In a recent article published in the Guardian (originally available on his personal website) George Monbiot looked at recent scientific evidence suggesting a link between ‘junk food’ and Alzheimer’s disease (1). This prompted me to think about the wider subject of nutrition and mental health. It’s an uncomfortable subject to consider especially if, like me, you enjoy a trip to the local takeaway and the ‘occasional’ alcoholic beverage. Nevertheless the availability and popularity of processed foods in modern industrial societies (2, 3) makes the impact of diet on brain function an issue that we all need to seriously consider.
Despite a significant amount of research being undertaken into how diet affects the brain, there appears to be little discussion of the subject in public discourse. This may due to the scientific uncertainties inherent in the study of diet and mental processes, especially when contrasted with the strong influence that the commercial interests of food manufacturers and retailers hold over government decision making. Here I intend to briefly review the difficulties researchers face in studying this topic, and what we know so far about how diet may alter mental health.
The problems of studying nutrition
A major problem with the study of diet is that it is really particular nutrients within food (e.g. vitamins and minerals) that influence our brains, rather than the foods themselves. As people can only really report their diets in terms of the foodstuffs they consume, and as each foodstuff contains a variety of chemicals in varying levels, each of which may be harmful, beneficial or neutral to our health to differing extents, it is not straightforward to map the relationship between foodstuffs and changes in health.
A second problem is that the impact of individual nutrients is likely to be mediated by other factors, such as the nutrient’s baseline level in the body, or the presence or absence of other nutrients. For example nutrients that are known to be beneficial to human health when consumed in food often fail to produce positive results when consumed in supplementary form (e.g. vitamin pills) an effect that is most likely due to the absence (in supplements) of naturally co-existing chemicals that facilitate the body’s uptake of the nutrient when it is consumed via foods (4). Likewise other factors that are independent of diet, such as age, genetics, and the level of physical activity, are likely to influence the effect of nutrition on health (e.g. 5). It is unethical to systematically control and manipulate a person’s entire diet over the period of time necessary to identify changes in mental processes likely to be triggered by diet. It is also impossible to fully control for the influence of other non-diet factors over a similar time frame. Therefore it is not possible to establish causality between individual foods and health outcomes with any certainty. Of course it is possible to perform such experiments on laboratory animals, but as such animals lack many of the cognitive functions that are disrupted in neurological diseases such as dementia, such studies are of limited use when considering the impact of nutrition on mental health in humans.
In light of these problems, the effect of nutrition on health is often studied via ‘cohort studies’, where large numbers of people are surveyed as to their dietary habits and health over an extended period of time. Such studies are not only expensive and time-consuming to complete, but also rely on potentially unreliable self-report measures (see (6) for a discussion). Alternatively, the influence of individual nutrients is sometimes studied by giving one group of participants supplements containing the nutrient, and others a placebo. This approach lacks the ecological validity of cohort studies, but allows a tighter control over the intake level of the nutrient involved, thus allowing its effects to be isolated. Neither method however overcomes the previously mentioned problems regarding establishing causality.
What we do know?
Given the complex relationship between food and nutrition, and the imprecision of self-report measures, diet is often characterised in cohort studies in broad terms. One relative common distinction that is used is between the so-called ‘Mediterranean Diet’ and the ‘Western Diet’. The former involves the high intake of fruit, vegetables, fish, cereals and unsaturated fats (e.g. the type of fat that tends to be found in nuts and seeds). In contrast the ‘Western Diet’ involves the frequent consumption of foods with high levels of saturated fats, such as red meats, dairy products as well as other processed foods such as confectionery and ‘convenience’ foods. Studies tend to show that those who have diets that more closely resemble the Mediterranean Diet have lower instances of both dementia and mild cognitive impairment, even after confounding factors like age, socio-economic status and physical activity are controlled for (7). More specifically it has been shown that high intake of fruit and vegetables, as well as omega-3 fats (dietary rather than through supplements) predict a reduced likelihood of dementia (8); dementia levels in those with diets high in fruit and vegetables being 2.6%, compared with 5.7% for those with diets poor in fruit, vegetables and omega-3 fats.
The neurological effects of diet are not just restricted to dementia however. There is increasing evidence that diets high in saturated fat and sugars may contribute to behavioural problems in children and adolescents, including ADHD (9, 10). Similarly artificial food additives, such as the colourings and preservatives commonly added to confectionery and soft drinks, appear to increase hyperactivity in children (11). For example in a double-blind placebo trial (12) it was found that children regularly given a drink containing additives became more hyperactive (as measured by parent and teacher ratings, and through performance on a computerised attention task) than those given a placebo drink with the same frequency. This effect was present in both 3 year old and 8 year old children, suggesting that the influence of additives is not restricted to one particular stage of development.
Evidence also exists which suggests that deficiencies in a variety of vitamins and minerals within the body may encourage depressive symptoms. For example double-blind placebo trials consistently show that Thiamine supplements improve mood (13) while other studies have suggested that low levels of vitamins B6 and E are implicated in depression (14). The effect of diet on mood may be self-reinforcing as depressed individuals often turn to ‘comfort eating’ (13) which is likely to involve foods that are high in saturated fats, and which in turn may promote obesity which could further depress mood and self-esteem over the long term.
In what way do nutrients affect the brain?
Due to the aforementioned complexities in identifying the contribution of different nutrients, it has proven difficult to identify the exact mechanisms by which the under or over abundance of certain nutrients might affect the brain. However two interrelated systems are thought to be most vulnerable to dietary factors; the neuroinflammatory response of brain neurons, and the processes surrounding insulin signalling within the brain (15). Neuroinflammation is the immune response to neuron damage. It acts to preserve the damaged neuron and promote its recovery, but it can also cause damage to surrounding neurons. It is thought that the beneficial effect of diets high in fruit and vegetables may partly be due to the polyphenols present in plant matter working to limit neuroinflammation in the brain (e.g. 16). In terms of the second system, Insulin is involved in regulating the uptake of glucose by neurons, as well as maintaining their function and structure (17). Diets that are high in saturated fats appear to promote ‘insulin resistance’ which reduces the body’s ability to utilise Insulin (hence the association between obesity and type II diabetes). This in turn negatively impacts on the ability of neurons to function properly and to adapt to changes in the signalling patterns of other connecting neurons. This leads to reduced neural plasticity and an increased likelihood of chronic, maladaptive neuroinflammation, both of which are likely to interfere with normal cognitive functioning. This may be the mechanism by which frequent consumption of junk foods leads to a greater risk of dementia (1).
Should I change what I eat?
While it is never possible to rule out the influence of confounding factors, the basic message one can take from these studies seems pretty intuitive. We are better off eating foods that can be thought of as ‘natural’ for humans to eat. Throughout history the human race have presumably mainly relied on fruits, vegetables, nuts and cereals, supplemented with small amounts of fish and meat. It therefore makes sense that these foods would be conducive to both our physical and mental health, as research seems to suggest. In contrast the convenience and affordability of seemingly unnatural foods such as confectionery, processed meats and ‘ready meals’ belies their damaging impact on our health. We could do our future selves a favour by avoiding the temptation these foods provide, and making the extra effort to eat healthily.
Image courtesy of www.freedigitalphotos.net
- http://www.monbiot.com/2012/09/10/the-mind-thieves/ (retrieved 24/09/2012).
- Popkin, B. M. (2004). The nutrition transition: An overview of world patterns of change. Nutrition Reviews, 62(7), S140-S143. <link>
- Thow, A. M. (2009). Trade liberalisation and the nutrition transition: mapping the pathways for public health nutritionists. Public Health Nutrition, 12(11), 2150-2158. <link>
- Morris, M. C. (2012) Nutritional determinants of cognitive aging and dementia. Proc Nutr Soc, 71(1), 1-13. <link>
- Dauncey, M. J. (2009). New insights into nutrition and cognitive neuroscience. Proceedings of the Nutrition Society, 68(4), 408-415 <link>
- http://www.sciencebrainwaves.com/uncategorized/the-dangers-of-self-report/ (retrieved 24/09/2012)
- Sofi, F., Abbate, R., Gensini, G. F., & Casini, A. (2010). Accruing evidence on benefits of adherence to the Mediterranean diet on health an updated systematic review and meta-analysis. American Journal of Clinical Nutrition, 92(5), 1189-1196. <link>
- Barberger-Gateau, P., Raffaitin, C., Letenneur, L., Berr, C., Tzourio, C., Dartigues, J. F., et al. (2007). Dietary patterns and risk of dementia – The three-city cohort study. Neurology, 69(20), 1921-1930 <link>
- Oddy, W. H., Robinson, M., Ambrosini, G. L., O’Sullivan, T. A., de Klerk, N. H., Beilin, L. J., et al. (2009). The association between dietary patterns and mental health in early adolescence. Preventive Medicine, 49(1), 39-44 <link>
- Howard, A. L., Robinson, M., Smith, G. J., Ambrosini, G. L., Piek, J. P., & Oddy, W. H. (2011). ADHD Is Associated With a “Western” Dietary Pattern in Adolescents. Journal of Attention Disorders, 15(5), 403-411 <link>
- Schab, D.W & Trinh, N.T. (2004). Do Artificial Food Colors Promote Hyperactivity
in Children with Hyperactive Syndromes? A Meta-Analysis of Double-Blind
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- McCann, D., Barrett, A., Cooper, A., Crumpler, D., Dalen, L., Grimshaw, K., . . . Stevenson, J. (2007). Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: A randomised, double-blinded, placebo controlled trial. Lancet, 370, 1560-1567. <link>
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- Lim, G. P., Chu, T., Yang, F., Beech, W., Frautschy, S. A., & Cole, G. M. (2001). The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci, 21(21), 8370-8377. <link>
- http://www.thealzheimerssolution.com/insulin-brain-function-and-alzheimers-disease-is-insulin-resistance-to-blame-for-alzheimers/ (retrieved 28/09/2012)