"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."
Key takeaway: higher fasting insulin and higher fasting blood sugar are both signs of being prediabetic or having type 2 diabetes, which is correlated with 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".
The correlate of my correlate is not... me. Or something like that.
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.
No, really. Insulin resistance and elevated fasted blood are clinical markers of diabetes and prediabetes. There is no arguing this.
Yes, non-obese individuals with type 2 diabetes exist, though they are rare. Obese individuals who are not prediabetic or already have pathological type 2 diabetes are unicorns.
Patients are already having their blood sugar monitored in a clinical setting, especially diabetic ones or ones likely to be prediabetic. And those patients are... obese.
There is no getting around his fact.
Non-obese patients also have this checked regularly. Clinicians frequently ask for fasting the night beforehand to check blood values. They are checking for this. Nothing here is new, even remotely.
I mentioned this in the other thread, but the really interesting part to me is "When fasting insulin and the natural logarithm of c-reactive protein were included in the model, an inverse association between BMI and mortality was present" which says that, if the study's findings are correct, that hyperinsulinemia and inflammation are the only material contributors to obesity-linked mortality.
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.
I don't know that that's very informative, clinically. How many obesity cases are there that don't have one of those two issues in some co-causal way? Likewise how do you treat these people to reduce their insulin swings in such a way that they... would fail to lose weight?
It seems almost like a joke, but "hyperinsulinemia and inflammation" seems more or less identical with "chronic overeating", right?
[Metabolic syndrome] doubles the risk of all vascular complications in patients often erroneously considered at lower CVD risk because of their normal BMI.
> How many obesity cases are there that don't have one of those two issues in some co-causal way?
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.
The linked article is about an epidemiological measurement often used to flag health risks. And it's pointing out that the real causality is likely due to other factors. I'm pointing out that those other factors are hopelessly conflated with the first anyway, so we might as well keep measuring BMI and treating it as a risk factor.
Are there other things we should measure? Of course there are. Propose a test and let's look at the tradeoffs. I'm just saying let's not stop treating BMI as informative, because it still is.
> 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?
There's not a good reason to think that those people are not already getting effective medical care. Medical practitioners are interested in their patients' health and longevity. Obesity and good long-term health outcomes have negative correlations. Here is one of many studies:
If there is such a population comprising even 1% of the world population (and that figure has almost no backing in any literature unless you include age 18-30 in that cohort, who are broadly too young to have seen longitudinal health effects from obesity affect their health yet), it's unfortunate that occam's razor may impede the quality of their care, but this is very much a hypothetical question without any meaningful evidence to the contrary.
> 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?
Uh, that's what insulin pumps and injectable insulin do. We really don't have to imagine it. But beta cells in the pancreas can literally get worked to death in type 2 diabetes, and type 1 diabetics never produced enough (or any) in the first place. So exogenous insulin is administered because without it (and sometimes with it), glucose will acidify the blood and cause neuropathy or ketoacidosis in the worst cases, and it impedes healing, so reduced feeling causes a small injury which heals more slowly to lead to an enormous ulcer and infiltration which the patient still may not feel, until amputation is a necessary lifesaving measure.
Science can directly manipulate lots of hormone levels, but it all has side effects versus letting your body manage itself, most of them profoundly negative.
> 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.
I don't think anyone in this thread wants to see fat people punished instead of happy and healthy. Rather, it's that obesity and being happy and healthy are incompatible in the long term, and this study doesn't change that at all. There's no moralizing or proselytizing in this thread, just a "hey dude, this isn't gonna work out in the long run, and you shouldn't fool yourself or others that it is".
If this were a study indicating that lung cancer actually wasn't linked to smoking, but was instead due to some environmental effect, and people were out here saying "wait, wait -- the study says that it was actually elevated levels of blood CO that caused it, but the number of people sucking on exhaust pipes is so low it doesn't move the needle, and this doesn't change COPD, heartattack, etc", nobody would be saying 'it's like there's an urge to see smokers punished rather than happy and healthy".
I used this as an example because the obesity rate in the US is that kind of public health crisis, with side effects that bad. Impotence, amputation, and blindness (among others) are nothing to minimize.
I am not a nutrition expert but I believe inflammation can be a problem without high BMI. For example, eating lots of highly processed foods but staying within your calorie limit, would have this outcome.
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:
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.
>It’s true that these groups are slightly more likely to suffer from heart disease and some other life-threatening conditions in the first place. But many factors influence the likelihood of a person getting heart disease. And a strong link between weight and disease only emerges among people with severe obesity.
That seems like a place where the article should maybe have a citation or two.
One possible explanation is that obese people lack adequate muscle mass. The lack of muscle -- protein -- is associated with insulin resistance and it may be lack of muscle rather than additional fat per se that is one of the actual root causes of health issues associated with obesity and routinely attributed to fat per se.
"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."