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Latest news on selenium

Claus Hancke

January 12, 2010

Intensive research is going on in utilization of selenium against cancer.
The public in Denmark do not hear much of it, but here is a selection of recent news.

The lack of television and newspaper information may give the impression that there is quiet on the antioxidant front concerning disease control. This is not the case. The news shortage is chiefly due to the censorship that has been introduced. Regarding selenium alone, being one of the major antioxidants, there were in 2009 published more than 900 scientific articles. Here we will mention a selection of recent articles about selenium in the fight against cancer.

A famous attempt to demonstrate whether antioxidants protect against cancer were performed in the years 1985-91 in the Chinese Linxian province. Nearly 30.000 participated in the study, which showed a strong decrease in cancer risk among those who received a supplement of selenium (50 micrograms) and Vitamin E and Beta Carotene (respectively 30 and 15 mg). Now it has been determined, what had happened to the participants 10 years later (2001). Even after so long a time, there were relatively more survivors in this group than among those who received other supplements (eg. Vitamin A + zinc, was of no benefit). In particular, the group had reduced incidence of cancer of the stomach, but it was the participants under 55 years of age who experienced the greatest gain – you must avoid lacking vital nutrients already from the youth.

Apparently this result is contradicted by another famous study, the SELECT trial conducted in the U.S. Here it appeared that you could not prevent prostate cancer using selenium, vitamin E or a combination of both. This study was in large scale and the result a huge disappointment.

One of the world’s leading selenium specialists, Margaret Rayman, did point out however, a few months ago what really is obvious: Supplementation with selenium is of no benefit if you already get enough! As a general rule you get enough in the U.S., where you typically get 3-4 times as much selenium in the diet as in Denmark. Sufficient selenium is essential for the body to form enough of the enzymes which we presume protects against cancer. Amongst others Rayman refer to another U.S. cancer trial where you just saw a massive impact in those who received the least amount of selenium, but no effect in those who got the most.

Heavy metals neutralized
One of the veterans in selenium research is Gerhard Schrauzer from San Diego University of California. He has been involved more than 20 years. Now he points out that selenium is able to detoxify numerous toxic metals that somehow during our civilized environment ends up in our bodies. This applies to lead, mercury, copper, cadmium, arsenic, etc. Selenium inactivates these metals by forming insoluble compounds with them. But, says Schrauzer, one must remember that at the same time selenium is used up, so we for that reason are less protected against cancer. In Europe we already get too little selenium, but heavy metals etc. increases the demand.

Taylor and associates have written an article on new advances in selenium research. They write that the renewed interest in selenium is linked to the fact that the anti-cancer effect is now very well documented in animal studies. This is worth noticing.

And precisely on animals a research team from San Diego University have demonstrated that the effect of chemotherapy (cisplatin) against cancer of the colon is reinforced considerably by large supplements of antioxidants (A and vitamin E and selenium) combined with fish oil. The group believes their achievement justifies that research is made with people. The result is very exciting because cancer doctors in this country often discourages in strong terms their patients from combining antioxidants with chemotherapy. The reason for this warning has hitherto been unclear.

Selenium and chemotherapy
Researchers from The Karolinska Hospital in Stockholm state without hesitation that it is well documented that selenium prevents cancer. They describe several experiments which have shown that selenium has strong anti cancer effects – especially against cancer, which no longer responds to chemotherapy. Normal cells will not be harmed by the selenium doses needed for this!

Italian researchers, however, stresses that people can get too much selenium (but living in Denmark you have take approx. two selenium tablets a day in order to get the same amount as a typical American). They argue that high doses may increase the risk of diabetes, an assertion, however, that is controversial.

In the Netherlands, like in China there has been an interest in selenium and cancer of the esophagus. More than 120,000 persons who was 55-69 years old in 1968, delivered at that time, a portion nail clips from their big toes. 16 years later it was found who and how many have got cancer of the esophagus or stomach in the meantime. Then the selenium levels in their nails was measured and compared with the levels in healthy subjects. It was found that the risk of both cancers was significantly higher among those who only had small amounts of selenium in their nails, and hence their body.

A curious study has been conducted in Japan. Here researchers cultivated broccoli-sprouts in a selenium-rich environment, so the sprouts got an extra high content of selenium. In a laboratory study the sprouts was investigated for their impact on prostate cancer tissue. The enriched sprouts inhibited cancer growth clearly better than normal sprouts. Now the Japanese suggests, that men eat that kind of sprouts to prevent cancer of the prostate.

Finally other Japanese mention, that it is well known that selenium can kill cancer cells from humans, but but precisely how this happens is still unclear. They have reached the conclusion that at least part of the effect is due to selenium starts off a cancer cell death process using the same mechanism (apoptosis) as when normal cells must be replaced and die. Such a mechanism is of course necessary, since almost all normal cells divide continuously. There would soon be twice as many, and we would grow indefinitely, if not worn-out cells were put out.

As you can see, the research is really alive. Much of our understanding of selenium is achieved in very recent years. More will undoubtly follow.

By: Niels Hertz, M.D.

References
1. Qiao YL et al. Total and cancer mortality after supplementation with vitamins and minerals: follow-up of the Linxian General Population Nutrition Intervention Trial. J Natl Cancer Inst. 2009 Apr 1;101(7):507-18. Epub 2009 Mar 24.
2. Lippman SM et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009 Jan 7;301(1):39-51. Epub 2008 Dec 9.
3. Rayman MP. Selenoproteins and human health: insights from epidemiological data.
Biochim Biophys Acta. 2009 Nov;1790(11):1533-40. Epub 2009 Mar 25.
4. Schrauzer GN Selenium and selenium-antagonistic elements in nutritional cancer prevention.
Crit Rev Biotechnol. 2009;29(1):10-7.
5. Taylor D. Recent developments in selenium research. Br J Biomed Sci. 2009;66(2):107-16; quiz 129.
6. Ma H. Bi Efficacy of dietary antioxidants combined with a chemotherapeutic agent on human colon cancer progression in a fluorescent orthotopic mouse model. Anticancer Res. 2009 Jul;29(7):2421-6.
7. Selenius M. Selenium and selenoproteins in the treatment and diagnostics of cancer.
Antioxid Redox Signal. 2009 Sep 21. [Epub ahead of print]
8. Vinceti M. Risk of chronic low-dose selenium overexposure in humans: insights from epidemiology and biochemistry Rev Environ Health. 2009 Jul-Sep;24(3):231-48.
9. Steevens J. Selenium status and the risk of esophageal and gastric cancer subtypes: the Netherlands cohort study. Gastroenterology.. [Epub ahead of print]
10. Abdulah R. Selenium enrichment of broccoli sprout extract increases chemosensitivity and apoptosis of LNCaP prostate cancer cells. BMC Cancer. 2009 Nov 30;9:414.

Fish oil reduces age-related blindness

Claus Hancke

October 14, 2009

New U.S. study shows that intake of fish oil may reduce the incidence of age-related blindness by 30%

There seems to be no end to blessings from fish oil.

Fish oil is the end stages in the development of omega-3 fatty acids which is transformed from alpha-linolenic acid in a number of processes to E.g. eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) which then are converted to prostaglandin E 3 with a wide range of health-promoting properties.

The fish oils EPA and DHA are some of the strongest anti-inflammatory nutrients, we can consume. This is probably one of the reasons why they reduce the risk of blood clots, but they also reduces blood triglycerides, reduces inflammation in rheumatic diseases, enhances children’s learning capacity, reduces the risk of pre-eclampsia (pregnancy–induced high blood pressure) and premature birth, and gives brighter children from pregnant women who took fish oil and much more.

It is indeed difficult to see the end of the health-promoting properties, we can get from fish oil, and new scientific findings seems to emerge all the time which support its use.

Thus, even last week when researchers from the National Eye Institute in Bethesda, MD, USA, 7 October published a study in the American Journal of Clinical Nutrition.
Scientists have over 12 years studied 1,837 people with moderate to severe risk of age-related central blindness in the form of central atrophy or macular degeneration.

For both types of blindness, it appeared that the incidence was 30% lower in the group that took the most fish oil (0.11% of total caloric intake) compared with the group that took the least.

Although previous studies have been uncertain in its conclusions, the authors believe that the figures can be generalized, this is both a cheap and readily available intervention opportunity against risk families with high incidence of these diseases.

In times when the collective consensus have shouted in our ears that we should eat less fat, it is important to use common sense, read the research properly and stand firm.

Fat is healthy, and fat is vital!

One should obviously not wallow in margarine, french fries and chips, but make sure to eat well from the healthy fats as olive oil and especially fish oil.

It can be ingested as a liquid, as capsules, or as very attractive food.

Fish is not only healthy but also tastes very good indeed. Many people are nevertheless troubled by the increasing presence of heavy metals in fish, but if you avoid the large predatory fish as swordfish and tuna, there is significantly less in for example salmon and trout, especially if they are caught in clean rivers and lakes.

There are however problems with farmed fish, which often contains pretty much omega-6 fat, due to the fish feed composition. And this we should avoid. We already get far too much omega-6, especially linoleic acid, found in the cheap cooking oils with corn and sunflower oil, so as to avoid further bias, we must select the oily fish that are caught in the wild and not farmed.

We must remind you that in a previous newsletter we described two studies that showed that even eggs contain substances that prevent the age-related central blindness, so it may be, we soon will see a Danish ban against bread with eggs and herring. In Denmark food is not allowed to prevent a disease!

Enjoy your meal.

By: Claus Hancke, MD 

References:

  • Sangiovanni JP, Agron E, et al. Omega-3 Long-chain polyunsaturated fatty acid intake and 12-y incidence of neovascular age-related macular degeneration and central geographic atrophy: a prospective cohort study from the Age-Related Eye Disease Study, Am J Clin Nutr, 2009 Oct 7 (E-pub. Ahead of print)
  • Mares JA, Larowe TL, et al. Predictors of optical density of lutein and zeaxanthin in retinas of older women in the Carotenoids in Age-Related Eye Disease Study, an ancillary study of the Women’s Health Initiative. Am J Clin Nutr., 2006, 84(5): 1107-1122.
  • Wenzel AJ, Gerweck C, et al. A 12-wk egg intervention increases serum zeaxanthin and macular pigment optical density in women. J Nutr., 2006; 136(10):2568-73.

Fat is beneficial for the eyes

Claus Hancke

June 15, 2009

Two new studies suggest that the most common cause of functional blindness is preventable with healthy fatty acids.

This newsletter has previously suggested that certain vitamins and other nutrients have a preventive effect against the age-related macular degeneration (AMD), meaning a degeneration of the cones in the macula. The cells of the retina responsible for our central vision and our color vision.

Recently two new scientific studies have appeared from Australia, which very convincingly make probable that it is the healthy fatty acids that prevent this frequent visual impairment.

The first study showed that high intake of omega-3 fatty acids and low intake of linoleic acid protect against AMD.

In this study, 2,454 people were followed for up to 10 years, where the incidence of AMD related to their intake of fish, nuts or fatty acids in the form of supplements was recorded.

The study showed a risk reduction of 31% and 35% in those who regularly ate fish and nuts or consumed n-3 fatty acids (fish oil and flaxseed oil) and the authors advise you to make an effort to attain this and avoid a diet rich in linoleic acid that occurs especially in the cheap cooking oils e.g. corn oil.

The second study showed that high intake of omega-3 fatty acids and olive oil reduces the risk of AMD, and that a high intake of trans fatty acids increase the risk.

Data from 6,734 people between 58 and 69 years was examined.
It turned out that the highest intake of trans fatty acids increased the risk of AMD by 76% compared to the lowest.

To the contrary a high intake of fish oil also here showed a reduced risk (15%).
But most compelling was that a high intake of olive oil reduced the risk of AMD with whole 52%.

The healthy essential fatty acids is beneficial for virtually every cell in the body and bad fats can cause just as much harm.

So again in these fat frightening times let´s strike a blow for the good fat we should eat much more of

By: Claus Hancke, MD

References:
• “Dietary fatty acids and the 10-year incidence of age-related macular degeneration: the Blue Mountains Eye Study,” Tan JS, Wang JJ, et al, Arch Ophthalmol, 2009; 127(5): 656-65.
• “Fat consumption and its association with age-related macular degeneration,” Chong EW, Robman LD, et al, Arch Ophthalmol, 2009; 127(5): 674-80

Selenium still helps preventing cancer

Claus Hancke

January 26, 2009

A huge U.S. study showed that supplementation of selenium do not prevent cancer of the prostate. But this result is only valid if you get plenty of selenium in advance.

12 years ago it aroused hope and optimism when American Larry Clark could tell that the mineral selenium prevents cancer, particularly prostate cancer, the second most common cause of death from cancer in men. He had to stop his trial before expiry when he learned that far fewer selenium-treated than placebo-treated patients (placebo: Inert tablets) got cancer.

Now a second, much larger, selenium trial has been stopped prematurely. Also in this case the focus of interest was the effect against prostate cancer. This was also an American study. But SELECT, as the trial was named, unfortunately showed that selenium had no effect. One could even not exclude an, admittedly very little, harmful effect. So, it was stopped.

In the meantime, Clark’s trial has been studied more closely. Was it really as convincing as was first believed? With 1.312 participants it was not nearly as large as SELECT where 35.000 attended. Very important was that the final report which came in 2003 showed that the benefit was smaller than first believed. Some cases of prostate cancer among selenium treated had for various reasons been overlooked.

What was left was a statistically significant benefit among those who at the beginning of the experiment had the least selenium in the blood and with most certainty did not have incipient cancer of the prostate. The latter could be concluded from the very low values of PSA (Prostate-Specific Antigen) in the blood of these people. In this group, while the trial was in progress, the incidence of cancer of the prostate was three times less than in the placebo group.

More selenium in the U.S.
Now the question is whether the much larger SELECT trial cancels Clark’s trial. It seems to be the general opinion as for example reflected in the leading article of the same issue of the American medical journal, JAMA, where SELECT was published. So far physicians should not recommend selenium as a prevention against prostate cancer, it says.

And yet one can rightly come to the diametrically opposite conclusion: There is every reason to believe that selenium prevents cancer of the prostate, and presumably also other kinds of cancer.

The fact is that Americans, but not all Americans, get far more selenium in their diet than we Scandinavians. In Clark’s study, participants were selected on the basis of consistently having relatively little selenium in their diet for U.S. standards. Two-thirds had less than 122 micrograms of selenium per. liter of serum. In the SELECT study only one in five had that low values. In other words, it is conceivable that most of the SELECT participants already got plenty of selenium so that additional supplementation would not benefit them. In Denmark almost everybody get less selenium than the participants of both the first and the second study mentioned. Our values are typically 80 micrograms per liter.

This is in excellent compliance with the fact that incredible few participants died from prostate cancer during the SELECT study. Statistically one would have expected 75 to 100 deaths for this reason, during the 5.6 years duration of the study. But only one died (!).

A contributory cause may have been that the vast majority of participants in the SELECT study on their own underwent PSA measurement annually. Possible prostate cancer was therefore detected and treated early. On the other hand, other studies have shown that annual PSA measurement does not reduce mortality. Therefore it is not recommended in Denmark.

Despite the termination of the SELECT study, as a Dane you should still remember that the research that involves us – as opposed to Americans we get very little selenium in our diet – suggests that supplementation with selenium in the order of 1-2 tablets (100-200 micrograms) per day seems to reduce the risk of prostate cancer to a third.

By: Niels Hertz, M.D.

References:
1. Lippman SM et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers. JAMA online December 9, 2008: E1-E13
2. Gann PH. Randomized trials of antioxidant supplementation for cancer prevention. JAMA online December 9, 2008: E1-E2.
3. Selenium supplementation, baseline plasma selenium status and incidence of prostate cancer: An analysis of the complete treatment of the Nutritional Prevention of Cancer Trial. BJU Int. 2003;91:608-12.

jama.ama-assn.org
www.bjui.org

Vitamin C slows cancer growth

Claus Hancke

August 13. 2008

More than 30 years of experience have shown the anti-cancer effect of vitamin C in both test tubes, animal tests and human trials.

Nevertheless, the Danish Cancer Society (Kræftens Bekæmpelse) does not consider it acceptable to apply yet.

Well-known effect on humans
As early as 1936, a young registrar at the Blegdam Hospital in Copenhagen published in the danish scientific journal “Ugeskrift for Læger” an experiment on two leukemia patients in which the disease improved on treatment with vitamin C (1). The young registrar was later to become the renowned professor of pediatrics, Preben Plum.

Forty years ago, researchers first found that vitamin C selectively kills cancer cells in tumors (2), and already 7 years later, Nobel laureate Linus Pauling and Scottish surgeon Ewan Cameron were able to publish a study in which they found an unprecedented survival time for cancer patients treated with vitamin C (3), and they could reproduce the results a few years later (4).

The Mayo Clinic in the USA quickly put a lid on the debate with a study on cancer patients with very small doses of vitamin C given as tablets, where, as you know, you can not consume very much until you get diarrhea; – the body’s natural “overflow valve”.

In 1982, Japanese researchers were able to reproduce Pauling and Cameron’s unusually long survival for cancer patients on Vitamin C (5).

Since then, numerous both animal and human trials have been published to treat cancer with vitamin C.

The new breakthrough
A few years ago, the National Institutes of Health (NIH) in the United States began to look at the old experiments extra carefully and found it relevant to retest them, and in 2006 they published a large-scale laboratory experiment that showed that when exposing cancer cells to vitamin C in the high doses that can be obtained by intravenous administration, it causes increased cell death in the cancer cells, that is without damaging the normal cells (6).

This prompted the NIH to move on, and last week we heard about their latest publication (7), where they had shown significant tumor size shrinkage in mice with implanted cancerous tumors treated with intravenous vitamin C.

The new skepticism
Now one would think that this news was received with enthusiasm and optimism in an organization like the Danish Cancer Society, whose main goal is probably best described in the name of the association; -but no.

We see in today’s newspaper BT that Anja Olsen from the Danish Cancer Society, who actually researches in diet and lifestyle’s significance for cancer, is absolutely not thrilled.

She tells BT: “It is ethically on the edge to treat with vitamin C. New treatments must be approved according to completely fixed rules, which means, among other things, that research must be carried out based on humans. “Until this is done, we do not know if it works, just as we can not rule out side effects,” she says.

Of course, it is easy for a researcher in the Danish Cancer Society to demand more research. That is what the Danish Cancer Society does. And how easy it is to spend more time on research when you have no illness yourself. But here “the film breaks off”.

The Danish Cancer Society (DCS) must wake up
For researchers far from patients and for administrators behind closed doors, of course, it is difficult to imagine; but as any general practitioner knows, the time factor for a cancer patient is of completely different dimensions than for the healthy.

The patient who has terminal supplements because “further treatment is hopeless” does not have a time frame of several years before it turns out whether a treatment works or not. He can not say “let’s wait and see”, because then he will never see.

He is looking for a way to prolong life and gain a little extra time. Shouldn’t he have that opportunity? And is it not better that he chooses a treatment which rests on evidence than anything else?

In addition, we have a treatment that has been free of side effects for 10-15 years of use, and a treatment that has numerous both animal experiments and human experiments as evidence.

Wake up DCS and stop moralizing. It can not be justified.

Denmark has a top position in cancer incidence and a bottom position in cancer treatment.

More clinics
A side-effect-free cancer treatment that selectively hits cancer cells without damaging normal cells at the same time is the ideal cancer treatment.

Once it seeps into the public health service and the Danish Cancer Society how good a palliative and life-prolonging treatment Vitamin C can be, then we must hope that large outpatient clinics will be established so that this treatment in the future can be offered for free to cancer patients in Denmark.

The Vitality Council.

References:
1. Plum P. Thomsen S. (1936) Remission under forløbet af akut aleukæmisk leukæmi iagttaget i to tilfælde under behandling med ascorbinsyre. Ugeskr. Læger (98):1062-67.
2. Benade L. Howard T. Burk D. (1969) Synergistic killing of Ehrlich ascites carcinoma cells by ascorbate and 3-amino-1, 2, 4, -triazole, Oncology, 23, 33–43.
3. Cameron E. Pauling L. (1976) Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci USA, 73, 3685–3689 .
4. Cameron E. Pauling L. (1978) Supplemental ascorbate in the supportive treatment of cancer: Reevaluation of prolongation of survival times in terminal human cancer, Proc Natl Acad Sci USA, 75, 4538–4542 .
5. Murata A. Morishige F. Yamaguchi H. (1982) Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate, International Journal for Vitamin and Nutrition Research, Supplement, 23, 101-113.
6. Chen et al. Proceedings of the National Academy of Sciences 20.Sep.2005;102:13604-9
7. NIH News (2008) Vitamin C Injections Slow Tumor Growth in Mice, Embargoed for Release, Monday, August 4,

Vitamin D against atherosclerosis

Claus Hancke

January 28, 2008

Vitamin D counteracts the development of atherosclerosis and prevents fatal complications of high blood pressure – but vitamin D deficiency is very widespread.

We are not done with vitamin D. More and more information is streaming in about this amazing substance, which is actually not a vitamin but a hormone created in skin exposed to sunlight.

Now we will look at vitamin D’s effects on the heart and circulation. It seems as though the risks of blood clots in the heart and the brain are far lower in people who get enough vitamin D, which is to say people who get more than most. This “vitamin” is especially effective at lowering the risk in people with high blood pressure.

This find appears in a recent report from Farmingham, a little town in Massachusetts where the health and lifestyles of thousands of people (and their descendents) has been registered since 1948 in order to find lifestyle related reasons for cardiovascular disease. The Farmingham study is, without a doubt, the most famous of its kind. When we today take for granted that exercise, healthy diet, and aspirin prevents cardiac death it is the Farmingham project that we should thank.

The report in question is on a part of the study involving 1,739 people aged 50 – 70 who were free of cardiovascular disease at the beginning of the study. From 1996 to 2000 their vitamin D status was measured with blood tests after which their health was monitored for an average of 5.4 years (up to 7.6 years). Who suffered blood clots?

Those who had the least vitamin D in the blood! After seven years blood clots in the heart or the brain (stroke) was registered in one in ten with vitamin D levels over 37 nmol/l, but in no less than one in four of those with levels under 37. After correcting for differences within the group such as age, sex, cholesterol levels, smoking, diabetes, and so on, the group with the highest vitamin D levels still had a cardiovascular risk 60 % less than that of the group with the lowest levels. If these numbers are right, vitamin D is more important for cardiovascular health than aspirin or cholesterol medicine.

Strong immune system
The beneficial effects of vitamin D seem to be even greater for those with high blood pressure, which is the most important cause of cardiovascular disease. Among participants with high blood pressure the risk for those with vitamin D levels over 37 was half that of those with levels under 37.

This result is similar to that of other studies which have shown that low vitamin D status and high blood pressure and clogged cardiac arteries are related. The Farmingham has an even stronger message: If you lack vitamin D you are at risk of a heart attack within the foreseeable future.

Does this mean that vitamin D prevents atherosclerosis? Yes, this seems to be the case. This fits in well with other known effects including: that vitamin D counteracts an important hormone (renin) which is responsible for raising blood pressure and that when heart cells which normally use vitamin D are prevented from using vitamin D (through genetic manipulation) in experiments on mice, blood pressure rises quickly.

Without eating fatty fish is you get almost no vitamin D from October to May. Deficiency is therefore very widespread. In a European study of teenage girls more than one out of every three had severe anemia (blood percent of under 25 nmol/l). Over 90% of these girls would have, if they lived in Farmingham, ended up in the study group with severe atherosclerosis.

How much vitamin D is it wise to take? There is no rule of thumb, but it should be considered that a typical vitamin pill contains 200 units whereas one out of every two adult Americans need 1,000 units in order to have an “acceptable” vitamin D status (which is a concentration of 75 nmol/l – most American researchers recommend 75 – 150 nmol/l). It is also understood that it is completely safe to take up to 2,000 units daily.

Luz Tavera-Mendoza and John White, two molecular biologists from the American McGill University have shown that vitamin D causes the skin and the immune system to form antibiotics (cathelicidin and more) which kill bacteria, including tuberculosis bacteria. This is probably the explanation for the earlier idea that it is possible to cure tuberculosis with sunlight. These two researchers have written an easy to read summery of recent research and even reveal what they take as supplements during the dark months.

Luz, who is a younger woman, takes 1,000 unites (25 micrograms).
John, who is a younger man, takes 4,000 units (100 micrograms).

By: Niels Hertz, MD

References:
1. Wang TJ et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117:000-000.
2. Tavera-Mendoza L, White J. Celle defences and the sunshine vitamin. Scientific American 2007 (11):36-44.

circ.ahajournals.org
www.sciam.com

Never Calcium Without Magnesium

Claus Hancke

January 17, 2008

Calcium tablets as monotherapy increase the risk of blood clots in the heart and brain.

Last year, the British Medical Journal in their web version published a scientific article with the above-mentioned gloomy message.

1,471 healthy women over 55 years were randomly divided into two groups, one with 732, who took a supplement of calcium citrate for 5 years and a group of 739 who took placebo.

During these five years, they were examined every six months, and for each year, the distance between the two groups increased with statistic significance.

It was found that in the group who took calcium tablets, there was a significant increase in the risk of blood clots in both the brain and the heart.

The authors are surprised by the result and have reservations until the matter has been investigated further with more studies.

But do we have to wait five years for a new study of this result?

Is not it predictable?

Most people who have experience with the use of minerals for disease prevention are well aware that you should never take calcium without taking magnesium at the same time.

Magnesium is the key
(If you think it becomes too biochemical, then just read the conclusion at the end).
Magnesium sits like a bolt in the calcium channel of the cell membrane.

The moment calcium wants to enter a cell, magnesium closes the door and when calcium wants leave the cell, magnesium will open up. It’s the opposite in bone cells.

Therefore, the cells in the soft tissues are almost empty of calcium. The calcium concentration outside of a cell is about 10,000 times as high as within a cell. Thanks to magnesium.

If we lack magnesium, the calcium channels will open.

This means that through the open calcium channels, calcium flows into the cells, causing the cell to cramp and, in the long term, (hours) destroy its mitochondria.

The cramp causes immediate contraction of the blood vessels due to the smooth muscle cells around the small arteries, resulting in increasing blood pressure and risk of brain hemorrhage and destruction of calcification plaque and thus risking a blood clot in the heart. At the same time, the energy production of the cell is minimized due to the destruction of the energy-producing mitochondria with their vital content of coenzyme Q10.

This not only results in less energy production in the cells, but also a smaller consumption of oxygen absorbed in the cell, which in turn means that a greater proportion of this oxygen are then used to produce harmful free radicals, IF there is iron present as a catalyst for this process, and this is precisely the case in this group of women who no longer menstruate.

Then the roulette runs with destruction of the cell membrane and the surrounding cells from within, because now the cell has suddenly had its own little “Chernobyl meltdown”.

If we lack magnesium, we have no control over the distribution of calcium, and it is distributed more or less evenly throughout the cell phase, ie. both in bone cells and in soft tissue cells, muscle cells, skin cells, connective tissues, etc.

But are we lacking magnesium?
Yes we are. More than 70% of the population do not even get the recommended daily allowance of 300 mg of magnesium.

Why not?

The food has gradually become more and more low in magnesium. In part, the industrialization of the diet has resulted in a large loss of magnesium in the finished product, and we eat less vegetables where we find this magnesium and when we cook the vegetables, we pour the magnesium out with the boiling water.

Furthermore, many elderly people loses magnesium because they take diuretic medicine or because they drink too much coffee.

70% of research participants with low intracellular magnesium are more than sufficient to explain the significant increased risk associated with calcium intake as monotherapy.

There is therefore no surprise in the achieved result, and it should not be necessary to wait a lot of years to take extra magnesium along with ones calcium supplement. This will not only benefit muscles, heart, brain and bones, but also a variety of processes in the body that rely on the more than 300 enzymes for which magnesium is required.

So: Never take calcium without magnesium!

By: Claus Hancke, M.D.

 

References

Mark J Bolland, P Alan Barber, Robert N Doughty, Barbara Mason, Anne Horne, Ruth Ames, Gregory D Gamble, Andrew Grey, Ian R Reid. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ published online 15 Jan 2008;doi:10.1136/bmj.39440.525752.BE

Promising treatment for macular degeneration

Claus Hancke

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.

Healthy and Safe

Robert Verkerk

October 25, 2007

There are over 480,000 published peer-reviewed research studies on food supplements or ingredients used in food supplements, and the vast majority of these show positive effects. There are only a small handful of studies that have shown negative effects, these generally being associated with high doses or synthetic forms of ingredients like vitamin A, beta-carotene and vitamin E.

In the case of vitamin A, there is no doubt that high doses of this fat soluble vitamin can be harmful and an upper safe level or maximum permitted level for this vitamin makes perfect sense.

There are three key studies showing negative effects of beta-carotene on diseased or high-risk patients, but these have all used synthetic beta-carotene, in the absence of natural carotenoid complexes found in natural carotenoid-rich fruits and vegetables which have been found to be potent cancer-fighting nutrients. Ironically, these natural ‘mixed carotenoids’ are disallowed by the Food Supplements Directive.

Finally, there are four key negative studies on vitamin E, all of them conducted with synthetic vitamin E, which comprises only one of the eight vitamin E forms found in nature, but in its esterified form. This form, alpha-tocopherol, the only vitamin E form allowed by the Directive, actually reduces the body’s absorption of gamma-tocopherol which is the key antioxidant form of vitamin E found in food sources.

By: Robert Verkerk, The Alliance for Natural Health, United Kingdom

Vitamin C inhibits cancer. But How?

Claus Hancke

September 18, 2007

New research sparks new theories about how vitamin C inhibits cancerous growth.

A great deal of research indicates that vitamin C has a considerable inhibitory effect on the growth of cancer cells.

The biochemical effect of high-dose treatment with vitamin C is reasonably understood; vitamin C acts as a pro-oxidant on cancer cells at such doses. This causes increased free radical strain on the cancer cells and thereby acts as a poison to the cancer.

In moderate doses, the kind of doses which we can get through our diets, vitamin C is an antioxidant. But even at these doses, vitamin C has shown an inhibitory effect on the growth of cancer cells.

It was therefore believed that vitamin C blocks the free radicals which cause the cancer forming mutations in the cells, and that the reason for its protective effects is that it protects the cells’ DNA.

This is presumably not the whole truth.

Many years ago a famous professor by the name of Warburg was among the first to maintain that cancer cells grow in oxygen poor tissue. Today this is common knowledge, but there lacks knowledge on how this occurs. Ten years ago Gregg Semenza of John Hopkins University found that cancer cells are dependent on a protein called HIF-1 (hypoxia induced factor), which helps the cells by compensating for lacking oxygen in the surrounding tissue and thus allows cancer cells to convert sugar to energy without oxygen. HIF-1 also catalyses the creation of new blood vessels so that hungry cancer cells can get fresh supplies of nutrients and oxygen. If a cancer grows aggressively, it quickly uses up its oxygen supply and becomes entirely dependent on HIF-1. The HIF-1 protein is dependent on the presence of free radicals, which are also necessary for many other processes in the body. A powerful antioxidant like vitamin C eliminates the surplus of free radicals, which causes HIF-1 to become ineffective and thus inhibits cancer growth.

This new theory is based on a study done by a research group at the centre of oncology at John Hopkins University in conjunction with Dean Felsher of Stanford.

They set out to study antioxidants’ roles in cancer growth and found, to their great surprise, that antioxidants destabilise the protein on which cancer cells are dependent. As professor Chi Dang from John Hopkins University wisely stated, “By uncovering the mechanism behind anti-oxidants, we are now better suited to maximize their therapeutic use.”

By: Claus Hancke, MD

Reference

HIF-Dependent Antitumorigenic Effect of Antioxidants In Vivo. Cancer Cell, Volume 12, Issue 3, 11 September 2007, Pages 230-238Ping Gao, Huafeng Zhang, Ramani Dinavahi, Feng Li, Yan Xiang, Venu Raman, Zaver M. Bhujwalla, Dean W. Felsher, Linzhao Cheng, Jonathan Pevsner et al.

www.cancercell.org