Early onset Alzheimer's disease that afflicts people younger than 65, usually in their 50s, is genetic. Late onset Alzheimer's disease is much more common; 95% of Alzheimer's is late onset Alzheimer's. It is not genetic. If genes do not cause late onset Alzheimer's, then what does? The answer? Nobody knows. However, there are risk factors. Age is the strongest risk factor: the older you are the more likely you are to get the disease. Age is not a modifiable risk factor.
But there are risk factors that are modifiable. Three of them are the subjects of this article. The first is obesity. Three studies on the relationship between obesity and Alzheimer's disease were published since 2003. The first of these found that older women who were overweight at age 70 were much more likely to develop Alzheimer's disease 10 to 18 years later. The study also found that each point increase in body mass index (equivalent to about 5 or 6 pounds) after age 70 led to a 36 percent increase in Alzheimer's risk. On February 14, 2005, a study was published on men that came to a similar conclusion. Men who had a body mass index of less than 20 or greater than 22.5 had an increased risk of dementia, and that risk increased as the body mass index increased. A study published in June 2005 found that obesity in middle age increased the risk of dementia in old age by 74%.
The second of the modifiable risk factors for Alzheimer's that is the subject of this article is diabetes. Since the 1990s there has been a flood of studies linking diabetes to dementia and Alzheimer's disease. One of these, a large study done in Rotterdam and published in 1999, found that type 2 diabetes almost doubled the risk of Alzheimer's disease. Another study published in January of 2000 found that older women (65 years and older) who had diabetes for 15 years or more had a 57% to 114% greater risk of cognitive decline than women without diabetes. A study done in May of 2004 found that subjects with diabetes mellitus had a 65% increase in the risk of developing Alzheimer's compared with those without diabetes mellitus. In researching this article, I came across fifteen major studies linking diabetes and Alzheimer's.
Insulin Degrading Enzyme
Why and how does diabetes increase the risk of Alzheimer's disease? One theory involves an enzyme that removes excess insulin from the blood. This insulin degrading enzyme is also responsible for removing beta-amyloid plaques from the brain, the beta-amyloid plaques that are the hallmarks of Alzheimer's disease. The excess insulin that is produced in type 2 diabetes, as well as the insulin used to treat diabetes, both type 1 and type 2, may demand more insulin degrading enzyme than the body is able to produce, leaving none to remove accumulating beta-amyloid plaques from the brain.
There is evidence in support of this theory because hyperinsulinemia (excess insulin in the blood) is a risk factor in its own right for Alzheimer's disease. In the Rotterdam study mentioned earlier, Alzheimer's disease was found to be more frequent in elderly diabetic patients treated with insulin; patients treated with insulin were at highest risk of dementia. In another study (1997), subjects with insulin resistance syndrome, in which high levels of insulin circulate in the blood, had an increased risk of Alzheimer's disease. A very recent study published July 25, 2005, found that higher insulin secretion may be related to worse cognition, even among those without diabetes. A study published on October 14, 2004, found the risk of Alzheimer's disease doubled in subjects with hyperinsulinemia and was highest in such subjects without diabetes.
Even more direct support of the theory can be found in a study published in October 2005, in which subjects were given infusions of insulin. Brain levels of beta-amyloid increased. And finally, a study published on May 5, 2003, found that beta-amyloid levels in the brain increased when insulysin, an insulin degrading enzyme, decreased.
The insulin degrading enzyme theory can also explain how obesity can cause Alzheimer's disease. As the body becomes more and more overweight, it becomes more and more resistant to the blood-sugar-lowering effects of insulin. To counter this insulin resistance, the body keeps making more insulin. Thus obesity, like type 2 diabetes, results in hyperinsulinemia, which in turn leads to a depletion in insulin degrading enzyme, which causes an increase in beta-amyloid plaques.
The good news is that these risk factors are modifiable. Having diabetes does not seal one's cognitive fate. In one of the studies linking diabetes to cognitive decline, the decline was strongest among diabetics who did not control their blood-sugar levels. Therefore, this decline should be preventable by normalizing blood sugar levels. In fact, in two studies where diabetic subjects were able to normalize their blood-sugar levels, they performed as well as subjects without diabetes on tests of cognitive ability. Normalizing blood sugar levels normalizes insulin levels, which in turn normalizes appetite.
All three of the risk factors for Alzheimer's disease discussed in this article - obesity, diabetes, and hyperinsulinemia - are really different perspectives of the same problem, and the solution to that problem is the same for all three. The first line of defense in normalizing blood sugar levels, normalizing insulin levels, and normalizing weight, is diet. That diet is a diet of unprocessed, fresh food in which refined carbohydrates are eliminated.
Mary Lou Williams, M. Ed., is a lecturer and writer in the field of nutrition. She welcomes inquiries. She can be reached at 267-6480.