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The Monkey Longevity Lesson

Longevity News Digest

Funding Aging Research

The Monkey Longevity Lesson

Dear Future Centenarian, 

I™m often asked¦ œWhat is your #1 longevity (or wellness) tip?

My answer™s simple, and it™s always the same: œDiet.

I usually add¦ œExercise is a close second."

To ignore either will shorten and diminish the quality of your life.

But what does œdiet mean in this context? I devote my longest chapter to it in Smart, Strong and Sexy at 100. But for the purpose of this discussion, let™s address how much you eat, rather than what you eat (both are important).

You must know by now that those who eat less tend to live longer¦ remarkably longer. And just as important, they tend to avoid most of the aging-related diseases such as heart disease, cancer, diabetes and a litany of others.

A recent article in examined even more proof that it™s good for animals all up and down the food chain.

It tells how calorie restriction (CR) improves health and extends life in nearly all shorter-lived species examined to date. In mice, life span can be extended by 40% or more this way. But it has much less of an effect on longer-lived species¦ such as humans.

Nonetheless, the CR response evolved very early on in the tree of life, and the short term effects in mice and humans are surprisingly similar. In human studies from recent years the practice of calorie restriction is shown to produce very favorable changes to metabolism and health, far greater and better than can be achieved with any present drug or medical technology.

If CR were a drug. it would outsell every pharmaceutical created to date.

But try telling people they should eat less, and see how far you get. We are short-term gratification critters for sure.

A pair of primate studies that record the effects of CR on health and life span started decades ago and are still underway. One runs under the auspices of the NIA, the other at the University of Wisconsin-Madison.

You may recall that the NIA researchers published results back in 2012 that suggested CR does not in fact have any significant effect on primate longevity. Some of the research community have in turn pointed out that the NIA study has potential issues, mostly covered in the article quoted below:

  • Considering a Negative Result for Primate CR
  • No Extension of Average Lifespan in Primate Study of CR


The latest results from the Wisconsin-Madison study have now been published, and they are more positive and more in line with what we'd expect based on short term response to CR in primates, humans included.

Monkey CR Study Shows Big Benefit; Contradicts Earlier Study

The latest results from a 25-year study of diet and aging in monkeys shows a significant reduction in mortality and in age-associated diseases among those with calorie-restricted diets.

The study was performed at the Wisconsin National Primate Research Center in Madison. When they were 7 to 14 years of age, the monkeys began eating a diet reduced in calories by 30 percent. The comparison monkeys, which ate as much as they wanted, had an increased risk of disease 2.9 times that of the calorie-restricted group, and a threefold increased risk of death.

Still, the effects of CR on primates have been debated. An influential 2012 report on 120 monkeys being studied at the National Institute of Aging (NIA) reported no differences in survival for CR animals and a trend toward improved health that did not reach statistical significance.

How can two prestigious institutions come to opposite conclusions?

The discrepancy may be a result of how the feeding was implemented in control animals in the NIA study. "In Wisconsin, we started with adults. We knew how much food they wanted to eat, and we based our experimental diet on a 30 percent reduction in calories from that point."

In contrast, the NIA monkeys were fed according to a standardized food intake chart designed by the National Academy of Science. The Wisconsin researchers concluded that the NIA controls were actually on CR as well. "At all the time points that have been published by NIA, their control monkeys weigh less than ours, and in most cases, significantly so."

Twenty monkeys entered the NIA study as mature adults, 10 in the test group and 10 in the control group, and five of these (four test monkeys and one control monkey) lived at least 40 years.

"Heretofore, there was NEVER a monkey that we are aware of that was reported to live beyond 40 years. Hence, the conclusion that CR is ineffective in their study does not make sense to me and my colleagues."

This should all be filed away under basic good health practices. Yet CR, including attempts to recreate its effects on metabolism through drugs and targeted manipulation of gene expression, is the not the path to greatly extended longevity.

It is among the best of presently available paths to raising your odds of having a better old age, which is good in and of itself, but you can't calorie restrict yourself to a decent chance of living to see 100.

The only thing that will make a significant difference to your prospects of great and healthy longevity is faster progress towards rejuvenation treatments - ways to prevent and reverse the course of aging.

That™s precisely why it™s so important to take every single step available to you now, such as cutting back on how much you eat¦ just like the healthy monkeys. If you miss the time when rejuvenative technologies are available to you by a day, it might as well be a miss by a century.

Is that side of fries really that important to you?

More Life,
David Kekich

Latest Headlines from Fight Aging!

A Telomere-Centric View of the Biochemistry of Aging - Monday, July 7, 2014
Telomeres are lengths of repeated DNA at the end of chromosomes that in part serve as a sort of clock to limit the life span of some cell types. Telomeres shorten with each cell division, but can be lengthened in longer-lived cells (such as stem cells) by the activity of telomerase.

Average telomere length tends to shorten in white blood cells with ill health and aging, but this is somewhat dynamic: go out and exercise more and your average telomere length will increase, for example. Looking at the average length is a smeared-out measure of numerous low-level processes in our biology, such as telomerase activity, the pace at which stem cells are generating new cells with long telomeres, rate of cell division, and so on and so forth.

For some years now there has been a contingent of researchers focused on telomeres: producing better ways to measure them, or more ambitiously trying to construct therapies that lengthen telomeres using telomerase.

It seems to me that most research indicates shortening telomere length to be a secondary marker of aging, and thus not a helpful target to either slow or reverse aging, but there exist studies in which mouse life span was extended by upregulating the activity of telomerase. This may, however, be one of those areas of biology in which mice are in fact significantly different from people, or it may be the case that telomerase has other effects independent of lengthening telomeres, such as acting to reduce levels of mitochondrial damage.

Read More

The Lack of Ambition that Characterizes Much of the Discussion of Aging and Longevity - Monday, July 7, 2014
Near all of the discussion on human aging and longevity that takes place even nowadays, in this age of revolutionary progress in biotechnology, is characterized by a profound lack of ambition.

People think about aging and wisely nod their heads and say things like "we should focus on our lifestyle choices" so as to marginally alter the outcome of disability and death. This is disappointing on many levels. It seems that the majority gravitate to tinkering with what is, to doing easy things simply because they are easy, rather than trying in earnest to change matters for the better.

The best lifestyle choices in the world will still lead to a 75% mortality rate by age 90: the only way to do better is the creation of new medical technologies, such as the SENS vision of periodic repair of the known forms of cellular and molecular damage that cause aging.

Here is one example of failing to reach far enough: a post on a new longevity blog that glances at the present range of theories of aging, and then concludes that we should focus on lifestyle and environment because that is what we have control over now. It is disappointing to see this sort of response from someone who has actually looked into the science.

Read More

Stochastic Mutations in Mitochondrial DNA are Commonplace - Tuesday, July 8, 2014
Certain forms of mitochondrial DNA damage are one of the causes of aging. Your mitochondria, the cell's power plants, are the remnants of ancient symbiotic bacteria. Most of their original DNA is lost or migrated to the cell nucleus, but a small number of genes remain.

This DNA is much more vulnerable to damage and has worse repair mechanisms than nuclear DNA, but if important parts are lost then the outcome can be dysfunctional mitochondria that overtake the cell because they are more resistant to being cleared out by quality control mechanisms. That cell will then cause harm to surrounding tissues by exporting damaged proteins and reactive molecules: this is the modern mitochondrial free radical theory of aging in a nutshell.

Since this is likely an important cause of aging we should expect to see that everyone has an appreciable load of stochastic damage to their mitochondrial DNA, and that this damage grows over time. As the cost of DNA sequencing continues to fall and thousands of human genomes are being sequenced, this data is becoming available.

Read More

TDP43 and Autophagy in Frontotemporal Dementia and ALS - Tuesday, July 8, 2014
Researchers have been looking into the biochemistry of TDP43 and failure of autophagy for a few years now in the context of some age-related dementias and amyotrophic lateral sclerosis (ALS).

The processes of autophagy are cellular housekeeping mechanisms, acting to recycle damaged components and remove unwanted waste. More autophagy is shown to occur in connection with many of the presently known methods of slowing aging and extending life in laboratory animals. The research community has been slow off the mark to make inroads into the development of treatments based on enhanced autophagy, however - there is nowhere near as much interest and funding for this goal as for, say, the production of calorie restriction mimetic drugs.

Still here is one example of this approach gaining traction, though here the aim is to treat conditions in which autophagy is impaired in a specific way, through the presence of too much TDP43. It is unclear as to whether a treatment to reduce levels of TDP43 would be of any application to boosting autophagy in an undamaged metabolism.

Read More

An Article on the Work of the Gerontology Research Group - Wednesday, July 9, 2014
The all-volunteer Gerontology Research Group is an online notable hub for the aging research community, thanks to a mailing list and a few highly connected scientists who keep things running along with a shoestring budget. This article takes a look at the offline work of the organization, the challenging process of accumulating reliable data on survival and mortality in extreme old age.

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Trapped by the Conviction that an Extended Life Means Older For Longer, Not Younger For Longer - Wednesday, July 9, 2014
The belief that extending life through new medical science will lead to people who spend their additional years becoming ever more decrepit and frail is widespread and hard to shake.

Scientists have told the public over and again that this is not going to be the outcome: any successful treatment for the causes of aging will produce patients who are younger than their years. Extending life will inevitably mean extending youthful, healthy life, because aging is just an accumulation of damage.

The medical conditions that we call age-related diseases are just late manifestations of very high levels of damage. The only sound way to extend life is through reduction or repair of this damage, and that extends the period of health, pushing back the onset of medical conditions and deterioration.

But it doesn't seem to matter how many times this is repeated by members of the research community. People just aren't listening. The article quoted below is a microcosm of this larger picture: an author who hears what is said about aging, medicine, and healthy life, and cruises right on past to conclude with the same fear of extended years of frailty that he started with.

Read More

Quantifying the Value of a Healthy Lifestyle - Thursday, July 10, 2014
As a companion piece to a recent post on the cost of obesity and lack of exercise, as determined by epidemiological studies, here is another study that looks at the costs and benefits of various lifestyle choices.

Read More

Aging, Klotho, and Skeletal Muscle - Thursday, July 10, 2014
Klotho is one of numerous genes demonstrated to influence longevity in several species of laboratory animal. Like all of the other genes it influences many fundamental cellular and metabolic processes, which makes deciphering how and why it all works to affect the pace of aging a real challenge.

There are probably a few core (and very complex) arrays of biological machinery that influence aging greatly enough to be easily measurable, established long ago in the deep evolutionary past, and thus shared across many different species. However influencing these mechanisms can be accomplished by altering any one of many varied genes, or changing the level of any one of many varied proteins in tissues, and all of these changes produce other effects as well. Biology likes reuse, and any one gene or protein might play a role in dozens of mechanisms.

Thus the low-level details of the progression of aging are a maze, poorly understood at present, even though the actual results in terms of differences between old tissue and young tissue are very well cataloged and understood. This is one of the reasons why attempting to produce age-slowing drugs that work through targeted metabolic manipulation is the slow, expensive road to marginal results.

More than a decade of work and upwards of a billion dollars have been poured into simply trying to recreate some aspects of one well-studied metabolic alteration that increases longevity in laboratory species, the response to calorie restriction. There is little to show for it so far but more knowledge. If that same billion dollars had been put into SENS-like repair strategies, aimed at reverting the known changes in tissues that occur with aging and letting metabolism take care of itself, we'd be most of the way towards a rejuvenation toolkit demonstrated in mice by now. But no-one said the world was rational.

Here researchers speculate on the relationship between klotho and muscle metabolism, suggesting that it might shed some more light on why exactly it is that exercise improves long-term health..

Read More

The Rejuvenation Research Advocacy of Aubrey de Grey - Friday, July 11, 2014
This is a decent article under an irrelevant linkbait title, which is about the best you can expect from the Huffington Post.

The author takes a look at the public advocacy of Aubrey de Grey, which in conjunction with coordinating the ongoing scientific programs of SENS Research Foundation keeps him quite busy. Perhaps the point to take away from this is that change and progress never happens as fast as we want it to, but it is happening nonetheless.

Read More

Promoting October 1st as Longevity Day - Friday, July 11, 2014
The International Longevity Alliance (ILA) is gearing up to promote longevity research on October 1st, presently the UN International Day of Older Persons, and also the date for this year's Eurosymposium for Healthy Ageing conference.

This is a step on the way towards establishing an officially recognized Longevity Day at some point in the years ahead, one of the traditional methods of long-term political advocacy for a cause that needs more attention. ILA chapters will be organizing meetings and events, and - coincidentally - here at Fight Aging! we will be kicking off the year-end SENS rejuvenation research fundraiser on October 1st of this year.

Read More


DISCLAIMER:  News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see

David A. Kekich
Maximum Life Foundation

"Where Biotech, Infotech and Nanotech
     Meet to Reverse Aging by 2033"


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