Author: Claus Hancke

Folic Acid Lowers Blood Pressure and Prevents Blood Clots

Claus Hancke

April 19, 2005

While folic acid lowers blood pressure, the dose must be large enough to have this effect. Diet alone will not provide a significantly large enough dose, so it is essential to take folic acid as a supplement. The vitamin also simultaneously protects the heart and brain against blood clots.

It has long been documented that the B vitamin, folic acid, prevents the birth defect Spina bifida. For eight years, Canada has fortified all flour with folic acid and has thus prevented 80% of these sad cases. Enrichment is also required in the United States, but in Denmark, expectant mothers must manage on their own. It’s their own problem to find out to take a supplement – before they get pregnant!

By: Vitality Council

References:
1. Forman JP, Rimm EB, Stampfer MJ, Curhan GC. Folate intake and the risk of incident hypertension among US women. JAMA. 2005 Jan 19;293(3):320-9.
2. American Heart Association’s 44th annual Conference on Cardiovascular Disease Epidemiology and Prevention. carole.bullock@heart.org
3. Endres M, Ahmadi M, Kruman I, Biniszkiewicz D, Meisel A, Gertz K. Folate deficiency increases postischemic brain injury. Stroke. 2005 Feb;36(2):321-5. Epub 2004 Dec 29.
4. Taivani A et al. Folate and vitamin B6 intake and risk of acute myocardial infarct in Italy. Eur J Clin Nutr 2004;58:1266-72.
5. Al-Delaimy WK, Rexrode KM, Hu FB, Albert CM, Stampfer MJ, Willett WC, Manson JE. Folate intake and risk of stroke among women. Stroke. 2004 Jun;35(6):1259-63.
6. Casas JP et al. Homocysteine and stroke: Evidence on a causal link from mendelian randomisation. The Lancet 2005;365: 224-32.
7. Klerk M, Verhoef P, Clarke R, Blom HJ, Kok FJ, Schouten EG; MTHFR Studies Collaboration Group. MTHFR 677C– T polymorphism and risk of coronary heart disease: a meta-analysis. JAMA. 2002 Oct 23-30;288(16):2023-31.
8. S Schwammenthal et al. Homocysteine, B-vitamin supplementation, and stroke prevention. From observational to interventional trials. Lancet Neurol. 2004;3(8):493.

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www.nature.com
www.stroke.org
www.thelancet.com
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Deficiency in B-vitamin Causes Dementia

Claus Hancke

April 18, 2005

According to one American study, folic acid weakens the memory of the elderly. According to another study, the opposite happens. Nearly all studies, however, indirectly indicate that folic acid prevents both arteriosclerosis and dementia.

It is a well-known fact that the B-vitamin folic acid prevents congenital neural tube defects. However, it can also lower the blood’s content of homocysteine; a biproduct in human metabolism that promotes atherosclerosis, among other things. Having an increased level of homocysteine is just as dangerous as cholesterol: Up to 40% of all individuals with premature atherosclerosis have increased blood levels of homocysteine.

The fact that homocysteine also damages the brain is indicated by more than 20 different studies. It has been found with almost unerring certainty that demented old people have more homocysteine in their blood than others and that the ones who score highest on memory tests are the ones with the least homocysteine in their blood. This is a clear argument for taking folic acid.

However, completely unexpectedly, a fly in the ointment has now appeared. A study at Rush University in Chicago has shown that the exact opposite might be the case. If you are elderly and you get more than the typical 0.4mg. of folic acid a day, your memory will decline more rapidly.

A total of 3,718 trial subjects over 65 years of age were followed for five to six years after having reported their eating habits. They were then mentally tested three times during the course of the 5 – 6 years. The results were the same whether they got folic acid from their diet or from dietary supplements: In the people taking folic acid, memory declined more rapidly than in the others.

Are these results the result of a coincidence? Anyhow, it does make you wonder that the 20% who got the most folic acid (0.7 mg. a day) did far better on the mental tests than the rest. Granted, their memory deteriorated more rapidly, but they obviously had a better memory to begin with. Why was that so, if folic acid is actually harmful?

In addition to this, doctors from the UCLA in February 2005 published results stating the exact opposite. Among 499 well-functioning 70 – 79 year-olds, most folic acid was found in the blood of the ones who had the best memory. And equally importantly: Seven years later, they were in better posession of all their faculties.

No explanation
What is true, then? If the truth lies in the Chicago study, it might be based on the co-operation between vitamin B12 and folic acid. Both vitamins reduce blood levels of homocysteine and the major task of both of them is to produce small, chemical units – which only contain a single carbon atom – for building other molecules.

Folic acid delivers its units to vitamin B12 which are then further delivered to – homocysteine. In this way, homocysteine is neutralized and is transformed into a harmless amino acid and the blood level of homocysteine will drop.

Whether you lack vitamin B12, folic acid, or both, the transport of the single-carbon units will be complicated. In all three cases, the result will be a specific type of anaemia (pernicious anaemia) which is characterized by the red blood cells being abnormally large.

However, the symptoms in vitamin B12 deficiency and folic acid deficiency are not quite similar. In folic acid deficiency, neuritis – i.e. nerve damage – will not occur. In vitamin B12 deficiency, it will. The anaemia in vitamin B12 deficiency can be removed by taking folic acid, but the neuritis cannot. Vitamin B12 has an affect on nervous tissue that folic acid cannot imitate.

In up to 30% of all elderly people, vitamin B12 deficiency can be demonstrated. Imagine large amounts of folic acid enhancing the B12 deficiency in the nervous system by blocking the small amounts of vitamin B12 with single-carbon compounds. This could correlate to another finding in the Chicago study: Memory declined by 25% less in the ones with the largest consumption of vitamin B12.

The leader of the study, Martha Clare Morris, believes that folic acid might mask the very common vitamin B12 deficiency in the elderly. This is more or less the same thing. In both cases, the consequence should be that the elderly get more vitamin B12 and not less folic acid which can have a protective effect in other areas.

This is the message – that is if you do not choose to believe that the new finding is a coincidence and that the truth is the exact opposite – which is actually also quite likely!

For the time being, however, Morris’ conclusion is simple: “We don’t know yet what is going on,” she says.

Up to every third elderly person may have demonstrable signs of mild vitamin B12 deficiency. If the results of the Chicago study are truthful, elderly persons possibly should not reduce their folic acid intake but rather focus on getting enough vitamin B12.

By: Vitality Council

References:
1. Morris MC et al. Dietary folate and vitamin B12 and cognitive decline among community-dwelling older persons. Arch Neurol 2005;62:641-5
2. Austin RC et al. Role of hyperhomocysteinemia in endothelial dysfunction and atherthrombotic disease. Cell Death and Differentiation 2004;11:S56-S64
3. Morris MS. Homocysteine and Alzheimers disease. Lancet Neurol 2003;2:425-8
4. Kado DM et al. Homocysteine versus the vitamins folate, B6, and B12 as predictors of cognitive function and decline in older high-functioning adults: Mac Arthur Studies of Successfull Aging. Am J Med 2005;118:161-7
5. Garcia A et al. Homocysteine and cognitive function in elderly people. CMAJ, Oct. 12, 2004; 171 (8).

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www.sciencedirect.com
www.cmaj.ca
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Depressed Due to Vitamin Deficiency?

Claus Hancke

April 11, 2005

Several reports show a connection between depression and Vitamin E deficiency. There is a similar relation between depression and lack of Vitamin C and selenium. So far this gives food for thought.

Could it be that lack of vitamin E plays a role in depression? Something in that direction according to a preliminary Australian survey.

By: Vitality Council

References:
1. Owen AJ et al. Low plasma vitamin E levels in major depression: Diet or disease? Eur J Clin Nutr 2005;59:304-6.
2. Tiemeier H et al. Vitamin E and depressive symptoms are not related. The Rotterdam Study. J Affect Disord 2002;72:79-83.
3. Maes M et al. Lower seriúm vitamin E concentration in major depression. Another marker of lowered antioxidant defense in that disease. J Affect Disord 2000;58:241-6.
4. Benton D et al. The impact of selenium supplementation on mood. Biol Psychiatry 1991;29:1092-8.

www.nature.com/ejcn/index.html
www.sciencedirect.com
www.iom.dk

The Emperor’s New Clothes: HOPE-TOO

Claus Hancke

April 5, 2005

Reputable American researchers claim that even large amounts of natural Vitamin E do not benefit established atherosclerosis. But their study do not reveal it. The participants got almost no Vitamin E.

Perhaps somebody have heard about the praised American HOPE study from 2000. It was to reveal that natural Vitamin E would not make any difference for people with atherosclerosis. This was a disappointment, and with it the issue could then have been dismissed.

That is not how it went. The HOPE study, which lasted 4,5 years and included 9,000 participants was prolonged with 2,5 years. They wanted to be absolutely sure, they said. In the follow-up study called HOPE-TOO only 4,000 people participated. Some did not want to participate, others had died, and others only wanted to be examined, but did not want any medication.

Half of the participants took 400 units natural Vitamin E daily (alpha-tocopherol), while the rest took placebo. They certainly had serious atherosclerosis: Every other one had had a heart attack, just as many suffered from angina pectoris (atherosclerosis ), and more than every third had diabetes.

The HOPE study showed that Vitamin E did not cause more or less cancer, more or less heart attacks, strokes, deaths or anything else. HOPE-TOO showed the same result, though with a single addition: Those who took Vitamin E slightly more often had heart failure; that is to say a decreased functioning of the heart.

The difference was so small that it could very well have been coincidental, even though it was statistically significant. Nevertheless the authors took the opportunity to strongly warn against dietary supplements. But yet they might as well have taken the opportunity to recommend them. They found that Vitamin E protected against lung cancer!

This finding, which was also statistically significant, was rejected, as an “error.” This conclusion was preceded by a lengthy discussion, in which reference is made to studies with beta-carotene, which as we all know, is something completely different.

No clothes on
But there is a far more serious surprise, which totally overshadows this biased opinion: During the whole study the participants did not have any more Vitamin E in their blood than all other people, who do not take supplements. The average value was 17,6 μmol/l. The normal value is 12 – 42. Despite the Vitamin E they only just managed to get their minimal need covered.

Before the study the participants actually had even lower values, averaging 10 μmol/l. This fits well with the fact that they were seriously ill, overweight heart patients who were kept on a low fat diet. A low fat diet may lead to deficiency of vitamin E.

Here we may also find the explanation of the low blood values. Vitamin E can only be absorbed from the intestine when fat is present. If you eat non-fat foods you might as well not take Vitamin E, even when you take 20 – 40 times the recommended dosage.

One is reminded of the Emperor’s New Clothes. HOPE-TOO has no clothes on. It claims to examine the effects of mega doses of Vitamin E, but the participants are only seemingly getting it. Strangely enough nobody has pointed out this almost ridiculous mistake before. In particular one wonders, why the authors themselves have not seen this mistake. Could it be that they do not know the normal values of Vitamin E in the blood?

This is not completely out of the question although it sounds strange. There are many examples of superficiality in scientific research. You do not have to look any further than the official commentary in the same issue of JAMA, which published the HOPE-TOO study. Here doctor Greg Brown by and large agrees with the conclusion of the study. He was also in charge of a similar study from 2001, which was supposed to show if antioxidants prevent atherosclerosis in the coronary arteries. This study concluded that antioxidants did not prevent atherosclerosis, even though the figures showed in black and white that the antioxidants halved the growth of atherosclerosis in the coronary arteries, compared to placebo.

By: Vitality Council

References:
1. The HOPE and HOPE-TOO Trial Investigators. Effects of long-term vitamin E supplementation on cardiovascular events and cancer. JAMA 2005;293:1338-47.
2. B Greg Brown. Is there any hope for vitamin E? JAMA 2005;293:1387-90.
3. Greg Brown et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med 2001;345:1583-92.

jama.ama-assn.org
content.nejm.org
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Perhaps Prostate Cancer may be a Rarity in the Future

Claus Hancke

April 1, 2005

Every forth man lives with a highly increased risk of getting cancer of the prostate, the next most frequent cause to cancer deaths in men. It does not have to be like that. Exactly these exposed men could easily decrease their risk to a tenth.

Researchers from Harvard University in Boston have published a landmark study. It strongly suggests that most cases of cancer in the prostate are due to lack of balance in the body’s defense against free oxygen radicals. And most importantly: This balance can be restored with antioxidants – especially with selenium, but also vitamin E and the red dye of the tomatoes, lycopene. Prostate cancer can thus become a rare disease.

The imbalance occurs especially in men who get too little selenium and who, for hereditary reasons, have a particularly effective antioxidant enzyme (manganese-containing SOD) in their mitochondria. The mitochondria are the cells’ internal energy factories, which are worn down by free oxygen radicals with age. This wear and tear, parenthetically noted, is believed to be a very significant cause of aging and age-related diseases.

One would therefore think that it was an advantage to have a particularly effective antioxidant enzyme in one’s mitochondria. But very often it is not. The SOD enzyme transforms free oxygen radicals into the less risky hydrogen peroxide, but this creates a new problem: the hydrogen peroxide must also be removed, since it also causes harmful oxygenation. The removal requires an enzyme (glutathione peroxidase), the quantity of which depends on the supply of selenium.

The more free oxygen radicals (e.g. from smoking) that need to be neutralized and the more efficient the SOD enzyme is, the more harmful hydrogen peroxide accumulates and the greater the need for selenium.

Balance in things
The Harvard study is part of a study of approx. 15,000 American doctors who have been followed since 1982. Around 1990, 275 of them had developed serious prostate cancer, and it was those who were primarily found interesting.

By: Vitality Council

References:
1. Haojie Li et al. : Manganese superoxide dismutase polymorphism, prediagnostic antioxidant status, and risk of clinical significant prostate cancer. Cancer Res. 2005;65:2498-2504.
2. Woodson et al. Manganese superoxide dismutase (MnSOD) polymorphism, α-tocopherol supplementation and prostate cancer risk in the α-Tocopherol, β-Carotene Cancer Prevention Study. Cancer Causes Control 2003;14:513-8
3. Niels Hertz. Selen – et livsvigtigt spormineral. Forlaget Ny Videnskab 2002.

www.aacr.org/cncrrea.htm
www.ingentaconnect.com/content/klu/caco;jsessionid=2sf53q49osdn1.victoria
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Supporting Evidence: B-vitamins Strengthen the Bones

Claus Hancke

March 18, 2005

A year ago a correlation between osteoporosis, folic acid and Vitamin B12 deficiency was discovered. It might have been a statistical coincidence, but a Japanese study discovered that the two vitamins reduced the risk of bone fracture by 80%.

Just a year ago, Dutch and American researchers demonstrated that at high homocysteine level – which is very common and most often a consequence of folic acid or vitamin B12 deficiency – the risk of breaking the hip doubles. It was only a statistical context, but was there also a causal link?

By: Vitality Council

References:
1. Sato Y, Honda Y, Iwamoto J, Kanoko T, Satoh K. JAMA. 2005 Mar 2;293(9):1082-8. Effect of folate and mecobalamin on hip fractures in patients with stroke: a randomized controlled trial.
2. Krumdieck CL et al. Mechanisms of homocysteine toxicity on connective tissues: Implications for the morbidity of aging. J Nutr. 2000;130:365S-368S.
3. Van Meurs Joyce B J et al. Homocysteine levels and the risk of osteoporotic fracture. N Engl J Med 2004;350:2033-41.
4. Mc Lean Robert R et al. Homocysteine as a predictive factor for hip fracture in older persons, N Engl J Med 2004;350:2042-9.

jama.ama-assn.org
content.nejm.org

Fried Herrings – Are They Really Good For The Heart?

Claus Hancke

March 15, 2005

An American study says that you can avoid heart flutter (atrial fibrillation) by eating fatty fish. Danish researchers have come to the exact opposite conclusion. Is that because the Danes like fried fish?

An American study concludes that you can avoid atrial fibrillation by eating fatty fish. Danish researchers have come to the exact opposite conclusion.

In the summer of 2004, researchers at Harvard University in Boston published an article stating that if you eat lots of fatty fish, your risk of atrial fibrillation will be reduced.

Atrial fibrillation is the most common cause of irregular heartbeat that will occur in a large number of elderly people and will require lifelong anticoagulant treatment.

To be precise, the American researchers had found that the risk of atrial fibrillation was reduced by 35% in people who consumed fatty fish at least five times a week and by 24% in the ones who consumed fatty fish 1 – 3 times a month – compared to people who only ate fish very rarely.

However, the matter is more complex than that: In January 2005, two Danish doctors published an article stating that a large consumption of fatty fish increases the risk of atrial fibrillation. They found the risk to be increased by 44% in the 20% who consumed the most fatty fish compared to the 20% who consumed the least.

Were do we go from that, then? If we take a rough average of the two studies, it will indicate that it does not matter whether or not you eat fatty fish.

But why are the results so conflicting? If we move below the surface, it turns out that the two studies are very different.

The American study included 5000 trial subjects with an average age of 73 years. The Danish study included 50,000 trial subjects with an average age that was 18 years less than the American study, i.e. 55 years.

Almost every fifth of the old Americans suffered atrial fibrillation during the 12-year duration of the American study. In comparison, the same was true for less than 2% of the Danes during the 6-year duration of the Danish study.

In total, the Americans observed more than twice as many trial subjects with atrial fibrillation compared to the Danes (980 and 456, respectively).

Frying distorts the fish oil
How were the person with atrial fibrillation indentified? The American trial subjects went through a cardiac examination every year in which all cases of atrial fibrillation were discovered. Contrary to this, information about the health state of the Danes was solely obtained from the hospitals – it was obviously assumed that all the trial subjects who had suffered atrial fibrillation had been hospitalized.

This discrepancy involves some uncertainty: Even though most trial subjects with atrial fibrillation were hospitalized, it is far from certain that this applied to everyone. Atrial fibrillation can very well be treated by a GP.

It was particularly important that the Americans observed that there is difference in the effect of fried fish and other kinds of fish. Fried fatty fish slightly increased the risk while non-fried (fatty) fish decreased the risk. Fried fatty fish neither increased the blood levels of fish oil (N-3 fatty acids) as non-fried fish does.

The Danish study does not explain how the fish were prepared. There was no distinguishing.

None of the studies explained how many and who took fish oil supplements: In the Danish study the trial subjects had not been given this question and in the American study, the information apparently did not alter the overall result.

To conclude: A detailed and precise American study has established that fatty fish reduces the risk of atrial fibrillation by approximately 33%.
A less detailed Danish study has established the opposite.

However, the size of the study is hardly decisive. It is probably more essential to pay some attention to how the fish was prepared. Fish oil is destroyed by high temperatures which, more or less, transforms the N-3 fatty acids into N-6 fatty acids, transfatty acids, and harmful oxidation products.

The American group has recently published some more news: Fatty fish – that has not been fried – reduces the risk of cerebral haemorrhage to approximately the same degree as is the case with atrial fibrillation. Fatty fish, on the other hand, increases this risk!

By: Vitality Council

References:
1. Dariush Mozaffarian et al. Fish intake and risk of incident atrial fibrillation. Circulation 2004;116:368-73.
2. n-3 Fatty acids consumed from fish and risk of atrial fibrillation or flutter : The Danish Diet, Cancer and Health Study. Am J Clin Nutr 2005;81:50-4
3. Mozaffarian D et al. Fish consumption and stroke risk in elderly individuals: the cardiovascular health study. Arch Intern Med 2005 Jan 24;165(2):200-6.

www.americanheart.org
www.americanheart.org/presenter.jhtml
www.ajcn.org
archinte.ama-assn.org
www.iom.dk

Magnesium May (Perhaps) Prevent Cancer

Claus Hancke

February 21, 2005

The less magnesium you get, the larger is the risk of colon cancer – plus asthma and imbalances in the muscle- and nerve function. Diuretic pills and empty calories is the major cause of magnesium deficiency.

Swedish researchers have discovered that a lack of magnesium seems to increase the risk of colon cancer which is one of the most common forms of cancer. The increased incidence was discovered in a group of 66,000 women of 40 – 70 years of age who were followed during a 3 year period.

The majority of the 66,000 women got less than the recommended 350 mg. of magnesium a day through their diet. Actually, if a woman got more than 255 mg. of magnesium a day, she would belong to the top 20% in regard to magnesium intake. This top 20% had a significantly reduced risk of colon cancer compared to the rest of the women, and the risk was inversely proportional to the intake of magnesium.

Why do so few people get enough magnesium? It should not be difficult to get enough, but it is estmated that at the beginning of the last century, an average adult person got more than 1000 mg. of magnesium a day. That is four times as much as the women who today get the most.

The explanation is obvious. At the beginning of the last century, the consumption of empty or half-empty calories in the form of sugar, margarine, and white flour was much smaller than it is today. In 100 g. of oatmeal, there is almost 300 mg. of magnesium while other whole grain products (and semisweet chocolate!) contain approx. 100 mg. of magnesium per 100 g. That is four times as much as in industrially manufactured white flour.

Lean meat which was rarely used 100 years ago does not contain more than about 25 mg. of magnesium per 100 g; which is about the same as in vegetables such as spinach, peas, and beans.

The comparison is interesting for other reasons than its relation to cancer. In numberous studies, a lack of magnesium has been linked to atherosclerosis and heart failure; diseases that were not all that common 100 years ago.

A number of years ago, for example, a Scottish study showed that when asthmatics were given a supplement of just 100 mg. magnesium, they suffered fewer asthmatic attacks and their mucous membranes were less irritable. It is a well-known fact that asthma is also a far more common disease today. The effect corresponds to the fact that you can stop an asthma attack by intravenously injecting magnesium sulphate.

Magnesium has many other effects as well: It inhitibs the tendency of the blood platelets to aggregate and increases the production of nitric oxide (NO) which keeps the blood vessels open, it lowers the blood pressure, and it maintains a normal circulation.

All these things can be assumed to reduce the risk of coronary thrombosis; a connection that is presumed but has yet to be finally confirmed. However, it is further supported by the fact that magnesium has several effects in common with the cholesterol-lowering drugs called statins – without having the side effects, that is.

The relaxing effect on the blood vessels might be connected to the generally relaxing effect on muscles and nerves for which magnesium is well-known. In earlier days, complete anaesthesia was induced by magnesium just as local anaesthesia can be achieved by injecting magnesium under the skin.

Magnesium is still the most important remedy against cramps in pre-eclampsia and can also be used against tetanus. Many people also benefit from a magnesium supplement that can relieve cramps in the legs which can be a nuisance to both pregnant women and elderly people.

It can seem alarming that we get so much less than we used to of a mineral with these properties. Not least because the widespread use of diuretics contribute to the lack of magnesium by excreting magnesium via the kidneys.

In addition to this, we can now add the possible anti-carcinogenic effects of magnesium. Of course, it might also be the result of a combination of other deficiencies which occurs at the same time as the magnesium deficiency. A poor diet will result in a lack of a number of essential nutrients, so the moral must be: Eat properly!

By: vitality Council

References:
“Magnesium Intake in Relation to Risk of Colorectal Cancer in Women”, Susanna C. Larsson, MSc; Leif Bergkvist, MD, PhD; Alicja Wolk, DMSc, JAMA. 2005;293:86-89.
“Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals”, Rosanoff A, Seelig MS, J Am Coll Nutr, 2004;23(5):501S-505S. (Address:Mildred S. Seelig, MD, E-mail: mgseelig(at)comcast.net ).
Ford Es, Mokdad AH. Dietary magnesium intake in a national sample of US adults. J Nutr 2003;133:2879-82
Goodman and Gilman’s The Pharmacological basis of therapeutics. Pergamon Press 1990. P. 704-6.

www.jacn.org
www.nutrition.org
www.iom.dk

St. John’s Wort Outdoes Antidepressant Drugs

Claus Hancke

February 14, 2005

It is better to take St. John’s Wort than Anti-Depressant Drugs, even when suffering from a moderate to a severe depression. It not only works better but it has fewer side effects. But every second patient needs a double dose.”…

Taking St. John’s wort is better than taking antidepressant drugs, even in the case of moderate to severe depressions. The effect is better and it has fewer adverse effects. However, every other patients needs a double dose for the herb to be effective.

The fact that St. John’s wort can be used for other things than making schnapps has been known for some time. As early as in 1994 it turned out that the plant can be used for even serious depressions, and St. John’s wort has been an unlicenced herbal remedy for some time now.

On account of the usual hypocrisy of the authorities, the remedy is only approved for treating “melancholy, despondency, and sadness”; concepts that are not used in the scientific world of approved licensed medical drugs. It has been documented, however, that St. John’s wort is effective against depression; but the hyprocrisy forbids informing about this even though it is specifically the word of “depression” that is used in the scientific articles.

In Germany, the authorities are truthful and here, St. John’s wort has been officially approved for “mental disturbances, depressive conditions, anxiety, and nervous restlessness” since 1984.

For this reason, German doctors have used far more St. John’s wort than their British colleagues and have spared their patients of nausea, tiredness, impotence, oral dryness, dizziness, sleeplessness, and what else might come from using antidepressants – also called SSRI preparations. In Germany, St. John’s wort is prescribed twice as often as standard antidepressants.

So far, it has been known that St. John’s wort is just as effective against light depression as SSRI preparations and other antidepressants. When it comes to severe depressions, there has been more doubt about its effectiveness even though a study indicated that the effect was fully equal to prescription drugs. However, the study was too small for the results to be valid.

This uncertainty has now been removed. An unusually well accomplished German study performed with typical German thoroughness has documented that not only is St. John’s wort fully equal to the SSRI remedies; it actually outdoes them. In a study involving 244 severely depressed patients, St. John’s wort had both a better effect and caused fewer adverse effects than the widely used SSRI preparation paroxetine.

The study showed that adverse effects only appeared half as often in the group receiving St. John’s wort as in the group receiving paroxetine. After six weeks, the patients who had been treated with St. John’s wort noted a decrease in depression score of 57% while the patients who had been treated with paroxetine could only note a decrease of 45% – scored on the basis of the so-called Hamilton depression rating scale.

In all respects, this study lives up to the highest standards. There are therefore very strong reasons for preferring St. John’s wort to other remedies – in both mild and moderate to severe depression.

You should be aware of two things, however: First of all, the recommended dose in the over-the-counter drugs is generally too small: They advise you to take e.g. 3 – 6 tablets which gives you a total of 900 – 1800 mg of hypericin if the content of hypericin is 300 mg per tablet. The 900 mg is too small a dose.

In the German study, 900 mg was the starting dosage. Approximately every other patient had that dosage doubled after 14 days due to a lacking effect. This means that with Danish pills (450 milligrams hypericum / tablet) you either have to start with 2 and possibly increase to 4 tablets a day to get the same effect as the German trial subjects!

The second thing you should know is that St. John’s wort reduces the effect of several kinds of drugs, including prescription drugs such as contraceptive pills and anticoagulants. The reason for this is that St. John’s wort promotes the breakdown of the drugs in the liver. If you are taking any kind of medicine, you should consult your doctor before starting self-treatment with St. John’s wort!

By: Vitality Council

References:
1. Szgedi A et al. Acute treatrment of moderate to severe depression with hypericum extract WS 5570 (St Johns Wort): randomised controlled double blind non-inferiority trial versus paroxetine. BMJ online 11.2.2005, page 1-6.
2. de Smet P.A.G. et al. St Johns wort as an antidepressant. BMJ 1996;313:241-2 (L).
3. Linde K et al. St Johns wort for depression – an overview and meta analysis of randomised clinical trials. BMJ 1996;313:253-7.

bmj.bmjjournals.com
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Folic Acid: It Seems Wise to Take a Supplement

Claus Hancke

February 7, 2005

Folic acid reduces the blood pressure, but only if you take a folic acid supplement, as you will not get enough simply through your diet. At the same time, folic acid protects your heart and brain from blood clots.

Since long, it has been documented that the B-vitamin folic acid (B9) prevents congenital neural tube defects. In Canada, all kinds of flour have been enriched with folic acid during the past 8 years, and 80% of the congenital neural tube defects have thus been prevented. In the USA, enrichment is also obligatory, but in Britain, expectant mothers are left to themselves. They have to figure out for themselves to take a supplement – before they become pregnant!

The main source of folic acid is leafy green vegetables (the latin “folium” means “leaf”). Many people do not like these leafy greens and folic acid deficiency is therefore more common than any other vitamin deficiency. Unfortunately, the deficiency probably does not only harm the unborn baby but does also increase the mortality of coronary thrombosis and cerebral apoplexy in adults. But this is not all: Folic acid deficiency probably also increases the risk of hypertension.

The connection between folic acid deficiency and hypertension that has been unknown till now was discovered when an eight-year study was concluded involving 156,000 American nurses *1). The risk of the nurses having hypertension while being 27 – 44 years of age was only half as great when they took 1 mg (1000 mcg.) of folic acid a day compared to when they took 0.2 mg. In both the US and Britain, 0.2 mg. is just below the average daily folic acid intake which is 0.25 mg. It is almost impossible to get 1 mg. of folic acid a day – which is four times as much – without taking a supplement.

With regard to apoplexy and coronary thrombosis, much interesting knowledge has been produced during recent years:
In the US, where enrichment of flour with folic acid began in 1996, the mortality rate following apoplexy has droppped dramatically – in all groups of society, that is, and for both men and women – so the results are rather regardless of lifestyle, etc.

Before 1996, the annual drop in mortality as a result of apoplexy was about 1%. This drop was the result of improved treatment and prophylaxis. However, in the succeeding three years, mortality rates dropped three times as fast, i.e. with a total of 10 – 15%! Statistically, this has been explained by the fact that the average American now has twice as much folic acid in his/her blood as before *2).

Moreover, apoplexy is far more dangerous if you are deficient in folic acid. This was recently demonstrated on mice. They were given an artificial apoplexy in that their cerebral artery was simply clamped. It turned out that the cerebral damage was only half as great in the mice that had been given enough folic acid *3).

Folic acid seems to be able to protect the heart as well. This appeared most recently when Italian doctors studied 900 patients hospitalized with or without coronary thrombosis. The patients were divided into three groups according to their estimated daily intake of folic acid. Among the patients admitted to the cardiology department, most of them belonged to the group that got the least folic acid!

The third of the patients that got the least folic acid had twice as great a risk compared to the third of the patients that got the most folic acid. When vitamin B6 intake was also taken into account (vitamin B6 collaborates with folic acid), the ones who got the most folic acid only had a relative risk of 29% *4).

It is not the folic acid itself that protects the heart and the brain. However, folic acid reduces the blood content of the harmful amino acid homocysteine which attacks the blood vessels.

About 10% of the population are unaware that they have a hereditarily increased homocysteine level in their blood (and therefore need more folic acid). Recently, it was discovered that these 10% suffer apoplexy significantly more often than others *5, 6). It was already known that these people already have an increased risk of suffering coronary thrombosis *7).

Nobody has yet performed a blinded study in which supplements have been used to efficiently lower the blood contents of homocysteine. However, this kind of research is now being encouraged *8). Yet, with our existing knowledge, it seems wise to take a folic acid supplement. The ideal dosage may be around 0.8 mg. (800 mcg.) a day.

By: Vitality Council

References:
1. Forman JP, Rimm EB, Stampfer MJ, Curhan GC. Folate intake and the risk of incident hypertension among US women. JAMA. 2005 Jan 19;293(3):320-9.
2. American Heart Association’s 44th annual Conference on Cardiovascular Disease Epidemiology and Prevention.carole.bullock@heart.org
3. Endres M, Ahmadi M, Kruman I, Biniszkiewicz D, Meisel A, Gertz K. Folate deficiency increases postischemic brain injury. Stroke. 2005 Feb;36(2):321-5.
4. Taivani A et al. Folate and vitamin B6 intake and risk of acute myocardial infarct in Italy. Eur J Clin Nutr 2004;58:1266-72
5. Al-Delaimy WK, Rexrode KM, Hu FB, Albert CM, Stampfer MJ, Willett WC, Manson JE. Folate intake and risk of stroke among women. Stroke. 2004 Jun;35(6):1259-63.
6. Casas JP et al. Homocysteine and stroke: Evidence on a causal link from mendelian randomisation. The Lancet 2005;365: 224-32
7. Klerk M, Verhoef P, Clarke R, Blom HJ, Kok FJ, Schouten EG; MTHFR Studies Collaboration Group. MTHFR 677C–>T polymorphism and risk of coronary heart disease: a meta-analysis. JAMA. 2002 Oct 23-30; 288(16):2023-31.
8. S Schwammenthal et al. Homocysteine, B-vitamin supplementation, and stroke prevention. From observational to interventional trials. Lancet Neurol. 2004;3(8):493-5.

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