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Nutrition and Neurology

By Andrea Arthofer '17

HONR-191: Food As Medicine

This assignment encouraged students to investigate an area of health around the general topic of food as medicine. Nutrition has gained a lot of attention in metabolic and cardiovascular diseases, but neurology is one area where the discussion of diet is nearly absent. While some research exists on the relationship between diet and the disorders multiple sclerosis and epilepsy, there is a severe lack of research on how nutrition affects other neurological disorders. This led Andrea to investigate the effect of dietary behaviors on brain function overall and apply this information to how nutrition may be a crucial missing piece to the treatment of many neurological disorders. This essay was written to call attention to the need for further research in this area.

-Sara Shuger Fox


This century has been the century of medical advancement. Worldwide, understanding of the pathology of many diseases has greatly increased, which has led to the development of more effective treatments. A view near the end of the twentieth century was that eventually, we could develop a medication for any disease in order to eliminate disease entirely from the population. However, this generation is beginning to realize that medication may not be what we should be relying on. Medicine, while capable of treating symptoms or even curing many diseases, also often presents miserable side effects for its users, as well as extreme financial burdens. One aspect of healthcare that is slowly attracting more attention is nutrition and lifestyle. Many researchers have investigated the relationship between diet and both chronic and acute illnesses. The main chronic illnesses that have been researched include type two diabetes and cardiovascular diseases. For these chronic diseases, diet has consistently shown to be a major factor in their incidence and prevalence. Another health concern that has recently gained a lot of attention is cancer, which has also been strongly linked to dietary behaviors. After learning of the high correlation between dietary patterns and chronic diseases such as these, it is important to examine how nutrition can affect the development and progression of other types of diseases. Specifically, nutrition’s impact on neurological diseases should be of particular interest.

Multiple sclerosis is one of the neurological diseases that can be greatly influenced by nutrition. This interaction was suggested by epidemiological studies stating that prevalence of multiple sclerosis is higher in areas where saturated fat intake is higher as opposed to polyunsaturated fat (Payne, 2001). In relation to this, in people already affected by multiple sclerosis, there is a significant decrease in death rate for people following a very low-fat diet, defined as less than twenty grams of fat per day (Payne, 2001). The type of fat being consumed is also something that has been investigated. Essential fatty acids (EFAs) are currently being recommended for patients with multiple sclerosis. However, three studies done on this topic have actually showed no real benefit from the consumption of n-3 or n-6 EFAs (Payne, 2001).

The low-fat diet’s effect on multiple sclerosis, while remarkable, can be enhanced by the supplementation of antioxidants. Mauriz et al. conducted a 42 day randomized prospective placebo-controlled trial on long-term residents with multiple sclerosis to investigate the effect this supplementation would have on cell metabolism and the inflammatory processes related to multiple sclerosis (2013). In this study, five participants were assigned to the experimental group, which was given a low-fat diet and antioxidant supplementation, while four participants were put in the control group, only receiving the low-fat diet and a placebo instead of the antioxidant supplements. Biomarkers were measured at baseline, then after the 42 days of the trial. At the end, participants in the intervention group had significantly reduced C reactive proteins and inflammatory markers isoprostane 8-iso-PGF2α and interleukine IL-6 as compared to the control group (Mauriz et al., 2013). Therefore, when treating multiple sclerosis through dietary interventions of a low-fat diet, it would be beneficial for antioxidant supplementation to be included.

While this presents the possibility that a lowfat diet and antioxidant supplementation can reduce progression and onset of multiple sclerosis, there are several drug side effects that may interfere with a patient’s ability to follow a proper diet. Drugs commonly prescribed for patients suffering from multiple sclerosis include skeletal muscle relaxants, urination frequency reducers, antibiotics due to frequent urinary tract infections, and corticosteroids. These medications can lead to nausea, dry mouth, diarrhea or constipation. All of these symptoms would cause an overall decrease in food intake, which would inhibit a patient’s ability to consume a proper diet. Additionally, some of these prescribed medications prevent sufficient nutrient absorption from food (Payne, 2001). Since these medications already cause a decrease in food consumption, inability to absorb nutrients will further destroy a patient’s ability to follow a diet that could delay the progression of this illness. These effects of drugs demonstrate their harmful side effects, only further reinforcing the idea that medication should be less heavily relied on and that nutrition interventions should be investigated as a primary treatment.

One nutrition intervention that has been employed as a primary treatment are specific diets for decreasing seizure prevalence in epilepsy patients. Contrary to the recommended diet for multiple sclerosis, the diets proposed for epilepsy treatment have promoted high-fat diets, particularly emphasizing the importance of medium-chain triglycerides. The ketogenic diet is the first of these proposed diets, suggesting epilepsy patients consume a diet consisting of 90% fats and 10% protein and carbohydrates combined. This led to the development of the modified medium-chain triglyceride ketogenic diet, which recommended a slightly lower percentage of fats, at a total of 71-75% of the diet composed of fat, 10% from protein, and 15-19% from carbohydrates. Further, this diet explained that 30-60% of the diet should specifically be from medium-chain triglycerides, while 11-45% should come from long-chain triglycerides, but no matter what, this breakdown should add up to at least 71% of the diet from fats. Newer, less frequently used diets include the low glycemic index treatment, which breaks the proper diet composition down to 60% from fat, 20-30% from protein, and only 10-20% from carbohydrates, and the modified Atkins diet, which strongly encourages the intake of high-fat and high-protein foods while limiting the intake of carbohydrates to 10 to 15 grams per day (Neal & Cross, 2010).

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Raigen Furness, “Congestion”, marker, 22” x 30”

Neal and Cross (2010) conducted a literature review of many studies examining the effectiveness of these diets. The ketogenic diet and medium-chain triglyceride ketogenic diets showed to be most effective. These, on average, resulted in nearly one-third of participants becoming seizure-free. Further, 30% to 100% of participants, depending on the particular study experienced a 50% or more reduction in seizure frequency. While these diets may be effective in reducing seizure prevalence, other health aspects should be considered in such an extreme diet. These diets revealed negative effects on children’s biomarkers. One study examined children’s biomarkers after six months of adherence to the diet. These effects included a significant blood plasma increase in LDL, VLDL, and non-HDL cholesterol as well as a significant decrease in HDL cholesterol. Additionally, triglyceride levels and apolipoprotein B significantly increased in the blood plasma of these children (Kwiterovich et al., 2003). In response to this, considerations from Johns Hopkins stated that children should adhere to this diet for only two years, after which their seizures may not return and their biomarkers should return to normal (Lawson, 2003).

The role of diet has been illustrated in these two specific neurological disorders. Further, there are links between nutrition and lifestyle and the brain’s health in general. The efficiency of the brain tends to decrease with age as part of the natural process of aging, which can lead to a decline in cognitive functioning, development of dementia or Alzheimer’s, or other neurological disorders. However, diet and lifestyle factors have been shown to prevent or reduce this neurodegeneration that occurs with age. This correlation can be explained by what is known about how the vascular system is affected by diet, which is important in the functioning of the brain because the brain consumes over twenty percent of the body’s oxygen and nutrients even though it only makes up approximately two percent of the body’s weight (Kalaria, 2010).

This relationship between thevascular system’s health and neurological health can be explained because pathological changes in the smooth muscle of the walls of the cerebral resistance arteries change the brain’s autoregulatory responses. For example, changes in circulation due to dilation or constriction of cerebral resistance arteries often results in hypertensive encephalopathy or cerebral hypoperfusion. Many links such as these exist between the cardiovascular system and the brain’s functioning. For example, hypertension is correlated with an increased risk of dementia, particularly Alzheimer’s disease, and adult onset type 2 diabetes mellitus leads to a 2 to 2.5 fold increased risk of dementia with aging (Kalaria, 2010). Further, the nutritional interventions that prevent neuronal degeneration are very similar to those that improve cardiovascular functioning.

Many nutrition interventions have been investigated for their effect on cognitive functioning and neurological deterioration. First and foremost, adherence to a Mediterranean diet, which promotes the consumption of moderate alcohol, olive oil, whole grains, and fish, has been significantly associated with a decrease in neuronal degeneration. Additionally, increased fish consumption alone has shown to have a similar effect of decreasing the rate of decline in cognitive functioning and lowering the risk of developing Alzheimer’s disease due to its anti-inflammatory properties, ability to develop vascular tone of the smooth muscle, and prevention of atherosclerosis. Aside from the overall diet, there is evidence that fruit and vegetable extracts serve to decrease the neuronal degeneration that leads to dementia and cognitive impairment. This is due to the polyphenols and B vitamins contained inside these fruits and vegetables. Therefore, when consumed as a concentrate, these extracts are rich in these, making deficiencies of these essential components of the diet nearly impossible (Kalaria, 2010).

More research must be done in order for nutrition interventions to be utilized as a primary treatment in neurological disorders such as multiple sclerosis, epilepsy, dementia and Alzheimer’s disease, and overall general cognitive impairment. However, there is sufficient evidence that nutrition plays a role in neuronal degeneration and other neurological deficits to reasonably rely on nutrition interventions as minimally a secondary treatment for these chronic diseases. Therefore, these dietary patterns should be promoted by medical doctors and other health professionals as supplementary to other treatments. Eventually, it may be possible for research to illustrate nutrition as the most effective treatment for these types of conditions.

Works Cited

Kalaria, R. N. (2010). Vascular basis for brain degeneration: faltering controls and risk factors for dementia. Nutrition Reviews, 68S74-S87. doi:10.1111/j.1753-4887.2010.00352.x

Kwiterovich, J. O., Vining, E. G., Pyzik, P., Skolasky, J. R., & Freeman, J. M. (2003). Effect of a high-fat ketogenic diet on plasma levels of lipids, lipoproteins, and apolipoproteins in children. JAMA: Journal Of The American Medical Association, 290(7), 912-920.

Lawson, W. (2003). Seizure Diet is Safe. Psychology Today, 36(6), 29.

Mauriz, Laliena, Vallejo, Tuñón, Rodríguez-López, Rodríguez-Pérez, García-Fernández. (2013). Effects of a low-fat diet with antioxidant supplementation on biochemical markers ofmultiple sclerosis long-term care residents. Nutrición Hospitalaria, 28(6), 2229-35. doi:
10.3305/nutr hosp.v28in06.6983.

Neal, E. G., & Cross, J. H. (2010). Efficacy of dietary treatments for epilepsy. Journal Of Human Nutrition & Dietetics, 23(2), 113-119. doi:10.1111/j.1365-277X.2010.01043.x

Payne, A. (2001). Nutrition and diet in the clinical management of multiple sclerosis. Journal Of Human Nutrition & Dietetics, 14(5), 349-357. doi:10.1046/j.1365-277X.2001.00308.x