There has been some discussion on the possibility of food addiction.
In the article below, the issue is explored by David Benton, a Professor of Psychology at the University of Swansea in the United Kingdom. He specialises in the study of the influence of nutrition on psychological functioning. Professor Benton helps us to understand why the NeuroFAST consortium, funded by the European Union, concluded that a single food substance cannot account for overeating and obesity.
A review that looked for the symptoms of addiction such as withdrawal, craving and tolerance could find no evidence of an association with sugar consumption (Benton, 2010).
There is currently no strong evidence that individuals become addicted to chemical substances in foods and the brain differs in the way it responds to food and addictive drugs such as heroin or cocaine.
Addiction is a powerful force that can take control of the lives of users. In the past, addiction was thought to be a weakness of character, but in recent decades research has increasingly found that addiction to drugs like cocaine and heroin is a matter of brain chemistry.
Addiction is a chronic, brain disease that causes drug seeking and use, despite harmful consequences to the addicted individual and to those around him or her. Although the initial decision to take drugs is voluntary for most people, the brain changes that occur over time challenge an addicted person’s self-control and hamper the ability to resist intense impulses to take drugs.
The way a brain becomes addicted to a drug is related to how a drug increases levels of the chemical dopamine. Dopamine controls movement, emotion, motivation and feelings of pleasure. The pleasure sensation that the brain gets when dopamine levels are raised creates the motivation for us to proactively perform actions that are indispensable to our survival (like eating or procreation). Dopamine is what conditions us to do the things we need to do.
Using addictive drugs floods the brain with dopamine—taking it up to as much as five or 10 times the normal level. With these levels elevated, the user’s brain begins to associate the drug with an oversized reward. Over time, by artificially raising the amount of dopamine our brains think is “normal,” the drugs create a need that only they can meet. That leads to the process of addiction, wherein a person loses control and is left with an intense drive to compulsively take the drug.
Human evolution has been associated with the development of a genetically based liking for a sweet taste. Breast milk is sweet: we are born liking a sweet taste. Such data puts the current worry that sugar may be addictive into perspective. It has been proposed that physical addiction to sugar may develop as it stimulates the release of dopamine which causes a “happy feeling” via the brain’s reward system. Yet although sweet foods stimulate reward pathways in the brain, such responses should not be confused with addiction. Drugs of abuse, such as cocaine, hijack the normal reward pathways and act in a different way to a normal response to a palatable food.
Those studying physical addiction to drugs of abuse distinguish ‘wanting’ from ‘liking’, two mechanisms that reflect different circuits in the brain. When addicted the release of dopamine is associated with ‘wanting’ a substance, it is motivating and may be associated with cravings. In contrast, ‘liking’, that is a resulting pleasant experience, is associated with the release of opioids by the brain. As any pleasant event, even a joke or a smile, will cause the release of dopamine release, inevitably palatable food releases dopamine. This is a normal response.
However, neurophysiological techniques, that monitor the firing of brain cells, have been used to study the impact of consuming sugar on the release of dopamine and find that the pattern differs from drugs of abuse. With sucrose less dopamine is released prior to consumption than with drugs of abuse. Once eating becomes a habit or when we adapt to eating, the initial release of dopamine declines and in addition the release of dopamine stops when eating begins. As the release of dopamine declines the motivation to eat ‘a second or third piece of cheesecake’ falls rapidly. With drugs of abuse, dopamine is released for longer, in larger amounts, and occurs both before and after consumption. This is an important difference as it is the presence of dopamine that induces the motivation to consume and the prolonged release of dopamine with drugs of abuse increases intake.
Particular attention has been drawn to brain imaging studies in which a low level of dopamine receptors has been found in the obese, in a similar manner to those addicted to drugs of abuse. However, a recent large scale study found that the number of dopamine receptors was not associated with obesity in either children or their mothers (Hardman et al., 2014).
A review that looked for the symptoms of addiction such as withdrawal, craving and tolerance could find no evidence of an association with sugar consumption (Benton, 2010). The NeuroFAST consortium, funded by the European Union, concluded that a single food substance cannot account for overeating and obesity (Hebebrand et al., 2014). There was no strong evidence that individuals become addicted to chemical substances in foods and the brain differs in the way it responds to food and addictive drugs such as heroin or cocaine. They suggested the term “eating addiction” rather than “food addiction”; that is some people develop a psychological compulsion to eat, driven by the positive feelings associated with eating: the focus should be moved from food itself towards the individual’s relationship with eating. Thus, attempts to deal with obesity should concentrate not so much with food but rather the individual’s relationship with eating. This is an important distinction as a ‘food addiction’ approach sees obesity as a passive process that befalls the individual when palatable foods are eaten. However, the incidence of obesity differs in those with a similar access to food: some are able to control their weight, whereas others cannot. The ‘eating addiction’ approach stresses the need to consider psychological differences in the ability to deal with food.
Benton (2010) The plausibility of sugar addiction and its role in obesity and eating disorders. Clinical Nutrition 29, 288-303.
Hardman et al. (2014) Lack of association between DRD2 and OPRM1 genotypes and adiposity. International Journal of Obesity 38, 730–736
Hebebrand et al. (2014). “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behaviour. Neuroscience & Biobehavioral Reviews 47, 295–306.