Mark S. Gold, MD & Drew W. Edwards, EdD, MS


The Disease of Addiction
In 1959, amid much skepticism and controversy, the American Medical Association (AMA) declared alcoholism a disease. “Alcoholism is a primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations.” In 1969 the World Health Organization (WHO) followed suit and in 1992 the American Society of Addiction Medicine (ASAM) stated. “The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic.” Over the past 4 decades we have witnessed groundbreaking research that has led to remarkable advances in education and treatment. For those in the business of treating addiction this was a game changer. For the millions of suffering alcoholics and their families this was a lifesaver.

In the 1970’s I (MSG) began looking for the mechanisms of drug reinforcement and withdrawal. In opiate addicted patients this looked straightforward. Those addicted to heroin, for example, would go to extreme lengths to avoid the agony of withdrawal. Our major contribution was discovering the importance of the nucleus locus coeruleus, norepinephrine hyperactivity and clonidine’s efficacy in opiate withdrawal. However, even successful and safely detoxed patients once let go, relapsed. Relapse was itself proof that addiction treatment was much more than detox. In the early 80’s we learned in this work and subsequent work with cocaine, that addiction is rooted in complex neuro-biological systems that are germane to human survival. Successful withdrawal and abstinence was associated with a rebound hyperphagia, overeating and weight gain. During early recovery these same patients now desired and consumed high volumes of sweet, highly palatable food. Through these observations and relevant research it became clear that
the drive for food and the drive for drugs of abuse may be related. Research by my friend, colleague and research collaborator Bart Hoebel, demonstrated that sugar is self-administered by lab animals as if it were a drug. Like heroin, sugar withdrawal could be provoked by naloxone or opiate antagonists. So, in humans, we thought food might become an object of intense interest and desire in much the same way as drugs of abuse.

In the mid 1990’s the University of Florida department of psychiatry began to offer treatment for obese patients in our specialty teaching clinics, believing that for many people overeating was an addiction. As patients described their relationship with food we began to see the symptoms of addiction and maladaptive, self-defeating behavior. What was remarkable to us was the continued consumption of highly palatable food beyond the point of physical satiety. As a result, we coined the phrase the Hungry Brain. Although their stomachs were full, their brains were starving. These obese individuals were clearly eating to change their mood. Like all addicts these patients reported a general feeling of angst and un-ease that was quickly mediated by eating. Not surprisingly, depression was the most common comorbidity in this clinical population. In 2000 we endeavored to document our observation, research, and theory in a popular book, titled, The Hungry Brain. Unfortunately, the publishers of the day told us that only books with diets will sell in this market. Fad diets may sell books but they will never make a dent in the underlying disease of obesity and addiction.

A New Day
It was certainly welcome news when the American Medical Association (AMA) shook up the world of medicine by recognizing obesity as a disease (June 2013). AMA board member Patrice Harris, MD stated. “Recognizing obesity as a disease will help change the way the medical community tackles this complex issue that affects approximately one in three Americans”.

Shortly thereafter, the American Association of Clinical Endocrinologists (AACE) Obesity Task Force affirmed their position on obesity in agreement with analysis and criteria put forth by the AMA. The AACE asserts that obesity is a “primary disease” that impairs normal functioning of some aspect of the body; has “definitive signs
or symptoms”; and “results in harm and increased morbidity including endocrine dysfunction (including leptin dysregulation) and insulin resistance, hypertension, appetite dysregulation, impaired endothelial function, nonalcoholic fatty liver disease, dyslipidemia, adipocyte produced inflammation, anatomical complications such as osteoarthritis, increased immobility, depression and sleep apnea.”

The New Plague
Obesity is a poorly understood, multifaceted disease. In a 2010 report by the Organization for Economic Cooperation and Development, obesity has tripled in the last 20 years in the developing world with 10% of the world’s children currently overweight or obese. In the United States over one-third (36.7%) of adults and nearly 17% of children and adolescents are obese. In adults, obesity is defined as having a body mass index (BMI) ≥ 30 kg/m². In actual numbers, 78 million adults above age 20 and 12.5 million children and adolescents in the US are obese.
Data from two National Health and Nutrition Examination Surveys (NHANES) show that among adults aged 20-74 years, the prevalence of obesity increased from 15% in the 1976-1980 surveys to its present rate of nearly 37 percent. This trend is confounding, considering the increased attention toward health and fitness observed in the United States over the same period. The resulting impact of obesity on morbidity, mortality, and healthcare cost is staggering. But why?
The Food Addicted Brain

Although doctors and scientists can now accurately describe the signs, symptoms and consequences of obesity, there is little understanding of the etiology or pathophysiology. The best available data suggest that obesity is not simply a problem of excess caloric intake and decreased energy expenditure or a lack of will power. Something else is happening. We know this because in spite of the wide spread knowledge regarding the serious health risks associated with obesity, competent and intelligent people continue to overeat. To us, and many addiction experts, this looks very much like addiction. Yet for many, the idea that someone could be addicted to food seems farfetched because unlike cocaine or alcohol, eating is necessary for survival. However, recent advances in neuroscience and neuroimaging reveal that overeating and drug abuse share common neurocircuitry. In other words, the reward associated with overeating is biologically similar to the reward experienced via abuse of alcohol and drugs.

In 2012, I (MSG) co-chaired the Yale Historic Conference on food addiction. Nearly forty experts convened to present evidence, discuss and debate the question of food addiction.

In 2013, Richard Shriner and I (MSG) published a comprehensive, evidenced description of food addiction:

Food addiction represents a pervasive and enduring pattern of both food perception and food-related behavior (leading to either excessive food ingestion or aversion) whose dual valence (i.e. perception and behavior) biases interaction with food in harmful and unhealthy ways. Such a biasing and unhealthy valence toward food continues, despite knowledge of its harmful consequences. Food addicts usually present both a tolerance (i.e. a need to increase participation in their harmful relationships with food over space and time) as well as a form of withdrawal (i.e. an inability to escape their addiction with food without suffering undue anxiety, craving, or other adverse neurochemical reactivity [which may include depression or anger]) when deprived of access to addictive foods. This latter emotional and behavioral reactivity must reliably occur during efforts to either alter or disrupt the food addict’s harmful and maladaptive pattern of eating.

Although the neurobiological mechanisms of addiction are unseen, they are essential to our understanding of the maladaptive and self-destructive behavior we encounter in addicted individuals. In 2009, neuroscientists Wang and Volkow found similarities between the brains of drug addicted subjects and obese subjects. Both groups had reduced striatal DA receptor availability, which may predispose obese subjects to, “seek food as a means to temporarily compensate for under stimulated reward circuits”. In other words, the angst, boredom and dysphoric mood state associated with addiction is temporarily mediated in obese individuals when they overeat or eat certain foods. Moreover, this investigation showed that obese subjects had decreased metabolism in the frontal and prefrontal regions of their brain which are involved in inhibitory control. This finding is key to understanding the inability of obese individuals to control food intake. Simply stated, the intrinsic reward from eating may override signals of fullness, satiety and the individual’s rational observation that they are indeed obese and unhealthy.

It’s helpful to remember that the end of the neurobiological cascade associated with drug and alcohol abuse is stimulation of opiate receptors, which is perhaps the most powerful reinforcement in nature. Our survival is inexorably connected to brain reward associated with food, water and sex. Addiction to drugs and alcohol is said to “highjack” the brain’s reward system by creating intrinsic pleasure for destructive behavior. In the case of food addiction, we now know that the same mechanisms are at work. What we didn’t understand until recently that for a subset of people food, or certain foods are overly rewarding in the same way that drugs and alcohol are. Recent research has shown that excessive carbohydrate intake is associated with endogenous opioid stimulation in some people.

There are certainly more questions than answers, but we are making progress. To date, neuroscientists have identified a number of brain messengers that are involved in the sensation of hunger and satiation. These include Leptin, Neuropeptide Y, Ghrelin, Dopamine, 5 HTP and others. These are some of the new targets for the development of new treatment, which may reduce hunger and overeating. But as we have learned from experience in dealing with addicts, a pill may reduce symptoms, but the underlying disease state of addiction is a stubborn thing. Certainly the frontier of neuroscience is promising but we must never lose sight of this truth. Attached to every addicted brain is an out of control addict who desperately needs help.

The Patient

On the clinical front, addressing the food addict requires understanding the metabolic issues of obesity and overeating, the addiction processes that deny, rationalize and distort; and, the emotional labiality; (mood swings, depression, obsession and compulsions)and lastly the relational consequences of addiction (loneliness, marital & family stress, abuse and separation or divorce). We must remember that losing weight does not cure food addiction. We mention this because working with food addicts requires another level of sensitivity to the plight of the obese addicts. Understanding compulsions of the hedonic brain in food addicts will require more research, education and more listening to our patients. In the meantime, our friends in Alcoholics Anonymous remind us that recovery is a simple program. Surrender, admit powerlessness, ask God for help, go to meetings and life gets better. Although we do not fully understand the pathophysiology of food addiction, we know that all addicts suffer from self-loathing, guilt and fear. The good news is that caring and compassion is always good medicine. We press on.

Mark S. Gold, MD is the Dizney Eminent Scholar, UF Distinguished Alumni Professor, and Chairman of Psychiatry at the University of Florida College of Medicine and McKnight Brain Institute. He has developed translational research models leading to new treatments and approaches to addiction during his 40 years as a researcher and inventor. Dr. Gold has also advanced the understanding of effects of tobacco, cocaine, other drugs, and food on the brain and behavior.

Drew W. Edwards EdD, MS is a healthcare researcher, author, clinician and consultant and is a forensic expert in the neurobiology of addictive disease. He has published over 250 peer reviewed and popular articles, curricula, and training resources on behavioral health, addictive disease, parenting and youth culture, as well handbooks for parents on childhood depression and selfesteem in children.