Trigger Events

August 29, 2014

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The term “trigger even” is commonly used by people struggling to understand what turns on their addictive thinking, ear lying warning signs (drug seeking behavior), and the strong attraction or need to bet involved in high risk situations. Recovering people intuitively understand the idea of relapse because it is linked to the metaphor of a gun. When you are holding a  load gun and pull the trigger it fires. Addiction, especially in early recovery, is very much a like a loaded gun with a sensitive trigger.

When you pull the addiction trigger, the disease of addiction fires off addictive thinking, automatic addictive or drug seeking behavior, and a craving or urge that pulls you toward high risk situations. One you are in a high risk situation you have put yourself in a HIGH RISK SITUATION which takes you away from recovery support, puts you around people, place, and things that support addictive use and make it easy for you to use. The high risk situation also provides social support to start using and social criticize if you refuse to start using. In a high risk situation there is also usually the false promise that goes like this: “I can use my addictive substance just this once, no one will know, and I can just renew my sobriety tomorrow. That, of course, is a very dangerous way from a recovering addictive to be thinking.

Most recovering people intuitively understand what a trigger is, and can describe exactly what pulled the trigger and what happened after the trigger fired off the movement toward addiction.  The problem is that very few recovering people or professional can tell you what a trigger is.  Events and situations that act as powerful triggers for some people have no effect on others. Even more confusing, on some days a certain situation, like have lunch in a restaurant that serves alcohol, activates a powerful trigger. On other days, haven lunch in the same place with the same people does nothing to pull the trigger that activates craving. Why is this?

Many people mistaken believe that the trigger lives in the external person, place or thing that sets it off. As a result addiction professionals teach recovering people to identify and avoid common trigger events. Rarely do recovery people get a clear explanation of psychobiological dynamics that that make triggers so powerful. Without a clear understanding of the psychobiological dynamics of a trigger event, the only way to learn to many them is through trial and error.

Bob Tyler, in his book Enough Already!: A Guide to Recovery from Alcohol and Drug Addiction, explains it this way:

“If we don’t know what makes a trigger a trigger, the only thing we can teach patients to do is to avoid them. Now, how much success do you think our patients will have avoiding triggers living in this society which is permeated by alcohol and drugs? Probably not very much! Therefore, it is essential that we are knowledgeable about how a trigger actually becomes a trigger so we can teach our patients how to recover from triggers?” Although Bob Tyler talks about “recovering from triggers, and I talk about identifying, managing, and disempowering triggers, our basic concept is the same. Recovering people can learn to identify avoid, manage, and eventual, turn off the ability of the trigger to activate craving and drug seeking behavior. This happens spontaneously as people get into long-term recovery. There are techniques and methods for pan aging and disempowering triggers that can make the process a lot easier.

Trigger Event – Defined

A trigger event as “any internal or external occurrence that activates a craving (obsession, compulsion, physical craving, and drug-seeking behavior)” (Gorski, 1988). let’s break down this definition:

  • “internal” occurrences are thoughts or feelings;
  • “external” occurrences involve the five senses: sight, sound, smell, taste, and touch.
  • In order for something to be a trigger, such an event must be connected in some way to the person’s using alcohol to other drugs.
  • The trigger is stronger if the event happen just before, or simultaneous to, the actual use (Gorski, 1988).
  • The most important thing to know about what makes a trigger a trigger is its connection to the use.

Bob  Tyler explains it this way: “A simple way of explaining this is by relating it to classical (or Pavlovian) conditioning. Ivan Pavlov was a Russian scientist who won the Nobel Peace Prize in 1904 for his research in digestive processes. While studying the relationship between salivation and digestive processes in dogs, he would show a dog meat powder and measure the resulting salivation level of the dog – they did this repeatedly. One day, Dr. Pavlov noticed that when he walked into the lab, that the dog started to salivate even before showing it the meat powder. There appeared to be some connection made for the dog between Dr. Pavlov and the meat powder which caused it to salivate. To study this phenomenon, he added a third variable (a bell) and rang it just prior to showing the dog meat powder and measured the resulting salivation level. He did this repeatedly: bell à meat powder à salivation, bell à meat powder à salivation, etc. He eventually found that he could ring the bell, not present the meat powder, and the dog would still salivate. Thus, there was a connection made for the dog between the bell and the meat powder that prompted the salivation (PageWise, 2002). For our purposes, the bell is the trigger for the dog’s drug of choice – meat powder, which caused the dog to salivate for, or crave, the meat powder. The challenge for the addicted is to identify the bells (triggers) that cause them to salivate (crave) their drug of choice. This will allow them to avoid or manage such triggers until the time in their recovery comes to start recovering from them.”

Disempowering (Recovering from) Triggers

There are three phases in disempowering  a trigger:

  • Phase 1: Avoidance: Make a list of the most powerful triggers that were associated with you drinking and drugging and plan to avoid them.
  • Phase 2: Gradual re-introduction with adequate recovery support: If consciously exposing yourself to a trigger it is best to have a friend in recovery to help you prepare, go through the experience with the trigger, be their to help you get out, and then talk about the experience and the thoughts and feelings that it stirred up.
  • Phase 3: Extinction. Phase I is to “eliminate as many of them as you can, for a limited period of time, until stable” (Gorski, 1988). As stated previously, in very early sobriety, you do not go to bars or other using places, you avoid people who use and drink, and you avoid any other triggers you identify.

“The second phase is a gradual reintroduction of the triggers so that the person can learn how to cope with them” (Gorski, 1988). This does not mean to gradually re-introduce the addict into the crack house or their favorite watering hole, but there are some trigger situations that you should be able to eventually participate in. As stated earlier, alcohol permeates our society and you would have to live a very sheltered life in order to avoid it over the long-term. Therefore, in order to lead any kind of normal life, gradual re-introduction to some trigger situations is necessary. This re-introduction process is best done with the addict’s sponsor or with a therapist or group if they have one. Following is an example of this process in my own sobriety.

The following story reported by Bob Tyler gives and excellent example:

“When I was about 90 days sober and still involved in the aftercare portion of my treatment program, we were invited to the wedding of my wife’s cousin in Chandler, Arizona. I thought: “I’d really like to go!” However, I had learned from past experience that decisions I made on my own in relation to my sobriety were typically bad ones. So I decided to leave it completely up to my group and put it out to them. The consensus was that since I was still working a very strong sobriety program, going to daily meetings, and going with my supportive wife, I could probably stay sober if I created a sobriety plan. The group then proceeded to help me put this plan together.

  • Suggestion 1: Carry a Big Book (Alcoholics Anonymous) onto the plane and read it: The thinking was that since flying on an airplane was a trigger for me to drink, it would be difficult to order a drink while holding a Big Book in my hand. The book has an embossed cover so nobody would know what it was and, if they recognized it, they probably have one and I might meet someone in the program.
  • Suggestion 2: Keep you recovery support system close. If traveling, find out where the lo=cal meetings are and make telephone contact with one or more local members. Have a written plan to go to 12-Step meetings each day and have an accountability system built-in.  I was in Arizona. They had me call the downtown Los Angeles Central Office of Alcoholics Anonymous (AA) to get the number of the central office in Chandler, Arizona. I was to get a meeting scheduled for each day I was there and, if possible, schedule a meeting for the time of the reception so if I got into trouble, I could simply leave the reception and go to a meeting. In fact, this actually happened – here’s a funny little story:
  • Suggestion 3: Have an Emergency Escape Plan if Craving Is Triggered: Bob Tyler went to the reception.  “I found myself talking to my wife’s uncle next to the wet bar at his home.” Bob said.  “Suddenly, someone plopped down a bottle of my favorite whiskey onto the bar right in front of me. After recovering from my slight panic, I excused myself and informed my wife  that I was going to a meeting. She was supportive because I had talked with her about this emergency plan before we left.   Fortunately, I got the address and directions to the from AA’s Central Office before I left. This made it easier for me to go.”

After the meeting, Bob went back to the reception where he noticed “everyone was having a great time dancing. This really looked fun to me, but I had never danced sober before. I always had to have at least a few drinks in me first because I was not a very good dancer and cared too much about what other people thought of me. When I had a few drinks, I felt like I danced like John Travolta and you didn’t think so – too bad!” It’s amazing how many recovering people won;t dance in recovery because they fear it will make them feel stupid and activate a craving. Bob is not alone here. So Bob developed a plan:

He waited for a fast song that he liked, and slid onto the dance floor while playing “air guitar” and, and starting to  dance. “A Van Halen song came on,” says Bob, and I was off and running. Little did I know that just after I left for my meeting, the bride and groom arrived, walked across the portable dance floor, and everyone followed tradition by throwing rice at them. You can imagine what happened next. As I attempted to slide onto the dance floor, my feet hit the rice and came right out from under me. I hit the floor, followed by two of my wife’s female cousins (one of them the bride!) who I managed to take down with me – one of them right onto my lap. I rose to my feet with my beet-red face and, as I looked around the dance floor, I could see my wife’s family’s reaction which I perceived as, “There he goes, he’s drunk again” – and I was probably the only sober person there!”

Alcoholics and other addicts carry with them a reputation for doing stupid things when they are drinking or using. AS a result, any time they make a mistake or try to have fun by being silly, many people with just assume they have stated drinking or drugging again. This can activate shame and guilt and bring back painful members. It’s also easy to feel unfairly judged and to question the value of your sobriety. “If this is how people will always react to me, why bother to stay sober?” Needless to say, this kind of thinking a serious warning that needs to be discussed with your therapist and sponsor.

The other elements of his sobriety plan helped Bob get though this situation sober. He called his sponsor each day discussing everything that happened and how he felt about it. He read the Big Book for a half-hour each evening to keep is sober-thinking brain circuits alive and active., and not going anywhere alone. Upon returning, my group and I processed what worked, and what additional program tools I might have used so I could use them the next time I might have to expose myself to triggers.

Through this process of gradual re-introduction, Bob was able to participate in increasingly more activities in my recovery to the point I can now do almost anything without being triggered. This is due to the third phase of the recovery process called the “extinction process” (Gorski, 1988). As mentioned earlier, triggers become extinguished when repeated exposure to them is connected with not using, rather than using.

Addiction professionals can learn to prepare recovering people for living in a society that is alcohol and drug centered.  The trigger management process, or as Bob Tyler Describes it, Trigger Recovery, can help many recovering people improve the quality of their sober life and reduce the fear and risk of relapse.

References:

Gorski, Terence T. (Speaker). (1988). Cocaine craving and relapse: A comparison
between alcohol and cocaine (Cassette Recording Number 17 – 0157).

Independence, Mo: Herald House/Independent Press.

Pagewise, Inc. (2002). This study in classical conditioning is one of the most renown for its incredible results. Learn about Pavlov’s dogs [Online]. Available Internet: http://ks.essortment.com/pavlovdogs_oif.htm.

Tyler, Bob. (2005) Enough Already!: A Guide to Recovery from Alcohol and Drug Addiction

Books by Terence T. Gorski

Gorski’s book Straight Talk About Addiction describes trigger events in detail.

Gorski, Terence T., Addiction & Recovery Magazine, April 10, 1991

Gorski, Terence T.,  Managing Cocaine Craving, Hazelden, Center City, June 1990


Addiction Can Be Understood and Treated

August 15, 2014

RECOVERY IS POSSIBLE
STRAIGHT TALK ABOUT ADDICTION

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Straight talk means giving clear, honest, and plain-English descriptions of important issues related to addiction, recovery, relapse prevention. Straight Talk means discussion the artistes for addiction — sobriety and responsible living.

This book tells it like it is without a great deal of concern for political correctness or the tentative guarded language that so often hides the truth about addiction, recovery, and relapse.

After 40 years of following the new research and treatment practices for addiction, Terry Gorski became frustrated at the misinformation about alcohol and other drug addictions and the narrow and incomplete approaches to treatment, recovery and relapse prevention.

In this book, Terry provides the best information on the current science-based upon an accurate understanding of what the core addiction syndrome is and what the an effective addiction treatment process needs to look like if it is to increase the chances of recovery and decrease the risk of relapse.

This book is easy to read and loaded with useful information. The book can be quickly read from beginning to end, and then kept as a handy reference to find specific information that can be used as a guide to manage the problems and crises that are so often a part of the addiction and recovery process.

The message is simple: addiction is a biopsychosocial disease. science-based understanding of what the core addiction syndrome is and what the core addiction treatment process needs to look like if it is to increase the chances of recovery and decrease the risk. Here are some of the key ideas developed in depth with the book:

Addiction is a biopsychosocial disease. Bio means biological or of the body, Psycho means psychological or of the mind, Social means the relationships that develop among people and with the social and legal systems that are needed for responsible living.

Biologically, addiction is marked by brain dysfunction that disrupts the reward chemistry of the brain creating cycles of intense euphoria and powerful craving.

Psychologically addicted people slowly adjust their ways of thinking, feeling, acting that allows them to deny and rationalize the problems caused by the it addiction.

Gradually, over time, an addictive beliefs develops that create a powerful denial system. This denial blocks the ability to recognize the addiction, interferes with the ability to ask for and accept help, and creates a deadly spiral of progressively more severe relapse episodes.

Socially, addiction pushes away sober and responsible people while attracting and feeling attracted to addicted and irresponsible people. The result is a tragedy. The addict abuses, disregards, and destroys those who love and try to help them. Active addicts set themselves up to be exploited by other addicted people and are vulnerable to predators who use and abuse them.

Most importantly Straight Talk About Addiction provides hope. Addiction and be understood, recovery is possible, and relapse can be prevented it effectively managed should it occur.

This book is easy to read and understand. It is loaded with useful information. Many people read it from beginning to end to get a comprehensive understanding of addiction, recovery, relapse, and related problems. Many people keep the book handy so they can use it as an easy-access reference to find useful information that can be used to effectively manage addiction-related problems.

The message is clear: Recovery is possible. Relapse can be prevented or effectively managed should it occur. There is hope.

LIVE SOBER – BE RESPONSIBLE – LIVE FREE

Get The Book By Terence T. Gorski
STRAIGHT TALK ABOUT ADDICTION


The Living Carcass: Zombies, Vampires, and Addiction

May 7, 2014

imagesBy Terence T. Gorski, Author

Addiction can turn an active addict into a living carcass — the empty shell of a real human person.

A carcass is “the outside part of a vehicle, building, or other object that is left when the rest of it has been destroyed.” In terms of addiction, it is the living shell of a person who has nothing left in life but their addiction.  The addiction has stripped them of the essence of being a human being and left a arational drug seeking creature in its place.

The zombie metaphor is very appropriate for addiction. The brain is attacked by the active addiction and the addict becomes a zombie, repeating the same addictive cycle without thought or self-control. Eventually zombies die or are killed or imprisoned by those who are still alive. The consequences of their own behavior condemns zombies to dwell in then land of the living dead and function on a subhuman level.

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I bite. You bleed. You may fight. I need to feed.

The vampire metaphor also applies to addiction. Vampires were once good people who were victimized by a predatory vampire. As the transformation from human to vampire progresses, need for blood grows. Even the vampires who still remember human sensibilities cannot resist the need to feed on blood, no matter what the consequence or how badly the act of feeding violates their values..

The analogy of the addict as vampire is best expressed in the book The Vampire Lestat by Anne Rice. It is a great book. Lestat is a likable vampire because he fights back against the inhuman need to feed on blood. He does not like being a vampire and goes to heroic lengths to rise above his nature and become human again. He hates himself for what he is and what he feels the compulsion to do. Yet he is what he is and cannot change his nature.

Fortunately, unlike Zombies and Vampires, people suffering from addiction can recover.

I have not seen any 12-Step for vampires. There is a book on the 12-Steps for Vampires by Michael Masden and a film entitled Vampires Anonymous.

LIVE SOBER – BE RESPONSIBLE – LIVE FREE

GORSKI BOOKS


Alcohol Facts and Statistics

May 7, 2014

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On The Internet
http://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-facts-and-statistics

Percentage of Drinkers:

In 2012,
– 87.6% of people aged 18 or older reported that they drank alcohol at some point in their lifetime;
– 71% reported that they drank in the past year; 56.3% reported that they drank in the past month.

Percentage of Binge Drinkers and Heavy Drinkers:

In 2012,
– 24.6 % of people aged 18 or older reported that they engaged in binge drinking in the past month (drinking 5 or more alcoholic drinks on the same occasion on at least 1 day in the past 30 days);
– 7.1% reported that they engaged in heavy drinking in the past month (drinking 5 or more drinks on the same occasion on each of 5 or more days in the past 30 days).

Alcohol Use Disorders:

An estimated 17 million Americans have an alcohol use disorder (AUD)—a medical term that includes both alcoholism and harmful drinking that does not reach the level of dependence.

Untreated AUDs:

Research shows that an estimated 15% of individuals with an AUD ever seek treatment.

Alcohol-related Deaths:

Each year in the U.S., nearly 80,000 people die from alcohol-related causes, making it the third leading preventable cause of death in our country.8

Economic Burden of Alcohol Problems:

In 2006, alcohol problems cost the U.S. $224 billion each year, primarily from lost productivity but also from health care and property damage costs. These issues affect all Americans, whether they drink or not.

Global burden of Alcohol Problems:

Globally, alcohol use is the fifth leading risk factor for premature death and disability; among people between the ages of 15 to 49, it is the first.10

Family consequences of Alcohol Problems:

More than 10% of U.S. children live with a parent with alcohol problems, according to a 2012 study.

Alcohol and College Students:

Each year —

– 1,825 college students between the ages of 18 and 24 die from alcohol-related unintentional injuries, including motor vehicle crashes.

– 696,000 students between the ages of 18 and 24 are assaulted by another student who has been drinking.

– 97,000 students between the ages of 18 and 24 are victims of alcohol-related sexual assault or date rape.

Alcohol and Adolescents:

– By age 15, more than 50 percent of teens have had at least 1 drink.
More adolescents drink alcohol than smoke cigarettes or use marijuana.

– In 2009, 10.4 million young people ages 12 to 20 reported that they drank alcohol beyond “just a few sips” in the past month.

Alcohol and Pregnancy:

– Among more than half a million pregnant women surveyed between 1991 and 2005, about 12% reported drinking and about 2% reported binge drinking.

– The prevalence of Fetal Alcohol Syndrome (FAS) in the U.S. is between 2 to 7 cases per 1,000;

– The prevalence of Fetal Alcohol Spectrum Disorders (FASD) in populations of younger school children may be as high as 2-5% in the U.S. and some Western European countries.

Alcohol and the Human Body:

– In 2009, liver cirrhosis was the 12th leading cause of death in the United States, with a total of 31,522 deaths—664 more than in 2008.

– Among all cirrhosis deaths in 2009, 48.2 percent were alcohol related. The proportion of alcohol-related cirrhosis was highest (70.6 percent) among decedents aged 35 to 44.

– In 2009, alcohol related liver disease was the primary cause of almost 1 in 3 liver transplants in the U.S.


Straight Talk About Addiction

May 4, 2014

 

Gorski_Addiction_Straight_TalkBy Terence T. Gorski
Author

Accurate and up-to-date. Easy to read and understand.

Books about addiction are boring! — REALLY?
Not when they’re written in STRAIGHT TALK ABOUT ADDICTION!

I have found my voice as a writer. It’s the same voice I use as a speaker: Direct! No nonsense! Factual! Authoritative!

My new voice is clear and easy to understand. Yet it’s engaging. I write as if I’m sitting directly in front of you and putting the information right in your face. You may not like what you’re hearing, but, believe me, you’ll listen.

Straight Talk is direct and entertaining; it explains useful information in clear and easy to understand language. I provide clear examples to back up th information. Yet with all of that, my sarcastic but “incredibly funny” sense of humor shines through.

I’m glad I finally learned how to write with the same clarity and impact in which I speak to audiences. I am proud of my new “writers voice” and, using this new voice, I am in the process of updating my previous works. The concepts have a new clarity, research findings are presented in an easy to understand way. The new works are just plain interesting and filled with useful information.

The First Books In The Straight Talk Series

The first book in the “Straight Talk Series” was Straight Talk About Suicide.” Not a fun topic, but a necessary one. Too many recovering people, especially out veterans, are dying at their own hand. This book is short, straight and to the point. It is written as if I am talking a suicidal person away from the ledge of a tall building while the crown is yelling “jump, jump, jump!” Its key message is brutally simple: Suicide is a permanent solution to a temporary problem! Wait and think it through. Even though it may not seem like it, there are better choices than killing yourself.

The second and newest book in the straight talk series is Straight Talk About Addiction. I talk to the reader in a clear and logical way that explains what addiction is, tells you how to figure out if you have it, and then explains how to b-pass your denial and motivate yourself to stand up and get moving ahead in recovery.

Why Straight Talk About Addiction Is Important

You don’t have to be bored to death to learn about addiction. As a matter of fact, the absolute worst way to learn about addiction is to read or listen to something boring. You learn best when you are engaged with what you are reading or listening too. things get interesting when the material smacks you right in the face because it explains your real life experiences in a new and more meaningful way – a way that gives you new choices in recovery.

The Biopsychosocial Addiction Model in presented in short and concise conceptual area that build upon one another to paint a complete picture. After reading the book you will be able to describe in a model of Addiction that has proven to be both accurate and memorial. In other words, a model that bas stood the test of time. Don’t take my word for it. Decide for yourself by reading some examples from the book.

Excerpts from the Book Straight Talk About Addiction

Excerpt #1: The Progression of Addiction:  Addiction is not something that suddenly happens.  It usually progresses just fast enough to start changing how you think, feel, act, and relate to other people; and just slow enough to make it difficult for you and others to notice the changes that are slowly developing into serious alcohol and drug related problems.

Excerpt #2: What Causes Addiction To Progress: The progression of addiction is caused by a complex interaction among four things. (1) The Addictive Brain Responses: This is the unique way the brain of addict responds to alcohol or other drugs; (2) Addictive Psychodynamics: This is the unique way the mind of an addict responds to alcohol and other drug use that results in denial and addictive thinking; (3) Addictive Behavior: This is the drug seeking habits that addicted people develop. Addictive behavior puts us around the people, places, and things and things where alcohol and other drugs are readily available and support for sober and responsible behavior is slim or nonexistent; and (4) Addictive Social Systems: These result from the way addicted people structure their lives. They are the social systems that make heavy, abusive, and addictive alcohol and drug use possible by driving away sober and responsible people while both attracting and feeling attracted to others who have alcohol and drug problems.

You must address all four of these areas simultaneously to increase your chances of recovery. So it’s suggested that you take ownership of this information. Taking ownership means finding what applies to you and then using it to make sense out of what is happening in your life. Reading this book with an open mind will help you to see the truth, either good or bad, about what alcohol and other drugs are doing in your life. The truths allows you to see new ways of solving your problems and moving ahead in recovery without relapse.

Excerpt #4: Mind Altering Substances: Mind-altering substances are chemical agents that alter how the brain works in a way that changes how we think, feel, act, and relate to other people. In other words, mind-altering substances physically change how our brain works.

The human brain is a complex chemical factory. Millions of nerve cells communicate with each other by releasing and absorbing chemicals called neurotransmitters. Mind altering substances have a powerful physical affect on how our brains function.  They can chemically change our thoughts, feelings, and behaviors by changing how our brain functions.  As a result mind-altering drugs can cause damage to the brain.  They make us feel better by disrupting the normal functioning of our brain, but we always pay a price.

Excerpt #5: The Gorski Simplified Drug Classification System: A useful drug classification systems need to be easy to understand for the person using it. A system based on the effect that most users experience when they use alcohol and other drugs. The Gorski Simplified Drug Classification System has four basic drug groups:

People tend to use drugs because they like their effects – they like the way the drug makes them feel. If the drug makes them feel good enough, many people are willing to risk the consequences of breaking the law in order to get and use the drug. Most people use alcohol or other drugs to experience one of four effects produced by drugs in one of four different groups. Here are the drug groups: (1) Uppers stimulate and excite. (2). Downers relax and sedate. (3) Pain Killers take away both physical and emotional pain. (4) Mind Benders that scramble consciousness and produce pseudo-spiritual and pseudo-intimate experiences. We that think that we are communing with God when in fact we are worshiping the effects of a drug! We believe that we are getting intimate with a partner when in fact we are making love to the effect of the drug effect. The drug effect makes our partner irrelevant.

Excerpt #5: The Addictive Brain Response. The Brains of people who are at high risk of addiction react to the use of alcohol and drugs differently than the brains of at low risk of addiction. This is because high risk people experience an addictive brain response when they use alcohol and other drugs. People at low risk experience a normal brain response.

When you have a Normal Brain Response, the drug makes you feel what it was designed to make you feel – an upper creates a feeling of energy, a downer creates a feeling of relaxation, and so forth.

The Addictive Brain Response causes a feeling of euphoria that enhances the mood altering effect the drug was designed to produce. In other words, you feel both the normal drug effect of the drug plus a euphoric effect caused by the drug tickling the pleasure centers of the brain causing a flood of pleasure chemicals. As a result the “hole in your disappears when using alcohol and other drugs and you feel whole and complete, maybe for the first time in your life. As a result you really like how the drug makes you feel, so you want to use it again and again.

So there it is – my new straight talk voice

You should have a good feel for Straight Talk About Addiction. Did you understand the concepts? Will you remember them? Can you see how this information applies to you?

These are only brief excerpts from a 245 page book that explains everything you need to know about alcohol and drug use, abuse, and addiction. I think you’ll like reading this book. I know the ideas will be easy to understand and stick in your mind. Reading this book may reorganize the way you understand and respond to addictive disease.

I’m proud of this book. I believe it is one of the best books I’ve ever written. I hope you will enjoy it and find the information useful.

Terence T. (Terry) Gorski

Live Sober — Be Responsible — Five Free

Gorski BooksGorski Training


Rules of the Workplace

May 4, 2014

By Terence T. Gorski, Author

Over the course of my career many people have discussed problems they are having at work. Many times these problems result from violating or failing to understand ten basic rules of the workplace.

1. STRESS: The workplace is always stressful. Learn how to manage it or stress-related problems will hurt your performance.

2. HABITUAL EARLINESS: Get in the habit of getting to work a little bit early and staying a little bit late. Being early gives you time to settle in and plan your day before the action starts. Staying a little late gives you the time to think through the day mark progress to build upon and problems to correct.

3. GOING THE EXTRA MILE: Get in the habit of doing a little bit more than expected without being asked to do it, without expectation of praise or gratitude and with a positive attitude.

4. ALL WORKPLACES ARE POLITICAL: Be aware of what goes on in the workplace that no one wants to see or talk about. Leave it hidden, unless it is is your explicit responsibility to expose and fix it. Avoid pointing out the problems hidden in plain sight. They are hidden and ignored for a reason.

5. THERE IS NO PERFECT WORKPLACE: Learn to accept the flaws and work around them. If the benefits don’t out way the problems inherent in your job, responsibly move on to something better without burning your bridges behind you. Remember, however, jobs always look better from the outside in than the inside out.

6. REMEMBER IT IS CALLED WORK FOR A REASON: You go to work to earn a living, do a job, add value to the business you work for, and improve your skills and resume. You don’t work for fun, personal growth, or to enhance your social life.

7. WORK IS STRESSFUL: Work by it’s very nature is stressful. This is because work relationships are conditional. You have your job on the condition you can successful perform your duties and meet your responsibilities.

8. CAREER PLANNING PRINCIPLES:
– Face the truth
– Set a goal,
– Make a plan,
– Work the plan.

9. YOUR REAL JOB: Your real job is to make you bosses job easier, build up the people who build you up, and ignore everyone else. Let your enemies die of their own stupidity.

10. KEEPING ROMANCE OUT OF THE WORKLACE: You go to work to build a career, not to fall in love or get laid. Romantic/Sexual Relationships with people in the workplace can literally screw-up even the best career plans.

GORSKI BOOKS: http://www.relapse.org


Eating Disorders and Substance Addiction

May 4, 2014

1. Less than 50% of recovering alcohol and drug addicts develop an eating disorder.

2. Although this is higher than in the general population, not all recovering chemical addicts develop eating disorders.

3. Alcoholism and EDs frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders.

4. Although such diagnostic co–occurrence suggests the possibility of shared factors in the etiology or maintenance of these problems, research has not established such links.

5. The clinical reality that eating and alcohol use disorders frequently co–occur has important implications for assessment, treatment, and research.

6. Comprehensive assessment is necessary for good treatment.

7. Concurrent treatment of both disorders is recommended as a best practice.

8. The most effective forms of treatment include Cognitive Behavioral Therapy (CBT), coping skills, and Dialectal Behavioral Therapy (DBT).

Here is a comprehensive research article that reviews the relationship.

http://pubs.niaaa.nih.gov/publications/arh26-2/151-160.htm

Full Text of the Article:

Numerous studies suggest that eating disorders (EDs) and alcohol and other drug use disorders (referred to throughout this paper as substance use disorders [SUDs]) frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders. This review will consider the extent and nature of such co–occurrences and whether research supports the possibility of common or shared factors in the etiology or maintenance of EDs and SUDs.

The reality that EDs and SUDs frequently co–occur has important implications for assessment, treatment, and future research.

Although this review will offer implications for clinicians and researchers in both fields, the presentation bias will be toward providing a more detailed discussion of the ED literature for professionals in the alcoholism field.

EATING DISORDERS

The current classification system, the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–IV) (American Psychiatric Association [APA] 1994) specifies three ED diagnoses. The formal diagnoses are anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). In addition, the DSM–IV includes a new ED category (binge eating disorder [BED]) as a research category. BED is a specific example of EDNOS. Brief descriptions of these EDs follow. See Grilo (2002a) and Becker and colleagues (1999) for detailed discussions of the clinical features and assessment issues of these disorders.

Anorexia Nervosa is characterized by a refusal to maintain normal body weight (defined as 15 percent below normal weight for age and height), an intense fear of becoming fat, and (in females) skipped menstrual periods (i.e., amenorrhea) for at least 3 months. People with AN have a severely distorted body image. They see themselves as overweight despite being overly thin, and they tend to deny the seriousness of their low body weight.

The DSM–IV specifies two subtypes of AN—a “restricting type,” characterized by strict dieting or exercise without binge eating; and a “binge–eating/purging type,” marked by episodes of binge eating and/or purging via self–induced vomiting or misusing laxatives, enemas, or diuretics. In severe cases, medical complications or death from starvation can occur.

Roughly 50 percent of people with AN may eventually develop bulimia nervosa (described below). AN is a rare disorder; it occurs disproportionately in women, and is estimated to have a prevalence of roughly 1 percent in adolescent and young adult women (Hoek 1993).

Bulimia Nervosa is characterized by recurrent episodes of binge eating (defined as consuming unusually large amounts of food in a discrete period of time plus a subjective sense of lack of control over eating). BN is further characterized by regular use of extreme weight control methods (e.g., vomiting; abuse of laxatives, diet pills, or diuretics; severe dieting or fasting; vigorous exercise) and by dysfunctional attitudes about weight or shape that unduly influence self–evaluation. For a diagnosis of bulimia nervosa, the DSM–IV requires both the binge eating and inappropriate weight control methods to have occurred, on average, at least twice per week during the past 3 months.

The DSM–IV specifies two subtypes of BN, a “purging type” and a “non–purging type,” which is limited to the severe dieting, fasting, or exercise forms of weight control behaviors. If either form of BN occurs during a current episode of AN, the assigned diagnosis is AN. BN, like AN, is more common in females and has an estimated prevalence rate of 2 percent to 3 percent in young females (Kendler et al. 1991; Kringlen et al. 2001).
Eating Disorder Not Otherwise Specified is generally considered the most prevalent form or category of ED and the least studied (Andersen et al. 2001; Grilo et al. 1997).

Outside of research centers with specific recruitment requirements, the majority of patients who present for treatment for eating–related problems are “partial syndrome” or EDNOS cases. That is, they fail to meet all the diagnostic requirements for one of the “formal” EDs but they have significant symptoms and associated problems. Indeed, researchers have questioned the significance of the failure to meet some of the specific criteria (such as the necessity that amenorrhea be present in female patients for a diagnosis of AN to be made). Investigators have also claimed that some of the diagnostic criteria for the formal EDs are too stringent (Andersen et al. 2001; Striegel–Moore et al. 2000). Many patients experience significant and clinically meaningful problems with eating and body image, but do not always fulfill the exact requirements for the diagnoses of AN or BN.

Binge Eating Disorder, included as a provisional category in the DSM–IV, is a specific example of an EDNOS. BED is characterized by recurrent episodes of binge eating (an average of 2 days with binge episodes per week over a 6–month period is required; marked distress exists because of the binge eating) without the compensatory weight control methods that are required for the diagnosis of BN (Grilo 1998, 2002a). BED, unlike AN and BN, is not uncommon in males or in people of color. It is most frequently seen in adults, and has an estimated prevalence of 3 percent in adults and roughly 8 percent in obese persons (Spitzer et al. 1993). BED is associated with increased risk for obesity and thus for the plethora of medical problems associated with obesity (Grilo 1998).

Age Ranges and Gender

Eating disorders most frequently develop during adolescence or early adulthood, but their onset can occur during childhood or much later in adulthood (Grilo 2002a).

The peak age range for onset of AN is 14 to 18 years, although some patients develop AN as late as their 40s (Frey 1999). Similarly, the peak age range for BN is adolescence through early adulthood (Lamb 1999). BED most frequently occurs in young to middle adulthood (Grilo 1998). Although developmental challenges and severe dieting generally predate AN and BN, it appears that a significant proportion of people with BED report no dieting prior to the onset of binge eating (Grilo 1998, 2002a).

Although AN and BN occur mostly in females and BED is more common in females than males, it is important to not overlook these EDs in men (Andersen 1995; Andersen and Holman 1997). Available research suggests that among ED patients, few gender differences exist in the specific features of the EDs (Barry et al. 2002; Woodside et al. 2001).

CO–OCCURRENCE OF SUBSTANCE USE DISORDERS AND EATING DISORDERS

Most studies have reported that EDs and SUDs frequently co–occur, with especially high rates observed among patients in treatment (e.g., Beary et al. 1986; Brewerton et al. 1995; Bushnell et al. 1994; Goldbloom et al. 1992; Grilo et al. 1995b; Higuchi et al. 1993; Suzuki et al. 1993; Taylor et al. 1993; see reviews by Grilo et al. 1995a and Holderness et al. 1994 for more complete listings of earlier studies).
Although research has generally reported high rates of co–occurrence between EDs and SUDs, perhaps most striking is the marked inconsistency or variability in the reported co–occurrence rates across studies.

A previous review (Holderness et al. 1994) noted that estimates of BN in patients with SUDs ranged from 8 percent to 41 percent and estimates for AN ranged from 2 percent to 10 percent. Methodological issues account, in part, for some of the inconsistencies in the reported co–occurrence rates and make interpretation of the literature ambiguous. Variations in recruitment methods (community versus treatment samples, and, if using treatment samples, the type of treatment facility [e.g., general psychiatric, substance or chemical dependency, eating disorder; inpatient versus outpatient]) and assessment and diagnostic methods (survey, self–report, diagnostic interview) account for some of the variability in the literature.

These important methodological limitations notwithstanding, research does suggest that EDs and SUDs frequently co–occur. Therefore, research seeks to determine the significance of the co–occurrence for informing (a) models of etiology and pathophysiology, and (b) approaches to treatment and clinical management. The remainder of this article will review this research, first examining the prevalence of the co–occurrence of EDs and SUDs in more detail and then exploring whether research supports the possibility of common or shared factors in the etiology or maintenance of EDs and SUDs.

Co–Occurrence versus Comorbidity

“Comorbidity” is a widely used term in psychopathology research but one that appears to reflect various meanings or definitions. Kendall and Clarkin (1992), among others (Grilo 2002b), noted numerous possible meanings of comorbidity, including random co–occurrence of disorders that are independent, co–occurrence of different disorders that share a common etiology, or different disorders that have a causal relationship between them.

Comorbidity may reflect, in part, artifacts of the diagnostic systems because of criterion overlap (e.g., one criterion for borderline personality disorder is “impulsivity,” which can be met in part by binge eating and/or by substance use). As demonstrated initially by Berkson (1946), and more recently by duFort and colleagues (1993), studies of treatment–seeking patients must be interpreted cautiously because of biases (i.e., people seeking treatment may have especially severe problems, people with multiple problems may seek treatment for one or several of the problems) that can make interpretation of comorbidity difficult and may limit generalizability to community samples. Thus, a starting point for possible comorbidity is when rates of co–occurring diagnoses are statistically different from those expected, given the base rates for the individual disorders (Kraemer 1995). Allison (1993) maintained the importance of selecting “relevant” control or comparison groups to provide a context for interpreting differences in co–occurrence patterns. Appropriate comparisons might include psychiatric patient groups without the eating and/or alcohol use disorders.

Recent research with both people in treatment (Grilo et al. 1995b; Wilfley et al. 2000) and in the general population (Dansky et al. 2000; von Ranson et al. 2002; Telch and Stice 1998; Yanovski et al. 1993) that used systematic recruitment methods, standardized diagnostic interviews (rather than self–report), and “relevant” comparison groups has revealed that, although EDs and SUDs co–occur, the co–occurrence is either not significantly greater or-if so-is only marginally greater than the co–occurrence rate in relevant comparison groups (i.e., patient groups of comparable severity chosen to provide a context as opposed to the frequently used “normal” control group). Grilo and colleagues (1995a, 1995b) found that, although EDs are frequently diagnosed among inpatients with SUDs, they are also frequently diagnosed in other psychiatric inpatients. In this controlled study, the frequency of AN and BN was not greater in patients with SUDs than without SUDs. Subthreshold manifestations of EDs (i.e., EDNOS; cases where insufficient criteria were present to warrant either BN or AN diagnoses) were diagnosed significantly more frequently in the patients with SUDs than without.

Some research has also suggested that patients with nonpurging AN may be less likely than patients with other forms of EDs, including AN purging subtype, to have SUDs. The increased possibility for SUDs to co–occur with atypical manifestations of EDs, rather than with AN and BN, is examined further in the following section.
The three studies of comorbidity in BED that used relevant comparison groups found high rates of lifetime alcohol use and SUDs but not higher rates than observed in the comparison groups (Telch and Stice 1998; Wilfley et al. 2000; Yanovski et al. 1993). Most recently, von Ranson and colleagues (2002) reported findings from a large community study of two groups (672 adolescent girls, 718 adult women) assessed using diagnostic interviews. The authors reported that EDs and substance use were positively related, but the association was not significant. They concluded that there is no strong overarching relationship between these problems. These findings suggest caution in interpreting comorbidity between different forms of EDs and SUDs.

Other Comorbid Psychiatric Disorders

Although this review focuses primarily on the co–occurrence of EDs and SUDs, both of these classes of disorders frequently co–occur with other forms of psychopathology. A large body of research has documented associations between

EDs and other psychiatric and personality disorders (Bulik et al. 1997; Grilo 2002b; Grilo et al. 1995a,b) as well as between SUDs and other psychiatric disorders (Grilo et al. 1997; Sher and Trull 2002).

Controlled studies (Dansky et al. 2000; Grilo et al. 1995a,b; Wiseman et al. 1999) have suggested that some of the apparent co–occurrence between EDs and SUDs may be related, in part, to other psychiatric comorbidities. Specifically, Dansky and colleagues (2000) reported that the relationship between BN and alcohol use disorders reported by the National Women’s Study was likely indirect and the result of associations with other psychiatric disorders, most notably major depressive disorder and post–traumatic stress disorder. Grilo and colleagues (1995b) compared inpatients who had ED with and without SUD with a comparison group who had SUD but not ED. In this controlled comparison, personality disorders characterized as cluster B (i.e., erratic or unstable) were diagnosed more frequently in the patients with co–occurring ED and SUD, whereas cluster C personality disorders (i.e., anxious or fearful) were diagnosed more frequently in patients with ED without co–occurring SUD.

This three–group comparison allowed for a finer distinction regarding potential comorbidity and raised the possibility of subgroups of patients (e.g., with borderline personality disorder) who might be most likely to have problems with both eating and substance use disorders. Consistent with this, Bulik and colleagues (1997) found that, although women with alcoholism and BN had higher rates of a variety of psychiatric problems than women with BN without histories of alcohol use disorders, multivariate analyses revealed that borderline personality disorder was the sole distinguishing variable between the two groups. Most recently, Wiseman and colleagues (1999) found that the order of onset of the two disorders might be important. Patients who developed EDs early and prior to SUDs had greater levels of psychiatric and personality disorder psychopathology compared with patients who developed the ED after the SUD and with patients who had an ED but no SUD.

These findings suggest that additional psychiatric disorders frequently co–occur with EDs and SUDs, and may play a role in their relationship to each other. In particular, these findings suggest that patients who suffer from both eating disorders and substance abuse disorders may have deficits in impulse control. Related to this line of investigation, recent years have witnessed increased attention to the potential role of childhood abuse, perhaps mediated by personality disorders, as a common factor in patients with both EDs and SUDs. Research, however, has not generally supported specific or strong associations between childhood abuse and specific disorders (Grilo and Masheb 2001; Smolak and Murnen 2002). Another issue to examine in the relationship between these disorders is the significant frequency with which ED symptoms occur with SUDs.
Eating Disorder Symptoms Among Women with Substance Use Disorders
Grilo and colleagues (1995a) have reported that EDNOS (but not AN or BN) was significantly more common in people with SUD than without SUD. This suggests that it is important for clinicians to consider and screen for subthreshold levels of EDs in addition to formal ED diagnoses. Moreover, assessment of co–occurring subthreshold eating problems may facilitate earlier intervention to prevent later development of the full–blown disorder.

A few studies have examined the specific features of EDs present among patients with SUDs (Sinha et al. 1996; Peveler and Fairburn 1990; Jackson and Grilo in press). Sinha and colleagues (1996) assessed eating behaviors and the attitudinal features of EDs in a community–based sample of 201 young women (ages 18 to 30) who comprised the following four groups: alcohol dependent, alcohol dependent with anxiety disorders, anxiety disorders only, and neither alcohol nor anxiety disorders. Women with alcohol dependence had significantly higher levels of the behavioral and attitudinal features of eating disorders and were more likely to meet the criteria for BN and EDNOS than women without alcohol dependence. Interestingly, these authors found that alcoholism was more closely related to the attitudinal features, whereas anxiety disorders were more closely associated with the behavioral features of eating disorders.

Eating Disorder Symptoms by Gender and Ethnicity

More recently, Jackson and Grilo (in press) examined the specific features of EDs and tested for gender and ethnic differences in a racially diverse group of outpatients with SUDs. Similar to previous studies with primarily Caucasian samples (Peveler and Fairburn 1990; Sinha et al. 1996), eating–related problems were not uncommon in substance abusers.

Roughly 20 percent of men and women reported binge eating, and 12 percent reported some form of inappropriate weight compensatory behaviors. Problematic attitudes about body shape were also common; 28 percent of the Jackson and Grilo (in press) sample reported overvalued ideas regarding shape at levels considered to be clinically significant-as compared with 28 percent in the study of young women reported by Sinha and colleagues (1996) and 26 percent in the study reported by Peveler and Fairburn (1990). Jackson and Grilo (in press) found no significant ethnic differences in obesity, in features of eating disorders, or in levels of body image dissatisfaction. Men and women were similar in terms of overweight and behavioral features, but women had significantly higher levels of attitudinal features of EDs. Thus, contrary to clinical lore, weight– and eating–related problems are not uncommon in males or in minority groups.

RESEARCH INVESTIGATING WHETHER COMMON FACTORS MAY UNDERLIE THE CO–OCCURRENCE OF EDs AND SUDs

The studies described above demonstrate that EDs and SUDs often co–occur and that ED symptoms are significantly more common in people with SUDs than without SUDs. Although research is ongoing, reasons for this co–occurrence have not been reported. One potential explanation is that these disorders are different manifestations of a common underlying factor. Three types of research provide support for this hypothesis: studies of dieting and substance use, studies of brain chemistry, and family and genetic studies.

Studies of Dieting Behavior and Substance Use

Research has documented significant associations between dieting and eating problems and substance use in younger populations. Krahn and colleagues (1992), for example, found that among college women, increasing severity of dieting and problems associated with EDs were associated with increased rates of alcohol, cigarette, and other drug use. Krahn and colleagues (1996) also found that dieting during pre–adolescence (among sixth grade students) predicted future alcohol use. Such findings, when considered with studies showing that food deprivation can increase self–administration of alcohol and other drugs in laboratory animals, are consistent with models positing that common mechanisms may play a role in EDs and SUDs (see Krahn 1991).

For example, Krahn (1991) suggested that food deprivation might cause alterations in the central nervous system’s reward pathways, thus increasing the consumption of reinforcing substances (e.g., alcohol).

However, as emphasized above, and by other reviews (Wilson 1993), the fact that these problems are associated does not demonstrate a specific or common cause.

Studies of Brain Chemistry

Animal studies of brain chemistry have provided some support for the view that EDs and alcohol use disorders may have some shared factors. Some research, for example, has suggested that both disorders may be related to atypical endogenous opioid peptide (EOP) activity. EOPs have been found to influence both alcohol and food consumption (see Mercer and Holder 1997) and may play roles in the control of eating behavior (Berridge 1996; Carr 1996; Cooper and Kirkham 1993; Gosnell and Levine 1996) as well as the development of alcoholism (Reid 1985; Reid et al. 1991; see also Froehlich 1995). In addition, brain neurotransmitter systems, including the serotonin, gamma–aminobutyric acid (GABA), and dopamine systems, are the focus of active research across a wide range of psychiatric and behavioral problems, including food and alcohol consumption (see Mercer and Holder 1997). Particularly active attention has been paid to the role of serotonin, which has been implicated in the control of eating, mood, and impulsivity (Brewerton 1995; Kaye et al. 1998). In addition, treatment studies have reported some support for the efficacy of selective serotonin reuptake inhibitors (SSRIs) across different EDs (Fluoxetine Bulimia Nervosa Collaborative Study Group [FBNCSG] 1992; Hudson et al. 1998; Kaye et al. 2001).

Family and Genetic Studies

Early research reported that people with eating disorders are more likely than those without EDs to have family histories of substance use disorders (e.g., Hudson et al. 1983; Jones et al. 1985). However, several recent large, carefully conducted studies have found that EDs (especially BN) and SUDs segregate independently in families-that is, eating disorders and substance use disorders most likely do not have the same genetic, familial, and environmental risk factors. For example, Kaye and colleagues (1996) reported that alcohol or other drug dependence was increased only in first–degree relatives of women with BN who themselves also had alcohol or other drug dependence. Schuckit and colleagues (1996), in a large study of alcohol–dependent people and their relatives, also reported weak evidence at best for familial transmission between alcohol dependence and BN. Lilenfeld and colleagues (1997) reported that women with co–occurring BN and SUD have higher rates of problems with anxiety, a variety of personality disturbances including antisocial behavior, and high rates of familial SUD, anxiety, impulsivity, and affective instability.

These authors hypothesized that a familial vulnerability for impulsivity and affective instability may contribute to the development of SUD in a subgroup of BN patients. Using data from a large epidemiological sample of female twin pairs, Kendler and colleagues (1995) demonstrated that most of the genetic factors associated with vulnerability to alcoholism in women do not alter the risk for development of BN.

TREATMENT OF CO–OCCURRING ALCOHOLISM AND EATING DISORDERS

Although alcoholism and other SUDs frequently occur with EDs, research has not established common or shared factors in the etiology or maintenance of this co–occurrence.

Nonetheless, the frequent co–occurrence of problems with eating and alcohol may signal greater psychiatric disturbances (Grilo et al. 1995b) and greater medical risk (Catterson et al. 1997; Mitchell et al. 1991). These clinical realities represent considerable challenges to practitioners and researchers. The most common questions include how to identify the presence of possible problems, which problem to focus on first, or whether/how to address both concurrently (Daniels et al. 1999; Wilson 1993; Mitchell et al. 1997).

These are important questions and there is a pressing need for research on these treatment issues (Grilo et al. 1997). Not only has little research been done on treating these co–occurring conditions, but many treatment studies with ED patients either exclude patients with substance dependence or enroll few such patients. Although the brief overview that follows will offer implications for clinicians and researchers in both fields, this section gives a more detailed discussion of the ED intervention literature for professionals in the alcoholism field.
Assessment and Screening for Eating Disorders

Good, comprehensive assessment of patients is necessary for good treatment. Assessment protocols should involve questionnaires (i.e., instruments) that are sensitive enough to flag patients with potential problems for further evaluation.

Failure to identify all problems may contribute to poor retention and treatment outcomes even for the targeted problem. Screening instruments for alcohol problems are described in detail elsewhere (Bradley et al. 1998). Although standardized interviews are generally thought to hold important advantages for accurate and thorough assessment of EDs (Grilo et al. 2001a), it may not be possible or practical for many types of clinical facilities to use them because of cost, time, and lack of training.

The authors of this article recommend two self–report instruments for the screening and preliminary assessment of EDs. The first is the Questionnaire on Eating and Weight Patterns–Revised (QEWP–R) (Yanovski et al. 1993), a well–established and easy–to–complete self–report instrument. The QEWP–R, widely used in research programs, screens for the presence of the specific ED categories and provides useful information about the frequency of problem eating and dieting behaviors. The second instrument is the Eating Disorder Examination–Questionnaire Version (EDEQ) (Fairburn and Beglin 1994), the self–report version of the Eating Disorder Examination interview (Cooper and Fairburn 1987). The EDEQ offers a number of advantages over other self–report measures and provides detailed information about the behavioral and attitudinal features of eating disorders. The EDEQ has received some support for its utility (Grilo et al. 2001a) and has been used with substance abusers (Black and Wilson 1996). The relative merits of different assessment methods are described elsewhere (Grilo et al. 2001a). Briefly, such instruments are generally thought to underestimate the frequency of some of the behavioral features of EDs (e.g., binge eating) and overestimate some of the cognitive or attitudinal symptoms, compared with interviews (Grilo et al. 2001a). These limitations notwithstanding, such screens are useful for efficiently identifying people with possible problems.

Of course, in addition, it is important for clinicians and researchers alike to consider comprehensive medical and psychiatric evaluations for these patient groups (see Grilo 1998). In particular, patients with these co–occurring problems require careful medical evaluation and followup (Mitchell et al. 1991).

In terms of followup, it may be particularly useful for repeated assessments to include the ED screens. Some clinical experience suggests the possibility that successful cessation of substance or alcohol use may be followed by the re–emergence of ED symptoms in some patients. Although this hypothesis awaits conclusive research, it highlights the usefulness of repeated assessments.

Pharmacological Treatments

Pharmacological treatments have generally been found to have little effect on AN either as the primary approach or as an augmentation approach (Attia et al. 1998), although the antidepressant fluoxetine was found to decrease frequency of relapse in one study (Kaye et al. 2001). In contrast, pharmacological treatments, particularly antidepressant medications, have generally been found to be superior to placebo for the treatment of BN (e.g., Agras et al. 1992; FBNCSG 1992; Mitchell et al. 1990) and BED (e.g., Hudson et al. 1998; McCann and Agras 1990; McElroy et al. 2000; see Grilo 1998). It is worth stressing that these studies generally find, particularly for fluoxetine, that high doses are required to produce effects (as high as 60 mg per day in the case of fluoxetine) (FBNCSG 1992).

Unfortunately, surveys have revealed that most patients with BN treated with pharmacotherapy by community practitioners received inadequate dosing (Crow et al. 1999).

Nevertheless, fluoxetine has also been shown to reduce depressive symptoms and alcohol consumption in depressed alcoholics (Cornelius et al. 1997). Controlled research testing the efficacy of this medication among women with both alcoholism and EDs is needed.

Medications designed to block the action of opioids (i.e., opioid antagonists) have demonstrated efficacy for reducing alcohol use and relapse, and increasing abstinence rates among alcoholic patients (Anton et al. 1999; Heinala et al. 2001; Mason et al. 1999; Monti et al. 2001; O’Malley et al. 1992; Volpicelli et al. 1992, 1997; see also Krystal et al. 2001). The opioid antagonist naltrexone (ReViaT) has also been studied as a treatment for ED.

One study that compared naltrexone, imipramine, and placebo among BED patients found that both medications produced reductions in binge eating but neither was superior to placebo (high placebo response occurred in this study) (Alger et al. 1991). One study found that naltrexone reduced the frequency of binge eating in patients with BN during the first few weeks of treatment but that the effects did not last (Jonas and Gold 1987). A rigorous controlled study is currently under way at Yale University to evaluate the efficacy of naltrexone among alcoholic women and women with both alcoholism and EDs.
Psychological Treatments of Eating Disorders

Cognitive behavioral therapy (CBT) has received the most consistent support of any psychological or pharmacologic treatment for EDs. Briefly, CBT is a focal and structured treatment that involves a collaborative effort between patients and clinicians (Fairburn et al. 1993a).

CBT for eating disorders can be delivered via individual or group approaches and generally follows three phases.

The first phase involves education and presentation of the treatment model, including expectations for treatment and homework, teaching behavioral strategies such as self–monitoring to identify problems, and a graded approach to normalization of eating.

The second phase involves the use of cognitive restructuring methods to identify, challenge, and modify maladaptive thinking. The final stage involves relapse prevention techniques and problem solving to generalize the skills to other areas and to consolidate improvements. CBT has been found to be superior to control conditions, to most other forms of psychological therapies, to behavioral therapies without the cognitive components, and to the pharmacological treatments (e.g., Agras et al. 1992, 2000; Fairburn et al. 1993a; see reviews: Wilson and Fairburn 1998; Grilo 1998, 2000).

Moreover, self–help versions (e.g., Fairburn 1995) of standard CBT therapist manuals (Fairburn et al. 1993b) have demonstrated efficacy (Carter and Fairburn 1998; Peterson et al. 1998; Treasure et al. 1996). This approach may provide general practitioners with expertise in CBT with the technology to help certain ED patients.

Although CBT is generally regarded as the first–line treatment of choice for ED (Agras et al. 2000; Wilson and Fairburn 1998), research is needed to determine its usefulness for patients with co–occurring alcoholism and eating disorders, and to develop integrated psychological treatment approaches for patients with alcoholism and eating disorders (Mitchell et al. 1997).

Although the data are sparse, the treatment literature has not suggested that alcoholism or a history of alcoholism diminishes CBT treatment effectiveness for BN or BED (Goldbloom 1993; Mitchell et al. 1990; Wilfley et al. 2000).

No available studies have examined whether eating disturbances influence the outcome of alcoholism treatment. Although clinical lore suggests that personality disorders—if present—are associated with negative treatment outcomes, this has not received empirical support in treatment studies of patients with EDs (Grilo 2002b), and findings from treatment studies of patients with SUD are mixed (Grilo and McGlashan 1999).

Based on clinical experience with both patient groups, the authors suggest that certain CBT–based treatments represent a good starting point for treating co–occurring alcohol use and eating disorders. Basic aspects of the cognitive behavioral approach (e.g., coping skills therapy) have been found effective for treating alcohol dependence (Kadden et al. 1992; Monti et al. 1989, 2001) and are useful for ED patients. However, as previously noted, behavioral therapies without the specific cognitive components of CBT have inferior long–term outcomes compared with CBT (Fairburn et al. 1993a).

Nevertheless, specific forms of behavioral and coping skills treatments (without the specific cognitive components of the CBT approaches for EDs) have been used successfully with substance abusers and seem to be readily integrated with pharmacological approaches (Monti et al. 2001; O’Malley et al. 1992; Sinha 2000).

Thus, an approach that targets alcohol use and pathologic eating behaviors may be especially appropriate for treating patients with both disorders. Treatment designed to teach new coping skills to patients with alcoholism could also have a beneficial effect on eating disorders even if the ED is not specifically targeted. Given the well–known ambivalence that characterizes many of these patients (e.g., Vitousek et al. 1998), another potentially relevant approach involves motivational enhancement interviewing (Rollnick and Miller 1995), which has received some support for SUDs (Project MATCH Research Group 1997) and EDs (Treasure et al. 1999).
Another promising approach is dialectical behavior therapy (DBT), which initial research supports for both BN (Safer et al. 2001) and BED (Telch et al. 2001). DBT, which focuses on awareness of problems and choices, mood regulation techniques, and coping skills, directly addresses many of the needs of both ED and alcohol use disorder patients, including the frequently co–occurring borderline personality disorder. Indeed, the initial treatment outcome findings for DBT for both BN (Safer et al. 2001) and BED (Telch et al. 2001) suggest that addressing a potential vulnerability (e.g., problems with mood regulation and coping) can lead to improvements in ED even without a direct focus on the eating behaviors, a finding that parallels that reported for interpersonal psychotherapy (Agras et al. 2000; Fairburn et al. 1993a; Wilfley et al. 1993).

Telch and colleagues (2001) speculated that DBT may be particularly helpful for ED patients characterized by high levels of negative affect. Recent studies with BN (Grilo et al. 2001b; Stice and Agras 1999) and BED (Grilo et al. 2001c) revealed two subtypes of these EDs: dietary and a mixed dietary–negative affect. The dietary subgroup was characterized primarily by eating–specific psychopathology without associated problems with self–esteem and depression (negative affect). Patients with the mixed dietary–negative affect subtype also had high rates of alcohol and other drug problems. It is possible that such patients, particularly if they have problems with impulsivity or have co–occurring borderline personality disorder, might benefit from affect regulation and coping skills approaches such as DBT.

CONCLUSION

Alcoholism and EDs frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders.

Although such diagnostic co–occurrence suggests the possibility of shared factors in the etiology or maintenance of these problems, research has not established such links.

The clinical reality that eating and alcohol use disorders frequently co–occur has important implications for assessment, treatment, and research.

Comprehensive assessment is necessary for good treatment.

Research on methods of treating people with co–occurring alcohol and eating problems represents a major need. Until further guidance is provided, the authors recommend concurrently addressing both disorders. CBT, coping skills, or DBT approaches seem to be reasonable starting points.

REFERENCES

AGRAS, W.S.; ROSSITER, E.M.; ARNOW, B.; et al. Pharmacologic and cognitive–behavioral treatment for bulimia nervosa: A controlled comparison. American Journal of Psychiatry 149(1):82–87, 1992.
AGRAS, W.S.; WALSH, T.; FAIRBURN, C.G.; et al. A multicenter comparison of cognitive–behavioral therapy and interpersonal psychotherapy for bulimia nervosa. Archives of General Psychiatry 57:459–466, 2000.
ALLISON, D.B. A note on the selection of control groups and control variables in comorbidity research. Comprehensive Psychiatry 34:336–339, 1993.
ALGER, S.A.; SCHWALBERG, M.D.; BIGAOUETTE, J.M.; et al. Effect of a tricyclic antidepressant and opiate antagonist on binge–eating behavior in normal weight bulimic and obese, binge–eating subjects. American Journal of Clinical Nutrition 53(4):865–871, 1991.
American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: APA, 1994.
ANDERSEN, A.E. Eating disorders in males. In: Brownell, K.D.; Fairburn, C.G., eds. Eating Disorders and Obesity: A Comprehensive Handbook. New York: Guilford Press, 1995. pp. 177–187.
ANDERSEN, A.E.; BOWERS, W.A.; and WATSON, T. A slimming program for eating disorders not otherwise specified. Reconceptualizing a confusing residual diagnostic category. Psychiatric Clinics of North America 24:271–280, 2001.
ANDERSEN, A.E., and HOLMAN, J.E. Males with eating disorders: Challenges for treatment and research. Psychopharmacology Bulletin 33:391–397, 1997.
ANTON, R.F.; MOAK, D.H.; WAID, L.R.; et al. Naltrexone and cognitive behavioral therapy for the treatment of outpatient alcoholics: Results of a placebo–controlled trial. American Journal of Psychiatry 156(11):1758–1764, 1999.
ATTIA, E.; HAIMAN, C.; WALSH, B.T.; and FLATER, S.R. Does fluoxetine augment the inpatient treatment of anorexia nervosa? American Journal of Psychiatry 155:548–551, 1998.
BARRY, D.T.; GRILO, C.M.; and MASHEB, R.M. Gender differences in patients with binge eating disorder. International Journal of Eating Disorders 31:63–70, 2002.
BEARY, M.D.; LACEY, J.H.; and MERRY, J. Alcoholism and eating disorders in women of fertile age. British Journal of Addiction 81(5):685–689, 1986.
BECKER, A.E.; GRINSPOON, S.K.; KLIBANSKI, A.; and HERZOG, D.B. Eating disorders. New England Journal of Medicine 340(14):1092–1098, 1999.
BERKSON, J. Limitations of the application of the four–fold table analysis to hospital data. Biometrics Bulletin 2:47–53, 1946.
BERRIDGE, K.C. Food reward: Brain substrates of wanting and liking. Neuroscience and Biobehavioral Reviews 20:1–25, 1996.
BLACK, C.M.D., and WILSON, G.T. Assessment of eating disorders: Interview versus questionnaire. International Journal of Eating Disorders 20:43–50, 1996.
BRADLEY, K.A.; BOYD–WICKIZER, J.; POWELL, S.H.; and BURMAN, M.L. Alcohol screening questionnaires in women: A critical review. JAMA: Journal of the American Medical Association 280(2):166–171, 1998.
BREWERTON, T. Toward a unified theory of serotonin dysregulation in eating and related disorders. Psychoneuroendocrinology 20:561–590, 1995.
BREWERTON, T.; LYDIARD, R.; HERZOG, D.; et al. Comorbidity of axis I psychiatric disorders in bulimia nervosa. Journal of Clinical Psychiatry 56:77–80, 1995.
BULIK, C.M.; SULLIVAN, P.F.; CARTER, F.A.; and JOYCE, P.R. Lifetime comorbidity of alcohol dependence in women with bulimia nervosa. Addictive Behaviors 22:437–446, 1997.
BUSHNELL, J.A.; WELLS, E.; MCKENZIE, J.M.; et al. Bulimia comorbidity in the general population and in the clinic. Psychological Medicine 24:605–611, 1994.
CARR, K.D. Opioid receptor subtypes and stimulation–induced feeding. In: Cooper, S.J., and Clifton, P.G., eds. Drug Receptor Subtypes and Ingestive Behavior. San Diego, CA: Academic Press, 1996. pp. 167–191.
CARTER, J.C., and FAIRBURN, C.G. Cognitive–behavioral self–help for binge eating disorder: A controlled effectiveness study. Journal of Consulting and Clinical Psychology 66:616–623, 1998.
CATTERSON, M.F.; PRYOR, T.L.; BURKE, M.J.; et al. Death due to alcoholic complications in a young woman with a severe eating disorder: A case report. International Journal of Eating Disorders 21:303–305, 1997.
COOPER, Z., and FAIRBURN, C.G. The Eating Disorder Examination: A semi–structured interview for the assessment of the specific psychopathology of eating disorders. International Journal of Eating Disorders 6:1–8, 1987.
COOPER, S.J., and KIRKHAM, T.C. Opioid mechanisms in the control of food consumption and taste preferences. In: Herz, A.; Akil, H.; and Simon, E.J., eds. Handbook of Experimental Pharmacology, Vol. 104 Part II. Berlin: Springer Verlag, 1993. pp. 239–263.
CORNELIUS, J.R.; SALLOUM, I.M.; EHLER, J.G.; et al. Fluoxetine in depressed alcoholics: A double–blind, placebo–controlled trial. Archives of General Psychiatry 54(8):700–705, 1997.
CROW, S.; MUSSELL, M.P.; PETERSON, C.; et al. Prior treatment received by patients with bulimia nervosa. International Journal of Eating Disorders 25:39–44, 1999.
DANIELS, E.S.; MASHEB, R.M.; BERMAN, R.M.; et al. Bulimia nervosa and alcohol dependence: A case report of a patient enrolled in a randomized controlled clinical trial. Journal of Substance Abuse Treatment 17:163–166, 1999.
DANSKY, B.S.; BREWERTON, T.D.; and KILPATRICK, D.G. Comorbidity of bulimia nervosa and alcohol use disorders: Results from the National Women’s Study. International Journal of Eating Disorders 27:180–190, 2000.
DUFORT, G.G.; NEWMAN, S.C.; and BLAND, R.C. Psychiatric comorbidity and treatment seeking sources of selection bias in the study of clinical populations. Journal of Nervous and Mental Disease 181:467–474, 1993.
FAIRBURN, C.G. Overcoming Binge Eating. New York: Guilford Press, 1995.
FAIRBURN, C.G., and BEGLIN, S.J. Assessment of eating disorders: Interview or self–report questionnaire? International Journal of Eating Disorders 16:363–370, 1994.
FAIRBURN, C.G.; JONES, R.; PEVELER, R.C.; et al. Psychotherapy and bulimia nervosa: Longer–term effects of interpersonal psychotherapy, behavior therapy, and cognitive–behavior therapy. Archives of General Psychiatry 50:419–428, 1993a.
FAIRBURN, C.G.; MARCUS, M.D.; and WILSON, G.T. Cognitive behavioral therapy for binge eating and bulimia nervosa: A comprehensive treatment manual. In: Fairburn, C.G., and Wilson, G.T., eds. Binge Eating: Nature, Assessment, and Treatment. New York: Guilford Press, 1993b. pp. 361–404.
Fluoxetine Bulimia Nervosa Collaborative Study Group (FBNCSG). Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo–controlled, double–blind trial. Archives of General Psychiatry 49(2):139–147, 1992.
FREY, R.J. Anorexia nervosa. In: Olendorf, O.; Jeryan, C.; and Boyden, K., eds. The Gale Encyclopedia of Medicine. Farmington Hills, MI.: Gale Research, 1999.
FROEHLICH, J.C. Genetic factors in alcohol self–administration. Journal of Clinical Psychiatry 56(Suppl. 7):15–23, 1995.
GOLDBLOOM, D.S. Alcohol misuse and eating disorders: Aspects of an association. Alcohol and Alcoholism 28(4):375–381, 1993.
GOLDBLOOM, D.S.; NARANJO, C.A.; BREMNER, K.E.; and HICKS, L.K. Eating disorders and alcohol abuse in women. British Journal of Addiction 87(6):913–920, 1992.
GOSNELL, B.A., and LEVINE, A.S. Stimulation of ingestive behavior by preferential and selective opioid agonists. In: Cooper, S.J., and Clifton, P.G. Drug Receptor Subtypes and Ingestive Behavior. San Diego, CA: Academic Press, 1996. pp. 147–166.
GRILO, C.M. The assessment and treatment of binge eating disorder. Journal of Practical Psychiatry and Behavioral Health 4:191–201, 1998.
GRILO, C.M. Self–help and guided self–help treatments for bulimia nervosa and binge eating disorder. Journal of Practical Psychiatry 6:18–26, 2000.
GRILO, C.M. Binge eating disorder. In: Fairburn, C.G., and Brownell, K.D., eds. Eating Disorders and Obesity: A Comprehensive Handbook. 2d edition. New York: Guilford Press, 2002a. pp. 178–182.
GRILO, C.M. Recent research of relationships among eating disorders and personality disorders. Current Psychiatry Reports 4:18–24, 2002b.
GRILO, C.M., and MASHEB, R.M. Childhood psychological, physical, and sexual maltreatment in outpatients with binge eating disorder: Frequency and associations with gender, obesity, and eating–related psychopathology. Obesity Research 9(5):320–325, 2001.
GRILO, C.M., and MCGLASHAN, T.H. Stability and course of personality disorders. Current Opinion in Psychiatry 12:157–162, 1999.
GRILO, C.M.; BECKER, D.F.; LEVY, K.N.; et. al. Eating disorders with and without substance use disorders: A comparative study of inpatients. Comprehensive Psychiatry 36:312–317, 1995a.
GRILO, C.M.; LEVY, K.N.; BECKER, D.F.; et al. Eating disorders in female inpatients with versus without substance use disorders. Addictive Behaviors 20:255–260, 1995b.
GRILO, C.M.; DEVLIN, M.J.; CACHELIN, F.M.; and YANOVSKI, S.Z. Report of the National Institutes of Health Workshop on the development of research priorities in eating disorders. Psychopharmacology Bulletin 33:321–333, 1997.
GRILO, C.M.; MASHEB, R.M.; and WILSON, G.T. A comparison of different methods for assessing the features of eating disorders in patients with binge eating disorder. Journal of Consulting and Clinical Psychology 69:317–322, 2001a.
GRILO, C.M.; MASHEB, R.M.; and BERMAN R.M. Subtyping women with bulimia nervosa along dietary and negative affect dimensions: A replication in a treatment–seeking sample. Eating and Weight Disorders 6:53–58, 2001b.
GRILO, C.M.; MASHEB, R.M.; and WILSON, G.T. Subtyping binge eating disorder. Journal of Consulting and Clinical Psychology 69:317–322, 2001c.
HEINALA, P.; ALHO, H.; KIIANMA, K.; et al. Targeted use of naltrexone without prior detoxification in the treatment of alcohol dependence: A factorial double–blind, placebo–controlled trial. Journal of Clinical Psychopharmacology 21:287–292, 2001.
HIGUCHI, S.; SUZUKI, K.; YAMADA, K.; et al. Alcoholics with eating disorders: Prevalence and clinical course—A study from Japan. British Journal of Psychiatry 162:403–406, 1993.
HOEK, H.W. Review of the epidemiological studies of eating disorders. International Review of Psychiatry 5:61–74, 1993.
HOLDERNESS, C.C., BROOKS–GUNN, J.; and WARREN, M.P. Co–morbidity of eating disorders and substance abuse: Review of the literature. International Journal of Eating Disorders 16:1–35, 1994.
HUDSON, J.I.; POPE, H.G., JR.; JONAS, J.M.; and YURGELUN–TODD, D. Phenomenologic relationship of eating disorders to major affective disorder. Psychiatry Research 9(4):345–354, 1983.
HUDSON, J.I.; MCELROY, S.L.; RAYMOND, N.C.; et al. Fluvoxamine treatment of binge eating disorder: A multicenter, placebo–controlled trial. American Journal of Psychiatry 155:1756–1762, 1998.
JACKSON, T.D., and GRILO, C.M. Weight and eating concerns in men and women in outpatient treatment for substance abuse. Eating and Weight Disorders, in press.
JONAS, J.M., and GOLD, M.S. The use of opiate antagonists in treating bulimia: A study of low dose vs. high dose naltrexone. Psychiatry Research 24:195–199, 1987.
JONES, D.A.; CHESHIRE, N.; and MOORHOUSE, H. Anorexia nervosa, bulimia and alcoholism: Association of eating disorder and alcohol. Journal of Psychiatric Research 19(2/3):377–380, 1985.
KADDEN, R.; CARROLL, K.; DONOVAN, D.; et al., eds. Cognitive–Behavioral Coping Skills Therapy Manual: A Clinical Research Guide for Therapists Treating Individuals with Alcohol Abuse and Dependence. Project MATCH Monograph Series, Vol. 3. DHS Publication No. (ADM) 92–1895. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1992.
KAYE, W.H.; LILENFELD L.R.; PLOTNICOV, K.; et al. Bulimia nervosa and substance dependence: Association and family transmission. Alcoholism: Clinical and Experimental Research 20(5):878–881, 1996.
KAYE, W.H.; GREENO, C.G.; MOSS, H.; et al. Alterations in serotonin activity and psychiatric symptomatology after recovery from bulimia nervosa. Archives of General Psychiatry 55:927–935, 1998.
KAYE, W.H.; NAGATA, T.; WELTZIN, T.E.; et al. Double–blind placebo–controlled administration of fluoxetine in restricting– and restricting–purging–type anorexia nervosa. Biological Psychiatry 49:644–652, 2001.
KENDALL, P.C., and CLARKIN, J.F. Introduction to special section: Comorbidity and treatment implications. Journal of Consulting and Clinical Psychology 60:833–834, 1992.
KENDLER, K.S.; MACLEAN, C.; NEALE, M.; et al. The genetic epidemiology of bulimia nervosa. American Journal of Psychiatry 148(12):1627–37, 1991.
KENDLER, K.S.; WALTERS, E.E.; NEALE, M.C.; et al. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women: Phobia, generalized anxiety disorder, panic disorder, bulimia, major depression and alcoholism. Archives of General Psychiatry 52:374–383, 1995.
KRAEMER, H.C. Statistical issues in assessing comorbidity. Statistics in Medicine 14:721–733, 1995.
KRAHN, D.D. The relationship of eating disorders and substance abuse. Journal of Substance Abuse 3(2):239–253, 1991.
KRAHN, D.; KURTH, C.; DEMITRACK, M.; and DREWNOWSKI, A. The relationship of dieting severity and bulimic behaviors to alcohol and other drug use in young women. Journal of Substance Abuse 4(4):341–353, 1992.
KRAHN, D.; PIPER, D.; KING, M.; et al. Dieting in sixth grade predicts alcohol use in ninth grade. Journal of Substance Abuse 8(3):293–301, 1996.
KRINGLEN, E.; TORGERSEN, S.; and CRAMER, V. A Norwegian psychiatric epidemiological study. American Journal of Psychiatry 158:1091–1098, 2001.
KRYSTAL, J.H.; CRAMER, J.A.; KROL, W.F.; et al. Naltrexone in the treatment of alcohol dependence. New England Journal of Medicine 345:1734–1739, 2001.
LAMB, J. Bulimia nervosa. In: Olendorf, O.; Jeryan, C.; and Boyden, K., eds. The Gale Encyclopedia of Medicine. Farmington Hills, MI: Gale Research, 1999.
LILENFELD, L.; KAYE, W.; GREENO, C.; et al. Psychiatric disorders in women with bulimia nervosa and their first–degree relatives: Effects of comorbid substance dependence. International Journal of Eating Disorders 22:253–264, 1997.
MASON, B.J.; SALVATO, F.R.; WILLIAMS, L.D.; et al. Double–blind, placebo–controlled study of oral nalmefene for alcohol dependence. Archives of General Psychiatry 56(8):719–724, 1999.
MCCANN, U.D., and AGRAS, W.S. Successful treatment of nonpurging bulimia nervosa with desipramine: A double–blind, placebo–controlled study. American Journal of Psychiatry 147:1509–1513, 1990.
MCELROY, S.L.; CASUTO, L.S.; NELSON, E.B.; et al. Placebo–controlled trial of sertaline in the treatment of binge eating disorder. American Journal of Psychiatry 157:1004–1006, 2000.
MERCER, M.E., and HOLDER, M.D. Food cravings, endogenous opioid peptides, and food intake: A review. Appetite 29(3):325–352, 1997.
MITCHELL, J.E.; PYLE, R.L.; ECKERT, E.D.; et al. A comparison study of antidepressants and structured intensive group therapy in the treatment of bulimia nervosa. Archives of General Psychiatry 47:149–157, 1990.
MITCHELL, J.; SPECKER, S.; and DE ZWANN, M. Comorbidity and medical complications of substance abuse: Review of the literature. International Journal of Eating Disorders 16:1–34, 1991.
MITCHELL, J.E.; SPECKER, S.; and EDMONSON, K. Management of substance abuse and dependence. In: Garner, D., and Garfinkel, P.E., eds. Handbook of Treatment for Eating Disorders. New York: Guilford Press, 1997. pp. 415–423.
MONTI, P.M.; ABRAMS, D.B.; KADDEN, R.M.; and COONEY, N.L. Treating Alcohol Dependence: A Coping Skills Training Guide. New York: Guilford Press, 1989.
MONTI, P.M.; ROHSENOW, D.J.; SWIFT, R.; et al. Naltrexone and cue exposure with coping and communication skills training for alcoholics: Treatment process and 1–year outcomes. Alcoholism: Clinical and Experimental Research 25:1634–1647, 2001.
O’MALLEY, S.S.; JAFFE, A.J.; CHANG, G.; et al. Naltrexone and coping skills therapy for alcohol dependence: A controlled study. Archives of General Psychiatry 49(11):881–887, 1992.
PETERSON, C.B.; MITCHELL, J.E.; ENGBLOOM, S.; et al: Group cognitive–behavioral treatment of binge eating disorder: A comparison of therapist–led versus self–help formats. International Journal of Eating Disorders 24:125–136, 1998.
PEVELER, R., and FAIRBURN, C. Eating disorders in women who abuse alcohol. British Journal of Addiction 85(12):1633–1638, 1990.
Project MATCH Research Group. Matching alcoholism treatment to client heterogeneity: Posttreatment outcomes. Journal of Studies on Alcohol 58:7–29, 1997.
REID, L.D. Endogenous opioid peptides and regulation of drinking and feeding. American Journal of Clinical Nutrition 42:1099–1132, 1985.
REID, L.D.; DELCONTE, J.D.; NICHOLS, M.L.; et al. Tests of opioid deficiency hypotheses of alcoholism. Alcohol: An International Biomedical Journal 8(4):247–258, 1991.
ROLLNICK, S., and MILLER, W.R. What is motivational interviewing? Behavioral and Cognitive Psychotherapy 23:325–334, 1995.
SAFER, D.L.; TELCH, C.F.; and AGRAS, W.S. Dialectical behavior therapy for bulimia nervosa. American Journal of Psychiatry 158:632–634, 2001.
SCHUCKIT, M.A.; TIPP, J.E.; ANTHENELLI, R.M.; et al. Anorexia nervosa and bulimia nervosa in alcohol–dependent men and women and their relatives. American Journal of Psychiatry 153(1):74–82, 1996.
SHER, K.J., and TRULL, T.J. Substance use disorder and personality disorder. Current Psychiatry Reports 4:25–29, 2002.
SINHA, R. Treatment for alcohol abuse and dependence: Special therapeutic needs of women. In: Zernig, G.; Saria, A.; Kurz, M.; and O’Malley, S.S., eds. CRC Handbook of Alcoholism: Clinical and Theoretical Approaches. Boca Raton, FL: CRC Press, 2000. pp. 151–164.
SINHA, R.; ROBINSON, J.; MERIKANGAS, K.; et al. Eating pathology among women with alcoholism and/or anxiety disorders. Alcoholism: Clinical and Experimental Research 20(7):1184–1191, 1996.
SMOLAK, L., and MURNEN, S.K. A meta–analytic examination of the relationship between child sexual abuse and eating disorders. International Journal of Eating Disorders 31:136–150, 2002.
SPITZER, R.L.; YANOVSKI, S.; WADDEN, T.; et al. Binge eating disorder: Its further validation in a multisite study. International Journal of Eating Disorders 13(2):137–153, 1993.
STICE, E., and AGRAS, W.S. Subtyping bulimic women along dietary restraint and negative affect dimensions. Journal of Consulting and Clinical Psychology 67:460–469, 1999.
STRIEGEL–MOORE, R.H.; DOHM, F.A.; SOLOMON, E.E.; et al. Subthreshold binge eating disorder. International Journal of Eating Disorders 27:270–278, 2000.
SUZUKI, K.; HIGUCHI, S.; YAMADA, K.; et al. Young female alcoholics with and without eating disorders: A comparative study in Japan. American Journal of Psychiatry 150(7):1053–1058, 1993.
TAYLOR, A.V.; PEVELER, R.C.; HIBBERT, G.A.; and FAIRBURN, C.G. Eating disorders among women receiving treatment for an alcohol problem. International Journal of Eating Disorders 14(2):147–151, 1993.
TELCH, C.F., and STICE, E. Psychiatric comorbidity in women with binge eating disorder: Prevalence rates from a non–treatment–seeking sample. Journal of Consulting and Clinical Psychology 66:768–776, 1998.
TELCH, C.F.; AGRAS, W.S.; and LINEHAN, M.M. Dialectical behavior therapy for binge eating disorder. Journal of Consulting and Clinical Psychology 69:1061–1065, 2001.
TREASURE, J.; SCHMIDT, U.; TROOP, N.; et al. Sequential treatment for bulimia nervosa incorporating a self–care manual. British Journal of Psychiatry 168:94–98, 1996.
TREASURE, J.L.; KATZMAN, M.; SCHMIDT, U.; et al. Engagement and outcome in the treatment of bulimia nervosa: First phase of a sequential design comparing motivation enhancement therapy and cognitive behavioural therapy. Behaviour Research and Therapy 37:405–418, 1999.
VITOUSEK, K.; WATSON, S.; and WILSON, G.T. Enhancing motivation for change in treatment–resistant eating disorders. Clinical Psychology Review 18:391–420, 1998.

Eating Disorders and Alcohol Use Disorders

Carlos M. Grilo, Ph.D., Rajita Sinha, Ph.D., and Stephanie S. O’Malley, Ph.D.

Carlos M. Grilo, Ph.D., is an associate professor in the Department of Psychiatry and director of the Eating Disorder Program; Rajita Sinha, Ph.D., is an associate professor in the Department of Psychiatry and director of the Substance Abuse Treatment Unit; and Stephanie S. O’Malley, Ph.D., is a professor in the Department of Psychiatry and director of the Division of Substance Abuse Research, all at Yale University School of Medicine, New Haven, Connecticut.

Preparation of this article was supported, in part, by National Institute on Alcohol Abuse and Alcoholism grants AA–10225 and AA–110171 and National Institute of Diabetes and Digestive and Kidney Diseases grant DK–49587.
Alcoholism and eating disorders frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders. Although this co–occurrence suggests the possibility of common or shared factors in the etiology of these two problems, research to date has not established such links. Regardless of the precise meaning of the association, the reality that eating disorders and alcohol use disorders frequently co–occur has important implications for assessment, treatment, and future research. Key words: eating disorder; personality disorder; AODD (alcohol and other drug dependence); comorbidity; anorexia nervosa; bulimia nervosa; gender differences; diet; coping skills; cognitive therapy; behavior therapy; psychosocial treatment method
Numerous studies suggest that eating disorders (EDs) and alcohol and other drug use disorders (referred to throughout this paper as substance use disorders [SUDs]) frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders. This review will consider the extent and nature of such co–occurrences and whether research supports the possibility of common or shared factors in the etiology or maintenance of EDs and SUDs. The reality that EDs and SUDs frequently co–occur has important implications for assessment, treatment, and future research. Although this review will offer implications for clinicians and researchers in both fields, the presentation bias will be toward providing a more detailed discussion of the ED literature for professionals in the alcoholism field.
EATING DISORDERS
The current classification system, the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–IV) (American Psychiatric Association [APA] 1994) specifies three ED diagnoses. The formal diagnoses are anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). In addition, the DSM–IV includes a new ED category (binge eating disorder [BED]) as a research category. BED is a specific example of EDNOS. Brief descriptions of these EDs follow. See Grilo (2002a) and Becker and colleagues (1999) for detailed discussions of the clinical features and assessment issues of these disorders.
Anorexia Nervosa is characterized by a refusal to maintain normal body weight (defined as 15 percent below normal weight for age and height), an intense fear of becoming fat, and (in females) skipped menstrual periods (i.e., amenorrhea) for at least 3 months. People with AN have a severely distorted body image. They see themselves as overweight despite being overly thin, and they tend to deny the seriousness of their low body weight. The DSM–IV specifies two subtypes of AN—a “restricting type,” characterized by strict dieting or exercise without binge eating; and a “binge–eating/purging type,” marked by episodes of binge eating and/or purging via self–induced vomiting or misusing laxatives, enemas, or diuretics. In severe cases, medical complications or death from starvation can occur. Roughly 50 percent of people with AN may eventually develop bulimia nervosa (described below). AN is a rare disorder; it occurs disproportionately in women, and is estimated to have a prevalence of roughly 1 percent in adolescent and young adult women (Hoek 1993).
Bulimia Nervosa is characterized by recurrent episodes of binge eating (defined as consuming unusually large amounts of food in a discrete period of time plus a subjective sense of lack of control over eating). BN is further characterized by regular use of extreme weight control methods (e.g., vomiting; abuse of laxatives, diet pills, or diuretics; severe dieting or fasting; vigorous exercise) and by dysfunctional attitudes about weight or shape that unduly influence self–evaluation. For a diagnosis of bulimia nervosa, the DSM–IV requires both the binge eating and inappropriate weight control methods to have occurred, on average, at least twice per week during the past 3 months. The DSM–IV specifies two subtypes of BN, a “purging type” and a “non–purging type,” which is limited to the severe dieting, fasting, or exercise forms of weight control behaviors. If either form of BN occurs during a current episode of AN, the assigned diagnosis is AN. BN, like AN, is more common in females and has an estimated prevalence rate of 2 percent to 3 percent in young females (Kendler et al. 1991; Kringlen et al. 2001).
Eating Disorder Not Otherwise Specified is generally considered the most prevalent form or category of ED and the least studied (Andersen et al. 2001; Grilo et al. 1997). Outside of research centers with specific recruitment requirements, the majority of patients who present for treatment for eating–related problems are “partial syndrome” or EDNOS cases. That is, they fail to meet all the diagnostic requirements for one of the “formal” EDs but they have significant symptoms and associated problems. Indeed, researchers have questioned the significance of the failure to meet some of the specific criteria (such as the necessity that amenorrhea be present in female patients for a diagnosis of AN to be made). Investigators have also claimed that some of the diagnostic criteria for the formal EDs are too stringent (Andersen et al. 2001; Striegel–Moore et al. 2000). Many patients experience significant and clinically meaningful problems with eating and body image, but do not always fulfill the exact requirements for the diagnoses of AN or BN.
Binge Eating Disorder, included as a provisional category in the DSM–IV, is a specific example of an EDNOS. BED is characterized by recurrent episodes of binge eating (an average of 2 days with binge episodes per week over a 6–month period is required; marked distress exists because of the binge eating) without the compensatory weight control methods that are required for the diagnosis of BN (Grilo 1998, 2002a). BED, unlike AN and BN, is not uncommon in males or in people of color. It is most frequently seen in adults, and has an estimated prevalence of 3 percent in adults and roughly 8 percent in obese persons (Spitzer et al. 1993). BED is associated with increased risk for obesity and thus for the plethora of medical problems associated with obesity (Grilo 1998).
Age Ranges and Gender
Eating disorders most frequently develop during adolescence or early adulthood, but their onset can occur during childhood or much later in adulthood (Grilo 2002a). The peak age range for onset of AN is 14 to 18 years, although some patients develop AN as late as their 40s (Frey 1999). Similarly, the peak age range for BN is adolescence through early adulthood (Lamb 1999). BED most frequently occurs in young to middle adulthood (Grilo 1998). Although developmental challenges and severe dieting generally predate AN and BN, it appears that a significant proportion of people with BED report no dieting prior to the onset of binge eating (Grilo 1998, 2002a). Although AN and BN occur mostly in females and BED is more common in females than males, it is important to not overlook these EDs in men (Andersen 1995; Andersen and Holman 1997). Available research suggests that among ED patients, few gender differences exist in the specific features of the EDs (Barry et al. 2002; Woodside et al. 2001).
CO–OCCURRENCE OF SUBSTANCE USE DISORDERS AND EATING DISORDERS
Most studies have reported that EDs and SUDs frequently co–occur, with especially high rates observed among patients in treatment (e.g., Beary et al. 1986; Brewerton et al. 1995; Bushnell et al. 1994; Goldbloom et al. 1992; Grilo et al. 1995b; Higuchi et al. 1993; Suzuki et al. 1993; Taylor et al. 1993; see reviews by Grilo et al. 1995a and Holderness et al. 1994 for more complete listings of earlier studies).
Although research has generally reported high rates of co–occurrence between EDs and SUDs, perhaps most striking is the marked inconsistency or variability in the reported co–occurrence rates across studies. A previous review (Holderness et al. 1994) noted that estimates of BN in patients with SUDs ranged from 8 percent to 41 percent and estimates for AN ranged from 2 percent to 10 percent. Methodological issues account, in part, for some of the inconsistencies in the reported co–occurrence rates and make interpretation of the literature ambiguous. Variations in recruitment methods (community versus treatment samples, and, if using treatment samples, the type of treatment facility [e.g., general psychiatric, substance or chemical dependency, eating disorder; inpatient versus outpatient]) and assessment and diagnostic methods (survey, self–report, diagnostic interview) account for some of the variability in the literature.
These important methodological limitations notwithstanding, research does suggest that EDs and SUDs frequently co–occur. Therefore, research seeks to determine the significance of the co–occurrence for informing (a) models of etiology and pathophysiology, and (b) approaches to treatment and clinical management. The remainder of this article will review this research, first examining the prevalence of the co–occurrence of EDs and SUDs in more detail and then exploring whether research supports the possibility of common or shared factors in the etiology or maintenance of EDs and SUDs.
Co–Occurrence versus Comorbidity
“Comorbidity” is a widely used term in psychopathology research but one that appears to reflect various meanings or definitions. Kendall and Clarkin (1992), among others (Grilo 2002b), noted numerous possible meanings of comorbidity, including random co–occurrence of disorders that are independent, co–occurrence of different disorders that share a common etiology, or different disorders that have a causal relationship between them. Comorbidity may reflect, in part, artifacts of the diagnostic systems because of criterion overlap (e.g., one criterion for borderline personality disorder is “impulsivity,” which can be met in part by binge eating and/or by substance use). As demonstrated initially by Berkson (1946), and more recently by duFort and colleagues (1993), studies of treatment–seeking patients must be interpreted cautiously because of biases (i.e., people seeking treatment may have especially severe problems, people with multiple problems may seek treatment for one or several of the problems) that can make interpretation of comorbidity difficult and may limit generalizability to community samples. Thus, a starting point for possible comorbidity is when rates of co–occurring diagnoses are statistically different from those expected, given the base rates for the individual disorders (Kraemer 1995). Allison (1993) maintained the importance of selecting “relevant” control or comparison groups to provide a context for interpreting differences in co–occurrence patterns. Appropriate comparisons might include psychiatric patient groups without the eating and/or alcohol use disorders.
Recent research with both people in treatment (Grilo et al. 1995b; Wilfley et al. 2000) and in the general population (Dansky et al. 2000; von Ranson et al. 2002; Telch and Stice 1998; Yanovski et al. 1993) that used systematic recruitment methods, standardized diagnostic interviews (rather than self–report), and “relevant” comparison groups has revealed that, although EDs and SUDs co–occur, the co–occurrence is either not significantly greater or-if so-is only marginally greater than the co–occurrence rate in relevant comparison groups (i.e., patient groups of comparable severity chosen to provide a context as opposed to the frequently used “normal” control group). Grilo and colleagues (1995a, 1995b) found that, although EDs are frequently diagnosed among inpatients with SUDs, they are also frequently diagnosed in other psychiatric inpatients. In this controlled study, the frequency of AN and BN was not greater in patients with SUDs than without SUDs. Subthreshold manifestations of EDs (i.e., EDNOS; cases where insufficient criteria were present to warrant either BN or AN diagnoses) were diagnosed significantly more frequently in the patients with SUDs than without. Some research has also suggested that patients with nonpurging AN may be less likely than patients with other forms of EDs, including AN purging subtype, to have SUDs. The increased possibility for SUDs to co–occur with atypical manifestations of EDs, rather than with AN and BN, is examined further in the following section.
The three studies of comorbidity in BED that used relevant comparison groups found high rates of lifetime alcohol use and SUDs but not higher rates than observed in the comparison groups (Telch and Stice 1998; Wilfley et al. 2000; Yanovski et al. 1993). Most recently, von Ranson and colleagues (2002) reported findings from a large community study of two groups (672 adolescent girls, 718 adult women) assessed using diagnostic interviews. The authors reported that EDs and substance use were positively related, but the association was not significant. They concluded that there is no strong overarching relationship between these problems. These findings suggest caution in interpreting comorbidity between different forms of EDs and SUDs.
Other Comorbid Psychiatric Disorders
Although this review focuses primarily on the co–occurrence of EDs and SUDs, both of these classes of disorders frequently co–occur with other forms of psychopathology. A large body of research has documented associations between EDs and other psychiatric and personality disorders (Bulik et al. 1997; Grilo 2002b; Grilo et al. 1995a,b) as well as between SUDs and other psychiatric disorders (Grilo et al. 1997; Sher and Trull 2002).
Controlled studies (Dansky et al. 2000; Grilo et al. 1995a,b; Wiseman et al. 1999) have suggested that some of the apparent co–occurrence between EDs and SUDs may be related, in part, to other psychiatric comorbidities. Specifically, Dansky and colleagues (2000) reported that the relationship between BN and alcohol use disorders reported by the National Women’s Study was likely indirect and the result of associations with other psychiatric disorders, most notably major depressive disorder and post–traumatic stress disorder. Grilo and colleagues (1995b) compared inpatients who had ED with and without SUD with a comparison group who had SUD but not ED. In this controlled comparison, personality disorders characterized as cluster B (i.e., erratic or unstable) were diagnosed more frequently in the patients with co–occurring ED and SUD, whereas cluster C personality disorders (i.e., anxious or fearful) were diagnosed more frequently in patients with ED without co–occurring SUD. This three–group comparison allowed for a finer distinction regarding potential comorbidity and raised the possibility of subgroups of patients (e.g., with borderline personality disorder) who might be most likely to have problems with both eating and substance use disorders. Consistent with this, Bulik and colleagues (1997) found that, although women with alcoholism and BN had higher rates of a variety of psychiatric problems than women with BN without histories of alcohol use disorders, multivariate analyses revealed that borderline personality disorder was the sole distinguishing variable between the two groups. Most recently, Wiseman and colleagues (1999) found that the order of onset of the two disorders might be important. Patients who developed EDs early and prior to SUDs had greater levels of psychiatric and personality disorder psychopathology compared with patients who developed the ED after the SUD and with patients who had an ED but no SUD.
These findings suggest that additional psychiatric disorders frequently co–occur with EDs and SUDs, and may play a role in their relationship to each other. In particular, these findings suggest that patients who suffer from both eating disorders and substance abuse disorders may have deficits in impulse control. Related to this line of investigation, recent years have witnessed increased attention to the potential role of childhood abuse, perhaps mediated by personality disorders, as a common factor in patients with both EDs and SUDs. Research, however, has not generally supported specific or strong associations between childhood abuse and specific disorders (Grilo and Masheb 2001; Smolak and Murnen 2002). Another issue to examine in the relationship between these disorders is the significant frequency with which ED symptoms occur with SUDs.
Eating Disorder Symptoms Among Women with Substance Use Disorders
Grilo and colleagues (1995a) have reported that EDNOS (but not AN or BN) was significantly more common in people with SUD than without SUD. This suggests that it is important for clinicians to consider and screen for subthreshold levels of EDs in addition to formal ED diagnoses. Moreover, assessment of co–occurring subthreshold eating problems may facilitate earlier intervention to prevent later development of the full–blown disorder.
A few studies have examined the specific features of EDs present among patients with SUDs (Sinha et al. 1996; Peveler and Fairburn 1990; Jackson and Grilo in press). Sinha and colleagues (1996) assessed eating behaviors and the attitudinal features of EDs in a community–based sample of 201 young women (ages 18 to 30) who comprised the following four groups: alcohol dependent, alcohol dependent with anxiety disorders, anxiety disorders only, and neither alcohol nor anxiety disorders. Women with alcohol dependence had significantly higher levels of the behavioral and attitudinal features of eating disorders and were more likely to meet the criteria for BN and EDNOS than women without alcohol dependence. Interestingly, these authors found that alcoholism was more closely related to the attitudinal features, whereas anxiety disorders were more closely associated with the behavioral features of eating disorders.
Eating Disorder Symptoms by Gender and Ethnicity
More recently, Jackson and Grilo (in press) examined the specific features of EDs and tested for gender and ethnic differences in a racially diverse group of outpatients with SUDs. Similar to previous studies with primarily Caucasian samples (Peveler and Fairburn 1990; Sinha et al. 1996), eating–related problems were not uncommon in substance abusers. Roughly 20 percent of men and women reported binge eating, and 12 percent reported some form of inappropriate weight compensatory behaviors. Problematic attitudes about body shape were also common; 28 percent of the Jackson and Grilo (in press) sample reported overvalued ideas regarding shape at levels considered to be clinically significant-as compared with 28 percent in the study of young women reported by Sinha and colleagues (1996) and 26 percent in the study reported by Peveler and Fairburn (1990). Jackson and Grilo (in press) found no significant ethnic differences in obesity, in features of eating disorders, or in levels of body image dissatisfaction. Men and women were similar in terms of overweight and behavioral features, but women had significantly higher levels of attitudinal features of EDs. Thus, contrary to clinical lore, weight– and eating–related problems are not uncommon in males or in minority groups.
RESEARCH INVESTIGATING WHETHER COMMON FACTORS MAY UNDERLIE THE CO–OCCURRENCE OF EDs AND SUDs
The studies described above demonstrate that EDs and SUDs often co–occur and that ED symptoms are significantly more common in people with SUDs than without SUDs. Although research is ongoing, reasons for this co–occurrence have not been reported. One potential explanation is that these disorders are different manifestations of a common underlying factor. Three types of research provide support for this hypothesis: studies of dieting and substance use, studies of brain chemistry, and family and genetic studies.
Studies of Dieting Behavior and Substance Use
Research has documented significant associations between dieting and eating problems and substance use in younger populations. Krahn and colleagues (1992), for example, found that among college women, increasing severity of dieting and problems associated with EDs were associated with increased rates of alcohol, cigarette, and other drug use. Krahn and colleagues (1996) also found that dieting during pre–adolescence (among sixth grade students) predicted future alcohol use. Such findings, when considered with studies showing that food deprivation can increase self–administration of alcohol and other drugs in laboratory animals, are consistent with models positing that common mechanisms may play a role in EDs and SUDs (see Krahn 1991). For example, Krahn (1991) suggested that food deprivation might cause alterations in the central nervous system’s reward pathways, thus increasing the consumption of reinforcing substances (e.g., alcohol). However, as emphasized above, and by other reviews (Wilson 1993), the fact that these problems are associated does not demonstrate a specific or common cause.
Studies of Brain Chemistry
Animal studies of brain chemistry have provided some support for the view that EDs and alcohol use disorders may have some shared factors. Some research, for example, has suggested that both disorders may be related to atypical endogenous opioid peptide (EOP) activity. EOPs have been found to influence both alcohol and food consumption (see Mercer and Holder 1997) and may play roles in the control of eating behavior (Berridge 1996; Carr 1996; Cooper and Kirkham 1993; Gosnell and Levine 1996) as well as the development of alcoholism (Reid 1985; Reid et al. 1991; see also Froehlich 1995). In addition, brain neurotransmitter systems, including the serotonin, gamma–aminobutyric acid (GABA), and dopamine systems, are the focus of active research across a wide range of psychiatric and behavioral problems, including food and alcohol consumption (see Mercer and Holder 1997). Particularly active attention has been paid to the role of serotonin, which has been implicated in the control of eating, mood, and impulsivity (Brewerton 1995; Kaye et al. 1998). In addition, treatment studies have reported some support for the efficacy of selective serotonin reuptake inhibitors (SSRIs) across different EDs (Fluoxetine Bulimia Nervosa Collaborative Study Group [FBNCSG] 1992; Hudson et al. 1998; Kaye et al. 2001).
Family and Genetic Studies
Early research reported that people with eating disorders are more likely than those without EDs to have family histories of substance use disorders (e.g., Hudson et al. 1983; Jones et al. 1985). However, several recent large, carefully conducted studies have found that EDs (especially BN) and SUDs segregate independently in families-that is, eating disorders and substance use disorders most likely do not have the same genetic, familial, and environmental risk factors. For example, Kaye and colleagues (1996) reported that alcohol or other drug dependence was increased only in first–degree relatives of women with BN who themselves also had alcohol or other drug dependence. Schuckit and colleagues (1996), in a large study of alcohol–dependent people and their relatives, also reported weak evidence at best for familial transmission between alcohol dependence and BN. Lilenfeld and colleagues (1997) reported that women with co–occurring BN and SUD have higher rates of problems with anxiety, a variety of personality disturbances including antisocial behavior, and high rates of familial SUD, anxiety, impulsivity, and affective instability. These authors hypothesized that a familial vulnerability for impulsivity and affective instability may contribute to the development of SUD in a subgroup of BN patients. Using data from a large epidemiological sample of female twin pairs, Kendler and colleagues (1995) demonstrated that most of the genetic factors associated with vulnerability to alcoholism in women do not alter the risk for development of BN.
TREATMENT OF CO–OCCURRING ALCOHOLISM AND EATING DISORDERS
Although alcoholism and other SUDs frequently occur with EDs, research has not established common or shared factors in the etiology or maintenance of this co–occurrence. Nonetheless, the frequent co–occurrence of problems with eating and alcohol may signal greater psychiatric disturbances (Grilo et al. 1995b) and greater medical risk (Catterson et al. 1997; Mitchell et al. 1991). These clinical realities represent considerable challenges to practitioners and researchers. The most common questions include how to identify the presence of possible problems, which problem to focus on first, or whether/how to address both concurrently (Daniels et al. 1999; Wilson 1993; Mitchell et al. 1997). These are important questions and there is a pressing need for research on these treatment issues (Grilo et al. 1997). Not only has little research been done on treating these co–occurring conditions, but many treatment studies with ED patients either exclude patients with substance dependence or enroll few such patients. Although the brief overview that follows will offer implications for clinicians and researchers in both fields, this section gives a more detailed discussion of the ED intervention literature for professionals in the alcoholism field.
Assessment and Screening for Eating Disorders
Good, comprehensive assessment of patients is necessary for good treatment. Assessment protocols should involve questionnaires (i.e., instruments) that are sensitive enough to flag patients with potential problems for further evaluation. Failure to identify all problems may contribute to poor retention and treatment outcomes even for the targeted problem. Screening instruments for alcohol problems are described in detail elsewhere (Bradley et al. 1998). Although standardized interviews are generally thought to hold important advantages for accurate and thorough assessment of EDs (Grilo et al. 2001a), it may not be possible or practical for many types of clinical facilities to use them because of cost, time, and lack of training.
The authors of this article recommend two self–report instruments for the screening and preliminary assessment of EDs. The first is the Questionnaire on Eating and Weight Patterns–Revised (QEWP–R) (Yanovski et al. 1993), a well–established and easy–to–complete self–report instrument. The QEWP–R, widely used in research programs, screens for the presence of the specific ED categories and provides useful information about the frequency of problem eating and dieting behaviors. The second instrument is the Eating Disorder Examination–Questionnaire Version (EDEQ) (Fairburn and Beglin 1994), the self–report version of the Eating Disorder Examination interview (Cooper and Fairburn 1987). The EDEQ offers a number of advantages over other self–report measures and provides detailed information about the behavioral and attitudinal features of eating disorders. The EDEQ has received some support for its utility (Grilo et al. 2001a) and has been used with substance abusers (Black and Wilson 1996). The relative merits of different assessment methods are described elsewhere (Grilo et al. 2001a). Briefly, such instruments are generally thought to underestimate the frequency of some of the behavioral features of EDs (e.g., binge eating) and overestimate some of the cognitive or attitudinal symptoms, compared with interviews (Grilo et al. 2001a). These limitations notwithstanding, such screens are useful for efficiently identifying people with possible problems. Of course, in addition, it is important for clinicians and researchers alike to consider comprehensive medical and psychiatric evaluations for these patient groups (see Grilo 1998). In particular, patients with these co–occurring problems require careful medical evaluation and followup (Mitchell et al. 1991). In terms of followup, it may be particularly useful for repeated assessments to include the ED screens. Some clinical experience suggests the possibility that successful cessation of substance or alcohol use may be followed by the re–emergence of ED symptoms in some patients. Although this hypothesis awaits conclusive research, it highlights the usefulness of repeated assessments.
Pharmacological Treatments
Pharmacological treatments have generally been found to have little effect on AN either as the primary approach or as an augmentation approach (Attia et al. 1998), although the antidepressant fluoxetine was found to decrease frequency of relapse in one study (Kaye et al. 2001). In contrast, pharmacological treatments, particularly antidepressant medications, have generally been found to be superior to placebo for the treatment of BN (e.g., Agras et al. 1992; FBNCSG 1992; Mitchell et al. 1990) and BED (e.g., Hudson et al. 1998; McCann and Agras 1990; McElroy et al. 2000; see Grilo 1998). It is worth stressing that these studies generally find, particularly for fluoxetine, that high doses are required to produce effects (as high as 60 mg per day in the case of fluoxetine) (FBNCSG 1992). Unfortunately, surveys have revealed that most patients with BN treated with pharmacotherapy by community practitioners received inadequate dosing (Crow et al. 1999). Nevertheless, fluoxetine has also been shown to reduce depressive symptoms and alcohol consumption in depressed alcoholics (Cornelius et al. 1997). Controlled research testing the efficacy of this medication among women with both alcoholism and EDs is needed.
Medications designed to block the action of opioids (i.e., opioid antagonists) have demonstrated efficacy for reducing alcohol use and relapse, and increasing abstinence rates among alcoholic patients (Anton et al. 1999; Heinala et al. 2001; Mason et al. 1999; Monti et al. 2001; O’Malley et al. 1992; Volpicelli et al. 1992, 1997; see also Krystal et al. 2001). The opioid antagonist naltrexone (ReViaT) has also been studied as a treatment for ED. One study that compared naltrexone, imipramine, and placebo among BED patients found that both medications produced reductions in binge eating but neither was superior to placebo (high placebo response occurred in this study) (Alger et al. 1991). One study found that naltrexone reduced the frequency of binge eating in patients with BN during the first few weeks of treatment but that the effects did not last (Jonas and Gold 1987). A rigorous controlled study is currently under way at Yale University to evaluate the efficacy of naltrexone among alcoholic women and women with both alcoholism and EDs.
Psychological Treatments of Eating Disorders
Cognitive behavioral therapy (CBT) has received the most consistent support of any psychological or pharmacologic treatment for EDs. Briefly, CBT is a focal and structured treatment that involves a collaborative effort between patients and clinicians (Fairburn et al. 1993a). CBT for eating disorders can be delivered via individual or group approaches and generally follows three phases. The first phase involves education and presentation of the treatment model, including expectations for treatment and homework, teaching behavioral strategies such as self–monitoring to identify problems, and a graded approach to normalization of eating. The second phase involves the use of cognitive restructuring methods to identify, challenge, and modify maladaptive thinking. The final stage involves relapse prevention techniques and problem solving to generalize the skills to other areas and to consolidate improvements. CBT has been found to be superior to control conditions, to most other forms of psychological therapies, to behavioral therapies without the cognitive components, and to the pharmacological treatments (e.g., Agras et al. 1992, 2000; Fairburn et al. 1993a; see reviews: Wilson and Fairburn 1998; Grilo 1998, 2000). Moreover, self–help versions (e.g., Fairburn 1995) of standard CBT therapist manuals (Fairburn et al. 1993b) have demonstrated efficacy (Carter and Fairburn 1998; Peterson et al. 1998; Treasure et al. 1996). This approach may provide general practitioners with expertise in CBT with the technology to help certain ED patients.
Although CBT is generally regarded as the first–line treatment of choice for ED (Agras et al. 2000; Wilson and Fairburn 1998), research is needed to determine its usefulness for patients with co–occurring alcoholism and eating disorders, and to develop integrated psychological treatment approaches for patients with alcoholism and eating disorders (Mitchell et al. 1997). Although the data are sparse, the treatment literature has not suggested that alcoholism or a history of alcoholism diminishes CBT treatment effectiveness for BN or BED (Goldbloom 1993; Mitchell et al. 1990; Wilfley et al. 2000). No available studies have examined whether eating disturbances influence the outcome of alcoholism treatment. Although clinical lore suggests that personality disorders—if present—are associated with negative treatment outcomes, this has not received empirical support in treatment studies of patients with EDs (Grilo 2002b), and findings from treatment studies of patients with SUD are mixed (Grilo and McGlashan 1999).
Based on clinical experience with both patient groups, the authors suggest that certain CBT–based treatments represent a good starting point for treating co–occurring alcohol use and eating disorders. Basic aspects of the cognitive behavioral approach (e.g., coping skills therapy) have been found effective for treating alcohol dependence (Kadden et al. 1992; Monti et al. 1989, 2001) and are useful for ED patients. However, as previously noted, behavioral therapies without the specific cognitive components of CBT have inferior long–term outcomes compared with CBT (Fairburn et al. 1993a). Nevertheless, specific forms of behavioral and coping skills treatments (without the specific cognitive components of the CBT approaches for EDs) have been used successfully with substance abusers and seem to be readily integrated with pharmacological approaches (Monti et al. 2001; O’Malley et al. 1992; Sinha 2000).
Thus, an approach that targets alcohol use and pathologic eating behaviors may be especially appropriate for treating patients with both disorders. Treatment designed to teach new coping skills to patients with alcoholism could also have a beneficial effect on eating disorders even if the ED is not specifically targeted. Given the well–known ambivalence that characterizes many of these patients (e.g., Vitousek et al. 1998), another potentially relevant approach involves motivational enhancement interviewing (Rollnick and Miller 1995), which has received some support for SUDs (Project MATCH Research Group 1997) and EDs (Treasure et al. 1999).
Another promising approach is dialectical behavior therapy (DBT), which initial research supports for both BN (Safer et al. 2001) and BED (Telch et al. 2001). DBT, which focuses on awareness of problems and choices, mood regulation techniques, and coping skills, directly addresses many of the needs of both ED and alcohol use disorder patients, including the frequently co–occurring borderline personality disorder. Indeed, the initial treatment outcome findings for DBT for both BN (Safer et al. 2001) and BED (Telch et al. 2001) suggest that addressing a potential vulnerability (e.g., problems with mood regulation and coping) can lead to improvements in ED even without a direct focus on the eating behaviors, a finding that parallels that reported for interpersonal psychotherapy (Agras et al. 2000; Fairburn et al. 1993a; Wilfley et al. 1993). Telch and colleagues (2001) speculated that DBT may be particularly helpful for ED patients characterized by high levels of negative affect. Recent studies with BN (Grilo et al. 2001b; Stice and Agras 1999) and BED (Grilo et al. 2001c) revealed two subtypes of these EDs: dietary and a mixed dietary–negative affect. The dietary subgroup was characterized primarily by eating–specific psychopathology without associated problems with self–esteem and depression (negative affect). Patients with the mixed dietary–negative affect subtype also had high rates of alcohol and other drug problems. It is possible that such patients, particularly if they have problems with impulsivity or have co–occurring borderline personality disorder, might benefit from affect regulation and coping skills approaches such as DBT.
CONCLUSION
Alcoholism and EDs frequently co–occur and often co–occur in the presence of other psychiatric and personality disorders. Although such diagnostic co–occurrence suggests the possibility of shared factors in the etiology or maintenance of these problems, research has not established such links. The clinical reality that eating and alcohol use disorders frequently co–occur has important implications for assessment, treatment, and research. Comprehensive assessment is necessary for good treatment. Research on methods of treating people with co–occurring alcohol and eating problems represents a major need. Until further guidance is provided, the authors recommend concurrently addressing both disorders. CBT, coping skills, or DBT approaches seem to be reasonable starting points.
REFERENCES
AGRAS, W.S.; ROSSITER, E.M.; ARNOW, B.; et al. Pharmacologic and cognitive–behavioral treatment for bulimia nervosa: A controlled comparison. American Journal of Psychiatry 149(1):82–87, 1992.
AGRAS, W.S.; WALSH, T.; FAIRBURN, C.G.; et al. A multicenter comparison of cognitive–behavioral therapy and interpersonal psychotherapy for bulimia nervosa. Archives of General Psychiatry 57:459–466, 2000.
ALLISON, D.B. A note on the selection of control groups and control variables in comorbidity research. Comprehensive Psychiatry 34:336–339, 1993.
ALGER, S.A.; SCHWALBERG, M.D.; BIGAOUETTE, J.M.; et al. Effect of a tricyclic antidepressant and opiate antagonist on binge–eating behavior in normal weight bulimic and obese, binge–eating subjects. American Journal of Clinical Nutrition 53(4):865–871, 1991.
American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: APA, 1994.
ANDERSEN, A.E. Eating disorders in males. In: Brownell, K.D.; Fairburn, C.G., eds. Eating Disorders and Obesity: A Comprehensive Handbook. New York: Guilford Press, 1995. pp. 177–187.
ANDERSEN, A.E.; BOWERS, W.A.; and WATSON, T. A slimming program for eating disorders not otherwise specified. Reconceptualizing a confusing residual diagnostic category. Psychiatric Clinics of North America 24:271–280, 2001.
ANDERSEN, A.E., and HOLMAN, J.E. Males with eating disorders: Challenges for treatment and research. Psychopharmacology Bulletin 33:391–397, 1997.
ANTON, R.F.; MOAK, D.H.; WAID, L.R.; et al. Naltrexone and cognitive behavioral therapy for the treatment of outpatient alcoholics: Results of a placebo–controlled trial. American Journal of Psychiatry 156(11):1758–1764, 1999.
ATTIA, E.; HAIMAN, C.; WALSH, B.T.; and FLATER, S.R. Does fluoxetine augment the inpatient treatment of anorexia nervosa? American Journal of Psychiatry 155:548–551, 1998.
BARRY, D.T.; GRILO, C.M.; and MASHEB, R.M. Gender differences in patients with binge eating disorder. International Journal of Eating Disorders 31:63–70, 2002.
BEARY, M.D.; LACEY, J.H.; and MERRY, J. Alcoholism and eating disorders in women of fertile age. British Journal of Addiction 81(5):685–689, 1986.
BECKER, A.E.; GRINSPOON, S.K.; KLIBANSKI, A.; and HERZOG, D.B. Eating disorders. New England Journal of Medicine 340(14):1092–1098, 1999.
BERKSON, J. Limitations of the application of the four–fold table analysis to hospital data. Biometrics Bulletin 2:47–53, 1946.
BERRIDGE, K.C. Food reward: Brain substrates of wanting and liking. Neuroscience and Biobehavioral Reviews 20:1–25, 1996.
BLACK, C.M.D., and WILSON, G.T. Assessment of eating disorders: Interview versus questionnaire. International Journal of Eating Disorders 20:43–50, 1996.
BRADLEY, K.A.; BOYD–WICKIZER, J.; POWELL, S.H.; and BURMAN, M.L. Alcohol screening questionnaires in women: A critical review. JAMA: Journal of the American Medical Association 280(2):166–171, 1998.
BREWERTON, T. Toward a unified theory of serotonin dysregulation in eating and related disorders. Psychoneuroendocrinology 20:561–590, 1995.
BREWERTON, T.; LYDIARD, R.; HERZOG, D.; et al. Comorbidity of axis I psychiatric disorders in bulimia nervosa. Journal of Clinical Psychiatry 56:77–80, 1995.
BULIK, C.M.; SULLIVAN, P.F.; CARTER, F.A.; and JOYCE, P.R. Lifetime comorbidity of alcohol dependence in women with bulimia nervosa. Addictive Behaviors 22:437–446, 1997.
BUSHNELL, J.A.; WELLS, E.; MCKENZIE, J.M.; et al. Bulimia comorbidity in the general population and in the clinic. Psychological Medicine 24:605–611, 1994.
CARR, K.D. Opioid receptor subtypes and stimulation–induced feeding. In: Cooper, S.J., and Clifton, P.G., eds. Drug Receptor Subtypes and Ingestive Behavior. San Diego, CA: Academic Press, 1996. pp. 167–191.
CARTER, J.C., and FAIRBURN, C.G. Cognitive–behavioral self–help for binge eating disorder: A controlled effectiveness study. Journal of Consulting and Clinical Psychology 66:616–623, 1998.
CATTERSON, M.F.; PRYOR, T.L.; BURKE, M.J.; et al. Death due to alcoholic complications in a young woman with a severe eating disorder: A case report. International Journal of Eating Disorders 21:303–305, 1997.
COOPER, Z., and FAIRBURN, C.G. The Eating Disorder Examination: A semi–structured interview for the assessment of the specific psychopathology of eating disorders. International Journal of Eating Disorders 6:1–8, 1987.
COOPER, S.J., and KIRKHAM, T.C. Opioid mechanisms in the control of food consumption and taste preferences. In: Herz, A.; Akil, H.; and Simon, E.J., eds. Handbook of Experimental Pharmacology, Vol. 104 Part II. Berlin: Springer Verlag, 1993. pp. 239–263.
CORNELIUS, J.R.; SALLOUM, I.M.; EHLER, J.G.; et al. Fluoxetine in depressed alcoholics: A double–blind, placebo–controlled trial. Archives of General Psychiatry 54(8):700–705, 1997.
CROW, S.; MUSSELL, M.P.; PETERSON, C.; et al. Prior treatment received by patients with bulimia nervosa. International Journal of Eating Disorders 25:39–44, 1999.
DANIELS, E.S.; MASHEB, R.M.; BERMAN, R.M.; et al. Bulimia nervosa and alcohol dependence: A case report of a patient enrolled in a randomized controlled clinical trial. Journal of Substance Abuse Treatment 17:163–166, 1999.
DANSKY, B.S.; BREWERTON, T.D.; and KILPATRICK, D.G. Comorbidity of bulimia nervosa and alcohol use disorders: Results from the National Women’s Study. International Journal of Eating Disorders 27:180–190, 2000.
DUFORT, G.G.; NEWMAN, S.C.; and BLAND, R.C. Psychiatric comorbidity and treatment seeking sources of selection bias in the study of clinical populations. Journal of Nervous and Mental Disease 181:467–474, 1993.
FAIRBURN, C.G. Overcoming Binge Eating. New York: Guilford Press, 1995.
FAIRBURN, C.G., and BEGLIN, S.J. Assessment of eating disorders: Interview or self–report questionnaire? International Journal of Eating Disorders 16:363–370, 1994.
FAIRBURN, C.G.; JONES, R.; PEVELER, R.C.; et al. Psychotherapy and bulimia nervosa: Longer–term effects of interpersonal psychotherapy, behavior therapy, and cognitive–behavior therapy. Archives of General Psychiatry 50:419–428, 1993a.
FAIRBURN, C.G.; MARCUS, M.D.; and WILSON, G.T. Cognitive behavioral therapy for binge eating and bulimia nervosa: A comprehensive treatment manual. In: Fairburn, C.G., and Wilson, G.T., eds. Binge Eating: Nature, Assessment, and Treatment. New York: Guilford Press, 1993b. pp. 361–404.
Fluoxetine Bulimia Nervosa Collaborative Study Group (FBNCSG). Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo–controlled, double–blind trial. Archives of General Psychiatry 49(2):139–147, 1992.
FREY, R.J. Anorexia nervosa. In: Olendorf, O.; Jeryan, C.; and Boyden, K., eds. The Gale Encyclopedia of Medicine. Farmington Hills, MI.: Gale Research, 1999.
FROEHLICH, J.C. Genetic factors in alcohol self–administration. Journal of Clinical Psychiatry 56(Suppl. 7):15–23, 1995.
GOLDBLOOM, D.S. Alcohol misuse and eating disorders: Aspects of an association. Alcohol and Alcoholism 28(4):375–381, 1993.
GOLDBLOOM, D.S.; NARANJO, C.A.; BREMNER, K.E.; and HICKS, L.K. Eating disorders and alcohol abuse in women. British Journal of Addiction 87(6):913–920, 1992.
GOSNELL, B.A., and LEVINE, A.S. Stimulation of ingestive behavior by preferential and selective opioid agonists. In: Cooper, S.J., and Clifton, P.G. Drug Receptor Subtypes and Ingestive Behavior. San Diego, CA: Academic Press, 1996. pp. 147–166.
GRILO, C.M. The assessment and treatment of binge eating disorder. Journal of Practical Psychiatry and Behavioral Health 4:191–201, 1998.
GRILO, C.M. Self–help and guided self–help treatments for bulimia nervosa and binge eating disorder. Journal of Practical Psychiatry 6:18–26, 2000.
GRILO, C.M. Binge eating disorder. In: Fairburn, C.G., and Brownell, K.D., eds. Eating Disorders and Obesity: A Comprehensive Handbook. 2d edition. New York: Guilford Press, 2002a. pp. 178–182.
GRILO, C.M. Recent research of relationships among eating disorders and personality disorders. Current Psychiatry Reports 4:18–24, 2002b.
GRILO, C.M., and MASHEB, R.M. Childhood psychological, physical, and sexual maltreatment in outpatients with binge eating disorder: Frequency and associations with gender, obesity, and eating–related psychopathology. Obesity Research 9(5):320–325, 2001.
GRILO, C.M., and MCGLASHAN, T.H. Stability and course of personality disorders. Current Opinion in Psychiatry 12:157–162, 1999.
GRILO, C.M.; BECKER, D.F.; LEVY, K.N.; et. al. Eating disorders with and without substance use disorders: A comparative study of inpatients. Comprehensive Psychiatry 36:312–317, 1995a.
GRILO, C.M.; LEVY, K.N.; BECKER, D.F.; et al. Eating disorders in female inpatients with versus without substance use disorders. Addictive Behaviors 20:255–260, 1995b.
GRILO, C.M.; DEVLIN, M.J.; CACHELIN, F.M.; and YANOVSKI, S.Z. Report of the National Institutes of Health Workshop on the development of research priorities in eating disorders. Psychopharmacology Bulletin 33:321–333, 1997.
GRILO, C.M.; MASHEB, R.M.; and WILSON, G.T. A comparison of different methods for assessing the features of eating disorders in patients with binge eating disorder. Journal of Consulting and Clinical Psychology 69:317–322, 2001a.
GRILO, C.M.; MASHEB, R.M.; and BERMAN R.M. Subtyping women with bulimia nervosa along dietary and negative affect dimensions: A replication in a treatment–seeking sample. Eating and Weight Disorders 6:53–58, 2001b.
GRILO, C.M.; MASHEB, R.M.; and WILSON, G.T. Subtyping binge eating disorder. Journal of Consulting and Clinical Psychology 69:317–322, 2001c.
HEINALA, P.; ALHO, H.; KIIANMA, K.; et al. Targeted use of naltrexone without prior detoxification in the treatment of alcohol dependence: A factorial double–blind, placebo–controlled trial. Journal of Clinical Psychopharmacology 21:287–292, 2001.
HIGUCHI, S.; SUZUKI, K.; YAMADA, K.; et al. Alcoholics with eating disorders: Prevalence and clinical course—A study from Japan. British Journal of Psychiatry 162:403–406, 1993.
HOEK, H.W. Review of the epidemiological studies of eating disorders. International Review of Psychiatry 5:61–74, 1993.
HOLDERNESS, C.C., BROOKS–GUNN, J.; and WARREN, M.P. Co–morbidity of eating disorders and substance abuse: Review of the literature. International Journal of Eating Disorders 16:1–35, 1994.
HUDSON, J.I.; POPE, H.G., JR.; JONAS, J.M.; and YURGELUN–TODD, D. Phenomenologic relationship of eating disorders to major affective disorder. Psychiatry Research 9(4):345–354, 1983.
HUDSON, J.I.; MCELROY, S.L.; RAYMOND, N.C.; et al. Fluvoxamine treatment of binge eating disorder: A multicenter, placebo–controlled trial. American Journal of Psychiatry 155:1756–1762, 1998.
JACKSON, T.D., and GRILO, C.M. Weight and eating concerns in men and women in outpatient treatment for substance abuse. Eating and Weight Disorders, in press.
JONAS, J.M., and GOLD, M.S. The use of opiate antagonists in treating bulimia: A study of low dose vs. high dose naltrexone. Psychiatry Research 24:195–199, 1987.
JONES, D.A.; CHESHIRE, N.; and MOORHOUSE, H. Anorexia nervosa, bulimia and alcoholism: Association of eating disorder and alcohol. Journal of Psychiatric Research 19(2/3):377–380, 1985.
KADDEN, R.; CARROLL, K.; DONOVAN, D.; et al., eds. Cognitive–Behavioral Coping Skills Therapy Manual: A Clinical Research Guide for Therapists Treating Individuals with Alcohol Abuse and Dependence. Project MATCH Monograph Series, Vol. 3. DHS Publication No. (ADM) 92–1895. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism, 1992.
KAYE, W.H.; LILENFELD L.R.; PLOTNICOV, K.; et al. Bulimia nervosa and substance dependence: Association and family transmission. Alcoholism: Clinical and Experimental Research 20(5):878–881, 1996.
KAYE, W.H.; GREENO, C.G.; MOSS, H.; et al. Alterations in serotonin activity and psychiatric symptomatology after recovery from bulimia nervosa. Archives of General Psychiatry 55:927–935, 1998.
KAYE, W.H.; NAGATA, T.; WELTZIN, T.E.; et al. Double–blind placebo–controlled administration of fluoxetine in restricting– and restricting–purging–type anorexia nervosa. Biological Psychiatry 49:644–652, 2001.
KENDALL, P.C., and CLARKIN, J.F. Introduction to special section: Comorbidity and treatment implications. Journal of Consulting and Clinical Psychology 60:833–834, 1992.
KENDLER, K.S.; MACLEAN, C.; NEALE, M.; et al. The genetic epidemiology of bulimia nervosa. American Journal of Psychiatry 148(12):1627–37, 1991.
KENDLER, K.S.; WALTERS, E.E.; NEALE, M.C.; et al. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women: Phobia, generalized anxiety disorder, panic disorder, bulimia, major depression and alcoholism. Archives of General Psychiatry 52:374–383, 1995.
KRAEMER, H.C. Statistical issues in assessing comorbidity. Statistics in Medicine 14:721–733, 1995.
KRAHN, D.D. The relationship of eating disorders and substance abuse. Journal of Substance Abuse 3(2):239–253, 1991.
KRAHN, D.; KURTH, C.; DEMITRACK, M.; and DREWNOWSKI, A. The relationship of dieting severity and bulimic behaviors to alcohol and other drug use in young women. Journal of Substance Abuse 4(4):341–353, 1992.
KRAHN, D.; PIPER, D.; KING, M.; et al. Dieting in sixth grade predicts alcohol use in ninth grade. Journal of Substance Abuse 8(3):293–301, 1996.
KRINGLEN, E.; TORGERSEN, S.; and CRAMER, V. A Norwegian psychiatric epidemiological study. American Journal of Psychiatry 158:1091–1098, 2001.
KRYSTAL, J.H.; CRAMER, J.A.; KROL, W.F.; et al. Naltrexone in the treatment of alcohol dependence. New England Journal of Medicine 345:1734–1739, 2001.
LAMB, J. Bulimia nervosa. In: Olendorf, O.; Jeryan, C.; and Boyden, K., eds. The Gale Encyclopedia of Medicine. Farmington Hills, MI: Gale Research, 1999.
LILENFELD, L.; KAYE, W.; GREENO, C.; et al. Psychiatric disorders in women with bulimia nervosa and their first–degree relatives: Effects of comorbid substance dependence. International Journal of Eating Disorders 22:253–264, 1997.
MASON, B.J.; SALVATO, F.R.; WILLIAMS, L.D.; et al. Double–blind, placebo–controlled study of oral nalmefene for alcohol dependence. Archives of General Psychiatry 56(8):719–724, 1999.
MCCANN, U.D., and AGRAS, W.S. Successful treatment of nonpurging bulimia nervosa with desipramine: A double–blind, placebo–controlled study. American Journal of Psychiatry 147:1509–1513, 1990.
MCELROY, S.L.; CASUTO, L.S.; NELSON, E.B.; et al. Placebo–controlled trial of sertaline in the treatment of binge eating disorder. American Journal of Psychiatry 157:1004–1006, 2000.
MERCER, M.E., and HOLDER, M.D. Food cravings, endogenous opioid peptides, and food intake: A review. Appetite 29(3):325–352, 1997.
MITCHELL, J.E.; PYLE, R.L.; ECKERT, E.D.; et al. A comparison study of antidepressants and structured intensive group therapy in the treatment of bulimia nervosa. Archives of General Psychiatry 47:149–157, 1990.
MITCHELL, J.; SPECKER, S.; and DE ZWANN, M. Comorbidity and medical complications of substance abuse: Review of the literature. International Journal of Eating Disorders 16:1–34, 1991.
MITCHELL, J.E.; SPECKER, S.; and EDMONSON, K. Management of substance abuse and dependence. In: Garner, D., and Garfinkel, P.E., eds. Handbook of Treatment for Eating Disorders. New York: Guilford Press, 1997. pp. 415–423.
MONTI, P.M.; ABRAMS, D.B.; KADDEN, R.M.; and COONEY, N.L. Treating Alcohol Dependence: A Coping Skills Training Guide. New York: Guilford Press, 1989.
MONTI, P.M.; ROHSENOW, D.J.; SWIFT, R.; et al. Naltrexone and cue exposure with coping and communication skills training for alcoholics: Treatment process and 1–year outcomes. Alcoholism: Clinical and Experimental Research 25:1634–1647, 2001.
O’MALLEY, S.S.; JAFFE, A.J.; CHANG, G.; et al. Naltrexone and coping skills therapy for alcohol dependence: A controlled study. Archives of General Psychiatry 49(11):881–887, 1992.
PETERSON, C.B.; MITCHELL, J.E.; ENGBLOOM, S.; et al: Group cognitive–behavioral treatment of binge eating disorder: A comparison of therapist–led versus self–help formats. International Journal of Eating Disorders 24:125–136, 1998.
PEVELER, R., and FAIRBURN, C. Eating disorders in women who abuse alcohol. British Journal of Addiction 85(12):1633–1638, 1990.
Project MATCH Research Group. Matching alcoholism treatment to client heterogeneity: Posttreatment outcomes. Journal of Studies on Alcohol 58:7–29, 1997.
REID, L.D. Endogenous opioid peptides and regulation of drinking and feeding. American Journal of Clinical Nutrition 42:1099–1132, 1985.
REID, L.D.; DELCONTE, J.D.; NICHOLS, M.L.; et al. Tests of opioid deficiency hypotheses of alcoholism. Alcohol: An International Biomedical Journal 8(4):247–258, 1991.
ROLLNICK, S., and MILLER, W.R. What is motivational interviewing? Behavioral and Cognitive Psychotherapy 23:325–334, 1995.
SAFER, D.L.; TELCH, C.F.; and AGRAS, W.S. Dialectical behavior therapy for bulimia nervosa. American Journal of Psychiatry 158:632–634, 2001.
SCHUCKIT, M.A.; TIPP, J.E.; ANTHENELLI, R.M.; et al. Anorexia nervosa and bulimia nervosa in alcohol–dependent men and women and their relatives. American Journal of Psychiatry 153(1):74–82, 1996.
SHER, K.J., and TRULL, T.J. Substance use disorder and personality disorder. Current Psychiatry Reports 4:25–29, 2002.
SINHA, R. Treatment for alcohol abuse and dependence: Special therapeutic needs of women. In: Zernig, G.; Saria, A.; Kurz, M.; and O’Malley, S.S., eds. CRC Handbook of Alcoholism: Clinical and Theoretical Approaches. Boca Raton, FL: CRC Press, 2000. pp. 151–164.
SINHA, R.; ROBINSON, J.; MERIKANGAS, K.; et al. Eating pathology among women with alcoholism and/or anxiety disorders. Alcoholism: Clinical and Experimental Research 20(7):1184–1191, 1996.
SMOLAK, L., and MURNEN, S.K. A meta–analytic examination of the relationship between child sexual abuse and eating disorders. International Journal of Eating Disorders 31:136–150, 2002.
SPITZER, R.L.; YANOVSKI, S.; WADDEN, T.; et al. Binge eating disorder: Its further validation in a multisite study. International Journal of Eating Disorders 13(2):137–153, 1993.
STICE, E., and AGRAS, W.S. Subtyping bulimic women along dietary restraint and negative affect dimensions. Journal of Consulting and Clinical Psychology 67:460–469, 1999.
STRIEGEL–MOORE, R.H.; DOHM, F.A.; SOLOMON, E.E.; et al. Subthreshold binge eating disorder. International Journal of Eating Disorders 27:270–278, 2000.
SUZUKI, K.; HIGUCHI, S.; YAMADA, K.; et al. Young female alcoholics with and without eating disorders: A comparative study in Japan. American Journal of Psychiatry 150(7):1053–1058, 1993.
TAYLOR, A.V.; PEVELER, R.C.; HIBBERT, G.A.; and FAIRBURN, C.G. Eating disorders among women receiving treatment for an alcohol problem. International Journal of Eating Disorders 14(2):147–151, 1993.
TELCH, C.F., and STICE, E. Psychiatric comorbidity in women with binge eating disorder: Prevalence rates from a non–treatment–seeking sample. Journal of Consulting and Clinical Psychology 66:768–776, 1998.
TELCH, C.F.; AGRAS, W.S.; and LINEHAN, M.M. Dialectical behavior therapy for binge eating disorder. Journal of Consulting and Clinical Psychology 69:1061–1065, 2001.
TREASURE, J.; SCHMIDT, U.; TROOP, N.; et al. Sequential treatment for bulimia nervosa incorporating a self–care manual. British Journal of Psychiatry 168:94–98, 1996.
TREASURE, J.L.; KATZMAN, M.; SCHMIDT, U.; et al. Engagement and outcome in the treatment of bulimia nervosa: First phase of a sequential design comparing motivation enhancement therapy and cognitive behavioural therapy. Behaviour Research and Therapy 37:405–418, 1999.
VITOUSEK, K.; WATSON, S.; and WILSON, G.T. Enhancing motivation for change in treatment–resistant eating disorders. Clinical Psychology Review 18:391–420, 1998.
VOLPICELLI, J.R.; ALTERMAN, A.I.; HAYASHIDA, M.; and O’BRIEN, C.P. Naltrexone in the treatment of alcohol dependence. Archives of General Psychiatry 49(11):876–880, 1992.
VOLPICELLI, J.R.; RHINES, K.C.; RHINES, J.S.; et al. Naltrexone and alcohol dependence: Role of subject compliance. Archives of General Psychiatry 54(8):737–742, 1997.
VON RANSON, K.M.; IACONO, W.G.; and MCGUE, M. Disordered eating and substance use in an epidemiological sample: I. Associations within individuals. International Journal of Eating Disorders 31:389–403, 2002.
WILFLEY, D.E.; AGRAS, W.S.; TELCH, C.F.; et al. Group cognitive–behavioral therapy and group interpersonal psychotherapy for the nonpurging bulimic individual: A controlled comparison. Journal of Consulting and Clinical Psychology 61(2):296–305, 1993.
WILFLEY, D.E.; FRIEDMAN, M.A.; DOUNCHIS, J.Z.; et al. Comorbid psychopathology in binge eating disorder: Relation to eating disorder severity at baseline and following treatment. Journal of Consulting and Clinical Psychology 68:641–649, 2000.
WILSON, G.T. Binge eating and addictive behaviors. In: Fairburn C.G., and Wilson, G.T., eds. Binge Eating: Nature, Assessment, and Treatment. New York: Guilford Press, 1993. pp. 97–120.
WILSON, G.T., and FAIRBURN, C.G. Treatment of eating disorders. In: Nathan, P.E., and Gorman, J.M., eds. A Guide to Treatments That Work. New York: Oxford University Press, 1998. pp. 501–530.
WISEMAN, C.V.; SUNDAY, S.R.; HALLIGAN, P.; et al. Substance dependence and eating disorders: Impact of sequence on comorbidity. Comprehensive Psychiatry 40:332–336, 1999.
WOODSIDE, D.B.; GARFINKEL, P.E.; LIN, E.; et al. Comparisons of men with full or partial eating disorders, men without eating disorders, and women with eating disorders in the community. American Journal of Psychiatry 158:570–574, 2001.
YANOVSKI, S.Z. Binge eating disorder: Current knowledge and future directions. Obesity Research 1:306–324, 1993.
YANOVSKI, S.Z.; NELSON, J.E.; DUBBERT, B.K.; and SPITZER, R.L. Association of binge eating disorder and psychiatric comorbidity in obese subjects. American Journal of Psychiatry 150:1472–1479, 1993.
Posted: November 2002


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