Tag: Alzheimer’s disease

Alzheimer’s disease: The third diabetes

Claus Hancke

May 4, 2006

According to a revolutionary theory, Alzheimer’s is caused by diabetes in the brain. The theory throws light on the need for antioxidants.

It has been one hundred years since the discovery of Alzheimer’s disease. Alzheimer’s is the most severe disease of dementia, and many of us will suffer from it if we become old enough. Those who get Alzheimer’s suffer from an unavoidable dementia which worsens until they loose contact with reality entirely. The brain shrinks and the spaces between the brain cells become filled with a peculiar substance called amyloid. A network of fibres is produced within the cells, decreasing the strength of the chemical signals that the cells use to communicate.

The medical treatment for Alzheimer’s is currently nothing to get exited about. Its function is to strengthen the chemical signals between the cells, but its effects are few. Now, one hundred years after the disease’s discovery, a surprising new theory has paved the way for new possibilities in the treatment of Alzheimer’s. According to the theory, Alzheimer’s is nothing more than a type of diabetes! The theory has such strong foundations that some already call Alzheimer’s “type 3 diabetes.”

Diabetics should not be alarmed by this find. Type 3 diabetes is in no way connected with either insulin requiring type 1 diabetes or the so called old age diabetes, type 2 diabetes. Type 3 diabetes only shows itself in the brain. How does it get there?

The explanation is simple when one knows a few facts about diabetes and insulin: With classic diabetes one lacks insulin, which is normally produced in the pancreas. This is unfortunate because insulin is necessary for the sugar I the blood to enter the cells, where it can be used for energy. The brain is especially dependent on insulin, because it can only metabolise blood sugar (fructose and glucose), not fat as in other tissues.

Therefore the brain needs insulin. But where does it get it? The new theory is based on new knowledge. The brain makes its own insulin! This occurs in the temporal lobes and in deep lying areas of the brain, namely the hippocampus and the hypothalamus. Insulin produced in the brain only affects blood sugar locally as it cannot leave the brain. Likewise, insulin produced by the pancreas cannot enter the brain. One can thus have diabetes in the brain without having it in the rest of the body and the reverse.

Q10 protects the brain
Multitudes of data have shown that there are signs of defect in the brain’s sugar metabolism already in the early stages of Alzheimer’s. Is this due to type 3 diabetes, seen as a lack of insulin and therefore sugar within the cells? A solid argument for this new theory is based on a recent animal study where the effect of insulin in the brains of the animals was blocked chemically by an injection of a special insulin toxin (streptozotocin). The animals not only became demented due to the resulting brain diabetes, but also produced fewer neurotransmitters, produced deposits of amyloid, and produced fibres within the nerve cells; just like one finds in Alzheimer’s.

Alzheimer’s could thus be the result of the brain lacking the energy it needs to perform its functions. According to a very prominent researcher in this field, Suzanne de la Monte from Brown University, lack of insulin in the brain causes the production of free radicals (causing oxidative stress) because the weakened cells cannot neutralize them because, for example, they cannot produce the necessary enzymes. The amassed free radicals cause the amyloid deposits, and fibre formation, and so on. They also kill the brain cells.

But if the free radicals are the central reason for the nervous damage, antioxidants should help. Is this the case? Yes; in another recent animal study utilizing the same insulin poison, the animals (rats) were given large doses of Q10 for three weeks following the injection of the poison. The treated animals were much better off in all of the subsequent tests. Their brain cells produced more energy, they were better able to find their way in a labyrinth, and they produced more signalling chemicals in their brains.

It is not unreasonable to mention here that there have been many studies which have shown that long time users of vitamins C and E have a considerably reduced risk of getting Alzheimer’s; or that there is a statistical link between low blood levels of selenium and the quick development of dementia. Vitamins E and C, as well as selenium and Q10, are antioxidants.

Is this comparison valid? This can be considered; studies using human subjects will take shape in the coming years.

By: Vitality Council

References:
1. Ishrat T et al. Coenzyme Q10 modulates cognitive impairment against intracerebroventricular injection of streptozotocin in rats. Behav. Brain Res. 2006; Apr 16;(Epub ahead of print)
2. Lester-Coll N et al. Intracerebral streptozotocin model of type 3 diabetes: Relevance to sporadic Alzheimer disease. J Alzheimers Dis. 2006;9:13-33.

Overlooked B-vitamin Might Prevent Alzheimer’s Disease

Claus Hancke

September 27, 2004

In the search for substances that might prevent Alzheimer’s disease, the focus has mainly been on antioxidants like Vitamin E and Gingko biloba as well as the B-vitamins B12, B6, and folic acid. However, an American study now indicates that the quite unnoticed B-vitamin Niacin as being able to play a role too.

For 90 years, it has been clear that niacin is important to the nervous system and that severe niacin deficiency can cause dementia – as part of the deficiency disease pellagra. The wonder is that, until now, nobody has made a link between this kind of dementia and Alzheimer’s disease.

So far, the study has involved 6158 inhabitants of Chicago. They were all above 65 years of age and the plan was to register their diet and follow them every third year with psychological tests for dementia. They succeeded in doing so with 3718 of the trial subjects. Among these, 815 people who did not have Alzheimer’s disease at the beginning of the trial were randomly chosen. They were divided into five groups according to their intake of niacin.

131 people in the latter group were diagnosed with Alzheimer’s disease during the following four years. It turned out, however, that in the 20% who had the lowest intake of niacin (on average 12.5 mg. a day), the incidence of Alzheimer’s disease was more than three times as high compared to the ones with the highest intake (22.4 mg. a day or more). This was the result after statistical adjustments for known or suspected causes of the disease had been performed.

Both dietary niacin and niacin from vitamin tablets were included in the study. Good dietary sources of niacin are whole meal, liver, meat, fish, milk, legumes, – and coffee! Brewer’s yeast is also a good source of niacin, but, unfortunately, the same does not apply for beer! The average Englishman gets 2/3 of his niacin from meat, beverages, milk, and cheese, while only 1/8 comes from vegetables.

By: Vitality Council

References:
1. Morris MC, Evans DA, Bienias JL, Scherr PA, Tangney CC, Hebert LE, Bennett DA, Wilson RS, Aggarwal N. Dietary niacin and the risk of incident Alzheimer’s disease and of cognitive decline. J Neurol Neurosurg Psychiatry. 2004;75(8):1093-9.
2. National Food Agency of Denmark (Levnedsmiddelstyrelsen): Nutrient recommendations, 1992 (Naeringsstofanbefalinger, 1992).

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