, acamprosate reduces the reinforcing (pleasurable) effects of alcohol to reduce craving. Oral dosing is two 333-mg delayed-release tablets three times daily [234,325]. Common side effects include diarrhea, anxiety, insomnia, nausea, dizziness, and weakness. Some research indicates that acamprosate may worsen depression and/or suicidal ideation; so, patients with a history of major depression should be monitored closely or prescribed a different medication [234]. Acamprosate is contraindicated in patients with severe renal impairment [234,325]. Due to risk of diminished renal function in patients 65 years of age and older, baseline and frequent renal function tests should be performed in this population. Dose reductions also may be necessary [325].

The effectiveness of acamprosate in promoting abstinence has not been demonstrated in individuals who have not completed detoxification or who have not achieved alcohol abstinence before beginning treatment [325]. An analysis of many studies of acamprosate showed a benefit in maintaining abstinence when coupled with CBT [343]. A systematic review found similar benefit [348]. Results of other research into the effectiveness of acamprosate have been mixed. One study showed no improvement in measures of psychological well-being or health status when compared to treatment with placebo. Another study demonstrated both safety and effectiveness of acamprosate for treating alcohol use disorder [349].

Baclofen

Baclofen is a GABA agonist that may prove to be a unique therapeutic alternative to reduce alcohol craving and consumption. In a small, 12-week trial, patients with alcohol use disorder were given 10 mg of baclofen three times daily paired with motivational enhancement therapy. Patients experienced a reduction in number of drinks, drinking days, anxiety, and craving [350]. In a study of patients with alcohol use disorder and liver cirrhosis, baclofen was also found to work favorably in maintenance of alcohol abstinence. Seventy-one percent of baclofen-treated patients maintained abstinence as compared with 29% of the placebo group [351]. A 2018 meta-analysis of 12 randomized controlled trials that compared the efficacy of baclofen to placebo found that baclofen was associated with higher rates of abstinence than placebo but that its effects were not superior to placebo in increasing the number of abstinent days or in decreasing heavy drinking, craving, depression, or anxiety [352]. A 2023 systematic review of 17 randomized controlled trials involving 1,818 participants found that baclofen reduces the risk of relapse to any drinking and increases the percentage of abstinent days, mainly among detoxified participants. The agent was not found to reduce the number of heavy drinking days or the number of drinks per drinking days [353].

Anticonvulsants

Research has demonstrated that topiramate is efficacious in decreasing heavy drinking among individuals with alcohol use disorder [354]. In a controlled study, topiramate produced significant and meaningful improvement in a wide variety of drinking outcomes [355]. Topiramate may suppress the craving and rewarding effects of alcohol [356]. In a double-blind, controlled trial, 150 patients with alcohol use disorder were randomized to escalating doses of topiramate (25–300 mg/day) or placebo. Those on topiramate had a reduction in self-reported drinking (number of drinks and drinking days), alcohol craving, and plasma y-glutamyl transferase (an indicator of alcohol consumption) [357]. Side effects of topiramate include numbness in the extremities, fatigue, confusion, paresthesia, depression, change in taste, and weight loss. Use of topiramate for alcohol use disorder is off-label [234].

Carbamazepine has proven effective for treating acute alcohol withdrawal [358]. Its side effects include nausea, vomiting, drowsiness, dizziness, chest pain, headache, trouble urinating, numbness in extremities, liver damage, and allergic reaction [234]. In a 12-month, double-blind, placebo-controlled trial, 29 patients were assigned to carbamazepine three times daily (to reach an average blood level of 6 mg/liter) or placebo. Those treated with carbamazepine showed a delay in time to first drink and a decrease in number of drinks and drinking days [359].

Oxcarbazepine is a carbamazepine derivative, with fewer side effects and contraindications, used to prevent relapse in patients with alcohol use disorder by blocking alcohol withdrawal [358]. A group of 84 patients with alcohol use disorder following detoxification were randomized to 50 mg naltrexone, 1,500–1,800 mg oxcarbazepine, or 600–900 mg oxcarbazepine for 90 days. Approximately 58.6% of the high-dose oxcarbazepine patients remained alcohol-free, a significantly larger number as compared to the low-dose (42.8%) and naltrexone groups (40.7%) [360].

Treatment in Special Populations

Ondansetron is a serotonin antagonist and antiemetic that may block the rewarding effects of alcohol, specifically in the early-onset alcoholic subgroup. Early-onset alcoholism differs from late-onset in its association with abnormal serotonin and antisocial behavior. In a double-blind, controlled trial of ondansetron as an adjunct to cognitive-behavioral therapy, ondansetron was shown to reduce self-reported drinking and increase abstinence as compared to placebo. These results were confirmed by measure of plasma carbohydrate deficient transferring, a biomarker of alcohol consumption [361]. One hypothesis suggests that ondansetron may reduce drinking in individuals with alcohol use disorder with the LL genotype [362].

Buspirone hydrochloride is a dopamine antagonist and partial agonist for serotonin, exhibiting anxiolytic properties. In a 12-week randomized, placebo-controlled trial among 61 patients with alcohol use disorder and anxiety, buspirone was associated with slower return to heavy alcohol consumption and fewer drinking days [363]. One study found buspirone to be effective in treatment of comorbid anxiety disorder and alcohol use disorder [364].

Clozapine is an atypical antipsychotic approved to treat schizophrenia and its resultant symptoms (e.g., hallucinations, suicidal behavior). In case studies, it has shown promise in the treatment of comorbid substance use. In a study of 151 individuals with schizophrenia with comorbid substance use, 36 were given clozapine [365]. Those who abused alcohol experienced a reduction in drinks and drinking days.

Other drugs under trial for use in the treatment of alcohol use disorder include varenicline and lithium. Varenicline does appear to help reduce drinking in some individuals with alcohol use disorder; however, concerns exist regarding reports of an association between the drug and an increased risk for suicidal thoughts and cardiovascular events [366]. Studies have demonstrated that varenicline helps reduce alcohol craving and consumption in patients with alcohol use disorder and in individuals with alcohol use disorder who also smoke [367,368,369]. None of the medications mentioned for alcohol use disorder are recommended for women who are pregnant or breastfeeding.

TREATMENT OF ALCOHOL WITHDRAWAL

Benzodiazepines have been used for 30 years in the United States as the primary medical treatment for alcohol withdrawal syndrome. All benzodiazepines appear similarly effective in the treatment of alcohol withdrawal syndrome [370]. Although benzodiazepines are the drugs of choice, there are concerns about the side effects and, as stated, problems of abuse, especially for outpatient detoxification. Benzodiazepines are sedatives and cause deficiencies in psychomotor abilities that, when combined with alcohol, can cause accidents and affect the ability to think clearly. However, benzodiazepines are, and have been, effective in treating alcohol withdrawal symptoms and preventing most seizures. Other regimens for alcohol withdrawal syndrome include barbiturates, propofol, and ethanol [371,372,373].

A desirable alternative to benzodiazepines would be a nonsedative anticonvulsant that has less potential for abuse and dependence. Valproic acid has been used in Europe safely and successfully for many years for alcohol withdrawal syndrome, but is only approved by the FDA for the treatment of mania, seizures, and migraines. Valproic acid should be used as an adjunctive therapy, not as monotherapy [370]. According to clinical reports, valproic acid is an anticonvulsant with no potential for abuse and is better tolerated by patients. Valproic acid also has less cognitive impairment and causes fewer deficiencies of psychomotor abilities than benzodiazepines; however, benzodiazepines have allowed for safe detoxification for patients with alcohol use disorder since they were approved. While detoxification is not treatment, and detoxification problems have not been the most important problem area in successful treatment of the patient with alcohol use disorder, these are important findings.

Recognizing that relapse prevention and harm-reducing medications are safe and effective in alcohol use disorders, fewer than 10% of these patients are given medication-assisted treatment. In a 2018 meeting of the American Psychiatric Association, experts suggested [374]:

- Naltrexone or acamprosate should be offered to those patients with moderate- to-severe alcohol use disorder that have a goal of reducing consumption or achieving abstinence, prefer pharmacotherapy, or have not responded to nonpharmacologic therapies, and have no contraindications.

- Disulfiram should be offered to patients with severe alcohol use disorder that seek to achieve abstinence, prefer the therapy, or have not responded (or are intolerant) to naltrexone or acamprosate, and have no contraindications. Additionally, patients must understand the risks associated with consuming alcohol while on disulfiram.

- Topiramate or gabapentin should be offered to patients with moderate-to-severe alcohol use disorder when they aim to reduce or achieve abstinence, prefer them to other medications, or have not responded to naltrexone or acamprosate and have no contraindications.

- Benzodiazepine use is discouraged except in patients with alcohol use disorder who require treatment for acute alcohol withdrawal.

MANDATORY TREATMENT

Even coerced or court-mandated treatment for alcohol use disorder can work. In a follow-up study (six months to one year) of Florida physicians with alcohol use disorder, 84% had positive outcomes, defined as positive counselor and physician assessment, negative alcohol testing, group attendance, and full return to work [375].

12. CONCLUSION

In a society where alcohol use is ubiquitous, it is important for healthcare professionals to recognize the signs and symptoms of alcohol abuse and intervene before a state of dependence is reached. It is critical to stress upon patients the negative health effects of excessive alcohol consumption, especially the synergistic effects of alcohol and tobacco use, beginning at an early age. Owing to the several benefits provided by low to moderate drinking as discussed in this course, certain patients can be advised to drink more regularly, provided alcohol use is not contraindicated due to drug or herb interactions.

13. RESOURCES

Al-Anon Family Groups

The mission of Al-Anon is to provide support for friends and families of problem drinkers.

https://al-anon.org

Alcoholics Anonymous

https://www.aa.org

American Society of Addiction Medicine (ASAM)

The nation's medical specialty society dedicated to educating physicians and improving the treatment of individuals suffering from alcoholism and other addictions. The mission of the ASAM is to:

- Increase access to and improve the quality of addiction treatment

- Educate physicians, medical and osteopathic students, other healthcare providers, and the public

- Promote research and prevention

- Promote the appropriate role of the physician in the care of patients with addiction

- Establish addiction medicine as a specialty recognized by the American Board of Medical Specialties

https://www.asam.org

301-656-3920

MedicAlert Foundation

https://www.medicalert.org

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Evidence-Based Practice Recommendations Citations

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