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Wednesday, May 23, 2012

Cutting-Edge Natural Health & Anti-Aging Products.


Organic Food Is Safer

Major Study of Pesticide Residues Shows Organic Food Is Safer May 7 — WASHINGTON — U.S. Newswire Following is a statement by Environmental Working Group (EWG) President Ken Cook: “”Conventionally grown food has significantly higher levels of pesticides, and is contaminated with residues of multiple pesticides, far more frequently than organic food. And those lower pesticide levels translate into lower risk of cancer and other health effects for consumers who eat organic food, particularly children.”"

“”These are the key findings of the first detailed study comparing pesticide residues on tens of thousands of samples of organic and conventional foods. The study also found that farming methods designed to use pesticides more sparingly also result in food residue levels that are lower than in regular food.

“”In recent years, the federal government has restricted or banned a number of pesticides out of a growing scientific recognition of the special risk these chemicals pose to children’s health. This study makes clear that the entire food supply can and should move in the direction of lower pesticide residues and thus lower health risks. The organic food industry is leading the way with a safer alternative.

“”Consumers know what to eat if they want to cut back on fat, calories or cholesterol. Now they know they should buy organic if they want to reduce pesticides in the foods they eat and feed their children.”"

The study was published in the current (May, 2002) issue of Food Additives and Contaminants, a scientific journal. It was authored by Brian Baker, Charles Benbrook, Edward Groth and Karen Lutz Benbrook.

EWG, a nonprofit environmental research organization, has published dozens of studies on the risks of pesticides to children.

PSA Test

PSA Test a Thing of the Past? MONDAY, May 10 (HealthDayNews) — The PSA test, long the gold standard for deciding who should have a biopsy for prostate cancer, may have outlived its usefulness for the most part.

Stanford University researchers say PSA (prostate specific antigen) levels bear little relationship to the severity of a cancer these days. They presented their finding May 9 at the American Urology Association’s annual meeting in San Francisco.

“”We need to recognize that PSA is no longer a marker for prostate cancer,”" said study author Dr. Thomas A. Stamey, a professor of urology at Stanford University School of Medicine. “”We urgently need to find a new marker for prostate cancer, and that marker must be proportional to how much cancer you have.”"

“”We have been so thorough and effective in screening for prostate cancer over this 20-year period that PSA no longer has a relationship to prostate cancer,”" Stamey said. “”Because we all develop the cancer, we’re now removing prostates from men whose cancer is so small that they do not need the procedure. We’re finding all these little cancers that are never going to be a danger to the patient.”"

“”In smaller cancers, the PSA test is not relevant anymore,”" Stamey explained. “”You might as well biopsy a man because he has blue eyes.”"

PSA is a protein produced by the cells of the prostate gland. Because blood levels of the antigen tend to rise as the gland enlarges, it has been used for years as a test of whether a person needs a biopsy for cancer. The test, however, is not foolproof.

“”People’s perceptions [are] that if your PSA is a certain level, you’re very likely or you do have prostate cancer, and that is incorrect,”" said Dr. Mark Soloway, chairman of the department of urology at the University of Miami School of Medicine.

“”The PSA test is a very good test. It’s not a perfect test, especially in younger men,”" added Dr. Jay Brooks, chief of hematology/oncology at the Ochsner Clinic Foundation in New Orleans.

To see how the efficacy of the PSA test might have waned, researchers in Stamey’s lab reexamined every prostate that had been removed since 1983 (1,317 of them) and compared the size of the cancer with blood PSA levels. None of the cancers had been treated with chemotherapy, radiation, or hormones before surgery.

Each cancer was rated on eight or 10 different parameters thought to indicate how aggressive the cancer was, including the size of the tumor and its grade.

Stamey then divided the samples into four five-year periods to see what had happened to the qualities of the cancers over time.

“”What we showed was that in the first five years, the cancers were related to the level of serum PSA,”" Stamey said. “”Then in the next five years, they were still bad but not as bad as the first five years. Then in the third five-year period, they were better and better. And in the last five years ending Jan. 1 of this year, the cancers were so small they had no relationship to serum PSA.”"

Twenty years ago, 80 percent of cancers were detected by digital rectal examination; only 20 percent of cancers are now detected that way, Stamey explained.

Instead, PSA levels today are driven by benign enlargement of the prostate, a condition that does not usually require surgery.

The concept that the PSA test is not foolproof is not an entirely new one. “”The point is well taken that in microscopic disease, the volume of cancer is clearly overshadowed by the volume of noncancer, so that the cancer cannot be the cause of the elevated PSA,”" said Dr. John Phillips, physician-in-charge of urologic oncology at Beth Israel Medical Center in New York City.

The question now is what can replace it. “”People are trying to find other ways of finding cancer,”" Phillips added.

As a matter of fact, University of Pittsburgh researchers who presented at the same conference reported that additional testing for a protein called early prostate cancer antigen (EPCA) might mean prostate cancer could be detected as many as five years earlier than with just the PSA test.

“”We would like a perfect test that would only find biologically significant cancers,”" Soloway said. “”Today we can’t distinguish between those with indolent cancer and those whose cancers threaten their life. We need another way. That’s going to be a difficult task.”"

In the meantime, the American Urological Association issued a statement that, for the time being, the PSA test in combination with a digital rectal exam and a full medical history is the best way to determine when a biopsy might be necessary

Scientists Learning More Why Aging Cells Fail to Repair Themselves

Why Aging Cells Lose Ability to Repair Themselves Study finds defect that could lead to new treatments for disease

FRIDAY, Sept. 5 (HealthWire) — A defect in the body’s self-defense mechanism against age-related genetic mutations has been identified by researchers at the University of Texas Medical Branch at Galveston.

The finding may help explain why the aging human body can’t defend itself against DNA damage in the mitochondria, the power plants that fuel the growth and activity of cells.

Finding ways to help aging cells repair their own damaged DNA could possibly lead to ways to prevent or treat cancer, Alzheimer’s disease, Parkinson’s disease and other health problems caused by genetic defects.

As cells age, they experience continuous genetic mutations, some of which are caused by the harmful byproducts of the oxygen we inhale. But the body’s repair mechanism is constantly at work fixing this DNA damage. However, this repair activity becomes less efficient as cells age.

In this study, the researchers analyzed why this DNA repair activity becomes less effective in the mitochondria as cells age. They found a biochemical “”roadblock”" that prevents much of the repair enzyme activity from reaching the site of the DNA damage in the mitochondria of aging cells.

In old cells, about half of the repair enzyme activity can’t reach the mitochondria DNA to repair it.

The study was published online this week in the Proceedings of the National Academy of Sciences.

Whole Grains Promote Healthy Weight

 

Bakers, Food makers and nutritionists are warning about the amazing popularity of the Atkins diet have a new tool in their fight against this food fad in a new study that reveals an inverse assocation between whole grains and weight gain.

It found that while women who ate a large amount of refined grain foods were more likely to be obese, those with the greatest whole grain consumption weighed less and are less likely to gain weight.

The study, published in November’s American Journal of Clinical Nutrition (vol 78, no 5, pp 920-927), investigated the relation between intake of dietary fibre and whole- or refined-grain products with weight gain over time.

They used a prospective cohort study on more than 74,000 US female nurses, aged 38-63 years in 1984 and free of known cardiovascular disease, cancer, and diabetes at baseline. Their dietary habits were assessed in 1984, 1986, 1990, and 1994 with validated food-frequency questionnaires.

Average weight, body mass index, long-term weight changes, and the odds ratio of developing obesity (BMI of 30) according to change in dietary intake were recorded.

The researchers from the Brigham and Women’s Hospital and Harvard Medical School found that women who consumed more whole grains consistently weighed less than women who consumed less whole grains.

Over 12 years, those with the greatest increase in intake of dietary fibre gained an average of 1.52 kg less than did those with the smallest increase in intake of dietary fibre independent of body weight at baseline and age.

Women in the highest quintile of dietary fibre intake had a 49 per cent lower risk of major weight gain than did women in the lowest quintile.

The team concludes that “”weight gain was inversely associated with the intake of high-fibre, whole-grain foods but positively related to the intake of refined-grain foods, which indicated the importance of distinguishing whole-grain products from refined-grain products to aid in weight control”".

Science Begins to Add Weight to CLA

 

The flurry of activity in CLA applications is being backed by a growing body of research to support the ingredient, particularly for its effects on weight loss. A review published in this month’s Journal of Nutrition supports conjugated linoleic acid’s action on weight management, concluding that it is at least in part due to regulation of glucose and fatty acid uptake and metabolism.

Conjugated linoleic acid is the common name of a group of fatty acids found in dairy products and meat. CLA isomers have been studied for their action on an impressive range of diseases, including cancer, atherosclerosis, obesity, and immune function. However as scientists begin to reveal their effects on reduction of body fat, food makers are increasingly looking at the ingredient for the valuable slimming market.

In Canada, where many of the patents for CLA are held, the dairy industry has long been studying the production of high-CLA milk. In Europe, a research centre in Ireland is studying the compound which could add significant value to its dairy industry, while in Italy, Techno Foods introduced a strawberry flavoured yoghurt naturally rich in CLA (conjugated linoleic acid) and omega-3 fatty acids this summer.

Specific CLA isomers have been shown to prevent the development of obesity in certain rodent and pig models and this has been attributed mainly to trans-10, cis-12 CLA, both in vivo and in vitro, write the University of North Carolina researchers in the review. However, CLA’s ability to modulate human obesity remains controversial because data from clinical trials using mixed isomers are conflicting.

In vitro studies by the team demonstrated that while trans-10, cis-12 CLA prevents triglyceride accumulation in human cells, cis-9, trans-11 CLA increases triglyceride content. The team concluded that the isomers’ regulation of glucose and metabolism must partly explain its mechanism on human fat.

The news is also good for supplement marketers who recently learned of research carried out by Cognis backing the long-term safety of its Tonalin CLA.

Brain Cell Growth Boosted By DHEA Supplements

‘Anti-aging’ hormone DHEA Found to Boost Brain Cell Growth August 24, 2004

Human neural stem cells, exposed in a lab dish to the steroid DHEA, exhibit a remarkable uptick in growth rates, suggesting that the hormone may play a role in helping the brain produce new cells, according to a new study published this week in the online edition of the Proceedings of the National Academy of Sciences (PNAS).

The new work, conducted by a team of scientists at the University of Wisconsin-Madison, provides some of the first direct evidence of the biological effects of DHEA on the human nervous system, according to Clive Svendsen, the study’s senior author and an authority on brain stem cells at UW-Madison’s Waisman Center.

“What we saw was that DHEA significantly increased the division of the cells,” said Svendsen, a UW-Madison professor of anatomy and neurology. “It also increased the number of neurons produced by the stem cells, prompting increased neurogenesis of cells in culture.”

DHEA or dehydroepiandrosterone is among the most abundant naturally occurring steroids in the blood of young humans, but levels decline with age and its physiological effects are poorly understood.

A synthetic form of the hormone is sold over-the-counter as a dietary supplement in the US, thought to have anti-aging properties and to offer prevention against cancer and heart disease, Alzheimer’s and other diseases. But scientists know relatively little about the drug and its basic biological effects on humans.

“We don’t know much about DHEA, but this new work adds a piece to the puzzle,” said Svendsen, who conducted the study with colleagues Masatoshi Suzuki, Lynda S. Wright, Padma Marwah and Henry A. Lardy, all of UW-Madison. “This is the first real evidence of DHEA’s effects on human neural cells.”

Svendsen and Suzuki carried out the experiments by growing human fetal neural stem cells in culture. The cells form aggregates known as ‘neurospheres,’ which were exposed to a cocktail of DHEA and growth and inhibitory factors, and observed a 29 per cent increase in new brain cells compared to cells grown in a medium with the same factors, but without DHEA.

“We saw such a pure effect of DHEA,” Svendsen said.

“It’s the only steroid we tested that had such a direct effect on stem cell growth and new neuron formation,” according to Suzuki.

The new work is important because it provides a direct window to the controversial hormone’s effects on critical human cells. Similar studies have been conducted in mice and rats, but those models have shortcomings that are difficult to address, Svendsen notes.

“There are previous studies in rats that suggest DHEA is neuroprotective, but the problem with DHEA in rats is that it is not a major metabolite in that animal so its effects may not be the same as those seen in humans,” he said. According to Lardy, metabolic products of DHEA hormone have also been shown to aid memory retention in old mice.

Despite hints from the studies in rodents that DHEA may play a role in enhancing the brain and memory, the new findings reported in the PNAS article were a surprise, he said.

“We assumed the compounds we were testing would be more active than DHEA in brain stem cells,” Lardy explains. In previous studies, Lardy, with Wisconsin biochemistry colleagues James Ntambi and Brian Fox, showed that DHEA blocked a step in fat synthesis.

“The effects of DHEA on brain stem cells is a completely new finding,” said Lardy. “The problem of whether DHEA itself is having this effect, or if there’s another metabolite of the hormone involved, still exists.”

One of the intriguing aspects of the new work, according to Svendsen, is the possibility that DHEA could have some positive effects on the adult human brain.

It is known that DHEA amounts fall progressively during aging, and reduced levels of DHEA have been reported in both adolescents and adults with major depressive disorders. And given the fact that adult humans have neural stem cells that continue to make new neurons in some parts of the brain, there is a possibility that DHEA could play a role in moderating the genesis of new brain cells.