CONTEXT: Increased dietary intake of marine omega-3 fatty acids is associated with prolonged survival in patients with coronary heart disease. However, the mechanisms underlying this protective effect are poorly understood. OBJECTIVE: To investigate the association of omega-3 fatty acid blood levels with temporal changes in telomere length, an emerging marker of biological age. DESIGN, SETTING, AND PARTICIPANTS: Prospective cohort study of 608 ambulatory outpatients in California with stable coronary artery disease recruited from the Heart and Soul Study between September 2000 and December 2002 and followed up to January 2009 (median, 6.0 years; range, 5.0-8.1 years). MAIN OUTCOME MEASURES: We measured leukocyte telomere length at baseline and again after 5 years of follow-up. Multivariable linear and logistic regression models were used to investigate the association of baseline levels of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) with subsequent change in telomere length.

They pass themselves off as an independent review site, but the truth is that this is just a portal to steer you to the sites that sell you this crap.

Resveratrol SCAM

Resveratrol (3,5,4 trans-hydroxy stilbene) was discovered about 70 years ago. It's hardly new. You see everyone selling resveratrol, so it must be good stuff, right? If so many people are buying it, then it must work, right?

Cancer Research UK is more forthright in condemning those who hype resveratrol for its cancer- inhibiting properties. "Many vitamin and mineral supplements were believed to be potent cancer fighters until trials and large studies showed they are usually ineffective and can even increase the risk of cancer in some cases," says the charity's Yinka Ebo. "Resveratrol has a few anticancer properties when tested in animals or cells grown in a lab. But, to date, there is no strong evidence that resveratrol supplements can prevent cancer in people."

Read the whole story at Wired

Caution Is Advisable

Although laboratory tests have demonstrated that resveratrol might help prevent cardiovascular disease and cancer, there are several reasons why a population-wide increase would be premature.

- The research on resveratrol has focused on its short-term effects and has been dominated by in vitro (laboratory) studies on non-human models.

- Not enough is known about the absorption and clearance of resveratrol, the identities of its metabolic products, or its effects on the liver.

- Resveratrol's role as a potentiator of breast carcinomas may significantly limit its use.

-  While taking resveratrol pills is certainly safer than heavy wine consumption, supplementing with unproven substances is generally unwise. At this point, occasional use of red wine seems far more prudent.

The Bottom Line

Via In the Pipeline, I see that research groups are suggesting that some of the data for resveratrol (and other possible calorie restriction mimetics developed by Sirtris) is invalid, and previously reported beneficial effects on mice cannot be replicated: "Last fall, a group at Amgen published a study suggesting that some of the SIRT1/resveratrol connections might be due an an experimental artifact caused by a particular fluorescent peptide. Now a group at Pfizer has piled on in the Journal of Biological Chemistry. They're looking over resveratrol and a series of sirtuin activators described by the Sirtris group in Nature. And unfortunately, they also find trouble due to fluorogenic peptides. The TAMRA fluorophore on their peptide substrates seems to pervert the assay. While the Sirtris compounds looked like activators initially, switching to the native peptide substrates showed them to be worthless. Further study (calorimetry) showed that the activator compounds bind to a complex of SIRT1 and the fluorescent peptide substrate, but not to SIRT1 itself (or in the presence of native substrate without the fluorogenic group).

Efforts to slow the march of old age with a pill have been dealt a blow. Drugs that might treat disease by tampering with the biology of ageing are being tested, but new research questions whether they work as thought.

The compounds include resveratrol, a much-touted component of red wine that is thought to prevent the cellular damage that underlies ageing. Also under test are several chemicals intended to mimic resveratrol's effects by activating SIRT1, a protein implicated in ageing. Experiments have led some to conclude that these drugs ramp up the protein's activity, but the new studies suggest that those experiments suffered from errors.

Genescient is the world's first computational biology company founded on the use of artificial biological selection to cure the diseases of aging. Our laboratory animals have been selected for longevity through 750 generations for the equivalent of 15,000 human years. I will describe Genescient's multiple pathways toward accelerating human longevity, with parallel enhancements of vigor and function. Genescient applies 21st century genomic technology to identify, screen and develop benign therapeutic substances at precise doses, to defeat the diseases of aging. Our singular approach addresses the complex genomic networks that underlie aging and aging-associated diseases such as cardiovascular disease, Type II diabetes and neurodegenerative diseases. I shall display some results and our first product, due in 2009.

BACKGROUND: Caloric restriction without malnutrition extends life span in a range of organisms including insects and mammals and lowers free radical production by the mitochondria. However, the mechanism responsible for this adaptation are poorly understood. METHODS AND FINDINGS: The current study was undertaken to examine muscle mitochondrial bioenergetics in response to caloric restriction alone or in combination with exercise in 36 young (36.8 +/- 1.0 y), overweight (body mass index, 27.8 +/- 0.7 kg/m(2)) individuals randomized into one of three groups for a 6-mo intervention: Control, 100% of energy requirements; CR, 25% caloric restriction; and CREX, caloric restriction with exercise (CREX), 12.5% CR + 12.5% increased energy expenditure (EE). In the controls, 24-h EE was unchanged, but in CR and CREX it was significantly reduced from baseline even after adjustment for the loss of metabolic mass (CR, -135 +/- 42 kcal/d, p = 0.002 and CREX, -117 +/- 52 kcal/d, p = 0.008). Participants in the CR and CREX groups had increased expression of genes encoding proteins involved in mitochondrial function such as PPARGC1A, TFAM, eNOS, SIRT1, and PARL (all, p < 0.05).

A team led by researchers at Albert Einstein College of Medicine of Yeshiva University has found a clear link between living to 100 and inheriting a hyperactive version of an enzyme that rebuilds telomeres -- the tip ends of chromosomes.

The findings appear in a recent issue of the Proceedings of the National Academy of Sciences.

Telomeres play crucial roles in aging, cancer and other biological processes. Their importance was recognized last month, when three scientists were awarded the 2009 Nobel Prize in Physiology and Medicine for determining the structure of telomeres and discovering how they protect chromosomes from degrading.

Telomeres are relatively short sections of specialized DNA that sit at the ends of all chromosomes. One of the Nobel Prize winners, Elizabeth Blackburn, Ph.D., of the University of California at San Francisco, has compared telomeres to the plastic tips at the ends of shoelaces that prevent the laces from unraveling.

Hidden from sight, our cells battle challenges such as their environment, bacteria, viruses, too much or too little oxygen, and physiological stressors. Molecular systems protect cells under assault, but those systems can break down, especially with age.

To better understand how cells are protected from stress and damage, a team led by Northwestern University researchers studied the effect of resveratrol, a beneficial chemical found in red wine, on human cells in tissue culture.

The findings may help explain what happens in neurodegenerative diseases, which are age-related, when cell protection fails, proteins misfold, lots of damage accumulates and the system falls apart.

The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, flies, and mice results in decreased lifespan. In this experiment, we examine the effect of eliminating each of the five individual sod genes present in Caenorhabditis elegans. In contrast to what is observed in other model organisms, none of the sod deletion mutants shows decreased lifespan compared to wild-type worms, despite a clear increase in sensitivity to paraquat- and juglone-induced oxidative stress. In fact, even mutants lacking combinations of two or three sod genes survive at least as long as wild-type worms.

Epigallocatechin gallate (EGCG), a main active ingredient of green tea, is believed to be beneficial in association with anticarcinogenesis, antiobesity, and blood pressure reduction. Here we report that EGCG extended Caenorhabditis elegans longevity under stress. Under heat stress (35 degrees C), EGCG improved the mean longevity by 13.1% at 0.1 microg/ml, 8.0% at 1.0 microg/ml, and 11.8% at 10.0 microg/ml. Under oxidative stress, EGCG could improve the mean longevity of C. elegans by 172.9% at 0.1 microg/ml, 177.7% at 1.0 microg/ml, and 88.5% at 10.0 microg/ml. However, EGCG could not extend the life span of C. elegans under normal culture conditions. Further studies demonstrated that the significant longevity-extending effects of EGCG on C.

For lean mice – and possibly for lean humans, the authors of a new study predict – the anti-aging strategy known as caloric restriction may be a pointless, frustrating and even dangerous exercise.

"Today there are a lot of very healthy people who look like skeletons because they bought into this," said Raj Sohal, professor at the University of Southern California's School of Pharmacy.

He and Michael Forster, of the University of North Texas Health Science Center, compared the life span and caloric intake of two genetically engineered strains of mice.

The "fat" strain, known as C57BL/6, roughly doubles in weight over its adult life. That strain benefited from caloric restriction, Sohal said.

The "lean" strain, DBA/2, does not become obese. Caloric restriction did not extend the life of these mice, confirming previous work by Forster and Sohal.