UNSW’s Labratory for Ageing Research. Left to right, Lindsay Wu, Myung-Jin Kang, Frank Stoddart, David Sinclair, Ashley Wong, Hassina Massudi. Credit: Britta Campion

Fighting the Aging Process at a Cellular Level

Original Article Here via Medical Xpress

It was about 400 BC when Hippocrates astutely observed that gluttony and early death seemed to go hand in hand. Too much food appeared to ‘extinguish’ life in much the same way as putting too much wood on a fire smothers its flames. If obesity led to disease and death, he thought, then perhaps restraint was the secret to a longer life?

It would be a couple of millennia before science confirmed, in 1935, a link between reducing and living longer. This discovery was just the beginning. In the , further advances have led to an extraordinary leap in ; a child born in Australia today can expect to live at least 25 years longer than a child born a century ago. Yet longer life has also unleashed a cocktail of diseases and , attacking us in tandem, to blight our final years.

Scientists are now increasingly focusing on the biology of ageing itself as the key to warding off this multitude of illnesses. “We currently study diseases in isolation, so we look, for example, at , cancer, diabetes, and Alzheimer’s separately,” said Dr Lindsay Wu, organiser of the recent inaugural Australian Biology of Ageing Conference, hosted by UNSW. “But they all have an underlying process of cellular ageing – so if we are able to treat the biological process of ageing, then we can have a huge impact on all sorts of diseases.”

Significant progress is being made on several frontiers. In New York, a human drug study is for the first time targeting ageing rather than a specific disease. US researchers have also recently managed to kill off age-damaged cells in mice to restore vitality, body function and extend life by up to 35%.

And at UNSW’s Laboratory for Ageing Research, and its sister lab at Harvard Medical School, scientists have identified and isolated a compound found in red wine that has prolonged life and improved health in animals as varied as worms, fruit flies and mice. Lead researcher, David Sinclair – who splits his time between his roles as head of the UNSW Lab and as Professor of Genetics at Harvard – has long been taking the compound himself.

Targeting ageing cells

Australian and international researchers are focusing on two key processes. One promising approach is to target naturally occurring ‘senescent’ cells, the label given to any type of cell as it acquires age-related damage or loss of function. Our immune systems should clear out these cells, but as we age this housekeeping function becomes less and less effective. This means senescent cells accumulate rather than divide, and in turn, they secrete inflammatory agents that can damage adjacent cells, causing the kind of chronic inflammation associated with age-related diseases.

Dr Darren Baker, of the US Mayo Clinic, who was in Australia for the Biology of Ageing conference, and colleagues, recently published their breakthrough results in Nature. Their study demonstrated the elimination of senescent cells in mice not only extended their lives but improved their general health, curiosity and energy levels, with no apparent ill effects.

“What we are thinking about is extending healthy life, not just extending life, per se … we don’t want to increase people’s time in care,” says Baker.

His Mayo Clinic group is now trying to develop components or compounds that can selectively kill senescent cells, without relying on the genetic manipulation used in the mouse study. “If you had asked me five years ago, I would have said we are decades away from human interventions, but we are now moving much faster than we anticipated.”

The loosening of DNA

A second prominent research area focuses on the anti-ageing molecules known as sirtuins, particularly the ‘SIRT1’ enzyme. “When we are young, our DNA is very tightly wound and it’s the SIRT1 molecules that keep this structure intact,” says Wu. “As we age, DNA structure naturally loosens and can turn on the wrong genes, causing dysfunction that can lead to diseases like cancer.” Researchers at UNSW are working on ways to energise the enzyme SIRT1, which Sinclair and his team have been working on for close to two decades, so it works more effectively.

“We think the loosening of DNA is driving whole-of-body ageing, so if we can boost the levels of fuel in our SIRT1 molecules to maintain our DNA in a youthful state, we can slow down ageing,” Wu says.

SIRT1 is also the key to Sinclair’s landmark discoveries about resveratrol, a naturally occurring compound found in red wine. In 2003, Sinclair first demonstrated that resveratrol made SIRT1 run faster and could extend the life of single organisms. In 2013, the prestigious Science journal published his work, proving this single anti-ageing enzyme could be effectively targeted, paving the way for the development of a new class of anti-ageing drug that could potentially prevent some 20 diseases ranging from cancer, to type 2 diabetes and Alzheimer’s disease.

The science of diet and exercise

It has also been uncovered that sirtuins (SIRT3 and 4) are behind the link between longevity and dietary restraint that has fascinated so many thinkers since Hippocrates. In the 1500s, the Venetian nobleman, Alvise Cornaro, famously refined Hippocrates’ theory and experimented on himself, limiting his daily intake of food to 12 oz (340 g) and 14 oz (397 g) of wine. He reportedly lived until 100, attributing his health, vigour and contentment to this regime.

Calorie restriction and exercise are now both known to activate sirtuins, explaining in part the protective nature of a good diet and regular physical activity. However, scientists have also greatly refined the link between diet and longevity. Professor David Le Couteur, from the University of Sydney, told the recent conference that a low-protein, high-carbohydrate diet is associated with a , with nutrients ideally balanced in a ratio of about 1:10. This ratio, he said, correlates with the traditional diet of the people of the Japanese island of Okinawa, famous for its high number of centenarians.

Sinclair is confident human life spans of 150 years are likely in the foreseeable future; other researchers suggest 100 will be more commonly attainable. Although Sinclair’s resveratrol is on the market as a supplement, it has not yet been formulated as an anti-ageing drug. However, the first human trials of a potential anti-ageing drug, metformin, are taking place in the US. Metformin is actually a common anti-diabetes drug that has been in use for some 60 years.

Research has consistently shown many diabetics taking metformin live longer than non-diabetics, even if they have additional risk factors, like being overweight. This association is so pronounced metformin is now being tested as an anti-ageing drug.

There are, however, simple steps everyone can take right now if they want to live longer, healthier lives, says Baker. “If you exercise a lot you have fewer senescent cells, and if you have a decent diet you also see fewer of these cells, so just by modifying your behaviour you can influence your rate of accumulation of these kinds of cells.”

“It is always better to look after yourself … than to just wait for an anti-ageing pill.”

Explore further: Anti-ageing drug breakthrough

More information: Darren J. Baker et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan,Nature (2016). DOI: 10.1038/nature16932


Mbah Gotho

Claim – Oldest Human In Recorded History – 145 Years Mbah Gotho

Original Article Here via Telegraph.co.uk

An Indonesian man who claims to be the longest living human in recorded history has described how he “just wants to die”.

Mbah Gotho, from Sragen in central Java, was born on December 31, 1870, according to the date of birth on his identity card.

Now officials at the local record office say they have finally been able to confirm that remarkable date as genuine.

Mbah Gotho's identity card, showing his date of birth as December 31, 1870

Mbah Gotho’s identity card, showing his date of birth as December 31, 1870. He is registered under his official name, Sodimejo; like many Indonesians he was only given one CREDIT: CEN

If independently confirmed, the findings would make Mr Gotho a staggering 145 years old – and the longest lived human in recorded history.

But despite his incredible longevity, Mr Gotho says he has little wish to remain on this earth much longer.

“What I want is to die. My grandchildren are all independent,” he told local media this week.

Mr Gotho has outlived all 10 of his siblings, four wives, and even his children. His nearest living relatives are grand children, great grand children, and great-great grandchildren.

One of Mr Gotho’s grandsons said his grandfather has been preparing for his death ever since he was 122.

He has even bought a burial site close to the graves of his children.

“The gravestone there was made in 1992. That was 24 years ago,” Mr Gotho’s grandson said.

Members of the family said Mr Gotho now spends most of his time sitting and listening to the radio because his eyesight is too poor to watch television.

He has had to be spoon-fed and bathed for the past three months as he has become increasingly frail.

When asked what his secret to longevity is, Mr Gotho replied: “The recipe is just patience.”

While record office staff say they have confirmed the birth date on his identity card, he will not make it into the record books until the findings are independently verified.

The current record holder, French woman Jeanne Calment, died in 1997 at the age of 122.

BioViva CEO Elizabeth Liz Parrish Younger

First Human To Increase Her Lifespan with Modern Science?

Elizabeth Parrish of Bioviva, may prove to be the first human being to benefit from anti-aging therapies. More Below.

Gene Therapy Makes BioViva CEO Elizabeth Parrish Younger, Blunter, and Resolute
We talked to the woman who claims to have reversed the aging process. She’s ready for a revolution.

Elizabeth Parrish, Chief Executive Officer and guinea pig for Bioviva, announced today that she has become the first human “successfully rejuvenated by gene therapy.” Using two proprietary processes, Parrish claims to have reversed two decades worth of telomere shortening, the process that leads to the breakdown of cell replications in the vast majority of living things. Telomere scores — measured using white blood cells — indicate that Parrish, who was 44 years old in September, has slowed a cellular process many scientists believe to be one of the root causes of aging.

That makes today a big day for Elizabeth Parrish. She’s publicly announcing a potential cure to the disease she feared would kill her: Time.

Parrish has become one of the leading lights of the biohacking movement by refusing to see aging as a fundamental fact of life. She described her highly experimental gene and cellular therapies as treatment targeted against an epidemic sometimes called the “silver tsunami.” She has made it very clear that, to her, “old” is a diagnosis. What she hasn’t always made clear — and seems to actively avoid addressing — are the moral, societal, and even medical ramifications of her work. Also the science.

Earlier this week, she spoke to Inverse about becoming her own patient zero, how human cells are like computers, and why she’s justified in evading the FDA.

“It will become so obvious why we haven't been able to ”cure“ the diseases of aging -- because we've been treating symptoms for so long,” Parrish told Inverse.

“It will become so obvious why we haven’t been able to “cure” the diseases of aging — because we’ve been treating symptoms for so long,” Parrish told Inverse.

What made you realize that aging was a disease and not a normal process?

I had actually gotten involved to cure childhood disease, so I wasn’t exactly entirely prepared to find out that biological aging was in fact a disease. I went to a very crucial conference that changed my mind: I ended up at the SENS (Strategies for Engineered Negligible Senescence) conference in Cambridge, U.K., and I became very interested in this idea that perhaps biological aging itself was a disease. I took the time to speak with many researchers after that and found out that some of the drivers of childhood disease were in fact accelerated aging.

That’s certainly a shift in the way we think about aging.

I basically had to change my thinking to realize that the body’s cells are very much like a computer, and the things that they’re programmed to do eventually land up with a lot of damage over time. Some people get that damage at a youthful age; that is, some people have programming issues — genetic problems — early on. Some people are born with them. But all of us are accumulating this damage that will eventually lead to the symptoms of the aging disease and kill us.

Framed that way, it seems like a much more daunting problem than dealing with the diseases we already know about.

The problem, I thought, would be much easier to solve: It was actually everyone’s problem. It wasn’t an orphan disease, it wasn’t a small subset of children. It’s actually everyone who has the disease. It’s inherent to our very selves. At that point I was really mobilized. In a sense, it was a bigger problem, but it seemed easier to solve.

How do you plan to study the disease of aging?

I thought that one of the most important things that we needed to do was to start collecting human data. It seemed to be what we were lacking; we were sitting on all sorts of mouse data for a slew of diseases that actually looked really good. I think we’ve cured cancer a hundred times in mice. We’ve reversed atherosclerotic plaques. We’ve reversed biological aging with telomerase inducers. We just weren’t using it in humans. So in order to get the safety data, I decided I would get behind them. I would prove that they were safe by taking them.

So you’re patient zero.

I am patient zero.

Last year, you went to Colombia to undergo the first round of your BioViva gene therapy treatment. That was a huge risk.

But living is very risky, and you’re guaranteed to die of these diseases. If we can start using these methods in end-stage patients — patients for compassionate care scenarios — and start getting good results, we can move them back into patients who are not in such critical shape, then we can move them back to preventative medicine, and then we really have something. We’ll have cost-saving measures, we’ll be actually saving lives before people get sick. Me, I’m feeling great, and we’ll be releasing some data on that sooner than later.

Why do you think there have been so many obstacles to human testing for anti-aging gene therapy?

The obstacles are in the regulatory framework. At this point, it’s not really starting a fight to say that the U.S. FDA and other countries have stifled innovation. That’s just obvious. It’s too much paperwork, it’s too far-reaching, the costs to get through the U.S. FDA are too high. And there’s no reason, at this point, that we have to mix safety and efficacy with a price tag of over $1 billion. Those two don’t need to go together. We need to find out how to efficiently get therapeutics through to the public that may be life saving.

That’s not going to happen until you convince the FDA that aging is actually a disease.

Here at home, we just cannot move quickly enough for patients. We’re losing over 100,000 people a day to biological aging. We’re not really treating this like the catastrophe that it is. Ebola came up and killed many people. It’s a big tragedy. But it didn’t kill anywhere near the number of people that die every month of biological aging.

As a matter of fact, if you start to look at that and extrapolate the numbers, millions of people are dying in a matter of months. We just think of this process as being very normal, but it’s actually a very costly process. It’s going to hinder our future significantly. The silver tsunami has already hit the industrialized countries and it’s about to hit the whole Earth.

How will you convince the FDA that investing in it now is a better idea than paying for it later?

On the Earth, by 2020, there will be more people over 65 than under 5 years of age. So the 5-year-olds become 5, then 25, then 35 — they become the workforce — while the 65-year-olds are retired and are in imminent danger of 20, 30, 40 years of needed accelerated healthcare. So it really doesn’t work. We’re actually at a point where it’s not just fashionable. It’s not a vanity issue. It’s “How do we save economies?” How do we keep people working longer? How do we save the trillions of dollars that we spend every four years on major diseases [which have led to] no cures? The government — your employer — you — everyone saves so much money by mitigating these diseases that there is no reason to hold this type of technology back.

If this actually happens; is everyone going to have equal access to these types of therapies?

Yeah, absolutely. It’s going to happen very similar to computers or cell phones. At first the technology is very expensive, because it’s new. First it’s kind of like building a supercomputer, and then eventually everyone gets an iPhone. In your life when you look at that, you don’t ever remember living without an iPhone. Certainly you like an iPhone better than you would have liked it if you had to pay for the first supercomputer because your iPhone is much more predictable than the supercomputer was. But it’s that model, and we will get there as quickly as we can to drive down the costs so that everyone does have access to it.

Are we going to have to shift the retirement age? What’s the limit here?

I don’t really get into those kinds of questions. My job is to mitigate the diseases we can mitigate. To create the mandate on the Earth that the minute we do that, we have to move forward. If we think we have something, it would be immoral not to move forward with it. How long people can live, I don’t know, but I want them to live as well and as healthy as they can live for as long as possible. That’s good for society, that’s good for the economy, that’s good for you and me, and it’s good for the future of our planet.

Won’t you run into a problem finding people willing to take part in your studies, if they’re so experimental?

We have no end of volunteers, both healthy and sick. As a reminder, as far as the FDA’s concerned, in the past 50 years they have passed, through their gold standard, 50 drugs that have been pulled from the market. Some of those drugs were actually harmful, if not fatal, to patients. We cannot pretend that their standard has kept anyone safe. It was there initially to keep people safe. It’s not actually doing a good job of that. It definitely serves a purpose, where we want drugs with safety and efficacy, we want to keep the public safe, but not to the point where they’re dying, waiting for treatment.

If you’re letting people die without access to experimental treatments, then your safety and efficacy administration is failing.

This interview has been edited for brevity and clarity.

Photos via Bioviva-Sciences.com, Getty Images

Greenland Shark

Oldest Vertebrate Lifespan? The Greenland Shark at 400 years.

Original Article Here

A new record has been set for the oldest vertebrate, and it’s not a giant tortoise orBowhead whale. Instead, the record-holder appears to be the Greenland shark, which new evidence suggests lives can live for 400 years, with average adults exceeding two centuries.

Greenland sharks live in the North Atlantic at both the surface and to depths of around 2 kilometers (at least 1.3 miles). They are poorly studied, although their status as among the slowest of sharks has been known for a while. A slow-moving lifestyle usually goes with a long lifespan, but no one knew just how long this meant for Somniosus microcephalus until Julius Nielsen of the University of Copenhagen collected the eye lenses of 28 female sharks caught as bycatch during scientific surveys of Greenland.

The ages of fish are usually calculated from calcified tissues, but Greenland sharks don’t have any that could be tested. The center of the eye is formed during embryonic development, and being made of inert crystalline proteins, does not experience a change of atoms through an individual’s lifespan. Consequently, radiocarbon dating of these proteins has been used to estimate the age of animals where this is hard to measure through other means.Females were chosen because they outgrow males, reaching typical sizes of 4 to 5 meters (13 to 17 feet).

A Greenland shark caught as by-catch by the research vessel Palmut. Julius Nielsen

In Science, Nielsen has revealed the average lifespan of the sharks was 272 years, and that they did not reach sexual maturity until 156 ± 22 years.

The oldest individual was estimated to be 392 years old, give or take 120 years. However, as this individual was 5 meters (17 feet) long, which is average for an adult female, some sharks almost certainly exceed four centuries.

Despite living on the other side of the world from most test sites, the younger sharks showed evidence of radioactive isotopes released during nuclear testing in the 1950s and ’60s. However, the eyes of sharks longer than 2.2 meters (7.3 feet) showed no such signs. The isotopic ratios at the center of the eye are consistent with the diet of an adult shark, rather than a young one that would feed on smaller prey. Together, these findings confirmed the theory that the proteins contain atoms laid down before the shark was born, and that the age estimates are reliable.

Although the Greenland shark is widespread across the North Atlantic, and only classified as “near threatened”, long-lived animals usually have low birthrates and struggle to recover from population shocks, suggesting the sharks may be vulnerable.

The findings make the Greenland shark easily the current record-holder for the oldest vertebrate, almost doubling the previous record of 211 years for a Bowhead whale. Invertebrates such as a clam named Mingand deep sea corals, still have the advantage, however, living for more than 500 years.

Not bad for a species whose Latin name means tiny brain.

A Greenland Shark in Disko Bay, Greenland. Julius Nielson


XX protection against age-related mutations

Original Article Here Via ScienceDaily

Rendering of hromosomes. A protective effect of the second X chromosome has been identified in fruit flies. Credit: © Giovanni Cancemi / Fotolia

Rendering of hromosomes. A protective effect of the second X chromosome has been identified in fruit flies.
Credit: © Giovanni Cancemi / Fotolia

Researchers at the University of Valencia’s Cavanilles Institute of Biodiversity and Evolutionary Biology have put the ‘unguarded X hypothesis’ to the test and confirmed that differences in lifespan between the sexes, a widespread phenomenon in nature, may indeed be due to the protective effect of having two copies of the X chromosome.

In this study, carried out in collaboration with the University of Oxford, researchers analysed the lifespans of male and female fruit flies (Drosophila melanogaster), having subjected both to different levels of inbreeding. The work, published in the journal ‘Biology Letters’, brings some much-needed empirical evidence in support of the ‘unguarded X hypothesis’, proposed 30 years ago to explain why, for instance, XY males ages faster than XX females. Specifically, the study targets one of its fundamental predictions: that inbreeding shortens lifespan more in females than in males.

Pau Carazo, director of the research team at the UV, explains: “the differences in lifespan between the sexes can be partly explained by the fact that the accumulation of mutations over the course of a lifetime, or passed on from generation to generation, has a larger affect on the sex that has just one ‘unguarded’ copy of the X chromosome; generally males, including in human beings.”

He adds, “if the guard effect is important, we can expect inbreeding to affect the lifespan of the homogametic sex (individuals with two of the same sex-determining chromosomes) to a greater extent than the heterogametic sex (with two different sex-determining chromosomes). This is because, in the latter group, the X chromosome is always ‘unguarded’, with or without inbreeding, while in the former group the X chromosome is only ‘guarded’ if the two X chromosomes are different, which is not the case after repeated inbreeding.”

The findings were consistent with this prediction.

The explanation for this ‘guard’ effect lies in the fact that most genetic mutations are by nature recessive. For XX individuals, this means they are only harmful when the same mutation occurs in both copies of the X chromosome, otherwise they are simply not expressed. However, in the case of XY individuals, with no ‘guard’, any recessive mutation present in either the X or the Y chromosome would be expressed unconditionally. So by making the two X chromosomes in female fruit flies the same through inbreeding, the researchers essentially cancelled out the protective effect of the second X chromosome, meaning that recessive mutations were expressed at the same rate among males as among females.

Story Source:

The above post is reprinted from materials provided by Asociación RUVID.Note: Materials may be edited for content and length.

Journal Reference:

  1. Pau Carazo, Jared Green, Irem Sepil, Tommaso Pizzari, Stuart Wigby.Inbreeding removes sex differences in lifespan in a population ofDrosophila melanogaster. Biology Letters, 2016; 12 (6): 20160337 DOI: 10.1098/rsbl.2016.0337
Basis by Elysium

This could be the beginning of More Years and Less Tears – Basis by Elysium Health

Time will prove the validity of this supplement, but time is ticking. I submit to you the first major commercial anti-aging supplement to be introduced by anti-aging research scientist since the inception of this blog.

Link to the product here.


Science has enabled us to focus on the cellular level to achieve optimal health, beyond what can be accomplished with diet and exercise. Basis is designed to optimize NAD+ levels and sirtuin function in our cells to support our most critical metabolic processes like cellular detoxification, DNA repair and energy production.


Basis exemplifies Elysium’s focus on providing direct access
to scientific breakthroughs in health.

The encapsulation of 35 years of research in a bottle.

For decades, scientists have been searching for answers to what internal mechanisms lead to ongoing health as well as health decline. This led to the discovery of a critical coenzyme called NAD+, which controls cellular communication, and sirtuin proteins, which play a key role in our long-term health. Sirtuin proteins require NAD+ to function, and our NAD+ levels naturally decline over time, leading to a decline in cellular health. With a focus on NAD+ and sirtuins, we can help to sustain their function over time and support the health of the building blocks of our body — our cells. This is the purpose of Basis.


Basis contains two novel compounds that support
the production of NAD+ and the activation of sirtuins.

“NAD is one of the most compelling bits of chemistry related to aging. Its presence in the body is directly correlated with the passage of time.”


  • Nicotinamide RibosideNR
  • PterostilbenePT

Nicotinamide Riboside Pterostilbene

The most direct precursor to NAD+. It is the most readily usable and effective building block for creating more NAD+ inside the cell. NAD+ plays a crucial role in regulating core metabolic functions including cell function, DNA repair and energy production. NAD+ supplies decline naturally with age, thus reducing a cell’s ability to function optimally and potentially impacting baseline health.


Learn more about Basis, designed for long-term use
in adults from our 20s onward.

Instructions Take two capsules every morning with or without food. Each jar contains a 30-day supply.
Lead Scientist Dr. Lenny Guarente, Elysium Co-Founder, Leads Science of Aging Lab at MIT.
Purity Assessment Basis undergoes rigorous third party testing to confirm its content accurately reflects the ingredients listed on our label. Two capsules of Basis in our current lot contain 109% of promised quantity of NR, 112% of promised quantity of Pterostilbene.
Analysis Through our established laboratory model, Basis meets standard measures of safety and tolerability.
Both primary ingredients in Basis are GRAS (generally recognized as safe) under intended conditions of use by qualified experts.
Feedback Subtle changes in overall feeling of well-being, sleep quality, energy consistency, cognitive function, and skin health are often reported within 4-16 weeks of starting. Note that cellular health may not always manifest results at the surface.
Dietary Basis is vegetarian, vegan, gluten-free, nut-free, and contains no artificial colors or flavors.
See ingredient information here.
Production Basis is created in the United States in adherence with the FDA’s Good Manufacturing Practices.


Review the scientific research that led to Basis
and how it can impact our cellular health.

  • Cellular DetoxificationCD
  • DNA RepairDR
  • Circadian Rhythm & SleepCRS
  • Protein FoldingPF
  • Mitochondrial Health & EnergyMHE
  • CognitionC
  • All Research Papers


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One’s ability to identify different smells may impact longevity

Original Article Here Via EurekaAlert!

In a recent study of older adults, those with a reduced ability to identify certain odors had an increased risk of dying during an average follow-up of 4 years. The mortality rate was 45% in participants with the lowest scores on a 40-item smell test, compared with 18% of participants with the highest scores.

The study included 1169 Medicare beneficiaries who scratched and sniffed individuals odorant strips and chose the best answer from 4 items listed as multiple-choice.

“The increased risk of death increased progressively with worse performance in the smell identification test and was highest in those with the worst smelling ability, even after adjusting for medical burden and dementia,” said Dr. Davangere Devanand, lead author of the Annals of Neurology study. “This was a study of older adults–the question that remains is whether young to middle-aged adults with impaired smell identification ability are at high risk as they grow older.”


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

under construction

Change to Site – Forums Gone – Papers Added

The forum section of the site has not yet taken off the way I had hoped. Also, when I switched hosts, I lost some of the more aesthetically pleasing attributes on the forum. I have also come to realize the site could benefit from a collection of published anti-aging papers. I have decided to replace the forum with this repository. I will return to the forum in the future.