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22 July 2011

Coffee and Tea Drinkers Less Likely to Carry MRSA

People who drink hot tea or coffee are less likely to carry the superbug known as methicillin-resistant Staphylococcus aureus (MRSA) in their noses, researchers found.

Drinking either beverage was associated with about a 50 percent relative reduction in the odds of nasal MRSA carriage, and drinking both was associated with a 67 percent reduction, according to Dr. Eric Matheson of the Medical University of South Carolina in Charleston and colleagues.

The findings, reported in the July/August issue of Annals of Family Medicine, "raise the possibility of a promising new method to decrease MRSA nasal carriage that is safe, inexpensive, and easily accessible," they wrote.

The clinical importance of the finding is not entirely clear, however, as the relationship between nasal MRSA carriage and the chances of systemic infection has not been resolved, they added.

Previous studies have shown that tea and coffee have antimicrobial properties when applied topically, and to find out whether drinking the beverages had systemic effects the researchers turned to the 2003-2004 National Health and Nutrition Examination Survey (NHANES).

The analysis included 5,555 individuals ages 2 and older, representing 182.1 million people. About half (48.6 percent) reported consuming hot tea over the past month and 60.8 percent reported drinking coffee over the past month.

Overall, 1.4 percent of the participants carried MRSA in their noses.

After adjustment for age, race, sex, poverty status, current health status, hospitalization in the past 12 months, and use of antibiotics in the past month, there were lower odds of nasal MRSA carriage among individuals who drank any amount of hot tea, coffee or both compared with those who drank none.

A separate analysis of just the adult participants provided similar results.

Consumption of iced tea, however, was not associated with nasal MRSA carriage. The reason is unclear, but it could be that iced tea has lower levels of polyphenolic compounds than hot tea, or that the volatile antimicrobial compounds in coffee and tea reach the nose in vapor form, according to the researchers.

Although the study -- cross-sectional in design -- could not establish a causal relationship between drinking coffee and tea and nasal MRSA carriage, there are some possible mechanisms to explain the finding.

"In the case of coffee, particular attention has focused on the potential antibacterial properties of trigonelline, glyoxal, methylglyoxal, and diacetyl," Matheson and colleagues wrote. "For tea, attention has focused on the antimicrobial properties of tannic acid and catechins."

In addition, they wrote, drinking both coffee and tea decrease iron absorption, which could affect the growth of S. aureus.

The authors acknowledged that the study was limited by the exclusion of some individuals because of missing data and the inability to determine when the participants last drank coffee or tea.

They noted that the study could not address the larger question of whether nasal MRSA carriage is associated with systemic infection.

"Given this debate, the benefits of any treatment for MRSA nasal carriage should be carefully balanced against the risk," they wrote.

Eggs' Antioxidant Properties May Help Prevent Heart Disease and Cancer, Study Suggests

While eggs are well known to be an excellent source of proteins, lipids, vitamins and minerals, researchers at the University of Alberta recently discovered they also contain antioxidant properties, which helps in the prevention of cardiovascular disease and cancer.

Jianping Wu, Andreas Schieber and graduate students Chamila Nimalaratne and Daise Lopes-Lutz of the U of A Department of Agricultural Food and Nutritional Science examined egg yolks produced by hens fed typical diets of either primarily wheat or corn. They found the yolks contained two amino acids, tryptophan and tyrosine, which have high antioxidant properties.

After analyzing the properties, the researchers determined that two egg yolks in their raw state have almost twice as many antioxidant properties as an apple and about the same as half a serving (25 grams) of cranberries.

However, when the eggs were fried or boiled, antioxidant properties were reduced by about half, and a little more than half if the eggs were cooked in a microwave.

"It's a big reduction but it still leaves eggs equal to apples in their antioxidant value," said Wu.

The findings were published in the peer-reviewed journal Food Chemistry.

The discovery of these two amino acids, while important, may only signify the beginning of finding antioxidant properties in egg yolks, said Wu, an associate professor of agricultural, food and nutritional science.

"Ultimately, we're trying to map antioxidants in egg yolks so we have to look at all of the properties in the yolks that could contain antioxidants, as well as how the eggs are ingested," said Wu, adding that he and his team will examine the other type of antioxidant already known to be in eggs, carotenoids, the yellow pigment in egg yolk, as well as peptides.

In previous research, Wu found that egg proteins were converted by enzymes in the stomach and small intestines and produced peptides that act the same way as ACE inhibitors, prescriptions drugs that are used to lower high blood pressure.

That finding defied common wisdom and contradicted the public perception that eggs increased high blood pressure because of their high cholesterol content. Additional research by Wu suggests the peptides can be formulated to help prevent and treat hypertension.

Wu is convinced the peptides also have some antioxidant properties, which leads him to suggest that when he completes the next step in his research, the result will likely be that eggs have more antioxidant properties than we currently know.

How Bright Promise in Cancer Testing Fell Apart

When Juliet Jacobs found out she had lung cancer, she was terrified, but realized that her hope lay in getting the best treatment medicine could offer. So she got a second opinion, then a third. In February of 2010, she ended up at Duke University, where she entered a research study whose promise seemed stunning.

Doctors would assess her tumor cells, looking for gene patterns that would determine which drugs would best attack her particular cancer. She would not waste precious time with ineffective drugs or trial-and-error treatment. The Duke program — considered a breakthrough at the time — was the first fruit of the new genomics, a way of letting a cancer cell’s own genes reveal the cancer’s weaknesses.

But the research at Duke turned out to be wrong. Its gene-based tests proved worthless, and the research behind them was discredited. Ms. Jacobs died a few months after treatment, and her husband and other patients’ relatives have retained lawyers.

The episode is a stark illustration of serious problems in a field in which the medical community has placed great hope: using patterns from large groups of genes or other molecules to improve the detection and treatment of cancer. Companies have been formed and products have been introduced that claim to use genetics in this way, but assertions have turned out to be unfounded. While researchers agree there is great promise in this science, it has yet to yield many reliable methods for diagnosing cancer or identifying the best treatment.

Instead, as patients and their doctors try to make critical decisions about serious illnesses, they may be getting worthless information that is based on bad science. The scientific world is concerned enough that two prominent groups, the National Cancer Institute and the Institute of Medicine, have begun examining the Duke case; they hope to find new ways to evaluate claims based on emerging and complex analyses of patterns of genes and other molecules.

So far, the Food and Drug Administration “has generally not enforced” its regulation of tests created by individual labs because, until recently, such tests were relatively simple and relied heavily on the expertise of a particular doctor, said Erica Jefferson, a spokeswoman for the agency. But now, with labs offering more complex tests on a large scale, the F.D.A. is taking a new look at enforcement.

Dr. Scott Ramsey, director of cancer outcomes research at the Fred Hutchinson Cancer Center in Seattle, says there is already “a mini-gold rush” of companies trying to market tests based on the new techniques, at a time when good science has not caught up with the financial push. “That’s the scariest part of all,” Dr. Ramsey said.

Doctors say the heart of the problem is the intricacy of the analyses in this emerging field and the difficulty in finding errors. Even well-respected scientists often “oversee a machine they do not understand and cannot supervise directly” because each segment of the research requires different areas of expertise, said Dr. Lajos Pusztai, a breast cancer researcher at M. D. Anderson Cancer Center at the University of Texas. As a senior scientist, he added, “It’s true for me, too.”

The Duke case came right after two other claims that gave medical researchers pause. Like the Duke case, they used complex analyses to detect patterns of genes or cell proteins. But these were tests that were supposed to find ovarian cancer in patients’ blood. One, OvaSure, was developed by a Yale scientist, Dr. Gil G. Mor, licensed by the university and sold to patients before it was found to be useless.

The other, OvaCheck, was developed by a company, Correlogic, with contributions from scientists from the National Cancer Institute and the Food and Drug Administration. Major commercial labs licensed it and were about to start using it before two statisticians from M. D. Anderson discovered and publicized its faults.

The Duke saga began when a prestigious journal, Nature Medicine, published a paper on Nov. 6, 2006, by Dr. Anil Potti, a cancer researcher at Duke University Medical Center; Joseph R. Nevins, a senior scientist there; and their colleagues. They wrote about genomic tests they developed that looked at the molecular traits of a cancerous tumor and figured out which chemotherapy would work best.

Other groups of cancer researchers had been trying to do the same thing.

“Our group was despondent to get beaten out,” said Dr. John Minna, a lung cancer researcher at the University of Texas Southwestern Medical Center. But Dr. Minna rallied; at the very least, he thought, he would make use of this incredible discovery to select drugs for lung cancer patients.

First, though, he asked two statisticians at M. D. Anderson, Keith Baggerly and Kevin Coombes, to check the work. Several other doctors approached them with the same request.

Dr. Baggerly and Dr. Coombes found errors almost immediately. Some seemed careless — moving a row or a column over by one in a giant spreadsheet — while others seemed inexplicable. The Duke team shrugged them off as “clerical errors.”

And the Duke researchers continued to publish papers on their genomic signatures in prestigious journals. Meanwhile, they started three trials using the work to decide which drugs to give patients.

Dr. Baggerly and Dr. Coombes tried to sound an alarm. They got the attention of the National Cancer Institute, whose own investigators wanted to use the Duke system in a clinical trial but were dissuaded by the criticisms. Finally, they published their analysis in The Annals of Applied Statistics, a journal that medical scientists rarely read.

The situation finally grabbed the cancer world’s attention last July, not because of the efforts of Dr. Baggerly and Dr. Coombes, but because a trade publication, The Cancer Letter, reported that the lead researcher, Dr. Potti, had falsified parts of his résumé. He claimed, among other things, that he had been a Rhodes scholar.

“It took that to make people sit up and take notice,” said Dr. Steven Goodman, professor of oncology, pediatrics, epidemiology and biostatistics at Johns Hopkins University.

In the end, four gene signature papers were retracted. Duke shut down three trials using the results. Dr. Potti resigned from Duke. He declined to be interviewed for this article. His collaborator and mentor, Dr. Nevins, no longer directs one of Duke’s genomics centers.

The cancer world is reeling.

The Duke researchers had even set up a company — now disbanded — and planned to sell their test to determine cancer treatments. Duke cancer patients and their families, including Mrs. Jacobs’s husband, Walter Jacobs, say they feel angry and betrayed. And medical researchers see the story as a call to action. With such huge data sets and complicated analyses, researchers can no longer trust their hunches that a result does — or does not — make sense.

21 July 2011


The sunshine vitamin beams in the health news spotlight with mega health benefits.
 By Deborah Tukua,

Sunshine on his shoulders made John Denver so happy he sang its praises.  When you read all the health benefits that keep vitamin D beaming in the health news spotlight, you should be singing its praises too.  A friend recently told me how much more energetic and happy she feels now that she’s spending time sunbathing outside this summer. My friend, Valerie also said, “I finally came to realize that the sun is natural. It’s there for our wellbeing.” Why was this fact something Valerie just recently accepted? Because like most consumers, she’s listened to the barrage of beauty and skin experts advise us for years to totally ban sun exposure. We are advised to slather on sunblock, sunglasses, hats and gear every time we step outside, as though we’re entering a toxic zone. Fortunately, there are health professionals willing to speak the truth despite current mainstream trends. 

A rise in malignant melanomas in the US heightened the scare of sun exposure in the 1970s and ‘80s.  It was assumed that skin cancers were the result of over exposure to UVB rays from the sun.   However, we have since learned that, “Skin cancer is also caused by UVA rays, which most sun blocks don’t block. Thus, by making people vitamin D deficient, they inadvertently increased people’s risk of developing all forms of skin cancer, including the deadly malignant melanoma,” states Dr. Russell Blaylock, MD, author of the Blaylock Wellness Report.

What is vitamin D and its Benefits

19 July 2011

'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"

17 July 2011

This Cooking Oil is a Powerful Virus-Destroyer and Antibiotic…

You've no doubt noticed that for about the last 60 years the majority of health care officials and the media have been telling you saturated fats are bad for your health and lead to a host of negative consequences, like elevated cholesterol, obesity, heart disease and Alzheimer's disease.
Meanwhile during this same 60 years the American levels of heart disease, obesity, elevated serum cholesterol and Alzheimer's have skyrocketed compared to our ancestors, and even compared to modern-day primitive societies using saturated fat as a dietary staple.
Did you know that multiple studies on Pacific Island populations who get 30-60% of their total caloric intact from fully saturated coconut oil have all shown nearly non-existent rates of cardiovascular disease?[1]
Clearly, a lot of confusion and contradictory evidence exists on the subject of saturated fats, even among health care professionals.
But I'm going to tell you something that public health officials and the media aren't telling you.
The fact is, all saturated fats are not created equal.
The operative word here is "created", because some saturated fats occur naturally, while other fats are artificially manipulated into a saturated state through the man-made process called hydrogenation.
Hydrogenation manipulates vegetable and seed oils by adding hydrogen atoms while heating the oil, producing a rancid, thickened oil that really only benefits processed food shelf life and corporate profits.
The medical and scientific communities are now fairly united in the opinion that hydrogenated vegetable and seed oils should be avoided.
These unsaturated fats, artificially manipulated into saturated fats, are also called trans fats, and no doubt you've heard about them lately. Some cities and states have now outlawed their use. There is no controversy anymore regarding the health dangers of these artificially saturated fats.
And guess what?
These are the same damaged trans fats that have been touted as "healthy" and "heart-friendly" for the last 60 years by the vegetable and seed oil interests!
But the truth finally came out. Trans fat was rebuked, debunked, and revealed as the true enemy to good health that it has always been, regardless of what the seed- and vegetable oil shills told the American public for the last half century.
Unfortunately, this rightful vilification of hydrogenated saturated fats has created a lot of confusion regarding naturally occurring saturated fats, including coconut oil.
If one form of saturated fat is bad for you, the argument goes, then all saturated fat must be bad.
Nothing could be further from the truth!