What does science say about food addiction?

Since 1995 there have been a number of lines of scientific research, each developed separately, that have established evidence of chemical dependency on food: human genetic research, controlled animal studies, comparative brain imaging of dopamine receptors, controlled human studies using opioid blockers, biochemical studies of the digestive processes, outcome surveys of those in voluntary food addiction recovery fellowships, and outcome studies of professional food addiction treatment programs.

There are a number of other lines of scientific investigation which could illuminate the complexity of food addiction: discovery of several other gene markers associated with obesity and digestive disorders, studies showing the role of leptin deficiencies in problems with satiation, the phenomenon of some celiacs craving gluten-based foods which keeps them from digesting food, the possibility that some with Praeder-Willi Syndrome have a form of addiction to large volumes of food, and many more. It is now clear that clinicians view food addiction as not just as one bio-chemical illness but rather as a cluster of several different chemical dependencies and other disorders.

Each of these lines of research have produced scientific evidence about food addiction from a different angle; combined, the research to date provides a confluence of informed scientific opinion confirming the existence of food addiction but also, in substantial detail, how a number of the chemical dependency processes regarding food work. There is now more scientific evidence establishing food as a chemical dependency, and a more complete understanding of the disease of food addiction as a whole than there was for alcoholism and other drug addictions when they were confirmed as substance use disorders by the medical establishment.

In 2009, the Food Addiction Institute created a bibliography of 2,733 peer reviewed studieson aspects of food addiction from over one-hundred different scientific journals. There have been hundreds of more research studies published since then. The Refined Food Addiction Foundation (ReFA) has a summary of thirty-four science review articles forming a consensus about one of the parts of this body of research. One can view streaming video of the Seattle Summit on the Obesity Crisis and Food Addiction where a number of the most prominent international researchers on food addiction summarize their work and its implications for clinicians and recovering food addicts.

More recently, members from the Institute’s International Advisory Board published “Physical Craving and Food Addiction” a science review article on the key question of whether or not there is a biochemical basis for some binge eating and obesity. (Cheren, et al, 2010) The conclusion is that some people can be addicted to a specific food, to several foods or to overeating on large volumes of almost any food. Another group from the Advisory Board is now working on a scientific review of research on “Loss of Control and Food Addiction.” These are the pivotal issues which establish chemical dependency on food as a disease that is distinctly different from obesity and other eating disorders.

Genetic Evidence: In the early 1990’s, Dr. Earnest Noble led a team of researchers at the Medical School of the University of California at Los Angeles in identifying a marker on the D2 Dopamine Gene associated with alcoholism and drug addiction. In 1994, the UCLA team published an article in the International Journal for the Study of Obesity showing that some obese adults who binged on dense carbohydrates and who showed no symptoms of alcoholism or drug addiction also had the same gene marker. (Nobel et al, 1994) In the article this was called the obesity gene, but at the First International Conference on Food Addiction in 1996, Dr. Noble clarified that it was more reasonable to think of the D2 gene marker as evidence of food addiction underlying some cases of obesity. (Summary of Proceedings for Food Addiction 2000, 1996). This research has since been replicated dozens of times leaving undisputed proof that some obese people carry a gene distinction statistically associated with chemical dependency and substance use disorders.

More recently, there has been research (not yet published) showing that some obese adults who have been clinically diagnosed as late stage food addicts do not have the D2 dopamine gene marker. One theory is that those food addicts without the marker are what the DSM 4 designates as “abusers” and those with the marker are “addicts.” In preparing for the DSM 5, the Substance Abuse Disorder Committee of the APA found that very few alcoholics or drug addicts have been diagnosed as abusers, (add comma) and that both abusers and addicts have been successfully treated in the same way. As a result, they are considering eliminating the “abuser” diagnosis. There is no reason to believe that this would be different for food addicts, but there is no formal study of this matter to date.

Another theory about this new research showing food addicts both with and without the D2 gene marker is that, as with diabetes, there are two types of food addicts. Type I food addicts, those with the gene marker, are genetically predisposed to food addiction from birth, and the potentiality for the disease will continue to be passed down genetically. Type II food addicts, those without the gene marker, develop a Substance Use Disorder from intensively eating chemically addictive foods over time. There is substantial research suggesting that prolonged, intense, gluttonous overeating can produce the brain biochemistry of addiction. Great increases in the consumption of sugar, flour, excess fat, salt and artificial sweeteners in recent decades, could reasonably account for some of the parallel increases in obesity and other related secondary diseases. If so, it would mean that in these cases, food addiction is the primary cause of obesity and related diabetes, high blood pressure, cancer and heart disease.

The genetic causes of obesity as a whole are quite complex. Two genes definitely needing further study regarding craving and loss of control are the ob gene, sometimes called the obesity gene, and the gene identified with a deficiency of the chemical leptin and problems with satiety. (Shell, 2002) The latter is a marker for some of those with out of control eating and a diagnosis of Prader Willi Syndrome. (Deneen et al, 2009) Another area where further research is needed is with celiac disease; in this disease, the ingestion of gluten causes a malfunction of the celia in the intestines and nutrients are not digested. In advanced stages, some celiacs experience a feeling of starvation even when eating great amounts of food. This is similar to the clinical experience of food addicts who are addicted to volume, and the fact that some food addicts are only able to achieve food abstinence after they eliminate wheat, the common grain in bread and processed foods with the most gluten. (Celiac.com 2008)

It is problematic that many scientific discussions of the genetics of obesity do not even include the research on the D2 dopamine gene or discuss the other genes which may be responsible for loss of control. (Beales, et al, 2009)

Evidence from Controlled Animal Studies: There is a long tradition of using carefully bred strains of mice in highly controlled animal studies and, in particular, there is an experimental methodology for determining whether a substance is addictive. These animal studies, the same type used to pretest medical drugs for safety in humans, have been highly reliable in predicting the results of addictive substances on humans. Over the last decade, Dr. Bart Hoebel, Chairman of the Department of Psychology and director of the animal research laboratory at Princeton University, led a research team in systematically testing for the addictive properties of sugar. In a review published in 2008 of all the research on sugar addiction to date, including that of the Princeton team, it was found that rats in carefully controlled experimental conditions show physical craving, loss of control, withdrawal, tolerance and chemical dependency for sugar; in summary, “some animals can become addicted to sugar”. (Averna et al, 2008).

Research by noted French psychologist Dr. Serge Ahmed took this one step further. Using artificial sweeteners in a different type of comparative research methodology, he found that “sweet taste” could be more addictive than cocaine. In mice already addicted to cocaine, he had them choose between sweetener and cocaine. They always chose the sweet substance. Even when it was made four times more difficult to choose sweet over cocaine, the animal chose the sweetener (Ahmed, 2009). Then at the Scripps Research Institute in Florida, researchers found that a wide range of high-calorie “junk food” was just as addictive to animals in a controlled setting. Reviewed in Childhood Obesity News, Pat Hartman concluded, “The studies involving rats conclude that over-consumption of high-calorie food can trigger an addiction response in the brain and high-calorie food can turn rats into compulsive eaters in a laboratory setting….Junk food may just be the socially (sic) acceptable form of drug dealing.” (ChildhoodObesityNews.com)

Brain Imaging Evidence for Humans: The relatively new technologies of CAT and PET scans of the human brain have provided a way to identify with precision the areas of the animal and human brain affected by addictive substances. Dr. Mark Gold, Distinguished Professor and Chair of Psychiatry, University of Florida College of Medicine in Gainesville, did the primary research to establish that cocaine is addictive and to place it on the registry of narcotic substances for humans. Over the last decade Dr. Gold turned his attention to the issue of sugar addiction, publishing a number of papers showing that people who binge on sugar develop brain images similar to those addicted to alcohol, cocaine and methamphetamine. As early as 2004, he edited a full volume of the Journal of Addictive Medicine devoted to the research on food addiction at Harvard University, Yale University, and the University of California at Los Angeles, University of Iowa, the Pennsylvania State University, the McKnight Brain Institute, Brookhaven National Laboratories, and the U.S. Department of Health’s National Institute for Drug Abuse. His conclusion: “Over a decade ago, we reported on the similarities of (some) overeating…to classic addictions. Since that time, neurological studies have supported the hypothesis that loss of control over eating and obesity produces changes in the brain which are similar to those produced by drugs of abuse… Overeating and obesity may be readily included in the DSM-5 by simply considering food as a substance in Substance Use Disorders. Loss of control, use despite diabetes and other consequences, changing priories” would fulfill the American Psychiatric Association’s diagnostic criteria. (Gold, 2004).

Evidence of Endogenous Opioids. One of the frequent secondary observations in the animal research is the bio-chemistry of addiction appearing in the brains of animals especially when they maintain a cycle of overeating and restricting. It is often observed that this pattern is frequently present in humans who binge and then restrict. In an effort to understand this, researchers have examined the blood chemistry of obese adults who diet and then regain their weight. In the general text The Way We Eat: a Six Step Path to Weight Control, Dr. David Katz, Director of the Center for Preventive Medicine at the Yale University School of Medicine, noted that in the process of digesting fats, there were opioid-like proteins produced in the human body. There was nothing the individual could do about these chemicals by conscious choice, and they were either “addictive or something very similar.” (Katz and Gonzales, 2002)

That same year, Dr. Carlo Colantuoni at Princeton University, reported on the findings of over a hundred peer reviewed studies on this subject and found “evidence that intermittent excessive sugar intake causes endogenous opioid dependence.”(Colantuoni et al, 2002) Dr. Neil Bernard, noted nutritional scientist at George Washington University, flushed out the implications for the lay person. Food “contains chemical compounds no one ever suspected were there – mild opiates that are released during digestion. Other researchers have added evidence that there is really something about sugar, chocolate, cheese and meat and certain other foods which set 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 other health problems.” (Bernard, 2003). Simply stated, some animals and humans on the “yo-yo” cycle of overeating and dieting can be triggering a process in their body that releases the same narcotic chemical which causes people to become addicted to cocaine, morphine and heroin.

Interestingly, it was an ingenious experiment at the University of Wisconsin in 1992 that showed the implications of endogenous opioid creation in humans. Dr. A. Drewnowski set up two groups of students: one group was given a chemical opiate blocker called naloxone and the other control group was given a placebo. Both groups were then brought into a large room with lots of food high in sugar, flour and fat. The control group ate freely of the treats at the same rate as previous test groups. The group given naloxone ate almost nothing. Those with the opiate blocker were just not interested; those in the control group were. (Drewnowski, et al, 1992) This was one of the early scientific indications that a proclivity for what we now know are potentially addictive foods could be inhibited by the same opiate blocker that was being used in some treatments of addiction to narcotics. It can now be seen as a confirmation that there is some sort of endogenous opioid in play regarding human interest in eating – and potentially overeating –highly palatable foods.

Many will ask: why don’t we use this as a medication for those with obesity caused by food addiction? In fact, there have been a number of recent experiments with this idea. So far, the “obesity drugs” using naloxone have had one of two problems: 1) they have either had secondary complications with consequences that the FDA decided were too dangerous for general use (dosages of naloxone that had any effect on weight loss at all had to be very much higher than dosages for blocking effects of external drug addiction) or 2) they produced little or no weight loss –- no more than ten pounds per person –which is not sufficient to justify the risk involved. In short, naloxone has the same problem as most other obesity drugs to date: too much risk and/or too little payoff. There is not yet a medicine truly helpful for obesity in general or the obesity caused by food addiction in particular. (Druglib.com, 2011) Those with knowledge of current research and what is in the pipeline of major pharmaceutical companies say it is very unlikely that a new experimental pill will be approved for human use until at least 2015.

Other Biochemical Evidence. There are several other lines of scientific research which point to food addiction:

  1. The information above has dealt with only research on the dopamine receptor biochemistry of food addiction. This focuses on the pleasure center of the brain. There is also substantial evidence of an obesity, eating disorders and food addiction relationship to the serotonin receptors. This focuses on the pain reduction function of the brain.
  2. A very different biochemical explanation of loss of control over food is the research on leptin deficiencies. Leptin is essential for a person to experience satiation. Some Praeder Willi Syndrome patients with extreme leptin deficiencies experience insatiable desires for food. Though not the conventional biochemistry of addiction, this could explain what many self-assessed food addicts call addiction to volume, i.e. overeating or bingeing on all foods.
  3. There is a great deal of research showing that the physical cravings of some people increase when foods are higher on the glycemic index. Experienced clinicians working with food addicts have suggested that spiking low blood sugar might create an experience of “false starving” in some overeaters.

More detail about these and other parts of the body of scientific knowledge about food addiction can be found in the Food Addiction Institute’s scientific review paper on “Physical Cravings and Food Addition.” (Cheren, et al, 2009) The conclusion of this research is a scientific consensus that people can become chemically dependent on certain foods just as they can become addicted to alcohol and drugs. (Volkow, et al, 2005)

Evidence of Outcomes for 12 Step and Professional Food Addiction Treatment: Medicine is a pragmatic science: if the treatment works, the disease exists. There is much we do not know about the biochemistry of cancer, for example, but we have cures that work for specific kinds of cancer, and we use them because there is evidence that they work. This is true in the area of food addiction, too. Long before most of the current scientific research was even contemplated, there were thousands of self-diagnosed and professionally diagnosed food addicts who have applied the addictive symptomology with some cases of obesity and eating disorders. They applied the addictive model of treatment, and it worked. This was sufficient evidence for the food addicts and the clinicians who have served them. There are tens of thousands of these cases; this can be seen as possibly the most important evidence that food addiction or something very much like it does truly exist.

Evidence from Food-related 12-Step Fellowships: In 1960, a suburban housewife in California, learned that a compulsive gambler had found relief from his destructive behavior by applying the principles of Alcoholics Anonymous. She decided to apply this method to her continual struggle with her eating and weight. The program she developed, Overeaters Anonymous, suggested complete physical abstinence, asking for help in a community of peers, and treating the underlying emotional, mental and spiritual problems with the 12-Steps. Over time, Overeaters Anonymous (OA) expounded upon its definition of abstinence and has supported its members to use a food plan tailored to each individual’s particular needs. From the beginning, some members of OA saw themselves as chemically dependent on specific foods, and the principle of “putting down one’s binge foods a day at a time” became widely accepted. Research on OA commissioned by the organization itself found that:

  • In 1992, 81% of a sample group reported “an improvement regarding preoccupation with food” and the group as whole lost an average of 40.8 pounds and kept it off to date for an average of 3.97 years. (OA, 1992).
  • In 2004, a larger and more rigorous OA self-survey, managed by members of the Southern Methodist University School of Business, found that 33% were abstinent at the time of the survey and another 45.6% reported significant improvement in eating behaviors; 56% reported “food obsessions had been lifted”; and 46% achieved a healthy body weight since joining OA. (OA, 2004)
  • In 2010, a third survey – with a return rate of 36% and a margin of error of 4.09% – found that 82% of respondents came to OA overweight; 69% lost weight so far (with an average loss of 45 pounds); and 51% were maintaining a healthy body weight; a large majority found that they had “significant improvement” in daily functioning, overall physical health, mental/emotional health, spiritual connection, and relationships as well as weight issues. In fact, a slightly lower percentage described success with physical recovery – 75% – than with inner recovery – 79-91%. (OA, 2010)

Members of OA are people who have usually tried many diets and failed. Seventy-four per cent (74%) had tried therapy but failed to find help for their food and eating problems before joining OA. The OA success rate is impressive considering the fact that most diets have a success rate of only 10-30% in the first yearTens of thousands of people have been recovering in OA for over fifty years, and most of these people have never had the opportunity to benefit from professional treatment using the addictive model as our counterparts in NA and AA have. OA certainly provides an effective solution for some obese and eating disordered adults, and this makes a strong case that compulsive overeating and food addiction are diseases that exist and can be treated successfully.

Within OA, there are “movements” for those who identify as “food addicts” and not just “compulsive overeaters” or “eating disordered.” Because their disease with food has advanced to a more critical level, they embrace a stricter program to deal with it. Some sub-groups within OA that have developed to suit the needs of critical level compulsive overeaters and food addicts are: OA-HOW, OA-90 Days, and former OA Grey Sheet. Since the turn of the century, substantial groups in each of these movements have created whole new fellowships where everyone identifies as a food addict and where community support is focused on the needs of those in the late and final stages of the disease. These new fellowships include: FAA, FA, CEA-HOW, RFA, and GSA. While there is not yet any self-initiated research from these sub-groups and new organizations, it is commonly known within the food recovery community that these disease-model recovery sub-groups and fellowships are generally more structured, more demanding and more successful with advanced food addicts. The percentage of members who are food abstinent, the amount of weight lost and the stability of recovery seems to be higher in many of these groups than in the rest of OA.

There is one independent academic study of OA in a geographical area where OA HOW is particularly strong. In her doctoral thesis at Virginia Polytechnic Institute, Dr. Kriz did a rigorous study of the effectiveness of 12-Step recovery for obesity and eating disorders. The findings included:

  • 68% of 162 respondents said they adhere to a food plan daily;
  • 70% were abstinent more than 30 days at the time of the survey;
  • 46% said they weighed and measured their meals 75-100% of the time;
  • 46% reported never or rarely relapsing;
  • 62% had completed a Fourth Step self-inventory;
  • 21% had completed making Ninth Step amends to others they had hurt; (Kriz, 2002)

Although Dr. Kriz did not make the distinction between those with eating disorders, food addiction or both, the large percentage who weighed and measured their food suggest many were using a more structured program designed for those with chemical dependency on food. There were no questions comparable to the OA surveys on weight loss.

Evidence from Professional Food Addiction Treatment Program: During the 1980’s and 1990’s there were over a hundred hospital-based treatment programs for food addiction using the medical model. Many did outcome research but did not publish it. There is one independent academic study of Glenbeigh Psychiatric Hospital of Tampa’s Residential Eating Disorder and Food Addiction Treatment Program. It is a doctoral dissertation by Dr. M. Theodora Carroll for the Department of Psychological and Social Foundations of the University of South Florida. The focus of the thesis is on evaluating the predictive value of the Eating Disorder Inventory in an inpatient treatment program for the bulimic and obese employing an addiction paradigm. More importantly perhaps, is the rigorous outcome survey done within the research to establish a basis for evaluating the testing instrument. It is the outcome data which provides evidence supporting the disease concept of food addiction:

  • 1/3 of the sample group had maintained rigorous and stable abstinence for at least a year, some up to five years; this entire group was maintaining or moving towards a healthy weight loss.
  • 1/3 had had at least one relapse for weeks or months, but each had regained their abstinence, and they too, were moving towards a healthy weight.
  • 1/3 had relapsed and was still in relapse at the time of the survey; most did not have an appreciable weight loss, but almost all were thankful for the experience of treatment and for the knowledge that they were chemically dependent on food.

Over 8,000 clients had participated in the six to eight week residential food addiction treatment program at Glenbeigh, and the research studied a random sample of alumni. The outcomes compare favorably with outcomes of drug and alcohol treatment and very favorably with outcomes of commercial weight loss programs.

When health insurance companies stopped reimbursement for all hospital-based primary treatment programs for food addiction, a new model of professional service was developed by private practitioners (e.g., Kay Sheppard, Judy Hollis and Anne Katherine) and private treatment programs (e.g., Shades of Hope and ACORN Food Dependency Recovery Services). Outcome research on the ACORN program was presented at the first “Promising Practices” conference of the International Association of Food Addiction Professionals in 2009. As of 2006, over 1,200 self-assessed food addicts had participated in the five day ACORN Primary Intensive – a residential workshop modeled after the program at Glenbeigh Hospital of Tampa. The samples in the study included 250 alumni of the Primary Intensive and 40 members of Overeaters Anonymous who were in long-time recovery and had not attended ACORN or other professional treatment programs.

Of the ACORN alumni sample, 95% identified themselves as food addicted and were not able to successfully diet, deal with their eating problems through therapy or to achieve and maintain food abstinence with the help of food-related 12-Step programs. Surveyed between one and five years after attending their first ACORN workshop: (add colon, remove comma)

  • Over two-thirds said that food addiction had had a strongly negative effect on their physical, emotional and spiritual lives prior to the workshop.
  • On the day they responded to the survey, most (76%) were abstinent; they had honestly committed to what they were going to eat that day and then followed through with it.
  • About one-third had been stably abstinent since treatment, and another third had relapsed but found their way back to abstinence and recovery on their own.
  • On average the ACORN group had lost 50 pounds from their highest weight. They had relief from secondary medical problems, and they judged their mental and emotional health to have improved.
  • Those in the ACORN group had similar recovery profiles to the non-ACORN long-timers from OA: a peer support group, a mentor or a sponsor, a spiritual practice of prayer and meditation and/or the 12-Steps.
  • None rated their overall ACORN experience negatively; 20% said “it helped a lot,” 59% said “it changed everything,” and 96% said they would “recommend ACORN to other food addicts.”

One of the most interesting outcomes was that all but six of the 1,200+ ACORN participants had become rigorously abstinent during the Primary Intensive, showing that this is a lower cost alternative to a treatment centers and a highly effective way of supporting detoxification for chronically relapsing food addicts. These findings also suggest that short-term residential detox for those chemically dependent on food(s) might make a substantial intervention in the obesity crisis.

Many of the most difficult cases of adult obesity and eating disorders can and do respond favorably to an addiction model of treatment, thus corroborating the scientific evidence for food addiction. The effective treatment for food addiction behooves us to make use of a diagnosis of chemical dependency on food, i.e., food as a substance use disorder. (Cheren, et al)

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