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(Health) Vitamin E from Palm Oil and Dermal Healing

 
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PostPosted: Thu Jan 05, 2006 7:55 pm    Post subject: (Health) Vitamin E from Palm Oil and Dermal Healing Reply with quote






Palm oil derived vitamin E ‘improves’ dermal healing
By Simon Pitman

15/12/2005- A Malaysian study has found that the vitamin derived from antioxidant-rich palm oil is more potent than other forms of vitamin E when used to improve the healing of dermal wounds.

The discovery could make the ingredient a useful alternative ito treat a host of skin care conditions such as eczema, dermatitis or acne that can often permanently scar or damage the skin.
The study was led by Musalmah Mazlan at the Universiti Kebangsaan, where a series of tests were carried out applying equal amounts of vitamin E palm oil (PVE) extract and alpha-tocopherol, the most biologically active form of vitamin E, on laboratory rats.

The antioxidant potencies of the two preparations were also evaluated to help determine the outcome of the experiment.

The research team interpreted the results by measuring the healing wound contractions in the diabetic rats as well as assessing protein contents.

The results revealed that both PVE and alpha-toc were potent antioxidants and helped to reduce lipid peroxidation levels in the wounds.

However, the researchers said that it was also clear that PVE had a significantly greater potency to enhance wound repair, which in turn helped to induce an increase in free radical-scavenging enzyme activity, when compared to the rats treated with alpha-toc.

Currently the farming of palm oil is one of the most important industries in Malaysia. Although widespread commercial plantings only began in the 1990s, the country is now the world's largest producer of palm oil, with Indonesia coming up as a close second. Last year Malaysia produced 14 million tons and Indonesia 11 million, on a global total of 30 million tons.

In an effort to increase production further, the Malaysian government has been increasing investment in a broad range of programmes aimed at developing the number of applications palm oil can be used for.

Vitamin E has long been an important ingredient in a variety of skin care products, due mainly to its healing and reparation properties. However, recent studies have found that its anti-oxidant properties also make it an important active ingredient for both sunscreen and anti-ageing formulations.

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Important Note: Unlike the other more well-known vitamins, Vitamin E is not yet fully understood and much study is still needed. News articles like the one above that describe Vitamin E effects should therefore receive some amount of skepticism.

Questions to explore further this topic:

What is Vitamin E?

http://ods.od.nih.gov/factsheets/vitamine.asp
http://pharmacy.auburn.edu/hea.....amin_e.pdf
http://lpi.oregonstate.edu/fw04/allaboute.html
http://www.umm.edu/altmed/Cons.....inEcs.html
http://lpi.oregonstate.edu/inf...../vitaminE/

Is it beneficial to take oral supplements of Vitamin E?

http://www.berkeleywellness.co.....taminE.php

Vitamin E and the skin:

http://www.news.uiuc.edu/scitips/01/09sunburn.html

What is palm oil?

http://en.wikipedia.org/wiki/Palm_oil
http://www.unu.edu/unupress/fo.....152E05.htm

Some of the latest news regarding Vitamin E:

Vitamin E possibly unsafe for Alzheimer's patients
http://www.naturalproductsinsi.....91334.html

Vitamin E and prostate cancer
http://www.nutraingredients-us.....ate-cancer

Vitamin E risky for some
http://www.cbsnews.com/stories.....0401.shtml

Vitamin E proves no cure-all
http://msnbc.msn.com/id/8618413/

Vitamin E Loses Luster: Nutrient tests show disappointing results
http://www.sciencenews.org/art.....9/fob6.asp
http://www.naturalproductsinsi.....91334.html


GAMES

http://www.coolfoodplanet.org/gb/kidz/
http://www.fda.gov/oc/opacom/kids/default.htm
http://www.exhibits.pacsci.org....._cafe.html


Last edited by adedios on Sat Jan 27, 2007 4:50 pm; edited 3 times in total
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PostPosted: Thu Mar 02, 2006 8:33 pm    Post subject: NUTRITIONAL FRIEND OR FOE? VITAMIN E SENDS MIXED MESSAGES Reply with quote

NUTRITIONAL FRIEND OR FOE? VITAMIN E SENDS MIXED MESSAGES
Ohio State University
2 March 2006

COLUMBUS , Ohio – One of the most powerful antioxidants is truly a double-edged sword, say researchers at Ohio State University who studied how two forms of vitamin E act once they are inside animal cells.

In the past couple of decades, a slough of studies has looked at the benefits of vitamin E and other antioxidants. While a considerable amount of this research touts the advantages of consuming antioxidants, some of the studies have found that in certain cases, antioxidants, including vitamin E, may actually increase the potential for developing heart disease, cancer and a host of other health problems.

This study provides clues as to why this could happen, say Jiyan Ma, an assistant professor of molecular and cellular biochemistry, and his colleague David Cornwell, an emeritus professor of molecular and cellular biochemistry, both at Ohio State.

The two men led a study that compared how the two most common forms of vitamin E –– one is found primarily in plants like corn and soybeans, while the other is found in olive oil, almonds, sunflower seeds and mustard greens – affect the health of animal cells. The main difference between the two forms is a slight variation in their chemical structures.

In laboratory experiments, the kind of vitamin E found in corn and soybean oil, gamma-tocopherol, ultimately destroyed animal cells. But the other form of vitamin E, alpha-tocopherol, did not. (Tocopherol is the scientific name for vitamin E.)

“In the United States we tend to eat a diet rich in corn and soybean oil, so we consume much greater amounts of gamma-tocopherol than alpha-tocopherol,” Cornwell said. “But most of the vitamin E coursing through out veins is alpha-tocopherol – the body selects for this version. We want to know why that is, and whether the selection of the alpha-tocopherol confers an evolutionary benefit in animal cells.”


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While the study doesn't get into the possible effects on health, the researchers raise the point that there is still a great deal that isn't known about how antioxidants act in the body.
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Cornwell and Ma explain their findings in this week's Early Edition of the Proceedings of the National Academy of Sciences. They conducted the study with several colleagues from the departments of molecular and cellular biochemistry and chemistry at Ohio State.

The researchers conducted laboratory experiments on cells taken from the brains of mice. They treated some of the cells with metabolic end products, called quinones, of alpha- and gamma-tocopherol.

When the body breaks down vitamin E, these end products are what enter and act on our cells. However, Ma said that our bodies get rid of most gamma-tocopherol before it ever has a chance to reach its quinone stage.

Still, some nutritional supplement companies make and sell gamma-tocopherol supplements, promoting this version of vitamin E as a good antioxidant source. In theory, taking a vitamin supplement – a concentrated form of the vitamin - increases the amount of that substance in the body.

Using laboratory techniques that allowed them to detect the activity of the quinones inside the cells, the researchers found that the gamma-tocopherol quinone formed a compound which destroyed that cell. It did so by preventing proper protein folding in the cells, which causes a cellular response that is involved in a variety of human diseases, including diabetes and Parkinson's disease.

However, the alpha-tocopherol quinone did not kill cells, nor did it interfere with protein folding. The researchers repeated their experiments on kidney cells cultured from monkeys and on skin cells cultured from mice and found similar results.

“We think that gamma-tocopherol may have this kind of damaging effect on nearly every type of cell in the body,” Ma said.

While the study doesn't get into the possible effects on health, the researchers raise the point that there is still a great deal that isn't known about how antioxidants act in the body. In order to get to that point, scientists must study how antioxidants and cells interact on their most fundamental levels.

This work was funded through grants from the National Science Foundation Environmental Molecular Science Institute and the Large Interdisciplinary Grants Program in the Office of Research at Ohio State.
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PostPosted: Sun May 21, 2006 9:08 am    Post subject: RESEARCHERS MAKE VITAMIN E OFFSHOOT A POTENT CANCER KILLER Reply with quote

RESEARCHERS MAKE VITAMIN E OFFSHOOT A POTENT CANCER KILLER
COLUMBUS , Ohio –

Ohio State University
19 May 2006

Researchers here have learned how a derivative of vitamin E causes the death of cancer cells. The researchers then used that knowledge to make the agent an even more potent cancer killer.


The compound, called vitamin E succinate, or alpha tocopheryl succinate, is taken by some people as a nutritional supplement, mainly for its antioxidant properties. In addition, it has a weak ability to kill cancer cells, and it has been tested as a cancer chemopreventive agent.

The substance kills cancer cells by causing them to undergo a natural process known as programmed cell death, or apoptosis. Until now, no one knew how the agent caused this to happen.

These findings answer that question and also indicate that the molecule's antitumor activity is separate from its antioxidant effect.

The study, led by researchers with The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC-James), is published in the April 28 issue of the Journal of Biological Chemistry.

“Our findings could lead to a potent chemopreventive agent that has both strong anticancer and antioxidant properties,” says principal investigator Ching-Shih Chen, professor of pharmacy and of internal medicine and a researcher with the OSUCCC-James.


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The scientists found that a relatively simple process of altering the molecule's structure – basically cutting the tail short – allowed a tighter fit and improved the agent's ability to kill cancer cells by five- to ten-fold in laboratory tests.
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“Such an agent might help reduce the risk of prostate, colon and other cancers.”

Chen and his collaborators found that vitamin E succinate works by blocking a protein called Bcl-xL. The protein, which is made by healthy cells, is often present at abnormally high levels in cancer cells and protects them from dying when they should.

Using computer modeling, the researchers found that the vitamin E derivative works because it lodges in a groove in the structure of the Bcl-xL protein, disabling it.

However, the vitamin E molecule has a long, coiled, protruding tail that keeps the molecule from fitting tightly, and more effectively, into the groove.

“Once we identified how the agent and the protein interact, we asked how we could improve that interaction,” Chen says.

The scientists found that a relatively simple process of altering the molecule's structure – basically cutting the tail short – allowed a tighter fit and improved the agent's ability to kill cancer cells by five- to ten-fold in laboratory tests.

“Overall, out findings are proof of the principle that this drug can kill cancer cells very effectively but does very little damage to healthy cells,” Chen says.

Chen is also the Lucius A. Wing chair of cancer research and therapy at the OSUCCC-James and the Kimberly professor of pharmacy

Funding from the National Cancer Institute supported this research.
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PostPosted: Fri Sep 01, 2006 9:37 am    Post subject: Low vitamin E intake during pregnancy can lead to childhood Reply with quote

American Thoracic Society
1 September 2006

Low vitamin E intake during pregnancy can lead to childhood asthma

Children whose mothers had a low intake of vitamin E during pregnancy are more likely to develop wheezing and asthma by age five.

This research appears in the first issue for September 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

Graham Devereux, M.D., Ph.D., of the Department of Environmental and Occupational Medicine at the University of Aberdeen in the United Kingdom, and seven associates assessed maternal nutrient and respiratory status in 1,253 mothers and children during a five-year period.

According to the authors, children born to mothers from the lowest quintile of vitamin E intake were over five times more likely to manifest early persistent asthma than children whose mothers were in the highest quintile.

"Our findings suggest that vitamin E has a dual effect on lung function and airway inflammation and that the effects could change at differing periods of prenatal and early life," said Dr. Devereux. "Lung function was associated with early vitamin E exposure independent of atopy, whereas allergic airway inflammation was associated with vitamin E exposure in later pregnancy."

However, the researchers also noted that the airways are fully developed by 16 weeks after conception and, consequently, vitamin E exposure in early pregnancy may be more likely to influence airway function than exposure later in pregnancy.

"The present study suggests that children's own nutrient intake at the age of five does not modify the associations between maternal nutrient intake and respiratory outcomes in the children," said Dr. Devereux.

The study cited vegetable oils (sunflower, rapeseed and corn), margarine, wheat germ, nuts and sunflower seeds as major food sources of vitamin E for mothers in the U.K.

In a prior report on this group of children, the researchers found that two-year-olds whose mothers' vitamin E intake during pregnancy had been relatively low were more likely to wheeze even when they had no cold.

For the previous study, the investigators recruited 2,000 pregnant women at 12 months gestation who were attending area antenatal clinics between 1997 and 1999. Plasma antioxidant concentrations were measured in 1,856 mothers at 12 weeks gestation. In addition, symptom questionnaire data was later obtained for 1,253 children. From that group, 478 children were able to provide a lung function test measurement.

In light of the new findings, the authors concluded that the relationship shown between mothers' vitamin E intake during pregnancy and the respiratory outcomes of their children were likely "underestimates of the true association."

"The results of the present study suggest that dietary modification or supplementation during pregnancy to reduce the likelihood of childhood asthma warrants further investigation," said Dr. Devereux.

The researchers added that vitamin E supplementation in adults with established asthma has not been shown to be of clinical benefit.
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PostPosted: Wed Aug 22, 2007 11:44 am    Post subject: Vitamin E's lack of heart benefit linked to dosage Reply with quote

Vanderbilt University Medical Center
22 August 2007

Vitamin E's lack of heart benefit linked to dosage

Nashville (Tenn.) - The reported failure of vitamin E to prevent heart attacks may be due to underdosing, according to a new study by investigators at Vanderbilt University Medical Center.

The findings, published early online in Free Radical Biology and Medicine, suggest that these earlier studies all had a fundamental flaw – the doses used weren’t high enough to have a significant antioxidant effect. In fact, no studies have ever conclusively demonstrated the dose at which vitamin E can be considered an antioxidant drug, the researchers report.

Oxidant injury, or oxidative stress, occurs when highly reactive molecules called free radicals attack and damage cellular proteins, lipids (fats) and DNA. Free radicals, which are byproducts of normal metabolism, are produced in excess in certain disease states, including heart disease.

Epidemiological data and animal studies suggested that antioxidant compounds like vitamin E, vitamin C and beta-carotene might offer some protection against heart attack in individuals at risk.

But subsequent controlled clinical trials of vitamin E – which showed little to no benefit from the vitamin – stymied that hope.

“Multiple human trials looking at the effect of vitamin E supplementation on coronary events and atherosclerosis have all failed,” said Jack Roberts, M.D., the T. Edwin Rogers Professor of Pharmacology, professor of Medicine, and lead author on the study.

“We’re talking about trials that examined quite high doses,” added Jason Morrow, M.D., F. Tremaine Billings Professor of Medicine & Pharmacology and chief of the Division of Clinical Pharmacology. “Short of a couple of studies, there was no benefit in terms of prevention of cardiovascular events and deaths.”

These results caused many to discount vitamin E supplementation as a cardioprotective treatment, but Morrow and Roberts suspected that the studies had been poorly designed. All of the trials simply gave a dose of vitamin E and looked for end points such as heart attack occurrence. But Morrow and Roberts found a critical piece of information missing.

“All of these studies were designed in a way that they never assessed the ability of the dose of vitamin E tested to effectively reduce oxidant stress,” Morrow said.

Without determining whether the dose of vitamin E given was exerting sufficient antioxidant effects, the previous clinical trial results were flawed, the researchers said.

In the new study, Morrow and Roberts determined the optimum antioxidant dose of vitamin E using an assay they developed to measure compounds formed by oxidative stress processes, called F2-isoprostanes. This measure, said Roberts, “has been independently validated as the best measure of oxidative stress status in vivo.”

The researchers first determined how long it took for a very high dose of vitamin E – 3200 IU/day – to suppress oxidative stress in individuals at risk for cardiovascular disease.

To their surprise, it took 16 weeks for this dose – which is more than 100 times the recommended daily intake and about four times higher than doses used in most previous clinical studies – to maximally suppress F2-isoprostane formation.

In another group with similar cardiovascular risk factors, the researchers administered varying doses (0, 100, 200, 400, 800, 1600, and 3200 IU/day) over the 16-week period to find the minimum effective dose.

They found that it was necessary to give at least 1600 IU per day to cause a significant reduction in oxidative stress – twice that used in some of the previous clinical trials.

“It was clear that large doses – and doses in excess of what all clinical studies had used – were necessary,” Morrow said.

“Even with this massive dose of vitamin E, you only observe a 50 percent reduction in F2- isoprostanes,” added Roberts. “So in my opinion, vitamin E is not the spiffy antioxidant everybody thinks it is – it’s a pretty poor antioxidant.”

Because the long-term safety of such high doses is unknown, “we are not touting taking vitamin E in large doses,” Morrow said. “We are saying that, in the design of clinical trials, one needs to have good surrogate biochemical markers.”

Based on their findings, the investigators suggest that measures like F2-isoprostane measurement should be incorporated into any future studies of antioxidants in atherosclerosis prevention.

And since oxidative stress has been linked to numerous other diseases, including Alzheimer’s disease, Morrow suggests that F2-isoprostane measurement “really ought to be incorporated into studies assessing disease prevention by antioxidants in general.”
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PostPosted: Sat Sep 22, 2007 9:56 am    Post subject: Vitamin E trials 'fatally flawed' Reply with quote

Oregon State University
21 September 2007

Vitamin E trials 'fatally flawed'

CORVALLIS, Ore. – Generations of studies on vitamin E may be largely meaningless, scientists say, because new research has demonstrated that the levels of this micronutrient necessary to reduce oxidative stress are far higher than those that have been commonly used in clinical trials.

In a new study and commentary in Free Radical Biology and Medicine, researchers concluded that the levels of vitamin E necessary to reduce oxidative stress – as measured by accepted biomarkers of lipid peroxidation – are about 1,600 to 3,200 I.U. daily, or four to eight times higher than those used in almost all past clinical trials.

This could help explain the inconsistent results of many vitamin E trials for its value in preventing or treating cardiovascular disease, said Balz Frei, professor and director of the Linus Pauling Institute at Oregon State University, and co-author of the new commentary along with Jeffrey Blumberg, at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University.

“The methodology used in almost all past clinical trials of vitamin E has been fatally flawed,” said Frei, one of the world’s leading experts on antioxidants and disease. “These trials supposedly addressed the hypothesis that reducing oxidative stress could reduce cardiovascular disease. But oxidative stress was never measured in these trials, and therefore we don’t know whether it was actually reduced or not. The hypothesis was never really tested.”

The level of vitamin E that clearly can be shown to reduce oxidative stress, new research is showing, is far higher than the level that could be obtained in any diet, and is also above the “tolerable upper intake level” outlined by the Institute of Medicine, which is 1,000 I.U. a day. OSU researchers are not yet recommending that people should routinely take such high levels, but they do say that controlled clinical trials studying this issue should be aware of the latest findings and seriously consider using much higher vitamin E supplement levels in their studies.

In lab, animal or human studies, there’s evidence that vitamin E can reduce oxidative stress, inhibit formation of atherosclerotic lesions, slow aortic thickening, lower inflammation, and reduce platelet adhesion. Some human studies using lower levels of vitamin E supplements, such as 100 to 400 I.U. a day, have shown benefits in reducing cardiovascular disease risk, and others have not. An underlying assumption was that these levels were more than adequate to reduce oxidative stress, since they far exceeded the “recommended dietary allowance” or RDA for the vitamin, a level adequate to prevent deficiency disease.

“What’s now clear is that the amount of vitamin E than can conclusively be shown to reduce oxidative stress is higher than we realized,” Frei said. “And almost none of the studies done with vitamin E actually measured the beginning level or reduction of oxidative stress.”

Proper studies of vitamin E, researchers say, must be done carefully and take into account the newest findings about this micronutrient. It’s now known that natural forms of the vitamin are far more readily absorbed than synthetic types. It’s also been discovered that supplements taken without a fat-containing meal are largely useless, because in the absence of dietary fat vitamin E is not absorbed.

Some clinical trials may wish to study the long term effect of vitamins on healthy individuals. But if a clinical trial seeks to learn the value of reducing oxidative stress, they should select patients in advance for those who have high, measurable oxidative stress – often people who are older or have a range of heart disease risk factors, such as obesity, poor diet, hypertension or other problems. Cognizance should also be taken of people with health issues that may further increase their vitamin needs, such as smokers.

“A pill count simply isn’t enough to determine the value of vitamin E,” Frei said. “We need to select people for trials properly, make sure they are taking the right form of the vitamin, at the right levels and at the right time, and then verify the metabolic results with laboratory testing.”

“Only when we do these studies right will we answer questions about the value of vitamin E in addressing cardiovascular disease,” he said. “So far we’ve been flying blind.”

A parallel, Frei said, would be presuming to test the value of a statin drug, which lowers cholesterol, without ever measuring cholesterol levels in the test subjects, neither at the beginning nor at the end of the study. Such trials would be ridiculed in the science community.

So far, that’s the way vitamin E has been studied.

The use and intake of vitamins, experts say, has traditionally been thought of in terms of overt deficiency – for example, not enough vitamin C causes scurvy. Much less research has been done on the levels that can help create optimum health. The issue is of special importance with modern populations that have very different diets, activity levels and increased lifespan, and are dying from much different causes – predominantly heart disease and cancer – than people of past generations.
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PostPosted: Wed Jan 23, 2008 1:30 pm    Post subject: Low vitamin E levels associated with physical decline in eld Reply with quote

Yale University

Low vitamin E levels associated with physical decline in elderly

Researchers at Yale School of Medicine have found that a low concentration of vitamin E in the blood is linked with physical decline in older persons.

Published in the January 23 issue of Journal of the American Medical Association, the study included 698 people age 65 or older who were randomly selected from the population registry in two municipalities close to Florence, Italy. The researchers, led by first author Benedetta Bartali of Yale, collected blood samples to measure the levels of micronutrients including folate, iron and vitamins B6, B12, D and E. They assessed physical decline in the study participants over a three-year period using an objective test of three tasks: walking speed, rising repeatedly from a chair, and standing balance.

“We evaluated the effects of several micronutrients and only vitamin E was significantly associated with decline in physical function,” said Bartali, a nutritionist and a Brown-Coxe Postdoctoral Fellow at Yale School of Medicine. “The odds of declining in physical function was 1.62 times greater in persons with low levels of vitamin E compared with persons with higher levels.”

Bartali added, “It is unlikely that vitamin E is simply a marker for poor nutrition because our results are independent of energy intake, and the effect of low levels of other micronutrients was not significant. Our results suggest that an appropriate dietary intake of vitamin E may help to reduce the decline in physical function among older persons. Since only one person in our study used vitamin E supplements, it is unknown whether the use of vitamin E supplements would have the same beneficial effect.”

Bartali stresses that vitamin E was the only antioxidant measured in the study and further studies are needed to determine whether low levels of other antioxidants would yield the same results.

As an antioxidant, vitamin E may prevent or reduce the propagation of free radicals in the human body, which are associated with physical decline. This may help reduce muscle or DNA damage and the development of pathological conditions like atherosclerosis. Bartali said further studies are needed to determine the mechanisms of how low levels of vitamin E contributes to a decline in physical function.


###

Other authors on the study included Edward A. Frongillo, Jack M. Guralnik, M.D., Martha H. Stipanuk, Heather G. Allore, Antonio Cherubini, M.D., Stefania Bandinelli, M.D., Luigi Ferrucci, M.D., and Thomas M. Gill, M.D.
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