Promising treatment for macular degeneration

December 22, 2007

New orthomolecular treatment named as the “first choice” for AMD, otherwise known macula degeneration.

In the November 28, 2006 edition of the Vitality Council Newsletter we reported on a study which indicated that eating eggs, which contain the antioxidants lutein and zeaxanthine, has positive effects on AMD.

Almost two years ago we described a maybe even more important study undertaken at the University of Rome. It showed that normal recommended doses of simple dietary supplements prevents the most common form of blindness, the age related degeneration of the retina otherwise known as “retinal calcification.” This is what medical professionals call AMD. About one in eight people over the age of 85 have AMD severe enough to cause vision loss.

This study has recently been published again, giving us grounds to discuss AMD in more detail.

One does not become completely blind due to AMD. Peripheral vision is still maintained, enabling one to orient themselves in a room or go for a walk. Even so, AMD does cause handicap. Central vision is lost, which means that the ability to see shapely is lost. Therefore reading is impossible, seeing the TV, cooking, using tools, working on the computer, and recognising friends and family is difficult. A grey dot in the middle of the field of vision replaces everyone’s faces.

Central sight is governed by a yellow spot on the eye’s retina where the highest concentration of colour registering cones is found. This is why one of the first things lost in AMD is colour vision.

The changes in AMD can be directly observed on the retina when one looks into the eye. In the early stages it is characterized by small or larger deposits of yellowish waste products in the eye. Every one of these deposits represents a hole in the field of vision. This is unnoticeable so long as these hoses are small. Almost everyone over the age of 50 has at least one of these deposits, but if there are many deposits of greater size, the risk for blindness is great.

Severe cases of AMD can be characterised by an accumulation of larger deposits alone. This is called dry AMD. Another, and more dangerous, form is the so called wet AMD. In this form “leaky” blood vessels grow in under the retina, possibly as the body’s effort to bring more energy to the retina. The result is that liquid seeps out of these vessels causing total destruction of central vision. This can occur very quickly, but with quick intervention of an ophthalmologist (eye doctor) the new blood vessels can be blocked with laser treatment and vision can be saved in many cases.

The deposits and new blood vessels lead to the creation of dents in the retina. In severe cases scars form and pull on the retina. This leads to vision where straight lines seem bent. Often, but not always, one can discover the beginnings of AMD by holding a piece of graph paper at a normal reading distance and looking at it one eye at a time. If the lines are curved, an eye doctor should be consulted immediately.

New methodology
The republished study mentioned earlier is a double blinded study that showed with statistical certainty an improvement in the sight of patients with early stage AMD after they received a combination of n-3 fatty acids, Q10, and L-carnitine. The improvement in sight, which was slight, was first present after 3-6 months, after which sight remained stable until the end of the study one year later. This effect lasted even longer in a following study. It was also observed that the number of deposits decreased! This is important and very promising. Improvement occurred primarily for those with mild cases, but also for some with more severe AMD. Early diagnosis is paramount.

The theory behind these finds is that AMD is a disease of the mitochondria, which means that it is a disease which affects energy production in the cells. This is supported by the fact that cells from AMD affected retinas have more damaged mitochondria than normal cells when viewed under and electron microscope. The logic behind the treatment used in the study is therefore the following:

The vitamin-like substance carnitine is necessary for mitochondrial fat uptake and metabolism.

The fat is added as n-3 fatty acids, like those found in fish oil. N-3 fats compose no less than 30% of the structure of the retina!

Q10 can be understood as the motor’s sparkplug. It optimises metabolism so that energy production can start. The body’s own Q10 production falls with age and because of this, and carnitine deficiency, there becomes less energy available. It is hardly coincidental that patients with wet AMD have less Q10 in their blood than normal.

This important study powerfully indicates that quick action can stop newly diagnosed AMD. The authors strongly believe that their treatment should be the treatment of choice for newly diagnosed AMD.

By: Vitality Council

References:
1. Feher et al. Metabolic therapy for early treatment of age-related macula degeneration. Orv Hetil 2007;148:2259-68.
2. Feher et al. Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl-L-carnitine and coenzyme Q10. Ophtalmologica 2005;219:154-66
3. Feher et al. Mitotropic compounds for the treatment of age-related macular degeneration. The metabolic approach and a pilot study. Ophtalmologica 2003;217:351-7
4. Blasi et al. Does coenzyme Q10 play a role in opposing oxidative stress in patients with age-related macular degeneration? Ophtalmologica 2001;215:51-54.
5. Feher J et al. Mitochondrial alterations of retinal pigment epithelium in age-related macular degeneration. Neurobiol Aging 2005;June 22: 15979212.

Again, uneasiness regarding the pill

July 31, 2006

The pill (contraception in pill form) drains the body of the antioxidants, vitamin E and Q10. This could mean that a supplement would make it much safer to take the pill.

More than 100 million women worldwide use the pill as contraception. The pill is believed to be remarkably safe, and it is easy to forget that it can have serious side effects. According to a Dutch report from 2003, users of the pill have a 3-6 times higher risk of developing blood clots in the veins, which is a dangerous condition. In addition, they have a 2-5 times higher risk of developing blood clots in the heart or of suffering from stroke. These numbers are the same for the modern forms of the pill, which have few other few side effects.

If the risk of disease is low, (because of being young and otherwise healthy) than a low percentage increased in risk does not so important. But why is there any increase at all? Light has been thrown on this question by researchers of the Albert Einstein College of Medicine in New York. They have proven that users of the pill have lower vitamin E and Q10 levels in their blood than women who do not take the pill. Vitamin E and Q10 are well known antioxidants.

This is nothing new. Already 15 years ago, researchers believed that vitamin E could reduce the risks associated with the pill. It was also known that the pill drains the body of antioxidants, which can be directly linked to an increased risk of blood clot formation. When one lacks vitamin E, the fats in the blood become oxidized, thereby stimulating the platelets to stick together causing the formation of blood clots. Logically, it was suggested that vitamin E should be combined with use of the pill.

The pill uses up the body’s vitamin E and Q10 reserves. This has been proven again, this time in a study where 15 users of the pill in their forties were compared with women in the same age group who did not take the pill. The differences found were statistically valid, and although this was a small study there were no doubts regarding the results. These results were known before the study was completed; the problem was that nobody had been paying any attention to them.

Unsolved problems
Why does the pill strain the bloods vitamin E and Q10 contents? The pill raises the body’s oestrogen levels. This is why the ovaries go into hibernation so that ovulation is inhibited. The body registers a hormone level high enough that the ovaries can take a break. Even normal (physiologic) levels of oestrogen stimulate the formation of free radicals and therefore cause an increased use of antioxidants. This has been shown in an American study of the cells which compose the inner walls of the blood vessels (endothelium cells). They also showed that free radicals resulting from the presence of oestrogen caused the cells to grow, causing the blood vessels to thicken. It is believed that this increases the risk of blood clots. It also indicates that antioxidants could prevent such side effects.

For practical purposes, women with an increased risk for side effects are advised not to take the pill. This includes women over the age of 35, women with high blood pressure, and so on. All women with an increased risk of blood clots should refrain from using the pill. This causes some amount of contemplation. Who knows if they are in the high risk group? Is their risk so low that a five fold increase in risk is acceptable?

Aside from these problems it is important to know that if you use the pill, your defence against the formation of free radicals is weakened. Even though this is well known, no one has, until recently, thought to reduce this risk with the use of antioxidants.

An important question follows: What is the long term prognosis for women who took the pill for many years when they were young? During the many years they took the pill, they had reduced levels of vitamin E and Q10 in their blood. In the short term, this increased the oxidation of the blood’s fats which increased the risk of blood clots. But does it cause problems in the long term like smoking and high blood pressure? As yet, we can only guess.

By: Vitality Council

References:
1. Palan PR Magneson AT, Castillo M, Dunne J, Mikhail MS. Effects of menstrual cycle and oral contraceptive use on serum levels of lipid soluble antioxidants. Am J Obstet Gynecol. 2006 May;194(5):e35-8. Epub 2006 Apr 21
2. Felty Q. Estrogen-induced DNA synthesis in vascular endothelial cells is mediated by ROS signaling. BMC Cardiovasc Disord 2006 Apr 11;6:16
3. Ciavatti M, Renaud S. Oxidative status and oral contraceptive. Its relevance to platelet abnormalities and cardiovascular risk. Free Radic Biol Med. 1991;10(5):325-38
4. Saha A, Roy K, De K, Sengupta C. Effects of oral contraceptive norethindron on blood lipid and lipid peroxidation parameters. Acta Pol Pharm. 2000 Nov-Dec;57(6):441-7.
5. Tanis BC, Rosendaal FR. Venous and arterial thrombosis during oral contraceptive use: Risks and risk factors. Semin Vasc Med. 2003 Feb;3(1):69-84
6. Crook D, Godsland I. Safety evaluation of modern oral contraceptives. Effect on lipoprotein and carbohydrate metabolism. Contraception. 1998 Mar;57(3):189-201

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.

Cholesterol reducing pills: Do they have a downside?

August 3, 2005

Medications taken against cholesterol may prolong life in the event of arteriosclerosis and perhaps even heart failure. However, new figures seem to indicate that many patients get serious side effects from taking such medications, which side effects could have been avoided had they also taken Co-enzyme Q10.

Millions of people worldwide use cholesterol reducing medicine in the form of statins. These people most often have clogged coronary arteries and the statins are used to protect them against further atherosclerosis, blood clots, and strokes. They work, but to a lesser degree than many people think.

If they are given to one hundred 40-80 year old people who are at high risk due to atherosclerosis or diabetes, they prevent about one coronary blood clot or one stroke per year. In the course of five years, about two deaths are avoided.

Many of the treated meanwhile develop heart failure, which is reduced pump function of the heart, because atherosclerosis damages the heart muscle permanently. They begin to complain of tiredness and increasing shortness of breath.

Is it risky to take cholesterol lowering pills in this situation? There can be debated. The debate is due to the way that the medicine works. It blocks the livers production of mevalonic acid, which is necessary for the production of cholesterol, but it also blocks the production of vital Q10! Not only does the blood’s cholesterol level fall, but also the bloods Q10 level.

Because Q10 is necessary for the tissues to create energy it is easy to imagine that a heart muscle which is weakened by heart failure, is further weakened when Q10 is removed.

Apparently statins work anyway. Statins are believed to lengthen life in heart failure. Not because they lower cholesterol, which may actually be damaging when suffering from heart failure, but because statins have other effects than reducing cholesterol. They are antioxidants and counteract inflammation. In addition they promote the creation of new blood vessels in the heart. None of these effects have anything to do with cholesterol.

Maybe the positive effects of statins outweigh the dramatic Q10 loss that they cause. Nonetheless, it is hard to believe that this loss is completely harmless, especially with heart failure.

The American cardiologist P.H. Langsjoen is one of those who warn that we find ourselves in an epidemic of heart failure with unclear reasons and who believe that statins could be one of the reasons.

At a congress in Los Angeles he put forth data which indicates previously unrecognised side effects. Two thirds of 51 newly referred statin treated patients complained of muscle pain, more than 80% were abnormally tired, and almost 60% had shortness of breath. When they stopped using statins and instead received Q10 (240 mg/day), most became symptom free.

At the same congress a randomised trial showed that muscle pain and tiredness was present in one out of every ten on those treated with statins, but disappeared when they took Q10 (100 mg/day). Just as important, more than half experienced an improved quality of life and many showed improved heart function.

Pills against cholesterol lengthen life, but it is necessary to take Q10 if quality of life also increases so that a longer life is a life worth living.

By: Vitality Council

References:
1. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: A randomised placebo-controlled trial. Lancet 2002;360:7-22.
2. Langsjoen PH et al. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 2003;18(1-4):101-11.
3. Liao JK. Statin therapy for cardiac hypertrophy and heart failure. J Investig Med. 2004 May;52(4):248-53.
4. Bandolier. Statins in heart faikure. http://www.jr2.ox.ac.uk/bandolier/booth/cardiac/statHF.html
5. Fourth Conference of the International Coenzyme Q10 Association. Los Angeles April 14-17 2005.

www.thelancet.com
www.iospress.nl/html/09516433.php
journalseek.net/cgi-bin/journalseek/journalsearch.cgi
www.jr2.ox.ac.uk/bandolier/booth/cardiac/statHF.html
www.coenzymeq10.it/home.html
www.iom.dk

Cholesterol Medicine Halves the Amount of Coenzyme Q10 in the Blood

August 16, 2004

Heart specialists normally shrug off the suggested recommendation that patients treated with cholesterol lowering drugs must take Coenzyme Q10. While it is common knowledge that such medicine interferes with the body’s ability to create Coenzyme Q10, and that Q10 is essential for life, conventional medical thinking still holds that supplementation is superfluous because of the belief that medical treatment is effective and increases life span!

Now this conventional thinking is being challenged by new studies showing that one of the most commonly used cholesterol lowering medicines not only decreases but actually halves the amount of Coenzyme Q10 in the blood.

By: Vitality Council

Reference:
Rundek T, Naini A, Sacco R, Coates K, DiMauro S. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Arch Neurol. 2004;61(6):889-92.

archneur.ama-assn.org
www.iom.dk

Q10 Prevents Migraine

July 26, 2004

The antioxidant Q10 is an efficient remedy for the treating of migraine without side effects. This has been demonstrated by Swiss researchers at the University Hospital in Zürich. The discovery was presented in San Francisco at a congress for neurologists immediately prior the summer holidays.

The Swiss study is the second successive study to show that Q10 prevents migraine. Two years ago, the treatment was tested in a so-called open trial at Jefferson University of Pennsylvania.

32 severely affected migraine patients were included – they had an average of eight migraine attacks a month. During the course of three months, they were each given 150 mg. of Q10 a day and the frequency of migraine attacks were gradually reduced to less than three a month.

The result from Pennsylvania made such a big impression that a more thorough study was found necessary. This study has now been completed in Switzerland as a randomized trial with 42 participants. Before the trial, the participants suffered an average of 4-5 migraine attacks a month.

During the trial, 50% of the participants were given placebo while the other 50% were given 300 mg. of Q10 divided into three doses a day. After three months, 48% of the ones who had been given Q10 had achieved a 50% reduction in the frequency of migraine attacks while only 14% of the placebo group achieved the same effect. As a net result, 36% had substancially benefited from the treatment. A result of this magnitude can certainly be compared with the best working of the presently used treatments.

The leader of the Swiss trial, the neurologist Peter S. Sandor, underlines the absence of adverse effects as a decisive factor – particularly to young women who might fear that the conventional treatment could have teratogenic effects.

However, the result also opens up to other interesting perspectives in the understanding of migraine. Q10 is a natural substance necessary to the cells’ energy production and the theory behind the study is that migraine may be caused by a lack of chemical energy in the nerve cells.

According to David Dodick, professor in neurology at the respected Mayo clinic in Arizona, this new study was well performed and the result is statistically robust. He believes that Q10 can be an attractive form of treatment to those who prefer a natural alternative to prescription drugs.

By: Vitality Council

Reference:
Sandor P. et al. Water-soluble Coenzyme Q10 demonstrates significant migraine prophylaxis. American Academy of Neurology. 56th Annual Meeting: Abstract S43.004, 2004.

www.aan.com/professionals
www.iom.dk

Q10 and Ginkgo biloba may be taken together with blood thinners

May 5, 2003

Q10 and Ginkgo biloba may be taken together with blood thinning medication. A Danish study shows that it is non-dangerous to take the two supplements together with the blood diluting substance Warfarin.

An article in the danish medical journal, Ugeskrift for læger, rejects the suspicion that the two supplements may either weaken or enhance the effect of Warfarin (Marevan), which is typically used in the prevention and treatment of blood clots, eg in the heart or brain.

By: Vitality Council

Reference:
Ugeskrift for Laeger, 28. April 2003, no. 18.

www.dadlnet.dk
www.iom.dk

Coenzyme Q10, Research references

January 1999

1. Battino M, Fato R, Lenaz G: Coenzyme Q10 can control the efficiency of oxidative phosphorylation.; Int J Tissue React 12, no. 3, pp. 137-144, 1990.
2. Chen Rou-Shayn et al. Coenzyme Q10 treatment in mitochondrial encephalomyopathies. Eur Neurol 37:212-18, 1997.
3. Folkers K et al. Biochemical rationale and the cardiac response of patients with muscle disease to therapy with coenzyme Q10. Proc Natl Acad Sci U S A 82;13:4513-16, 1985.
4. Folkers K, Wolaniuk J, Sinonsen R, et al, in K. Folkers, Y Yamamura, Eds. Biochemical and Clinical Aspects of Coenzyme Q10, Vol. 5. Amsterdam, Elsevier Science Pub. 353-8, 1985.
5. Folkers K, Langsjoen P, Nara Y, et al. Biochemical deficiencies of coenzyme Q10 in HIV-infection and exploratory treatment. Biochem Biophys Res Commun 153:888-96, 1988.
6. Folkers K, Hanioka T, Xia LJ, et al. Coenzyme Q10 increases T4/T8 ratios of lymphocytes in ordinary subjects and relevance to patients having the AIDS-related complex. Biochem Biophys Res Commun 176; (2):786-91, 1991.
7. Folkers K, Morita M, McRee Jr. J. The activities of coenzyme Q10 and vitamin B6 for immune response. Biochem Biophys Res Commun 193: 88-92, 1993.
8. Fryburg DA et al. The immunostimulatory effects and safety of beta-carotene in patients with AIDS. VIIIth Int Conf on AIDS, Amsterdam, 1992.
9. Sato K. Pharmacoklinetics of coenzyme Q10 in recovery of acute sensorineural hearing loss due to hypoxia. Acta Otolaryngol Suppl (Stockh.) 458: 95-102, 1988.
10. Simonsen R, Folkers K, Komorowski J, et al, in K Folkers, GP Littarru, T Yamagami, Eds. Biochemical and Clinical Aspects of Coenzyme Q10, Volume 6. Amsterdam, Elsevier Science Publ., 363-73, 1991.
11. Sobreira C et al. Mitochondrial encephalomyopathy with coenzyme Q10 deficiency. Neurology 48:1238-43, 1997.
12. Yamabe H, Fukuzaki H, in K Folkers, GP Littarru, Y Yamagami, Eds. Biochemical and Clinical Aspects of Coenzyme Q10, Vol. 6. Amsterdam, Elsevier Sci Pub., 1991: 541-5, 1991.
13. Zeppilli P, Merlino B, DeLuca A, et al, in K Folkers, GP Littarru, Y Yamagami, Eds. Biochemical and Clinical Aspects of Coenzyme Q10, Volume 6. Amsterdam, Elsevier Science Pub. 541-5, 1991.

 

Sources
Joseph E. Pizzorno Jr., Michael T. Murrey & Melvyn R. Werbach.