Cross-Addiction: From Morbid Obesity to Substance Abuse

Eating dysfunctions: A choice or addiction?

Eating disorders are considered by some experts to be a form of drug addiction since the characteristics satisfy the definition of an addiction: first, there is a progressive, compulsive component, even when dire health and safety consequences are present or looming; second, the continual exposure to the food stimulus typically increases obsessive craving even after a prolonged period of abstinence; and, third, there is typically a requirement for more of the substance to experience the previous level of reinforcing effects. ⁵²

Some clinical researchers advocate that a common set of personality traits predisposes a person to a range of behaviors that can become excessive in nature. Based on a composite of her research studies, Davis found that drug- and alcohol-addicted subjects and subjects who had an eating disorder demonstrated similar scores on a research tool that measured addictive personality characteristics. Current research studies on addiction and eating disorders support that there is a substantial lifetime comorbidity between eating disorders and other forms of addiction, and there is strong evidence to suggest that eating disorders are a form of an addiction. ⁵²

Research shows that it has been determined, to a degree, that drugs and palatable food activate common reward brain circuitry. Obesity and substance addictions result in ingesting habits that continue even after the introduction of negative, possibly life-threatening consequences. Although some classes of obesity can be linked to genetic polymorphisms, the recent prevalence of obesity is clearly correlated with the increased availability of desired foods, which have powerful, reinforcing properties. ⁵³

The intake of food has been found to be regulated by two complementary mechanisms: (1) the homeostatic pathway, and the (2) hedonic pathway. The homeostatic pathway responds to the energy demands of the body, while the hedonic responds to the reward-based desires of the individual. The hedonic pathway only motivates the imbibing of drugs of abuse. Extensive research has evidenced that exposure to drugs of abuse affects neuronal functioning and increases the motivation to seek and use these substances. ⁵⁴

There is a strong argument to suggest that eating disorders are a form of addiction. Clinically, the behaviors that characterize eating and substance abuse are very similar, and biologically, similar mechanisms account for the compulsively progressive nature of both entities. Psychobiological vulnerability for both conditions is indicated, and there is evidence to suggest that a variety of rewarding behaviors to self-medicate occurs. ⁵²

Binge eating, which is defined as the intake of excessive amounts of calories in a short period of time (such as 2 hours) and the experiencing of a lack of control over eating during this episode, has been identified as an issue for some morbidly obese individuals. ⁵⁵ Bingeing has not been classified as a specific eating disorder by the DSM-IV-TR; instead, it is identified as one of the symptoms of bulimia nervosa, which is an accepted diagnostic entity in the DSM-IV-TR. ⁵⁶

DiLeone states that the loss of control over food intake is comparative to the loss of control that a drug addict experiences. It is possible that common neural mechanisms underlie both food and drug intake behaviors. Recent studies have shown direct leptin effects on dopamine neuronal functioning and behavior. This finding provides a new dynamic in that peripheral hormones contribute to a more definitive model of neural control over food intake. ⁵⁷

Leptin is recognized as a feedback signal to the central nervous system that affects eating behavior and energy homeostasis. The few published studies examining leptin concentration in obese patients who have binge eating disorder (BED) present conflicting results. In an attempt to determine the relationships between leptin and eating patterns, a study of 30 morbidly obese women was conducted. In this study, 14 morbidly obese women who had BED and 16 morbidly obese women who did not meet the clinical criteria for the diagnosis of BED and reportedly never engaged in binge eating were examined. Subjects and controls were matched for body weight, body composition, and resting energy expenditure. The Eating Inventory and the Eating Disorder Inventory were administered to all the subjects, who were also assessed on several different physiological dimensions, such as resting energy expenditure and serum leptin concentration. A non-parametrical statistical method, the Mann-Whitney U-Test, was used for analyzing independent data, and the relationships between data were assessed using the Spearman coefficient. The outcomes of the study suggest that both body fat size and eating behavior influence serum leptin concentration, but a low level of value of leptin does not appear to trigger binge eating in BED patients. ⁵⁸

Although eating disorders exhibit similar features to substance abuse and dependence, there is a lack of conclusive data to support that a food addictions model exists since neither tolerance nor dependence factors to food are unambiguously demonstrated. ⁵⁹

Suspected etiologies of obesity

Talvi states, “Over 60% of all Americans are now overweight and experts agree that fast food, television, office jobs, lack of fresh fruit and vegetables in school lunches and genetic factors have all conspired to make Americans of all ages fatter.” ⁶⁰ The ABO concurs with Talvi that genetics are an etiological agent of obesity, and the ABO adds that other recognizable etiological factors of obesity include social, behavioral, cultural, metabolic, physiological, and genetic factors. ⁵⁰

Medical conditions and obesity

Excess body weight is the sixth most important risk factor in the overall contribution to diseases worldwide. Major adverse consequences of obesity include cardiovascular disease, several types of cancer, and type 2 diabetes. The average life expectancy is decreased with obesity and the associated comorbidities require ongoing clinical assessment. Long-term weight loss is dependent upon permanent changes in dietary quality, energy consumption, and activity. ⁶¹

Neurobiochemical factors and obesity

Neurochemical changes occur in the brain with drugs of abuse and addiction, and with overeating. A deficiency in leptin signaling may lead to overfeeding and may account for some genetic and acquired forms of obesity. ⁶² Experts purport that overeating can be classified as an addiction since dopamine, a neurotransmitter, plays a significantly rewarding role in both food and drug intake mechanisms. The most clearly established commonality of the mechanisms of food and drug intake is their ability to activate the dopaminergic link in the brain. Brain dopamine has been found to play an important role in reinforcement in the ability of food to act as a reward and in response habits and conditioned preferences. ⁶³ It can be speculated that different drugs can establish different levels of compulsive behavior; so, too, different foods may establish different levels of compulsivity.

Addictive foods, like addictive drugs are believed to activate the brain circuitry involved in motivation, reward seeking, and decision making. In the addictive process, it appears that the brain seems to respond to drugs almost as it would to food under conditions marked by severe deprivation. Obesity and addiction both result from foraging and ingestion behaviors that persist and become stronger despite the risk of a catastrophic outcome. Overeating and drug usage involve behaviors that are learned habits and preferences that are concretized by the reinforcing properties of repetitive and powerful rewards. Attractive foods, such as refined sugars, can lead to a loss of control that conforms to the DSM-IV-TR criteria for substance use disorders. ⁶⁴ Food, like drugs, can activate brain circuitry, which some hypothesize may lead to neurobiological adaptations that make associated behaviors increasingly compulsive in nature, resulting in an additional loss of control over food or drugs. ⁵³

Genetic factors and obesity

Genetic causes of obesity have been established by the existence of disorders such as Prader-Willi syndrome, Cohen syndrome, and Bardet-Bidel syndrome, but these three syndromes do not explain the worldwide pervasiveness of obesity. ⁶⁵ There does seem to be a relationship between heredity and obesity. Often-quoted studies include (1) a research study in which adults were adopted as children but, nevertheless, their body weights were closer to the body weight of their biological parents rather than the adoptive parent; ²⁴ and (2) a study of identical twins who, when raised apart from one another, still had similar body mass indices much more frequently than fraternal twins who were raised together, suggesting the influence of genes and DNA. ²³ The results of both of these studies suggest that genetics appears to have influence upon weight. Scientists have found several single-gene mutations in animals shown to cause obesity in animals, but the most common forms of human obesity seem to arise from a complex etiology of environment, genetics, and behavior. ⁶⁶

Formal genetic data based on family, twin, and adoption studies lead to the conclusion that at least 50% of the interindividual variance of the BMI is attributable to genetic factors. Recent studies have discovered the first polygenes involved in body weight regulation. Additional studies will be necessary to determine the contribution of genetic and environmental factors upon obesity. ⁶⁷

Studies have identified a number of loci at which genetic variation is associated with obesity and related phenotypes, and the identification and characterization of monogenic obesity syndromes have been very productive. There is widespread belief and acceptance that hereditary factors might predispose an individual to obesity. All identifiable monogenic defects cause human obesity by disrupting the hypothalamic pathways, which have a major effect on satiety and food intake. The evidence on obesity to date suggests that the major impact of genes on human obesity likely impacts hunger, satiety, and food intake rather than metabolic rate or nutrient portioning. Human obesity appears to be less driven by metabolic dysfunctioning and more influenced by neurobehavioral disease. ⁶⁸

An extensive research study of 5,092 twin pairs measuring BMI and waist circumference indicated that genes appear to determine the subjects' risk for obesity and that environmental factors seemed to be less important. Researchers from the University College London assessed BMI and waist circumference of twin pairs, age 8–11 years, born between 1994 and 1996. Genetically identical twins were much more similar as far as BMI and waist circumference than non-identical twins. This finding is representative of a 1997 study of adult twin and adoption studies that found variation in BMI seems to be related to a heritability estimate in adults ranging from 55% to 85%. The authors conclude that the significant rise in obesity in the last 15 years is attributable to the environment, not genetics, because genetics have not changed in this time period. ⁶⁹

Other studies have stated that approximately as much as 50–70% of the variability of BMI and 40–60% of the vulnerability to addiction may be attributed to genetic differences under specific circumstances. Volkow and Wise state it is important to state that estimates of habitability for one set of circumstances are not necessarily valid for other circumstances. ⁵³

Obesity has been hypothesized to be the result of genetic and environmental factors. Polymorphisms in various genes control metabolism and appetite and may predispose an individual toward obesity when sufficient caloric intake occurs. A comprehensive review of published studies in the MEDLINE database and the Obesity Gene Map Database indicates that obesity-related phenotypes vary from 6% to 85% among various populations. ⁷⁰ As of 2003, more than 41 genetic sites have been linked to obesity when a favorable food environment is present for this malady. ⁷¹

A study that attempted to address the influence of genetics and environment upon obesity chose to study 23 Finnish identical twins who had significantly discordant Body Mass Indices. The mean BMI for the overweight twins was 29.5, while the BMI for the normal-weight twin counterparts was 22.9. Over a three-day inpatient stay, interviews were conducted and standardized questionnaires were administered to obtain information about energy and nutrient intake, physical activity history, smoking, eating behavior, and other background information. The results showed that overweight co-twins had higher disinhibition scores (P = 0.007) and hunger scores (P = 0.0005) in the 3-Factor Eating Questionnaire than their normal-weight co-twins. Additionally, difficulty in controlling eating in both sexes and high-energy intake in women were related to having an overweight status. It is suggested that varying living conditions, such as family- and work-related factors, and eating behaviors may have led to different weight gains in monozygotic twin pairs. ⁷²

A literature review on the origins of obesity suggests that both genetic and environmental factors contribute to the development of obesity. A study utilizing articles from PubMed and OMIM was conducted to determine if a relationship exists between obesity and the effects of genetics and the environment. An examination of twin and family studies suggests that there appear to be genetic influences on body weight and that environmental changes seem to have promoted the development of obesity for individuals who are genetically at risk. ⁷³

It is speculated that both addiction and obesity appear to be possibly under the auspices of polygenetic control. Genetic and environmental factors are not simply addictive factors; instead, these factors appear to interact in complex and counterintuitive manners. ⁵³ Brownell poses that 25% to 40% of the variability in population body weight can be explained by genetics, but at least 60% or more is attributable to an environment that is inundated with readily available, non-nutritious foods. ⁷⁴

Current research continues to suggest that both obesity and addiction appear to have contributory genetic components. ⁷⁵ This information may help to dissipate beliefs that obese people are lacking willpower and suffering from a character defect that leads them to make the choice to overeat, take drugs, or abuse alcohol. Evolving research results may support the influence of genetics upon obesity and addictions, which will, hopefully, aid in the alleviation of obesity-, alcohol-, and drug-related stigmatizations.

Sorensen advocates that there is no doubt that obesity is influenced by genetics, as indicated by his review of studies of monozygotic and dizygotic twins in which it was shown that monozygotic twins have a much greater resemblance in the degree of obesity than dizygotic twins. For family members, analyses of the distributions of obesity suggest a few genes have a discernible effect upon obesity but none of the genes have been definitively proven to cause obesity. Sorensen concludes that obesity is the result of an interaction between genetic and environmental factors, although he adds the specific factual evidence for these interactions is weak. ⁷⁶

Environmental factors and obesity

A comprehensive review of the research results on the etiology of obesity seems to suggest that environmental and genetic factors appear to be intertwined. The Western lifestyle of low activity levels, coupled with the consumption of energy-dense foods that are readily and cheaply available, seems to contribute to the rising rates of obesity. ⁷⁴ Flancbaum contends that the genetic contribution to obesity is only about 40%, and the remaining 60% may be attributable to environmental causes. ¹

The availability of food varies significantly among regions and countries. ⁷⁷ While starvation is an everyday reality in some countries, Americans are consuming more calories than they did three decades ago, and the rate of this increase is three times greater for women versus men. Between 1971 and 2000, women increased their daily caloric consumption from 1,542 calories to 1,877 calories, while men in the same time period increased their daily caloric consumption from 2,450 calories to 2,618 calories. ⁷⁸ The U.S. population ranks number one in obesity rates. ⁷⁹

Each individual, on average, in the United States uses or discards 3,770 calories each day, according to data from the United Nations Food and Agriculture Organization that was collected in 2001–2003, compared with 2,440 calories per person per day in India, ⁸⁰ and the obesity rate in the United States increased from 14.5% to 30.9% during 1971–2000. ⁸¹ During this same period, an increase in the amount of calories consumed was 335 calories per day for women and 168 calories per day for men. Most of the increase in caloric consumption is carbohydrate based, not fat based.

Obesity is a major cause of morbidity and mortality in the United States, and each year an estimated 300,000 adults die of causes related to obesity. Genes related to obesity cannot explain the dramatic incidence of obesity between 1991 and 1999. There has been a report that indicates a 33% increase in diagnosed diabetes from 1990 to 1998. Environmental factors need to be addressed in the form of a national, comprehensive plan. ⁸²

USDA survey data for 1977–1996 indicate that factors that contribute to increased caloric consumption in the United States include consumption of food away from home; increased energy consumption from salty snacks, soft drinks, and pizza; and increased portion sizes. ⁸³ The consumption of calorie-laden beverages has significantly increased over the last two decades in the United States and accounts for 20–24% of dietary consumption across all age groups. ⁸⁴

Between the time period of 1977 and 1995, it has been found that many Americans are eating out. This trend is expected to continue, and it is also expected that this choice will result in the continuing overconsumption of fat and saturated fat and the underconsumption of calcium, iron, and fiber, unless strategies to improve the American diet are implemented. ⁸⁵

Additionally, larger portion sizes and unit packaging are major contributors to the rising obesity rates. It is unlikely that biology is causing the rocketing obesity rates; instead, the super-sizing of food in the forms of muffins that weigh a half-pound, pasta bowls that hold more than two pounds of pasta, and movie popcorn containers that holds 16 cups of popcorn with a caloric content of up to 1,000 calories, among many high-caloric food and drink options, contributes to the obesity epidemic. Calorie-dense units of food can result in people eating more calories. If there is one cookie in a package, it would be likely that the consumer eats one cookie; if there are three cookies in a unit package, it is likely that the consumer will eat three cookies. People tend to eat in units; therefore, bigger portions in one unit typically mean that more calories will be consumed. ⁸⁶

Many experts state that environment contingencies, such as palatable foods, are a major contributor to obesity. To examine this hypothesis, a research study examined the response of 12 normal-body-weight subjects who were deprived of food before the study. Positron emission tomography and fluorodeoxyglucose were utilized to measure the metabolic brain changes when food was presented. Food presentation significantly increased (P is less than 0 .01) metabolism in the entire brain, and changes were most notable in the superior temporal, anterior insula, and orbitofrontal cortices. Research results shows a marked increase in brain metabolism when food is presented, and this sensitivity likely contributes to the motivation to obtain food and the obesity epidemic; furthermore, the motivation to seek food may be subjectively experienced as a desire for food and hunger when presented with food stimuli, and palatable and readily available food feeds this motivation. ⁸⁷

A sedentary lifestyle has also increased the rate of obesity. It is estimated that at least 60% of people worldwide do not participate in an adequate exercise program. ⁸⁸ It appears that readily available technology can also contribute to a sedentary tendency. A 2008 meta-analysis found that in 63 of the 73 studies examined (a total of 86% of the studies), the increase in obesity is shown as being linked with increased media exposure, and the rate of childhood obesity proportionally increased in relationship to time spent watching television. ⁸⁹ In contrast, Bouchard states that there is some indication that individual differences in habitual physical activity may be characterized by a significant genetic component. ⁷³

It is not unusual for individuals to remark that they cannot control their eating. The environmental contingencies of overeating cannot be ignored. There is a plethora of fast-food options that feed this appetite. Goodrick adds that overeating is intimately associated with lack of self-control and other factors, such as social influence, food environment, usage of food to mediate negative moods, and a rebound in appetite that can emerge from restrictive dieting. Overeating according to Goodrich does not support the existence of an addiction model of obesity; but he suggests, instead, that overweight and obese individuals demonstrate a lack of self-control in their food consumption. ³⁹

Brownell, in his book Food Fight, concludes that the environmental versus genetic controversy regarding obesity can be illustrated by the fact that our biology seeks out an energy-dense diet, the environment provides it, and the result is a proliferation of obesity. The personal investment costs of poor diet and being sedentary are low, while the investment costs of being active and eating a healthier diet are high. In order to rein in the obesity epidemic, fundamental economic changes and physical activity need to be instituted in everyday life. ⁷⁴

Psychosocial theories of obesity

Stress of an acute or chronic nature has been identified as a factor that may be a driving factor of obesity. Psychosocial stress and weight gain were assessed by analyzing a nationally representative longitudinal sample from 1995 to 2004 of 1,355 men and women in the United States. For both men and women with high baseline BMI, stress was associated with increasing levels of psychosocial stress related to job-related demands (P less than 0.001) for interaction with baseline BMI. ⁹⁰

For children and adolescents, stress appears to be linked to weight issues. Emotional eating may arise from a negative affect. A sample size of 666 middle school students from diverse backgrounds was examined to determine if there is a link between specific emotions or moods and emotional eating. Cross-sectional analyses revealed no gender difference in emotional eating. For boys emotional eating seemed to be driven by confused mood, while for girls emotional eating appeared to be activated by stress, worries, and tension and anxiety. These findings suggest that the implementation of stress reduction techniques may help to promote a more positive affect and decrease emotional eating. ⁹¹

Schachter, a prominent social psychologist, proposed an internal-external model of obesity that overweight people had a different style of eating, dependent on external cues that tell them when and when not to eat. Based on his research, Schachter originally theorized that cognitive and environmental stimuli, not somatic cues, motivate the obese person to eat. ⁹² As his research progressed, Schachter's viewpoint of overeating leaned in the direction of a physiological basis for overeating. ⁹³ Mela states that internal and external cues can trigger the immediate desire to eat or to select a specific food item. It has been found that individual differences in food likes and dislikes develop throughout life. Overweight and obese individuals show a greater tendency to like and consume energy-dense foods. ⁹⁴

Obesity is dangerous: Fact or fiction?

The importance of addressing the health-related aspects of obesity is emphasized by medical research that shows that obesity is dangerous to an individual's health status. ⁹⁵ Specifically, obesity has been linked to several serious medical conditions, such as heart disease and strokes, diabetes, cancer, hypertension, gallbladder disease and gallstones, osteoarthritis, gout, and breathing disorders, including asthma and sleep apnea. ⁹⁶

Obesity rates in China have increased 30-fold in 15 years, and the urban areas of China typically have a higher obesity rate than rural areas. One in five people in the world who are obese are Chinese, and they seem to be predisposed to earlier medical problems related to obesity in comparison to their European and American counterparts. ⁹⁷ Overconsumption has thus superseded malnutrition as the world's number one food problem. ⁷⁴ This is the first time in human evolution that the number of adults with excess weight surpassed the number of those who were underweight. ⁹⁹

Industrialization and urbanization have been identified as factors in the obesity epidemic in the United States. ⁷⁴ In more developed countries during the twentieth century, the genetic potential for height is being reached and individuals are gaining proportionally more weight than height, resulting in an increase in the average BMI. During the 1930s, insurance companies established a positive correlation between weight and life expectancy and they increased the premiums for obese individuals. In the 1950s, Breslow identified that body weights continued to increase in developed countries and that heart and kidney diseases also increased. ⁹⁸

The Centers for Disease Control and Prevention formally stated that obesity is a worldwide epidemic, ¹⁰⁰ and the World Health Organization (WHO) concurs with this statement and adds that obesity is also a public health issue. ¹⁰¹ Efforts need to be made to correct the environmental factors identified as being responsible for the increasing rise of obesity, such as offering federally sponsored healthy meal programs in school, limiting direct junk food marketing to children, ¹⁰² and decreasing the availability of sweetened beverages in the school system. ¹⁰³ Additionally, urban environment planning efforts need to be directed to increase access to parks and to plan pedestrian routes. ⁷⁴

Not everyone agrees that obesity results in negative health outcomes. Many books challenge the health risks of obesity, and one such book, The Diet Myth, states that the association of obesity with increased health risks is unproven and the real issue that is not addressed is the social stigma that obese individuals experience on a daily basis. ¹⁰⁴ Gard labels the obesity epidemic as fictitious and states that obesity is an ideological and moral phenomenon, not a health problem. ¹⁰⁵ The Center for Consumer Freedom (CCF) also challenges the hypothesis that obesity has adverse effects on health. The CCF advocates that the “obesity epidemic” is exaggerated, it is the right of adults and parents to choose what they want to eat and drink, and the consumer is the “king” or the “queen” of their food choices. ¹⁰⁶ It is important to note, however, that the CCF reportedly receives financial support from the food and restaurant industry. ⁷⁴

Food addiction: Fact or fiction?

The conceptual construct of a “food addiction” engenders controversy and debate, and it has been a long-standing and long-rejected phenomenon. The DSM-IV-TR, a manual that provides a list of diagnostic criteria for mental disorders, only recognizes the following eating disorders: (1) anorexia nervosa, (2) bulimia nervosa, and, (3) eating disorder not otherwise specified. ⁵⁶ None of these three eating disorders is listed as an addiction, and currently obesity and eating disturbances are not classified as mental disorders or addictions.

Presenters and committee members of a 2007 “Food and Addiction” conference sponsored by the Rudd Center for Food Policy and Obesity of Yale University have posed the inclusion of “food addiction” in the DSM-V. It is suggested by a contingent of conference members that “food addiction” could qualify as a DSM-V diagnostic entity based on the following clinical criteria: an occurrence of three or more counterproductive food behaviors that persist for a one-year period, such as increases in food consumption, a history of attempts to stymie eating that fail, and the exclusion or neglect of other activities because the food addiction is predominant. A select constituency of the membership involved in finalizing the DSM-V, pending 2012 publication, is reportedly in the throes of determining whether or not “food addiction” qualifies as a diagnostic category. ¹⁰⁷ Volkow and O'Brien remark that the symptoms of compulsive eating and the inability to restrain eating seem to parallel the criteria in the DSM-IV of substance abuse and drug dependence, which suggests that obesity may be considered to be a food addiction. ¹⁰⁸

Despite the DSM-IV-TR not recognizing “food addiction” as a diagnostic entity, numerous research studies have defined this syndrome. There are a multitude of food addiction models that try to specify the etiology of obesity. The addictions model of eating suggests that some features of compulsive overeating mirror aspects of conventional substance addiction. The premise that food consumption can be addictive is controversial; nevertheless, research articles continue to pose this possibility. Haddock and Dill reviewed the literature on the alleged psychoactive qualities of foods; they conclude that the addictions model of eating shares numerous characteristics with substance abuse disorders, but they did not conclude that overeating could be considered an addiction. It has been posed that overeating most likely stems from a combination of abnormal cognitive and neuroendocrine processes. Emotional states have been demonstrated to mediate reward processing. ³⁶

Two major theories purported to support the construct of food addiction are the following: (1) the “thrifty gene” theory established in 1962 suggests that those who have the obesity gene will consume more calories than their bodies need because this is an instinctive response to the possibility of an upcoming famine; and (2) the rational addiction theory poses that overeating fats and simple sugars happens because the individual is trying to avoid the effects of withdrawal from these addictive foods.^109,110 Foods that contain simple sugars and fat serve as a trigger for uncontrolled eating for some individuals. ¹¹¹

An important study of Pima Indians focused upon their consumption of foods high in simple sugars and their subsequent health issues. The Pima Indian group has a much higher incidence than normally found in the general population of morbid obesity and type 2 diabetes. A total of 50% of the Pima Indian adults have diabetes, and an overwhelming majority of these individuals who have diabetes are overweight. This outcome is contended to support two major theories of food addiction: the rational addiction theory and the thrifty gene theory. It is posed that the lower prices of foods high in simple sugars lead to the overconsumption of these foods in the Pima Indian group and other groups, which supports the rational addiction theory. The lower consumption of cheaper, lower-quality foods by non-Pima Indians and higher consumption of foods with simple sugars by the Pima Indian populations support the thrifty gene theory, which appears to be a genome that has essentially remained unchanged for 10,000 years. This theory poses that certain ethnic groups may be more prone to obesity when food is readily available because their bodies have the rare ability to store fat when there is a food scarcity, which aids their survival in times of famine. Stable food supplies confound this tendency and lead to obesity for the Pima Indians in lieu of a food scarcity. The readily available supply of inexpensive food is considered to be a factor related to obesity and exemplary of the rational addiction theory, while some people choosing to primarily eat a healthy low-fat diet is representative of the thrifty gene theory. Exposure to a Western lifestyle and the consumption of foods high in sugar content has led the Pima Indians to have one of the highest obesity rates in the world. ¹⁰⁹ Mounting evidence suggests that ethnic differences in cardiovascular risk are partially mediated by adipose tissue biology. Effort has been dedicated to searching for the genetic markers of thrifty metabolism, and this search will likely continue. ¹¹⁰

In a symposium on whether food addiction is a fact or fiction, it was stated that the ingestion of different nutrients, such as sugars and fats, generally produces different effects on the brain, behavior, and physiology. With respect to eating disorders and obesity, it was posited that fat may be the macronutrient that results in excess body weight, and sweet taste in the absence of fat may be largely responsible for producing addictive-like responses that include a withdrawal syndrome. ¹¹¹

Other research experts contend that obesity is not congruent with the parameters of the addictions model. Haddock and Dill, in their article “The Effects of Food on Mood and Behavior: Implications for the Addictions Model of Obesity and Eating Disorders,” ² question the addictions model of obesity, which suggests that people gain weight because of their dependence on and inability to properly regulate their consumption of certain foods. After their review of the related literature, Haddock and Dill remark that under specific situations, some foods may have minimal effects upon mood and behavior but these effects do not mirror the psychoactive effects of nicotine or alcohol, nor can these foods be considered to be addictive in nature. Therefore, the authors pose that the addictions model of obesity is not likely to be helpful in understanding the complexities of obesity. ³⁶ Goodrick offers additional challenges to the food addictions model. ³⁹ He concludes that overeating is not consistent with the operational definition of an addiction, but nevertheless he believes that the lack of self-control that overeaters experience necessitates treatment interventions. ³⁹ Some researchers conclude that although individuals may believe that they are powerless over their food consumption, this conviction does not confirm that overeating or obesity constitutes an addiction.^40,41

Volkow and Wise say that obesity can stem from compulsive eating, just as an addiction to substances of abuse arises from compulsive usage. Food and drugs are habit-forming, due to the fact that they activate a common brain mechanism, a reward mechanism that when overutilized leads to appetite dysfunctioning. Obesity has been linked with dopamine, which is associated with pleasure and reward, and this is one of the suspected culprits in obesity. The most clearly denoted commonality of the mechanisms of food and drug intake is their ability to activate the dopamine-containing link in brain reward circuitry. When there is impairment in the brain dopamine functioning, compulsive eating can ensue and this can lead to obesity. As this process advances, compulsive eating interferes with other rewarding activities and becomes a primary focus, thereby interfering with the individual's everyday activities, health, and sense of well-being. This state of compulsive eating has addictive-like, powerful reinforcers that can drive eating behaviors. The person who is addicted to drugs or alcohol persists, like the compulsive eater, in his or her quest to ameliorate the discomfort. When the addict's drug of choice is not available or he or she is in the recovery process, the experiencing of withdrawal symptoms is likely. Food, like drugs and alcohol, can be used to treat an addictive affliction. ⁵³

A recent article contends that the evidence for the addictive properties of food is advancing based upon animal model research and human subject research. It is posited that just as drugs can take over the brain, so too food can demonstrate a similar, albeit weaker and less dramatic, effect. The addictive dynamics of substance dependence include tolerance, withdrawal, and loss of control. Clearly, some people report loss of control in their food consumption as a significant contributor to their overweight or obese status. Furthermore, some individuals report failure in their attempts to abstain from certain categories of food, such as fats and sugars, even when they know their actions jeopardize their health status. Repeated failure in attempts to reduce food intake and loss of control over consumption of food are not uncommon dynamics for the obese and overweight individual. ¹¹²

Obesity is gaining recognition as being a neurobiological disorder. The neurobiological mechanism in the understanding of addiction poses that substantial progress has been accomplished in the understanding of the molecular and cellular operations of tolerance, dependence, and withdrawal, but much remains to be learned about the neural substrates of compulsive drug use. A significant element of addiction is the long-lasting risk of relapse, which is frequently activated by exposure to drug-related cues. ¹¹³ There is increasing evidence that compulsive overeating shares commonalities with conventional drug addiction; however, not all overeating behaviors automatically qualify as an addiction. One entity that is congruent with the designated parameters of an addiction is the phenotype of binge eating disorder. Davis and Carter conclude that obesity and addiction are not always intrinsically linked, but the recognition of the similarities provides recommendations for treatment modifications for both conditions. ¹¹³

Additional support for labeling BED, a biologically based subtype of obesity, as an addiction is offered by Carter who concludes after a comprehensive review of the literature that the phenomenon of compulsive eating has striking similarities to conventional drug addiction. ¹¹⁴ A study examining genetic and psychological indicators of hedonic (pleasure-oriented) eating in 66 obese subjects who were determined to have BED indicators and 70 obese subjects without indicators of BED. Three functional polymorphisms related to the dopamine 2 receptor gene as well as the functional A118G polymorphism of the mu-opioid receptor gene were examined in this subject group as well. Analyses of opioid genetic markers and dopamine were conducted since these factors are associated with the brain reward mechanisms. A relevant finding of this study based upon a chi square analysis revealed that BED subjects had significantly higher scores on a self-report measure of hedonic eating. The findings suggest that, as mentioned above, BED is a biologically based subtype of obesity, and it may be influenced by a hyperreactivity to the hedonic properties of food. It is surmised that this predisposition is likely heightened by the highly visible and readily available surplus of sweet and fatty foods in everyday life. ¹¹⁵

Research examining the relationship of dopamine and food intake using positron emission tomography as an examination method with pathologically obese subjects and drug-addicted subjects was conducted. It was found that reductions in striatal dopamine DA D2 receptors were similar in both groups. They postulate that these levels of DA D2 receptors predispose subjects to seek reinforcers; specifically, obese subjects seek the reinforcer of food, and drug-addicted subjects seek drugs as their reinforcer. A review of Wang's neuroimaging studies examines the role of brain dopamine in normal food intake and pathological food intake. The research results found that obese individuals have a reduction of dopamine receptors in conjunction with an enhanced sensitivity to the palatability of food as their most salient reinforcer. This dynamic may place the obese individual at risk for overconsuming food. ¹¹⁶

In 1990, the cDNA for the dopamine D3 receptor was isolated. Studies, thereafter, indicated that D3 receptors as well as D3 receptor mRNA are primarily localized in the limbic regions in mammals. This finding led to the postulation that D3 receptors may be involved in drug addiction and drug dependence. Research examined the effects of various putative D3 receptors selective compounds in animal models of drug dependence and drug addiction. The results indicate that central D3 receptors may play an important role in drug-induced reward, drug-taking’, and cue-induced, drug-induced, and stress-induced reinstatement of drug-seeking behavior. These results have yet to be extrapolated to human subjects according to this 2005 published research study . ¹¹⁷

At the 2007 “Food and Addiction” conference, Volkow focused on neuroimaging, the reward circuitry of the brain, and its connection to obesity. Dopamine, a neurotransmitter, has been denoted as being active in food and drug intake mechanisms; and, related to the motivation to consume both food and drugs, dopamine also plays a major role in the reward system related to food and drug abuse. Based upon current research, Volkow poses that the act of compulsive overeating shares many of the same characteristics as drug addiction. ⁵³

Wilson contends that although eating disorders demonstrate some features of substance use and dependence, there is a lack of data to support classifying eating disorders in the category of addiction based on the following: (1) evidence for carbohydrate craving is lacking; (2) neither tolerance nor withdrawal reactions to food have been clinically substantiated; and (3) independent familial transmission of eating and substance abuse disorders indicates that there is not a single, shared etiological mechanism. ⁴¹

Research continues to be conducted with animal models and human subjects to determine whether or not food addiction is a viable construct. The potentially addictive quality of some sugars has been an extensively explored research area. A comprehensive review of the research literature with laboratory rats supports the hypothesis that the ability to abuse and become addicted to sugar exists as determined by behavioral and neurochemical effects when intermittent, excessive sugar is consumed. The label of food addiction seems plausible because addictive drugs also activate brain pathways that respond to natural rewards, such as sugar. Sugar releases opioids and dopamine, and this may lead to an addictive potential. The evidence supports the hypothesis that under certain circumstances laboratory rats became sugar dependent, and these findings may be transferable to humans, based upon the research literature results on disorders and obesity. ¹¹⁸

The 2007 “Food and Addiction” conference states that dopamine has an important role in the overall reward systems, and bingeing on sugar everyday on a consistent basis produces dopamine. A comparison between sugar and fat bingeing upon animal models found that the ingestion of these two substances produces different effects on the brain, behavior, and physiology. Bingeing episodes release excessive dopamine, which is comparable to the effects of drugs of abuse upon the brain. The question of whether or not sugar could be implicated as promoting a “food addiction” was suggested for some sugar substances because of the addictive-like behaviors that sugar creates, including a withdrawal syndrome that was observed. ¹⁰⁷

Popular media have a history of suggesting that one can become addicted to sugar, particularly chocolate. A comparison between 16 “chocolate addicts” and 15 control subjects found that in the presence of external chocolate cues, those designated to be “chocolate addicts” reported greater cravings, voiced more negative affective states, and also ate more chocolate than the control subjects. Heart rate and salivation were measured in the presence of external chocolate cues for both the control group and the “chocolate addict” group, and self-report measures on body image, depression, eating attitudes, and behaviors were assessed. A relationship was found to exist between chocolate addiction and problem eating, in that chocolate addicts demonstrated more abnormal eating patterns and were found to be significantly more depressed than the control subjects. These research findings suggest that “chocolate addicts” may be considered to be on a plateau with drug addicts, in respect to their “chocolate addiction,” because of their marked craving for chocolate, aberrant eating behaviors, disturbed eating attitudes, and marked depression in comparison to the control subjects. ¹¹⁹

Pelchat examines the concept of food addiction and offers the following observations: (1) healthy-weight individuals do not suffer from food addiction; and (2) overweight and obese persons could be considered to be suffering from food addiction, since palatable and nonpalatable foods become desired and overconsumed. She adds that it may be the manner in which the food is consumed rather than the sensory properties that lead to an addictive pattern of eating. ¹²⁰ Corwin and Grigson concur that food can have addictive-like properties, especially sugar and fats, because of their neuron-changing qualities. These highly palatable foods can become associated with a restriction–binge pattern and can lead to addiction because of how they are consumed. ¹²¹

Gold says that there is no definitive diagnostic category known as “food addiction”; however, he voices that some foods may be more “addictive” than others, because of their brain reward factor. He adds that eating too much food, despite the consequences; being preoccupied with food; trying to reduce food intake; and feeling guilty about the overconsumption of food have the components of a substance dependence or addiction. ¹²²

Wilson reports that while eating disorders exhibit similar features to substance abuse and dependence, this does not validate that eating disorders are an addiction. ⁴¹ He adds that clinical evidence for “carbohydrate craving” is sparse and a consistent association between eating disorders and substance abuse and dependence remains unfounded. Goodrick poses that the current food environment, social influences, and the use of food to mediate negative affective states may lead to overeating but not necessarily a food addiction. ³⁹

In the 2007 “Food and Addiction” conference, a major question addressed was “Can food addiction be considered a meaningful concept?” To answer this question, clinical observations with scientific evidence were presented with an emphasis upon the connection of food to chemical, physiological, and psychological dependence. Some of the findings reported included the following: (1) the existing research on food addictions shows striking similarities in the withdrawal and usage patterns of sugar and classic drugs of abuse; (2) the reciprocal relationships found among food and other substances, such as alcohol and nicotine, indicate the possibility that food and addictive substances compete for the same brain pathways; (3) the continuum of behavior related to addiction ranges from tolerance to withdrawal; (4) the possibility of food addiction is plausible considering it fits into the continuum paradigm of addiction and can lead to weight gain; (5) the body of scientific evidence points to food and food components as being possibly addictive; (6) the increased incidence of a “food culture” and plentiful food environment supports overeating; and (7) the influence of marketing is seen in food choices and the amount of food consumed. ¹⁰⁶

In 2009, an article in the Journal of Addiction Medicine states that the evidence for stating that food has addictive qualities is accumulating as shown by research results with animal models of research and human subjects. Just as classic drugs of abuse activate the brain, certain foods seem to have a similar, albeit weaker, effect on the brain. ¹²³ Gold states that some foods appear to be more “addictive” than other foods. ¹²²

In the process of trying to establish whether or not food addiction meets the diagnostic criteria of dependence, it is important to state that some people experience a loss of control over food consumption, experience repeated failures in trying to reduce food intake, and incur failures in attempts to abstain from certain types of food. Some evidence exists to support the label of food addiction, but further research is necessary to examine tolerance and withdrawal properties to high-fat sweets; time spent in obtaining, using, and recovering from excess food consumption; and the effects upon activities of daily living. ¹²³

Pelchat, who focused upon the specific area of food craving, critically examined whether or not the premise of food addiction is a fact or fiction. Her review of the literature was prompted by a desire to provide a more comprehensive understanding of the neural mechanisms that underlie food cravings. Studies on the effects of neurotransmitters on ingestive behaviors and drug cravings, neuroimaging studies on drug and alcohol cravings, and neuroimaging studies on feeding and the chemical senses were examined.

After reviewing this information, Pelchat advocates that palatable food is not the cause of obesity since even non-palatable food can be overconsumed. She advanced the following hypotheses: (1) there are common brain mechanisms for food and drug cravings, (2) these brain mechanisms may have evolved to promote the seeking of natural rewards, and (3) palatable foods are not causing the problem of obesity since non-palatable foods can be desired and overconsumed. Pelchat concludes that the manner in which food is consumed, such as alternating availability and food restricting, may lead to an addictive eating pattern. Meanwhile, the availability of low-cost, high-fat, high-carbohydrate food has exponentially multiplied. Genomes have changed little, if at all, over an extended time period, while obesity has reached epidemic proportions. Genes that were favored under conditions of food scarcity have now become a liability in cultures where highly refined foods are overconsumed. ¹²⁰ Healthy, normal-weight individuals generally do not have a food addiction, but overweight and obese people could meet the clinical criteria of an addiction. ¹¹⁹

The categorization of food as being addictive in nature is debated in a comprehensive review of this topic in the book Food as a Drug by Poston, Poston, and Haddock. Although the authors do not conclusively state food addictions exist within the addictions model concept, they advise that food addictions as a viable construct can be utilized to provide effective treatment for patients who are experiencing obesity or eating disorders. ¹²⁴

It is expected that the controversy of whether food addiction is seen as a viable entity will continue, and whether this potential diagnostic category is included in the 2012 DSM-V remains to be seen. An operational definition of food addiction would likely include the following components: (1) a style of compulsive eating; (2) an obsession with body image; (3) an obsession with weight; (4) an obsession with food, indicated by cravings and a preoccupation with obtaining food; (5) an overusage of food for pleasure and comfort; and (6) a lack of ability to monitor food intake. ¹⁰⁷

Besides the issue of determining whether food has addictive properties, the DSM-V committee has another issue to tackle: defining the terms addiction versus dependence. These terms are often interchanged by the public and in research studies, but they are not equivalent entities. During the 1980s, the DSM-III-R committee struggled with the label of addiction since it could be viewed as a pejorative term that could lead to further stigmatization of people with substance abuse disorders. ¹⁰⁷

Dependence, which is defined by the experiencing of withdrawal symptoms when the drug is discontinued, was judged to be a more neutral term, and this term was chosen for inclusion in the DSM-III-R. At the last meeting of the committee, which was debating the addiction versus dependence labeling, the term dependence was chosen over and to the exclusion of addiction by one vote; thus, addiction was not included as an entity in the DSM-III-R. The DSM-V committee is currently attempting to decide how to remediate and address the harm that occurs when, for example, pain medication is withdrawn or withheld from a patient or stopped by a patient because of a fear of becoming “addicted” when, in fact, the patient may become dependent, which is a normal physiological process that occurs when medication is repeatedly given. Some members of the committee deciding if addiction should be included in the DSM-V pose that the exclusion of the term addiction in this next manual could further contribute to a patient not getting proper treatment. ¹²⁵

Characteristics of food addiction

Signs of a food addiction may include the following:

Eating to alleviate negative emotions, such as stress

One of these signs does not automatically constitute a food addiction; however, the endorsement of several signs may indicate dysfunctional eating, which unrecognized and untreated could have serious, deleterious effects upon the individual's health.

Cross-addiction: Fact or fiction?

Having one addiction does not provide an immunity status from adding on another addiction. WLS does not cure eating issues, nor does it eliminate the emotional underpinnings of unhealthy eating. Although many patients acknowledge that WLS is “just a tool,” sometimes people are looking for a cure for their eating dysfunctions and emotional difficulties. Being cut off from a readily available and reliable source of support, namely, food, for some WLS patients can lead to a conscious or unconscious search for a substitute. In this state, the patient may be vulnerable to an unhealthy substitute, or a cross-addiction: one compulsive behavior is exchanged for another compulsive behavior, and a cross-addiction emerges. In the case of the WLS patient, overeating or bingeing may no longer be an issue; instead, the patient may be abusing alcohol or another substance.

The phenomenon of cross-addictions or addiction transfers has been explicated in the media and in the scientific literature. On July 18, 2006, a Wall Street Journal article, “The New Science of Addiction,” reported that GBS patients were experiencing a higher than average incidence of addictive issues than the general population. At U.S. Bariatric, a weight loss surgery center, therapists estimated that approximately 20% of the WLS patients acquired new addictive behaviors. Moorehead estimated that about 30% of WLS patients struggle with new addictions after surgery, but she acknowledges that further studies on cross-addictions need to be conducted before firm conclusions are drawn. ¹²⁶

On October 24, 2006, an episode of Oprah entitled “Suddenly Skinny” warned that after GBS, patients often experience alcohol absorption quicker than their pre-surgery absorption rate. Furthermore, it was stated that some patients have an “addiction transfer” that occurs when an individual exchanges one addiction for another, such as exchanging a food addiction for an alcohol addiction. In the case of morbidly obese patients who have had GBS, binge eating, a prior dysfunctional eating behavior, may be transferred to an alcohol addiction. The Oprah show concluded that up to 30% of GBS patients have struggles with alcohol. ¹²⁷

Not everyone agrees with the construct of cross-addiction, however, and Philip Schauer voices his opposition to the premise that cross-addictions are a side effect of WLS. Schauer, who is president of the Society for Bariatric Surgery and director of the Bariatric and Metabolic Institute at Cleveland Clinic, says that only about 5% of all WLS patients develop a new compulsive behavior, such as alcoholism or compulsive shopping, and there is no established causal link between WLS and the development of a compulsive behavior. ¹²⁸

Sogg advocates that addiction transfer or cross-addiction is not an accepted scientific phenomenon and that there is a lack of credibility in the belief that an untreated symptom, such as a food addiction, will reemerge in another symptom, such as alcohol abuse, unless the psychological rationale for the original problem is resolved. There is insufficient evidence to unequivocally state that WLS increases the risk of substance abuse or addictive behaviors. ¹²⁹

While many experts dispute the phenomenon of cross-addictions as a serious side effect linked to GBS, other experts recognize substitute addictions or cross-addictions as being the fallout that may occur after GBS.^{130,131,132,133} It is speculated that when an addiction is not quelled, symptom substitution or a cross-addiction can arise.

When an individual is suffering from a “hunger disease,” attempts to eliminate this “hunger” may take the form of compulsive usage of substances, such as food, alcohol, technology, or gambling. When the preferred drug of choice is not available, one or more activities, persons, behaviors, or objects may be compulsively used. For example, when food is no longer available as the drug of choice, the loss of this self-medication, may, for example, lead to an increase in alcohol usage for some WLS patients.

Various studies suggest that disturbed eating patterns are prevalent among women in treatment for alcohol issues. ¹³⁴ Sussman and Black define cross-addiction as any addictive behavior that accomplishes at least one key function formerly achieved by the ingestion or usage of another addiction. ¹³² This new addictive behavior might result in the induction of pleasure, excitement, or relaxation, or in the reduction of a negative affect. ¹³³ Schaef proposes that a typology of substance addictions exists that involves the direct manipulation of pleasure through the ingestion of substances (such as alcohol, nicotine, heroin, and the overeating of food) or overspending, among other substances of abuse. ¹³⁵

The risk of cross-addictions when terminating an addictive behavior is recognized by the millions of participants in 12-step programs such as Alcoholics Anonymous (AA), Narcotics Anonymous, and Overeater's Anonymous. This risk is called 13th stepping, which refers to the tendency to replace a preferred drug of choice with another addictive substance or behavior. Replacing a food addiction with an alcohol addiction or a dysfunctional relationship are examples of 13th stepping or a cross-addiction. ¹³⁶

The 12-step programs can sometimes serve as a cross-addiction or the “drug of choice” for its participants, dependent upon the individual's level and ferociousness of commitment. Conversely, it has been suggested that the 12-step programs can be a reasonable treatment option.^137,138 Vaillant, in his discussion of the AA program, questions if AA offers a cure or a cult group. He concludes that AA helps in the process of relapse prevention by providing external supervision, new caring relationships, increased spirituality, and a substitute dependency. This substitute dependency is another name for cross-addiction when taken to the extreme; nevertheless, AA has been found to be equal to or better than other conventional treatment methods for alcoholism. ¹³⁹

Biblically based, self-help groups such as Weigh Down attempt to have overeaters reconnect with God as a means of addressing their weight issues. Weigh Down, like AA, has been labeled with a cult-like status that can evolve to a cross-addiction. Shamblim advises that women substitute their hunger for food with a hunger for God ¹⁴⁰ to the extreme that this substitution can evolve to the status of a cross-addiction. Adherents to the Weigh Down Program challenge this labeling and state that their participation in this group has changed their life for the better. In contrast, Oliver has written a book, Fat Politics: The Real Story behind America's Obesity Epidemic, which insists that the Weigh Down Program, like other similar women-based programs, has a sexist tinge and is one of several “evangelical diet plans” based on “guilt” that advocates submission not just to God but also to one's husband. ¹⁴¹

It has been advanced that specific foods, especially foods rich in fat or sugar, are capable of promoting addictive-like behaviors and neuronal change under certain conditions. These highly palatable foods are not addictive per se, but become so because of a restriction–binge pattern of consumption. The ingestion of foods that contain fats and sugars generally produces different effects on the brain, physiology, and behavior. When these substances are taken in excess amounts known as binges, compensatory changes that are comparable to drugs of abuse can emerge. These binges can result in excessive dopamine release comparable to the effects of drugs of abuse. ¹¹⁹

When food is no longer a dominant reinforcing feature of the WLS patient's existence, a replacement of an unhealthy constituency may emerge. Underlying psychological conflicts may reemerge, and a cross-addiction may be activated. Depression, anxiety, fear, and stress can occur as food recedes into the background as a maladaptive coping mechanism, and WLS patients may employ alcohol, gambling, overspending, sex addiction, eating disorders, or excessive exercising or Internet usage, among other dysfunctional behaviors, as a substitute, and a cross-addiction or symptom substitution may become established. ¹⁴² In a cross-addiction, the initial addiction may be suppressed and a new addiction may be expressed. The opponent–process theory helps to explain the process that can occur when this cycle happens. In this theory, there is an emotional pairing of pleasure and pain in drug addiction. Initially, there is a high level of pleasure from the drug usage and a low level of pain. With the continuance of the drug usage, pleasure decreases and the level of pain increases, thereby encouraging the continuing usage of the drug to avoid withdrawal. ¹⁴³ The WLS patient has to permanently change his or her relationship with food, and this can result in a withdrawal-like reaction, which may set the stage for a cross-addiction. Using food as a coping mechanism is suppressed, and the addition of a cross-addiction could be expressed.

Kay Sheppard states that for certain individuals, refined carbohydrates can trigger the addictive process and the effects can lead to depression, among other psychological difficulties. ¹⁴⁴ Sheppard concludes that for some people, food can be as addictive as alcohol.

Cross-addiction: Exchanging food for alcohol?

The National Center on Addiction and Substance Abuse at Columbia University published a groundbreaking, comprehensive study that examined the correlation of substance abuse and eating disorders. This three-year study found that up to 50% of individuals with eating disorders also abuse alcohol or drugs compared with 9% of the general population, and up to 35% of substance abusers have an eating disorder compared with 3% of the general population. Based on the results of this extensive research study, the following directive was given: if an eating disorder coexists, and if substance abuse is present, assess whether or not an eating disorder is present. ¹⁴⁵

A personal struggle with a cross-addiction from food to alcohol is shared by Carnie Wilson, signer, television star, and gastric bypass patient, in her book I'm Still Hungry: Finding Myself through Thick and Thin. Carnie Wilson readily admits and recounts that after her GBS, she found that her history of an eating disorder led to an alcohol addiction, saying that she exchanged her food addiction for an alcohol addiction. Specifically, she recounts that she was aware that the recommended limit of alcoholic drinks for the gastric bypass patient is two drinks per week or less, but she drank much more alcohol than the recommended amount. Wilson acknowledges that she moved from food to alcohol, and she was in the throes of a cross-addiction. ¹⁴⁶

A mixture of science and popular media regarding cross-addictions occurred following the aforementioned Oprah presentation entitled “Suddenly Skinny,” which suggested that some WLS patients transferred from food to alcohol as their drug of choice. ¹²⁷ Based on the information provided in “Suddenly Skinny,” John Morton and his associates decided to conduct a study on GBS patients and their alcohol usage. Morton, who is director of bariatric surgery at Stanford University, states that he was inundated with questions from past, current, and potential WLS patients about the information shared on the “Suddenly Skinny” segment, which linked GBS with alcohol abuse. These questions led Morton, who has performed over 1,000 gastric bypass surgeries, to examine 19 GBS patients who had GBS at least one year ago and 17 control subjects who were drawn from the general population and had not had GBS. The control subject group had a mean age of 37 and a mean weight of 150 pounds, while the GBS group had a mean age of 47 and a mean weight of 201 pounds. Subjects in this research, after not eating anything for 2 hours, were asked to drink 5 ounces of red wine within 15 minutes. Once consumed, all subjects had an alcohol breath analysis every 5 minutes until their level registered a zero. The GBS patients had a peak alcohol level of 0.08 percent versus the 0.05 percent for the control subjects (P = .004). The GBS patients needed an average of 108 minutes to reach zero, while the control subjects needed an average of 72 minutes (P = .001). For GBS patients, the alcohol level peaked higher and lasted longer. Morton stated that GBS patients seem to have a susceptibility to alcohol because GBS allows alcohol to bypass the stomach, which is one of the two places where alcohol dehydrogenase, the enzyme that metabolizes alcohol, is present. By bypassing the stomach, due to GBS, Morton said the ability to metabolize alcohol is minimized. ¹⁴⁷

Morton presented these research results at the June 14, 2007 annual meeting of the American Society for Bariatric Surgery. The research findings were presented under the following cautionary banner for GBS patients who consume alcohol: (1) GBS patients should never consume one alcohol drink and drive; (2) GBS patients should be aware that one drink of alcohol can be metabolized quicker and the effects last longer than their pre-surgical drinking of one drink of alcohol; (3) GBS patients may find that they become more social as they lose weight, and this could result in more exposure to alcohol and more drinking; (4) GBS patients have a fundamentally altered alcohol metabolism, whereby there is a reduction of the enzyme alcohol dehydrogenase; (5) GBS patients need to be aware that usage of alcohol leads to a decrease in the lower esophageal sphincter tone, and gastric emptying increases, potentially allowing for the consumption of more food; (6) GBS patients in this study did not typically report recognizable feelings of warmth or euphoria, which could signal the overconsumption of alcohol; (7) GBS patients seem to have a longer and quicker response to the alcohol consumption; (8) GBS patients may drink more alcohol to get the same subjective experience they obtained from alcohol consumption prior to GBS; and (9) GBS patients might be at risk for experiencing an “addiction transfer” in which they substitute binge eating, an issue for many GBS patients, for an alcohol addiction. Morton concludes that although the study was small, a power analysis shows that the sample was sufficient to detect a measurable difference in how GBS patients are affected by alcohol versus non-GBS patients. ¹⁴⁸

The significance of Morton's findings on the effects of alcohol upon the GBS patient and the implications have been examined by Philip Schauer. Schauer acknowledges that WLS produces profound changes in patients, and he states that only about 5% of WLS patients develop a compulsive disorder. Furthermore, Schauer says most bariatric centers exclude patients who have problems with alcohol dependency from having weight loss surgery. ¹²⁸

Neil Hutcher, director of surgery at Bon Secours St. Mary's Hospital in Virginia and past president of the American Society of Bariatric Society, states that Morton's study was a small, inconclusive study that lacks scientific validity since breath analysis was used instead of directly analyzing blood alcohol levels. Furthermore, Hutcher added that an automatic presumption that GBS patients are in danger of becoming alcoholics or incurring any other type of addiction is not supported by the results of the study. ¹⁴⁹ The results of several other studies suggest that sensitivity to blood alcohol level (BAL), peak BAL after drinking, and the elimination of blood alcohol are not correlated with family histories of alcoholism.^25,26

Contrasting research results to the findings offered by Morton were found in a study that examined the relationship between obesity, overeating, and addiction. It was hypothesized that drugs of abuse compete with food for the rewarding sites of the brain. A total of 298 female subjects' medical charts were examined in a pre-bariatric evaluation. A detailed summation of alcohol use, abuse, and dependence history was present in these medical records. A significant (P is less than .05) inverse relationship between BMI and alcohol usage was determined. Specifically, the more obese the subject, the less alcohol she consumed according to the medical record information. Overall, the subject pool of 298 women had a lower rate of alcohol usage than found in the general population. A tentative conclusion of this study is that overeating competes with alcohol for brain reward sites and results in alcohol having less reinforcing properties. ¹⁵⁰

The results of a study of 9,125 men and women subjects, labeled as a nationally representative sample of U.S. adults, indicated that obesity is associated with an approximately 25% decrease in the odds of developing a substance abuse disorder and an approximately 25% increase in the odds of developing anxiety and mood disorders. ¹⁵¹

A comprehensive research study examining the usage of alcohol by WLS patients was conducted 6–10 years after surgery. Subjects completed the Post-Bariatric Surgery Appearance Questionnaire, and the results of the analysis revealed that a statistically insignificant percentage of the research sample developed spontaneous alcohol abuse or dependence. The researchers pose that additional research is necessary to further establish or negate the risk of alcohol abuse and dependence for WLS patients. ¹⁵²

It has been found that gastric bypass surgery may enhance alcohol sensitivity by quickening the rate at which alcohol is absorbed into the bloodstream or metabolized, as supported by the research results of Morton and his research team. ¹⁴⁷ A website questionnaire designed to assess post-operative changes in alcohol consumption and effects was presented in the October 2007 issue of the Bariatric Times. A total of 318 responded to this questionnaire, and it was found that 28.4% of the gastric bypass patients said they had issues with alcohol, while only 4.5% of this population reported that they had alcohol control issues prior to their WLS. ¹⁵³

From 1998 to 2005, weight loss surgeries quadrupled and there has been a 900% increase in these surgeries for patients between the ages of 55 and 64. ¹⁵⁴ Typically, compliance with post-bariatric WLS recommendations has shown that weight loss will occur, but the weight of unresolved psychological issues may continue. This burden may translate to a cross-addiction, such as alcohol abuse or alcohol dependence.

Cross-addictions: Identifying the risk factors

As a healthcare provider, you are intimately involved in the victories and struggles of bariatric patients who have elected to have weight loss surgery. You bear witness to the dramatic changes and multiple costs that constitute the price of success. Some of the obvious costs that patients incur come in the form of saying goodbye to the ongoing emotional comfort that food used to provide; exercising when it would be preferable to just sit and read the newspaper; eating enough protein and following the food plan outlined by the registered dietician; continuing to attend and participate in regularly scheduled appointments with the nurses, doctors, and other members of their bariatric team; and attending the local bariatric support group. All of these changes, and many more, represent essential building blocks that provide a beginning foundation for healthy living for the WLS patient.

Sometimes, even when patients are making considerable progress in their everyday lives, healthy newly established habits start to short-circuit. Underneath the guise of apparent success, irrefutably proven by the patient's weight loss, there is evidence to suggest that the WLS patient is slightly “modifying” his or her diet plan, increasing intake of pain pills, reintroducing cigarettes back into the daily life plan, working more and more hours, exercising to the point of exhaustion, drinking alcohol until feelings of being “tipsy” are experienced, or shopping, shopping, and more shopping without respect to budgetary concerns. The patient underplays and labels his or her changes as “minor,” but an intensive assessment process alerts the healthcare provider to the contrary. An underlying addiction or a cross-addiction may be brewing, and the patient's defensive responses may indicate this issue.

Questioning patients about the adjustments that they are introducing into their program may result in a nonchalant reaction that this is “no big deal” and they are just “customizing” their program to fit their individual needs. Further rationalizations may flow forth as patients reiterate that they are continuing to lose weight and everyone comments on how great they look. Clinical observations suggest that some people experience a food addiction that, left untreated, can lead to a cross-addiction in which there is a transference or substitution of any other addiction for the old addiction. The knowledge that a cross-addiction or the substitution of unhealthy behavior is a genuine possibility for the WLS patient is essential for the identification of addictive risk factors.

Cross-addiction risk assessments

Impulsivity is associated with risk taking, and it is characterized by a person's tendency to engage in spontaneous, unpremeditated behaviors. It is speculated that individuals who are impulsive are more likely to engage in risky behaviors. ¹⁵⁵ Impulsivity is also related to self-control in the conditional sense that it is expected that high impulsivity is linked with low self-control and low impulsivity is linked with high self-control. Sensation-seeking behavior seems to be linked with risk-taking behaviors. The pursuit of novelty of an intense nature is sought by the sensation seeker. Addictions involve impulsivity, dysfunctional self-control, and sensation-seeking behavior. ¹⁵⁶ Loss of control has been identified as being a characteristic of addiction. In a study of bariatric WLS patients, it was found that 46% of post-operative patients reported a loss of control when eating, and these patients also showed significant post-operative weight regain, after maximum weight loss, than patients who did not voice a loss of control. ¹⁵⁷ A review of the influence of binge eating on WLS outcome was conducted by searching PubMed and MEDLINE through April 2006 for related articles. Many of the subjects who binged before the surgery endorsed that they felt a loss of control when eating small amounts of food after surgery. It was found that pre-surgical WLS patients who had a binge eating disorder were more likely to retain the eating pathology and have poorer surgical outcomes. ¹⁵⁸

In addition to risk-taking behaviors, it is important to identify any mental health issues the WLS patient may be experiencing. Evidence-based guidelines on the psychological and behavioral screening of WLS candidates and the impact of psychosocial factors on behavior change after GBS were developed after an examination of 198 abstracts from 1980 to 2004. A total of 17 papers were examined in detail. The members of the Behavioral and Psychological subgroup of the Multidisciplinary Care Task Group conducted searches of MEDLINE and PubMed for publications related to WLS, behavior changes, and mental health, including quality of life (QOL) and behavior modification. The results indicated a high incidence of depression, negative body image, and eating disorders, and low QOL in morbidly obese patients. Rates of anxiety and depression were three to four times for obese individuals what they were for leaner individuals. The task subgroup recommended that all WLS candidates have a psychological assessment evaluation to determine their psychological level of functioning prior to WLS. ¹⁵⁹

It is important to have a structured assessment process to aid in the discovery of any underlying addictions. To begin a risk assessment, the following steps are recommended: first, prior to meeting with the patient, it will be important to review the patient's initial psychological evaluation, if one has been conducted. If a psychological evaluation is within the medical record, make a notation of any history of drug or alcohol usage, mental health issues, food issues, or any other addictive behaviors. An identification of the patient's psychological assets and liabilities that could influence treatment progress may be helpful for the healthcare provider to have to aid the patient during his or her recovery process and to identify potential compliance issues. Additional clinical information will likely include the patient's history and other pre-surgical WLS evaluations that can be instrumental in customizing the patient treatment process.

Second, while performing a review of the medical chart, identify if any risk factors exist for cross-addictions. Any of the risk factors listed below may signify that the patient is at a heightened risk for cross-addictive or dysfunctional health behaviors.

Risk Factors Influencing Successful Weight Loss Surgery

History of addiction(s)

Healthcare workers will sometimes alter the recommended bariatric treatment program to fit their perceived needs. Since these individuals often have some medical knowledge, they may be at risk for overextending this knowledge in the belief that they can make adjustments to their program without severe consequences. Shift workers may have irregular eating patterns due to the hours they work, and this may impact their ability or willingness to follow a prescribed bariatric treatment program.

Third, once the meeting with the bariatric patient begins, take this opportunity to gather additional information regarding an endorsement of any of the potential risk factors for cross-addiction or dysfunctional health behaviors that were identified by the review of the medical chart. Knowledge of the patient's strengths and liabilities can help the healthcare provider to formulate relevant questions, assess the accuracy of the patient's responses, and identify potential risk factors that indicate cross-addictive or dysfunctional health behaviors.

While in the process of conducting the assessment of the WLS patient's level of emotional functioning and addictive risk, establish an atmosphere that encourages psychological safety denoted by the provision of direct eye contact, empathic listening, and open-ended questions. Stop, look, and listen to the patient's verbalizations and nonverbal communication, and identify and explore if there is an occasion when the patient hesitates or avoids answering a posed question. These reactions, among others, may denote that a cross-addiction or dysfunctional health pattern exists. It is also important to determine if the patient believes that WLS will provide a magical cure for his or her problems or the patient expects that WLS will easily lead to fast, long-term weight loss without much effort. Either one of these premises will be counterproductive to the pursuit of healthy weight loss.

Cross-addictive potentiality questionnaire

The following ten questions are designed to identify the likelihood of cross-addictive potentiality or dysfunctional health patterns:

Do you have a prior history of any addictive behaviors?

A response of yes to any of the ten prior question merits further investigation.

Fourth, in the current and ensuing clinical appointments, the following questions can serve as a working template to determine if a cross-addiction is occurring and to assess the patient's level of treatment program compliance. Please ask the patient to respond to the following statements during the appointment, or if time is limited, ask the patient to complete this inventory and bring it back to the next session to review.

Post-Surgical Weight Loss Surgery Inventory

_____ I use food, alcohol, or other substances to help me cope with everyday stresses.

Any response of true to the quiz indicates that there is a risk of non-compliance with the bariatric treatment program. When reviewing the patient's responses to this assessment tool, remember that one response of true along with the accompanying repetitive dysfunctional habits and behaviors could lead to health problems, a reoccurrence of a buried addiction, or the addition of a new cross-addiction.

The following three recommendations will help to elicit the patient's cooperation in elaborating upon the associated parameters of any yes responses. First, it continues to be essential to establish an atmosphere of safety that promotes communication. Asking questions about the patient's expectations and compliance with his or her bariatric treatment program can engender stress, particularly if the questioning procedure is delivered in a rapid-fire and judgmental manner. It can be helpful to begin the risk factor assessment with a leading statement, such as “Some weight loss patients find that following their weight loss program recommendations is harder than they expected, so I would like to ask you some questions to see how you are doing … ?” This general approach provides an opening for the patient to share his or her concerns. Second, it is important to ask the patient to elaborate on any answers that indicate or endorse a response of yes. Additional information can provide the health caregiver with data that can aid in the process of customizing treatment interventions. Third, it is necessary to provide the WLS patient with an educational basis that can be utilized to help the patient identify early warning signs of non-compliance with the post-operative WLS program. A patient who is armed with the knowledge that underlying addictions may arise or cross-addictions can occur may be able to identify early warning signs of impending trouble.

Utilizing the information you have collected to date regarding your patient's bariatric treatment program compliance and comparing the responses of your bariatric patient within the paradigm that defines substance abuse and substance dependence can be accomplished by determining if the patient's clinical profile shows any of the following attributes: (1) emotional, and sometimes physical, dependence on the substance; (2) failure to meet major obligations; (3) dysfunctional habits and behaviors; (4) denial of these dysfunctional habits and behaviors; (5) recurrent social, interpersonal, or legal problems; (6) inordinate amounts of time spent in obtaining the substance; (7) continual use of substance despite adverse consequences; and (8) unsuccessful efforts to decrease the substance. ³⁶

Offering self-monitoring as an intervention can help offset the “lifelong threat” of weight regain following any WLS. It is surmised that behavioral components have a modulating role in weight regain. To test this hypothesis, 1,117 post–Roux-en-Y gastric bypass (RYGB) patients who were one or more years post surgery were given a survey. A total of 203 surveys (24.8%) were returned, completed, and judged to be suitable for analysis. Baseline data, which included, demographic information and the pre-operative Beck Depression Inventory (18 scores), were abstracted from the patient's medical records. Pre- and post-operative well-being scores were also compared. The independent predictors of significant weight gain were increased food urges, decreased post-operative well-being, and concerns over alcohol or drug usage indicated by a significance level of P = .01. A total of 15% of the subjects reported significant weight regain, which was defined as an increase of 15% or more from the nadir. Identified predictors of significant weight regain after RYGB patients include the following: (1) increased food urges, (2) severely decreased post-operative well-being, and (3) concerns over drug or alcohol usage. Importantly, self-monitoring was identified as a preventive-like factor in regaining weight post surgery, and self-monitoring appears to be associated with decreased weight regain (P = .01). ¹⁶⁰

A lack of self-monitoring can provide a pervasive platform of vulnerability that allows and may encourage the practice of addictive behavior that can compromise the success an individual achieved in his or her efforts to quit a dysfunctional habit. ³⁰

A significant study investigating the characteristics associated with frequent self-monitoring of one's weight and the relationship between weight loss maintenance and self-weighing was conducted. A sample size of 3,003 subjects who were members of the National Weight Control Registry, had lost 30 pounds or more, kept this weight off for one year or more, and had completed the self-weighing frequency assessment at baseline participated. These subjects completed self-report questionnaires at the initial phase of participation and at a one-year follow-up. It was found that 36% of the successful weight loss subjects weighed themselves daily, and overall 79% of the subjects weighed themselves at least once per week. The results of the study suggest that frequent self-weighing appears to be associated with better weight loss outcomes, and it may be instrumentally helpful with long-term weight loss maintenance. Self-monitoring appears to be an active component associated with weight loss success. ¹⁶¹

Every meeting with the WLS patient provides an opportunity to gather information regarding the patient's treatment compliance and the related triumphs and difficulties. As treatment progresses, it is important to have patients make a transition from totally relying on their healthcare providers for their weight loss success to taking on more and more responsibility for their treatment outcome. An essential intervention in helping WLS patients make this transition is self-monitoring. The acquisition of this skill by patients enhances their active participation in their recovery program and reinforces their progress. Teaching patients how, when, and why it is essential to add self-monitoring to their armature is a gradual endeavor that can be addressed in each session. Elucidation and amplification of the self-monitoring process can be accomplished by utilizing examples that patients provide regarding their progress. If the patient mentions that certain foods, even though they are allowable on the treatment program, cause indigestion, the patient can be directed to make a list of foods that are difficult to digest and then be instructed to identify healthy substitutes. Another frequent example voiced by WLS patients is that they are losing weight slower than they expected or have reached a weight plateau. Asking the patient to keep a food journal and conducting a comparison with the recommended WLS surgery nutritional plan can be an illuminating experience for the patient and an effective self-monitoring technique. Self-monitoring necessitates an active involvement by the WLS patient, and this process can enhance treatment success.

With the institution of self-monitoring comes the decay of debilitating and destructive denial, and the stage is set for the beginning of positive changes. Addictions and dysfunctional health behaviors thrive in dark, unexplored, and unacknowledged regions. By giving your patients the tool of self-monitoring, in addition to their “tool” of having had WLS, patients can identify and treat their dysfunctional behaviors, thereby increasing their chance of having a successful WLS outcome. Self-monitoring appears to be an important component of becoming and continuing to be a successful WLS patient.

The “Self-Monitoring Guidelines for Weight Loss Surgery Patients,” in the next section, can provide a pathway for patients to abandon the psychological and physical weight of denial and provide an active mechanism for integrating functional behaviors into their everyday lives. Once the assessment process has been completed, providing patients with a list of interventions to monitor their WLS progress can help in the identification and possible prevention of addictive or dysfunctional health behaviors. The following list of interventions shared with WLS patients can enhance their recognition of personal compliance issues, and steps toward recovery can begin.