Till startsida
University of Gothenburg
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Does Food Addiction Exist?

The concept that people might be addicted to food has been widely touted in the popular press and wider media by way of (partial) explanation of some interactions with contemporary palatable foods, the overconsumption of calories, and the attendant onward march of the obesity epidemic in the developed world. However, this is an area of considerable scientific controversy, with many international scientists being uncomfortable with the casual manner with which the terminology ‘food addiction’ is bandied about. This brief article attempts to explain some of the background knowledge that has seen this concept take hold, and why we should probably be cautious in how we attach this label and discuss this issue and its implications. This is still an area of active research effort, as exemplified by the funding from the European Union for the current ‘NeuroFAST’ research programme, which was designed to expand the evidence base for or against food addiction and answer the question “Does food addiction exist?”. The scientific content of the NeuroFAST project reflects the common ground in terms of neurochemical pathways and brain regions between eating behaviour, including eating disorders, and addiction biology.

What is beyond dispute is that the growing obesity epidemic is driven by over-consumption of calories relative to energy expenditure. The evidence strongly implicates processes beyond homeostatic energy balance, i.e. the matching of energy intake and energy expenditure, in this over-consumption, with the rewarding properties of palatable food appearing to over-ride purely energy demand-led processes. It is the engagement of palatable food with reward systems within the brain, with similarities in mechanism, molecule and anatomy to responses to addictive chemicals, that underlies the food addiction concept. For example, brain imaging studies in obese or drug addicted individuals have shown similar activation patterns when subjects are exposed to palatable food or drugs of abuse.

Many of the neural signals involved in addictive behaviour also appear to be active in food reward. Naturally occurring opioids in the brain (including endorphins, enkephalins, dynorphins, and endomorphins) play an important role in neural reward processes that can lead to addictive behaviour. Both homeostatic and reward-based feeding mechanisms involve opioid peptide systems and opioid receptors, and opioid receptor blockers (antagonists) inhibit consumption of both addictive drugs and palatable food. Clinical trials targeting opioid receptors have revealed weight loss potential for opioid antagonists in obese patients. These relationships suggest the existence of a form of opioid-related addiction focused on palatable foods, although there are still major gaps in our knowledge of the molecular mechanisms through which opioids influence the hedonic properties of food. The dopamine system in the brain is also involved in obesity and meal feeding, with changes in dopamine D2 receptors in obesity. Similar changes in these receptors are also observed with substance addiction, and may precede changes in behaviour, although it is premature to conclude that common mechanisms determine emotional food dependency and chemical addiction. Brain activity at a regional level is differentially influenced by the perceived palatability of food and in response to food ingestion.

One of the primary issues of concern in the use of the term ‘food addiction’ relates to the current circumstantial evidence in support and how this compares to the medically-recognised forms of addiction that categorise substance use disorders. The latter are specific conditions with distinct definitions and diagnostic features. The medically-established psychiatric classifications of substance abuse are enshrined in the Diagnostic and Statistical Manual for Mental Disorders (DSM IV; American Psychiatric Association), recognised by psychiatrists and scientists worldwide as the standard reference work for the classification of mental health disorders. The Manual is currently under revision. This proposed revision (DSM V) suggests replacing the previous category “Substance-Related Disorders” with “Addiction and Related Disorders”, which may allow the diagnosis of behavioural addictions for the first time. This change is supported by the broad overlap in psychological characteristics between so-called ‘chemical’ and ‘behavioural’ addictions, and the common properties of addictive substances or activities. An integration of overeating into substance use disorders, under the current criteria, would imply a form of chemical addiction for which an evidence base does not exist, whereas there is evidence to suggest that food addiction might be viewed as a specific form of behavioural addiction in a subgroup of obese individuals. Currently, addictive-like behavioural patterns such as pathological gambling (a likely addition to DSM V), kleptomania or pyromania, are classified as impulse control disorders. Food addiction, however, is not included. It is almost certainly inappropriate to invoke food addiction in the gradual accumulation of excess weight gain over prolonged periods of time that characterises the development of overweight and obesity in the majority of the population so affected. In contrast to such marginal overeating, clinically significant and regular overeating i.e. abnormal eating behaviour (currently classified as eating disorders) does warrant consideration as ‘food addiction’. However, although eating disorders such as binge eating disorder (BED) have characteristics that more closely resemble addiction, they do not always lead to obesity.

A summary of the arguments for or against a convergence between overeating and drug and alcohol addiction may assist the reader in forming their own opinion. Palatable food is appealing to us because it activates reward centres in the brain, triggering signalling molecules in the opioid and dopamine systems. These same systems are triggered when we use drugs or alcohol. This food activation of the brain is likely to have developed through our evolution – where the instant energy high sugar foods give the body, and the density of energy fat gives the body, made these dietary components of choice. In morbid obesity we see changes, for example, in the dopamine systems in the brain which are similar to the changes in the dopamine system of a person who is addicted to drugs or alcohol. Conversely, we have to eat in order to survive – food is not a lifestyle choice that can then be avoided, although many people will have first hand experience of permanently changing their diet. Whereas drugs and alcohol are made of just one identifiable chemical molecule, foods are made of a mix of hundreds or thousands of different chemicals, making direct comparison problematical. Importantly, to date, there is no scientific evidence for a single nutritional compound or mixture of compounds, exerting addictive-like behaviour, as nicotine, alcohol or heroin would. Eating behaviour itself is a complex combination of internal and external factors. Eating behaviour that might resemble addictive behavioural patterns observed in substance dependency could well be the result of dysfunctional coping strategies and therefore the result of learning, rather than a substance-driven form of behavioural addiction.

Currently, the greatest behavioural and neurobiological similarity between an abnormal food consumption behaviour and drug addiction exists in Binge Eating Disorder (BED), which is prevalent within the obese human population. Even this conservative interpretation of the status of food addiction requires further development of the evidence base, which will likely involve both study of appropriate volunteer and patient groups, and animal models from the drug addiction and feeding fields. In the event that food addiction is established in the future as a route to overeating, binge eating or obesity, even in a small subgroup of individuals, and is classified in similar terms to drug or alcohol addiction, this could result in changes in clinical treatments and in public policy surrounding the obesity epidemic.

Public engagement
Page Manager: Erik Schéle|Last update: 12/4/2012

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