Does food addiction exist?

Close your eyes and think about your favourite food, the one you most enjoy eating because it’s the tastiest. Think about that moment when it enters your mouth: you savour the flavour, you bite into it and slowly start chewing, perceiving that complex in-mouth aroma, and then you swallow, sensing the wonderful aftertaste that lingers for some time. Think about the enjoyment you’d get from savouring that intense and pleasurable taste. Ok, stop there. Now, with this in mind, ask yourself the following question: if you’ve got that food somewhere in your kitchen, are you capable of staying where you are right now and forgetting about it or are you prepared to get up and go and do whatever’s necessary to get your hands on it? Do you feel almost uncontrollable cravings for certain foods? Is this the exception or the rule for you, and do you live it with only one or more than one particular food?

For most of us, the situation described above would probably seem exaggerated. Thinking about a particular food and then feeling an irrepressible need to actually have it? Perhaps you could associate this type of behaviour with smokers and their need for a cigarette, as we all know that nicotine is addictive, but when we think of the term addiction, or at least from the medical perspective, we don’t associate it with eating or food but with highly complicated pathologies and substances, such as tobacco, alcohol, cocaine and heroin, considered to be toxic and very dangerous for our health, especially if consumed continuously over time. After all, eating is a physiological necessity for all of us every day: if we don’t eat, our health will most likely take a turn for the worse. All of which inevitably raises the following question: does it really make any sense to relate food with addiction?

The truth is that in recent years, finding these two words together in the same sentence has become increasingly common, even in scientific texts. The number of publications with references to food addiction has increased exponentially from practically none to quite a lot (1): see for yourself by running the term through the search engine Pubmed. More and more experts believe there are aspects in common and parallels to be drawn with how our body, metabolism and brain react to drug consumption and to eating certain foods.

This idea is not new. Far from it, in fact. In the 1940s and 50s, a groundswell of medical opinion arose that drew parallels between substance addiction and binge eating (2). Unfortunately, however, this initial idea was ahead of its time and proved to be counterproductive; in those times, when scientific studies and public awareness and sensitivity towards human rights did not exactly abound, the stigma attached to substance addiction was enormous. Neither was there any kind of effective treatment to deal with this type of situation. All of which meant that for some overweight people, the stigma they already suffered as binge eaters was now exacerbated by the prejudices and rejection associated with addiction, with nothing in exchange in terms of new therapeutic approaches designed to solve or mitigate their problem.

Fortunately, medical progress in both scientific and social terms has made the modern-day approach to this subject far more encouraging and relevant, though, as we shall see later in this article, there is still a long way to go.

What does psychiatry have to say about this?

The criteria used by psychiatry, the medical speciality normally associated with dealing with and treating  addictions, is as good a place as any to begin looking into what science and medical consensus have to say about potential food addiction. The starting point could be the diagnostic phase of identifying the symptoms and the existence, or otherwise, of a pathology. Psychiatrists generally turn to what is probably the most commonly used book in their speciality, the Diagnostic and Statistical Manual of Mental Disorders, or DSM, a reference book published by the American Psychiatric Association (APA), now in its fifth edition. Chapter 2 of the DSM contains a comprehensive list of disorders and the criteria for their diagnosis, including a section on Feeding and eating disorders which mentions well-known pathologies such as anorexia nervosa and binge eating and other less-known ones such as pica and rumination.

However, disorders related to substances such as coffee, tobacco, alcohol, heroin or painkillers, and addiction to them, can be found in a totally different section.

Comparison of the two chapters (substance-related disorders and eating disorders) reveals significant differences in terms of approaches and diagnostic criteria. The section on eating disorders includes identifying pathological and uncontrolled behaviour but, conversely, does not use terms and concepts closely associated with the phenomenon of addiction and used in diagnosing substance addiction, such as tolerance and abstinence, or make reference to potential intoxicating scenarios. It could, therefore, be concluded that to date, psychiatry does not officially contemplate the existence of food addiction: binge eating would come nearest to it.

However, some experts have long been saying that the consumption of certain foods may have a lot in common with substance consumption (3). They believe there are many parallels to be drawn between the relationship many obesity sufferers have with food and the situation of people suffering from substance addiction. Many of the symptoms coincide.

To give you a better understanding of this, below are the 11 symptoms of reference the DSM-V has established for diagnosing substance addiction disorders (4):
  1. Consumption in large amounts or over a long period.
  2. Persistent desire or unsuccessful efforts to cut down consumption.
  3. A great deal of time spent on activities necessary for consumption, on consumption itself or on recovery from its effects.
  4. Craving or a strong desire or urge to consume.
  5. Recurrent consumption resulting in a failure to fulfil major role obligations at work, school or at home.
  6. Continued consumption despite persistent and recurrent personal or interpersonal problems brought on or exacerbated by the substance.
  7. Important social, professional or leisure activities are given up or reduced because of consumption.
  8. Consumption in physically hazardous situations.
  9. Continued consumption despite knowledge of having persistent or recurrent physical or psychological problems probably brought on or exacerbated by the substance.
  10. Tolerance, understood as the need to increase consumption over time to achieve intoxication or the desired effect, or a markedly reduced effect after continuous consumption of the same amount of the substance.
  11. Withdrawal syndrome, manifest as any one of the following: the existence of withdrawal effects or substance (or very similar substance) consumption to relieve or avoid the effects of withdrawal. 
Anyone familiar with the effects of tobacco, alcohol or caffeine will recognise many of these symptoms, and doctors who have treated someone for obesity will also recognise certain symptoms this list has in common with what they have observed in relation to being overweight. Conversely, other symptoms are much less applicable. For example, when speaking of food, it’s difficult to talk of toxicity, and the definition of tolerance and abstinence is likely to need fine tuning when applied to food as there’s a fine line between what can be considered as “normal” hunger and abstinence. The same can also be said of substances recognised on the DSM-V list: examples of a “traditional” intoxication through tobacco would be hard to find, as would cases correlated to all 11 symptoms in relation to caffeine, hallucinogenic substances and inhalants, all of which figure in the section on addictions. Another thing to bear in mind is that, according to the diagnostic criteria of the DSM, not all the symptoms have to be present. The frequent and continued presence over time of two or three of these symptoms is enough for the diagnosis of a mild addiction disorder, whilst four or five of them would point to a moderate addiction disorder.

A little over 20 years ago, one group of experts clearly subscribing to this theory drew up, within the framework of the fourth edition of the DSM, a list of symptoms of “addiction” adapted to the context of food. As this initiative originated in the University of Yale, it has became known as the YFAS (Yale Food Addiction Scale), and was recently reviewed and updated to bring it into line with the latest edition of  the DSM (5). The YFAS is a questionnaire containing 35 different items designed to assess the presence (or otherwise) of one or more of the previously mentioned eleven symptoms but in relation to food, using very similar criteria to those used with substances (with a minimum presence of 2-3 symptoms).

Though yet to be officially recognised, the YFAS is nowadays probably the best known and most widely used and effective tool in raising awareness and popularizing the concept of food addiction, and has already been used on several occasions to assess the potential prevalence of this same phenomenon (6, 7, 8). Though relatively few studies have been conducted on the issue to date, some research has shown that 20% of overweight people could, according to this scale, be categorised as suffering from food addiction, and, logically, the greater the degree of obesity, the higher the percentage.

These results have only served to further polarise opinion on the issue. Advocates of the concept believe these findings to be significant, especially taking into consideration the enormous amount of people affected by this epidemic of obesity. Conversely, opponents of this theory believe there is as yet insufficient evidence for this alarming increase in obesity to be attributed to the idea of food addiction, and that a lot more scientific evidence is required before this theory can be validated (9, 10).

In short, though clinical psychiatry remains sceptical about the concept of food addiction, debate on the issue is more vibrant than ever.

The neurobiological perspective

Another strategy to bring to light more evidence on the subject may be to analyse the issue from a more biological perspective, looking into what happens on a biological level with “traditional” addictions – especially on a neuronal level – to see how this compares with eating. To do so, a brief explanation must first be given of what an addiction really is, of what goes on at that moment at a microscopic level in our body and in our brain and what drives us to lose control.

Evolution has progressively shaped and given rise to a mechanical drive in human beings to do certain things. This includes our brain, which is to some extent mechanically programmed to ensure a series of particularly important habits essential for our existence, such as reproduction and eating. The logic behind this programming is remarkably simple: offer some kind of reward in the form of pleasure or satisfaction and provoke a desire to obtain that pleasure. In short, a very basic but highly effective and widely used method in the animal world to arouse motivation.

In the 1950s, a group of American scientists conducting experiments with mice discovered that pleasure could be triggered by activating certain areas of the brain (11). Those areas have progressively been identified and are now encompassed within what is referred to as the reward circuit.

Subsequent research has been focused on trying to understand the biological mechanisms involved in producing reward. It could be said that the neuronal activity of the reward circuit is capable of generating two situations: on one hand, motivation to look for or to do something, provoking a feeling of intense desire (or craving), and on the other, pleasure, as the consequence of a certain process or happening. The two situations feed off each other: the sense of pleasure develops and consolidates expectations, which in turn strengthen the desire and motivation to behave in such a way as to provoke the afore-mentioned sense of pleasure.

Experts also found that the neurotransmitter dopamine plays a key role in both situations, though particularly in the case of motivation and desire (12). Researchers concluded that these same motivational processes are the drivers of addiction (which could be considered an extreme case of this reward mechanism), whereby the self-replenishing circuit of motivation and pleasure goes into overdrive and culminates in a destructive spiral difficult to escape from. After conducting a further series of tests focused on the properties of dopamine, the same experts proposed a series of models designed to explain the biochemical origin of addictions. In this respect, the basic idea put forward was that repeated and continuous consumption over time of a substance could provoke a desensitisation of the corresponding neuronal receptors (which, in turn, would lead to “tolerance”, or the need to consume in greater quantity to obtain the same sense of pleasure or the same effect). At the same time, dopamine secretion levels would increase (triggering “abstinence”, or an ever-increasing prior activation of dopaminergic neurons), thereby arousing motivation and the craving to obtain and consume the substance in question.

However, and as is invariably the case when we begin studying how the brain works, several lines of research have subsequently revealed that things are considerably more complex than originally thought. It would seem that all substance addictions are not the same, and that, as well as dopamine, there are other neurotransmitters involved (such as opioids) which play a key and, at the same time, quite specific role in these addiction processes (13, 14). The models developed to explain the activity of the different addictive substances also differ amongst each other and are providing us with a clearer understanding of the multiple ways they interfere, and the mechanisms they interfere with, in the normal functioning of the different neurotransmitters, altering their concentration and modifying neuronal activity and, eventually, giving rise to recognised symptoms.

Furthermore, things may turn out to be even more complicated than that. New hypotheses envisage the possibility of the existence of biological mechanisms and processes of another nature associated with addiction, such as certain mechanisms related to gene expression (epigenetics) (15).

So, taking all these ideas into account and notwithstanding the current limitations and the complexity involved in their further study at a molecular level, certain parallels could be sought between substance addiction and possible food addiction. Such an approach would be far from straightforward, as numerous neurotransmitters are involved in both processes, and many of them are common to both. The best-known and most studied is dopamine but opioides, cannabinoides, serotonin, histamine and GABA all have a part to play. What’s more, a fair amount of hormones (ghrelin, melanocortin, NPY and leptin, amongst others) also impact on both perspectives, and to make matters even more complicated, all these neurotransmitters and hormones may also interact amongst each other, weaving a highly intricate network of interrelations.

A review of relevant literature on this subject would suggest that, as research on the issue develops, more and more experts find coincidences and overlapping parallels in the neurobiological systems related to addictions and overeating. However, they also find differences, and a lot of work remains to be done in this field (16, 17, 18, 19).

On a more microscopic level, modern fMRI techniques enable neuronal activity in different parts of the brain to be analysed in considerable detail, and to draw comparison between the neuronal activity of people suffering from addictions and those suffering from obesity or eating disorders. In this case too, study findings reveal that both the signals related to addictive substances and those related to food provoke particularly intense and exceptional activity in certain common areas of the brain, especially in people who suffer respectively from an addiction and obesity. It must be said that little research has been done to date on this issue and that, although must studies do find certain parallels, important differences are also sometimes detected, with significant variability depending on the methodology used and the approach of the study. (20, 21, 22, 23)

Genetics (the study of genes) is also contributing significantly to the argument, as genes are responsible for codifying the receptors of the neurotransmitters involved. For example, in the analysis of genes related to the dopaminergic system and to leptin, opioid and melanocortin 4 receptors, the two perspectives have been found to have certain points in common, though research findings are as yet few and far between and inconclusive (24, 25).

Food as a drug?

As can be seen from the above, research strategies are diverse and have drawn in a number of disciplines. There can be little doubt that within few years, research findings will progressively shed ever greater light on the appropriateness (or not) of the parallels being drawn between overeating and addictive substances. In the meantime, and to continue filling in the gaps in our knowledge, it is important for research to be focused and seen to be coherent, particularly with respect to the type of foods under study. It doesn’t make much sense to focus discussion on whether the food we’ve traditionally and/or always eaten may become addictive: these foods have never been addictive in the history of mankind and there’s no reason to think they’re going to become so now. Furthermore, this type of food is eaten less and less nowadays. Logic would tell us to focus on some of the “new” foods, those which reveal very different and particular characteristics. Researchers often talk of highly palatable foods, but some studies also contain characterisations and descriptions based on high calorie content or sugar, salt or fat-rich foods.

This lack of consensus regarding the typology of problematic foods becomes patently obvious when looking for studies that reveal which types of foods provoke most addiction-related symptoms. Very little research has been conducted in this field, and that which has been is normally limited to identifying those foods which are craved the most and most frequently (26, 27, 28, 29, 30), namely:
  • Chocolate, sweets, pastries, biscuits, ice-cream and desserts.
  • Highly flavoured and rapidly absorbed snacks (crisps, corn and potato-based snacks, crackers, etc.).
  • Fast food (pizza, battered and ready-made foods, etc.).
  • Sugary drinks.
  • Pasta, white bread and rice.
All these foods are highly processed and manufactured using ingredients and components which have been extracted and refined in bulk (especially from plants and vegetables) and subsequently combined and subjected to various processes of transformation. The end objective of this exercise is to produce a foodstuff with highly intense taste sensations and which is highly digestible, i.e. which can be absorbed very quickly into the bloodstream. Some studies associate this type of food with long-term neuronal and metabolic adaptations which may later be related to certain symptoms of addiction (31, 32, 33). From this perspective, parallels can be drawn, for example, with what happens in the case of nicotine and the other components added to tobacco to make smoking such a “rewarding” and addictive experience for our brain, or with the process of producing alcoholic drinks.

The fact that these heavily processed and highly palatable foods are targeted by research studies –particularly to identify exactly which foods we are talking about and to obtain a more in-depth insight into the characteristics and properties of those foods responsible for undesirable alterations and effects – is a major handicap, since most research on nutrition is funded by the food industry. In other words, the very sector responsible for manufacturing this type of foodstuff. It’s hardly surprising, then, at least for the moment, that the industry has little or no interest in publicising the idea that some of its products may become “addictive”.

To cap it all, all these foods are readily available at a low price in all types of shops and heavily and attractively advertised – including for children – using the most sophisticated and effective marketing strategies. This bombardment of publicity and the signals it sends out infiltrate our brain and trigger the release of neurotransmitters which activate the areas of our brain comprising the reward circuit and subsequently drive us to take unfortunate dietary decisions (34). What would happen if smoking were once again allowed to be mass-advertised and cigarettes became readily available on a grand scale, like 20 or so years ago?

A promising approach

The relentless epidemic of obesity challenging the health of people in the developed world requires new approaches if we are seriously going to address the multiple aspects and myriad causes of this highly complex issue. Alongside several other approaches, the theory of food addiction, though still at a fledgling stage requiring considerably more research and evidence, can be considered of interest in helping to identify innovative interventions and solutions. It’s high time we went beyond the traditional mantra of “eat less and do more exercise”, which is nothing more than a misguided simplification of little clinical use.

As is often the case in the world of nutrition, it’s quite possible that a lot of time and energy is being spent arguing about the initial ideas in an attempt to establish whether foods may or may not provoke something akin to addiction. As a result, these efforts may be turning the issue into a kind of confrontation of polar ideas, of black and white standpoints, when the reality is that the issue contains many different shades of grey. The different substances accepted and known to be addictive do not coincide in all their effects and characteristics (pathological gambling, included as an addictive disorder in the DSM-V, is not associated with any particular substance), so what they do have in common with each other may be significant enough to begin to consider constructive approaches of mutual benefit and learning for both sides of the argument. It may even be an appropriate moment, always on the basis of an eminently rigorous scientific approach, to think about the introduction of possible treatments. Such treatments would doubtlessly require multidisciplinary support, combining the efforts and knowledge of different branches of science.

Taking all this into consideration, I’m hopeful that we’ll have more weapons at our disposal in the near future to fight this complicated battle.


(1) Salamone, Dopamine and food addiction: lexicon badly needed, 2013

(2) Rasmussen, Stigma and the Addiction Paradigm for Obesity- Lessons from 1950s America, 2014

(3) Meule, Food Addiction in the Light of DSM-5, 2014

(4) «Alcohol consumption disorder», DSM-V,.

(5) Gearhardt, Development of the Yale Food Addiction Scale Version 2.0., 2016

(6) Meule,How Prevalent is “Food Addiction”?, 2011

(7) Pursey, The Prevalence of Food Addiction as Assessed by the Yale Food Addiction Scale: A Systematic Review, 2014

(8) Flynt, Food-addiction scale measurement in 2 cohorts of middle-aged and older women, 2014

(9) Ziauddeen, Is food addiction a valid and useful concept?,2013

(10) Hebebrand, Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior, 2014

(11) Milner, Brain-stimulation reward: A review, 1991

(12) Schultz, Predictive Reward Signal of Dopamine Neurons, 1998

(13) Koob, The Neurobiology of Addiction: Where We Have Been and Where We Are Going, 2009

(14) Feltenstein, The neurocircuitry of addiction: an overview, 2008

(15) Nestler, Epigenetic mechanisms of drug addiction, 2013

(16) Wolkow, Obesity and addiction: neurobiological overlaps, 2012

(17) Blumenthal, Neurobiology of food addiction, 2010

(18) Dagher, The neurobiology of appetite: hunger as addiction, 2009

(19) Murray, Food and Addiction among the Ageing Population, 2016

(20) Tang, Food and drug cues activate similar brain regions: a meta-analysis of functional MRI studies, 2012

(21) Avena, Further Developments in the Neurobiology of Food and Addiction: Update on the State of the Science, 2012

(22) GarcĂ­a, Reward processing in obesity, substance addiction and non-substance addiction, 2014)

(23) Tomassi, Striatocortical pathway dysfunction in addiction and obesity: differences and similarities, 2013

(24) Carlier, Genetic Similarities between Compulsive Overeating and Addiction Phenotypes: A Case for “Food Addiction”?, 2015

(25) Heber, Addictive Genes and the Relationship to Obesity and Inflammation, 2011

(26) Weingarten, Food Cravings in a College Population, 1991

(27) Chao, Food cravings, food intake, and weight status in a community-based sample population, 2014

(28) Komatsu, Rice and sushi cravings: A preliminary study of food craving among Japanese females, 2008

(29) Zellner, Food liking and craving: A cross-cultural approach, 1999

(30) Keser, A new insight into food addiction in childhood obesity, 2014

(31) Gearhardt, The Addiction Potential of Hyperpalatable Foods, 2011

(32) Ifland, Clearing the Confusion around Processed Food Addiction, 2014

(33) The Influence of Palatable Diets in Reward System Activation: A Mini Review, 2016

(34) Wansink, Mindless Eating: The 200 Daily Food Decisions We Overlook, 2007

Note: This post was first published in spanish at NextDoor Publisher