This website will never die. However, the frequency with which I update it will always be tied to the public’s interest and my current available time. It will always have a future.
No longer considered an inevitability, growing older should be and is being treated like a chronic condition.
November 1, 2016|
In a biological sense, the mere passage of time is pathological.
To complicate matters, the human body comprises a number of different systems that each develop at its own pace. The nervous system seems to reach full maturity in our 20s, for instance, while the skeletal system may peak a decade later. Of course, this physiologic natural history is subject to environmental influence. For example, a diet rich in calcium and vitamin D, along with weight training, can increase bone density and strength. Nevertheless, these environmental factors ultimately act on a foundation that, beyond a certain age, is inexorably deteriorating. There is a finite limit beyond which environmental factors cannot save us.
The changes of aging vary in their specifics from one system to another, but common mechanisms are at work. For instance, wear-and-tear of joints results from depletion of articular cartilage, just as the thinning of skin is due to a loss of elastic connective tissue. Other age-related changes arise from errors in cellular activity or the accumulation of metabolic by-products, the probabilities of which rise over time.
As these natural changes proceed, they lead to readily recognizable disease. The accumulation of fat in blood vessel walls provides a particularly good demonstration of this. Lipids are an essential part of our diet, but as processed lipids continue to accumulate in vessel walls, these vessels harden and narrow, eventually failing to supply the heart with enough blood. If the narrowing blocks vessels entirely, the heart is starved of blood, causing heart muscle death, or heart attack.
This simplified example illustrates that perfectly normal processes that are critical to survival will quite naturally lead to disease. In a biological sense, the mere passage of time is pathological. Importantly, most of the early changes in this progression, such as high cholesterol, are symptomless. Yet they are precursors to life-threatening illness and are therefore considered pathologic entities in their own right, to be prevented and treated. The same can be argued of the more subtle and gradual damages of aging.
There are countless other conditions subject to this dynamic. They include some of the most common and debilitating ailments, such as osteoporosis, arthritis, stroke, diabetes, dementia, and even many forms of cancer. Given enough time, myriad diseases will afflict us as a direct result of the natural aging process.
We can and should view these diseases, whose prevention and treatment are standard medical practice, as the clinical manifestations of natural age-related changes. Doctors have long targeted such changes to prevent disease. For instance, by recommending their patients limit the fat and carbohydrate content of their diets or take statin medications, doctors have strived to stave off heart disease. In so doing they unknowingly have been battling aging itself.
Yet there are those who find this view of aging contentious, a reaction that likely stems from the misperception that the terms “natural” and “pathologic” are conflicting. There’s a common yet unwarranted sense that these two terms are mutually exclusive; that what is natural can only be right, and what is pathologic cannot be natural. This is untrue. Because “natural” typically describes what conforms to the usual course of events, and “pathologic” describes what is harmful, the question posed in the opening paragraph presents a false dichotomy. Both “natural” and “pathologic” describe aging fairly.
Thus, the controversy is largely semantic. If I were to replace the call for a “fight against aging” with an invitation to “combat age-related changes,” I would expect a far more positive response. A call to “prevent the early stages of disease” would surely receive virtually unanimous support. I contend that the three phrasings are synonymous.
Mutaz Musa is a physician in the Department of Emergency Medicine at Albert Einstein College of Medicine/Montefiore Medical Center, a health-care consultant, and an entrepreneur in New York City.
Original Article Here Via Medical Xpress
(Medical Xpress)—A large team of researchers with members from several Europeans countries and the U.S. has found that mice fed a compound called spermidine lived longer than ordinary mice and also had better cardiovascular heath. In their paper published in the journal Nature Medicine, the researchers describe experiments they carried out with the compound and mice, what they found and why they believe the compound might provide benefits for humans.
Prior research has found that ingestion of spermidine—which was first discovered in semen samples, hence its name—led to longer lifespans in simple organisms such as fruit flies, yeast and roundworms. In this new study, the researchers sought to find out if the same would prove true for more complex creatures.
The researchers chose mice as their target, feeding some groups water with spermidine mixed in, while other groups received plain water. After observing the rodents over the course of their lifespans, the researchers discovered that those who had been given spermidine lived longer than those who had not—even if the supplement was not given to them until middle age. Closer examination of the rodents revealed that those given the supplement also had better heart function and lower blood pressure. They also found that rats fed a high-salt diet, which causes high blood pressure, had lower pressure readings when given spermidine.
Prior research had also suggested that the means by which spermidine extended lifespan was by inducing autophagy in heart cells, which is where cells naturally disable parts of themselves that are dysfunctional or no longer necessary. To find out if this might be the case for rodents, the researchers conducted the same experiments usingmice that had a genetic defect that prevented autophagy from taking place and found that feeding them spermidine did not cause them to live longer or to have improved cardiovascular health, suggesting that autophagy may, indeed, be involved in the process.
The researchers acknowledge that there is thus far little evidence that suggests humans might receive the same benefits from consuming the compound, but note that they did conduct a survey of approximately 800 people regarding their diets and found that those that reported eating foods that contained a fair amount of the compound (mushrooms, whole grains, aged cheese, etc.) had fewer cardiovascular disease symptoms including lower blood pressure. They suggest a much larger study should be undertaken before any real conclusions can be made.
Explore further: Healthy ageing—longer healthspan with spermidine
More information: Tobias Eisenberg et al. Cardioprotection and lifespan extension by the natural polyamine spermidine, Nature Medicine (2016). DOI: 10.1038/nm.4222
Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation. Spermidine feeding failed to provide cardioprotection in mice that lack the autophagy-related protein Atg5 in cardiomyocytes. In Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congestive heart failure, spermidine feeding reduced systemic blood pressure, increased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart failure. In humans, high levels of dietary spermidine, as assessed from food questionnaires, correlated with reduced blood pressure and a lower incidence of cardiovascular disease. Our results suggest a new and feasible strategy for protection against cardiovascular disease.
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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 calorie intake and living longer. This discovery was just the beginning. In the 21st century, further advances have led to an extraordinary leap in life expectancy; 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 chronic conditions, 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 cardiovascular disease, cancer, diabetes, heart disease 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 longer life, 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
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.
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.
Elizabeth Parrish of Bioviva, may prove to be the first human being to benefit from anti-aging therapies. More Below.
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.
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
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
Original Article Here Via ScienceDaily
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.
- 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
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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.
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“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
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.
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|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.|
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“A new generation of commercial entities is beginning to explore opportunities for new types of interventions and services in a graying world.”
“Their new supplement – with the backing of some of the world’s foremost authorities on aging – could change how you get older”
“[Between] high-end prescription drugs and nutraceuticals…there’s this vast space in between that could be filled in a way that’s useful for health maintenance.”
“Leonard Guarente, one of the best-known anti-aging researchers in the region, and the roster of eminent scientists have formed Elysium Health.”