I am hoping it was advice specifically given for wait loss, emphasising that just adding light exercise will not see large results in many cases. As an independent observation it would be terrible.
Yes, but that shows that Eliezer probably misremembered what the 40% referred to. In that study, “40%” refers not to how many didn’t benefit, but rather to the maximal benefit on a particular measure of fitness received by any of the participants:
For example, the team found that training improved maximum oxygen consumption, a measure of a person’s ability to perform work, by 17% on average. But the most trainable volunteers gained over 40%, and the least trainable showed no improvement at all. Similar patterns were seen with cardiac output, blood pressure, heart rate and other markers of fitness.
Alternately, he might’ve been rounding the subsequent statistic:
Bouchard reported that the impact of training on insulin sensitivity – a marker of risk for diabetes and heart disease – also varied. It improved in 58% of the volunteers following exercise, but in 42% it showed no improvement or, in a few cases, may have got worse.
So, how many is many? What fraction of the subjects were resistant on the various metrics? Unfortunately, the NS article doesn’t give exactly what we want to know, so we need to find the original scientific papers to figure it out ourselves, but the NS article doesn’t give citations either, forcing us to fact-check it the hard way (a long time in Google Scholar punching in names and keywords).
Tracking down sources for this article is quite difficult. Bouchard quickly pulls up a bunch of papers all revolving around similar data from what is called the HERITAGE Family Study, which has apparently been running since 1995 (the abstract to “The HERITAGE family study: Aims, design, and measurement protocol”, 1995, describes it as in-progress) and there are a lot of papers on various minutia of it. So we need to search with ‘HERITAGE’.
VO2_max: “The average increase reached 384 mL O 2 with an SD of 202 mL O 2”; citing:
BOUCHARD , C., P. A N , T. RICE , et al. Familial aggregation of VO2max response to exercise training: results from the HERITAGE Family Study. J. Appl. Physiol. 87:1003–1008, 1999.
heart-rate during exercise, “heart rate during submaximal exercise at 50 W” ; “A mean decrease of 11 beats·min −1 was observed
among the 727 subjects with complete data. However, the
SD reached 10 beats.”
original to this review, it seems
blood lipids, HDL-C: “They found that when the distribution of the
percent changes in HDL-C was broken down into quartiles,
the first quartile actually experienced a decrease in HDL-C of
9.3%, whereas the fourth quartile registered a mean increase of
18%.” Cited to:
LEON , A. S., T. RICE , S. MANDEL , et al. Blood lipid response to 20 weeks of supervised exercise in a large biracial population: the HERITAGE Family Study. Metabolism 49:513–520, 2000.
blood pressure, “systolic blood pressure during
exercise in relative steady state at 50 W”; “Among these subjects, the mean decrease in SBP during cycling at 50 W was 8.2 mm Hg (SD
11.8)”
original to this review
So that covers 4 of the markers mentioned in the NS link. In those 4 cases, going by the graphs (the data is highly non-normal so you can’t just estimate from the mean/SD), I’d guesstimate that 5-20% of each show <=0 benefit from the 20-weeks of endurance exercise.
(The papers don’t seem to include any correlation matrixes, but this is definitely a problem which calls out for dimensionality reduction: presumably resistance on all 4 measurements correlates and you could extract a ‘exercise resistance factor’ which would be more informative than looking at things piecemeal. Since correlations between the 4 measurements are not given, it’s possible that they are independent and so only ~0.2^4 or <1% of the subjects were exercise-resistant on all 4 measures, but that would surprise me: it would be strange if one’s insulin improved but not VO2_max or cholesterol. I don’t have any guesses on how large this ‘exercise-resistant factor’ might be, though.)
Not all of these are as important as one another and weight does not seem to be included judging by Bouchard’s silence on individual differences w/r/t that. He does cite some interesting studies on resistance of body weight to change like two twin studies.
So going by the HERITAGE data described in that NS link, exercise resistance is a thing in maybe a fifth of the population but mostly on invisible things. 40%, however, is too high, since only 1 of the 5 measured things seemed to go that high, and the specific fractions were not mentioned, so most likely Eliezer was misremembering the other two stats as the more important stat.
I recall originally reading something about a measure of exercise-linked gene expression and I’m pretty sure it wasn’t that New Scientist article, but regardless, it’s plausible that some mismemory occurred and this more detailed search screens off my memory either way. 20% of the population being immune to exercise seems to match real-world experience a bit better than 40% so far as my own eye can see—I eyeball-feel more like a 20% minority than a 40% minority, if that makes sense. I have revised my beliefs to match your statements. Thank you for tracking that down!
I recall originally reading something about a measure of exercise-linked gene expression and I’m pretty sure it wasn’t that New Scientist article
That’s certainly possible. Bouchard and others, after observing that some subjects were exercise-resistant and finding that like everything else it’s heritable, have moved onto gene expression and GWAS hits. Any of those papers could’ve generated some journalism covering the earlier HERITAGE results as background.
20% of the population being immune to exercise seems to match real-world experience a bit better than 40% so far as my own eye can see
Another study suggests it’s more like 7%. Probably hard to get a real estimate: how do you do the aggregation across multiple measured traits? If someone appears to be exercise resistant on visceral fat, but not blood glucose levels, do you count them as a case of exercise resistance? On top of the usual sampling error.
Do you have an opinion concerning whether this is better characterized as “non-response to the benefits of exercise due to pathology” vs. “immunity to the harmful effects of a sedentary lifestyle”?
Basically, is being a non-responder good or bad? Eyeballing that graph it does look like untrained non-responders might be a bit fitter than responders—but of course the first thing we should assume is ceiling effect.
(And of course there’s many 3rd options—orchid/dandelion trade offs and such)
I don’t have a specific link on hand, but I remember the term being “metabolic set point”. The idea is that some low level feedback loop in the old brain sets your weight, and it can easily compensate for exercise. Along with that theory goes the idea that only dietary changes may be effective.
Where did you read that?
(I’d be pretty surprised if that turned out not to be untrue, overstated, or overgeneralized.)
I am hoping it was advice specifically given for wait loss, emphasising that just adding light exercise will not see large results in many cases. As an independent observation it would be terrible.
I was skeptical as well, but Googling for “immune to exercise” produced this: http://www.newscientist.com/article/dn6735-some-people-are-immune-to-exercise.html. It seems like an area that could really use further research; if the universally-dispensed advice is ineffective for nearly half the population, that’s a huge problem.
Yes, but that shows that Eliezer probably misremembered what the 40% referred to. In that study, “40%” refers not to how many didn’t benefit, but rather to the maximal benefit on a particular measure of fitness received by any of the participants:
Alternately, he might’ve been rounding the subsequent statistic:
So, how many is many? What fraction of the subjects were resistant on the various metrics? Unfortunately, the NS article doesn’t give exactly what we want to know, so we need to find the original scientific papers to figure it out ourselves, but the NS article doesn’t give citations either, forcing us to fact-check it the hard way (a long time in Google Scholar punching in names and keywords).
Tracking down sources for this article is quite difficult. Bouchard quickly pulls up a bunch of papers all revolving around similar data from what is called the HERITAGE Family Study, which has apparently been running since 1995 (the abstract to “The HERITAGE family study: Aims, design, and measurement protocol”, 1995, describes it as in-progress) and there are a lot of papers on various minutia of it. So we need to search with ‘HERITAGE’.
The final paragraph about the 51⁄72 genes seems to be sourced from “Endurance training-induced changes in insulin sensitivity and gene expression”, which was published around 2004, consistent with the NS date. The general stuff about responses to exercise is much harder to track down, but after quite a bit of browsing through Google Scholar, I think it’s all summarized in “Individual differences in response to regular physical activity”, Bouchard & Rankinen 2001, which sounds promising since its abstract mentions “For example, Vo2_max responses to standardized training programs have ranged from almost no gain up to 100% increase in large groups of sedentary individuals”.
This review covers 4 major categories:
VO2_max: “The average increase reached 384 mL O 2 with an SD of 202 mL O 2”; citing:
BOUCHARD , C., P. A N , T. RICE , et al. Familial aggregation of VO2max response to exercise training: results from the HERITAGE Family Study. J. Appl. Physiol. 87:1003–1008, 1999.
heart-rate during exercise, “heart rate during submaximal exercise at 50 W” ; “A mean decrease of 11 beats·min −1 was observed among the 727 subjects with complete data. However, the SD reached 10 beats.”
original to this review, it seems
blood lipids, HDL-C: “They found that when the distribution of the percent changes in HDL-C was broken down into quartiles, the first quartile actually experienced a decrease in HDL-C of 9.3%, whereas the fourth quartile registered a mean increase of 18%.” Cited to:
LEON , A. S., T. RICE , S. MANDEL , et al. Blood lipid response to 20 weeks of supervised exercise in a large biracial population: the HERITAGE Family Study. Metabolism 49:513–520, 2000.
blood pressure, “systolic blood pressure during exercise in relative steady state at 50 W”; “Among these subjects, the mean decrease in SBP during cycling at 50 W was 8.2 mm Hg (SD 11.8)”
original to this review
So that covers 4 of the markers mentioned in the NS link. In those 4 cases, going by the graphs (the data is highly non-normal so you can’t just estimate from the mean/SD), I’d guesstimate that 5-20% of each show <=0 benefit from the 20-weeks of endurance exercise.
That leaves the insulin sensitivity one, which seems to be “Effects of Exercise Training on Glucose Homeostasis: The HERITAGE Family Study”, Boulé et al 2005. The graphs are hilarious, almost exactly 50-50 looking, and so correspond to the NS summary of 58%/42%.
(The papers don’t seem to include any correlation matrixes, but this is definitely a problem which calls out for dimensionality reduction: presumably resistance on all 4 measurements correlates and you could extract a ‘exercise resistance factor’ which would be more informative than looking at things piecemeal. Since correlations between the 4 measurements are not given, it’s possible that they are independent and so only ~0.2^4 or <1% of the subjects were exercise-resistant on all 4 measures, but that would surprise me: it would be strange if one’s insulin improved but not VO2_max or cholesterol. I don’t have any guesses on how large this ‘exercise-resistant factor’ might be, though.)
Not all of these are as important as one another and weight does not seem to be included judging by Bouchard’s silence on individual differences w/r/t that. He does cite some interesting studies on resistance of body weight to change like two twin studies.
So going by the HERITAGE data described in that NS link, exercise resistance is a thing in maybe a fifth of the population but mostly on invisible things. 40%, however, is too high, since only 1 of the 5 measured things seemed to go that high, and the specific fractions were not mentioned, so most likely Eliezer was misremembering the other two stats as the more important stat.
I recall originally reading something about a measure of exercise-linked gene expression and I’m pretty sure it wasn’t that New Scientist article, but regardless, it’s plausible that some mismemory occurred and this more detailed search screens off my memory either way. 20% of the population being immune to exercise seems to match real-world experience a bit better than 40% so far as my own eye can see—I eyeball-feel more like a 20% minority than a 40% minority, if that makes sense. I have revised my beliefs to match your statements. Thank you for tracking that down!
That’s certainly possible. Bouchard and others, after observing that some subjects were exercise-resistant and finding that like everything else it’s heritable, have moved onto gene expression and GWAS hits. Any of those papers could’ve generated some journalism covering the earlier HERITAGE results as background.
Another study suggests it’s more like 7%. Probably hard to get a real estimate: how do you do the aggregation across multiple measured traits? If someone appears to be exercise resistant on visceral fat, but not blood glucose levels, do you count them as a case of exercise resistance? On top of the usual sampling error.
Do you have an opinion concerning whether this is better characterized as “non-response to the benefits of exercise due to pathology” vs. “immunity to the harmful effects of a sedentary lifestyle”?
Basically, is being a non-responder good or bad? Eyeballing that graph it does look like untrained non-responders might be a bit fitter than responders—but of course the first thing we should assume is ceiling effect.
(And of course there’s many 3rd options—orchid/dandelion trade offs and such)
I don’t have a specific link on hand, but I remember the term being “metabolic set point”. The idea is that some low level feedback loop in the old brain sets your weight, and it can easily compensate for exercise. Along with that theory goes the idea that only dietary changes may be effective.