Addiction seems to be widespread these days. We are addicted to mobile phones, computer games, shopping, sex… and, of course, junk food. Obviously, there is a vast difference between these and serious clinical addictions. There is no doubt that we must eat to live, but can we become addicted to certain foods in the same way that we can to drugs? This is an important debate to hold and resolve because of the potential role of food addiction in the current obesity epidemic.
For addiction to occur, the brain must go through a series of changes, beginning with recognition of pleasure and ending with a drive toward compulsive behaviour.
Like addictive drugs, highly palatable foods trigger feel-good brain chemicals such as dopamine in the nucleus accumbens, a cluster of nerve cells lying underneath the cerebral cortex, also known as the brain’s pleasure centre.
Dopamine interacts with another neurotransmitter, glutamate, to take over the brain’s system of reward-related learning. This system has an important role in sustaining life because it links activities needed for human survival, such as eating and sex, with pleasure and reward. Repeated exposure to an addictive substance causes nerve cells in the nucleus accumbens and the prefrontal cortex (the area of the brain involved in planning and executing tasks) to communicate in a way that couples ‘liking’ something with ‘wanting’ it. This, in turn, drives us to go after it.
Over time, dopamine has less impact on the brain’s reward centre and more of the substance is needed to obtain the same dopamine “high”.
The hippocampus and the amygdala store information about environmental cues associated with the desired substance. These memories help create a conditioned response – intense craving – whenever the person encounters such environmental cues. Cravings contribute not only to addiction but also to relapse during periods of abstinence.
Once people experience pleasure associated with increased dopamine transmission in the brain’s reward pathway from eating certain foods, they quickly feel the need to eat again. The reward signals from highly palatable foods may override other signals of fullness and satisfaction. As a result, people keep eating, even when they are not hungry. People who show signs of food addiction may also develop a tolerance to food; they eat more and more, only to find that food satisfies them less and less.
Many of the human studies into food addiction have been based around the Yale Food Addiction Scale [1], a questionnaire used to determine whether someone could be classified as a food addict. Ashley Gearhardt, the co-creator of this scale, has shared the foods people find most problematic: crisps and chips, sweets, chocolate and biscuits crop up, as do white bread and pasta. But the number one culprit seems to be ice-cream. None of these come as a surprise as they all are high in fat, sugar and/or salt.
By far, the most convincing evidence for food addiction comes from animal studies where rats exposed to high-sugar, high-fat and a combination of high-sugar high-fat (cafeteria) diets develop behaviours that resemble addiction. These behaviours include binge eating, compulsive food-seeking and withdrawal symptoms.[2][3] However, it appears that fat and sugar produce different responses in the brain’s reward system. With sugar, rats showed clear signs of withdrawal: shaking, sweating, changes in body temperature and anxiety, which are accompanied by measurable changes in neural chemicals such as dopamine and the opioids. [4] Whereas fat, or combined high-fat high-sugar, didn’t have this effect.[5] Although this doesn’t necessarily mean that fat is less potent than sugar. In short, it appears as though the animals were addicted to a drug, to the extent of tolerating running over an electric grid to get their fix.
However, Paul Fletcher [6], professor of health neuroscience at Cambridge University, believes that it is way too early for food addiction to be taken as a valid or useful concept. While the rat studies are sound, the degree to which they can be extrapolated to humans is limited. And the results in human studies so far are inconsistent and sometimes conflicting.[7] Furthermore, tolerance and withdrawal are not convincingly observed in humans. [8]
Up to now there is only one type of eating disorder where it is thought addiction plays a role: Binge Eating Disorder (BED). This condition is characterised by recurrent episodes (‘binges’) of uncontrolled, often rapid consumption of large amounts of food, usually in isolation, even in the absence of hunger. This eating persists despite physical discomfort and binges are associated with marked distress and feelings of guilt and disgust. Binges can be triggered by negative mood states which are not necessarily ameliorated by the binge. [9] It must be highlighted that, although BED is associated with obesity, a substantial number of people who show binge eating behaviour are not obese and most obese people do not have BED [10]. This observation emphasises the importance of avoiding the use of body mass index (BMI) as a general marker for compulsive overconsumption and addiction-like behaviour.[6] Treatments for BED include anti-depressants and cognitive therapies.
Researchers are clearly divided on this subject. For some, the fact that food may affect addiction centres in the brain is strong evidence that eating can be addictive. Others believe that the label of addiction can be unhelpful for those who overeat as it removes personal responsibility and hinders recovery. But one thing most agree on is that the possible relationships between food and addiction are incredibly complicated and there is a lot we do not yet understand. Clearly more research is needed to examine the concept of food addiction, its potential link to obesity and its treatment. While, for obvious reasons, it is not possible or advisable to abstain from eating, with the right treatment and guidance abstaining from overeating should be achievable.
Written by Victoria Trowse.
References
1. Gearhardt AN, Corbin WR and Brownell KD. (2009). Preliminary validation of the Yale Food addiction Scale. Appetite 52: 430-436.
2. Johnson PM and Kenny PJ. (2010). Dopamine D2 receptors in addiction like reward dysfunction and compulsive eating in obese rats. Nat Neurosci 13: 635-641.
3. Avena NM, Rada P and Hoebel BG. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 32: 20-39.
4. Colantuoni C, Rada P, McCarthy J et al. (2002). Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obes Res 10: 478- 488.
5.Bocarsly ME, Berner LA, Hoebel BG and Avena NM. (2011). Rats that binge eat fat-rich food do not show somatic signs or anxiety associated with opiate-like withdrawal: implications for nutrient specific food addiction behaviors. Physiol Behav 104: 865-872.
6. Ziauddeen H and Fletcher PC. (2013). Is food addiction a valid and useful concept? Obes Rev. 14(1): 19-28.
7. Ziauddeen H, Farooqi IS and Fletcher PC. (2012). Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci 13: 279-286.
8. Gearhardt AN, Corbin WR and Brownell KD. (2009). Food addiction: an examination of the diagnostic criteria for dependence. J. Addict. Med. 3: 1-7.
9. Stein RI, Kenardy J, Wiseman CV, Dounchis JZ, Arnow BA and Wilfley DE. (2007). What’s driving the binge in binge eating disorder?: A prospective examination of precursors and consequences. Int J Eat Disord 40: 195-203.
10. Striegel-Moore RH, Cachelin FM, Dohm FA, Pike KM, Wilfley DE and Fairburn CG. (2001). Comparison of binge eating disorder and bulimia nervosa in a community sample. Int J Eat Disord 29: 157-165.