Vitamin E in Diet Protects Against Many Cancers

Researchers find form commonly used in supplements has no such benefit. 

Vitamin E in vegetable oils and nuts prevents cancer, according to research done at Rutgers University and the Cancer Institute of New Jersey.

Next time you need to choose between vegetable oil and margarine in that favorite recipe, think about your health and reach for the oil.

While the question of whether vitamin E prevents or promotes cancer has been widely debated in scientific journals and in the news media, scientists at the Center for Cancer Prevention Research, at Rutgers Mario School of Pharmacy, and the Cancer Institute of New Jersey, believe that two forms of vitamin E – gamma and delta-tocopherols – found in soybean, canola and corn oils as well as nuts do prevent colon, lung, breast and prostate cancers.

“There are studies suggesting that vitamin E actually increases the risk of cancer and decreases bone density,” says Chung S. Yang, director of the center. “Our message is that the vitamin E form of gamma-tocopherols, the most abundant form of vitamin E in the American diet, and delta-tocopherols, also found in vegetable oils, are beneficial in preventing cancers while the form of vitamin E, alpha- tocopherol, the most commonly used in vitamin E supplements, has no such benefit.”

Director of the Center for Cancer Prevention Research at Rutgers Ernest Mario School of Pharmacy

Yang and colleagues, Nanjoo Suh and Ah-Ng Tony Kong, summarized their findings recently in Cancer Prevention Research, a journal of the American Association for Cancer Research. In a Commentary, Does Vitamin E Prevent or Promote Cancer? the Rutgers scientists discuss animal studies done at Rutgers as well as human epidemiological studies that have examined the connection between vitamin E and cancer.

Yang says Rutgers scientists conducting animal studies for colon, lung, breast and prostate cancer found that the forms of vitamin E in vegetable oils, gamma and delta-tocopherols, prevent cancer formation and growth in animal models.

“When animals are exposed to cancer-causing substances, the group that was fed these tocopherols in their diet had fewer and smaller tumors,” Yang says. “When cancer cells were injected into mice these tocopherols also slowed down the development of tumors.”

In researching colon cancer, Yang pointed to another recently published paper in Cancer Prevention Research indicating that the delta-tocopherol form of vitamin E was more effective than other forms of vitamin E in suppressing the development of colon cancer in rats.

This is good news for cancer research. Recently, in one of the largest prostate cancer clinical trials in the United States and Canada, scientists found that the most commonly used form of vitamin E supplements, alpha-tocopherol, not only did not prevent prostate cancer, but its use significantly increased the risk of this disease among healthy men.

This is why, Yang says, it is important to distinguish between the different forms of vitamin E and conduct more research on its cancer preventive and other biological effects.

“For people who think that they need to take vitamin E supplements,” Yang says, “taking a mixture of vitamin E that resembles what is in our diet would be the most prudent supplement to take.”

 

Reference

Yang CS, Suh N, Kong AN. Does Vitamin E Prevent or Promote Cancer? Cancer Prev Res (Phila). 2012 Apr 16. [Epub ahead of print]

 

High Blood Levels Of Vitamin E Reduces Risk Of Alzheimer’s

High levels of several vitamin E components in the blood are associated with a decreased risk for Alzheimer’s disease (AD) in advanced age, suggesting that vitamin E may help prevent cognitive deterioration in elderly people.

“Vitamin E is a family of eight natural components, but most studies related to Alzheimer’s disease investigate only one of these components, ±-tocopherol”, says Dr. Francesca Mangialasche, who led a study on AD and vitamin E. “We hypothesized that all the vitamin E family members could be important in protecting against AD. If confirmed, this result has implications for both individuals and society, as 70 percent of all dementia cases in the general population occur in people over 75 years of age, and the study suggests a protective effect of vitamin E against AD in individuals aged 80+.”

The study was conducted at the Aging Research Center (ARC), Karolinska Institutet, Stockholm, Sweden, in collaboration with the Institute of Gerontology and Geriatrics, University of Perugia, Italy. The study included a sample of 232 participants from the Kungsholmen Project, a population-based longitudinal study on aging and dementia in Stockholm (Kungsholmen parish). All participants were aged 80+ years and were dementia-free at the beginning of the study (baseline). After 6-years of follow-up, 57 AD cases were identified.

The blood levels of all eight natural vitamin E components were measured at the beginning of the study. Subjects with higher blood levels (highest tertile) were compared with subjects who had lower blood levels (lowest tertile) to verify whether these two groups developed dementia at different rates. The study found that subjects with higher blood levels of all the vitamin E family forms had a reduced risk of developing AD, compared to subjects with lower levels. After adjusting for various confounders, the risk was reduced by 45-54%, depending on the vitamin E component.

Dr Mangialasche notes that the protective effect of vitamin E seems to be related to the combination of the different forms. Another recent study indicated that supplements containing high doses of the E vitamin form ±-tocopherol may increase mortality, emphasizing that such dietary supplements, if not used in a balanced way, may be more harmful than previously thought.

“Elderly people as a group are large consumers of vitamin E supplements, which usually contain only ±-tocopherol, and this often at high doses”, says Dr Mangialasche. “Our findings need to be confirmed by other studies, but they open up for the possibility that the balanced presence of different vitamin E forms can have an important neuroprotective effect.”

 

Reference

Mangialasche F, Kivipelto M, Mecocci P, Rizzuto D, Palmer K, Winblad B, Fratiglioni L. High plasma levels of vitamin E forms and reduced Alzheimer’s disease risk in advanced age. J Alzheimers Dis. 2010; 20 (4): 1029-37.

‘Gifted’ Natural Vitamin E Tocotrienol Protects Brain Against Stroke In 3 Ways

COLUMBUS, Ohio – A natural form of vitamin E called alpha-tocotrienol can trigger production of a protein in the brain that clears toxins from nerve cells, preventing those cells from dying after a stroke, new research shows.

This process is one of three mechanisms identified so far that this form of vitamin E uses to protect brain cells after a stroke, meaning that this natural substance might be more potent than drugs targeting single mechanisms for preventing stroke damage, according to Ohio State University scientists who have studied the nutrient for more than a decade.

These researchers previously reported that the tocotrienol form of vitamin E protects the brain after a stroke by blocking an enzyme from releasing toxic fatty acids and inhibiting activity of a gene that can lead to neuron death.

Vitamin E occurs naturally in eight different forms, and all of this work is focused on the tocotrienol form, also known as TCT. The commonly known form of vitamin E belongs to a variety called tocopherols. TCT is not abundant in the American diet but is available as a nutritional supplement. It is a common component of a typical Southeast Asian diet.

In this new study, the researchers first clarified the role of a protein called MRP1, or multidrug resistance-associated protein 1. This protein clears away a compound that can cause toxicity and cell death when it builds up in neurons as a result of the trauma of blocked blood flow associated with a stroke.

They then determined that TCT taken orally influences production of this protein by elevating the activity of genes that make MRP1. This appears to occur at the microRNA level; a microRNA is a small segment of RNA that influences a gene’s protein-building function.

This is one of the first studies to provide evidence that a safe nutrient – a vitamin – can alter microRNA biology to produce a favorable disease outcome,” said Chandan Sen, professor and vice chair for research in Ohio State’s Department of Surgery and senior author of the study. “Here, a natural nutritional product is simultaneously acting on multiple targets to help prevent stroke-induced brain damage. That is a gifted molecule.”

The research appears online and is scheduled for later print publication in the journal Stroke.

Over the past decade, Sen has led numerous studies on how the TCT form of vitamin E protects the brain against stroke damage in animal and cell models, and intends to eventually pursue tests of its potential to both prevent and treat strokes in humans. Approximately 795,000 Americans suffer new or recurrent strokes each year, and stroke is the third-leading cause of death in the United States, according to the American Stroke Association.

These latest research findings in mice follow a recent Food and Drug Administration certification of TCT as “Generally Recognized as Safe.” The scientists conclude in the paper that even before clinical trials can take place, “TCT may be considered as a preventive nutritional countermeasure for people at high risk for stroke.”

To determine the role of MRP1 in protecting brain cells, the researchers compared the effects of an induced stroke in two groups of mice: normal mice and animals that were genetically modified to be deficient in the MRP1 protein.

Both groups of mice showed comparably decreased blood flow in the area of the stroke, but the mice deficient in MRP1 had a larger volume of tissue death than did normal mice.

The mice with the protein deficiency also had a 1.6-fold higher level of a toxin that is cleared by MRP1. This toxin is called GSSG, or glutathione disulfide, and these researchers have previously shown that a failure to clear this toxin appears to trigger neuron death in the brain after stroke.

“The protein has the effect of dredging out the toxin,” said Sen, who is also a deputy director of Ohio State’s Davis Heart and Lung Research Institute. “A significant finding in this work is the recognition that MRP1 is a protective factor against stroke. Thanks to tocotrienol, we were able to identify that path.”

The presence of GSSG is linked to an excessive amount of glutamate that is released in the brain after a stroke. Glutamate is a neurotransmitter that, in tiny amounts, has important roles in learning and memory. Too much of it triggers a sequence of reactions that lead to the death of brain cells – the most damaging effects of a stroke.

This experiment showed for the first time that the loss of MRP1 function impairs the clearance of GSSG, and that MRP1 cells were recruited to the site of the stroke in normal mice, indicating this protein has a protective role in the brain after a stroke.

The researchers searched databases containing genomic data for a microRNA that appeared to have potential to influence production of MRP1. MicroRNAs bind to messenger RNA, which contains the actual set of instructions for building proteins. When that connection is made, however, the microRNA inhibits the building of protein from messenger RNA. So an inverse relationship exists between a microRNA and a protein it controls.

The researchers saw this very relationship in the cell study in which they manipulated the candidate microRNA levels and observed the effects of changing those levels on the presence of the MRP1 protein.

Finally, the researchers compared mice that were treated with TCT supplements or corn oil as a control for 13 weeks before a stroke was induced. The amount of damaged brain tissue was smaller in the mice that received TCT supplementation than in the mice receiving corn oil. In addition, TCT supplementation was associated with a lower level of the candidate microRNA in the damaged brain tissue, as well as an increase in the abundance of MRP1 cells at the stroke site.

“Essentially what we are showing with mechanistic explanation is that tocotrienol protects neural cells. It is anti-neurodegenerative,” Sen said. “This form of vitamin E helped us identify three major checkpoints in stroke-related neurodegeneration that were not known before we began testing tocotrienols against neurodegeneration”
Reference
Park HA, Kubicki N, Gnyawali S, Chan YC, Roy S, Khanna S, Sen CK. Natural Vitamin E α-Tocotrienol Protects Against Ischemic Stroke by Induction of Multidrug Resistance-Associated Protein 1. Stroke. 2011 Jun 30. [Epub ahead of print].