http://www.guardian.co.uk/commentisfree/2012/sep/10/alzheimers-junk-food-catastrophic-effect
Excerpts from this article: A large body of evidence now suggests that Alzheimer's is primarily a metabolic disease. Some scientists have gone so far as to rename it: they call it type 3 diabetes.
New Scientist carried this story on its cover on 1 September; since then I've been sitting in the library, trying to discover whether it stands up. I've now read dozens of papers on the subject, testing my cognitive powers to the limit as I've tried to get to grips with brain chemistry. Though the story is by no means complete, the evidence so far is compelling.
About 35 million people suffer from Alzheimer's disease worldwide; current projections, based on the rate at which the population ages, suggest that this will rise to 100 million by 2050. But if, as many scientists now believe, it is caused largely by the brain's impaired response to insulin, the numbers could rise much further. In the United States, the percentage of the population with type 2 diabetes, which is strongly linked to obesity, has almost trebled in 30 years. If Alzheimer's, or "type 3 diabetes", goes the same way, the potential for human suffering is incalculable.
Insulin is the hormone that prompts the liver, muscles and fat to absorb sugar from the blood. Type 2 diabetes is caused by excessive blood glucose, resulting either from a deficiency of insulin produced by the pancreas, or resistance to its signals by the organs that would usually take up the glucose.
The association between Alzheimer's and type 2 diabetes is long-established: type 2 sufferers are two to three times more likely to be struck by this form of dementia than the general population. There are also associations between Alzheimer's and obesity and Alzheimer's and metabolic syndrome (a complex of diet-related pathologies).
Researchers first proposed that Alzheimer's was another form of diabetes in 2005. The authors of the original paper investigated the brains of 54 corpses, 28 of which belonged to people who had died of the disease. They found that the levels of both insulin and insulin-like growth factors in the brains of Alzheimer's patients were much lower than those in the brains of people who had died of other causes. Levels were lowest in the parts of the brain most affected by the disease.
Their work led them to conclude that insulin and insulin-like growth factor are produced not only in the pancreas but also in the brain. Insulin in the brain has a host of functions: as well as glucose metabolism, it helps to regulate the transmission of signals from one nerve cell to another, and affects their growth, plasticity and survival.
Experiments conducted since then seem to support the link between diet and dementia, and researchers have begun to propose potential mechanisms. In common with all brain chemistry, these tend to be fantastically complex, involving, among other impacts, inflammation, stress caused by oxidation, the accumulation of one kind of brain protein and the transformation of another.
Home 
