Nutritional requirements in AlzHEimer’s disease


Specific nutritional needs

The link between nutrition and the risk of developing Alzheimer’s disease is supported by an increasing level of epidemiological evidence. This evidence highlights distinct nutritional requirements that originate from low levels of several key nutrients, metabolic alterations related to absorption of nutrients and endogenous production of various intermediates from nutrients, and increased nutrient requirements for synapse formation.

If the distinct nutritional requirements of people with Alzheimer’s disease are not addressed, this can aggravate known risk factors such as circulating homocysteine levels, oxidative stress, diminished blood flow to the brain and neuronal membrane health, all of which contribute to the pathophysiology of Alzheimer’s disease.

Low levels of several key nutrients

A systematic review and meta-analysis conducted by Lopes da Silva et al [1] demonstrated that people with Alzheimer’s disease have significantly lower plasma levels of docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), vitamins A, C, E, folate and vitamin B12 compared with cognitively intact elderly controls. Furthermore, these nutritional deficiencies are observed in the absence of any signs of protein and energy malnutrition, which is known to be a common occurrence in Alzheimer’s disease, and therefore suggests that compromised nutritional status in Alzheimer’s disease patients may precede protein and energy malnutrition.

Altered nutrient absorption and metabolism

The compromised nutritional status observed in Alzheimer’s disease patients typically cannot be met by the diet alone, and occur because of physiological and metabolic disturbances.

Endogenous DHA synthesis in the liver is reduced in people with Alzheimer’s disease, which may be attributable to age related decline in liver function [2,3]. DHA and uridine monophosphate synthesis may be further impaired by accelerated age related liver dysfunction due to increased oxidative stress, which is often observed in people with Alzheimer’s disease [4].

Choline uptake from the circulation into the brain decreases with age [5], which may result in increased degradation of membrane phosphatidylcholine (main phospholipid present in neuronal cell membranes) in order to produce sufficient amounts of acetylcholine [6], an important neurotransmitter in learning and memory processes. It is suggested that this contributes to the increased degradation of neuronal cell membrane observed in Alzheimer’s disease patients [7].

A decrease in B vitamins is associated with increased plasma homocysteine levels [8], which is associated with decreased mobilisation of DHA from the liver into plasma [9,10], and increased metabolic use of choline [11]. Elevated homocysteine levels has been associated with increased brain atrophy in elderly subjects, but is even more prominent in people with mild cognitive impairment and Alzheimer’s disease [12-16].



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