Can you trust your own judgment about health/fitness?

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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Just wanted to highlight a book excerpt that ran in the New York Times Magazine over the weekend, from Nobel Prize-winning psychologist Daniel Kahneman’s forthcoming book “Thinking, Fast and Slow.” It’s about our general tendency to place great faith in our own explanations for things, regardless of whether the facts bear them out:

The confidence we experience as we make a judgment is not a reasoned evaluation of the probability that it is right. Confidence is a feeling, one determined mostly by the coherence of the story and by the ease with which it comes to mind, even when the evidence for the story is sparse and unreliable. The bias toward coherence favors overconfidence. An individual who expresses high confidence probably has a good story, which may or may not be true.

[…] When a compelling impression of a particular event clashes with general knowledge, the impression commonly prevails.

The main example he discusses in the excerpt is the world of finance — many, many people (including just about everyone I know, seemingly) are convinced that they or their financial advisors are capable of outperforming the market, despite ample evidence that this is nearly impossible to do on a consistent basis. But the good stock picks they’ve made over the years make such a vivid impression that they remain convinced of their abilities.

The reason I’m blogging about this here is that I think this phenomenon is also nearly universal when it comes to health and fitness. Of course, there are many people who either don’t believe in or don’t understand the scientific method. They trust their instincts in figuring out which potions and pills are helping them in vague and unquantifiable ways. This is not surprising at all. What is surprising to me is the number of people who understand and profess belief in the scientific method, who murmur all the right catchphrases about “correlation is not causation” and “of course n=1 anecdotes don’t mean anything,” and yet are still absolutely convinced of their ability to determine which stretch has enhanced their power or saved them from injury, or which pill makes them feel more energetic, or which type of training has enhanced their lactate clearance.

There is some good news at the end of Kahneman’s excerpt: it is possible to have real intuitive expertise. (“You are probably an expert in guessing your spouse’s mood from one word on the telephone,” he notes. Chess players and medical diagnosticians are other example.) But there’s a necessary condition:

Is the environment in which the judgment is made sufficiently regular to enable predictions from the available evidence? The answer is yes for diagnosticians, no for stock pickers.

Maybe I’m just a particularly complicated human, or unusually incapable of reading my body’s signals. But given the huge number of factors, both intrinsic and extrinsic, that affect the day-to-day variation in my mood, energy and physical performance, I don’t consider my own body “sufficiently regular” to be able to make accurate judgements about the efficacy of any particular single intervention.

Aging: does the average decline as much as the extremes?

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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My Jockology column in today’s Globe and Mail takes another look at aging and physical decline:

It’s the chicken-and-egg question of aging: Do we become less active as we get older because our bodies start to break down, or do our bodies start to break down because we allow ourselves to become less active?

For years, it was widely accepted that humans would start getting slower, weaker and more fragile starting in their 30s. But new studies on topics ranging from the cellular mechanisms of aging to the time-defying performances of masters athletes are forcing researchers to question this orthodoxy. It seems increasingly likely that the first signs of decline are more a function of lifestyle than DNA: If you keep using it, you’ll be well into middle age before you start losing it. [READ THE WHOLE ARTICLE…]

One of the studies discussed in the article is this analysis of the finishing times of 900,000 German marathoners and half-marathoners, published last year. The researchers argue that the rate of decline of mid-packers is a better way of judging “natural” aging processes compared to the outliers who set age-group world records. For fun, I plotted the average finishing times of the runners in the German study, and superimposed the curve that you’d get if they declined at the same rate as age-group records. It’s pretty clear that this group of midpackers does decline at a slower rate:

 

Stress fractures: is it weak bones or muscles?

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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A new study from researchers at the University of Calgary, published in the November issue of Medicine & Science in Sports & Exercise, looks at bone quality and leg muscle strength in a group of 19 women who have suffered stress fractures in their legs, and compares them to a group of matched controls. The basic results:

  • the women who got stress fractures had thinner bones;
  • at certain key locations, the quality of the bone was lower in the stress fracture group;
  • the stress fracture group also had weaker leg muscles, particularly for knee extension (lower by 18.3%, statistically significant) and plantarflexion (lower by 17.3%, though not statistically significant).

Now, this sounds very similar to the results of a University of Minnesota study published a couple of years ago. Here‘s how I summed up the conclusions reached by those researchers:

What’s interesting, though, it that the bone differences were exactly in proportion to the size of the muscles in the same area, and there was no difference in bone mineral density. What this suggests is that the best way to avoid stress fractures is to make sure you have enough muscle on your legs — presumably by doing weights and (it goes without saying) eating enough.

What I don’t understand is that, in the new Calgary study, even though they mention the Minnesota study repeatedly in their discussion, they don’t discuss at all this idea that it’s the lower muscle strength that dictates the reduced bone size and thus the stress fracture risk — even though that was the primary conclusion of the Minnesota study. Instead, they say “the role of muscle weakness in [stress fractures] is unclear from previous studies,” and suggest that weaker knee extension might change running form to produce a “stiffer” running stride or somehow alter the direction of forces on the bone during running — both of which seem like unnecessarily complex and speculative ideas compared to the straightforward link between muscle strength and bone strength.

It’s entirely possible that I’m missing something here, because the paper is quite complex. But what I take away from it is, once again, that strengthening your legs is likely (though not yet proven in a prospective trial) to reduce your stress fracture risk.

Good diet trumps genetic risk of heart disease

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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I posted last week about “epigenetics” — the idea that, while the genes you’re born with are unchangeable, environmental influences can dictate which of your genes are turned “on” or “off.” A few days later, I saw a mention of this PLoS Medicine study in Amby Burfoot’s Twitter feed. It’s not an epigenetic study, but it again reinforces the idea that the “destiny” imprinted in your genes is highly modifiable by how you live your life.

The study mines the data from two very large heart disease studies, analyzing 8,114 people in the INTERHEART study and 19,129 people in the FINRISK prospective trial. They looked at a particular set of DNA variations that increase your risk of heart attack by around 20%. Then they divided up the subjects based their diet, using a measure that essentially looked at either their raw vegetable consumption, or their fresh veg, fruit and berry consumption. Here’s what the key INTERHEART data looked like:

Breaking it down:

  • The squares on the right represent the “odds ratio,” where the farther you are to the right (i.e. greater than one), the more likely you are to have a heart attack.
  • The top three squares represent the people who ate the least vegetables, and the bottom three squares are those who ate the most vegetables.
  • Within each group of three, GG are the people with the “worst” gene variants for heart attack risk, AG are in the middle, and AA are the people with the least risk.

So if we look at the top group first, we see exactly what we’d expect: the people with the bad genes are about twice as likely to suffer a heart attack as the people with the good genes. But if you look at the middle group (i.e. eat more vegetables), the elevated risk from bad genes is down to about 30%. And in the group eating the most vegetables, there’s essentially no difference between the good and bad genes.

How does this work? The researchers don’t know — partly because no one’s even sure exactly how the bad gene variants cause higher risk. (There are some theories, e.g. that it affects the structure of your veins and arteries.) But the practical message is pretty clear: if you eat your veggies, you don’t have to worry about this particular aspect of your genetic “destiny.”

How quickly is water absorbed after you drink it?

THANK YOU FOR VISITING SWEATSCIENCE.COM!

As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

I’ve always been curious about this. Sometimes, after drinking a big glass of water, it seems like I pee it all out literally just a few minutes later. Is this just in my head, or is ingested fluid really processed that quickly? A new study by researchers at the University of Montreal, published online in the European Journal of Applied Physiology, takes a very detailed look at the kinetics of water absorption and offers some answers.

The study gave 36 volunteers 300 mL of ordinary bottled water, “labelled” with deuterium (an isotope of hydrogen than contains a proton and a neutron instead of just a proton) to allow the researchers to track how much of that specific gulp of water was found at different places in the body. They found that the water started showing up in the bloodstream within five minutes; half of the water was absorbed in 11-13 minutes; and it was completely absorbed in 75-120 minutes.

Here’s what the data looks like:

On the left, it shows how quickly the water was absorbed in the first hour, measured in the blood. On the right, it shows the gradual decay of deuterium levels over the subsequent 10 days, measured from urine samples. This, of course, shows that when I pee after drinking a glass of water, I’m not peeing out the same glass of water! Within ~10 minutes, fluid levels in my blood will have risen sufficiently to trigger processes that tell me to pee — but, according to this data, it takes about 50 days for complete turnover of all the water in your body.

The other wrinkle in this data is that the subjects showed two distinct absorption patterns (shown on the bottom and top), with about half in each group. In the top group, the water is very rapidly absorbed into the blood (possibly because these people get water out of the stomach and into the small intestine very quickly) before running into a slight bottleneck as the water is then distributed throughout the body to all the extremities. The second group, on the other hand, doesn’t hit this bottleneck: the flow of water out of the stomach and into the small intestine is slow enough that extra water doesn’t have a chance to build up in the blood before being distributed throughout the body.

So what does this all mean? I don’t have any particular practical applications in mind — I just thought it was kind of cool.