Thank you for sharing that but I do have to say it is a pretty weak analysis.
Assuming that the populations used in studies chosen for their analysis were normally distributed before and after interventions (which they implicitly do) we would expect 2.5% of all those measured to have changes in a negative direction by chance. Indeed the numbers they came up with, 8.4 to 13.3% depending on the study and the item, were more than that. Statistically significantly so? They offer no such analysis. But of course there is no reason to assume a normal distribution either before or after intervention. The only way to support the claim that a number outside 2 S.D. of test range above 2.5% represents an adverse response would be to compare it to the percent outside of that range for the control population after the same amount of time. Do the studies cited show that? They don’t say. So let’s look at the studies themselves:
The HERITAGE study: notably had no nonexercise control group, showed variable magnitude of response that, in other analyses, do seem to link with particular genes, and none the same one whose testing kits is being sold by Timmons.
The DREW study: actually failed to show any difference on blood pressure between the control and the experimental exercise groups and such was not its intent. It set out to show that even mild exercise could impact measures of fitness and did so. It also would be expected that if movement in the negative direction was an effect of exercise (rather than statistics and effect of time on a cohort) that the negative movements would be more frequent in the higher than lower exercise groups; such was not seen.
The INFLAME study: Another one that found no difference from exercise alone without weight loss on CRP. Indeed a certain percent had increases in CRP after the exercise intervention … about the same percent as in the control group - “The shape of the distribution of change values was similar between groups …” OTOH “there was a strong association between fat loss and change in CRP and that the individuals in the exercise group who lost the most weight (and fat) had a significant decrease in CRP. Our data suggests that exercise training-induced reductions in CRP are due primarily to fat loss …”
STRRIDE also without a control group, found aerobic training resulted in a mean improvement in metabolic parameters that was not seen in resistance training alone.
So on.
One of the weakest analyses I’ve read in a while. Really. And if Timmons is somehow even implying that his product will identify who would be in those alleged adverse responder group (other than for the narrow result of lesser VO2 max response to aerobic training) than is he way out of line.
One of the articles you posted mentions how in a group of 1000 people about 48 vascular events are prevented by statins among people with existing CHD. Studies I’ve seen say it is closer to 2 out of 100. The treatment groups are possibly different, I don’t know.
Other studies I’ve seen show about 2 events per 100 in a 5 year period. It says ‘taking all years together’ but later says 5 years. I’m confused by that.
But if among high risk patients you have to treat 100 people to prevent 2 vascular events, and I’m not even sure what % of those vascular events are debilitating or fatal that still doesn’t sound uber impressive to me. Granted I’m not a physician but a person is likely to be in that group of 98 who sees no benefits than they are to be in that group of 2 who does see a benefit.
Granted, among people with existing CHD the numbers are a little better, treat 100 people and prevent 5 events. But again, it is like with aspirin. Aspirin can help prevent heart attacks, but not fatal ones. So the mortality rating isn’t much different between the treatment group and the placebo group.
Those studies as they say seem to be about middle aged men w/o heart disease. The study you posted finding 48 prevented per 1000 was among people with CHD.
All in all, I’m happy to be educated about this subject. I have a background in chemistry but not in medicine, and I’ve become jaded about medicine in the last few years. But I’m still just not seeing a reasonable benefit unless you are in a very high risk group, and even then you are highly likely not to see a benefit and not be one of the people whose vascular event is prevented.
I’m honestly so ignorant I don’t even know how CHD is even diagnosed. Do you have to have certain anatomical issues to have that diagnosed (arteries that are % clogged, issues on an ekg, stress test) or can they just diagnose you based on family history, weight, lifestyle, metrics readings, age?