Oh, I’m guessing based on purely correlational studies, with all the uncertainty and fuzziness that implies. Added a disclaimer to the relevant section to this effect, since it’s worth calling out.
That said, I’d be shocked if the whole effect was due to confounders, since there are so many negative conditions comorbid with obesity, along with the existence of some animal studies also pointing in the direction of improved lifespan with caloric restriction.
Unfortunately, we don’t have the ability to run controlled studies over a human lifespan, so we end up needing to do correlational studies and control for what we can. It seems like a bad idea to simply throw up our hands in complete epistemic helplessness and say that we don’t know anything for sure; we need to act in the presence of incomplete information.
Also, re: the specific point of
Diet might fix these, while drugs might not.
Keep in mind that these drugs cause weight loss by way of causing dietary changes.
Is that really how all of them work? In the case of ECA, I thought it was due to increased metabolism. But it might also have an effect on appetite.
And even when it is, is that good enough? It’s possible for dietary changes to promote weight loss, but still be unhealthy. If you just eat junk food, and then the drugs reduce your appetite so you eat less food, but it’s still junk food, then technically that’s “dietary changes”, but you’re still not getting the micronutrients, fiber, prebiotics, and possibly bacteria that you would from fruits and vegetables. To the extent that the poor health is caused by excess Calories, it helps. But to the extent that poor health is caused by eating the wrong things, then simply eating less of them can only go so far.
Of course, I expect that using the prescription drugs as directed would be a last resort after dietary improvements prove insufficient, but doctors can only do so much to influence behavior.
Whoops, sorry, I don’t actually know anything about ECA. Possibly that’s how it works, at least partially! I’m pretty sure it’s true that stimulants are appetite suppressants, but it’s also possible it has another mechanism of action having to do with non-exercise activity thermogenesis or similar.
Anyway: the way I was thinking about this is, obesity is caused by excess calories. That being the case, there’s no particular reason to anticipate obese people wouldn’t be getting appropriate amounts of fiber/micronutrients/etc; or at very least, I have not heard anyone make such a case.
So while it’s definitely true that drugs wouldn’t help with nutritional deficiencies, it’s also not clear to me that this is necessarily relevant to the health impacts of obesity.
It seems like a bad idea to simply throw up our hands in complete epistemic helplessness and say that we don’t know anything for sure; we need to act in the presence of incomplete information.
Pretending you know something that you don’t is not something you want to do in the presence of incomplete information.
In this case you would want to look for studies that actually look at the lifespan effects of successful weight loss. Estimating confidence intervals to be more explicit about one’s uncertainty is also helpful.
>[Note: as pointed out by comments below, extrapolation to life-years saved is very speculative, since all the studies on this in humans are going to be confounded all to hell by healthy user bias and socioeconomic correlations and the like. That said, it feels like a fairly reasonable extrapolation given the comorbidity of obesity to various extremely problematic medical conditions. Be warned!]
should be sufficient to exempt me from charges of “pretending to know things.”
The confidence intervals thing is probably a good idea, but I have no idea where to start on that, really, since the confidence intervals would be mostly driven by “how confident am I feeling about using correlational studies on health outcomes to make causal claims about the effects of a treatment” more than any objective factor.
I’m not actually sure about whether a study looking at the effects of successful weight loss on mortality would be all that helpful for this conversation, since that would still end up being a totally correlational study with enormous error bars and confounders, and successful long-lasting weight loss isn’t very common (itself which will introduce yet more confounders). Also I don’t think such a study exists.
The confidence intervals thing is probably a good idea, but I have no idea where to start on that, really,
Basically you have no idea about which extrapolations are reasonable to make and do them anyway in spite of having no idea what’s reasonable to do.
If you don’t think you understand the subject well enough to give confidence intervals I don’t think you understand it well enough to give any extrapolations that have any usefulness.
The idea that an “objective” number that’s clearly wrong is better then a more subjective that factors in more knowledge is also flawed.
Oh, I’m guessing based on purely correlational studies, with all the uncertainty and fuzziness that implies. Added a disclaimer to the relevant section to this effect, since it’s worth calling out.
That said, I’d be shocked if the whole effect was due to confounders, since there are so many negative conditions comorbid with obesity, along with the existence of some animal studies also pointing in the direction of improved lifespan with caloric restriction.
Unfortunately, we don’t have the ability to run controlled studies over a human lifespan, so we end up needing to do correlational studies and control for what we can. It seems like a bad idea to simply throw up our hands in complete epistemic helplessness and say that we don’t know anything for sure; we need to act in the presence of incomplete information.
Also, re: the specific point of
Keep in mind that these drugs cause weight loss by way of causing dietary changes.
Is that really how all of them work? In the case of ECA, I thought it was due to increased metabolism. But it might also have an effect on appetite.
And even when it is, is that good enough? It’s possible for dietary changes to promote weight loss, but still be unhealthy. If you just eat junk food, and then the drugs reduce your appetite so you eat less food, but it’s still junk food, then technically that’s “dietary changes”, but you’re still not getting the micronutrients, fiber, prebiotics, and possibly bacteria that you would from fruits and vegetables. To the extent that the poor health is caused by excess Calories, it helps. But to the extent that poor health is caused by eating the wrong things, then simply eating less of them can only go so far.
Of course, I expect that using the prescription drugs as directed would be a last resort after dietary improvements prove insufficient, but doctors can only do so much to influence behavior.
Whoops, sorry, I don’t actually know anything about ECA. Possibly that’s how it works, at least partially! I’m pretty sure it’s true that stimulants are appetite suppressants, but it’s also possible it has another mechanism of action having to do with non-exercise activity thermogenesis or similar.
Anyway: the way I was thinking about this is, obesity is caused by excess calories. That being the case, there’s no particular reason to anticipate obese people wouldn’t be getting appropriate amounts of fiber/micronutrients/etc; or at very least, I have not heard anyone make such a case.
So while it’s definitely true that drugs wouldn’t help with nutritional deficiencies, it’s also not clear to me that this is necessarily relevant to the health impacts of obesity.
Pretending you know something that you don’t is not something you want to do in the presence of incomplete information.
In this case you would want to look for studies that actually look at the lifespan effects of successful weight loss. Estimating confidence intervals to be more explicit about one’s uncertainty is also helpful.
I feel my disclaimer in the post:
>[Note: as pointed out by comments below, extrapolation to life-years saved is very speculative, since all the studies on this in humans are going to be confounded all to hell by healthy user bias and socioeconomic correlations and the like. That said, it feels like a fairly reasonable extrapolation given the comorbidity of obesity to various extremely problematic medical conditions. Be warned!]
should be sufficient to exempt me from charges of “pretending to know things.”
The confidence intervals thing is probably a good idea, but I have no idea where to start on that, really, since the confidence intervals would be mostly driven by “how confident am I feeling about using correlational studies on health outcomes to make causal claims about the effects of a treatment” more than any objective factor.
I’m not actually sure about whether a study looking at the effects of successful weight loss on mortality would be all that helpful for this conversation, since that would still end up being a totally correlational study with enormous error bars and confounders, and successful long-lasting weight loss isn’t very common (itself which will introduce yet more confounders). Also I don’t think such a study exists.
Basically you have no idea about which extrapolations are reasonable to make and do them anyway in spite of having no idea what’s reasonable to do.
If you don’t think you understand the subject well enough to give confidence intervals I don’t think you understand it well enough to give any extrapolations that have any usefulness.
The idea that an “objective” number that’s clearly wrong is better then a more subjective that factors in more knowledge is also flawed.