Is this more or less saying there's no definitive link between obesity and mortality risk?
You're letting the word "are" carry a lot of weight where "often" or "can be" might be more accurate.
They're correlated with obesity, which means that they're more likely to be present in obese patients. But they exist independent of it: not being present for all obese patients and sometimes being present for non-obese patients. And since they're measurable on their own, it's kind of a big deal to draw them out as obesity-associated factors more closely correlated with all-cause mortality than obesity as a whole.
Can you more specifically characterize what you mean by that and what your references are?
Because you're taking a statistical correlation and a hypothesized mechanism and turning it into logical entailment. It's hard to believe that even a extremely high correlation is anywhere near 100% but I would love to see real data saying otherwise.
I think I took it to mean you saying the study hadn't meaningfully narrowed down mortality risk to less noisy factors than obesity, when I see now that you may have just been helping the prior commenter see that obesity itself is still correlated with mortality through these. Probably because I can't even grok how they got to that idea. :)
The OP actually says that BMI is negatively correlated with mortality if you control for insulin levels, so that would mean that thin people with high fasting blood sugar would have more mortality than fat people in the same situation.
Weight gain is caused by an overconsumption of calories, barring a narrow range of medication side effects.
Insulin tells your body to uptake glucose into cellular bodies. If glycogen stores aren't depleted (in the liver from normal/basal metabolism, in muscular tissue from activity) and there's nowhere for it to go, it's converted via de novo lipogenesis and stored in adipose tissue. If there's no free room, new fat cells are created. Lipogenesis and the creation of new adipose tissue are not instantaneous processes.
Insulin resistance is because your body has continued to see that blood glucose is high because it cannot be taken up quickly enough, so it sends out more insulin. As high circulating levels become more normal, the alpha channel on the insulin receptor requires more insulin to activate a signal transduction pathway to open the GLUT4 transporter for glucose.
Very strictly, excess blood glucose causes insulin resistance. That excess blood glucose is caused by caloric overconsumption, which causes obesity. It is not the inverse.
Carbohydrates have poor satiety, so when the stomach is empty (fats and proteins have a longer processing time in the stomach), ghrelin is released, which stimulates hunger, and the person eats again. Probably more simple carbohydrates, possibly before the previous ones have been taken up by cells.
Caloric overconsumption -> obesity
Insulin resistance is a side effect here, one which is seen because simple carbohydrate consumption is part and parcel of obesity in the western world. It's very hard to become clinically obese without cheap sugar. The same mechanisms (overconsumption of calories) cause obesity and insulin resistance, so they're two sides of the same coin.
This is still a useful study though! It's useful to know that the cause is almost entirely through those factors. Though this is also an epidemiological study with no randomization and some of the hazard ratios are not particularly high.
> Higher fasting insulin and higher c-reactive protein confound the association between BMI and the risk of all-cause mortality. The increase in mortality that has been attributed to higher BMI is more likely due to hyperinsulinemia and inflammation rather than obesity.
Isn’t high BMI interchangeable with obesity in most studies?