Can We Delay Aging?

by Brad Gibson, Ph.D.

The Damsel of the Holy Grail
by Dante Gabriel Rosetti

“No, we cannot “prevent aging”… but what if we could delay it?

Unfortunately, the deterioration that comes with aging is part of a fundamental aspect of the universe, so it cannot be eliminated. Recent research suggests, however, that the rate of deterioration is indeed malleable, at least in many different animal models. So why not in people?” — Dr. Felipe Sierra

Dr. Felipe Sierra's post Can We Delay Aging? on the Next Avenue site is a reasonable and thoughtful response to what is actually a very difficult question. While, some researchers in the aging field have gone so far as to talk about extending one’s life to 200 years or more, or even becoming immortal, Dr. Sierra sidesteps these assertions and instead tackles the more practical, and the less politically charged issue, of targeting an increase in “‘healthspan,” or what is known in the field as “compression of morbidity.”

“Traditionally, research on aging has focused on longevity, but we all recognize that longevity without health is a hollow goal. As the field has matured, we are paying more attention to healthspan — the proportion of lifespan spent in reasonably good health.

Many of the interventions identified in animals lead to improved healthspan. Not only do the animals die later, they die with fewer diseases and debilitating conditions than their control counterparts. This suggests that, at least in mice and other species, it might be possible to attain the Holy Grail of aging research: compression of morbidity.”

This “compression of morbidity” hypothesis, first proposed by James Fries at Stanford Medical School back in 1980, states that the “Extension of adult vigor into a fixed life span compresses the period of senescence near the end of life” (J. F. Fries, The New England Journal of Medicine July 17, 1980). From the NIH and governments budget perspective, this is a laudable goal, as it would potentially lead to less healthcare expenditures in the later years of one’s life, which currently consume over 50% of all medical costs. It would also have the obvious advantages of reducing chronic illness and diseases associated with aging, such as cancer, Alzheimer’s disease, and diabetes.

But can it be achieved? Evidence in model organisms from worms to flies to mice suggest that many of the underlying molecular pathways that appear to have an effect on the lifespan of an organism also tends to improve other phenotypic traits, such as movement, and cognitive and behavioral functions. This is important, as many of the early studies just examined lifespan extension in these model organisms without a close examination of whether there was also an increase in the health or robustness of the organisms. Clearly, the last thing we want to experience for ourselves is an increase of 10-20 years of our lifespan if it was to be lived in a chronic state of debilitation. And while we all know that improved exercise and diet can have significant effect on our health or robustness, the question of whether this will lead simply to an increase in our lifespan but not a compression of morbidity or an increase in our healthspan. 

The jury is still out with respect to unequivocal evidence of the compression of morbidity hypothesis, but several published studies suggest that it may be achievable. Indeed, the term “geroscience” that Dr. Sierra invoked in his essay as a new field of research devoted to answering this question was first coined by scientists at my own institute, the Buck Institute for Research on Aging. It was the title of a successful NIH proposal, “Geroscience” to the NIH to “support interdisciplinary approaches to solving significant and complex biomedical problems, particularly those that have been resistant to traditional approaches.” The essential notion of geroscience was that processes that drive aging and the diseases of aging overlap. And if we are to make any real progress in understanding aging, scientists need to study age-related diseases in the context of aging in a truly interdisciplinary manner. 

This may seem like an obvious statement, but most basic science research into diseases that occur late in life were not, and are still not, conducted with aging as a major variable in the overall experimental design. For example, the vast majority of studies of neurodegenerative diseases, such as Alzheimer’s or Parkinson’s diseases, where mouse models were used, the age of the mice were typically 6 months old, or about late-adolescence in human terms. But this is changing, and there is now an emerging consensus in the scientific community that we need to study these diseases in aging models to gain the insight we will need to find cures. So where are we in this process? Dr. Sierra concludes by saying:

“When will people benefit from this?

It is definitely too early to say, which is why I have refrained from even mentioning the interventions that work in animals. So, despite the thriving industry of “anti-aging” treatments, nothing that we know of today has been shown to prevent or delay the aging process in people. Thus, the current generation may not benefit from this groundbreaking research. But maybe our children and grandchildren will.”

Indeed, there are no anti-aging treatments available today that have proven effects on delaying aging despite some interesting studies in animal models. And I mostly agree with him that progress will be slow and we are unlikely to benefit from this basic research in our own lives. So in the meantime we are left with what we know can affect our general health: diet, exercise, reducing stress, etc. So instead of waiting for the miracle cure or fountain of youth—when and if it ever comes—there are plenty of non-pharmacological ways to improve your health, whether or not that they will delay the rate of your aging.

Subscribe to Yoga for Healthy Aging by Email ° Follow Yoga for Healthy Aging on Facebook ° Join this site with Google Friend Connect

Read More

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

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook

Read More

Confusion About Nutrition Confusion: More Answers and Questions

by Nina and Brad

Peaches by Edouard Manet

I guess we should have known that even a post about nutrition confusion would cause further confusion. After all, the question of what you eat can literally be a life or death one, as you’ll see below. A few days after the post Nutrition Confusion!, we received an email from a friend of ours who is a regular reader. This led to a little email conversation between Brad and our reader, which I thought would be worth sharing with you, in case you had some of the same concerns our reader did. —Nina

READER EMAIL:

Hummmmm...
Well this hits home with my husband and I. It's been 3 weeks since his near, fatal heart attack and almost 2 weeks since we have gone Vegan--cardiologist's orders. 

I forwarded you blog to my husband. Here are a couple more books that might add to the confusion, or clear it up. I can say this in taking out dairy and meat to date-- we both feel really great. Even my menopause symptoms have subsided. 

My husband’s question of who funded her research is one to look into. Did the dairy or meat industry fund her work? Have you guys watched or read, Forks over Knives? 

BRAD’S RESPONSE:

Yes, this is all very confusing. I don't think there is a field of scientific inquiry that's as screwed up and contradictory as the nutrition sciences, especially when it comes to recommendations for dealing with being overweight, or for people with “bad” blood chemistry (high cholesterol, etc.).

In regards to the author, one should always be suspicious about motives. I suspect it has nothing to do with her funding (if she has any) but rather with making her claims more sensational than is justified. You know, “sell more books and be on more talk shows.” Never underestimate self-promotion as an explanation. That said, I've been following the real data behind this story for some time, and there is scientific merit to it. The long held conventional wisdom of avoiding saturated fats and high-cholesterol foods combined with the multi-billion dollar (cholesterol lowering) statin drugs industry, is a big problem. More confusion than good data.

I just had a phone conversation with a colleague at Harvard who runs the Joslin Diabetes Center. They're looking into fructose as a serious driver of not only diabetes, but possible cardiovascular problems as well. It turns out not all sugars are the same in how they are metabolized and absorbed by the body (insulin production etc.) , and we should probably all severely limit our consumption of drinks (and other foods) containing added sugars, especially those high in fructose*. And there are a lot of them out there—and not just in soft drinks. A study just came a few days ago (Hochuli  et al., 2014. J Clin Endocrinol Metab) that showed that just one 12oz sugar-containing soft drink a day for one week led to negative changes in liver function in young healthy male volunteers. The researchers concluded that drinks supplemented with fructose, sucrose or glucose all showed signs of impaired beta-oxidation pathways (not a good thing), but fructose drinks showed the largest increase in fatty acid synthesis (an even worse thing for the liver).  I’ve only mention the liver here—this is what this particular study focused on—but there are well-documented effects on muscle tissues and the cardiovascular system a well. 

Also, fried foods, vegan or otherwise, should also be avoided. Too many inflammatory effects from oxidized fats. This has been known for some time.

Personally, I'm sticking to my diet = vegan + poultry/fish, with the (very) occasional eggs/cheese. However, I probably will try to further reduce my overall carbohydrate intake (bread, pasta, rice)—at least a little—and shift more to vegetables. I may still eat an occasional hamburger or steak, but probably not more than once a month.

A vegan diet for you guys sounds like a good idea, as I know you're eating lots of fresh/real foods. It will help make some choices much easier and more clearly defined. But I've seen some people who eat a vegan diet that made me cringe. Yes, no meat and dairy, but way too much carbohydrates and junk foods.

Sorry for the rambling email...

*One clarification: High-fructose corn syrup (HFCS, a mixture of fructose and glucose, typically higher in fructose) is made from corn versus fructose, the naturally occurring sugar found in fruits. Fructose, while chemically and metabolically different than the common table sugar sucrose (a disaccharide obtained from cane or beet sugar that is metabolized into equal parts fructose and glucose after ingestion), has some of the same problems as HFCS. But if it is consumed as whole fruit this is probably not an issue as most fruits don’t contain that much fructose  and their digestion and absorption is very different than that in drinks. But too much fruit juice or fruit-juice sweetened beverages that you often find in health stores could lead to some of the same problems—or possibly worse—than those seen with drinks containing high-fructose corn syrups. There is some very reasonable data on this, although still a highly contentious debate. 

READER EMAIL: 

Good, level headed comments.
This all makes such interesting conversation. I love it.

BRAD’S EMAIL:

With so much misinformation out there, false (or at least poorly supported) claims, hundreds of diet books with conflicting advice, and badly designed scientific studies, nutrition a topic that Nina, Baxter and I have been reluctant to go into in the blog. But it’s also one of the most important issues of healthy aging, and something that affects everybody—every day—in the choices we make. We'll see where we take all this....

But I too enjoyed our conversation.

Reference: “Sugar-Sweetened Beverages With Moderate Amounts of Fructose, but Not Sucrose, Induce Fatty Acid Synthesis in Healthy Young Men: A Randomized Crossover Study.” Michel Hochuli,* Isabelle Aeberli,* Adrienne Weiss, Martin Hersberger, Heinz Troxler, Philipp A. Gerber, Giatgen A. Spinas, and Kaspar Berneis. J Clin Endocrinol Metab, in press.

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook 

Read More

An N of One and an N of All: Personalized Medicine and Personalized Yoga

by Brad

Patterns in Nature by Melina Meza

A couple months ago I attended a conference in Seattle sponsored by US HUPO (Human Proteome Organization) called “From Genes to Function.” Afterward, while I was mulling over the talks, I was reminded of some earlier posts I’ve written where I discussed studies that were “under powered,” that is, they didn’t have enough subjects and controls to come to any firm, or statistically validated, conclusions. These included the papers that looked at reduced IL-6 levels (an inflammatory cytokine) or the effect on telomere length (the ends of DNA sequence that correlate with age) in practioners of yoga (see Science, Aging and Yoga).  In another post, I discussed the issue of the “N of one (N = 1),” a reference to anecdotal cases or one’s own experience. I have often felt that we should not be overly tough on the lack of data on some aspects of our behavior before embarking on changes, as the bar for scientific proof is often simply too high—and the likelihood of someone carrying out the rigorous study needed to obtain a higher level of confidence is not likely to happen any time soon.

So, it was interesting to be reminded of two important trends taking place in the health sciences these days: the “N of one” and the “N of all.”  Both of these concepts came up in the talk by Leroy Hood, CEO of the Institute of Systems Biology, a major leader in the field of integrated “omics” technologies in medicine, i.e., genomics, proteomics, etc.  His point was that with new technologies becoming cheaper, we could envision a situation in the very near future of routine genomic sequencing and other data intensive methods to follow one’s own health (the N of one) as well as this data being integrated with thousands of patients for a virtual cloud of data (the N of all).  The N of one concept was reiterated in a fascinating talk from Michael Snyder of Stanford in which he discussed a project where such efforts are being carried out longitudinally to monitor precise changes in one’s microbiome and other parameters.  This idea stemmed in part from his own self-diagnosis of type 2 diabetes from information he was collecting on himself (talk about personalized medicine!). It is now expanding into larger, but still relatively small cohort of 50 pre-diabetics, to identify genes and other factors that contribute to type 2 diabetes. This project is already underway and will likely be expanded to include several thousand subjects if successful. Such technology innovations would allow you to have vast information about your own DNA, blood and microbiome status from which to make more informed health decisions.

Obviously the N of all concept is related to the N of one, but refers to an even larger amount of medical data that is now becoming available to researchers, as these data from thousands, if not millions, of people become available. Access to such a trove of information would allow scientists to identify genes for rare diseases, as well as to better pinpoint behaviors that are linked to diabetes or Alzheimer’s, for example. These data would also allow individuals to make better-informed decisions about what drugs they should or should not be taking, as well as what behavioral modifications would be best for their personalized health. As this idea really gets traction, maybe we will be able to better assess how the practice of yoga affects our health (and contributes to healthy aging), both from a personalized view  (N of 1) as well as that gleaned from thousands of people (N of all). Until then, using your subjective experience along with input from your yoga teachers and colleagues to evaluate which yoga practices are beneficial to you is a perfectly valid way to make decisions about what and how to practice.

One last thought: This scenario may seem like a dystopian future to many of you, as there are clear issues of privacy and how much information we really want to know about ourselves or others to know about us. Not surprisingly, these issues are being hotly debated among scientists, medical ethicists, and policy makers—and we should be participating in this discussion as well. There are already some pretty serious guidelines in place to insure privacy and remove personal identifiers from much of this data, but things are changing rapidly. The explosion of medical and behavioral information about ourselves and others will almost certainly happen as the technology become cheaper and more widely available. It will be very interesting to see how this plays out—and whether the rewards of personalized medicine will lead us to better ways to manage our health.

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook 

Read More

Nutrition Confusion!

by Nina and Brad

Still Life with Apples, Meat and a Roll by Vincent van Gogh

One of the most important decisions we make each day to foster healthy aging is deciding what to eat. But what if our ideas about which foods are healthy (and which are not) are misguided? What if some of the advice we’ve been receiving from our doctors for the last 50 years is actually wrong?

I’ve already written a post for this blog Healthy Diets for Healthy Aging, in which I discussed why the field of nutrition is so confusing. But a few days ago Brad read me an article from the Wall Street Journal The Questionable Link Between Saturated Fat and Heart Disease that kind of blew my mind. In this article, Nina Teicholz, who has been researching dietary fat and disease for nearly a decade (and whose book The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet will be published by Simon & Schuster on May 13) claimed that the "very cornerstone of dietary advice for generations has been that the saturated fats in butter, cheese and red meat should be avoided because they clog our arteries" was based on theory that has never actually been proven. She wrote:

“The fact is, there has never been solid evidence for the idea that these fats cause disease. We only believe this to be the case because nutrition policy has been derailed over the past half-century by a mixture of personal ambition, bad science, politics and bias.”

She says that our distrust of saturated fat can be traced back to the 1950s to the work of  scientist named Ancel Benjamin Keys, whose research was flawed but who relentlessly (and successfully) championed the idea that saturated fats raise cholesterol and, as a result, cause heart attacks. She concludes by saying,  “More than a billion dollars have been spent trying to prove Ancel Keys's hypothesis, but evidence of its benefits has never been produced. It is time to put the saturated-fat hypothesis to bed and to move on to test other possible culprits for our nation's health woes.”

She goes on to speculate that our increased intake of carbohydrates (even fruit!) as well as food fried in vegetable oil could be the real villains, leading to increased obesity rates and other health problems. While I’ve spent some time explaining why we’re not going to be giving dietary advice on this blog (see Healthy Diets for Healthy Aging), I decided to ask Brad to comment on this article in case some of you out there had read it (or related articles) and were feeling as confused as I am.

NINA: You read this article to me, so what do you make of it? 

BRAD: Of course, we couldn’t help but notice that the author of the article has a forthcoming book. So, as with most authors on these topics, some bias is almost certain to exist to make the story more sensational, so one always has to keep that in mind. That said, the article was fascinating in its take on saturated fats and heart disease.  It made me consider why I generally push to the side of the plate some of the fat on a side of pork belly—the very few times I even eat it at all anymore. Or the guilty pleasure at eating bacon, knowing it’s “bad for me” but that it tastes so good. Or looking for the low-fat milk for on cereal (I won’t go near non-fat milk as it simply tastes awful).  However, I have pretty much forgone eating muffins, scones and donuts—which still appear to be villains in this new take on healthy and unhealthy foods.  As a scientist, I, of course, love to see doctrine upturned, especially when it's based on a lot of poorly constructed experiments with too many underlying assumptions, which both appear to have been in full play in the nutritional epidemiology studies such as the ones described in this article.

NINA: What do you think we should make of this analysis?  And how should we incorporate it into our thinking about a healthy diet?

BRAD: The question is: is this analysis to be believed, or somehow put in the space with all those other studies that seem to pop up with greater regularity—such as too much protein in your diet can cause cancer? That also reminds me that the author did not really consider cancer, neurodegeneration,  gastrointestinal diseases, and other things that are associated with aging in her analysis. I guess it confirms what I suspected all along, that we know surprisingly little about how diet really effects our health, particularly when our basic nutritional needs are being met. So, when I next confront a hamburger on my plate, do I take off the bun, eat the patty only, leave off the cheese, or add extra raw (or grilled) onions? Or do I just eat it with all the trimmings (and medium rare—the way I like it), and remind myself that I probably shouldn’t be eating mammals all that often (you know, for all the obvious and very real ethical and environmental concerns), and make sure my next meal is mostly vegetables (and not deep fried)...

NINA: Ack!

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook 

Read More

Osteoporosis, Balance and Yoga

by Brad

A couple weeks ago, I attended a very interesting seminar on “Bone Marrow Adiposity:  An Age-Associated Phenotype; What's between bone and fat?  New insights into age-related osteoporosis” by Dr. Clifford Rosen, MD.  Dr. Rosen is the Director of the Center for Clinical and Translational Research at the Maine Medical Center Research Institute in Scarborough.  His talk was fairly technical and had to do with the regulation of fat in bone and how it increases slowly with age, as well as being affected by other environmental and genetic factors. His data showed that as fat accumulates in bone with age, it appeared to be related to a decrease in bone density, and therefore could be a driver of osteoporosis in both men and woman. He also stated that the clinical manifestation of osteoporosis is bone breakage, and therefore as your bone density decreases, it is the fall and inevitable bone fracture that typically turns people into patients. Avoiding a fall in the first place is possibly the best and for some the only way to avoid the adverse effects of this age-related decline in bone density.

After his seminar, I had a chance to talk with him after his research and asked him whether yoga might help by decreasing the risk of falling. He immediately said yes, and added that the yoga and tai chi were the two things that he knew that had been shown to have the greatest benefits in reducing this falling and bone fractures (see, for example, the Mayo Clinic web site's Exercising with osteoporosis: Stay active the safe way by choosing the right form of exercise and the New York Times article Ancient Moves for Orthopedic Problems). He implied that this was primarily through an increase in balance as opposed to strength. Indeed, while there is plenty of evidence that strength training is important, an increase in balance and flexibility can make all the difference between a stumble or misstep and a full-fledged fall.

As I sit on my flight to Seattle, I am reminded of how much variation exists in flexibility and balance among adults. Squeezing out of an aisle seat to make your way to the restroom or retrieving a suitcase from the overhead bin can easily become an awkward and precarious—and at times dangerous—act. And it is often not the oldest passengers, but the middle-aged and muscle-bound adults who induce serious cringing from neighboring passengers. Imagine how much more agile they would be if they all practiced yoga!

And for those of us who already do yoga, this is yet another compelling argument that working on balance is critical as we age. So if you haven't done so already, check out Shari's post last week about how to create a yoga practice to improve your balance (see Planning a Practice for Improving Balance).

Read More

Caloric Restriction: Comment and Response

by Nina and Brad

Brad’s post on caloric restriction (see Caloric Restriction and Longevity) prompted an interesting comment from Kathleen Summers MD PhD that I thought it worthwhile to share with you. Rather than having Brad respond in the comments section (I'm not sure how many of you actually read the comments), I asked him to reply to her comment at the end of this post. So have a look! This debate is a very good example of how little scientists currently understand about the aging process (a theme we return to periodically) and provides a hint of some of the many issues surrounding the controversy regarding the best diet for healthy aging.

Posted by Kathleen Summers MD PhD to YOGA FOR HEALTHY AGING

The biggest lesson here is that an excess of energy intake brings disease, disability, and early death. Restricting intake protects against cancer - and also diabetes, arthritis, and heart disease to some degree, although the numbers in the latest study didn't reach significance for the latter (potentially due to limited sample size). Teasing out just what the optimal amount of intake is takes time and research. And it's complicated - there's nutritional, environmental, mental/emotional health, and genetics among other factors playing a role.

The monkeys in both groups of the Wisconsin study ate more and weighed more than the NIH monkeys. The researchers used different sources for their proteins, fats, and carbs as well as a different approach to vitamin and mineral supplementation.

We have one primate study showing extended life span with calorie restriction and one not showing the same but yet other positive results. Let's not jump to absolute conclusions about what the latter study means.

Response from Brad Gibson PhD

Kathleen,

You make some good points, and I agree that this most recent NIA caloric restriction study needs to be considered within the context of other published work. There are undoubtedly many nuances in experimental design and interpretation that future experiments will need to address. That said, my major point is that the data for CR in primates is weak at best.  Many of my colleagues were very critical of the earlier Wisconsin study on two counts: the fact that they fed the control group a fairly high caloric diet and that they removed animals from their final analysis on the basis that they died from non age-related reasons. The removal of animals in the final statistical analysis was a very dubious call. And, as it was pointed out in the NYT article—and by many critics of the Wisconsin study—if those animals were included there was no difference in longevity between the two primate groups. Combined with other studies on more diverse genetic backgrounds in mice that show very mixed effects of CR, one really has to wonder how much traction the CR models has left in it, at least in mammals. Oddly, the data on other model organisms (flies, worms etc.) remain strong.  But one can only push these conserved evolutionary arguments so far.

While there may be benefits in a CR diet as you indicate (e.g., cancer and heart disease), one needs to make a distinction between a low calorie diet and caloric restriction. Many years ago a very prominent scientist in the field of aging who practiced the CR diet stated at the end of his seminar that "we scientists" needed to make a case to the public about the benefits of CR. I challenged him on this assertion, saying that American's relationship to food is so screwed up as it is, that to send a message that food is your enemy is not good advice. There is no evidence that CR in humans is beneficial. In contrast, there's plenty of evidence that a sound, balanced, healthy, low-to-moderate caloric diet (especially one that limits or avoid meat and dairy) is good for you. I suspect we are in agreement on that point.

I also agree that we are still far from drawing a final conclusion on the benefits of CR on human longevity. I was a bit flippant on this point in my last blog post. Guilty as charged. And there is little doubt that there will be more NIH studies examining CR and longevity in various mammalian and primate models as there is still compelling and interesting evidence that needs to be sorted when all animal models of CR and longevity are considered. However, I for one, will be placing my bets elsewhere.

Read More

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.

Read More

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….

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook 

Read More

Successful Aging and the Thinking-Moving-Feeling Triad

by Brad

Early this month I attended a symposium sponsored by the Longevity Consortium at the Buck Institute for Research on Aging on “Environmental, Developmental, and Genetic Factors in Aging and Longevity.” There were lots of interesting presentations, especially on the search for genetic determinants for longevity, or what we call genome wide association studies (GWAS). It turns out that almost nothing survives rigorous statistical scrutiny at this level, suggesting that the genetic factors for long life are very complex and highly dependent on a host of environmental factors.

However, there was one talk on a very different subject that was of particular interest. Dr. Dilip Jeste from UCSD gave a lecture on the meaning of successful aging, and why almost no one asks patients directly to assess their views of their own aging experience.  Almost all definitions of successful aging (and again, many prefer the term “healthy aging”, although they are often used interchangeably) are based largely on the absence of age-associated physical disabilities, such as cardiovascular disease, diabetes, neurodegenerative disease, etc. Dr. Jeste made a compelling case that self-assessment of one’s physical and psychological well-being at advanced age is critical for a better determination of what constitutes “successful aging.” Interesting concept, and one that may be more in sync with the yogic idea of the mind-body connection and mindfulness.

Larch Tree in Autumn by Philip Amdal

Intrigued by this, I went on to look at some of Dr. Jeste’s publications on these topics, and came across a very recent editorial published last year in BMJ titled, “Promoting successful aging through integrated care” (see here). I was struck the following statement:

“Another way of dealing with physical and mental health comorbidity may be through use of interventions that simultaneously increase physical activity, cognitive stimulation, and positive affect, thereby affecting all three components of the thinking-moving-feeling triad implicated in poor health related quality of life.”

As I read this I thought this is a pretty good definition of yoga, a “thinking-moving-feeling triad.” Maybe not an especially elegant summation, but pretty succinct. But what followed next took me back a bit:

An example of such an approach is the use of “exergames”—entertaining video exercise games. If such approaches were specifically adapted to the needs of older people, they could conceivably affect obesity, diabetes, heart disease, and depression simultaneously.”

Exergames? Not exactly sure what the meaning of this is (I confess to a horrible vision of a group of seniors playing bingo while clapping their hands to a Lady Gaga video), but if that's the best example they can come up with then something is wrong. Is yoga still met with such suspicion in the medical and academic community that such an obvious and natural connection is not made here? Is it going to take another generation for the current (and aging) yoga practitioners to retire before this can go more mainstream?

As I wrote in my last blog entry, one of the main reason I started practicing yoga at the age of 50 was that I was looking for a more age-appropriate exercise routine that would provide me with more flexibility, balance and core strength without exposing me to injuries. Sounds to me like yoga would be a much better fit here addressing all three of these goals (“thinking-moving-feeling triad”) in a much more integrated and natural fashion….

Read More

Does Yoga Wreck Your Body? A Scientist's Perspective

by Brad

There’s been a lot of buzz after the Sunday Times article on yoga and injuries, "How Yoga Can Wreck Your Body." My own take on this is that this is pretty shoddy journalism. The writer should have looked no further than the New York Times own Science Times format for Q&A.  Maybe a question like “Does yoga cause more injuries than similar exercise regimens?” would have been more appropriate? I suspect the answer would have been “no.”

In any case what’s the control here? No exercise at all, running, or lifting weights at the gym? All of these have both intended and unintended consequences on your physical well-being and injury status, especially as you get older. When I was a graduate student at MIT, I remember one of my professors invoking his own law to explain missteps in some scientific papers: “if you think you know the answer beforehand, you will undoubtedly find it.”  He used this to explain why some scientists misinterpreted their results by either overly fitting data to some preconceived notion, or ignoring or explaining away other types of information that was inconsistent. Makes for a good story, but this is not good science. Not good reporting, either.

My own experience with yoga suggests a different perspective on this question. I started yoga when I turned 50 because I thought that it would be more age-appropriate and not lead to as many injuries. In my case (Caution! N=1), I never injured myself in nine years of practice.  One reason was I had a good teacher (Baxter Bell), who did not push his students too far, and who also paid attention to preexisting injuries to tailor their practice. He was also well-trained and knew about anatomy and physiology. Not all yoga teachers have the appropriate training, so this is one of the most important first decisions in your practice:  choose a good teacher.  Finally, I did not push myself beyond what I thought was appropriate (if it hurts, back off a bit—you're not trying to prove anything to the teacher or other students).

A Crow by Philip Amdal

While I did not injure myself in yoga these last nine years, I can’t say the same about other activities. I have suffered from tennis elbow injury (overzealous gardening and foosball), heel pain (bad shoes as a kid leading to something called Haglund’s deformity), and lower back pain (digging all day with a shovel a year ago to clear a section of the yard).  What’s interesting is how yoga has helped to alleviate and moderate these injuries. Downward Dog and other similar poses have helped stretch my Achilles heel and tendon, considerably reducing my foot pain. I use a strap around my arms now for various positions, and this has seemed to both strengthen and better align my arms and elbows. And, lastly, I have noticed that my lower back feels better after a yoga practice than before—as long as I don’t overdo things.  So, at least in my case, I can honestly say that yoga has helped alleviate injuries, not caused them. Maybe someone should write a follow up article, “How Yoga can Help You Recover from Injuries?” Not as sensational, but....

And speaking of shoddy journalism, Dr. Timothy McCall tells us that although he was quoted in the article, he was not actually interviewed by the author and that the quote from him was taken out of context, from an old article. To read his rebuttal and his advice about practicing headstand, see his website http://www.drmccall.com/ and read the article "How to Not Wreck Your Body Doing Yoga or, How I Really Feel about Headstand" on the home page.

Read More

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….

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook

Read More

What is a Yoga Practice?

by Brad

From The Poetry of the Body by Yee and Zolotow

A year or so ago I was talking with a colleague about a genomics study he was planning that was going to look at exercise and aging. Previously, he and his colleagues had shown that resistance exercise training had a significant effect on the genes that were transcribed in muscle tissue, and that the older people undergoing this training had gene transcription profiles that resembled much younger people. This time around they were planning a more nuanced study and would look at several exercise regimens, including yoga. I remembered asking him what type of yoga practice they planned to use, and was met with a slightly confused look. He wasn’t sure, but thought it was a “standard practice” involving some stretching and aerobic components. When I inquired further about whether it was Iyengar style or one of those high-energy aerobic practices (like Ashtanga Vinyasa), I realized that our discussion had reached a dead end. He had no idea what I was talking about.

So when I ran across another article today on Yoga for Back Pain that was mentioned in the Science Times section of this weeks NY Times (see here), I decided to take a little closer look at what the actual practice was. I also looked back at the Ornish and Blackburn study I discussed a couple weeks ago (see here), as well as a few other studies I had run across. I was interested in seeing how well the practice was described and whether it made in sense.

I was surprised to find that the most high profile of these studies, the 2008 Ornish and Blackburn study (see here), had the least detail. What they described as yoga for stress management consisted of “gentle yoga-based stretching, breathing, meditation, imagery, and progressive relaxation techniques 60 min/day, 6 days/week”. In contrast, a study published this summer by Dr. Fishman on osteoporosis and yoga (see here ) was considerably more comprehensive, listing all 10 yoga poses by both Anglicized and Indian names, e.g., “Upward and Downward Dog poses (Adho Mukha Svanasana and Urdhva Mukha Svanasana),” as well providing an appendix of 13 figures illustrating each poses. It should be pointed out that the lead author of this study was extremely familiar with yoga, having practiced it in India for three before attending medical school.

Another group that was fairly thorough in their description was Sherman et al. which just appeared on-line a couple days ago (see here) in their study of chronic low back pain, where they describe a viniyoga practice consisting of 5-11 poses (with pictorial diagrams referenced from earlier 2005 paper by this same group (see here). Interestingly, these authors also provided the credential for the teachers as “instructors with at least 500 hours of viniyoga training, 5 years of teaching experience, and familiarity with the selected postures and who were briefed by our yoga consultant.” This paper also gave a defense of their yoga style (viniyoga), as “a therapeutically oriented style of yoga that emphasizes safety and is relatively easy to learn.”

Iyengar-style yoga was used in another study examining stress and inflammation by Kiecolt-Glaser, et al (see here) because it ”emphasizes the use of props to help students achieve precise postures safely and comfortably according to their particular body types and need”. In this latter study, the 12 poses and timing of each were well described and was constant, and apparently selected “based on their purported relationship to immune function and/or restorative effects.”

Obviously not everyone is going to agree with what is a good or best yoga practice for stress, back pain, osteoporosis or whatever. But what is clear is that these studies need to provide a through description of the regimen (time, poses, teacher qualifications) and their overall rationale, so that if someone wanted to reproduce this study or compare it with another, they shouldn’t be in the dark as to what the yoga practice was. In the end, it’s you who is going to have to decide on what to believe, as the standards for comparing these practices, pose sequences, and yoga styles are confusing at best. Maybe Nina and Baxter can comment on this, as I’m not an expert.

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook

Read More

Science, Aging, and Yoga

by Brad

Paris in the Rain by Brad Gibson 

So I promised I would get back to the question of how one would use science to study the effects of yoga on aging. As a starting point, let’s look at one highly publicized study that appeared a few years ago in Lancet Oncology (see here).

This work was collaboration between Elizabeth Blackburn, a prominent and highly respected biochemist at UCSF and recent Nobel Prize winner in Medicine, and Dean Ornish, a clinician at UCSF and well-known author of books and articles linking better nutrition to health and disease prevention, especially for coronary heart disease. The basic premise of their 2009 Lancet study was to examine whether relatively short-term lifestyle changes consisting of a low-fat diet, moderate exercise and yoga-based stress management could effect telomerase activity in circulating blood peripheral blood mononuclear cells (PBMCs) that are largely cells involved in immunity. 

The authors enrolled 30 men with a pre-diagnosed low-risk for prostate cancer for a three-month regimen. They measured telomerase activity, an enzyme present in certain class of replicating cells that maintains the length of telomeres. Telomeres are repetitive stretches of DNA at the ends of chromosomes that protect the integrity of chromosomes, and with each cell division gets shorter. Telomere shortening has been shown to negatively affect a cells capacity to replicate and general maintenance. Telomere shortening has been suggested as a biomarker of aging, acting as a type of clock for cellular aging. This so-called “telomere theory of aging” has gone out a favor among some scientists in recent few years, and its role in aging is controversial. Nonetheless, the basic premise underlying this study is that higher telomerase activity will lead to longer telomere lengths, which will set back the aging clock a bit in some way, or at least lead to healthier immune cells.

The author’s conclusions were as follows: “Comprehensive lifestyle changes significantly increase telomerase activity and consequently telomere maintenance capacity in human immune-system cells. Given this finding and the pilot nature of this study, we report these increases in telomerase activity as a significant association rather than inferring causation. Larger randomized controlled trials are warranted to confirm the findings of this study.”

What they mean here is that the number of patients in the study was low (N=30 is very small for a study of this type, and only 24 of these could actually be followed up the multiple times needed over this three-month period for technical reasons), the patients were pre-selected as having a clinical diagnosis of possible “low-risk prostate cancer” (that is, not a random group and probably motivated for a positive outcome), and that the results can at best be interpreted as an association and not necessarily a cause of the three-month lifestyle change (that is, just because thus group showed an increase in their telomerase activity, it doesn’t mean it resulted from the lifestyle intervention, but it could be the result of any one of a number of variables that were unaccounted for during this period, sometimes referred to as “confounders”).

But larger randomized properly controlled trials are expensive to run, and without a serious backer—the government or a drug company—don’t expect to see a follow-up any time soon. Just think about the large-scale trails of vitamin E that after many years and millions of dollars not only failed to establish a link but also showed a possible negative association. This is part in parcel of the tough love and art of large-scale clinical trials that are required if you want to prove something using rigorous scientific methods. 

So what did this study actually show? At minimum they showed what was needed for carrying out a larger study (power calculation) to actually determine a causal relationship. No mechanism was defined for why telomerase activity increased, although several were suggested (reduction in oxidative stress and inflammation, for example). Otherwise one shouldn’t draw too many conclusions from this study, especially since three independent variables were introduced (diet, exercise and yoga) and the study group was so small and biased. And one has to also keep in mind that the telomere length was not directly measured, as the authors themselves pointed out that telomere length changes would likely to be too small to measure in such a short time (three months). So I guess there’s another message to take home: some things take time.

Reports like these remind me of one of the reasons I have sympathy for the “N of 1” studies, that is, experimenting on yourself. Not real science, but you’ve got to try something. Take up yoga, improve your diet, have a walk everyday, and see what happens. 

Subscribe to YOGA FOR HEALTHY AGING by Email ° Follow Yoga for Healthy Aging on Facebook

Read More

Clarification: Aging, Yoga and Science

by Brad

Winter Trees by Brad Gibson

Today’s post is largely in response to the question: How would one go about investigating the effects of yoga on aging scientifically? Before tackling this question—which I will get to in the next week or two—I will first attempt to define or at least discuss a few key terms and assumptions. The reasons for this will hopefully become clear.

In the broadest the terms, “aging” applies to how systems or entities change with time. To inanimate objects, such as your new car or jacket, this begins right after it’s manufactured or, more relevantly, after you bought it. This process of aging can be rapid or slow (weeks, months, or years), and depends a lot on what the object is and what it was designed for. In biological systems (including us), we typically think of aging as starting after development, or post-puberty in our case. We also tend to associate aging with a decline and/or loss of functions, both physical and mental. However, aging can include more positive properties or phenotypes, such as increased knowledge and skill sets, and it isn’t all that hard to name a few that fit into this category. But in most biological scientific studies of aging, we refer to aging mostly in the former sense, i.e., an accumulation of mostly pathological properties, such memory loss, frailty, neurodegenerative diseases, bone loss, muscle loss, and so on. Surprisingly there are quite a few competing theories of basic aging, such as error accumulation, telomere shortening, antagonistic pleiotrophy, free-radical theory, and entropy, just to name a few. What all (or most) of these theories seek to address is the underlying molecular and physiological event that drives these largely negative processes. 

The term “successful aging” is more recent, having come into wide use in the last few decades. If you want to read more about this concept, I found the first chapter in the book Successful Aging: Perspectives from the Behavioral Sciences by Paul and Margaret Baltes quite useful (for information see Cambridge ebooks). 

Even last week as I read the science section of the New York Times (see NY Times), I came across a short review of a just-published study on “Alcohol Consumption at Midlife and Successful Ageing in Women: A Prospective Cohort Analysis in the Nurses Health Study” (see PLOS). In this prospective correlative study, researchers at Harvard demonstrated that a modest increase in successful aging for women who consumed small, but regular amount of alcohol at mid-life. (Maybe a glass of wine after yoga class isn’t such a bad idea after all?). Here they defined "successful aging" in a more precise manner: "as being free of 11 major chronic diseases and having no major cognitive impairment, physical impairment, or mental health limitations." Of course, this more operational definition to successful aging made it easier to make clear and objective distinctions among the woman in this group, typical of population based epidemiological studies. 

When we chose the term ‘healthy aging’ for this blog, the purpose was to provide information not on just how practicing yoga might help to avoid or reduce your chances of acquiring one or more of these age-related losses, but also to better manage and minimize their impact when they occur. Indeed, this is the position most of us are in, whether is through the vagaries of our genetic background, chance, past behavior, or whatever. (This reminds me of the joke: Q: What’s the best thing you can do to insure a long life? A: Choose your parents well.) So as I go back and reconsider the original question on how science can study the relationship of yoga and aging, I will reframe this question a bit: How can science study the effects of yoga on our overall physical and mental health as we age? I’ll tackle this question next time…. But as a preview, there are few good places to start, including the 2009 pilot study in Lancet on comprehensive lifestyle changes and telomere length (a biomarker of aging and cellular senescence) and several recently funded NIH studies examining yoga’s effects on depression, fatigue, and menopause. 

And please leave any questions for the Friday Q&A in the comments.

Subscribe to Yoga for Healthy Aging by Email ° Follow Yoga for Healthy Aging on Facebook ° Join this site with Google Friend Connect

Read More