Science of Food Addiction

© Phil Werdell, M.A.

Photo of Raindrop on Food Addiction WebsiteThis paper contains excerpts from Phil Werdell’s newly published book: Bariatric Surgery and Food Addiction: Pre-Operative Considerations.

Until about a decade ago, there were a few theories about the science of food addiction, but no hard evidence to support its existence. Scientists and doctors who take their cues from medical journals were not easily convinced. This is no longer the case. In fact, there is a great abundance of evidence in the peer-reviewed professional medical literature which has scientifically established the existence of something “very much like” food addiction. (For a detailed bibliography, please see the end of this article.)

This research is widespread and the findings from it are appearing in many different specialized medical journals. But, a great deal of these studies are categorized as being about the disease of obesity—not food addiction. In most cases, the obesity is claimed to be the result of a psychologically-based eating disorder.

Calling food addiction obesity is like calling alcoholism drunkenness or drug addiction a problem caused solely by trauma. Today there is a growing body of research that more correctly explains obesity and some eating disorders (especially bulimia and binge eating disorder) as being based in chemical dependency. This is quite similar to what happened when earlier studies showed that alcoholism and drug addiction were chemical dependencies, recognized as such by the American Medical Association and the American Psychiatric Association. Food dependency, it seems, is finally catching up to its fellow addictions.

In the last decade, however, as the obesity epidemic in the United States has exploded, research into several possible root causes, including food addiction, has re-emerged and has begun to bring us new evidence in support of food dependency as a bona fide addiction. The primary areas of this research are in the fields of genetics, brain imaging, opioids, cross addiction, serotonin malfunction, and endorphin overstimulation. If we examine each area, we soon see sufficient proof that the human body can, indeed, become addicted to food.

Genetic Evidence

Food Addiction: Genetic EvidenceA recent UCLA College of Medicine study of obese people who binged out of control on simple carbohydrates and were not alcoholic showed that they had at least one gene marker that was exactly the same as that found in diagnosed alcoholics and other drug addicts. This evidence helped corroborate the long-standing suspicion that the problem of addiction—and food addiction in particular—has a genetic basis.

In the families of alcoholics and drug addicts, there are often many more blood relatives who also have addictions to alcohol and/or drugs than would be possible by chance. For a long time it was assumed that less than 10 percent of the US population was alcoholic. But in single families with one diagnosed alcoholic, frequently half of the blood relatives are alcoholic or otherwise addicted. These are exactly the types of statistical patterns which were first used to deduce the existence of genetic inheritance of specific biochemical traits.

Similar statistical evidence supports the existence of a genetic factor with regard to compulsive overeating and food addiction. A survey of Overeaters Anonymous members conducted in the early 1990s found similar percentages of people who identified as compulsive overeaters or food addicts who had at least one blood relative also addicted to food or alcohol. This outcome was statistically highly improbable, unless there were some causal relationship within the family.

Until recently there was a serious scientific debate about whether the causal link was genetic or environmental. Like with many other diseases, such as mental illness, you could see how patterns often ran in families. But was this because some trait was passed on genetically, similar to eye color? Or, in the case of addiction, was it that one or more heavy drinking or overeating parents passed their habits and attitudes down to their children via their parenting patterns? It was a classic nature versus nurture dilemma.

Some scientists argued that nature, i.e. genetics, was the cause. Other scientists argued that different patterns of nurture, parental influence or any number of social-environmental factors were to blame. Still others argued that food addiction was an outcome of both nature and nurture.

The discovery of DNA and the ability to isolate specific differences in DNA which were causally linked with biochemical differences was the beginning of the end of many of these controversies. In the late 1980s, the argument about the genesis of alcoholism ended when scientists found a single genetic marker for those diagnosed with chemical dependency on alcohol. In short order, they found that other addictive drugs had the same gene marker as alcoholism.

In the early 1990s, researchers tested a sample of non-alcoholics who were obese and who craved and binged on simple carbohydrates. What they found was that these subjects had the same genetic aberration that had been established as a genetic marker for alcoholism and other drug addictions. This finding first appeared in the International Journal of Eating Disorders in l994 and it was heralded in newspaper accounts as “the obesity gene.” A year later at the first international conference on food addiction, Earnest Noble, M.D., the lead researcher on the study, made clear that the genetic marker was not for the external presence of obesity but rather for an underlying internal chemical dependency on food.

Obesity is a consequence of overeating, just as becoming intoxicated is a consequence of drinking too much alcohol. To call genetic differences noted in the above study as genetic markers for obesity you would need to change all the diagnoses for alcoholism and drug addiction to the diseases of “getting drunk” and “getting high.” Or, you would have to acknowledge, based on the research, that obesity in these cases is a secondary side effect of a chemical dependency on food.

Common sense clearly directs us to the latter conclusion. As David Katz, M.D., head of the Yale School of Medicine’s Preventive Research Center, and Maura Harrigan Gonzalez, M.S., write in The Way We Eat, fat is “if not actually addictive, then at least alarmingly close … this is not a matter of choice; it’s built right into our cells.” At this time, the genetic difference in non-alcoholic, carbohydrate-binging obese people can easily be seen as biological evidence of the existence of chemical dependency on food.

There is, however, an important qualification to this evidence. No one as of yet has duplicated the results of Noble’s study. Until someone accomplishes this task and reports the results in a professional peer-reviewed journal, the scientific community will remain unconvinced of the validity of food addiction as having a basis in physiology.

Of equal importance, the genetic basis for food addiction is likely to be much more complex—a condition driven by more than one gene marker. Researchers at Rockefeller University, where nutritional research is a major focus, have, in fact, identified 21 genes related to food digestion. There are likely many more. Several of these gene markers are quite likely connected to biochemical processes which offer explanations of obesity and eating disorders. Their functioning, however, is beyond the scope of this discussion.

Brain Imaging Evidence

Several neurological imaging studies from research centers at the University of Florida McKnight Brain Institute, Brookhaven National Laboratory, Pennsylvania State University Department of Psychology and Rehabilitation, Harvard University Medical School, Iowa University Department of Psychology, Yale University Department of Psychology, Massachusetts General Hospital and the U.S. Department of Health show ways that loss of control over eating and obesity produce changes in the brain which are similar to those produced by drug abuse.

Addiction counselors agree that a true chemical dependency is defined, in part, as a problem of perception that centers in the addict’s mind. Thus with someone addicted to food, he or she can develop food cravings after just one bite, and the problem is then exacerbated by what is commonly understood as biochemical denial created by the addicted mind.

Food addicts frequently experience what is referred to as euphoric recall—remembering the good experiences of taste and the mitigation of pain, but forgetting the negative emotional and physical consequences. They also suffer obsessions of the mind, such as rationalizing the eating of addictive foods and/or bingeing based on irrational thoughts. Finally, they encounter what are often called mental blank spots, unexplained absences of any logical thinking that would serve to prevent one from engaging in behaviors known in the past to inflict pain.

At Brookhaven National Laboratory in New York and at the University of Florida McKnight Brain Institute, brain imagining using computed tomography (CT) and positron emission tomography (PET) scans has shown that the brains of alcoholics and drug addicts can be accurately identified. There is visible proof that specific parts of the brain are regularly and progressively affected by alcohol and/or drugs. Recent research conducted at Brookhaven National Laboratory shows a strong similarity between the brains of drug addicts and those who are obese and have very strong food cravings. Additional research at the University of Florida shows the exact interaction in the brain between satiety and the reward response to food stimulation.

These studies serve to demonstrate a pattern not unlike that among those addicted to alcohol, cocaine and other drugs. Some of the research explains obsessive attraction to food before eating, while other studies focus on showing how the binge cycle can be activated after the first bite of an addictive food. Most important, this research helps demonstrate the interaction between a food addicted mind and out-of-control eating.

These studies on brain imagining research are summarized in the book Eating Disorders, Overeating and Pathological Attachment to Food: Independent or Addictive Disorders by Mark S. Gold, M.D. For more than 30 years, Gold has been working on models for understanding the connections between and effects of cocaine, nicotine and other drugs on the brain and the addict’s behavior. His research on cocaine led to that drug’s being reclassified as dangerous and addictive. Regarding food addiction he concludes:

“Over a decade ago, we reported on the similarities of overeating and obesity to classic addictions. Since that time, neuro-imaging studies have supported the hypothesis that loss of control over eating and obesity produced changes in the brain, which are similar to those produced by drug abuse. Food, highly palatable and energy dense, has become a substance of abuse.”

All the intricacies of the model for how this happens have not yet been discovered and documented. Gold calls for further research on “newly discovered [brain chemical] messengers,” but it is fair to say that there is more evidence now that someone can become chemically dependent on food than there was at the time when alcoholism was classed as a disease of chemical dependency and when various street and prescription drugs were classified as narcotics.

Brain imaging evidence shows, as Gold attempts to summarize for the lay reader, that the brain’s “cortex changes with overeating and obesity so that the mouth and tongue increase in geographical area,” and “the hypothalamus senses that eating has occurred with a time delay that increases with body mass.” In other words, it may be likely that weight gain leads to increases in the sensory power of food and to decreases in the time it takes to experience satiety.

Evidence of Opioid Dependency

Several studies by professors of psychology at the University of Washington, Princeton University, the University of Los Andes (Merida, Venezuela), the Yale University School of Medicine and the National Institute on Drug Abuse have shown that the excess intake of sugar can produce what is called endogenous opioid dependency. This means that the brain of a food addict is creating its own opium-like drug. He or she then experiences the same effects as if they had ingested any other opium-like substance.

One of the earliest clues as to the addictive nature of some foods comes from the basic text of AA, the book Alcoholics Anonymous, first published in 1939. There is a single paragraph inserted after the writing of the initial draft that suggests that the alcoholic giving up liquor eat sweets and chocolate as a way to combat the physical craving for a drink. This passage is worth quoting here:

“One of the many doctors who had the opportunity of reading this book in manuscript form told us that the use of sweets was often helpful, of course dependent on a doctor’s advice. He thought all alcoholics should constantly have chocolate available for its quick energy value at times of fatigue. He added that occasionally in the night a vague craving arose which would be satisfied by candy. Many of us have noticed a tendency to eat sweets and have found the practice beneficial.”

Over the next decades, however, one group of sober alcoholics had some trouble. They started to eat more than the recommend one piece of candy or chocolate. As a result, they began gaining weight they could not take off and keep off, and they had to admit they were eating much the same way they used to drink. As we mentioned above, many ended up in Overeaters Anonymous where they found a way to be healthy with both food and alcohol.

What these alcoholics did not know—and the medical community did not understand until recently—was that sugar can create a mild addictive reaction as it is digested, and this can affect a person’s brain chemistry in the same way that alcohol and other addictive drugs do. Opioids are a key chemical compound in this reaction, and in many of the most powerful addictive drugs, such as cocaine, morphine and heroin. Neil Bernard, M.D., in his book Breaking the Food Seduction: The Hidden Reasons Behind Food Cravings—and 7 Steps to End Them Naturally, summarizes the scientific research demonstrating that there are selective foods which break down into addictive ingredients.  He writes:

“[These foods] contain chemical compounds no one ever suspected were there—mild opiates that are released during digestion. Other researchers have added evidence that there really is something about sugar, chocolate, cheese, meat and certain other foods that sets them apart. They don’t just tickle the taste buds. It appears they actually stimulate the brain in such a way that it is easy to get hooked and tough to break free, even if you find yourself gaining weight or lapsing into health problems.”

It’s no wonder that in the early days of AA, sober alcoholics felt sugar satisfied their physical cravings. It did. Moreover, those who began snacking on these mild-opiate foods all day or binge eating them frequently discovered that the addictive agents in these foods when sufficiently concentrated can actually be a much stronger narcotic than some of the commonly recognized addictive substances. Since it is the nature of untreated addictive diseases to progress to more serious levels, it should come as no great surprise that many alcoholics who started with the occasional piece of candy or chocolate soon found themselves binge eating out of control.

We find complementary clinical evidence in two other sources, Eating Right to Live Sober by Katherine Ketcham and L. Ann Mueller, M.D., and Seven Weeks to Sobriety: The Proven Program to Fight Alcoholism Through Nutrition by John Mathews Larson, Ph.D. These authors have found that the success rate for alcoholism increases 300 percent when the sober alcoholic also abstains from sugar and other simple carbohydrates. Not only can sweets lead some sober alcoholics to acute food dependency, the use of sugar and other drug foods in early sobriety can lead a significant number of alcoholics back to the bottle. This is not all that surprising when one looks at the basic dietary content of most liquor—two primary ingredients are usually sugar and refined grains.

There are studies, too, which trace some of the differences in biochemistry between the normal drinker and the alcoholic to different enzymes in each that are produced by the pancreas. There is also a great deal of evidence pointing to the fact that a large percentage of alcoholics produce a chemical called tetrahydrolsoqulnoline (THIQ) during the digestion of alcohol that normal drinkers do not.

THIQ was discovered in the brains of alcoholics in a study by a scientist named Virginia Davis of Houston, Texas. She was doing cancer research and needed fresh human brains. She used the bodies of homeless alcoholics who had died during the night and were picked up by Houston police in the morning. What she discovered in the brains of these chronically alcoholic subjects was a substance closely related to heroin. When a person shoots heroin into their body, some of it breaks down and turns into THIQ, yet these alcohol abusers had not used heroin.

Is it this chemical, THIQ, which eventually and progressively finds its way through the bloodstream to the frontal lobes of the brain where the opioids have their impact? If this is truly the biology of chemical dependency on alcohol, there may be a similar body process that creates dependency in the minds of food addicts. On this topic, more research is indicated before we can say for certain that THIQ plays a role in food addiction.

Evidence of Malfunction of Serotonin

In addition to the phenomenon of opium-like chemicals being created inside the brains of addicts, there is a body of research pointing to what is called a malfunction of serotonin production. This is explained in very understandable terms in Ann Katherine’s Anatomy of a Food Addiction and I would encourage anyone interested in learning more to consult her writings.

In brief, just as the biochemistry of one addiction may differ slightly from that of another, it is useful to look at the differences in foods commonly experienced as addictive, starting with the food most often considered as potentially dangerous—sugar. The science of addiction points to an explanation of chemical dependency on sugar as a result of a malfunction in the production of the brain chemical serotonin, or in its use in the body.

Serotonin synapses in the brain signal the alleviation of physical and emotional pain, and someone without enough serotonin can be quite anxious or depressed. The highs become too high and the lows become too low. When refined carbohydrates (sugar, flour, alcohol) are ingested, serotonin is manufactured and released. This was first presented to the general public as a problem of addiction by Kay Sheppard in Food Addiction: The Body Knows. The current science on this is best summarized by Katherine in her more recently revised Anatomy of a Food Addiction: The Brain Chemistry of Overeating. Katherine explains:

“So if your serotonin level is functioning poorly and your life becomes stressful, you can get some relief by eating sugar. We all learn pain relief very quickly. When something stops pain we repeat it. If sugar stops pain for you, you will eat it again.”

Use can lead to abuse and ultimately to addiction: when the use of sugar becomes unconscious, a person is food dependent. If one cannot stop the process of self-medicating with food, one has crossed over the line of food addiction. Katherine continues:

“Will you stop eating? If serotonin reaches certain concentrations, it is supposed to tell you to stop eating. It’s suspected that some people have a malfunction in the feedback loop. So these folks can eat a whole loaf of bread without triggering the ‘stop eating’ message.”

When someone cannot stop using a food drug by reason and will power alone, this is chemical dependency on food—or something else amazingly similar.

Evidence of Overeating Stimulated by Endorphins

We find a second biological explanation for sugar addiction in the functioning of what are called beta-endorphins. Endorphins are often called brain chemicals that create a natural “high.” Beta-endorphin is produced by the pituitary gland and is reported to produce a more intense sense of well-being than any of the other endorphin types. Beta-endorphin levels are increased whenever a person craves sugar, simple carbohydrates and some fats.

The degree of increased craving and the specific foods that induce these cravings vary from person to person. Thus, just as there are those who are more sensitive to pain and more receptive to being medicated by internal chemicals such as serotonin, there are those who are more or less susceptible to becoming addicted to their own endorphins. As Anne Katherine states:  “they eat to trigger release, because when the endorphins are released they feel better.”

This is yet another way food can become a drug since the next step is the increased use of this means of “getting high,” leading ultimately to a chemical dependency on sugar and refined carbohydrates which quickly become simple sugars during the process of digestion.

Kathleen DesMaisons, Ph.D., writes in The Sugar Addict’s Total Recovery Program:

“When the sugar-sensitive person tries to stop using the sugar that evokes this wonderful beta-endorphin response, the receptors start screaming. This is called withdrawal. The person experiencing withdrawal may feel cranky, irritable, and out of sorts but never knows it was last night’s sugar binge creating the horrible feelings. Cravings loom large as the beta-endorphin receptors scream and relief is as close as a can of soda or a doughnut. The physical dependence on sugar to relieve the discomfort of withdrawal reinforces the need to use more and more. The addiction grows into a real problem.”

It is also true that the body’s beta-endorphin reaction is accentuated during fasting, dieting and other stresses. Thus, food addicts who try to control their weight by will power and behavior modification—as they see normal eaters around them doing all the time—often are actually enabling the progression of their biochemical dependency. For those who are genetically pre-inclined to food dependency or who already have crossed the line into addiction by overeating on mood altering foods for long periods of time, dieting may help them lose weight in the short term, but make them actually more chemically dependent on sugar in the long run.

Another stressor can be at work here as well. In our culture, those who are overweight or obese are often taunted or made fun of. Chronic stress of this type, created by the internalized shame of not being able to live up to cultural norms of thinness, leads to more overeating as a way to relieve the pain of being outcast. Overeating itself creates increased stress, whether it be the result of discomfort with one’s own body or from the pain of external criticism both real and imagined. Ironically, the food addict overeats to deal with the effects of overeating, and thus becomes trapped in a never-ending vicious cycle.

Cross-Addiction Evidence

The final body of evidence supporting the reality of food addiction comes from work with alcohol and other substance abusers. Studies have shown that that those who are addicted to alcohol and drugs are often helped in their recovery by abstaining both from alcohol/drugs and sugar. We actually have clear evidence that cross-addiction from alcohol and other drugs to specific foods is a significant problem in the recovery community.

We have known for a long time that many alcoholics in early treatment will gain weight—and some need to, given the ravages to their bodies many have experienced by forgoing nutritious eating in favor of a diet of almost exclusively nothing but alcohol.. It also is common knowledge that many members of Alcoholics Anonymous, while sober, use cigarettes, coffee and sugar/flour/fat products in abundance both in and out of meetings. All of these substances have similar, sometimes identical, biochemically addictive ingredients.

What is not as well known is that there exists a large subset of members of Overeaters Anonymous and other food-related recovery programs made up of recovered alcoholics and drug addicts. Oftentimes after a few years of sobriety from drinking and using drugs, members of this group not only find themselves gaining weight (or using anorexic or bulimic methods to try to control their weight), but also eating in very similar ways to how they once used alcohol and drugs—by obsessing, bingeing, isolating and lying. A complementary research finding is that as bingeing on food increases, there is a tendency for alcohol and drug use to decline.

Considering bariatric surgery for a moment, in recent years we have seen a new and disturbing trend in the addictions field: 6-8 percent of those who have had some form of intestinal surgery have developed alcoholism serious enough to warrant in-patient treatment. Their secondary chemical dependency on alcoholism has universally been classified as a cross-addiction. Unfortunately, even this has had little effect in calling for the diagnosis and treatment of possible food addiction prior to making the decision to undergo bariatric surgery.

Today, food addiction remains a medical problem fully established by scientific research, but not yet officially accepted by the medical and health insurance industry. Amy Teeple writes on www.docshop.com:

“A recent topic of debate, food addiction is now viewed by many scientists as a disorder as real as a drug or alcohol addiction. Although most people’s weight problems are not caused by an addiction, some people … [do] seem to gain weight because they are addicted to food.”

If, as Teeple contends, addiction or dependence can be defined as “the compulsive reliance on a behavior or substance by an individual,” anyone considering bariatric surgery would be well advised to look at least for the possibility that they may be struggling with something beyond the reach of simple will power. She states firmly:

“Addictive behavior will remain after bariatric surgery if the patient does not address the issues that led to the original addiction.”
Perhaps even more convincing is this comment the writer captures from a gastric bypass surgery patient with “no regrets” for having had the operation: “I really think that I would be dead if I hadn’t had it … [but] to do it without counseling built in, as I did, is stupid because you aren’t addressing the issues. Your issues with food are still going to be there …”

Teeple’s writings are echoed by those of Katie Jay, MSW. Jay is a nationally recognized expert on weight-loss and weight-loss surgery and the author of Dying to Change: My Really Heavy Life Story: How Weigh-Loss Surgery Gave Me Hope for Living. She comments:

“Weight loss surgery can be a great tool to help control your eating, but if you had trouble with food before surgery, there is high risk of eating compulsively, overeating or even just obsessing about food after surgery.”

Two additional authors (today there are hundreds) clearly support the notion that food addiction is real and is not treated by bariatric surgery alone. On www.beyondchange-obesity.com, Cynthia Buffington, Ph.D., reports that studies by bariatric psychologists found that “nearly 80 percent of gastric bypass pre-surgical patients suffer from food addiction.” She adds:

“Our collaborative studies found that more than 90 percent of pre-surgical morbidly obese patients use avoidance stress coping behavior to handle emotions, seeking comfort from negative feelings and stressful situations through the use and, sometimes, abuse of food.”

Buffington goes on to support brain chemistry as a primary factor in the etiology of food addiction:

“Serotonin defects … in the brain cause depression and anxiety. Smokers, alcoholics, drug addicts, and the obese (particularly females) have serotonin defects … Low serotonin and stress-induced activation of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis … are known to increase, by an unknown process, the risk for substance-abuse and food addiction through another ‘feel good’ pathway, the dopamine reward system. The euphoria or pleasure derived from the use of heroin, amphetamines, cocaine, alcohol and nicotine are, in part, due to stimulation of the actions of dopamine. Eating foods high in sugar or fat, or even the smell or taste of an individual’s favorite food, activates the dopamine reward system, producing pleasure and satisfaction … It is possible, therefore, that individuals with food addictions may be eating more and more food to increase dopamine activities and improve their mood.”

Although like my colleagues and me, Buffington passes no judgment on the efficacy of bariatric surgery and in fact sees it as a viable alternative for those who are morbidly obese, she offers this note of caution:

“Abstinence from the abused substance helps to reverse or improve many of the neurochemical defects associated with addictions. Bariatric surgery, by limiting the amount of food and type of food that can be consumed, and by enhancing mood through the euphoria of weight loss, is also effective in improving neurochemical defects contributing to addictive behavior. However, such improvements are often short-lived. Food cravings, as well as depression, may reoccur over time, along with weight regain.

“The neurochemical defects contributing to food dependency among post-bariatric surgical patients may reappear over time because the behaviors responsible for initiating the cascade of events leading to such defects are not resolved by the surgery.”

In his 2007 article titled “Addiction: From Drugs to Donuts, Brain Activity May be the Key,” Paul Park offers further support for the actuality of food addiction. He comments that a “particularly significant set of findings shows that obese subjects exhibit qualities of addiction, not unlike those of individuals who engage in substance abuse.” He goes on to quote Dr. Mark S. Gold of the University of Florida (mentioned in an earlier section):

“Today there is a convincing convergence of evidence … that supports the hypothesis that there are important similarities between overeating highly palatable and hedonic foods and the classic addictions.”

A final expert mentioned in Park’s writing is Dr. Gene-Jack Wang, head of a team of researchers from the U.S. Department of Energy’s Brookhaven National Laboratory. Wang conducted experiments to “observe how the brain’s chemistry encouraged overeating by associating positive feelings with consumption,” he writes. What Wang learned is that “the same brain circuits that trigger cravings play a substantial part in consumption behaviors linked to comforting negative emotions.” Wang summarizes an interesting “chicken and egg” question with regard to brain chemistry and food addiction that has yet to be answered:

“It’s possible that obese people have fewer dopamine receptors because their brains are trying to compensate for having chronically high dopamine levels, which are triggered by chronic overeating. It’s also possible that these people have low numbers of dopamine receptors to begin with, making them more vulnerable to addictive behaviors including compulsive food intake.”

Despite the mounting evidence supporting a direct relationship between brain activity and tendencies toward abnormal eating patterns, Dr. Wang stresses that obesity is a complex disease with a host of factors—genetics, cultural background, and cerebral mechanisms among many others—that contribute to its presence in those who are overweight. “However, the results of these various tests affirm that, when overeating is an addictive behavior, the treatment is similar to rehabilitation from drug use.”

Treatment for Food Addiction

Once treatment has begun for the food addict, what happens? When overeaters are separated from their primary binge foods, the first change is that they stop having physical cravings or, at minimum, the cravings are lessened to the point where they are no longer overpowering. Even more important for long-term success, the mind of the detoxified food addict begins to change in remarkable ways. Where once they believed their own rationalizations (read: lies) about food, detoxification helps the food addict begin to see his or her past thinking as distorted.

Food addicts who previously believed they had to eat foods that made them fat, sick or just plain miserable begin to have a change in perspective. Those who were once adept at hiding their eating from others or who, like the drug addict who thinks life without heroin or cocaine is not worth living, can’t imagine a day without ice cream, bread, pasta, or desserts, now start to see the self-destructiveness of their own internal messages. For the food addict accustomed to being drunk on sugar, flour or excess fats, detoxification helps to break the grip of the disease on his or her mind while creating the possibility for seeing, telling and believing the truth.

In our ACORN groups we work with food addicts who participated in a variety of treatment programs. This provides us with the opportunity to observe, closely, the changes that occur in food addicts who are actively working on recovery.

The first thing we learn from these participants is that psychologically based eating disorder programs utilizing behavior modification to teach moderate eating practices do not work for those whose food addiction is substantially evolved. In these cases, only complete abstinence from addictive foods and behaviors works. Even when a food addict is physically detoxified, they still need to be supported to do the deeper emotional work of learning skills to cope with difficult feelings, and to break their denial of their own food addiction.

The most advanced cases also need to accept that recovery work will be ongoing for life. Like the recovering alcoholic or drug addict, most approach this through Twelve Step fellowships, the oldest and largest of which is Overeaters Anonymous (OA). Newer and smaller fellowships work better for some people: Food Addicts Anonymous (FAA), Foods Addicts in Recovery Anonymous (FA), GreySheeters Anonymous (GSA) and Compulsive Eaters Anonymous (CEA-HOW). Helping those who are food-addicted find the needed support to help break their addiction, stay out of food addicted denial and become willing to use these fellowships is probably the most difficult challenge of treatment.
In summary, the key issues to keep in mind when treating obesity and food-related symptoms for people who also may be food addicts are as follows:

  1. Dieting—and more dramatically, bariatric surgery—is an entirely physical solution to the problems of an overweight or obese patient. It works well when the problem being dealt with is only a physical problem. Like a very sophisticated plumber, the bariatric surgeon repairs the pipes, and that’s all there is to it. Problem solved.
  2. When people use food to medicate feelings, they need to develop alternatives to overeating to cope with difficult emotions. When unresolved trauma makes this difficult, as in psychologically-based anorexia, bulimia and/or binge eating disorder, an individual becomes unable not to use food to control their feelings, and they often need outside help to develop new coping behaviors.
  3. Food addiction is not a trauma-based eating disorder. People who become dependent on food experience changes in instinct, motivation and attitude that are primarily biochemical. Their instincts have become distorted by the food rather than by external events, and the only answer is complete abstinence, outside support to stay food abstinent, and emotional work to move toward acceptance and the willingness to do the work required to recover.
  4. A majority of food addicts also have trauma-based eating disorders, so they need to work on both. The alcoholic or drug addict cannot do effective work in therapy while drinking or using drugs, and a food addict cannot deal with underlying feelings if their instincts are distorted or their emotions are being medicated by food.

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