New research supports a thesis that makes us feel all warm and fuzzy inside – and that feeling itself is good for our health and longevity.  People who seek gratification through personal aggrandizement and accumulation of wealth may achieve a kind of hedonistic satisfaction, but this leads to negative health consequences and shorter life span.  Meanwhile, people who seek fulfillment through service, dedication to cooperative efforts and shared values tend to have better health and longer lives.

The dominant theme of my research this last dozen years is that aging arose from an evolutionary conflict between that which is best for the individual and that which is best for the community.  Best for the individual is to go on living and reproducing, the longer the better.  Best for the ecosystem is to have a stable death rate to help avoid overpopulation, leading to collapse.  Without aging, everyone would likely be dying at once in times of overcrowding and severe scarcity.  Better is a fixed life span that stabilizes the population dynamics.  Even better is an adaptive life span which rises and falls in such a way as to complement the cycles of “external” deaths from starvation and disease.

Typically, life spans are not fixed, but plastic in response to environmental cues.  Almost always we can find some communal benefit in the relationship between life span and external conditions.  The best example is the Caloric Restriction effect, which is an adaptation to help protect the community from population collapse in times of famine.  Aging also responds to other environmental challenges, and to crowding.

Man is a social animal, and a significant piece of our evolution has occurred in the hundreds of thousands of years since primates began to live in structured social groups or tribes.  That suggests we might expect our life span to depend on social factors.  It is an effect worth looking for to see if leaders and important community members live longer than “disposable” rank-and-file workers.  There is some indication this is true, including a new study this week that connects aging to the satisfaction derived from constructive engagement with the community.

Thirty years ago, the British Whitehall Study first documented a relationship between mortality and status among civil servants.  The British system ranks public employees in a detailed grading system.  The mortality rate among men at the lowest grade was more than three times as high as the rate at the highest grade.  Differences in mortality persisted into retirement, producing a marked effect of social station on life expectancy.  The disparity was too large to be explained by differences in access to health care, or by the better self-care associated with education.  Right up into the highest employment grades, status was a predictor of life expectancy.

This suggests to me that we sense our importance in the community, and that our bodies respond by modulating our aging according to how much the community needs us.

Marital status is another well-known link to longevity.  “The unmarried live a relatively isolated existence that lacks the close interpersonal ties that the data suggest are a factor in maintaining a sense of well-being,” [Gove, 1973] and this translates into a mortality risk, larger for men than for women.  This table gives the mortality risk of various categories of unmarried people compared to married at different ages.  The numbers translate to several years’ difference in life expectancy, just a little smaller than the difference associated with smoking status.

Depression is a big risk factor for mortality, not just because of the risk of suicide, but also for association with increased rates of heart disease and cancer.  Of course, those who suffer depression tend to take care of themselves less well; but even accounting for all these factors, there appears to be a substantial physiologic response to depression that predisposes depressed people to all the diseases of old age.  Here is a meta-analysis concluding that people diagnosed with depression have an age-adjusted risk of dying that is 1.8 times as high as those who are not.

In a paper last year, UCSF psychologists linked depression to lower social status.  They theorized that oppressed people have bottled-up anger which it is objectively dangerous to express, so they learn to suffer quietly and depression is the price they pay.  Some research has linked depression to accelerated aging through telomere shortening, though this is disputed.

I have wondered about the evolutionary meaning of depression.  What adaptive purpose could it serve to put us into a passive state, with deadened senses and a narrow range of emotional responses?  Certainly depression is not good for individual survival or reproduction.  My guess is that depression evolved as a way to make feudal social orders tolerable for the serfs.  Depression is a response to powerlessness that prevents rebellion and promotes an imposed social cohesion.  I assume that much of the natural selection on early humans was tribe-vs-tribe competition, and those tribes in which the peons were depressed and subservient were able to out-produce and to prevail in armed conflict against those tribes in which every individual was thinking independently.

This week’s news

Your vocabulary word for the day is eudaimonic, an adjective that describes the feeling of happiness and well-being that is derived from engagement with a social mission.  The contrary is hedonic happiness, which refers to success in pursuit of more selfish ends.  A Florida research team looked at gene-expression profiles associated with inflammation and auto-immune responses that are associated with most of the pathologies of old age.  Our genes don’t change through a lifetime, but the patterns of which genes are turned on and off show an age dependence.  As we get older, inflammation and auto-immunity are part of a program of gradual self-destruction.  The Florida team found a link between hedonic happiness and expression of these self-destructive gene patterns.  Eudaimonic happiness had the opposite association, a link to younger, healthier gene expression profiles.  It seems that virtue provides its own reward.

I read the evolutionary context for this loud and clear: aging is a social adaptation, self-destruction whose purpose is to help keep the community stable and dynamically adaptive.  Everyone must take his turn making this sacrifice, but the community does well to hold on longer to those who are contributing most to robust and cohesive social functions.

But I notice that Steven Cole, the behavioral geneticist from UCLA who wrote up this work, tries to interpret his results in terms of individual benefit which mysteriously fails, rather than attributing to it a group selective purpose.

“This response likely evolved to help the immune system counter the changing patterns of microbial threat that were ancestrally associated with changing socio-environmental conditions; these threats included bacterial infection from wounds caused by social conflict and an increased risk of viral infection associated with social contact,” said study senior author Prof Steven Cole of the University of California, Los Angeles.

“But in contemporary society and our very different environment, chronic activation by social or symbolic threats can promote inflammation and cause cardiovascular, neurodegenerative and other diseases and can impair resistance to viral infections.”

This attitude is all too common in a pattern stretching back to the 1970s when evolutionary scientists began imposing an ideological purity that excludes group selection.  There is now a substantial minority of evolutionists who have taken a professional stance in support of group selection, but around the periphery of the field, few researchers are willing to pay the price of pushing back against this prejudice.

The Message

Get out there and work, in cooperation with others, for a better world.  Better yet, become a leader in progressive social movements.   You’ll feel better and live longer.

_______________

 Notice
I am traveling in Europe this next week, and may not post anything.
But the following week I will be at Aubrey de Grey’s SENS conference, Re-imagine Aging in Cambridge, and you’ll get a full report on Sept 8.  Stay tuned also for a major update in September to my Aging Advice page.

       “If I meditate, will I live longer?”

I am passionate about my own longevity.  I have a daily meditation practice.  I teach a weekly yoga class (a small part of my time, a large part of my life).  As a scientist, I study aging from a  practical as well as an evolutionary perspective.  I would dearly like to answer “yes” to this question.  But in my readings the last few days, the best answer I can offer is, “there are some data that hint in that direction.”  I can’t justify a more definite answer, and in fact I suspect that the question cannot be posed in experimental terms.  Still, there’s a lot more that could be done.

Imagine designing an experiment – even an idealized experiment – to test the effect of meditation on life span.  Animal models are useless.  Best would be to take a diverse group of people, divide them into two statistically-matched subgroups, and instruct one group to meditate and the other not to.  Everything else about their lives should be kept the same.  But meditation doesn’t work that way.  Over any substantial period of time, meditation practice is likely to change attitudes and habits and occupations.  These two groups of people will no longer be comparable.

This is just one of the pitfalls in trying to scientifically evaluate claims about meditation and life expectancy.  Of course, experiments with real human subjects must respect their freedom.  Realistically, all we can do is to compare a set of people who meditates with another set who do not meditate.  We can select them in such a way to match their ages, their sexes, their weights, diets, exercise habits, incomes and ethnicities.  But these groups will have had different life experiences, different social environments, and their attitude toward life will not be similar.  People who choose meditation have a take on the world and a set of values that likely leads them to pay more attention to care for themselves and others.  The culture and pratice of meditation are both conducive to that.  These social determinants of longevity are quite important, and any epidemiological study of meditation must use a combination of selection and ANOVA to compensate for inevitable differences between the two groups.  (ANOVA stands for Analysis of Variance, and it is a common mathematical procedure for separating and evaluating various contributing causes of one outcome.)  There would be inevitable ambiguity in how to translate the question into statistical terms.  For example, a person may tell you that his meditation practice led him to give up smoking.  Do we compare this against a matched control who continues to smoke, or to a subject who quit smoking without practicing meditation?  Do we count the benefits of improved self-care as part of the benefit of meditation, or do we factor it out as if it were an independent decision?

The study we are imagining would have to include a large number of subjects with detailed information about each individual’s health and life style.  It has never been attempted, to my knowledge.  The studies that have been done are far more modest, and so the evidence that we have is at best tentative and indirect.

 

The studies that we do have fall in three categories:

• Meditators tend to be healthier.  But how much of this is because people who make a commitment to meditation are more likely to care for themselves better in other ways?

For example, in a new article (Hoge 2013) naively measures telomere length in people who meditate and people who don’t. While they find a significant difference, it’s not warranted to interpret this as an effect of the meditation, because people who meditate are likely to take care of themselves better in other ways as well.

• Before/after comparisons of physiology of meditators.  This is very helpful and suggestive, but we must always be careful about imputing long-term benefits from a short-term response, because there are short-term challenges (like exercise and fasting) to which the body responds in ways that slow aging in the long run.

• A large but questionable scientific literature that is funded by the Transcendental Meditation establishment, which has cash to spend and a product to sell.  I regard this research with the same skepticism as drug trials sponsored by the drug’s manufacturer.  Walton reviewed this literature a few years ago.

The best work in the field comes out of the AME center at UCSF (Aging, Metabolism and Emotion).  I was impressed with one study for its clean design and significant outcome.  30 participants in an intensive meditation retreat were compared with a matched group of 30 people on a waiting list for the same retreat.  Telomerase activity was measured to be 40% higher on average in the retreatants.  I have written in this column and elsewhere that I believe telomere length is not just a predictor but a cause of aging and mortality.  A 40% increase in telomere activity sounds like a very significant number, but the catch is that the base telomerase in humans is very low.  For the most part, telomere length is in free-fall through a lifetime, and it is not clear that 40% more telomerase is enough to help that.

From the TM literature, here is a study (Walton, 2002) that demonstrates a reduction in blood pressure from meditation.  Now, it’s true that high blood pressure predicts heart attacks, but it’s not necessarily true that lowering blood pressure addresses the root cause of the problem, as I’ve argued a few weeks ago in this column. Atherosclerosis increases blood pressure and atherosclerosis increases risk of a heart attack.  But decreasing blood pressure without addressing the underlying atherosclerosis may not have a benefit.

The most relevant of the studies from the Maharishi Institute looked at a group of 202 older people identified as elevated risk for heart disease.   They were trained in Transcendental Meditation, and Schneider et al found a 23% reduction in all-cause mortality over 7 years.  This sounds impressive, until you realize how small the sample was.  The result was barely statistically significant.

Here is a study by Richard Brown of Columbia that finds health benefits from yogic breathing exercises, and extrapolates from there to speculate on life expectancy.

There’s a column in Huffington Post this week by Aditi Nerurkar that parallels some of my conclusions.

 

My Own Suggestions for Studies I Would Like to See

#1

Collect vital statistics from a variety of meditation studios and Buddhis sanghas for members who have died in recent years, and compare to similar statistics from selected church groups.

#2

Train a group of cancer patients in healing meditations focused on their particular ailment, and compare outcomes to a control group trained in a generic meditation technique.

#3

Here’s a thought: as real-time assays for telomerase become more practical, perhaps it will be possible to measure an individual’s telomerase levels while she is meditating.  In biofeedback therapy, people have learned to control a great many body functions that were previously thought to be autonomic: heart rate, temperature of a particular body part, electrical activity in a specific part of the brain.  Most people can learn to do this, though they can’t tell you how.  The protocol is simply to provide the person with real-time feedback about any measurable property of his body, and very often the person learns after a number of sessions to make the meter move in the desired direction.

Maybe we could learn to express telomerase.  Maybe there are other markers of the rate of aging that we could learn to modulate if only they were measured so that we could be offered real-time feedback.

 

The Bottom Line

I think there probably is a benefit from meditation for health and longevity, but it is difficult to substantiate this from the available studies.  All the evidence is indirect.  Perhaps the best justification for my position is that meditation has been found to increase positive affect, and people who are happier live a lot longer (“the nun study”).  There seems to be a connection between chronic stress and aging, but it’s not about the objective pressures a person is under, but rather the attitude and the way in which the challenges of life are perceived.  This is a central theme in the work of Elissa Epel, who first discovered the stress/telomere connection.

Studies that come out of Maharishi University are not of high quality, and aside from these there is a regrettable lack of attention to a practice for which there is preliminary evidence of broad psychological and physiological benefits and no down side.

For many of us, it is difficult to muster the consistent determination to focus our minds for a practice that we know will make our lives better. Maybe it will help to have the additional motivation that it will also make our lives longer.

Low-dose daily aspirin was an idea born in the 1960s, based on the insight that aspirin prevents blood clots and blood clots are the proximate cause of heart attacks and stroke.  Millions of people were advised by their doctors to take aspirin daily, and as a result there was a large group of people available for long-term health studies.  This led to an accidental discovery that aspirin slashes risk of many kinds of cancer and may have benefit preventing Alzheimer’s Disease.  Today, the medical consensus still favors daily aspirin, but the benefit for heart health is secondary.

Back in October, I reported on an article in Science Magazine claiming that daily aspirin can lower your risk of mortality by 13%.  I calculated this might add 2 years to life expectancy – and it’s easy and essentially free.  By the time it gets to Science Magazine, this is a mainstream position, meaning that although there is dissension (also here), the pro-aspirin view is now the majority.

The benefits of aspirin come from two quite different mechanisms, and my purpose in this column is to tease them apart.  One might legitimately be called “anti-aging”.  The other is more analogous to wearing seatbelts. Seatbelts lower your risk of dying but it would be a stretch to say that they make you younger.

The first benefit of aspirin is that it “thins the blood”.  (More technically, it inhibits the chemistry that makes blood clot.)  It turns out that, though chronic damage to the arteries sets the stage for heart attacks and strokes, the precipitating incident is usually a blood clot that gets snagged in the wrong place and denies blood supply to either the heart or the brain (“ischemia”), until, after just a minute or two, they suffocate.  Blood clots in the brain are the principal reason for stroke, and blood clots in the coronary artery can cause sudden cardiac death.  To the extent that these actions are responsible for its benefits, aspirin should be described as a “safety drug” rather than an anti-aging tonic.

The second mechanism, the one that I think of as “anti-aging” is to lower inflammation.  As we get older, our bodies slowly destroy themselves, and one of the principal mechanisms is to turn the inflammation process against healthy tissue.  All the diseases of old age are linked to chronic inflammation.

• Inflammation can turn normal cells into cancer cells.

• Inflammation in the arteries causes the damage that leads to plaques and then strokes and heart attacks.

• Inflammation in the joints causes arthritis.  (There was a time when osteo-arthritis was distinguished from rheumatoid arthritis, and the former was blamed on abrasion building up over a lifetime, while only the latter was attributed to inflammation.  But the modern view is that they are not so different, and that osteo-arthritis is also an inflammatory disease.)

• Inflammation is linked to brain damage and dementia.

So just by dialing down inflammation in a dumb, non-specific way, aspirin can lower risk of all these diseases.  In the young body, inflammation is an essential part of our immune defense, and has an important role in replacing damaged tissue.  But by the time we get to be 50+, inflammation is already causing more harm than good.  In this sense, anti-inflammatory is close to anti-aging.

If aspirin’s benefit comes from reducing inflammation then if you take aspirin from age 50 to age 80, say, then you are functionally a year or two younger than you might have been at the same age had you not taken aspirin.  If you stop taking aspirin on your 80th birthday, your body is that much younger, and the benefit stays with you still.  But if the only benefit comes from preventing fatal blood clots, then if you were to stop taking aspirin at age 80, your mortality risk would jump quickly back up where it would have been had you never taken aspirin at all.  You might attribute your survival for those 30 years in part to the benefit of aspirin, but you would not be better off than if you had survived to age 80 by sheer luck.

Separating these two effects of aspirin is not so easy because there is a strong physiological connection between the them.  Inflammation is suppressed by inhibiting COX-2, and blood clots are suppressed by inhibiting COX-1.  These are abbreviations for two forms of the enzyme cyclooxygenase.  Aspirin, like most NSAID drugs act on both COX-1 and COX-2.

(Rofecoxib=Vioxx is the only one that is completely specific to COX-2, without affecting COX-1.  Vioxx worked well against inflammation, but was found to increase risk of heart attack, and was withdrawn from the market in 2004.  But why should inhibiting COX-2 without COX-1 increase risk of heart attacks?  In the infamous VIGOR study, hidden data showed 4x as many heart attacks in patients taking Vioxx.  I have found no attempts to answer this question.)

Another interesting footnote:  Ibuprofen, the second most common NSAID, inhibits clotting in the same league with aspirin.  But the anti-clotting effect of aspirin lasts 5 days, and of ibuprofen just 1.  Here’s the curious part: if you take aspirin and ibuprofen together, the effect lasts just 1 day.  Evidently, ibuprofen blocks the long-term effects of aspirin.

By my reasoning, aspirin’s action in lowering heart risk ought to be a combination of these two kinds of actions.  But the message from Vioxx suggests that this benefit comes entirely from the first benefit, COX-1 and “blood thinning”.

But to the extent that aspirin lowers risk of cancer and Alzheimer’s disease, the effect must be due to COX-2 and the anti-inflammatory action.  There is powerful evidence that aspirin lowers risk of gastro-intestinal cancers and lung cancer.  There is also evidence for a less dramatic effect on other important cancers, including breast and prostate cancers.

Daily intake of NSAIDs, primarily aspirin, produced risk reductions of 63% for colon, 39% for breast, 36% for lung, and 39% for prostate cancer. Significant risk reductions were also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after five or more years of use and were stronger with longer duration. Observed protective effects were also consistently stronger for gastrointestinal malignancies (esophagus, stomach, and colon). Results for pancreatic, urinary bladder, and renal cancer were inconsistent. Initial epidemiologic studies of malignant melanoma, Hodgkin’s disease, and adult leukemia also found that NSAIDs are protective. A few studies suggest that ibuprofen has stronger anticancer effects than aspirin, particularly against breast and lung cancer. – (from  R.E. Harris et al, 2005)

There are still researchers who claim that aspirin offers no benefit at all for cancer.  Here is a study that found no reduction in cancer risk for a low dose of 1 baby aspirin every other day.

Results from this large-scale, long-term trial suggest that alternate day use of low-dose aspirin (100 mg) for an average 10 years of treatment does not lower risk of total, breast, colorectal, or other site-specific cancers. A protective effect on lung cancer or a benefit of higher doses of aspirin cannot be ruled out.

Conclusion

Aspirin’s blood-thinning and anti-inflammatory effects both contribute substantially to disease prevention.  The first is primarily associated with COX-1 and roughly 10% reduction of heart disease and stroke.  The second is assoiated with COX-2 and roughly 40% reduction in risk of cancer.