The Worm & Fly & Science Problem

by Nina

Just a part of NY Times Diagram

As some of you may know by now, my husband, Dr. Brad Gibson, is a medical researcher who works at a research institute where the focus is on aging and age-related diseases. So I hear about a lot of studies that claim to have discovered this or that supplement or food that will slow aging or lengthen our life spans. We are often quite skeptical, especially when we learn about how the studies were done. Because it is expensive and time-consuming to test human beings (and sometimes unethical), these studies are often done on worms and flies. And concluding that the effects are going to be the same on human beings is rather a stretch. 

I was motivated to write about this today after seeing a wonderful graphic in the Sunday New York Times in the article A Handy Guide to Longer Living Through Science! (I'm pretty sure the title is ironic.) I actually started to laugh when I read that the study that proved green tea extends life was done on flies (and the one that proved that it won’t was done on mice). A lot of the other studies on supplements were done on worms.

There’s a reason for this. Worms and flies have very short life spans and also visible signs of aging. Yes, older worms get quite wrinkly, for example. So it’s easy to change something about their diet and then see an obvious result, either in a longer-than expected life span or some other physical change. But does that mean the same thing would happen in a human? 

Brad says:

"I suppose its no accident that the artist who created the graphic used a "mouse maze" of conflicting, supporting or just plain absurd experimental results that have been published in the last three years alone to illustrate the disarray of lifespan research. While we all would have our favorites, for example, "worms live longer in outer space" or "men decrease women's life spans" (sorry, dear), these studies point to several underlying assumptions (or misassumptions) about how scientists go about studying longevity or health span. For one, we use a number of model organisms, with worms, flies and mice being the favorites. This is obvious to anyone thinking about conducting such a study, as these animals live anywhere from a couple of weeks to 2-3 years at most. Two, as we compare results of similar regimens across these organisms, we get a lot of contradictory results—maybe not a huge surprise. However, the more troubling truth is that even when we use the same model organism, the results can be very different (Rapamycin slows aging in mice, Rapamycin doesn't slow mice aging). The reasons behind this are complex, but could be due to differences in mouse strain, or the lab they are raised in (different gut microbiome!). My read on this? Here goes: avoid gimmicky lifespan-increasing supplements and drugs and, of course, get plenty of exercise like yoga, as all studies seem to indicate a big beneficial effect in daily exercise." 

So have fun looking at this graphic summary of recent studies on aging. I myself was thrilled to see that the study that showed coffee extends life was done on humans! But wait—there was another study done on humans that shows coffee decreases life spans. Sigh. 

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Can Meditation Delay Aging?

by Brad and Nina 

Gaudi Ceiling by Brad Gibson

Since the early days of Yoga for Healthy Aging, we’ve been blogging about the research of Dr. Elizabeth Blackburn, who studies the effects of stress on cellular aging (see Stress, Telomeres and Aging). Dr. Blackburn is so convinced that chronic stress affects aging on a cellular level that she is studying the effects of meditation and yoga on aging, thinking that these practices might actually slow aging and lengthen life.

In particular, Dr. Blackburn has been studying the affects of meditation and yoga on telomere length. Throughout your life, your cells may reproduce many times to repair and strengthen their host organs, to grow or to fight disease, and the telomere at the end shrinks each time the cell divides and duplicates itself. A chemical called telomerase helps restore a portion of the telomere with each division, but after 10 to 50 divisions or so (the number varies by tissue type and health, and biologists still do not understand the system well), the telomere gets so short that the cell is no longer able to replicate. Because some cells or tissues in our body (skin, blood cells, etc.) continue to replicate and be replaced as we age, or to be repaired after injury, if the progenitor cells needed for these processes cannot replicate due to telomere shortening, this can contribute to the aging process and increase our susceptibility to disease.

Dr. Blackburn’s research has demonstrated that chronic stress actually accelerates telomere shortening and that anti-stress practices such as meditation and yoga can in turn slow the process by “boosting” telomeres. A recent BBC article Can Meditation Delay Aging?  gives a good overview of Dr. Blackburn’s current research. Here’s an excerpt that explains why meditation and yoga might boost telomeres.

Theories differ as to how meditation might boost telomeres and telomerase, but most likely it reduces stress. The practice involves slow, regular breathing, which may relax us physically by calming the fight-or-flight response. It probably has a psychological stress-busting effect too. Being able to step back from negative or stressful thoughts may allow us to realise that these are not necessarily accurate reflections of reality but passing, ephemeral events. It also helps us to appreciate the present instead of continually worrying about the past or planning for the future.

But while telomeres are still getting a lot of buzz these days, I for one know that this is only one of many theories of aging out there (see What is Aging, Anyway?). So I turned to Brad for his take on the article (and the issue of telomeres in general). 

—Nina

Overall, this a reasonable, well-written and—for the most part—balanced article. I think when it gets into how the established medical profession and scientists are reluctant to get into this area, it is largely correct. However, there is so much confusion and outright snake oil sales in the “anti aging” field right now that it’s no big mystery why people (and scientists) are cautious. In addition, it is important to keep in mind that the role of telomeres in aging is still very controversial. This statement late in the article is a bit problematic:

"Conventional medical tests give us our risk of particular conditions - high cholesterol warns of impending heart disease, for example, while high blood sugar predicts diabetes. Telomere length, by contrast, gives an overall reading of how healthy we are: our biological age. And although we already know that we should exercise, eat well and reduce stress, many of us fall short of these goals."

For one, the role of cholesterol levels is (surprise!) being hotly debated again. And some of the longstanding wisdom about what levels are good or bad—especially for women—may be wrong.  The idea that telomere length is a read-out of our “biological age” is simply not supportable by solid scientific evidence. It is telling us something, but it’s not exactly clear what that is precisely. There are some big efforts going on right now to identify new “biomarkers” of aging, and I'm under the impression that telomere length is no longer being considered as major player in these efforts.

—Brad

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The Key to Reversing Aging. Or Not.

by Nina

A Mouse as a Monk by Shibata Zeshin

“It is quite possible that it will dramatically increase the incidence of cancer,” said Irina M. Conboy, a professor of bioengineering at the University of California, Berkeley. “You have to be careful about overselling it.” —New York Times

As if to prove one of the points I made in my post just last Monday What is Aging, Anyway?, a recent article in the New York Times announced a new study on aging research Young Blood May Hold Key to Reversing Aging. Yes, they went right ahead and used the “r” word, one of the words that I said should set of alarm bells.

But I try to keep up with the latest developments in research on aging and the article was the New York Times after all, so I went ahead and read it (oh, the things I’m forced to do for this blog). Of course, the “young blood” thing turned out to be more complex than headline implied. In fact, the research was specifically about adult stem cells—in mice, of course.

Adult stem cells keep our tissues healthy. When there is damage to a part of the body, stem cells move in and produce new cells to replace the dying ones. But as we—and mice—get older, our stem cells don’t work as well. (Have you noticed how much longer it takes to for you to heal after a muscle tear or even a simple scrape?) It’s not that the number of stem cells is lower in older bodies, it’s just that, as Thomas A. Rando, professor of neurology at Stanford University School of Medicine put it, “They just don’t get the right signals.”

Wondering what signals the old stem cells would receive if they were bathed in young blood, Dr. Rando and his colleagues experimented by joining old and young mice for five weeks (literally joining them together—see NY Times article for the gruesome details). After five weeks, the muscles of the old mice had healed about as quickly as those of the young mice, and the old mice had grown new liver cells at the rate of younger mice. What could be causing this? A member of Dr. Rando’s team, Dr. Wagers continued to study the blood of young mice after she moved in 2004 to Harvard, and last year she and her colleagues demonstrated that the young blood could rejuvenate the hearts of old mice. After they found that a protein called GDF11 that was abundant in young mice and scarce in old ones, the scientists injected GDF11 into old mice. And they found that even on its own, GDF11 had the same positive effective the hearts of the old mice. Then they did a similar experiment on skeletal muscle in mice, and found that GDF11 revived stems cells in old muscles as well, making old mice stronger and increasing their endurance.

At this point, I was actually feeling—despite the ultra gross details of how the old and young mice were sewn together—a bit excited. Imagine if we could take some kind of GDF11 supplement that would rejuvenate our aging organs, muscles and bones? But, WAIT! At the very end of the article, the author concluded by saying that scientists would need to take care in rejuvenating old body parts—waking up stem cells might lead to their multiplying uncontrollably. Hence the Conboy quote at the beginning of this post, warning of possible increases in cancer. Skepticism turned back to the ON position, I consulted our resident expert on aging Dr. Brad Gibson for his opinion on this latest claim about “Reversing” aging. And here’s what he said:

"I would agree with Conboy about the possibility for adverse effects. Especially cancer, as there is growing evidence for the role of dormant stem cells that become activated in breast and other cancers leading to metastasis.  And if young blood—now containing among other things an elevated level of GDF11—is introduced into an aged background, are we going to be stimulating (previously dormant) cancerous stem cells as well?

"It's akin to if we just now had discovered human growth hormone (hGH) and realized that it too goes down with age, and increasing would restore some young phenotype (more energy, more muscle mass, etc.). Turns out hGH has lots of bad side effects—including an increased risk of cancer as well as cardiovascular diseases —and it also was once (and still is to some) claimed as a 'rejuvenating" or 'anti-aging' substance.  Overall, very interesting and potentially ground breaking science, but it begs the question why we feel compelled to go around making absurd and/or over-reaching claims before we really know about its other effects? It’s possible that GDF11 levels go down with age to limit cancer stem cell becoming activated, albeit at a high price of a loss of tissue repairs capabilities. Or not..." 

Excuse me while I go practice a yoga for upper body strength sequence now….

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What is Aging, Anyway?

by Nina

Death and Life by Gustav Klimt

We all experience aging as we move through time, from that first gray hair to the need for reading glasses or a twinge of arthritis to more dramatic changes. Eventually our bodies just don’t work as well as they did when we were young. (A formal definition of aging is “the process of a system’s deterioration over time.”) But have you ever wondered what causes aging? Or why human beings have the life span that they do? After all, a worm lives for only 10 days, a mouse for one or two years, and a dog typically over 10 years. Some kind of clockwork causes all living things to gradually age—yes, even worms get wrinkly when they get “elderly”— according to an apparent built-in schedule. But why does this all happen? And is there anything we can do about it?

When Dr. Bradford Gibson first joined the Buck Institute for Research on Aging, he was looking forward to finding the answers to those questions. Much to his surprise, he discovered that there are many different and often conflicting theories of aging. He had somewhat naively assumed that there must be some general consensus on the basic questions of how and why we age. But, he says:

“As I examined theories such as the free radical theory of aging to antagonistic pleiotrophy, it became readily apparent that this was still early days of this discipline. While many of the processes described in these competing theories seemed plausible, they couldn’t all be correct. So working in this field was going to be much more confusing— and interesting — than I had originally imagined.”

Since you might have read about telomere shortening or caloric restriction in the news, here’s a list of some of the theories of aging that Dr. Gibson confronted when he first joined the Buck Institute (with the ones he currently thinks most likely to be important in bold).

• Wear and Tear theory
• Error and Repair theory
• Neuroendoncrine theory
• Redundant DNA theory
• Genetic Control theory
• Free Radical theory
• Caloric Restriction/Nutrition
• Cross-Linking
• Waste Accumulation
• Gene Mutation
• Limited No. of Cell Divisions/Telomere Shortening
• Rate of Living
• Hayflick’s Limit theory
• Order to Disorder (entropy)
• Death Hormone
• Thymic-stimulatory theory
• Mitochondrial theory
• Autoimmune theory
• Antagonistic Pleiotrophy

That’s quite a list, isn’t it? But that’s not all; newer data have emerged in the last few years that have shown the importance of stem cell maintenance, modifications to your DNA (epigenetics), and senescence-associated inflammation as playing key roles in the aging process. I’m sharing all this with you for a couple of reasons. First of all, if someone out there tells you they can “stop” or even “reverse” aging—I've heard both claims myself—you should be very skeptical. Because right now with so much unknown about aging, there is no proof that any of these anti-aging solutions are effective (and, in some cases, like overuse of certain supplements or human growth hormones, they could actually harm you). And, second, I want to set your expectations. This blog has always been about healthy aging, never about stopping or reversing aging.


I’m going to be defining “healthy aging” and writing more about what it means in future posts, but, for now, you can check out my post Longevity vs. Morbidity (Ill Health). 

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Aging, Telomeres, and Yoga: New Study by Elizabeth Blackburn and Dean Ornish

by Baxter

A while back, we reported on an interesting potential marker in the body for aging of the cells connected to the genes called a telomere (see Stressed Mind, Stressed Cells and Science, Aging and Yoga). A telomere is like a tail on the end of DNA strands found in our cells, and an enzyme called telomerase influences the length and activity of the telomere. Studies done a few years ago by a Dr. Elizabeth Blackburn at UCSF in San Francisco began to show a connection between telomeres and cell longevity—the longer the telomere, the longer the cell life. Her work garnered her a Nobel Prize in Medicine.

Telomere Caps

Now Dr. Blackburn has teamed up with Dr. Dean Ornish to see what effect his life-style changes approach to prostate cancer has on telomeres and telomerase activity. Dr. Ornish has already shown that a combination of dietary changes (vegan diet with less than 10% fat per day), exercise in the form of walking for 30 minutes most days, and stress management tools that include regular yoga asana and breath work, mindfulness meditation and once a week group stress reduction sessions can reverse heart disease and diabetes, and can stabilize prostate cancer and stop its progression.

In their most recent study, published in Lancet Oncology (see Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study), the two researchers looked at how the lifestyle program impacted the cellular genetic level in regards to telomere length and enzyme activity. What they found was that the 10 men studied had longer telomeres in the short (as quickly as three months!) and long run, if they stuck to the program, and the 25 men who were controls had shorter telomeres. And they also looked at gene activity in their ten study subjects, and found that 500 genes were turned on, and all were beneficial, according to Ornish. 

Even though telomeres may be an indicator of longer cell life, and by extension, longer overall lifespan, this has not been definitively concluded, so more studies will need to be done, looking at much larger numbers of people. But the early evidence is promising, and even if the telomere/aging cell theory does not pan out, it seems evident that yoga, diet, exercise and stress management do have significantly positive impacts on health, disease progress or remission, and are therefore worth the effort. And as Dr. Ornish noted, his study participants found the lifestyle plan easy to follow, with 85-90% compliance, much better than most pharmaceutical based treatment plans. Why, you might ask? Well, has he says, it’s because it’s pleasant and comprehensive and “most people feel so much better they change their lifestyle.”

To read more, you can check out articles at ucsf.edu and today.com—among others—which reported these new findings.

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Probability, Aging and a Pain in the Neck....

by Brad

It seems appropriate to discuss "probability" as I wait in my seat for takeoff on my flight to Vancouver on a sunny day in San Francisco in mid-may.  First probability calculation: what’s the likelihood that it will be sunny in Vancouver, a city a thousand miles north but also on the Pacific Coast? Better than the average expectation, but probably not by much given the low correlation between weather in the Pacific Northwest with that of the Bay Area, especially in late spring and summer.

Vancouver's Chinese Garden in the Rain by Nina Zolotow

I’m not sure how many calculations of this type most people make in a day, but I tend to think this way a lot (probability calculation #2: am I an outlier in this regard, say in the 5% fringe, or is this more common that I imagine?).  The reason to bring up probability with respect to aging is that most people don’t think about probabilities and randomness in looking at their future health—or their present state for that matter—and how it might change, for better or worse.  Or more to the point, how do changes you make right now influence your health, both in the near term as well as 10 or 20 years out (probability calculation #3: I expect to live say another 25 years or so to about 85, but 90 or so seems considerably more uncertain, even with a exercise, yoga and a good diet). 

Several months ago I was aghast to read a letter to the editor in the New York Times from a woman who couldn’t understand why she unable to get pregnant in her late thirties since she had been taken care of herself, had been eating well, and practiced yoga daily.  She apparently believed that her (good) behavior would insure health and fertility through her thirities.  Probability calculation #4: what is the likelihood that a woman in her late thirities can get pregnant relatively easily, and how much is this is improved if she's in relatively good health? I suspect the answer is that the improvement is small, despite what one might expect. This is just one of thousands of puzzling, fascinating, and at times callous probabilities that govern our lives in a world governed by processes that are themselves inherently random. Try as we might to make rational decisions that we believe will influence our present and future selves in predictable ways, this is clearly not the full story. 

The birth of modern quantum physics over one hundred years ago taught us that even the most basic particles that make up our universe—electrons, protons, light, etc.—are governed by rules that are probabilistic.  Einstein’s famous lament that “God doesn’t play dice with universe” was a last stand against the onslaught of quantum weirdness and other concepts that now dominate our thinking on the physical laws of the universe.  But biology is also subject to these same probabilities, such as the underlying molecular principles of random DNA mutations in evolutionary theory.  Biological aging also has many random elements, or stochastic processes. Indeed, some theorists have resisted any notion of programmed aging or defined biological process of aging per se, and rather believe that aging is inherently driven by the sum of hundred and thousands of random events every second that ultimately contribute to the overall aging process. As Yogi Berra once said, “If you see a fork in the road, take it.”

So as I sit in my airplane seat waiting for this trip to start, I also feel the pain in my neck that hasn’t gone away after a 23-day stretch of 10-12 hour days in front of computer working on grants and papers.  Oddly, I’ve done this many times before in my academic career, but hadn’t any neck pain that didn’t take more than a day or two go away. But I’m 59 now, and this time is different.  Probability calculation #6: if I just ignore this and take some ibuprophen for a few days, will it go away on its own?  As it turned out, no such luck….  It had seemed a reasonable bet since I had done nothing I hadn’t done many time before in the last 30 years.  But of course I hadn’t factored in the "aging" component in this calculation, or the probability that this behavior was now going to come at a price.  So now I’m looking at how I can change my yoga practice to help alleviate this new and unwanted development.  Calculation #7: what’s the chance that if I spend 20-30 minutes a day in a few key poses (Downward-Facing Dog with a wall, Standing Forward Bend, a passive backbend over a rolled blanket ) that my neck pain will improve or, better yet, heal completely?  I’ll let you know in a few weeks.

And one last thing, the weather in Vancouver was beautiful when we arrived, but was followed by five days of overcast skies and intermittent rain. It was a great trip.

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Aging: Terms and Theories

by Nina

I’m old enough that I’ve started to focus on doing some of the things I’ve always wanted to do but never got around to. Some are big (writing a novel!) and some are rather trivial. One of the more trivial things that I somehow never got around to was listening to my husband and fellow blogger, Professor Brad Gibson, give a talk. He’s kind of infamous for talking really fast, jumping around the room a lot, and packing his talks with lots of information and jokes. Recently I got the perfect opportunity to finally check him out in action when he gave a talk on his research on aging and age-related diseases at a scientific symposium.

And, yes, dear readers, Brad was a hyper and funny as I’d been told. And since you haven’t heard from Brad in a while, I thought I’d take the opportunity to tell you a little about what I learned from his talk. He began by defining some basic terms that I thought might be useful for you to hear as well.

Aging is the process of a system’s deterioration over time.

Aging and Age-Related Diseases is the (mostly) undefined relationship of “normal” aging and diseases known to be highly associated with aging, such as cancer, Alzheimer’s and Parkinson’s diseases, and type 2 diabetes.

Healthspan is the period during a person’s life during which they are generally healthy and free from serious or chronic illness. This is what most researchers in the aging field are focusing on increasing (as opposed to lifespan).

Compressed Morbidity is “The compression of morbidity occurs if the age at first appearance of aging manifestations and chronic disease can increase more rapidly than life expectancy. — James Fries (My translation: compressed morbidity means shortening the period of ill health that precedes a person’s death.)

Scientists understand that healthspan and compressed morbidity are important concepts because what would extending life be worth if it only meant 20 more years of serious illness and disability?

Muddy Road by Brad Gibson

Brad did make a number of jokes, but the thing that made me (and some of the audience) laugh the most was a slide about the theories of aging. He prefaced this slide by saying to his audience, as he’s said to you, that when he first came to the Buck Institute for Age Research, he assumed that scientists had a basic understanding of aging. Instead, he found that very little was currently known about aging. Then he showed a slide listing the following theories (those in bold are theories he considers the most compelling).

What is Aging?

Wear and Tear theory
Error and Repair theory
Neuroendoncrine theory
Redundant DNA theory
Genetic Control theory
Free Radical theory
Caloric Restriction/Nutrition
Cross-Linking
Waste Accumulation
Gene Mutation
Limited No. of Cell Divisions
Rate of Living
Hayflick’s Limit theory
Order to Disorder (entropy)
Death Hormone
Thymic-stimulatory theory
Mitochondrial theory
Autoimmune theory
Antagonistic Pleiotrophy
Senescence and Inflammation (SASP)Telomere Shortening
Others (Insulin, mTOR, etc.)

I don’t know about you, but I had no idea there were so many theories of aging and neither did most of the scientists in the room! (That's certainly something to keep in mind when you read about the latest anti-aging diet or supplements that are based on some theory of aging that some expert claims is fact.) Of course, while scientists don’t yet know the why of aging, we are all familiar with many of the what’s. For example, most of us understand that human beings typically lose strength and flexibility as they age (things yoga can help with, by the way). And I hope to have some posts from Shari Ser on this subject—what happens to us as we age—in the near future.

The next slide made people laugh, too, because it showed a worm looking young and fresh at 3 days and then old and wrinkly (for real) at 10 days

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Stressed Mind, Stressed Cells?

by Brad

Ferns by Joan Webster

Last Friday I attended a talk by Dr. Elissa Epel called “Telomeres, telomerase and mental states: Stressed mind, stressed cells?” According to the abstract Dr. Epel supplied in advance of her seminar:

"I will discuss our UCSF research on the telomere/telomerase maintenance system and relationships to stress and other psychological states and lifestyle factors. The length of our telomeres is a predictor of health status – early disease and mortality, and may serve as an index of biological aging. We now know from 8 years of research that shorter telomere length is related to states of suffering—anxiety, depression, trauma exposure, and chronic stress. Just how much can people stabilize their telomere length through interventions such as exercise and meditation? I will discuss initial findings, suggesting that this marker appears somewhat malleable."

Dr. Epel is an Associate Professor in the Department of Psychiatry at UCSF.  She is also a co-founder of Telome Health, Inc., a relatively new company located in the Bay Area to promote the use of telomere testing as a measure of biological age and overall health status. The basic idea that Dr. Epel was promoting is that chronic stress has a negative impact on telomere length, and that stress reduction through diet, exercise, and possibly other lifestyle changes can have preserve telomere length.

You may remember I posted a piece on this subject a couple months ago that discussed telomeres, yoga and aging ("Science, Aging and Yoga"). As a recap, telomeres are sequence of nucleotides or base pairs at the ends of your DNA that serve cap off and protect DNA integrity. One of the theories of aging asserts that decreased telomere length resulting from the failure of certain cell type in the body (immune cells, stem cells, etc.) to properly renew their telomere length after rounds of cell division via the action of telomerases (enzymes that add back lost telomere DNA) can lead to cellular senescence (a terminal, not dividing state) that could play a role in aging, acting as a sort of molecular clock. The question as to whether a reduction or low telomere length is responsible human aging or diseases is still hotly debate (see NY Times article here), despite many studies showing a correlation of shortened telomeres with cancer, diabetes, osteoporosis, Alzheimer’s and other chronic diseases of aging.

Personally, I found much of the data presented by Dr. Epel not especially convincing, as it was mostly correlative, and did not provide much if any mechanistic insight. However, I was intrigued by her attempt to link the physical and mental state of “stress” that we experience daily (you know, “I’m so stressed out”) to cellular stress and damage (alteration in the physiological state of cells or tissues that can lead to damage at the molecular and cellular level). Although we are all familiar with the former use of the term “stress,” this second usage of the term “stress” is quite different, and its effects can remain hidden until it manifests into a pathological or disease state.

It is well known that emotional stress can lead to an increase in cortisol and insulin levels, as well as increases in catecholamines and inflammatory cytokines. What is less clear is how these signals are integrated at the cellular and tissue level, especially under chronic stress, some of which are not at all obvious. Most studies measuring telomere length are on carried out on immune cells present in blood, as these cells are relatively easy to collect and originate from actively dividing cells. 

The notion that chronic stress could alter telomerase activity in these proliferating immune cell types, resulting in the shortening of the telomeres and causing these cells to lose their capacity to divide (“Immunosenescence”) is certainly an interesting hypothesis. Indeed, immunosenescence is increasingly being seen as a new target for drugs and/or biologics therapy by both pharmaceutical and biotech companies. According to data presented by Dr. Epel, one group of people that apparently has a statistically significant decrease in telomere length are long-term primary caregivers, a group that is regarded as suffering from chronic stress. People with long-term depression apparently also have a similar phenotype.

And as I have discussed in an earlier post, meditation and mindfulness practices have been proposed as ways to ward off the presumed negative effects of telomere shortening. (I say presumed, because it’s still not clear to what extent shortened telomeres are by definition a bad thing, or how much shortening of telomeres is required for any negative consequences.) The science on all this is still in the very early days. It may turn out that telomere length will be one more false lead in the ongoing search for biochemical measures of biological aging. And I would be extremely wary of any company advertising to measure your telomere length or that suggests that taking supplements to increase telomere length makes any sense at all. Unfortunately, there are a growing number of companies out there they do indeed make such claims. (To their credit, Telome Health appears to be considerably more circumspect in their claims and services than most.)

I suppose what interested me the most from Dr. Epel’s seminar is that it once again reminded me of the many avenues of medical research that are converging on the notion that chronic stress is a negative factor in human health and possibly a driver in premature or accelerated aging. While the details of how this actually happens is unclear, it is interesting to consider that one of the main, if not primary, benefits of practicing yoga might be to reduce stress.  Who knows, maybe it will turn out that yoga reduces stress at both the psychological and cellular level? Too early to tell, but stay tuned….

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Okay. Back to Aging.

by Brad

Manzanita by Brad Gibson

Okay. It’s been a while, as I’ve been busy with writing NIH grants and papers, as well as traveling. So it's time to get back to one of the central points of this blog: what is aging? It turns out this is no more clear than trying to define yoga. When I joined the Buck Institute for Research on Aging some 11 years ago, I was surprised and a little chagrined to discover how unsettled and wide open this central question of aging biology was.

This was not my original field of study, but as a chemist and structural biologist working at a major teaching university, I saw a prime opportunity to make a career shift by joining the Buck Institute and using my skill to elucidate molecular mechanisms of aging. But I had no idea how many competing theories existed on this subject, ranging from rather oblique terms like ”antagonistic pleotrophy” to more familiar ones—at least to a chemist—like “entropy” and “free radical damage.” So the other day when there was some news coverage in the New York Times of a breakthrough in aging research (see NY Times article here), I saw this as a chance to tackle this subject. The article, titled “In Body’s Shield Against Cancer, a Culprit in Aging May Lurk,” came out of the Mayo Clinic and looked at the role of senescent cells in aging (see original research here).

When cells reach a point of pathological state, either through telomere shortening or some other aberration or damage, a sequence of events are put into place that either sends these cells into a cell death pathway, or into a state of senescence, a kind of limbo non-dividing state. One reason this occurs is to avoid the formation of a cancerous cell, which the organism obviously wants to avoid. Cells that become senescent were usually thought of as sequestered cells that no longer posed a problem to the organism, but were also no longer productive. However, what this new study showed is that these senescent cells appear to have more damaging effects on neighboring cells and tissues, possibly through a secreted inflammatory signal.

By constructing a mutant mouse strain where the researchers could target and kill these senescent cells without harming the healthy cells, researchers found that it had a significant beneficial effect on the health of the mice, and that they lived longer. There is a lot of follow-up work to be done to confirm these studies in “normal mice” as well as in humans. In any case, the data are highly intriguing. It is also worth pointing out that when asked whether this would cure aging, the scientists were much more cautious, as they clearly understood that this is probably only one of many mechanisms that are contributing to aging. Nonetheless, it is interesting to see how inflammation comes up repeatedly as a cause or at least a driver of many age-related disease, from Alzheimer’s disease to diabetes.

One question that I would like to get back to is: what can we do as individuals to influence this process? What are the conditions that lead to cellular senescence versus cell death, for example, and what are the physiological and environmental determinants that cause as a cell to enter this critical state in the first place? If we knew the answers to these questions and as well other questions of this type, we might be able to critically examine how we can influence are own rate of aging. This question is related but separate from how we can reduce and/or cope with various age-related losses and pathologies as they emerge. Both questions will be critical to answer to reach an understanding on the practice of healthy aging.  How yoga might be a part of that practice is what we are trying to address here….

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