Training and nutrition linkfest, vol. 5

First of all, we are cautioned to be skeptical of results that are too spectacular.  (Where have I heard that before?)  Chris over at Conditioning Research points out that the famous triathlete CT scans may not be all that they seem.  He quotes Renaissance Exercise thus:

There are amazing CAT scans contrasting the muscularity of triathletic and sedentary elder men. It is apparent that destroying your body in a triathlon can, at least, maintain your muscularity. Or, perhaps the difference is completely due to a genetic aberration whereby the above-average muscularity of the elder man merely enables him to destroy his body in the triathlon. Of course, it is also true that such activities are sarcopenic.

(Emphasis his.)

In other words, the scans tell us that (some) 70yo triathletes are in much better shape than (some) 70yo sedentary individuals.  Whether they’re in better shape because they’re triathletes or whether they’re triathletes because they’re in better shape (and whether their vastly increased lean muscle mass is due to diligent exercise or random chance) is not indicated by the CT scans.  In any case, we should not take triathlons to be anabolic.


Next, Karl Smith points us to a potential breakthrough:

The “obesity molecule” in question is our good friend and xenoestrogen bisphenol-A.  Definitely not something you want to consume in large (or even in small) quantities, but is it responsible for the obesity epidemic?  Karl advocates caution, but thinks it’s plausible:

BPA looks exactly like what we would expect the obesity molecule to look it from a macro point of view. Its something that was suddenly everywhere. It works on a key channel. Even without any direct empirical evidence it would a plausible candidate for “metabolic lead.”

According to Wikipedia, BPA entered mainstream use in the 1940s.  My favourite chart ever —

— seems to indicate that the “obesity epidemic” really took off in the late 1970s.  Is this a matter of 30 years of BPA accumulation being necessary to bring about critical changes (the 1971 datum shows no deviation from previous trend; I’d expect something like a xenoestrogen to have effects proportional to its prevalence and/or accumulation, but then again I’m just a glib dilettante), or an indication that while BPA isn’t exactly something you want to seek out it’s not the smoking gun Karl’s looking for?

Either way, yes, (xeno-)estrogen levels and adipose tissue are correlated.


Speaking of warnings, Peter at Hyperlipid reminds us that unsaturated fats are far from the happy friendly substances they’ve been made out as:

“NASH” here expands to “Non-Alcoholic SteatoHepatitits”, or fatty liver disease without all the drinky-drinky.  Seems that a bunch of lab mice were fed a high-fat (ketogenic) diet and developed a rather nasty case of cirrhosis.  Poking around, Peter discovers that the mice were fed rather a lot of polyunsaturated fats, and digs up another paper to support this advisory:

If you are going to eat a very high fat diet in the long term, you should pay serious attention to PUFA creep. Having cirrhosis is not likely to help you make old bones in good shape. Perhaps go easy on the commercial mayonnaise and just spread some butter on your cheese… Actually I tend to add butter to my beef if it’s too lean (only happens when eating out, no way we would choose lean beef to cook at home!)…

It makes me wonder about saturophobes who might be swilling PUFA to lower their LDL and triglycerides, with or without a LC diet… More potential victims of the cholesterol hypothesis I suppose.

Those of you eating paleo, primal, archevore, or some other variant of “meat, leaves, and berries” may wish to note that chicken and pork, particularly if factory farmed, tend to have rather worse n3:n6 ratios than ruminants or seafood (can’t find the source for that, but it was probably on the Whole9 blog somewhere).  This may tempt you to add in more and more fish-oil caps to compensate.  Peter’s findings suggest that this isn’t a great long-term plan.


Next, a modern classic: Martin Berkhan debunking a huge whack of Conventional Wisdom and bro-science about intermittent fasting:

Click through and RTWT, then send it to all your friends.


Finally, here’s a lessons-learned article from Eric Cressey:

Points 1. and 7. (“The generalist is a dying breed” and “The basics are more important than ever”) make an interesting contrast.  If I read point 7 correctly, Eric’s saying that as athletes specialize in certain movement patterns to reach the highest levels of their sport, they (necessarily?) neglect other forms of athleticism which need to be trained at a more basic level.  Seems to me that the same thing holds for specialist trainers and practitioners — and for their clients.


10 Responses to “Training and nutrition linkfest, vol. 5”

  1. February 17, 2012 at 14:41

    I am guessing that xenoestrogen is a catalyst.
    Some people can eat tons of metabolism-destroying non-food and not get fat. Indeed, I seem to be one of them.
    What if, before xenoestrogens, that was most people? it seems pretty clear that estrogen should have fat-accumulating effects.
    What would that chart have looked like if the food pyramid had came in the 40s, and BFA in the 70s?

    I’m caricaturing the hypothesis somewhat; using a simplified, exaggerated version and adding in complications only as necessary. Because it should hold up in the caricature phase, if true. Whereas if even a caricature is obviously false…

    • February 17, 2012 at 15:08

      I am guessing that xenoestrogen is a catalyst.

      Good call. I don’t think it’s initiating the obesity cycle, but I’ll cheerfully believe that it’s speeding up the feedback loop by encouraging adipose tissue accumulation, which is itself estrogenic.

      A third variable that neither hypothesis considers is food abundance. If food is cheap enough to make its availability basically a non-issue, people can eat all they want (which is all the time once insulin- and leptin-resistance set in), which not only cranks up the insulin/leptin-resistance feedback loop but may also increase exposure to xenoestrogens like BPA.

      Furthermore, it keeps mTOR active at the cellular level, which (briefly) keeps the cells in “gimme moar!” mode. This is among other things a major cancer risk. I’m just starting to skill up on the mTOR/AMPK cycle, which my intuition says is somewhat similar to the leptin/ghrelin cycle but on an intracellular level. Once I’m less ignorant about it I’ll write something up.

      So you’ve got three events all showing up roughly at once: The presence of xenoestrogens in the food supply; the ability to eat basically whenever you damn well please; and a shift in Common Wisdom towards foods that are highly insulinogenic and non-satiating. My intuition tells me that BPA is the least of these factors, but that doesn’t mean it isn’t significant.

      How do you fix it? Archevory, intermittent fasting, resistance training for skeletal muscle hypertrophy, and sprinting. Restore insulin/leptin sensitivity and get the mTOR/AMPK cycle back on track. Minimizing chronic inflammation fits in here somewhere, too.

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