Obes Facts. 2012;5(2):165-79. doi: 10.1159/000338310. Epub 2012 Apr 19.
Albayrak O1, Wölfle SM, Hebebrand J.
Abstract
Classification of Chemical (Substance) Addiction
The medically established forms of addiction pertain to substance use disorders. The National Institute on Drug Abuse [4] provides the following definition: ‘Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences’. In Chapter V ‘Mental and Behavioral Disorders’ of the International Statistical Classification of Diseases and Related Health Problems, 10th Revision (ICD-10; World Health Organization, 1992 [5]) ‘Mental and Behavioral Disorders due to Psychoactive Substance Use’ (F10-F19) constitute one of the ten major diagnostic categories. ICD-10 specifically refers to mental and behavioral disorders (see table 1). In the second frequently used psychiatric classification scheme termed Diagnostic and Statistical Manual of Mental Disorders (DSM), 4th Edition, Text Revised (DSM-IV-TR), published by the American Psychiatric Association (APA) in 2000 [6], ‘Substance-Related Disorders’ also represent one of the major diagnostic categories. According to both classification schemes each substance-related disorder is subdivided into major clinical states (table 2; see table 3 and table 4 for the respective DSM-IV classification criteria). The symptoms of intoxication and withdrawal can differ by substance as can the physical and psychological consequences of substance use.
DSM-V [7] will replace the current DSM version (DSM-IV-TR) in 2013; currently different workgroups are discussing how to best categorize and operationalize mental disorders and their criteria as based on current empirical findings. After extensive discussions of the word ‘addiction’, the DSM-V Substance Use Disorders Workgroup has proposed to tentatively re-title the previous category Substance-Related Disorders with Addiction and Related Disorders [8]. The use of the word ‘dependence’ is now limited to physiological dependence, which is a normal response to repeated doses of many drugs and medications. If appropriate, medical treatment with prescribed drugs entails tolerance and/or withdrawal symptoms; these are not to be counted for the diagnosis of substance use disorder. Importantly, the DSM-V Substance Use Disorders Workgroup recommends combining abuse and dependence into a single disorder of graded clinical severity to be termed Substance Use Disorder, with two criteria required to make a diagnosis (table 5). This recommendation was, among other factors, based on problems differentiating abuse from dependence and the lower reliability of the DSM-IV diagnosis Substance Abuse. The current DSM-IV abuse and dependence criteria can be considered to form a unidimensional structure, with abuse and dependence criteria interspersed across the severity spectrum [8].
As illustrated by the discussion within the DSM V Substance Use Disorders Workgroup, classification of psychiatric disorders is subject to change reflecting advances in empirical findings. In the first edition of the APA’s Diagnostic and Statistical Manual of Mental Disorders (1952) [9], alcohol and drug abuse were grouped under Sociopathic Personality Disturbances, which were considered to result from deeper psychological disorders or moral weakness. Over the past 60 years we have witnessed the medicalization of addiction to the two major legal (nicotine and alcohol) and all illegal drugs. Thus, the biomedical concept of addiction as underlying excessive use of nicotine or alcohol has in itself led to the delineation of the respective substance use disorders with tremendous implications for the societal perception of these addictions, their treatment, direct and indirect health care costs, and prevention. The medicalization was, among other factors, boosted by the realization of the dire medical consequences of nicotine and alcohol dependency. Efforts of for example the tobacco industry to negate or mitigate the risks of smoking-induced diseases such as lung cancer and cardiovascular disorders are well known; the influence of the tobacco industry on policy is ongoing [10]. Accordingly, understanding how corporations influence policy therefore forms an essential part of public health research into addictions to legal drugs [11].
Classification of Behavioral Addiction
The term behavioral addiction has more recently been invoked; it has as yet not gained official recognition in medicine: Thus, neither ICD-10 nor DSM-IV-TR includes a respective diagnostic category. Psychiatrists and psychologists have been somewhat reluctant to systematically delineate and classify such disorders. We believe that several factors contribute to this reluctance:
i) The recent history of substance use disorders indicates that the transition from the concept of a behavioral problem as representing a personal flaw to that of an addictive disorder takes time; the process requires both a discussion and merging consensus within medicine and society as a whole.
ii) There is a general reluctance to medicalize and even more so to psychiatrize addictive behaviors, because they can be viewed as partially representing the extreme end of quantitative distributions of time spent pursuing everyday behaviors. Thus, the delineation of distinct disorders requires the definition of threshold or cut-off criteria. In contrast to chemical addiction, the intake of a specific substance, which can readily be verified (i.e., determination of concentrations of diverse drugs and/or their metabolites in serum and urine), is not required. Obviously, soft cut-offs for such disorders would result in high percentages of the population fulfilling the diagnostic criteria for the respective behavioral addiction disorders. Such individuals would then be eligible for a diagnostic evaluation and treatment potentially entailing high costs to national health care systems.
iii) Similar to the situation for legal drugs, the respective behaviors are pursued by a high percentage of the population, thus entailing difficulties at both the individual and societal levels to perceive quantitatively excessive behaviors as disorders. It is difficult to appreciate that some individuals who over-engage in specific activities can be seriously functionally impaired in their daily lives.
iv) Modern technologies and media with their easy access account for some of the ‘behavioral addictions’ (internet) or greatly facilitate them (internet based access to pornographic websites). As such, the problem of their excessive use is rather new and rapidly developing into novel directions; research accordingly lags well behind in comparison to that into substance use disorders.
v) Over-engagement in specific activities is frequently encountered in different psychiatric disorders, which are not considered within the realm of addiction. For example, excessive gambling or internet use may appear within the context of a major depressive episode or an obsessive compulsive disorder; accordingly, the excessive behavior appears to be a symptom or epiphenomenon of the underlying disorder. One view posits addictive behavioral disorders as lying along an impulsive-compulsive spectrum, with some classified as impulse control disorders [12].
The DSM-V Substance Use Disorders Workgroup [8] has recently proposed that the diagnosis of Pathological (Disordered) Gambling (table 6) be reclassified from Impulse-Control Disorders Not Elsewhere Classified’ to the novel category Addiction and Related Disorders [13]. Pathological (Disordered) Gambling was judged as having commonalities in clinical expression, etiology (including genetics), comorbidity, physiology, and treatment with Substance Use Disorders, thus warranting this reclassification [e.g. [14,15]. This proposal indicates a crucial turning point in the official psychiatric conceptualization of this disorder, which is additionally accompanied by the renaming of the diagnostic category. Currently, pathological gambling is to be the only behavioral addictive disorder within the novel DSM V diagnostic category ‘Addiction and Related Disorders’. However, this re-classification will undoubtedly boost research and discussions as to the delineation of additional behavioral addictions within this diagnostic category.
Table 6
Proposed DSM V criteria for pathological (disordered) gambling within the new diagnostic category addiction and related disorders [8]
Addiction can be defined as an abnormal tolerance to and dependence on something that is psychologically or physically habit-forming [16]. Behavioral addiction implies the continued involvement with an activity despite the negative consequences associated with it; pleasure and enjoyment would have originally been sought, however over a period of time involvement with the activity is needed to feel normal [17]. Accordingly, the respective activities have an addictive potential (e.g. gambling, internet, computer games, work, exercise, sexual activity, overeating), some of which pertain to natural homeostatic needs (e.g. eating). A behavior that can function both to produce pleasure and to provide relief from internal discomfort is pursued in a pattern characterized by i) recurrent failure to control the behavior (powerlessness) and ii) continuation of the behavior despite significant negative consequences (unmanageability) [15]. The terms that are used to characterize an addictive disorder are ‘dependence’ and ‘compulsion’. Dependence involves a repetitive pattern of behavior that aims to achieve a pleasurable internal state via gratification of needs. In the terminology of learning and behavior theory, the process by which dependence gratification motivates behavior is termed positive reinforcement. Compulsion involves an attempt to evade or avoid an unpleasant/aversive internal state (e.g. anxiety, grief, guilt, shame, rage). This corresponds to a negative reinforcement paradigm, whereby negative consequences are roughly taken into account. Among the distinguishing features of addictive disorders is this combination of gratification and escape from internal discomfort. Hence, the concept of addiction represents a synthesis of dependence and compulsion [15].
Obesity
Obesity is an exceedingly complex disorder, which evidently requires an environment that promotes a high energy intake and/or a low level of physical activity. In societies with diverse, tasty, cheap, and readily available foods a genetic predisposition is presumably also required to put on excess weight. The heritability of body weight is high – it is assumed that 50% or more of the variance of the BMI in the general population can be explained by genetic factors. However, currently known polygenic loci only explain a small percentage of the BMI variance [42,43]. Overeating implies an energy intake in excess of energy expenditure. Individuals with a low resting energy expenditure and/or a low physical activity level can overeat and thus gain weight despite intake of normal portion sizes. In many obese individuals excess weight gain occurred over prolonged periods of time; accordingly, obesity rates in young adults are substantially lower than in middle-aged adults [44,45,46,47,48]. If for example the daily energy excess is a mere 20 kcal, relative body weight will increase slowly over the life span [45]. Reference to addiction as an explanation for the common occurrence of this type of obesity seems totally inappropriate. Addiction also cannot readily be inferred as an explanation for the well-known difficulties of maintaining weight loss after a diet. Renewed weight gain largely results from physiological adaptations, including increased appetite and hunger and a reduced energy expenditure as a reaction to a prolonged curtailment of energy intake. Psychological health and long-term behavior monitoring characterize those individuals who successfully maintain a reduced body weight [49.]
Due to the insight we have gained into regulation of food intake and body weight, it is difficult to draw a line between food addiction and a biologically driven increased appetite or hunger. Thus, leptin-deficient patients show food craving, withdrawal, and overeat from infancy on [50]; their behavior throughout the day centers on seeking and ingesting food. They would obviously fulfill criteria for a diagnosis of a substance use disorder (table 7) except for the fact that their addiction applies to food in general, and not to a specific ingredient, substance, or ‘chemical’.
Mutations in the melanocortin receptor 4 gene have also been found to result in overeating [51], albeit to a lesser extent than in leptin-deficient subjects. Potentially, polygenic effects also add up and entail an increased appetite/hunger, overeating, and the development of obesity. If due to genetic or other reasons (e.g. hypoxia entailing brain damage, brain tumor) appetite/hunger of a human is in the uppermost range of the normal distribution, this could render his/her reward system particularly dependent on the input of the neuropeptides, neurotransmitters, and hormones involved the regulation of eating behavior. As such, ‘addictive behavior’ could ensue.
Currently, bulimia nervosa (BN) and binge eating disorder (BED), which will presumably receive the status of a formal eating disorder in DSM V [52], are the only psychiatric disorders which have features that bear resemblance to addiction (see table 7 for proposed DSM-5 diagnostic criteria for BED). The core features of these eating disorders are based on binge eating episodes associated with the subjective experience of a lack of control. However, in contrast to patients with BED, counter-regulation (e.g. purging) is a prominent feature of BN [7,53]. In clinically ascertained BED patients obesity is common. However, the association with obesity is diluted in the community; according to an epidemiological study, only two thirds of BED subjects were obese [for review see [53,54]. Other types of aberrant eating behaviors such as night eating and grazing have been described, which can potentially be viewed within the context of addiction. The current classification scheme DSM-IV-TR however only allows the diagnosis of an Eating Disorder Not Otherwise Specified for BED and other disordered eating patterns of clinical significance. It is of interest to discuss implications of classifying BED as a form of addictive behavior in DSM-V. This would encourage researchers to investigate more extensively the overlap with addiction and to apply therapeutic principles, which are more commonly used in addictive medicine [33].
The excessive overconsumption of palatable foods and fluids as seen in binge eating episodes may be indicative of an underlying neurobiological process similar to that seen in addiction [55,56]. This conclusion is drawn from a growing body of evidence that substance-related disorders and obesity both share common neural mechanisms [57]. Thus, in obese rats, hypofunctionality of the reward system occurs due to a blunted dopamine transmission in the reward center of the brain following high-caloric excess, which leads to compulsive-like eating in such rodents [58]. These maladaptive behavioral responses in obese rats likely arise from diet-induced deficits in striatal dopamine D2 receptor signaling. Overconsumption of drugs of abuse similarly decreases striatal dopamine D2 receptor density, induces a profound state of reward hypofunctionality, and triggers the emergence of compulsive-like drug-taking behaviors [59,60]. Similarly, human imaging studies have shown that obese subjects may have impairments in dopaminergic pathways that regulate neuronal systems associated with reward sensitivity, conditioning, and control [61]. But currently it is unclear if these findings are indicative of predisposing factors or represent the consequence of overeating.
The release of endorphins upon excessive exercise [62] reveals that the general term chemical addiction by itself does not necessarily require the substance to be an exogenous chemical. If endogenous ‘chemicals’ can be addictive in specific circumstances and/or in thus predisposed individuals, such neural mechanisms may represent a link between drug and behavioral addiction. The link of appetite, hunger, satiation, and satiety with the reward system can be viewed as the basis for the development of addictive eating. Even individuals who overeat despite not being hungry trigger alterations in complex central regulatory systems, which in theory could suffice to initiate and maintain addiction. The respective psychological cues could encompass boredom, perceived stress, a negative mood, and the like. Nevertheless, it should be clearly pointed out that, in light of the absence of an operational definition of food addiction, it is currently not possible to evaluate its validity and reliability as a diagnostic category. It is thus premature to consider food addiction within the psychiatric diagnostic classification systems. Studies are required to precisely delineate the symptoms, associated psychopathology and response to treatments [33].
We have mainly discussed food addiction as a subtype of behavioral addiction. However, because the term ‘food’ refers to a heterogeneous composite of a variety of dietary components, be it natural nutrients (e.g. fat, sugar) or synthetic food additives (e.g. preservatives), it is critical for the understanding of the nature of the underlying processes pertaining to food addiction to investigate whether these single nutrient components in itself display reinforcing behavioral properties and thus bear the possibility to lead to neurobiological alterations in the reward system, equivalent to substances of abuse such as heroin, cocaine, alcohol, or nicotine. As such, the nutrient component ought to be absorbed in the oro-gastro-intestinal tract itself or as a direct metabolite cross the blood-brain barrier and unfold its reinforcing effects via activation of the reward system. Indeed, various animal studies center on the effects of sugar on the mesolimbic dopamine projections from the VTA to the NAcc which is implicated in reinforcement functions [63] and attributed to display an incentive effect on the motivation in the process of getting addicted [64]. Extracellular dopamine in the NAcc increases after intake of drugs that are abused [65,66]. Rats intermittently food-deprived and fed with 10% sucrose dilution and chow develop a binge eating behavior. Similar to the intake of drugs, these rats release extracellular dopamine in the NAcc, every time they binge sugar (i.e., sucrose), whereas this dopamine response upon sugar feeding is blunted in control animals fed ad libitum sugar and chow [67]. Intermittent intake of 25% aqueous glucose and chow in rats revealed behavioral and neurochemical signs of opioid dependency [68,69].
The aforementioned animal studies used glucose or sucrose with chow in combination with intermittent food deprivation. Although these experiments could point toward the addictive potential of sugar, unlike in drugs of abuse, there is no evidence for a specific chemical structure of a nutrient unequivocally leading to neurobiological mechanisms underlying addiction. Excluding studies based on intermittent food deprivation, we are not aware of a series of animal studies, albeit human trials, that repeatedly demonstrated a defined nutrient component with a given chemical structure to cause changes in the reward system similar to those described for drugs. Humans who excessively overeat usually do not continuously resort to a single food molecule or a specific monotonous diet; diets rich in carbohydrates and/or fat contain multiple ingredients.
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