More is not always better

November 13, 2020

Dose response is diverse

Our body and cells react differently to the chemical substances we come into contact with. Our body’s reaction (response) to different concentrations (doses) is called dose-response. Small variations in the structure of substances can be decisive for the body’s reaction to the substances. For several groups of substances, it is known that they can be problematic, but theoretically it is not possible to predict how cells or organisms will react to a chemical substance.

As low doses of chemical substances are studied scientifically, more and more otherwise well-known substances are shown to have unexpected effects at low doses. Since the early 1990s, it has been clear that one cannot theoretically – based on a general dose-response formula – predict the response of cells to low concentrations of a substance.

In everyday life, we regularly experience that there is a linear relationship between dose and effect: Twice as much sugar tastes twice as sweet. Such is the case with the drugs and within the doses we normally use. The graph to the right shows 0-4 teaspoons of sugar in the coffee. It is the linear dose-response that we know best and that we often take for granted in daily life

From everyday life we also know of a decreasing effect on a larger dose. Double the dose of sugar in the coffee does not keep giving double effect. When the tongue’s sensation of sweetness is completely filled, an extra dose cannot be sensed. The body’s relationship to a variety of vitamins and minerals works in the same way. The graph to the right shows the experience of sweetness at 1-14 teaspoons of sugar in coffee.

Many substances first have a measurable effect above a certain threshold value as is known from e.g. alcohol. Below the threshold, no poisoning occurs – if you drink an alcoholic beverage with 7,5 ml or 6 grams of alcohol per hour, it has no effect, but if you drink an alcoholic beverage with 30 ml or 24 grams of alcohol per hour, you exceed the liver’s threshold value for continuously breaking down alcohol, after which alcohol continuously accumulates in the blood and you become drunk.

Some substances used as medicines inhibit processes in the body, so that higher doses inhibit the process more, but only within certain limits. With increasing dose, the inhibitory effect diminishes and eventually disappears. Well-known examples are statins, which lower the blood’s cholesterol content, and drugs that inhibit the stomach’s production of stomach acid.

Some drugs, including several hormones, have a bell-shaped dose-response curve. In addition to the fact that the substances are often active at very low doses, they are also only active within a “window”, so that they have a hormone-like or endocrine disrupting effect above a certain concentration, and then lose effect at higher concentrations. Several hormones and more proteins tested for cancer treatment have this type of dose-response (Reynolds, 2010; Diamond, 2004).

Some drugs have a U-shaped effect curve, so that the drug has a stimulating effect at low doses, but with decreasing effect at slightly higher doses, and then again has a stimulating effect at even higher doses. Several drugs with U-shaped dose-response curves are endocrine disruptors, or promote or inhibit cancer. (Almstrup et al., 2002; Davis & Svendsgaard 1990 and Vadenberg et al., 2012).

Living organisms – including humans – are extremely complex, and the “unexpected” types of non-linear toxic effects can e.g. is due to interactions where a chemical substance can affect sensors on or in the cells, immune reactions, enzymes in the liver, etc.,

In addition, the toxic effects of substances on humans can be determined by individual and often inherited genetic differences. For heavy metals such as mercury and copper, both individual differences and non-linear relationships are known (Andreoli & Sprovieri, 2017; O’Doherty et al., 2019).

In scientific research, organisms’ reactions to chemical substances are often assumed to be linear, so that researchers look for linear relationships without actually knowing if they are relevant. Non-linear contexts are also often overlooked in authorities’ risk assessments of substances. Overall, this means that researchers and authorities often disregard the toxic effects of substances on the basis of a rationale that when a clear toxic effect at low doses was not found at higher doses – well then one can simply ignore these results.

In the EU’s risk assessments of pesticides, GMOs, etc. one often disregards the concrete measurements or experiments that do not meet the requirement of linear and increasing toxicity at higher doses.

Not least Danish researchers such as Almstrup, Grandjean, Skakkebæk and Svendsgaard have helped to focus on non-linear dose response and toxic effects at low and extremely low doses. The same researchers are generally not impressed by the authorities’ ability or willingness to take this new knowledge seriously (Grandjean 2019, Hill et al 2018, Davis and Svendsgaard 1990); – neither is the Vitality Council.

Klaus Sall, cand.scient. in biology

References and further reading

Almstrup K; Fernández MF; Petersen JH; Olea N; Skakkebaek NE and Leffers H. (2002). Dual effects of phytoestro­gens result in u-shaped dose-response curves. Environ Health Perspect. 2002 August; 110(8): 743–748. LINK
Andreoli, V., Sprovieri, F., (2017). Genetic Aspects of Susceptibility to Mercury Toxicity: An Overview. Int J Environ Res Public Health 14. LINK
Davis JM og Svendsgaard DJ. 1990 U-shaped dose-response curves: their occurrence and implications for risk assessment. J Toxicol Environ Health. 1990 Jun;30(2):71-83. LINK
Diamond, D. M. 2004. Enhancement of Cognitive and Electrophysiological Measures of Hippocampal Functioning in Rats by a Low, But Not High, Dose of Dehydroepiandrosterone Sulfate (DHEAS). Nonlin. Biol. Toxicol. Med. 2004 Oct.; 2(4): 371–377. LINK
Grandjean, P., Abdennebi-Najar, L., Barouki, R., Cranor, C. F., Etzel, R. A., Gee, D., Heindel, J. J., Hougaard, K. S., Hunt, P., Nawrot, T. S., Prins, G. S., Ritz, B., Soffritti, M., Sunyer, J., & Weihe, P. (2019). Time scales of developmental toxicity impacting on research and needs for intervention. Basic & Clinical Pharmacology & Toxicology, 125(Suppl. 3), 70-80. LINK
Hill C. E., Myers J. P., Vandenberg L. N. (2018). Nonmonotonic dose-response curves occur in dose ranges that are relevant to regulatory decision-making. Dose Res. 16, 155932581879828. 1559325818798282–82. LINK
Lagarde, F., Beausoleil, C., Belcher, S. M., Belzunces, L. P., Emond, C., Guerbet, M., & Rousselle, C. (2015). Non-monotonic dose-response relationships and endocrine disruptors: a qualitative method of assessment. Environmental health 14, 13 (2015), LINK
Montévil M, Acevedo N, Schaeberle CM, Bharadwaj M, Fenton SE, and Ana M. Soto AM. 2020. A Combined Morphometric and Statistical Approach to Assess Nonmonotonicity in the Developing Mammary Gland of Rats in the CLARITY-BPA Study. Environ Health Perspect. 2020 May; 128(5):57001. LINK
Reynolds, Andrew R. 2010. Potential Relevance of Bell-Shaped and U-Shaped Dose-Responses for the Therapeutic Targeting of Angiogenesis in Cancer. Dose Response. 2010; 8(3): 253–284. LINK
O’Doherty, C., Keenan, J., Horgan, K., Murphy, R., O’Sullivan, F., Clynes, M., 2019. Copper-induced non-monotonic dose response in Caco-2 cells. In Vitro Cell.Dev.Biol.-Animal 55, 221–225. LINK
Vandenberg et al. 2012. Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses. Endocrine Reviews March 14, 2012 er.2011-1050 LINK
Zoeller RT, Brown TR, Doan LL, Gore AC, Skakkebaek NE, Soto AM, Woodruff TJ, Vom Saal FS. Endocrine-disrupting chemicals and public health protection: a statement of principles from The Endocrine Society. Endocrinology 2012; 153:4097 – 110; LINK

Fat is beneficial for the eyes

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

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

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 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.

………………..

References:
1. Plum P. Thomsen S. (1936) Remission under forløbet af akut aleukæmisk leukæmi iaggtaget 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

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

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

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

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?

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

Vitamin D inhibits cancer

June 26, 2007

An overlooked but very sensational study suggests that vitamin D could inhibit almost 80% of all cancer cases. We just need much more than we normally get (1).

One out of every three people in Britain die of cancer and a world without this feared disease seems utopian. But if an American study is correct, we can approach this unattainable goal with a historic leap forward. We just need more, much more, vitamin D, and maybe also more calcium. According to the study, a combination of calcium and vitamin D can reduce the risk of cancer by about 60%. Additionally, it seems that if cancer is avoided during the first year of taking supplements, then the risk of cancer the following year is reduced by nearly 80%! It is hard to expect more.

It is strange that such sensational news has received almost no official consideration. Especially because it comes from a highly trustworthy double blind, randomised trail published by highly respected researchers.

The participants in the study were 1,180 women with an average age of 67. They were from Nebraska, which is just as far south as southern Italy and receives a lot of sun. Not surprisingly the women had on average good blood levels of vitamin D before the study.

In the study 446 of the women received an advantageous daily supplement of as much as 1,100 units (27.5 micrograms) vitamin D. This is at least five times more than the contents of a normal vitamin pill and about three times the recommended dosage for people over age 60. They also received 1.5 gr. calcium (as carbonate or citrate), which is about the amount of calcium in a litre of milk.

Another 445 women received only calcium and 288 received placebo. Neither the women nor the researchers knew who got what. The study lasted for four years while it was noted who and how many got cancer.

We now have the results. The group which received the vitamin D and calcium was subject to many fewer cases of cancer than the group which received placebo. The difference was not coincidence! It was statistically extremely solid. The biggest difference (77% lower risk) was shown during the last three years of the study. The researchers surmised that this was because some of those who got cancer in the beginning of the study already had undetected cancer before the study started.

It could be true
The women who just received calcium also had a lower risk of cancer (40%). This finding was not completely certain statistically. The cancer risk for these women did not, as in them who received both vitamin D and calcium, become more reduced after the first year. It is therefore uncertain if this effect is actual or just the result of coincidence.

On the other hand, at least two further arguments indicate that vitamin D actually works. The first is that the women who had the poorest vitamin D status before the study, were those helped the most, their risk was the most reduced. The vitamin D status of the participants during the study also played a role, the lower the status, despite the supplements, the larger the cancer risk. The second argument that vitamin D has this effect is that the risk was directly link to the amount of vitamin D used.

Can it really be true that something as cheap as vitamin D can be so beneficial? We know that the vitamin regulates at least 200 genes, many of which control the cells’ growth and degree of specialisation. Animal studies have shown that vitamin D deficiency promotes cancer growth. For more than 60 years it has been known that cancer is less common in countries where the sun is high in the heavens leading to the production of more vitamin D in the skin. It has also be proven time and time again that low vitamin D status and high cancer risk in people go hand in hand (2,3).

The only thing that has been missing is a proper study with sufficient supplements so that cause and effect could be analysed. We now have just that study!

The women in Nebraska had a typical vitamin D status (25-hydroxy-vitamin-D3 in the serum) of 71 nanomolsl/L before the study. This is a very acceptable value. But the supplement increased this value to an average of 96. This is normally regarded as too high.

Vitamin D status is measured with a blood test! It is most important during the winter, when it is the lowest. According to the Nebraska study, this level should be no less than 100.

By: Vitality Council

References: 

1) Lappe J M et al. Vitamin D and calcium supplementation reduces cancer risk: Results of a randomized trial. Am J Clin Nutr 2007;85:1586-91.

2) Feskanich D et al. Plasma vitamin D metabolites and risk of colorectal cancer in women. Cancer Epidemiol Biomarkers Prev 2004;13:1501-8

3) Ahonen M H et al. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels (Finland). Cancer Causes Control 2000;11:847-52

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