Healthy Life Extension

Funding Aging Research

Study Shows Supplements Slow Aging

posted on January 24th, 2012

Dear Future Centenarian,

Recently, we™ve seen an increasing number of popular media articles citing studies discrediting nutritional supplements. This is contrary to the many tens of thousands of studies supporting beneficial effects of vitamins, minerals and herbs.

Why is that? Are we suddenly uncovering new data in new studies? Or might this be part of the FDA™s œwar on unregulated products and big pharma™s not so hidden agenda of wanting to control the supplement industry?
When flaws are pointed out in the study protocols, do we see them in the media? No. Even if rebuttals were published, they are usually buried somewhere deep in the publications™ body.

When articles are published in newspapers such as the NY Times, the general public tends to take the info as gospel, even though popular media is well-known for slanted and often inaccurate stories. Sensationalism and fear mongering sell newspapers.

It™s refreshing to see positive articles for a change.

CBC News examines how close we are to finding cures for aging, obesity, diabetes, the common cold and cancer in a series of special reports called CHASING CURES.


It might be possible to cure aging, say scientists who’ve found that lab mice get smarter and more agile as they age when fed a mix of nutritional supplements.

The diet and supplement plan isn’t a conventional “cure.” But the animal results at McMaster University in Hamilton, Ont., illustrate how investigators aim to slow down the aging process to avoid the physical and mental declines that often come as more candles are added to the birthday cake.

At Prof. David Rollo’s biology laboratory, mice that ate bagel bits soaked in a cocktail of supplements such as B vitamins, vitamin D, ginseng and garlic lived longer than those not taking the special mice chow.

“If you put them on a supplement, they actually learn better as they age,” Rollo said. “They still don’t live much longer but their brain function is remarkable.”

The mice also acted like restless teenagers showing “spontaneous motor function” that fades in humans in a universal sign of aging, Rollo added.

The supplemented mice maintained their memory function in tests, such as remembering a familiar object. Their learning abilities were like those of very young mice, he said. Mice of the same age that were not supplemented behaved in lab tests like a frail 80-year-old woman.

Investigators turned to the cocktail of ingredients based on their suspected ability to offset five key mechanisms involved in aging.

The researchers have also doubled the lifespan of crickets using a combination of dietary restriction and supplements, and other investigators have found similar results in other animal models.

Most of the supplements Rollo and his team use are sold at health food stores. But he cautioned they are not something to be toyed with because the cocktail hasn’t been tested to see if it is safe for people. The supplements cross the blood-brain barrier to affect the mitochondria “furnaces” in the brain in a fundamental way, he noted.

Scientists still don’t how the supplements actually work and interact in the body.

Live to 1,000?


Like Rollo, British gerontologist Aubrey de Grey of Cambridge is optimistic about the potential to extend human life span, but he takes a different approach. He’s not trying to eliminate aging but to extend how long people can be fit and healthy.

For a full text of this article, including the formula they used in the study, see

Long Life,
David Kekich


A bold set of claims from this group working on the genetics of natural variation in longevity for humans: “Like most complex phenotypes, exceptional longevity is thought to reflect a combined influence of environmental (e.g., lifestyle choices, where we live) and genetic factors. To explore the genetic contribution, we undertook a genome-wide association study of exceptional longevity in 801 centenarians (median age at death 104 years) and 914 genetically matched healthy controls. Using these data, we built a genetic model that includes 281 single nucleotide polymorphisms (SNPs)

Consistent with the hypothesis that the genetic contribution is largest with the oldest ages, the sensitivity of the model increased in the independent cohort with older and older ages. Further [analysis] suggests that 90% of centenarians can be grouped into clusters characterized by different ‘genetic signatures’ of varying predictive values for exceptional longevity. The different signatures may help dissect this complex phenotype into sub-phenotypes of exceptional longevity.” The researchers are claiming some moderately common sets of SNPs found in centenarians (but not so common in the general population) can predict exceptional longevity with odds of 70% or higher, with the much more predictive combinations of SNPs – some at 95% odds of exceptional longevity – being correspondingly very rare. The caveat here is that this is heavily statistical work, and we’ve already seen one paper from this group withdrawn last year for issues with the statistics.

A brief overview of one of the lines of work advocated by the Science for Life Extension Foundation: “Aging biomarkers are parameters that always, and in all people, change during aging. It is possible to evaluate and improve therapies that are aimed at slowing down aging, using the biomarkers of aging. The value and changing dynamics of aging markers provides information about the intensity of aging processes in the cells of the patient. Aging biomarker monitoring allows us not only to diagnose various diseases, but also to prevent their development. Aging can be slowed down. At the moment, there are already several scientific approaches that could lead to slowing down aging, and extending life. Scientists have been able to significantly extend the lifespans of model animals.

Now, it is time to apply the biogerontology knowledge in clinical practice. To understand if a given therapy is effective or not, first of all we compile data via conventional clinical tests to create the ‘electronic health passport.’ After that, we can perform measurements of the aging biomarkers listed in the table. The indicators will inform us if the therapy is working. Soon we will be able to look at thousands of parameters, obtained using genome and transcriptome sequencing, epigenome mapping and analysis of proteome and metabolome. The additional data will make the anti-aging therapies more precise. View our entire booklet that lists twenty (20) aging bio-markers.”

TELOMERES AND OSTEOARTHRITIS Wednesday, January 18, 2012
Another telomere length correlation, adding data to a relationship known for some years: “A process linked to natural cell aging has now also been associated with knee osteoarthritis, researchers say. Telomeres – lengths of DNA on the ends of chromosomes, sometimes described as being like the plastic cap on a shoelace tip – naturally shorten with age, but can also shorten due to sudden cell damage. Abnormally short telomeres have been found in some types of cancer and preliminary research has suggested that the average telomere length is also shortened in osteoarthritis. In this new study, Danish researchers used new technology to closely examine the telomeres of cells taken from the knees of osteoarthritis patients who had joint replacement surgery.

The cells had abnormally shorted telomeres and the percentage of cells with ultra-short telomeres increased with proximity to the damaged area in the knee joint. The telomere story shows us that there are, in theory, two processes going on in osteoarthritis. Age-related shortening of telomeres, which leads to the inability of cells to continue dividing and so to cell senescence [deterioration], and ultra-short telomeres, probably caused by compression stress during use, which lead to senescence and failure of the joint to repair itself. We believe the second situation to be the most important in osteoarthritis. The damaged cartilage could add to the mechanical stress within the joint and so cause a feedback cycle driving the progression of the disease.”

A possibly interesting position is put forth in this blog post, an attempt to merge a package of right to end of life decisions and acceptance of death with the urge to extend healthy life through biotechnology – an argument that the present cultural debate that places these two things in opposition is misguided: “People who try to fend off death are being selfish, are in denial, and are pouring money down the drain for cockamamy schemes to preserve their frozen heads for some fingers-crossed future, which will never arrive. At the same time, we shouldn’t let people die, particularly (and ironically) if they really want to. Choosing death is untenable. It’s against nature.

No, death is good only when death decides it’s ready for you. Or so go the arguments of many who oppose anti-aging technology. But just because we accept death as good and necessary, that doesn’t necessarily mean we have to say the same about aging. Can we argue for anti-aging technology, for 2,000-year lifespans of perpetual youth, and admit death can be good at the same time? Not only can we; we must. We can accept death yet also seek to live vastly longer, healthier, and happier. Death is good, but so too is a long, long, long life. We can attain long lives of quality by rejecting extreme ‘life-saving measures,’ embracing euthanasia, and accepting that there are just some things we cannot cure. Death has got to be our closest kept enemy if we want to be ageless. Baffling as it may seem, wanting to live to be a thousand years old is inextricably connected to the ability to decide when it’s time to give up the ghost.” I can’t say as I agree with the rush to incorporate acceptance of death, but I’m certainly very much on the side of the right to choose when and how you die. One of the many great and horrible cruelties in our present culture is the sadistic enforcement of prohibition against the choice of euthanasia – not least because it is the source of most of the challenges and costs that attend the organization of a successful cryopreservation.

The pace has picked up for discovery of longevity-correlated genetic and epigenetic variations in humans; there are too many for each and every new publication to be noted individually here – and we should expect there to be, ultimately, a very great many minor correlations between genes and natural variations in longevity. Here is an example: “The Leiden Longevity Study consists of families that express extended survival across generations, decreased morbidity in middle-age, and beneficial metabolic profiles. To identify which pathways drive this complex phenotype of familial longevity and healthy aging, we performed a genome-wide gene expression study within this cohort to screen for mRNAs whose expression changes with age and associates with longevity.

The expression of 360 probes was found to change differentially with age in members of the long-lived families [and] we confirmed a nonagenarian specific expression profile for 21 genes out of 25 tested. Since only some of the offspring will have inherited the beneficial longevity profile from their long-lived parents, the contrast between offspring and controls is expected to be weak. Despite this dilution of the longevity effects, reduced expression levels of two genes, ASF1A and IL7R, involved in maintenance of chromatin structure and the immune system, associated with familial longevity already in middle-age. The size of this association increased when controls were compared to a subfraction of the offspring that had the highest probability to age healthily and become long-lived according to beneficial metabolic parameters.”

Limited forms of Lamarkian inheritance, such as in the operation of metabolism, seem to be a reality, passed down through generations by epigenetic modifications. Here is a popular science article on the topic: researchers “described a series of experiments that caused nematodes raised under the same environmental conditions to experience dramatically different lifespans. Some individuals were exceptionally long-lived, and their descendants, through three generations, also enjoyed long lives. Clearly, the longevity advantage was inherited. And yet, the worms, both short- and long-lived, were genetically identical.

This type of finding – an inherited difference that cannot be explained by variations in genes themselves – has become increasingly common, in part because scientists now know that genes are not the only authors of inheritance. There are ghostwriters, too. At first glance, these scribes seem quite ordinary – methyl, acetyl, and phosphoryl groups, clinging to proteins associated with DNA, or sometimes even to DNA itself. There is increasing evidence that epigenetic modifications are transgenerational (inherited through multiple generations) in a variety of species. Examples include coat color in mammals, eye color in Drosophila, symmetry in flowers, and now longevity in C. elegans. There seems to be a renewed acceptance for the Lamarckian concept (in limited cases). This could change our understanding of inheritance in that it would add another component, probably minor, but present, in addition to Mendelian genetics.”

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