Food Addiction

Policy Position

FDF supports the findings from recent scientific reviews[i] [ii]which show that the current body of evidence does not demonstrate that people can be addicted to food, either as specific nutrients (with the exception of caffeine) or combinations of ingredients in foods; nor that ‘food addiction’ is responsible for the prevalence of obesity witnessed globally.

The causes of obesity are multifactorial and demonising individual ingredients and food groups does not help consumers to build a realistic approach to their diet. The key to good health is a balanced and varied diet in the context of a healthy lifestyle that includes plenty of physical activity.

This is supported by Public Health England’s recent review of the evidence in Sugar Reduction: The evidence for action.


The theory of obesity being caused by ‘food addiction’ has been growing in popularity recently, both in the media but also in scientific literature. There has been particular focus on the notion of sugar addiction, in part due to some evidence of sugar dependence in rat models (where the feeding regimes were highly controlled and not comparable to human feeding patterns) Given the differences between human and rat brains (including the lack of executive control in the decision-making process of rats), it is unclear how relevant these models are to the study of human obesity or ‘food addiction’.

Recent reviews on the topic indicate that addiction to a specific nutrient (with the exception of caffeine), does not exist in humans. A NeuroFAST report suggested that ‘addictive-like eating behaviours’ could be displayed towards foods (with a focus on behaviour rather than specific food components) but this is a relatively new theory.

The word addiction is commonly used and is often taken to mean little more than people assigning a high priority to a particular activity (such as never missing an episode of their favourite TV programme). Medically however, scientists no longer use the term addiction – preferring to use ‘substance-related and addictive disorders’ (Diagnostic and Statistical Manual of Mental Disorders 4th Edition [iii](DSM-5), which is sub-divided into ‘substance-related’ and ‘non-substance-related’ disorders. They also differentiate between physical and psychological dependence. Currently the only ‘non-substance related disorder’ recognised within the medical profession is gambling disorder.

Most of the scientific research undertaken to date on ‘food addiction’ is based on the notion that food addiction and drug addiction share behavioural and biological traits. Two theories for the underlying mechanism of ‘food addiction’ have been put forward, and are discussed in more detail below:

  1. Foods activate the same reward pathways in the brain as addictive drugs and thus may be considered as addictive substances;
  2. ‘Food addiction’ is a behavioural phenotype seen in some obese people which manifests itself as binge eating and this resembles the same patterns witnessed in drug addiction.

1) Food Activates Reward Pathways

Food is essential to survival and the brain has systems in place to ensure there is sustained motivation for eating. Dopamine is released within the brain when food is consumed, producing sensations of pleasure and satisfaction which encourage the behaviour of eating[iv].

Substances which have addictive properties also stimulate the release of dopamine and for this reason, the theory has been put forward that food could be considered an addictive substance. However, dopamine release in response to food is the normal response to a component essential for survival and addictive drugs hijack these natural reward pathways.

A WHO report[v](2004) recognised that dependence-producing substances differ from conventional reinforcers (e.g. food) in that their stimulant effects on dopamine release are significantly greater. Food increases dopamine levels in the brain by 45% whereas amphetamine and cocaine increase dopamine levels by 500%. In other words, the effect of food on dopamine release is ten times less that of these drugs. This would therefore not support the theory of food as an addictive substance. These findings are backed by a summary of results from neuroimaging studies which explored altered brain responses to food-related stimuli (e.g. images) and actual food stimuli in people with obesity or altered eating patterns and which showed no consistent results that could be interpreted as food addiction[i].

It has also been hypothesised that it is specifically processed foods that are addictive because they have nutrient profiles that are not found in naturally-occurring foods i.e. they are high in fat, sugar or salt. However, this classification of processed versus non-processed foods is very general and to date there is insufficient evidence to label any food (with the exception of caffeine), ingredients, micronutrient or combination of ingredients as addictive.

2) Obesity, Binge Eating and Addiction

A second theory which has been put forward is that the characteristic pattern of behaviours displayed by people with substance dependencies (as defined by the DSM-5) are similar to behaviours shown by obese people.

Whilst some criteria from the ‘substance dependency’ definition can be applied to overeating, others, in particular tolerance and withdrawal, are not observed in human studies of eating. Any overlap is limited and as such, a profile of obesity which resembles a ‘substance abuse or addictive disorder’ has not emerged.

A narrower view of ‘food addiction’ in obesity is that it may represent a subset or sub-type of individuals with binge-eating disorder (BED), which consists of repeated binges of uncontrolled consumption of large amounts of food. However, the presence of BED is not always accompanied by obesity; and obesity is not always accompanied by binge-eating episodes.

NeuroFAST consensus opinion on food addiction

Researchers at NeuroFAST (the Integrated Neurobiology of Food Intake, Addiction and Stress, a large multidisciplinary research project looking into the neurobiological and socio-psychological causes of overeating and substance use disorders) met in February 2013 to discuss addiction in the context of food intake and to develop a common consensus.

After a thorough discussion of issues related to the potential existence of food addiction as a disorder, the research group agreed on the following consensus statements:

  • Current evidence does not allow us to conclude that a single food substance via a single specific neurobiological mechanism (e.g. specific brain receptors or specific neuronal pathways) can account for the fact that people overeat and develop obesity.
  • In humans, there is no evidence that a specific food, food ingredient or food additive causes a substance based type of addiction (the only currently known exception is caffeine which via specific mechanisms can potentially be addictive). Within this context we specifically point out that we do not consider alcoholic beverages as food, despite the fact that one gram of ethanol has an energy density of 7 kcal.
  • Addictive (over)eating is clearly distinct from substance use disorders that cause addiction via specific mechanisms (e.g. nicotine, cocaine, cannabinoids, opiates etc).
  • An addiction-like eating behaviour may, in rare instances, be caused by mutations in single genes which entail an elevated feeling of hunger and reduced satiety.

The researchers also highlighted that food addiction cannot be diagnosed according to any set of criteria which have gained general medical or psychological recognition with the result that the term ‘food addiction’ appears inappropriate (although a recent review[vi] postulated that certain behaviours surrounding eating could become addictive in some individuals under specific environmental conditions – for this sub-group the term ‘addictive-like eating behaviour’ may be more appropriate).


In summary the current body of scientific evidence does not support the theory for physical addiction in humans to any food or specific nutrient (with the exception of caffeine); nor is there evidence that the widespread prevalence of obesity in the UK and elsewhere can be attributed to food addiction.


  1. Ziauddeen, H., Farooqi, I.S., and Fletcher, P.C. Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci. 13, 279-286 (2012).
  2. Benton, D. The plausibility of sugar addiction and its role in obesity and eating disorders. Clin Nutr. 29, 288-303 (2010).
  3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders 4th Edition. (American Psychiatric Association, Washington, DC, 2000).
  4. Barry, D. et al. Obesity and its Relationship to Addictions: Is Overeating a Form of Addictive Behaviour? Am J Addict 18, 439-451 (2009).
  5. World Health Organization. Neuroscience of psychoactive substance use and dependence. WHO, Geneva (2004).
  6. Hildebrand, J. et al, “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behaviour (2014) Available online at: cience/article/pii/S0149763414002140 [Accessed 19/09/2014]

Last reviewed: 21 Aug 2018