Alzheimer’s disease: The third diabetes

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

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.

Vitamin E May Be Diabetic’s Saviour

December 20, 2005

About one out of every two diabetics has a five times larger than average risk of dying from heart disease. This risk can be cut in half by vitamin E. This is a well justified theory which is now being tested in a large Israeli study.

It is well known that the heart’s of diabetics become easily atherosclerotic, often causing them to die due to blood clots in the heart. Therefore, health officials work hard to combat atherosclerosis in diabetics. For example, diabetics are encouraged to take cholesterol reducing medicine, even when their cholesterol levels are very low. Diabetics’ blood pressure should also be low.

If one believes the Israeli researcher, Andrew Levy, the lives of even more diabetics can be saved by taking 400 units of vitamin E daily. Levy’s theory is now being tested in Israel in a large randomised study with 5,000 middle aged diabetics. Half of them will receive vitamin E for the next four years while the other half will not. If it goes as is hoped, the result will have enormous significance for public health.

It is optimistic to implement such an expensive study with vitamin E. As every (Danish, ed.) TV watcher knows, vitamin E doesn’t work against anything. Why would Levy and his co-workers from the Israeli Technion Technical Institute, where many Nobel prise winners can be found, go against the flow?

The explanation involves an antioxidant which few non-experts know of. It is called haptoglobin and is a protein which is created in the body. Haptoglobin binds the blood’s colouring agent, the iron rich haemoglobin, if it becomes detached from the red blood cells. In this way it prevents iron poisoning and therefore against overloading of free radicals in a long list of conditions where red blood cells die.

Disregarded effects of vitamin E
Levy and his co-workers have shown time and time again that haptoglobin works as an antioxidant. There is more to the story; haptoglobin is found in two forms, which are not equally effective antioxidants. Type 1 haptoglobin works much better than type 2. If one has type 2 haptoglobin (like 40% of the Israeli diabetics) the risk of death due to heart disease is five times higher than normal! In other words, a very large part of diabetics’ high death rate due to heart disease is because one out of every two of them has an insufficiency defence against oxidation because of ineffective haptoglobin.

The logical consequence of this enormous difference is, according to Levy, that the poorly protected diabetics with type 2 haptoglobin should take supplementary antioxidants. This is where the vitamin E study comes in. Vitamin E should be able to help. On the other hand, if it does help, why have other studies with vitamin E not previously shown this effect?

Levy believes that this is presumably because they have not been analysed with this effect in mind. He studied serum from a large sample of the ca. 10,000 participants in the Canadian HOPE study, where atherosclerotic participants received 400 units of vitamin E daily. The people behind the HOPE study found no effect of the vitamin E. But what about the 1,000 diabetics in the study? About a year ago, Levy proved that vitamin E reduced the risk of heart disease by 50% in the diabetic participants who had type 2 haptoglobin.
This surprising result was hidden in the HOPE study and was apparently unknown. This is quite educational. If the most threatened diabetics’ very high risk of heart disease can be halved with a cheap, harmless, vitamin E pill, the signification is very large.

Until 2010 we only have these results. There are no other results to turn to. It is not even possible to find out which kind of haptoglobin you have. If you wish to prevent heart disease, you have to do it in the dark. It is however risk free.

By: Vitality Council

1. Andrew P. Levy et al. The Effect of Vitamin E Supplementation on Cardiovascular Risk in Diabetic Individuals With Different Haptoglobin Phenotypes. Diabetes Care 27:2767, 2004.
2. Levy AP et al. Strong Heart Study. Haptoglobin phenotype is an independent risk factor for cardiovascular disease in individuals with diabetes: The Strong Heart Study. J Am Coll Cardiol. 2002 Dec 4;40(11):1984-90.
3. Suleiman M, et al. Haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction. Diabetes. 2005 Sep;54(9):2802-6.
4. A survey of the study can be found at Clinical