If you look at a bunch of variables, including BMI, and then you remove the impact of well known negative health impacts of obesity (prediabetes/T2D), then you see that high BMI doesn't not correlate well with mortality. IMO, what this indicates to me is that (1) BMI is not a good indicator of obesity in this study. There are many healthy people with low body fat and high BMI, I am one of them. All you need to do is be tall and lift weights occasionally. If you remove the obesity related negative health signals, you also remove obesity(2) Being fat in and of itself is not the issue, the issue is prediabetes/T2D which is extremely reliably caused by obesity, and the treatment for prediabetes/T2D is weight loss.
That suggests that there is no other material contributor to mortality from obesity[1], which is a somewhat unexpected result.
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[1] it is possible that there are negative contributions to mortality associated with obesity which could potentially "hide" other positive contributors
(Leaving out the discussion: effects to environment, sedentary lifestyle, etc)
For example, tall people tend to have higher BMI, as if 2 is not the right power to raise height to. But you barely need a 4-op calculator to calculate that. Good luck calculating BMI if the power were 2.18 or whatever gives best fit.
Measuring body fat is not exactly hard but much less straightforward and a touch unpleasant. If you're running a large study, it's much easier to measure BMI than anything else. At population level, I'd imagine correlation to obesity is easily 80-90%.
I guess it is also easier for doctors to say "your BMI is too high" rather than "you're too rounded".
Fat is not the only way to be heavy, body builders have very high BMI value yet have very different risk profiles.
` 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.`
"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."
This takeaway is basically "the increase in mortality that has been attributed to fluid in the lungs is likely due to a lack of blood oxygenation rather than being submerged underwater".
There exist obese individuals that are not positive for those markers, and there exist non-obese individuals that are.
In a clinic, that might look like more proactively monitoring an obese patient for these indicators but not focusing as much on their obesity if those are doing well. Likewise, it might look like adding these tests to a 5 year physical (or whatever) for non-obese patients, since they appear to be especially suggestive of concern.
It's not surprising to find these causes are significant factors in obesity-linked mortality, but it is moderately surprising, at least to me, to find that they're the only significant ones.
It seems almost like a joke, but "hyperinsulinemia and inflammation" seems more or less identical with "chronic overeating", right?
https://www.ahajournals.org/doi/10.1161/circ.128.suppl_22.A1...
[Metabolic syndrome] doubles the risk of all vascular complications in patients often erroneously considered at lower CVD risk because of their normal BMI.
You can't imagine there are a few million people like that out of the billions in the world, and that we might want to give effective medical care to those people also?
> Likewise how do you treat these people to reduce their insulin swings in such a way that they... would fail to lose weight?
Is this an actual question asking about the state of the research, or do you think that it's unimaginable that science could ever be able to directly manipulate people's insulin levels?
I get the impression from most of the top level comments on this thread that some people would be upset if fat people's mortality could be reduced or normalized without weight loss. Like there's an urge to see fat people punished rather than happy and healthy.
In recent years there has been a back-and-forth discussion about whether being overweight is bad for your health. Intuitively one might think that being overweight is bad. But in 2015, for example, there was this article, which reflected a story making the rounds at the time:
https://qz.com/550527/obesity-paradox-scientists-now-think-t...
What I take this study to be saying is that obesity in itself is not really the problem, but it is (presumably) highly correlated with high A1C measurements and inflammation, which do indicate a poor state of the endocrine system (i.e., Type 2 diabetes), which can in turn lead to heart disease and stroke if not treated.
I'm hoping that someone who knows more than I do will poke some holes in what I have just written so as to give you a better answer.
However, both elevated CRP and higher fasting insulin are correlated with obesity, so controlling for these variables seems misleading.
Well: https://en.wikipedia.org/wiki/Multicollinearity
Summary: highly correlated variables don't fundamentally mess up the inference (coefficient estimates are still unbiased), the estimation becomes numerically unstable, however, and individual coefficients might be messed up because of that. This is reflected in the standard errors, so you're more likely to miss effects (type II error).
And what if they don't eat that much? They die or what?
The data shows that there is a better measure than BMI which doesn't carry all the stigma, so why not use that one?
Taking any of the more accurate measurements of body composition requires effort, unlike BMI. It's easy and lazy and not yet acknowledged as an ineffective practice so doctors do it. It's also not always wrong, just because BMI and obesity do correlate.
It also means that if we can control people's reactions to sugar, their weight becomes irrelevant (or possibly even protective.) Losing weight is usually the way to fix your sugar, but plenty of people who aren't fat have sugar problems, and sugar problems might not be reversed by weight loss in a particular individual.
There are a plethora of studies correlating a change in diet with improved blood markers for fasting blood glucose and insulin response. Sugar "problems" are resolved by diet, and resolving diet goes along with reversing weight loss. It cannot be any other way.
There is no evidence that obese BMIs are negatively correlated to mortality, only the opposite. Obese BMIs still come with increased arterial plaque, complications in anesthesia and surgical healing for medical interventions, fatty liver disease, ocular pressure, lung function, cardiovascular health, and so on.
Obesity is up with smoking as a cause of preventable death. Let's not try to put a pretty face on it. A spade is a spade.
Insulin resistance/high fasting glucose and obesity are inseparable peas in a pod.
That's encouraging because I've been able to fix the hyperinsulinemia and inflammation, but not all of the excess BMI. Maybe fit & fat aren't mutually exclusive.
https://www.youtube.com/watch?v=wadKIiGsDTw
Taking someone sick with high inflammation and putting them in a hospital bed is terrible for their recovery.
We have created an environment devoid of it and we reap the consequences: increase amount of chronic autoimmune diseases and many other things.
Personally I had to deal with eczema every winter that I got rid of with a simple infrared heater. A friend of mine was dying of IBS in the hospital, he say f*ck it if I am going to die it will be under the sun. He checkout of hospital (Canada), went to mexico and healed himself while ditching the medication.
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.
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?
That's basically tautological. Outliers are outliers because they don't fit the model.
Waist measurement is a stronger measure but still flawed.
for folks like yourself with T2D, noting changes. Keep on keeping on (i.e. follow current medical advice)
No, it is not. We should be very clear that high BMI is, in fact, life shortening.
High BMI is, in fact, strongly correlated with atherosclerosis. It is, in fact, strongly correlated with decreased lung volume and risk pulmonary edema. It is correlated with clot formation and stroke. It is correlated with fatty liver disease. It is correlated with decreased bone density, which leads to a heightened risk of throwing embolism-causing clots if a fall leads to a break. It is correlated with a variety of cardiac events, mostly around hardening valves and fat buildup in cardiac tissue causing lessened output while there is more circulating blood volume. It is correlated with difficulties administering anesthesia or intubating patients in case of emergency. It is correlated with...
Being obese is still horrifyingly unhealthy even if high fasting glucose is just a proxy for some of those factors (which it is not, as this study is terrible).
~20.3 here
and we chose not to justify or explain those parameterizations in any way, because what we probably actually did was diddle SAS until the model did what it was supposed to.
yawn.
"Don't be snarky."
