Implications of Food Addiction for Understanding and Treating Binge Eating Disorder

Drugs as Food

Conventional evolutionary mismatch views of addiction propose that substance use is a relatively recent phenomenon in the history of our species and that it occurs largely because of the availability of purified and synthetic drugs and their direct routes of administration. In other words, it is the ubiquity and concentrated doses of these substances that have contributed to widespread human drug abuse. By contrast, Sullivan and Hagen have pointed out that human beings shared a coevolutionary relationship with psychotropic plant substances in prehistory for millennia. Indeed, they frequently ate them as food because their ingestion solved a recurrent problem faced by our ancestors.

The neurotransmitters that are essential for normal human functioning—and most implicated in substance use—are dopamine and serotonin, the precursors of which must be provisioned externally from high-quality nutrients such as protein. During most of our history, due to famines and seasonal food shortages, these precursors were nutritionally constrained and, consequently, people experienced neurotransmitter deficits with considerable regularity. Depletions of this sort tend to affect critical behaviors and emotions adversely, including motor activities, cognitive abilities, and mood.

In addition, it is generally believed that over our evolutionary history, certain plants developed chemical defenses against mammalian predators by producing neurotransmitter substitutes, which had toxic effects when ingested. Sullivan and Hagen argued that in response to this threat, “behaviourally sophisticated hominids” evolved to counterexploit the potential benefits of plant toxins. For example, because these “neurotransmitter analogues” imparted energy, prevented fatigue, diminished appetite, and increased tolerance for hunger, they helped to avoid the maladaptive “behavioral sequelae of stress” in the absence of adequate food sources. In other words, plant substances served the dual purpose of substituting for more costly energy and buffering against the biological ravages of prolonged stress.

Thus, it seems reasonable and sensible to conclude that organic compounds in our environment can only be categorized as beneficial or harmful when we take account of dosage and the relevant characteristics of those who partake of them.

Food as Drugs

This last point is particularly relevant when considering the typical macronutrient intake in current Western societies. Diets high in concentrated fats and sugars are not only dense in calories, but metabolically efficient because a large proportion of their energy is provided to the consumer. They also tend to elevate mood by releasing neuropeptides, which reinforce their selective preference. Evolutionary biologists believe that cravings for sugar and fat evolved to enhance human energy intake in unpredictable nutritional environments, which were universally the norm until relatively recently. However, in the quantities that many people ingest them today, they have an abuse potential rivaling that of popular addictive drugs.

The food industry has become especially savvy in exploiting our natural human desire for sugar and fat by increasing many-fold their dose in much of our daily foods. For instance, there was a 42% per capita increase in the consumption of added fats and a 162% increase in cheese relative to only a 20% increase in fruits and vegetables between 1970 and 2000. The sharply reduced cost of sugar and vegetable oils worldwide has greatly contributed to the production of highly palatable processed foods. The incidence of snacking, especially in the form of carbohydrates, has also increased over the past 25 years, in tandem with the increase in daily energy intake. Junk foods, which are the principal type of snack, have little nutritional value, but are highly appealing because of their high fat and sucrose content.

In the case of conventional drugs, greater potency tends to increase their addictive potential. Directly parallel to the notion of drug dosage is the size of the meals we are presently served. Wansink and Van Ittersum described the “portion-distorted embarrassment of food” in today’s supermarkets and restaurants. To illustrate, a fast-food restaurant meal—a burger, fries, soft drink, and dessert—can provide almost all of one’s daily caloric requirements in a single serving. Moreover, the annual growth rate of fast food dining has increased threefold in the past generation compared with that of at-home consumption. The sizes of plates, bowls, and glasses in our homes have also increased steadily over the years, and the serving size of some entrees has virtually doubled in recipe books since the 1930s.

In summary, just as different drugs promote different degrees of dependence, foods also differ in their capacity to promote abuse. Experts are now confident in claiming that the nutrients composing fast foods are inherently addictive because of their concentration and high volume of fats and sugars. In addition, like drugs of abuse, they have the ability to alter brain mechanisms in ways that contribute to their increasingly compulsive use (see Del Parigi et al., Grigson, and Spring et al. ).

Loss of Control

Perhaps the most clear-cut feature of addiction is the increasingly compulsive use and abuse of the addictive substance or behavior, even in the face of detrimental consequences to health, safety, social relationships, and financial stability. In animal studies, for example, cocaine dependent and binge-prone animals will tolerate higher levels of foot shock to obtain cocaine and palatable food, respectively. Similarly, animals maintained on a palatable cafeteria diet will continue to consume food even when it has been laced with a bitter tasting substance.

BED is characterized by recurrent episodes of binge eating without the regular use of compensatory behaviors such as purging, fasting, or excessive exercising. Feeling out of control of one’s eating behavior is a defining feature of binge eating. BED also appears to be a chronic and stable condition with strong links to obesity. Although initially believed to be a disorder of adulthood, there is growing evidence that BED also occurs in children and adolescents. In addition to clinical research, there are good experimental paradigms whereby a subset of rats fed an intermittent diet of sugar have developed a pattern of copious consumption resembling human cases of BED (e.g., Avena et al. and Colantuoni et al. ).

BED sufferers typically report distress and guilt about their eating habits, but they have great difficulty controlling these behaviors despite weight gain and ensuing medical problems such as diabetes and hypertension. As a society, we are generally informed and knowledgeable about the negative consequences of poor nutrition and obesity and are sentient of dietary recommendations for good health, so we must conclude that binge eating—like drug addiction—exists despite an awareness of its poor health outcomes.

Tolerance and Withdrawal

In the most general sense, tolerance occurs when a stimulus of a particular magnitude elicits an increasingly diminished response with each repeated exposure and an increasingly higher dose is necessary to achieve the desired effect. This phenomenon is a key characteristic of all drug addictions—and one of the factors that fosters the escalation of intake. Animal studies have demonstrated that a sugar-enhanced diet is associated with increased daily food intake over time, and decreased striatal dopamine response. Individuals who report frequent ice-cream consumption also demonstrate decreases in striatal activation in response to an ice-cream–based milkshake, suggesting similar neuroadaptations following prolonged exposure to highly palatable food in humans.

Direct evidence of tolerance in BED, however, arises primarily from clinical reports of individuals consuming more and more food in each binge as the disorder becomes more chronic. The finding that higher body weight correlates with the frequency and severity of binge eating episodes also provides indirect evidence of tolerance effects. As well, a high proportion of adults with BED reported being overweight before the onset of their disordered eating, suggesting that over time, high-calorie diets prompt greater subsequent intake and may contribute to binge eating.

The impact of tolerance on the progression of addictive behaviors is made more poignant by its synergy with the debilitating symptoms of withdrawal. Certain foods—particularly sugar—can cause pronounced withdrawal symptoms when removed from the diet, and these effects most clearly resemble the physical signs of distress seen in opiate withdrawal. The most compelling evidence comes from animal research in which rats were initially maintained on a 25% glucose solution (e.g., Avena et al. and Wideman et al. ) or high sucrose diet. Following removal of the palatable diet, animals showed aggression, anxiety, a drop in body temperature, teeth chattering, forepaw tremor, head-shaking, and depressive-like behaviors—all symptoms associated with withdrawal from drugs such as heroin. Parallels have also been drawn between amphetamine and sugar withdrawal, both of which induce signs of increased impulsivity. Although there is human evidence of sugar withdrawal, it comes mostly from clinical observation, self-help books, and Internet sites promoting weight-loss diets. They are, however, uniform in describing headaches, irritability, and flu-like symptoms among heavy sugar consumers who become abstinent.