Every few years research on the effects of deuterium on life span in lower animals surfaces, by way of exposing them to heavy water, D2O rather than H2O. The presence of deuterium rather than hydrogen results in an uptake of deuterium atoms into biological molecules, subtly and slightly changing their behavior. Too much of that and you fall over dead - the mechanisms of life do not have a high tolerance for such tinkering, and heavy water is effectively toxic. At lower levels, however, species such as flies and nematodes live longer as a result of exposure to deuterium. A few articles and papers were published back in 2007-2009, which together give a fair grounding as to where the science stands:

• Eat Isotopes to Live Longer
• Deuterium Again
• SENS4, Session 1, Combating Oxidation

Dr Shchepinov's theory is based on deuterium, a naturally-occurring isotope, or form of hydrogen, that strengthens the bonds in between and around the body's cells, making them less vulnerable to attack. He found that water enriched with deuterium, which is twice as heavy as normal hydrogen, extends the lifespan of worms by 10 per cent. And fruitflies fed the 'water of life' lived up to 30 per cent longer.

There is some skepticism and debate amongst various parties regarding the mechanisms by which deuterium uptake extends life span, but it's clear that exposure to heavy water at lower levels does in fact extend life in flies, worms, and so forth. Not too many people are working on this, so there is a lot of room for speculation and a lack of hard evidence that can rule out possibilities such as increased resistance to oxidative damage in important proteins. Given the evidence backing the membrane pacemaker theory of longevity, this is an attractive idea - there is plenty of support for the hypothesis that differences in the proteins that make up cell membranes are responsible for large differences in life span between various otherwise similar species. But robust evidence for the much smaller difference of a little extra deuterium substituted for hydrogen atoms - as opposed to completely different proteins - is lacking.

On this topic, I see that a new paper has arrived in the prepublication queue at Rejuvenation Research. It adds more data to the current thin stack on deuterium and fly life span:

Brief Early-Life Non-specific Incoporation of Deuterium Extends Mean Lifespan in Drosophila melanogaster Without Affecting Fecundity

We have investigated the effects of brief, non-specific deuteration of Drosophila melanogaster by including varying percentages of 2H (D) in the H2O used in the food mix consumed during initial development. Up to 22.5% D2O in H2O was administered, with the result that a low percentage of D2O in the water increased mean lifespan, while the highest percentage used (22.5%) reduced lifespan. After the one-time treatment period, adult flies were maintained ad libitum with food of normal isotopic distribution.

At low deuterium levels, where lifespan extension was observed, there was no observed change in fecundity. Dead flies were assayed for deuterium incorporation ... Isoleucine and leucine residues showed a small, linear dose-dependent incorporation of deuterium at non-exchangeable sites. Although high levels of D2O itself are toxic for other reasons, higher levels of deuterium incorporation, which can be achieved without toxicity by strategies that avoid direct use of D2O, are clearly worth exploring.

Hormesis is a possible (and disappointingly ordinary) explanation for this sort of result. Given the range of ways to make flies, worms, and rodents live longer by exposing them to adversity in early life, this almost seems like the first place to be looking. Perhaps lesser degrees of heavy water exposure, entirely separately from any deuterium uptake into proteins, have a hormetic effect, causing enough damage and disarray to spur repair mechanisms into greater efforts and leading to a net gain in life expectancy.

Well, either way, we shall hear more in future years. As the researchers point out above, you can conduct similar studies without the need for heavy water, and those should produce a more useful set of data.

Source:
http://www.fightaging.org/archives/2013/01/deuterium-and-lifespan-in-flies.php

Exercise correlates with all sorts of better measures of health, but there is some debate and conflicting evidence on whether more is better past the point of moderate regular exercise. This ties in to questions of causation - to what degree are endurance athletes drawn to their activities because they are already more robust than their peers, for example?

Telomeres are the molecular caps on chromosomes. They shorten with each successive cell division and are thus linked to aging. The shortening rate also varies among people. Shorter telomeres have been linked to increased disease risk as well as shortening of lifespan.

Chronic endurance training is at least modestly linked with long lifespan, though there are some controversies about whether it may increase the risk of some heart diseases. In the current study researchers sought to determine if chronic endurance training is associated with telomere length in older aged individuals. To perform the trial they measured the length of telomeres in four groups of individuals: young people and older people who did or did non engage in chronic endurance training. For the endurance training the researchers chose participation in a 58 km cross country ski competition.

They found that indeed the older people who were chronic endurance trainers had significantly longer telomeres than moderately active older controls. There was no difference in telomere length in the younger subjects whether they did endurance training or not. There was also an association in older people between VO2 max and telomere length.

Link: http://extremelongevity.net/2013/01/10/chronic-endurance-training-linked-to-longer-telomeres-in-older-adults/

Source:
http://www.fightaging.org/archives/2013/01/endurance-training-associated-with-longer-telomeres.php

Over at In Search of Enlightenment you'll find an unpublished interview where the questions somewhat illustrate the point that most people don't look much beyond trivial matters when it comes to aging and longevity. Biotechnology like SENS and similar research projects are given no thought at all in most quarters, and even amongst advocates many favor the snail's pace path of trying to slow aging rather than working to repair its root causes to reverse it. This all means that there is much yet to accomplish in advocacy and education.

The field of research known as biogerontology, which studies the biology of aging, is a truly fascinating, though often misunderstood, area of scientific research. In 2011 the genome of the naked-mole rat was sequenced. This rodent is only the size of a mouse, and one might wonder what the significance of sequencing its genome could possibly be. But the naked-mole rate is the longest living rodent, it has a maximum lifespan exceeding 30 years and an exceptional resistance to cancer. Understanding the biology of this species could help unlock the mystery of healthy aging. A variety of experiments on fruit flies, mice and other species have demonstrated that the rate of aging can be manipulated, either by calorie restriction or by activating particular genes. Such research could eventually lead to the development of a drug that safely mimics the effects of caloric restriction (which delays the onset of disease) or actives the "longevity genes" that help protect against the diseases of late life.

The lion's share of funding for medical research is spent on disease research, such as research on cancer, heart disease or Alzheimer's disease. This approach, which I call "negative biology", assumes that the most important question to answer is "what causes disease?". Unfortunately this is a severely limited approach, especially for older populations. Even if you cured all 200+ forms of cancer (and we have not yet eliminated even just one cancer despite investing enormous sums of money for decades now), one of the other diseases of aging would quickly replace cancer as the leading cause of death because most people in late life are vulnerable to multiple diseases. So "positive biology" takes a different intellectual starting point. It assumes that the puzzles of exemplar health are just as important to understand as the development of disease. How can some (very rare) humans live over a century of disease-free life? Understanding these exemplar examples of health might prove to be more significant than trying to understand, treat and cure every specific disease of late life.

Link: http://colinfarrelly.blogspot.com/2012/12/readers-digest-interview-on-aging-and.html

Source:
http://www.fightaging.org/archives/2013/01/unpublished-readers-digest-interview-on-aging-and-longevity.php

Over at In Search of Enlightenment you'll find an unpublished interview where the questions somewhat illustrate the point that most people don't look much beyond trivial matters when it comes to aging and longevity. Biotechnology like SENS and similar research projects are given no thought at all in most quarters, and even amongst advocates many favor the snail's pace path of trying to slow aging rather than working to repair its root causes to reverse it. This all means that there is much yet to accomplish in advocacy and education.

The field of research known as biogerontology, which studies the biology of aging, is a truly fascinating, though often misunderstood, area of scientific research. In 2011 the genome of the naked-mole rat was sequenced. This rodent is only the size of a mouse, and one might wonder what the significance of sequencing its genome could possibly be. But the naked-mole rate is the longest living rodent, it has a maximum lifespan exceeding 30 years and an exceptional resistance to cancer. Understanding the biology of this species could help unlock the mystery of healthy aging. A variety of experiments on fruit flies, mice and other species have demonstrated that the rate of aging can be manipulated, either by calorie restriction or by activating particular genes. Such research could eventually lead to the development of a drug that safely mimics the effects of caloric restriction (which delays the onset of disease) or actives the "longevity genes" that help protect against the diseases of late life.

The lion's share of funding for medical research is spent on disease research, such as research on cancer, heart disease or Alzheimer's disease. This approach, which I call "negative biology", assumes that the most important question to answer is "what causes disease?". Unfortunately this is a severely limited approach, especially for older populations. Even if you cured all 200+ forms of cancer (and we have not yet eliminated even just one cancer despite investing enormous sums of money for decades now), one of the other diseases of aging would quickly replace cancer as the leading cause of death because most people in late life are vulnerable to multiple diseases. So "positive biology" takes a different intellectual starting point. It assumes that the puzzles of exemplar health are just as important to understand as the development of disease. How can some (very rare) humans live over a century of disease-free life? Understanding these exemplar examples of health might prove to be more significant than trying to understand, treat and cure every specific disease of late life.

Link: http://colinfarrelly.blogspot.com/2012/12/readers-digest-interview-on-aging-and.html

Source:
http://www.fightaging.org/archives/2013/01/unpublished-readers-digest-interview-on-aging-and-longevity.php

Regenerative medicine is not an all or nothing field of research. There are many useful waypoints on the road to being able to grow perfectly formed organs, blood vessels, muscle, and other tissues to order and from a patient's own cells. The partial results and half-way houses include a range of potential therapies and technologies that will be a great improvement over the present clinical state of the art.

Roadmaps in this sort of research tend to look like this:

• Gain knowledge of the underlying mechanisms: cell signaling, stem cell life cycles, and so forth.
• Use this new knowledge to better understand the workings of existing therapies, and perhaps optimize them a little.
• Produce new tools for diagnosis and testing procedures based on what is now known.
• Develop a helpful therapy that meets some fraction of the end goal: healing damage in an organ rather than growing a new organ; growing cells to populate a bioartificial system that carries out some of an organ's function, for use in dialysis for example; and so forth.
• Build poor versions of the end goal and find uses for them. The ability to grow small masses of tissue that can carry out some of the functions of a liver or a kidney may be very helpful as implants for those suffering organ failure, for example.
• Finally, the end goal: organs grown from a patient's cells that are good enough for transplant.

Below is an example of one type of waypoint in tissue engineering that is presently under widespread development: the use of cell transplants to spur regeneration and regrowth that would otherwise not have happened. This is a logical application of some of the knowledge gained regarding organ formation and growth; which cells are important, how they work together, and how they signal one another.

Stem cells found to heal damaged artery in lab study

[Scientists] have for the first time demonstrated that baboon embryonic stem cells can be programmed to completely restore a severely damaged artery. These early results show promise for eventually developing stem cell therapies to restore human tissues or organs damaged by age or disease.

Researchers completely removed the cells that line the inside surface from a segment of artery, and then put cells that had been derived from embryonic stem cells inside the artery. They then connected both ends of the arterial segment to plastic tubing inside a device called a bioreactor which is designed to grow cells and tissues. The scientists then pumped fluid through the artery under pressure as if blood were flowing through it. The outside of the artery was bathed in another fluid to sustain the cells located there.

Three days later, the complex structure of the inner surface was beginning to regenerate, and by 14 days, the inside of the artery had been perfectly restored to its complex natural state. It went from a non-functional tube to a complex fully functional artery. "Just think of what this kind of treatment would mean to a patient who had just suffered a heart attack as a consequence of a damaged coronary artery. And this is the real potential of stem cell regenerative medicine - that is, a treatment with stem cells that regenerates a damaged or destroyed tissue or organ."

Source:
http://www.fightaging.org/archives/2013/01/cells-derived-from-embryonic-stem-cells-rebuild-an-artery.php

Mitochondrial transcription factor A (TFAM) plays a number of important roles and shows up in connection with protofection research aimed at mitochondrial repair. Separately, researchers observe benefits by removing it from the fat tissue of mice:

Mutations in genes involved in the electron transport chain that cause mitochondrial dysfunction can sometimes paradoxically lead to improved health and/or enhanced longevity. One example is the situation in mice with conditional knockout of the mitochondrial transcription factor A (TFAM) specifically in fat. These F-TFKO mice exhibit mitochondrial dysfunction with increased energy expenditure, but are protected from age- and diet-induced obesity, insulin resistance and hepatosteatosis, despite increased food intake.

Mitochondrial DNA (mtDNA) is maternally inherited with multiple copies in each mitochondria. TFAM plays a critical role in maintenance and expression of mtDNA, and reductions of mtDNA copy number usually correlate with reduction of mitochondria content and function. So, how does a reduction in TFAM in fat have this beneficial effect?

Upon high fat diet, [the F-TFKO] mice develop a build-up of long chain acyl carnitines in both adipose tissue and the circulation. In addition, markers of oxidative stress are observed at the level of DNA and lipids in adipose tissue of F-TFKO mice on high fat diet, indicating overload of the ROS protection system. Despite this mitochondria stress, the mice remain lean and insulin sensitive even at 10 months of age. Although no formal aging studies have been conducted in these mice, we also noted that by 18 months of age, an age at which the control mice have started to die, the F-TFKO mice are still thriving, suggesting this knockout may be beneficial to aging mice as well.

Link: http://impactaging.com/papers/v4/n12/full/100518.html

Source:
http://www.fightaging.org/archives/2013/01/fat-tissue-knockout-of-mitochondrial-transcription-factor-a-is-beneficial-and-may-extend-life-in-mice.php