Simply Psychology...Food addiction

When it comes to food addiction there are two possible forms, substance specific or behavioural. One form would occur when specific food substances are eaten (e.g. sugar), such that the food substance itself is addictive. The alternative form suggests that it is the eating behaviour that is addictive (rather than a specific food substance).

So, what is a food addiction?

Under the DSM -IV-TR, substance dependence has seven criteria, three of which must be met to be classed as addicted (Toates, 2010). Tolerance, withdrawal, larger consumption, desire, spending time obtaining, giving up normal activities and continuing use despite knowledge of harm. Six of these criteria would be met with a food addiction. However, little time would be spent trying to obtain food as its easily available (Toates, 2010). Thus, a food addiction has the potential to be diagnosed as substance dependence.

The changes in the brain seen shortly after an addictive food substance is obtained and consumed, would be an initial increase in dopamine levels. This is due to the appetitive phase increasing dopamine in the mesolimbocortical pathway and driving incentive motivation (Dommett, 2010). According to some biomedical theories, such as the exposure models, long term brain changes in the addicted individual would be due to incentive sensitisation as suggested by Robinson and Berridge (1993) cited in Dommett (2010). This is where the mesolimbocortical pathway responds more strongly to the addictive substance than it would do in someone who was not addicted. This is because after repeated exposure to the object of addiction, the dopaminergic neurons eventually become more sensitive to its effects. In addition, the addicted person may experience a type of dopamine see saw where they need to consume more of the addictive substance to reach a state of equilibrium. As suggested by Solomon and Corbit (1974) cited in Dommett (2010) with the opponent motivation model. The dopamine pathways in the addictive individual would eventually start operating outside of the normal range, as the dopamine levels decrease significantly when the effects of the sugar wares off. This dip in dopamine would not be as prevalent in someone who was not addicted to sugar (Dommett, 2010).

Is addiction just an excuse for bad behaviour or is it really a disease?

The exposure models of addiction can be used to support that addiction is a disease. For example, the incentive sensitisation model suggests that the drug becomes increasingly wanted over time after repeated use. This is due to the mesolimbocortical pathway responding more strongly to the addictive substance, and the dopaminergic neurons becoming more sensitive (Dommett, 2010). In addition, incentive salience can further reinforce the addiction (Dommett, 2010). This is because the dopamine activity becomes a drive towards the conditional stimulus, like the environment where food is consumed, increasing the appetitive motivation for the substance. Pecina et al. (2006) cited in Dommett (2010) found corticotropin-releasing factor (CRF) to play a role in increasing incentive salience during stressful situations. This shows the long term neurological changes in the brain ultimately affecting the addicted individual’s control over their behaviours, making the addiction more of a disease rather than a conscious choice. The treatment process according to this model would then be to reverse the neurological changes that have occurred (Dommett, 2010). This could be achieved by reducing the exposure of the conditional stimulus that the individual has associated with the addictive substance. In addition, to reduce the reinforcing factor that CRF plays, stress management and reduction could be taught as part of the treatment process.

Is it possible to apply a preventative treatment approach to the development of food addiction?

To apply preventative treatment in the reduction of food addictions, the best intervention would be a reduction in the availability of energy dense, and potentially addictive foods. However, this may be possible for select individual’s, but applying this measure to the wider population would be seemingly difficult. This is mainly due to the marketing and food manufactures, who would be reluctant stop selling their products. Therefore, other measures could be used such as prevention interventions aimed at shoppers, parents, and school children. Psychological models of addiction such as rational choice assumes addiction can be a result of poor cost-benefit analysis (Dommett, 2010). Therefore, knowledge interventions could be used to build negative attitudes towards junk foods and make people aware of the health costs (Dommett, 2010). In addition, it could raise awareness of the importance and benefits of a healthy diet, further deterring people from unhealthy food. Another form of prevention could be legal schemes (Dommett, 2010). For example, increasing the tax for potentially addictive foods and making it a legal requirement for manufactures to sell their products with awareness information. Although little evidence has been shown in the effectiveness of these types of interventions (Dommett, 2010), it would be a productive step towards raising awareness to the larger population about the potentially damaging and addictive ingredients in energy-dense processed foods.

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Reference list

The Open University (2010) SDK228 Book 3: Addictions, Milton Keynes, The Open University.