Fight Aging! Newsletter, April 8th 2013

April 8th 2013

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!



- Video: Why Isn't Longevity Science the World's Greatest Concern?
- Deploying the Argument from Authority for SENS Research
- On Costs and Opportunity Costs of Aging
- Technological Progress, Hope, and Human Longevity
- Discussion
- Latest Headlines from Fight Aging!
    - Another Step Towards Early Artificial Cells
    - Longer Life or Unlimited Life?
    - Within a Species, Larger Size Tends to Mean a Shorter Life
    - An Example of Mitohormesis
    - On Hunger Without Calorie Restriction
    - A Trial of Very Small Embryonic-Like Stem Cells for Bone Regrowth
    - Pharmacology Lags Behind Genetic Engineering and Environmental Causes of Longevity
    - Old Blood Versus Young Blood From a Programmed Aging Perspective
    - The Importance of Autophagy for Mitochondria
    - Height Loss Correlates Well With Other Aspects of Aging


Without the biotechnologies of human rejuvenation that could be created over the next twenty years given a fully funded crash program of development, we and our descendants will all die due to the effects of aging, exactly as did our ancestors. Aging to death has never been a choice - but now it is, and every needless day of delay comes at a cost of 100,000 lives. Everyone presently alive will suffer greatly due to aging and age-related conditions unless new medical technologies of the sort envisaged by the SENS Research Foundation are developed to repair and reverse the low-level biological damage that causes of aging. So why isn't this front and center on everyone's list of concerns? Why does longevity science and the elimination of age-related suffering barely even register in the public eye?

Follow the link above to view a talk on this subject given at the Stanford Advancing Humanity Symposium last month by Maria Konovalenko of the Russian Science For Life Extension Foundation, an advocacy initiative.


Arguments from authority are frowned upon in most forms of formal debate, since the purpose of said debate is to argue and build upon facts firsthand - as opposed to merely repeating other people's consideration of those facts. But for the purposes of advocacy and informal discussion, invoking authority is tremendously useful for getting past knee-jerk rejection of new ideas. Most people are quick to bypass anything that they are unfamiliar with; in this information-dense age some sort of filter is needed to keep a focus on important matters, but folk in every era have been reluctant to engage with the new and the unusual.

Thus one of the necessary activities for any growing concern in any field of human endeavor is to convince influential, knowledgeable people to publicly provide their blessing. On the one hand this is all part and parcel of networking: if you're working on a disruptive new approach to aging research, say, then at some point you have to convince a sizable fraction of the existing research community leadership that you are right, and that your approach is indeed better than the established dogma. You need to build a network, and bootstrap your support.

In most cases, great new ideas can be easily discerned in hindsight, but in the early days it's a matter of a hundred rejections for every cautious expression of interest. You have to kick down a lot of doors. No good idea is accepted without a fight - and that is the human condition for you.

The disruptive and vastly better new approaches to aging research and extending human longevity that I favor are (as I'm sure you all know by now) collectively known as SENS: the Strategies for Engineered Negligible Senescence. SENS is is an assembly of tremendously good ideas expressed in the form of detailed research plans for medical biotechnology, and is (to my eyes) enormously better than the sort of work presently undertaken by the mainstream of longevity science. I say this meaning that it will most likely produce better outcomes at far lower cost in time and money. The present mainstream seeks only to slightly slow aging, and is moving glacially and at great expense. SENS aims to achieve rejuvenation of the old, and can be proven to work or not for a fraction of the amount it would take for the mainstream to develop a single drug to safely and modestly slow down aging through metabolic reprogramming.

Needless to say, with SENS being such a great idea and better plan of action, it's been a struggle this past decade to get it to its present level of respect and adoption. No good plan goes unchallenged in this madhouse world of ours. Congratulations should go to the Methuselah Foundation and SENS Research Foundation teams over the years, most of whom have worked tirelessly behind the scenes and for little recognition. The public at large, however, lagging behind some years in following the scientific conversation, remain suspicious of anything that presents itself as SENS does - new ideas, involving only a small portion of the scientific community at first, talking about human longevity, the existence of public scientific debates over validity in past years, and so forth. It's easy for the fellow in the street to knee-jerk and reject, just as he does for any new idea that has yet to take over the mainstream.

This is where the argument from authority is useful and indeed often necessary in the real world give and take of advocacy for a cause. It launches you past the first hurdle of immediate rejection, to a point at which people might actually start to consider factual arguments - i.e. start to give any sort of fair consideration to your position at all. For SENS, the resource of first recourse for the argument from authority is the SENS Research Foundation scientific advisory board. Again, this is not primarily why the advisory board exists: an initiative grows by networking. But it is enormously helpful when in casual discussion or debate for someone like such like myself to be able to point to that advisory board and say "look at these leading scientists in the fields of aging research, genetics, regenerative medicine, cancer research, and others: they have evaluated the scientific merits and goals of SENS and support it."


ew people seem terribly interested in noting the opportunity costs of aging, for all that a great deal of work goes into trying to build models for the direct costs. Insurers, government program administrators, and so forth, are all eager to put numbers to their potential future outlays - but they have fewer incentives to work on better numbers for the lost ability to earn that comes with advancing age. Here are some figures from a recent paper on dementia in the US, for example:

"The estimated prevalence of dementia among persons older than 70 years of age in the United States in 2010 was 14.7%. The yearly monetary cost per person that was attributable to dementia was either $56,290 (95% confidence interval [CI], $42,746 to $69,834) or $41,689 (95% CI, $31,017 to $52,362), depending on the method used to value informal care. These individual costs suggest that the total monetary cost of dementia in 2010 was between $157 billion and $215 billion. Dementia represents a substantial financial burden on society, one that is similar to the financial burden of heart disease and cancer."

If you go digging around in US census data on income, or the quick summaries thereof, you'll see that median income sits somewhere a little under $40,000/year in the prime earning years of life. It tapers off to a little more than half of that for surviving members of the 75 and older demographic. So while one of seven completely median older people incurs costs of roughly $40,000/year for dementia, all seven completely median older people suffer an opportunity cost of roughly $20,000/year as a result of becoming old. A range of income that might have been earned if still healthy and vigorous is no longer within reach.

These are very rough and ready comparisons, but you can see that even piling in a bunch of other direct medical costs for the rest of the population - cancer, diabetes, cardiovascular disease, and the other common foes - the opportunity costs of being old still look sizable in comparison. In another study that gives average medical costs over time for people in Japan aged between 40 and 80 followed over 13 years, the average yearly expenditure was in the ~$3,500 range, rising to more like ~$25,000 in the last year prior to death. The error bars for casual use of any of the numbers mentioned in this post is large - probably a factor of two, given all of the oddities and politics that goes into medical expenditures and recording of income, and especially when comparing data between different regions on the world. But you can still draw very rough conclusions about relative sizes.

Lastly, I should note that all of the above only considers the living. Once you get to the age 75 demographic in the US, half of the original population is dead, give or take. The dead accrue even higher opportunity costs than those mentioned above, as they have (for the most part) lost all ability to earn or contribute to building new things.

So aging causes a largely unseen cost to go along with what is seen, the cost of what might have been but for disability and death. As is often the case, the cost of research and development to build the means of rejuvenation is small in comparison to what is lost to aging - and also in comparison to what is spent in coping with the aftermath of loss rather than trying to prevent it.


Forecasting is really hard, especially when it involves the future - or so they say. One of Ray Kurzweil's more noteworthy achievements has been, I think, to help popularize the idea that technological progress can be predicted fairly well at the level of general capabilities (as opposed to specific implementations). This is not a new idea, but despite - or because of - the sweeping, glittering changes transforming our society, at a pace that is only getting faster, it hasn't achieved any great adoption in the public eye, at least beyond some few narrow and often misquoted instances such as Moore's law for computing power.

If the outcome of technological progress only meant smaller widgets and brighter lights, then I probably wouldn't be as interested in it as I am. In the grand scheme of things, does it much matter that you can be modestly confident in predicting whether widgets will be half the size and a tenth of the cost in twenty years versus forty years? If you're in the widget business for the long haul, it matters. If not ... well, everyone has their own specialty to attend to.

There is one branch of technology which is now of great importance to everyone, however, and that is medicine. We stand on the verge of being able to extend human life by reversing the underlying biological damage that causes aging. "On the verge" means that either you die just a little later than your parents, or you live for centuries or longer, depending on whether or not you live long enough to benefit from the first therapies capable of actual rejuvenation. The early rejuvenation therapies will be poor in comparison to what comes afterwards, but they will give you time to wait for better treatments: you just have to be young enough at the outset to stay ahead of the curve of improvement.

This is vastly more important than widgets: being able to more or less predict the course of electronics, computing, or space flight gives you an idea of what you might see before you die. Predicting the course of capacities in medicine even at a very high level may show you whether you will have to age to death at all, should things progress as expected. On this topic, here is an open access paper that delves into historical technologies to suggest that progress is predictable:

"Using a new database on the cost and production of 62 different technologies, which is the most expansive of its kind, we test the ability of six different postulated laws to predict future costs. We discover a previously unobserved regularity that production tends to increase exponentially. Our results show that technological progress is forecastable, with the square root of the logarithmic error growing linearly with the forecasting horizon at a typical rate of 2.5% per year."

I point you to the research quoted above as a form of reassurance: progress will continue in medicine, and via efforts such as the Methuselah Foundation and SENS Research Foundation the medical research community is presently being brought around to the idea of extending human life via rejuvenation biotechnology. The uncertainty in timelines at present all lies in how long it will take for SENS-style rejuvenation research to gather a firm, mainstream, well-funded position: once that happens then progress is inevitable and tends to unfold as outlined above. Prior to that point there is much uncertainty, with things progressing in fits and starts - the standard tyranny of progress under minimal funding and participation.

Thus the present goal for advocates is to persuade enough people and funds to make progress inevitable from that point on. The sooner that happens, the higher the fraction of those presently alive who will live to see and benefit from human rejuvenation. If you're in mid-life like I am, you only have forty years or so of grace - and less if you're not taking care of your health, or are just plain unlucky in the cancer lottery. Four decades is probably only enough time if things go very well over the next ten to twenty years, and SENS or SENS-like programs colonize a large enough chunk of the life science research community in a short enough space of time.

So: hope or help. One of the two, but the letter is generally a better plan.


The highlights and headlines from the past week follow below. Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!



Friday, April 5, 2013
It is worth keeping an eye on progress towards the creation of artificial cells and cell-like structures, as they are potentially useful in a very broad range of biotechnologies relevant to longevity science, regenerative medicine, and so forth. The first swarms of medical microrobots will quite likely be modified cells or artificial cells, packed with specific forms of molecular machinery to achieve some sort of effect in the body - such as manufacturing signaling compounds in response to local conditions, so as to steer the activities of surrounding cells. "A custom-built programmable 3D printer can create materials with several of the properties of living tissues. The new type of material consists of thousands of connected water droplets, encapsulated within lipid films. Because droplet networks are entirely synthetic, have no genome and do not replicate, they avoid some of the problems associated with other approaches to creating artificial tissues - such as those that use stem cells. Each droplet is an aqueous compartment about 50 microns in diameter. Although this is around five times larger than living cells the researchers believe there is no reason why they could not be made smaller. The networks remain stable for weeks. "We aren't trying to make materials that faithfully resemble tissues but rather structures that can carry out the functions of tissues. We've shown that it is possible to create networks of tens of thousands of connected droplets. The droplets can be printed with protein pores to form pathways through the network that mimic nerves and are able to transmit electrical signals from one side of a network to the other.""

Friday, April 5, 2013
This article looks past the immediate challenges of aging and early medical biotechnologies aimed at extending human longevity, and into the future of merged molecular manufacturing and biotechnology, when it will become possible to replace our biology with far more robust and long-lasting machinery: "If we're talking far-future, non-biological approaches to life-extension will win out over biological approaches, due mainly to their comparative advantages (e.g. ease of repair and modification). [I] think that the distinction between non-biological and biological systems (especially if Drexlerian nanotech - that is, using mechanosynthesis - is implemented with any ubiquity) will increasingly dissolve. If a system exhibits the structural, functional and operational modalities of a biological cell, tissue, organ or organism, yet consists of wholly inorganic materials, is it not closer to a biological system than to what we would typically consider a non-biological system? Either the distinction between the two will eventually dissolve, or we will use the term "biological" to designate systems exhibiting the structural, functional, and/or operational modalities of biological systems. I make a distinction between life-extension therapies and indefinite-longevity therapies, and I'd like to elaborate more on this distinction here. Life-extension therapies extend longevity, but for various reasons fail to make it necessarily indefinite or unlimited. Often this is because such therapies aren't comprehensive - a given therapy solves one contributing factor of aging, but not all of them. Others, like SENS (which I'm in no way discounting), fix the major causes of damage, but use a different methodology for each respective source of damage or aging; the drawback of this approach is that if previously overshadowed causes of aging now begin to make a non-negligible impact on aging, in the absence of the more predominant causes, then we have no methodology to combat it. Because each strategy is tied intimately to the cause it seeks to ameliorate, the techniques often cannot be applied to the new source of molecular damage. Indefinite or unlimited longevity therapies, on the other hand, use one comprehensive approach to mitigate all sources of aging. One example is Drexlerian nanotech (and to a shared but somewhat lesser extent Robert Freitas's nanomedicine - only because it has specifically-tailored strategies not dependent on the feasibility of Drexlerian molecular assembly or "mechanosynthesis", in addition to the more comprehensive ones). This approach fixes not the source of the damage but the damage itself, iteratively, and can thus be used to combat any source of molecular damage using the same tools, technologies and techniques. With such therapies we wouldn't need to come up with a second wave of strategies to combat those sources of aging that might crop up in the future, and which remained unnoticed until such a time only because their impact couldn't be seen (or allowed to take effect) while the first wave of sources was still predominant." I'm not totally convinced that this last point is the case; I think it's more that a designed replacement for tissue can be made to have far fewer and more comprehensibly understood forms of aging (which can be repaired on an ongoing basis). But there will still be the unknowns, pushed into an ever-smaller corner, and ever less important. Yet by the time it is possible to build artificial tissue and cell replacements in this way, will we not have come to understand biology so well that the unknowns in biological aging are already equally small?

Thursday, April 4, 2013
You might look at this research on size and longevity in the context of what is known of growth hormone and aging. The presently longest lived mice, for example, are those in which growth hormone is removed or blocked, and they are small in comparison to their peers. Also worth considering are analogous rare human lineages with non-functional growth hormone receptors, such as those exhibiting Laron-type dwarfism. "Large body size is one of the best predictors of long life span across species of mammals. In marked contrast, there is considerable evidence that, within species, larger individuals are actually shorter lived. This apparent cost of larger size is especially evident in the domestic dog, where artificial selection has led to breeds that vary in body size by almost two orders of magnitude and in average life expectancy by a factor of two. Survival costs of large size might be paid at different stages of the life cycle: a higher early mortality, an early onset of senescence, an elevated baseline mortality, or an increased rate of aging. After fitting different mortality hazard models to death data from 74 breeds of dogs, we describe the relationship between size and several mortality components. We did not find a clear correlation between body size and the onset of senescence. The baseline hazard is slightly higher in large dogs, but the driving force behind the trade-off between size and life span is apparently a strong positive relationship between size and aging rate. We conclude that large dogs die young mainly because they age quickly."

Thursday, April 4, 2013
Mitohormesis is a process by which a low dose of some toxic substance or environmental effect causes mitochondria in cells to emit a little more in the way of damaging reactive oxygen species, which in turn causes cellular maintenance mechanisms to ramp up their efforts. The end result is a net gain in health and longevity: "Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. This requires two transcription factors, namely DAF-16 and SKN-1, which employ the metallothionein MTL-2 as well as the mitochondrial transporter TIN-9.1 to extend life span. Taken together, low-dose arsenite extends lifespan, providing evidence for non-linear dose-response characteristics of toxin-mediated stress resistance and longevity in a multicellular organism." SKN-1 and DAF-16 are already well known as longevity-related genes in nematodes - more data for the importance of mitochondria in aging.

Wednesday, April 3, 2013
It is suspected that some fraction of the benefits of calorie restriction for health and longevity are keyed to the hunger response in some way - i.e. that being hungry more often is necessary to gain the full effects. There's not all that much work on this so far as I'm aware, however. You might look at one study suggesting increased levels of ghrelin, the hunger hormone, are linked to an improved immune system response, for example. Studies investigating the contribution of hunger to the benefits of calorie restriction would have to run by manipulating the hunger response separately from calorie intake to try to isolate its effects. Here is one recently published example of such a study. It is unfortunately focused only on aspects of Alzheimer's disease rather than on longevity, but it is still intriguing. The reduced inflammation is a sign that the researchers might be on the right track: "It has been shown that caloric restriction (CR) delays aging and possibly delays the development of Alzheimer's disease (AD). We conjecture that the mechanism may involve interoceptive cues, rather than reduced energy intake per se. We determined that hunger alone, induced by a ghrelin agonist, reduces AD pathology and improves cognition in [a] mouse model of AD. Long-term treatment with a ghrelin agonist was sufficient to improve the performance in the water maze. The treatment also reduced levels of amyloid beta (Aβ) and inflammation (microglial activation) at 6 months of age compared to the control group, similar to the effect of CR. Thus, a hunger-inducing drug attenuates AD pathology, in the absence of CR, and the neuroendocrine aspects of hunger also prevent age-related cognitive decline."

Wednesday, April 3, 2013
"Very small embryonic-like stem cells" (VSELs) is one name given to populations of stem cells in the adult body that appear to share some characteristics with embryonic stem cells - such as the ability to differentiate into multiple cell types. If this pans out, these cells will be useful in therapy - and here is news of an upcoming trial: "Preparations are underway for the first known human trial to use embryonic-like stem cells collected from adult cells to grow bone. [The] research partners hypothesize that the VSEL stem cells, which mimic properties of embryonic stem cells, can provide a minimally invasive way to speed painful bone regeneration for dental patients and others with bone trauma. Within a year, researchers hope to begin recruiting roughly 50 patients who need a tooth extraction and a dental implant. Before extracting the tooth, [researchers] harvest the patient's cells, and then NeoStem's VSEL technology is used to purify and isolate those VSEL stem cells from the patient's other cells. This allows [researchers] to implant pure populations of the VSEL stem cells back into test patients. Control patients receive their own cells, not the VSELs. After the new bone grows, researchers remove a small portion of it to analyze, and replace it with an implant. "We're taking advantage of the time between extraction and implant to see if these cells will expedite healing time and produce better quality bone. They are natural cells that are already in your body, but NeoStem's technology concentrates them so that we can place a higher quantity of them onto the wound site.""

Tuesday, April 2, 2013
This is a somewhat obvious point, but seems worth making once or twice. The primary methods of extending life in laboratory animals involve genetic engineering and environmental line items such as calorie restriction - these are how new metabolic states that lead to increased longevity are discovered in the research mainstream. The process of then developing drugs to try to recapture some of these effects inevitably lags behind in effectiveness: it's a complex process with many dead ends and only partial successes, whereas testing new genetic alterations in lower animals proceeds fairly rapidly these days. This recent paper illustrates the point: "The regulation of animal longevity shows remarkable plasticity, in that a variety of genetic lesions are able to extend lifespan by as much as 10-fold. Such studies have implicated several key signaling pathways that must normally limit longevity, since their disruption prolongs life. Little is known, however, about the proximal effectors of aging on which these pathways are presumed to converge, and to date, no pharmacologic agents even approach the life-extending effects of genetic mutation. In the present study, we have sought to define the downstream consequences of age-1 nonsense mutations, which confer 10-fold life extension to the nematode Caenorhabditis elegans - the largest effect documented for any single mutation. Such mutations insert a premature stop codon upstream of the catalytic domain of the AGE-1/p110α subunit of class-I PI3K. As expected, we do not detect class-I PI3K, [nor] do we find any PI3K activity as judged by immunodetection of phosphorylated AKT, which strongly requires PIP3 for activation by upstream kinases, or immunodetection of its product, PIP3. We tested a variety of commercially available PI3K inhibitors, as well as three phosphatidylinositol analogs (PIAs) that are most active in inhibiting AKT activation, for effects on longevity and survival of oxidative stress. Of these, GDC-0941, PIA6, and PIA24 [extended] lifespan by 7-14%, while PIAs 6, 12, and 24 (at 1 or 10 μM) increased survival time [under oxidative stress] by 12-52%. These effects may have been conferred by insulinlike signaling."

Tuesday, April 2, 2013
The programmed aging camp points to experiments such as this as supportive of their view that aging is a genetic program that gives rise to damage and change, rather than resulting from damage that causes epigenetic changes to arise in reaction. The data could be interpreted either way, however, and there are other reasons to believe that aging is caused by damage: "In a 2005 experiment, one old mouse and one young mouse became artificial Siamese twins. For control, [researchers] also paired two old mice and two young mice. After the surgery, they injured one mouse from each pair, and monitored the healing process at a cellular level. As expected, the young mice recovered from injury much more efficiently than old mice. The surprise was that old mice that were paired with young mice healed as if they were young. "Importantly, the enhanced regeneration of aged muscle was due almost exclusively to the activation of resident, aged progenitor cells, not to the engraftment of circulating progenitor cells from the young partner." In other words, it was not young cells that implanted themselves in the old mice; it was signal proteins in the blood that told the old mouse tissue to go ahead and heal as if it were young. [A recent paper] culminates in a proposal for whole-body rejuvenation that might be practical in the near term. Fortuitously, its safety in humans has already been established, so people might be willing to try it if a course of animal experiments shows promise. The idea is simply to transfuse older subjects with blood plasma from a young donor, repeated often enough to sustain levels of signaling proteins that control gene expression." The mainstream view on why stem cells and tissue maintenance decline with age is that it is an evolved response to rising levels of damage that reduces cancer risk. Flooding an old system with young signaling overrides that response, but would probably be accompanied by an increased risk of cancer - though in the case of a short-term signal change as a therapy to promote regeneration of a specific injury, that may be an acceptable risk. In the long term, however, the underlying damage has to be repaired, rather than just forcing our biochemistry to continue as though it didn't exist.

Monday, April 1, 2013
Mitochondria are the powerplants of the cell, bacteria-like entities that produce chemical stores of energy to power cellular processes. The accumulation of damaged mitochondria is thought to cause a fair portion of degenerative aging, and differences in the ability of mitochondria to resist damage appear to play an important role in determining variation in life span between similar species. Autophagy is one of the processes by which damaged mitochondria are removed from consideration, in this case by destroying them and freeing up the materials for recycling. Autophagy also removes other damaged cell components and unwanted metabolic byproducts. Mitochondria-specific autophagy is often called mitophagy or macromitophagy, and a large pile of evidence suggests that it is this aspect of autophagy that is most responsible for the association between increased levels of autophagy and increased longevity in a range of laboratory species and different methods of life extension. At some point in the near future, development will be underway in earnest on drugs to boost autophagy. Here researchers add more evidence to considerations of autophagy and longevity while examining mitophagy in yeast under calorie restriction (CR), a well-known method of life extension: "In this study, we provide the first evidence that selective macroautophagic mitochondrial removal plays a pivotal role in longevity extension by a CR diet in chronologically aging yeast; such a diet was implemented by culturing yeast cells in a nutrient-rich medium initially containing low (0.2%) concentration of glucose, a fermentable carbon source. It should be emphasized that under these longevity-extending CR conditions yeast cells are not starving but undergo an extensive remodeling of their metabolism in order to match the level of ATP produced under longevity-shortening non-CR conditions. Moreover, our study also reveals that in chronologically aging yeast limited in calorie supply macromitophagy is essential for longevity extension by LCA. This bile acid is a potent anti-aging intervention previously shown to act in synergy with CR to enable a significant further extension of yeast lifespan under CR conditions by modulating so-called "housekeeping" longevity pathways. In sum, these findings imply that macromitophagy is a longevity assurance process that in chronologically aging yeast underlies the synergistic beneficial effects of anti-aging dietary and pharmacological interventions (i.e., CR and LCA) on lifespan. Our data suggest that macromitophagy can maintain survival of chronologically aging yeast limited in calorie supply by controlling a compendium of vital cellular processes known for their essential roles in defining longevity. [It] is conceivable that in chronologically aging yeast limited in calorie supply macromitophagy selectively eliminates dysfunctional mitochondria impaired in vital mitochondrial functions that define longevity."

Monday, April 1, 2013
Aging is a global phenomenon throughout the body, and thus we should expect the pace of progression of any one aspect to correlate well with the others. So it is for height loss - meaning that you have the same modest level of control via lifestyle choices such as exercise and calorie restriction as is the case for aging in general: "Using unique data from a new massive longitudinal survey of 17,708 adults beginning at age 45, the researchers show for the first time that lifestyle choices we make in adulthood - and not just the hand we're dealt as children - influence how tall we stand as we age. While prior work has looked for the connection between height and health - both in childhood and adulthood - the researchers are the first to examine height loss as we age. They show that regardless of your maximum height, the loss of height over time is also an important indicator for other health issues as we age. For example, the research reveals an especially strong relationship between height loss and cognitive health. Those who had lost more height were also much more likely to perform poorly on standard tests of cognitive health such as short-term memory, ability to perform basic arithmetic and awareness of the date. All humans go through physical changes with age, including an increase in body fat and decrease in bone mass. But a decrease in height can be further exacerbated by certain kinds of arthritis, inflammation of spine joints or osteoporosis, which other studies have shown are associated with such lifestyle choices as diet, exercise and smoking."



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