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

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.

Lipoic Acid. Perhaps The Medicine Of The Future?

January 25, 2006

Lipoic acid is a simple fatty acid which is produced in all human cells. It is considered to be the ideal antioxidant and it may actually be highly beneficial against diabetes, neurological damage, and more. However, it is banned in Denmark.

Is lipoic acid the medicine of the future? There are many who believe this is so. One of the worlds leading experts in the field of antioxidants, Lester Packer of Southern California University, has emphasized that lipoic acid is the ideal antioxidant and a recent article by Polish researchers cautiously comes to the same conclusion.

Packer maintains that “from a therapeutic viewpoint, few natural antioxidants are ideal.” He continues by indicating that an ideal antioxidant should fulfil many demands: It should be absorbable by the intestines, occur in a form useful to the cells and have many antioxidant effects (including interaction with other antioxidants) in both cell membranes and the organism’s aqueous phase. It also must be completely non-toxic. Packer believes that lipoic acid is unique among antioxidants because it fulfils these demands. Lipoic acid is a potentially very effective medicine in many situations where free oxygen radicals are implicated.

Lipoic acid is a small sulphur containing fatty acid. It was discovered in 1950, but its special anti-oxidative properties were first noticed during the 1980’s. It is a very strong antioxidant, considerably stronger than vitamin C. It is also both fat and water soluble, which means that it can enter and have effects both outside and inside the cells. When other antioxidants such as vitamins E and C are used up, they can be “recharged” by lipoic acid so that they can be used again. It is also necessary for the cells’ metabolism and for a period it was considered to be a vitamin, but when laboratory animals did not suffer damage from lipoic acid deficiency, this idea was dropped.

Diabetes and nerve damage
The question of whether or not it is a good idea to take lipoic acid supplements should be addressed. The previously mentioned Polish researchers analysed some of the as yet very limited knowledge in this area and found that lipoic acid may be especially interesting for diabetics. Studies on animals with type II diabetes have shown strong improvement of their diabetes with lowered blood sugar levels and better utilization of their bodies own insulin with lipoic acid supplements. Many studies have shown that lipoic acid improves nerve function in diabetics with nervous inflammation.

Just as interesting, lipoic acid may be an effective weapon against the protein damage caused by heightened blood sugar. In a process called protein oxidation the proteins change structure in a way which is similar to what happens when an egg is boiled. This oxidation is an important part of the explanation for diabetics’ tendency to get cataracts, where the lens of the eye becomes clouded. In animal studies this is counteracted by lipoic acid.

The apparent nerve protective properties have lead to studies in Alzheimer’s treatment. In two studies it was found that the disease was halted by lipoic acid, but these results should be considered as provisional. The same result has been found in studies of Parkinson’s disease.

Does lipoic acid prevent cancer? The Polish researchers are uncertain. Their tissue studies indicate that small doses promote growth, while large doses inhibit growth. Dare we claim that this effect speaks for supplementation? We produce small doses of lipoic acid without help.

Only about 1,000 articles on lipoic acid can be found in the medical database, Medline. Research is still in its infancy. Even so, entering lipoic acid into Google gives over two million links (search “lipoic acid”).

By: Vitality Council

Reference:
Bilska A et al. Lipoic acid – the drug of the future? Pharmacological Review 2005;57:570-77.

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

References:
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 Trials.gov: www.clinicaltrials.gov/ct/gui/show/NCT00220831.

care.diabetesjournals.org
www.cardiosource.com/jacc/index.asp
www.clinicaltrials.gov/ct/gui/show/NCT00220831
www.iom.dk

Vitamin E Lowers Cholesterol Levels in Diabetics

December 13, 2005

There are at least eight different kinds of Vitamin E, but typically we only get one of those in vitamin pills. One of the other kinds prevents arteriosclerosis, while a third kind has been shown to effectively lower the blood cholesterol levels of diabetics.

When you buy vitamin E in pill form, you almost always get alpha-tocopherol. Alpha-tocopherol (natural and sometimes, unfortunately, synthetic) has also been used exclusively in almost all of the studies on vitamin E’s effectiveness against cardiovascular disease.

There are other tocopherols than alpha-tocopherol. They all share the same basic chemical structure but differ in their side chains. Tocopherol can come in alpha, beta, gamma, or delta forms depending on the position of its side chains. Apha-tocopherol, the type used in vitamin pills, has the greatest effect as a vitamin.

Tocotrienols, another vitamin E form, are less well known. They differ from the other forms by having three double binds in their side chain. They are found in palm oil as well as grains such as oats, barley, rice, and corn. Tocotrienols can also be found in alpha, beta, gamma, and delta forms.

These tocotrienols are coming into the spotlight. For many years, on the basis of animal studies and small studies using humans, there has been the suspicion that they are effective against atherosclerosis. For example, ten year ago an American randomised study with 50 test subjects showed that tocotrienols from palm oil definitely counteracted atherosclerosis of the carotid arteries. Unfortunately no follow up study has been preformed.

Recently an Indian randomised study has surfaced. It shows that tocotrienols from rice sources sink the cholesterol concentration in the blood of type 2 diabetics (old age diabetes). In this study 19 diabetics received placebos for a period of 60 days. Before or after this 60 period they received, for a similar period, capsules containing rice with high concentrations of tocotrienols (each participant received 3 mg tocotrienol per kilo bodyweight per day). The study was designed so that no one knew which participants received which pill at what time until the study was completed.

Unsolved problems
The results showed that the tocotrienols reduced the total cholesterol levels of the participant’s blood by no less than 30%. Even more encouraging, the “bad” cholesterol, (LDL cholesterol) which can become oxidised and cause atherosclerosis, fell by an astonishing 42%. This effect is just as pronounced as seen with traditional cholesterol lowering medication, the so called statins.

It seems that anyone who can get a hold of tocotrienols is free from seeking traditional cholesterol lowering treatment. But before this is certain and becomes common practice, a few things should be further looked analysed.

First and foremost, can the results of the aforementioned study be reproduced? As stated earlier tocotrienols were effective against atherosclerosis in the carotid arteries, but in the study which showed this effect, the participants’ total cholesterol was unchanged! Tocotrienol does not always lower cholesterol. But does it always counteract atherosclerosis? At best the answer is maybe, we don’t know. After looking at the results of the two studies we can hypothesise that the differences in their results could be the result of the different tocotrienol blends used. The first study used a palm oil extract while the second used a rice source. The differences between alpha, beta, gamma, and delta tocotrienol is sufficient, their effects should differ.

Other things which we understand even less could also play a role. The likely cholesterol lowering effect of the rice tocotrienol should also be tested for possible side effects and the results of this should be compared with the side effects of traditional cholesterol medicine. A big job awaits researchers.

Meanwhile, the studies have shown with certainty that (apart from that oatmeal and brown rice are healthy) we are not finished with vitamin E or, more to the point, the E vitamins. There are many of them, and they have different effects. Their potential is very promising.

By: Vitality Council

References:
1. Tomeo AC, Geller M, Watkins TR, Gapor A, Bierenbaum ML. Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotid stenosis. Lipids. 1995 Dec;30(12):1179-83.
2. Qureshi AA, Salser WA, Parmar R, Emeson EE. Novel tocotrienols of rice bran inhibit atherosclerotic lesions in C57BL/6 ApoE-deficient mice. J Nutr. 2001 Oct;131(10):2606-18.
3. Baliarsingh S, Beg ZH, Ahmad J. The therapeutic impacts of tocotrienols in type 2 diabetic patients with hyperlipidemia. Atherosclerosis. 2005 Oct;182(2):367-74. Epub 2005 Apr 20.

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www.nutrition.org
www.athero.org
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