Can Diet Accelerate the Development of Alzheimer’s Disease?




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The Western diet or the standard American diet has been recognized as one of the most common food diets in the world. An increasing number of studies have shown that it could be connected to an increased risk for Alzheimer’s disease.

The Western diet is generally characterized by increased levels of refined and processed foods, with elevated content of simple sugars such as sucrose and fructose, sodium, saturated fat, and red meat-derived protein, and with decreased levels of monounsaturated and polyunsaturated fatty acids, protein from plants and fiber.

Links to obesity and metabolic diseases

This type of diet has been identified as a leading factor in the development of metabolic and obesity-related diseases such as type 2 diabetes. Four features of this diet are suggestive of increased risk for various diseases. These features are increased fat and phosphate content and decreased calcium and vitamin D levels. One well-publicized study demonstrated that the human Western diet induces tumors in the colon of normal mice.

More studies have shown that elevated mortality from diseases such as breast cancer is linked to the Western diet. This type of food intake also increases plasma levels of sex hormones while decreasing sex hormone-binding proteins and the formation of mammalian lignans and isoflavonic phytoestrogens. This, in turn, affects hormone production and degradation by decreasing the excretion of these compounds in feces and minimizing the intestinal metabolism and regulation of the enterohepatic circulation.

Another study also showed that increased acid levels in Western diet causes increased bone resorption and bone calcium loss resulting to osteoporosis and calcium nephrolithiasis.

Along with a sedentary lifestyle, obesity is characterized by chronic accumulation of excessive fat in the adipose tissue. It is widespread in both developing and developed countries and has become a leading public health concern followed by under-nutrition and infectious disease. The cardiovascular and metabolic effects of obesity have been understood for a long time; recently, however, increasing number of studies have shown that Western diet and its health implications such as obesity are also connected to the increased risk for Alzheimer’s disease.

The Western diet & Alzheimer’s disease

Alzheimer’s disease is a chronic progressive neurodegenerative disease brought about by deposition of beta-amyloid protein and neurofibrillary tangles. Characterized by declining cognitive processes such as lapses in memory and reasoning, it is the most common form of dementia and often occurs concomitantly with increasing age.

The Western diet significantly affects cognitive functions, particularly the hippocampal area, which involves areas of learning and memory functions, attributed to increased intake of simple carbohydrates and saturated fats present in Western diet. Another study has also shown that Western-style diet affects hippocampal size by decreasing its volume. This diet is also associated with disrupting blood-brain barrier integrity. Excessive food intake, strongly related to obesity, interferes with hippocampal-dependent memory inhibition which is responsible for controlling animal responses to environmental signals that imitate food, eventually driving a vicious cycle of excessive calorie intake.

Associations between Western diet consumption and Alzheimer’s disease have been established by some recent studies. One particular study which utilized a “Western diet” preparation (foodstuffs with increased amounts of animal products, fats, and low-nutrient density sugars to be consumed by mice) found out that long periods of consumption of this diet increase microglial activity in both non-Alzheimer’s and Alzheimer’s brain models. This strongly suggests increased susceptibility to Alzheimer’s disease in the presence of chronic inflammatory conditions. Due to this increased immune response in the brain, TREM2, a regulatory protein present during increased microglial activity, is also elevated. TREM2 is significantly associated with increased risk for Alzheimer’s disease and other age-linked neurodegenerative conditions. The study also showed that increased levels of beta-amyloid plaques correlates with elevated TREM2 level in mice brain.

So what’s the link?

As mentioned previously, obesity is a major risk factor in the development of type 2 diabetes, which is generally characterized by increased resistance of insulin receptors to insulin. A study has shown that insulin resistance is implicated in the development of Alzheimer’s disease. Insulin reaches the blood-brain barrier from the peripheral system and competes with beta-amyloid for the brain’s insulin degrading enzyme. This eventually causes the increased levels of beta-amyloid protein.

Another study has shown that young individuals who possess the apo-E4 allele have a seven-fold higher risk of developing Alzheimer’s disease if exposed to high-fat diet, such as a Western-style diet, in comparison to individuals who consume the same diet but don’t have this allele. The Apo-E protein is a transport protein responsible for the mobility of cholesterol in the body and one of its forms, apo-E4, is associated with the development of Alzheimer’s disease.

A number of studies have shown that the risk of age-related cognitive decline can be reduced by consumption of foods containing polyunsaturated fatty acids, monounsaturated fatty acids and fish meat. There is increasing evidence that unsaturated fatty acids have a neuroprotective effect, although no specific molecular mechanism is yet clearly identified. Nevertheless, unsaturated fatty acids help to maintain the integrity of neuronal membranes and regulate neuronal transmission. Increased consumption of polyunsaturated fatty acids such as docosahexaenoic acid (DHA) is shown to increase cognitive ability in Alzheimer’s disease model rats, at the same time inhibiting cognitive decline.

Recent scientific data clearly indicate that wrong diet can accelerate the cognitive decline and progression of Alzheimer’s disease. On the other hand, increased consumption of protein-derived plant protein, vegetable oils and fat from fish meat helps to decrease the risk of developing both early- and late-onset Alzheimer’s disease in non-genetically susceptible individuals. These new findings definitely need to be taken into account when considering the care for individuals at higher risk of neurodegenerative conditions.

References

Adlercreutz, H. (2011). Western diet and Western diseases: Some hormonal and biochemical mechanisms and associations Scandinavian Journal of Clinical and Laboratory Investigation, 50 (sup201), 3-23 DOI: 10.1080/00365519009085798

Creegan, R., Hunt, W., McManus, A., & Rainey-Smith, S. (2015). Diet, nutrients and metabolism: cogs in the wheel driving Alzheimer’s disease pathology? British Journal of Nutrition, 113 (10), 1499-1517 DOI: 10.1017/s0007114515000926

Graham, L., Harder, J., Soto, I., de Vries, W., John, S., & Howell, G. (2016). Chronic consumption of a western diet induces robust glial activation in aging mice and in a mouse model of Alzheimer’s disease Scientific Reports, 6 DOI: 10.1038/srep21568

Kanoski, S., & Davidson, T. (2011). Western diet consumption and cognitive impairment: Links to hippocampal dysfunction and obesity Physiology & Behavior, 103 (1), 59-68 DOI: 10.1016/j.physbeh.2010.12.003

Maurer, M., Riesen, W., Muser, J., Hulter, H., & Krapf, R. (2003). Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans American Journal of Physiology – Renal Physiology, 284 (1) DOI: 10.1152/ajprenal.00212.2002

Mody, N., Agouni, A., Mcilroy, G., Platt, B., & Delibegovic, M. (2011). Susceptibility to diet-induced obesity and glucose intolerance in the APP SWE/PSEN1 A246E mouse model of Alzheimer’s disease is associated with increased brain levels of protein tyrosine phosphatase 1B (PTP1B) and retinol-binding protein 4 (RBP4), and b Diabetologia, 54 (8), 2143-2151 DOI: 10.1007/s00125-011-2160-2

Newmark, H., Lipkin, M., & Maheshwari, N. (1990). Colonic Hyperplasia and Hyperproliferation Induced by a Nutritional Stress Diet With Four Components of Western-Style Diet JNCI Journal of the National Cancer Institute, 82 (6), 491-496 DOI: 10.1093/jnci/82.6.491

Newmark, H., Yang, K., Lipkin, M., Kopelovich, L., Liu, Y., Fan, K., & Shinozaki, H. (2001). A Western-style diet induces benign and malignant neoplasms in the colon of normal C57Bl/6 mice Carcinogenesis, 22 (11), 1871-1875 DOI: 10.1093/carcin/22.11.1871

Odermatt, A. (2011). The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease AJP: Renal Physiology, 301 (5) DOI: 10.1152/ajprenal.00068.2011

Solfrizzi, V., Panza, F., Frisardi, V., Seripa, D., Logroscino, G., Imbimbo, B., & Pilotto, A. (2014). Diet and Alzheimer’s disease risk factors or prevention: the current evidence Expert Review of Neurotherapeutics, 11 (5), 677-708 DOI: 10.1586/ern.11.56

Image via Meditations / Pixabay.

Viatcheslav Wlassoff, PhD

Viatcheslav Wlassoff, PhD, is a scientific and medical consultant with experience in pharmaceutical and genetic research. He has an extensive publication history on various topics related to medical sciences. He worked at several leading academic institutions around the globe (Cambridge University (UK), University of New South Wales (Australia), National Institute of Genetics (Japan). Dr. Wlassoff runs consulting service specialized on preparation of scientific publications, medical and scientific writing and editing.
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