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BLOG: May 2008

Obesity and the brain

Obesity's bad reputation of causing or aggravating diseases has recently been expanded to include significantly higher risk for developing dementia and even Alzheimer's. Obesity and brain? Yes, you read it right. And it seems to be making a lot of sense.

According to the results of a recently published study (Whitmer et al, Neurology journal, March 2008) on over 6500 individuals within 36-year time span, those that were obese, with large belly, were

3.6 times more likely to develop dementia

than those with normal body weight and belly size (obesity without large belly increased the risk 2.7 times).

One of the reasons why it shouldn't be surprising - except, perhaps, for the magnitude - is that obese folks are much more likely to have elevated glucose level or full-blown diabetes. While the specifics of how exactly the elevated glucose level damages memory are yet to be explained, recent evidence of it being a significant factor in developing dementia and Alzheimer's is conclusive. Neural cells, in general, are

more sensitive to the restriction in production of cellular energy

due to inefficient insulin function (with glucose, as a result, accumulating in the blood instead of being transferred into the cells and burned for energy). Impaired memory being one of its longer-term consequences only seems logical.

Another reason has to do with obesity being restricting mobility. It is known for some time now that regular physical activity stimulates production of new neural cells in the portion of hippocampus - the curved ridge of neural tissue in the middle of each brain hemisphere - where the memory is processed. Both, dementia and Alzheimer's sufferers have

 significantly reduced hippocampus volume,

although the node that is affected is not identical for the two. The one affected in dementia is where neural cells production continues throughout the lifetime. Reduced physical activity could result in a slower growth of this node, its smaller size and, possibly, lower functional capacity.

Are these two factors - elevated blood glucose and reduced mobility, typical for obese individuals - really causing dementia, or only contributing to it? Elevated blood glucose, indicating its compromised cellular supply and energy production, implicates compromised functionlity of the brain cells. If severe enough, could contribute to

accelerated rate of dying of brain cells,

and longer-term impairment in the memory function resulting from it.

Also, lower energy level can certainly make the cells more vulnerable to both, chemical toxins and effects of nutritional deficiencies. The consequence could be the onset of dementia, as well as Alzheimer's, as this recent research suggests.

As for the reduced production of neural cells in the hippocampus due to low physical activity, it alone is probably not likely to result in dementia. But if your cells begin to die at an accelerated rate due to any of a number of possible factors, the fewer total of cells you have in this part of brain, the sooner you'll feel the consequences.

In all, seems that we can add one more legitimate reason - keeping brain function from accelerated onset of dementia - to already quite extensive list of reasons why not to take on, and accept, too many extra pounds.