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The European Journal of Internal Medicine just published a paper discussing "Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet." Authors Seneff, Wainwright, and Mascitelli provided this abstract:
"Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause." [Emphasis added]
The idea certainly echos findings that type 2 diabetics (i.e. people with high blood sugar) have an increased risk of diabetes. In search of an explanation for the link between diabetes and Alzheimer's, Salk Institute researchers did some experiments discussed in this article at Science Daily:
To get at the bottom of the question why diabetes predisposes people to Alzheimer's disease as they age, the Salk researchers Schubert, Burdo and Qi Chen, in collaboration with diabetes expert Nigel Calcutt, a professor in UCSD's Department of Pathology, induced diabetes in young mice, whose genetic background predisposes them to acquire the symptoms of Alzheimer's with old age.

These [high blood sugar] mice suffered damage to blood vessels well before any overt signs of Alzheimer's disease such as nerve cell death or the acquisition of amyloid deposits, the hallmark of the disease, could be detected in their brains. Further experiments revealed that the vascular damage was due to the overproduction of free radicals, resulting in oxidative damage to the cells lining the brain's blood vessels.
"While all people have a low level of amyloid circulating in their blood, in diabetics there may be a synergistic toxicity between the amyloid and high level of blood glucose that is leading to the problems with proper blood vessel formation," says Burdo. [Emphasis added]
Some researchers have even proposed that Alzheimer's disease is a novel third form of diabetes:
Now scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin resistant...
With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer's disease, the Northwestern study sheds light on the emerging idea of Alzheimer's being a "type 3" diabetes.
Although I would love to outright endorse the idea that a high-carbohydrate, fructose-rich, low-fat diet drives the development of Alzheimer's disease, I can't because we have data from Kitava contradicting it.

The Kitavans appear immune to Alzheimer's while consuming considerably more carbohydrate than the typical American. Kitavan diets supply nearly 70% of calories as carbohydrate largely from various starchy roots (sweet potatoes, cassava, yam, taro), including a fairly large dose of fructose (perhaps as much as 36 g daily) from tropical fruits (bananas, guava, watermelon, pineapple).

Comment: Research has shown that a diet high in carbohydrates is responsible for many health problems experienced around the world while a diet high in healthy fats and meat is the diet humans are naturally beneficial.

The Kitavan experience suggests that the source of carbohydrate may matter. Traditional Kitavans don't eat grains or legumes, sources of toxins like gluten and lectins that might serve as neurotoxins to which we aren't adapted.

Other factors may modify the effect of high carbohydrate diets. Kitavans get plenty of sun exposure, don't have the types of mental stress encountered in modern civilization, and inhabit a far less chemically toxic environment than us.

We have some evidence that vitamin D deficiency may promote Alzheimer's disease. That study suggests that people with suboptimal D due to inadequate sun exposure have twice the risk of dementia compared to people with optimal D levels. Unfortunately, this study only shows a correlation between low D levels and Alzheimer's, which could be confounded by the so-called healthy subject effect. That means that people who spend more time in the sun and get more vitamin D might also do something else--like eat less sugar--that would protect them from dementia.

We also have evidence that stress promotes Alzheimer's disease:
Stress hormones appear to rapidly exacerbate the formation of brain lesions that are the hallmarks of Alzheimer's disease, according to researchers at UC Irvine. The findings suggest that managing stress and reducing certain medications prescribed for the elderly could slow down the progression of this devastating disease.
The researchers injected four-month-old transgenic mice with levels of dexamethasone similar to the level of hormones that would be seen in humans under stress. At this young age, there would be little formation of plaques and tangles in the brains of the mice. After one week, the scientists found that the level of beta-amyloid in the brains of the animals compared to what is seen in the brains of untreated eight- to nine-month-old mice, demonstrating the profound consequence of glucocorticoid exposure. When dexamethasone was given to 13-month-old mice that already had some plaque and tangle pathology, the hormone again significantly worsened the plaque lesions in the brain and led to increased accumulation of the tau protein.
Finally, to name a few explored by researchers, exposure to the following environmental neurotoxins (rare or absent in Kitava) might contribute to the development of Alzheimer's disease:

About the last item, although having a large number of amalgam fillings appears to increase the risk of Alzheimer's, I do have to comment that having a large number of amalgam fillings would also be a marker for consumption of a high carbohydrate diet, so it could be that both the fillings and the dementia are caused by diet.

All that aside, I wouldn't choose a Kitavan-style diet to prevent Alzheimer's disease because I don't like the gastrointestinal effects of eating that amount of carbohydrate. I prefer a meat-based diet.

We have evidence that a meat-based, low-carb diet may prevent or reverse Alzheimer's. Gasior, Rogawski, and Hartman reviewed the evidence here, stating:
Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury.
Moreover, in a murine model of Alzheimer's disease, Van der Auwera et al showed that a short-term, high saturated fat, ketogenic diet reduced deposits of toxic amyloid-ß plaque by 25%.

Thus, a low-sugar, high-fat, meat-based diet may serve as both preventive and remedial medicine for Alzheimer's disease, especially if combined with intermittent fasting (which also boosts ß-hydroxybutyrate levels).