Is food addiction a valid phenomenon through the lens of the DSM-5?

Recent literature has seen a rise in interest in the phenomenon of food addiction. Nolan (2013) highlighted that Medline has had a sevenfold increase in the number of papers indexed by the term food addiction since 2008. However, a lack of consensus regarding the entity of food addiction and whether it constitutes a ‘true’ and valid addiction pervades.

Clearly the ideology of food addiction and its accompanying nosological status (if such a status should exist) has vast implications. Especially in the context of the current global epidemic of overweight and obesity with its associated health, psychological, economic and social consequences, as logically food addiction would be a significant aetiological factor fuelling this epidemic (Lindberg, et al., 2011).

This viewpoint seeks to briefly highlight the debate regarding whether food addiction is a ‘true’ and valid addiction, through the lens of the recently released DSM-5 (American Psychiatric Association, 2013). Firstly, the status of food addiction as a ‘true’ addiction in relation to the DSM-5 generally will be discussed, before moving on to a discussion of food addiction in relation to the nosology of substance use.

Is food addiction a ‘true’ addiction: Through the lens of the DSM-5 generally?

The DSM-5 introduced the first non-substance related addictive disorder namely Gambling Disorder, as well as including Internet Gaming Disorder as a condition warranting further study (American Psychiatric Association, 2013). The inclusion of these non-substance related, behavioural or process addictions is noteworthy in the context of food addiction, as food addiction is considered by some to be a behavioural addiction akin to gambling and internet gaming disorders (Zhang et al., 2012). Thus the inclusion of such a disorder for the first time sets the foundation for the potential future inclusion of food addiction, providing further support for the validity of the concept.

Readers of the DSM-5 that are familiar with the food addiction literature, may be left wondering why food addiction was excluded based upon the rationale for the inclusion of Gambling Disorder; espoused in the introduction to the substance-related and addictive disorders chapter (American Psychiatric Association, 2013). Specifically, that gambling activates the same reward and motivation pathways as drugs of abuse.

In regards to food addiction there is copious research indicating the neurological overlap that exists between drugs of abuse and the ingestion of hyperpalatable food stuffs both in the animal model and human research (Avena et al., 2012; Nolan, 2013; Volkow et al., 2013; Zhang et al., 2012). Most recently Volkow (2013) recounted that drugs of abuse are known to impact upon the same neuronal pathways that regulate the motivation to seek and consume food, and that in both obesity and drug addiction the dopamine pathways are disrupted.

Conversely others such as Zaiuddeen and Fletcher (2013) oppose the notion of food addiction being a behavioural or process addiction and instead being comparable to a substance addiction (Zaiuddeen and Fletcher, 2013). Moreover Zaiuddeen and Fletcher (2013) question the validity of the food addiction concept noting that there are inconsistencies in human studies of the phenomenon. That, in their opinion, does not support an addiction model of food addiction or a model denoting altered neural reward mechanisms in obesity at the present time; with further research being necessary to validate the entity at the neurobiological level.

Is food addiction a ‘true’ addiction: Through the Lens of the DSM-5 substance use nosology?

The following section briefly discusses the validity of food addiction as it relates to each of the four broad categories of substance use criteria espoused in the DSM-5.

The criteria pertaining to impaired control refer to a general lack of control relating to regulating the use of the substance, as well as the new DSM-5 addition of craving (American Psychiatric Association, 2013).

In regards to food addiction the substance is clearly food, however it is not foods that are high in nutritional value that are implicated; rather it is energy dense hyperpalatable food stuffs such as chips, lollies, fast food, soft drinks, etc. In naturally occurring foods, the concentration of carbohydrate, fat and sodium are balanced with other macronutrients and micronutrients that are important for health. However, with the artificial development of many of these products containing high concentrations and combinations of sugar, fat, and salt, individuals may be attracted to seek large amounts of these hyperpalatable, refined foods.

This is clearly apparent with the association between the rise in hyperpalatable food stuffs and the growing rates of obesity that are well documented (Allen et al., 2012). As well as research demonstrating that overweight and obese individuals display a strong preference for hyperpalatable and energy dense food stuffs (Allen et al., 2012; Lennerz et al., 2013).

Recently Lennerz and Colleagues (2013) conducted a clinical trial investigating the effect of high versus low glycemic index (GI) shake meal replacements with palatability controlled for; on the neurological activity of obese men in the postprandial period. They found that men who consumed the high-GI shake displayed greater activation in the brain areas associated with reward and craving than those who consumed the low-GI shake. These findings are significant as this striatal activation combined with the physiological consequences of a high-GI meal produced strong cravings for high-GI food and stimulated the cycle of overeating.

Conversely from an evolutionary perspective; humans may seek out energy dense foods and binge-eat in order to maximise energy stores to prepare for periods of famine (Gearhardt et al., 2009). Thus the drive to consume energy dense food stuff may not stem from the addictive properties of the food and the addictive predisposition of the individual but rather an innate ancestral drive.

The criteria relating to social impairment refers to the addiction impacting upon the major role obligations of the individual as well as leading to a reduction in other activities thus creating social and interpersonal problems. While the criteria pertaining to risky use relates to continued use of the substance despite physical and psychological problems (American Psychiatric Association, 2013).

In comparison to other substance use disorders; food addiction may not have as strong an impact upon the social functioning of individuals. As all individuals need to eat to survive and food (including hyperpalatable food stuffs) is both legal and socially acceptable. Further, many social events are planned around food. Thus from this perspective food addiction may not be a ‘true’ and valid addiction. However, the secondary impact of food addiction, namely obesity, can lead to social withdrawal and isolation due to the stigma associated with obesity (Allen et al., 2013; Gearhardt et al., 2009).

Furthermore, the health consequences of obesity and the continued use of the substance (hyperpalatable food stuffs) despite significant physical consequences, has the potential to heighten the impairment of the individual coupled with potentially lethal health implications. Although, the development of nutrition related chronic health issues such as obesity are multifaceted, it is important to recognise the role that food addiction might play. Dopamine, the primary neurotransmitter of addiction, has a site-specific action to both regulate the intake and reinforce the effects of food. Studies suggest that disruptions in dopamine production and/or structure may predispose individuals to addictive behaviours and obesity (Liu et al., 2010).

Obesity related health impairment has been widely studied to determine morbidity and mortality. Obesity has also been investigated in order to determine the impact on health related quality of life (HRQL), which considers measurable changes in health parameters, disease status, costs of care and medical/health-related outcomes from a patient perspective. The literature demonstrates a strong dose dependant relationship between higher degrees of obesity and greater functional impairment, as well as, significant detriments to wellbeing (Fontaine and Barofsky, 2001).

The pharmacological criteria specified by the DSM-5 are tolerance and withdrawal. The notion of tolerance refers to the need for increased amounts of the substance in order to achieve the desired effect (American Psychiatric Association, 2013). In relation to food addiction research has indicated the development of tolerance both in the animal model and in humans as evident through reductions in dopamine (Allen et al., 2012; Lui et al., 2010; Wang et al., 2001). Wang and Colleagues (2001) found that the availability of the dopamine D2 receptors was significantly decreased in obese individuals in comparison to controls. This reduction may contribute to overeating in order to achieve the same effect upon the neural pathways associated with reward as normal weight controls. However, it is unclear whether this disruption in dopamine receptors results initially from overeating or some other factor.

The concept of withdrawal is defined by the physiological and psychological effects that occur when the use of a substance is ceased or an alternative substance is consumed in order to negate these effects (American Psychiatric Association, 2013). In relation to food addiction results from the animal model demonstrate neurochemical changes associated with withdrawal from hyperpalatable food stuffs (Allen et al., 2012; Gearhardt et al., 2009). While evidence from humans remains largely anecdotal; withdrawal symptoms including agitation, insatiable cravings, fatigue, headaches, palpitations, poor mood and cold sweats have been reported (Allen et al., 2012; Gearhardt et al., 2009). As nutrition is the human energy source, it is difficult to differentiate withdrawal symptoms from the normal drive for consumption; thus it is difficult to delineate whether food addiction is a ‘true’ and valid addiction.

Conclusion

In summary it is apparent that there is compelling evidence for the notion of food addiction as a ‘true’ addiction. Conversely it seems premature to make a definitive conclusion about the validity of the phenomenon; as validity ultimately depends upon an understanding of the aetiology of the condition (Phelps, 2008). However, Phelps (2008) ascertains that the primary justification of a diagnostic system is its utility; this is especially pertinent in relation to food addiction with the continually rising rates of obesity internationally and the associated health consequences.

From a nosological perspective the phenomenon of food addiction relates to the underlying criteria of addiction espoused in the DSM-5. This is evident in the relationship between food addiction and the concept and rationale for the inclusion of a non-substance use disorder; as well as the diagnostic criteria of substance use disorder. With the change away from considering withdrawal and tolerance as essential features of dependence, food, akin to substances of abuse now meets the ideology of addiction.

Other factors such as the denial of both the severity and the presence of disorder, along with the loss of allaying negative affect the use of the substance once had, also highlights the potential for food to be addictive. Moreover the social isolation, secretiveness, craving and maintenance of problem behaviour (excessive eating of hyperpalatable food stuffs) despite the adverse consequences similarly corresponds to the criteria of addictive disorders. Thus food addiction should be seen as a ‘true’ addiction while requiring further research to delineate the aetiology of the condition and subsequently verify the validity of the disorder. As the utility of such a diagnosis has the potential to assist with circumventing the current obesity epidemic and the associated consequences.