FOOD, FACTS and FADS

Exploring the sense and nonsense of food and health

Diet and Alzheimer’s Disease – Some Evidence

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Drawing comparing how a brain of an Alzheimer ...

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Another win for healthy diets – this time it’s a low-saturated fat, low glycemic diet.  And the latest study suggests that that this type of diet consumed early in life may lower the risk of Alzheimer’s Disease (AD). Alzheimer’s disease is characterized by the presence of beta-amyloid plaque development as well as neurobrillary tangles.

Research on foods and whole diets on the prevention of AD has been sparse or disappointing.  Nutrition always gets a bad rap when it comes having a curative effect against various established diseases.  But nutrients cannot cure directly – they are more effective before a disease has progressed, i.e. in the prevention stage. Often it is more successful if the practice of eating healthy is done in midlife or earlier.  Most animal studies are done on young animals before the disease in question has already developed.

There is certainly no solid proof that diet can prevent AD; although a new study suggests that diet can make a difference.  AD is a disease primarily of the elderly, but there are some earlier onset cases more than likely due more to genetics than lifestyle

In the study mentioned above, a group of healthy individuals and a group of patients with mild cognitive impairment that could be predictive of AD followed either a high-saturated-fat, simple carbohydrate diet with a glycemic index of greater of greater than 70 or a low-saturated-fat diet, simple carbohydrate diet with a glycemic index of less than 55.  A glycemic index for foods measures the degree of how a food or diet can elevate blood sugar levels and thus insulin levels when compared to pure glucose.  A good thing about this study was that the participants were only fed foods provided by the researchers, so the compliance to the diet was very good.

Cerebrospinal fluid Abeta42 and tau proteins are biomarkers of AD-associated pathologic changes in the brain. The combination of abnormally low CSF Abeta42 level and abnormally high CSF tau level predicted the presence of AD pathologic features with high accuracy. This combination assay may be helpful in diagnosing the presence of AD pathologic changes in the brain. The study’s primary outcome measure was to measure only Beta-amyloid-42 concentrations in the cerebral spinal fluid (CSF).

What were the results? The high-saturated fat high glycemic diet raised levels of Abeta42 in the CSF of healthy group, raising them in the direction that could contribute to presymptomatic AD before plaque deposition in the brain. The high-saturated fat high glycemic diet had no effect in the mild memory group levels of Abeta-42.

The results of the low-sat-fat /low glycemic diet in the healthy group resulted in the diet lowering Abeta42 levels in the CSF which may have moved them away from “the tipping point that corresponds with the start of amyloid deposition in the neurons.  But in the impaired group, the diet raised Abeta42 in CSF (which is usually in low concentrations in AD patients).

In both groups, the high- fat diet produced unhealthy changes in serum cholesterol and insulin profiles while the low-fat diet produced healthy changes in these measures.

In both groups, the low-fat diet reduced F2-isoprostane concentrations; increased apolipoprotein E, which aids with B-amyloid clearance and was associated with improved delayed memory, a hallmark cognitive deficit in mild cognitive impairment and Alzheimer’s disease.

The isoprostanes compounds and their value as markers of oxidative injury (free radical) have been well documented.  Numerous studies carried out over the past decade have shown that these compounds are extremely accurate measures of lipid peroxidation and have illuminated the role of oxidant injury in a number of human diseases including atherosclerosis, Alzheimer’s disease and pulmonary disorders.

So what can we take away from the group differences?  From the authors: “ these results support further investigation into the possibility that consumption of a diet high in saturated fat and simple carbohydrates may contribute to the pathological processes in the brain that increase the risk of Alzheimer’s disease, while a diet low in saturated fat and simple carbohydrates may offer protection against dementia and enhance brain health.

 

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3 thoughts on “Diet and Alzheimer’s Disease – Some Evidence

  1. It is implied that both groups received the same amount of carbohydrates, but that the difference lies in the glycemic index of the carbohydrates – one high and one low. The glycemic index is controversial in itself; probably a better measure is the glycemic load.

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  2. In this study the group given higher amounts of saturated fat were also given higher amounts of carbohydrate. How is it possible to then conclude that the increased markers of disease were caused by the excess fat and not the excess carbohydrate? This is just another piece of junk science that has been (not very skillfully) manipulated to produce a politically correct result.

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  3. Pingback: Diet and Alzheimers Disease

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