The American health care system wastes billions of dollars each year on diseases and conditions that are a direct cause of obesity.
I assume you meant “a direct consequence of obesity”. Here’s a quote from the original interview that contradicts your claim:
Paul: The correlations between higher weight and greater health risk are weak except at statistical extremes. The extent to which those correlations are causal is poorly established. There is literally not a shred of evidence that turning fat people into thin people improves their health. And the reason there’s no evidence is that there’s no way to do it.
Now, if your point of view is informed, the right way forward in the argument would be producing citations.
Also, the part of your comment that deals with evolution seems confused to me. Hunter-gatherers don’t get obese because they don’t have access to cheap food, not because natural selection kills off obese people. If the latter were the case, modern people (who evolved from hunter-gatherers, after all) would have genetic safeguards against obesity.
Now, if your point of view is informed, the right way forward in the argument would be producing citations.
I am literally so baffled by the thesis presented above I can’t bring myself to disagree with it because I must be missing something. I mean, within five minutes on Google I found five studies showing strong correlations between various measures of body fat and coronary heart disease:
If I was willing to give it an hour, I’m sure I could have found sixty of them, and I know there are many similar studies about type II diabetes, cerebrovascular disease, et cetera. Because many of these are prospective studies, they have a better ability to show causality than longitudinal studies (although still not perfect). And another five minutes on Google find me several interventional studies about how turning fat people into thin people improves their health:
So what exactly is the thesis? That all of these studies are flawed in the same way? That there’s some vital causal step that’s been left out? Surely the author must know about these, right?
I think the story goes like this: there are correlations between weight and health. There are disputes, but let us skip that and assume for the sake of argument that thin people live longer than fat people. The next question is whether this is causal. If a fat person makes a big effort and becomes thin, will he have a long life, just like a person who was thin to begin with?
We can fill in the details of what the experiment looks like. We start with 200 fatties who want to get thin, and a random assignment of 100 to the control group, who get the usual crap advice about diet and exercise. Since this doesn’t work they remain fat. The others get special good advice about diet and exercise. They diet and exercise sucessfully and become thin. Then we wait.
Later (10 years? 20 years?) we follow up. Did the newly thin live longer? It is hard to be sure of the outcome in advance, the observed correlations do not guarantee it.
This is where Paul Campos jumps in a says “hey wait a minute, we cannot do that experiment because we do not have special good advice to hand out.”
Data from the scientific community indicate that a 15-wk diet or diet plus exercise program produces a weight loss of about 11 kg with a 60-80% maintenance after 1 yr. Although long-term follow-up data are meager, the data that do exist suggest almost complete relapse after 3-5 yr.
Think about planning the experiment that I sketched earlier. The key to getting a crisp, clear result is a ten or twenty year follow up measuring all-cause morbidity and mortality. The designer of the experiment needs to chose an intervention for the trial group, but the weight loss interventions that follow up five years later are reporting almost complete relapse for all interventions. So design of the experiment shudders to a halt.
I assume you meant “a direct consequence of obesity”. Here’s a quote from the original interview that contradicts your claim:
Now, if your point of view is informed, the right way forward in the argument would be producing citations.
Also, the part of your comment that deals with evolution seems confused to me. Hunter-gatherers don’t get obese because they don’t have access to cheap food, not because natural selection kills off obese people. If the latter were the case, modern people (who evolved from hunter-gatherers, after all) would have genetic safeguards against obesity.
I am literally so baffled by the thesis presented above I can’t bring myself to disagree with it because I must be missing something. I mean, within five minutes on Google I found five studies showing strong correlations between various measures of body fat and coronary heart disease:
In a 14-year prospective study, middle-aged women with a BMI >23 but 25 but <29 had a 72% increased risk
When participants with the highest waist-to-hip ratio were compared with those having the lowest ratio, there was an 80 percent increase in risk.
The risk of any CHD event, a nonfatal event, and a fatal event among adults was positively associated with BMI at 7 to 13 years of age for boys and 10 to 13 years of age for girls.
These prospective cohort studies employed simple indices of body-fat distribution such as waist-to-hip circumference ratio or subscapular skinfold. Their similar results suggested that increased abdominal obesity conferred a two-fold increased risk of ischemic heart disease among middle-aged men.
IAF and trunk fat were consistently positively related to CVD risk factors, whereas leg fat was consistently negatively related to CVD risk, indicating that IAF and trunk fat may put women at increased risk of developing CVD.
If I was willing to give it an hour, I’m sure I could have found sixty of them, and I know there are many similar studies about type II diabetes, cerebrovascular disease, et cetera. Because many of these are prospective studies, they have a better ability to show causality than longitudinal studies (although still not perfect). And another five minutes on Google find me several interventional studies about how turning fat people into thin people improves their health:
Our study has shown that weight loss of as little as 6.5 percent in individuals with [metabolic syndrome] results in substantial reductions in blood pressure, glucose, triglycerides and total cholesterol, all factors that lead to heart disease,’ MDBHVC director Christie Ballantyne said. These impressive results occur early in the weight loss, well before individuals even begin to approach their ideal body weight,’ Ballantyne said.
Weight loss was significantly associated with lower rate of the composite outcome after adjustment for age, sex, smoking, dyslipidemia, diabetes, hypertension, myocardial infarction, and obese status [hazard ratio (HR)=0.62; P=0.018]. Subgroup analysis showed that patients who lost weight had favorable outcomes both in patients with BMI <25 (HR=0.32; P=0.035) and those with BMI ≥25kg/m2 HR=0.64; P=0.032.
So what exactly is the thesis? That all of these studies are flawed in the same way? That there’s some vital causal step that’s been left out? Surely the author must know about these, right?
I think the story goes like this: there are correlations between weight and health. There are disputes, but let us skip that and assume for the sake of argument that thin people live longer than fat people. The next question is whether this is causal. If a fat person makes a big effort and becomes thin, will he have a long life, just like a person who was thin to begin with?
We can fill in the details of what the experiment looks like. We start with 200 fatties who want to get thin, and a random assignment of 100 to the control group, who get the usual crap advice about diet and exercise. Since this doesn’t work they remain fat. The others get special good advice about diet and exercise. They diet and exercise sucessfully and become thin. Then we wait.
Later (10 years? 20 years?) we follow up. Did the newly thin live longer? It is hard to be sure of the outcome in advance, the observed correlations do not guarantee it.
This is where Paul Campos jumps in a says “hey wait a minute, we cannot do that experiment because we do not have special good advice to hand out.”
That is a controversial position, and the key issue seems to be the duration of follow up. Qutoing from How effective are traditional dietary and exercise interventions for weight loss?
Think about planning the experiment that I sketched earlier. The key to getting a crisp, clear result is a ten or twenty year follow up measuring all-cause morbidity and mortality. The designer of the experiment needs to chose an intervention for the trial group, but the weight loss interventions that follow up five years later are reporting almost complete relapse for all interventions. So design of the experiment shudders to a halt.