Associations of body mass index, fasting insulin and inflammation with mortality
nature.comThis is interesting in a "of course" kind of way.
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.
What is interesting here is their finding that the two specific known major causes of obesity-linked mortality that they considered (c-reactive protein and high resting insulin -- effectively "obesity-linked diabetes") explained slightly more than all of the increased mortality associated with obesity.
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
If you do a study of the mortality rates of driving cars and control for crashes, it’s probably near zero.
This may have been meant in a tongue-and-cheek way but assuming that were true it would still be useful information: signifying that crash-prevention is where the focus should be.
(Leaving out the discussion: effects to environment, sedentary lifestyle, etc)
I'm guessing BMI is not really a considered obesity metric, but rather a good approximation which any GP can calculate in seconds.
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".
I think I'm a little confused by your definition of obesity. As far as I know, obesity is defined by BMI measure which is defined by a specific ratio of weight and height, so I don't understand how being tall would affect your being obese or not. [Unless you're saying the measurement doesn't work for tall people?]
The usual argument is that the scaling of the power wrt height is wrong (people aren't spherical basically). I don't buy it though. So many people say they have a high BMI but "they just lift weights". If you aren't on PEDs it is very unlikely that you can be BMI > 30 with low body fat.
My son is 15, 182 cm and weights 81 kg. According to BMI charts he is in the 94th percentile and it's categorized as obese.
But he is an athlete with almost no fat (he is not aiming at muscles so he does not have a diet that minimizes fat, he is looking for sheer power and explosivity (gym, martial arts)). He is very built up (muscular) though.
So I wonder how the BMI can give any kind of reasonable indication when the fat level is not taken into account.
He is only BMI = 24 though? What crazy redefinition of obese is going on there.
If you input these values at https://www.nhs.uk/live-well/healthy-weight/bmi-calculator/ you get the "obese" suggestion.
Without any consideration for fat BMI doe snot make much sense I guess.
182 cm isn't even that tall. I'm 193 CM and athletic build and at my recommended weight range by body composition measurements had me at like 26 BMI or "overweight".
Ehhh I'm not sure I'd go that far, but the person who has >30 BMI with muscle mass is going to look completely different than the person doing it with body fat.
Sure BMI can be more or less accurate depending on the person, but for those few who have actually rendered it inapplicable to them it's going to be blatantly obvious. No one will confuse them with being obese.
It seems like you’re moving the goalposts a bit by talking about “low” body fat. I don’t have “low” body fat but I know my bmi would be significantly lower if it weren’t for the 30+lbs of extra muscle mass I’ve put on in the last 5 years.
I wouldn’t have been obese before, but I technically am now (with reduced bodyfat %).
Ronnie Coleman has BMI of 38.9 while having less than 1% body fat. Bit of an extreme example, but "light weight baby!"
He also lifted weights to the point that he put himself into a wheelchair in his 50s. I also highly doubt the no PEDs part.
Ronnie was never less than 1% body fat, or even 1%. Stage ready bodybuilders are more like 3-5%. People are just poor at estimating bodyfat, and the media throwing out nonsense numbers doesn't help.
Obesity implies high BMI, but not vice versa.
Fat is not the only way to be heavy, body builders have very high BMI value yet have very different risk profiles.
The poster above states outright that you don't have to be a bodybuilding to have high BMI though. You just have to be tall and lift occasionally? Thus my confusion.
Also, I'm still confused. My previous understanding was that bodybuilders are classified as obese without having excess body fat because they fit into that ratio because the ratio doesn't account for exceptions. Not that obesity actually incorporates more than just a ratio.
As other commenters noted, BMI is just a low fruit metric to open the door for more investigations (or not). And when you see the person I bet you'll know immediately whether it applies or not. The word "obesity" existed well before BMI.
BMI uses an exponent of 2, for physical reasons it needs to be around that value, but the "correct" value might be different; it appears that GP believes it should be higher.
The point about body builders is that BMI as a metric assumes a fixed muscular profile, so doing (an healthy amount of) muscle training can wildly affect your BMI independently of your fatness.
If is still likely a good measure at a population level as very few people that have BMI > 30 are also fit. But you need to contextualize it to your own case.
To be more precise, my problem with this study is when you select for people with BMI>30 and filter for those who do not have obesity related health issues, you’re going to have a lot more of the pathological case, like body builders, tall folks who are overweight but not obese, etc.
This is a bit like saying "after accounting for inseam and glove size, height does not predict the probability of hitting your head on low doorways".
Right? I mean if I can be tall without having long legs, surely I can be morbidly obese without having inflammation and insulin response disorder
I can't read the study directly (and it's not my field, which makes reading it directly challenging), but this is the abstract conclusion:
` 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.`
Excess fat -> insulin resistance -> higher fasting insulin.
This is mentioned in the article, I must admit I previously thought it was as you say, but:
"available evidence in humans suggests that hyperinsulinemia precedes weight gain (rather than the other way around)"
Key takeaway:
"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?
You're missing the other direction: those people who have insulin resistance and inflammation and aren't clinically obese.
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.
> 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.
That's a very unfair strawman.
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:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963496/
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.
I’m not getting it? Can you dumb it down?
First off, I'm no doctor or even close.
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.
>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.
The researchers tried to subtract out the mortality risk of elevated C-reactive protein (aka CRP, inflammation market) and higher fasting insulin.
However, both elevated CRP and higher fasting insulin are correlated with obesity, so controlling for these variables seems misleading.
> 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).
This isn't surprising. BMI increases bring reduced insulation sensitivity, which in turn is what causes the issues. The fix is to diet and exercise. At the end of the day we don't care about BMI, we care about insulin sensitivity - but it is easier to measure BMI than blood insulin. BMI isn't a perfect indicator but it's a pretty good one.
"The fix is diet and exercise" is not correct at all. There is no evidence on population level data or studies that diet and exercise produce durable BMI loss on a population level. From a "calories in calories out" perspective it is naively true, but in practice it doesn't work at all. The issue is that when people have BMI>30, their bodies endocrine system gets pretty messed up and their bodies will basically request 3500 calories per day. There have been a number of breakthrough medicines in the past few years that disrupt this cycle and reliably produce weight loss on a population level through hormonal changes that reduce appetite and delay gastric emptying. Some examples of these drugs are Tirzepatide and Semaglutide.
A caloric deficit will produce weight loss. If you're arguing that this isn't sustainable due to the amount of calories being "requested" by people's subjective desires and experiences, that's a completely different (and also incorrect) argument.
There are many double blind studies on this. On a 2+ year time horizon, the huge majority of obese people who follow a "eat less exercise more" regime lose weight and then gain it back. This happens because the people never stop being hungry due to the disruption that obesity puts on their endocrine system. There are a number of medicines (saxenda, liraglutide, ozempic, mounjaro, wegovy) that produce reliable robust weight loss on a 2+ year time horizon. These medicines work best with a change in diet and exercise habits, but reliable weight loss on a population wide scale is not something you treat with "diet and exercise" advice.
Not really?
Yes a lot of crash diets fail, for obvious reasons, but once a diet has stabilized the cravings will go away.
It does for many people mean they will need to cut out or dramatically cut down the eating out, drinking and instant meals. Most people don't want to do that.
Substantial weight loss is possible across a range of treatment modalities, but long-term sustenance of lost weight is much more challenging, and weight regain is typical1–3. In a meta-analysis of 29 long-term weight loss studies, more than half of the lost weight was regained within two years, and by five years more than 80% of lost weight was regained (Figure 1)4. Indeed, previous failed attempts at achieving durable weight loss may have contributed to the recent decrease in the percentage of people with obesity who are trying to lose weight5 and many now believe that weight loss is a futile endeavor6.
Obesity is a problem of modernity and specific cultures made up of people who didn't used to be obese generations ago. Are the populations around the world in which people aren't generally obese just filled with a large subset of the population constantly starving...or we agree that no such large subset is simply destined to obesity.
If we agree on this, then your argument isn't that people are destined to obesity, but rather that once they're obese, they have patterns of behavior that are extremely hard to break over a long term basis. That isn't the same as saying that weight loss is a futile endeavor, it's just saying that people who are obese are very often going to fail to stick to the patterns of behavior that resulted in weight loss.
My argument is that in 2022, the medical advise and consultation of “diet and weight loss is the solution to obesity” is not true on a population level. We now have other tools to address obesity that are both pharmacological (GLP-1/GIP acting) or surgical (bariatric surgery). We should stop admonishing patients for not following treatment guidance (eat less, exercise) and instead provide them with solutions that actually work reliably. I have nothing to add to the causes of obesity, and eating properly and maintaining a high level of activity are clearly good at preventing people who have never been obese from becoming obese.
Sure a caloric deficit will produce weight loss. Obviously. But reducing calorie intake alone does not guarantee a calorie deficit. While there is of course some level of unavoidable caloric expenditure, the average person has a fair bit of expenditure that is quite avoidable.
It is not hard for the body to discourage unnecessary caloric expenditure in response to a notable caloric deficit. Indeed, doing just that is a basic famine survival instinct.
Now given the decidedly non-famine conditions, eventually things should restablize, but it does mean for a person at caloric equilibrium, reducing caloric intake by say 500 Calories, will often not result in a 500 calorie deficit, but a smaller one for for quite some time until the body adjusts to this being the new normal.
In the mean time, the person likely feels like shit. Furthermore, If there actually is food available, the body and subconscious mind is doing everything it can to encourage the person to eat more.
This substantial resistance of the body to attempts to run meaningful caloric deficits for an extended period are a not insignificant portion of why "dieting" often fails. People don't stick with it, since it majorly sucks.
> Results: Despite heterogeneity across studies, we observed reductions in pooled effects for overall food cravings (-0.246 [-0.490, -0.001]) as well as cravings for sweet (-0.410 [-0.626, -0.194]), high-fat (-0.190 [-0.343, -0.037]), starchy (-0.288 [-0.517, -0.058]) and fast food (-0.340 [-0.633, -0.048]) in the meta-analysis. Baseline body weight, type of intervention, duration, sample size and percentage of female subjects explained the heterogeneity. > > Conclusions: Calorie restriction is associated with reduced food cravings supporting a de-conditioning model of craving reductions. Our findings should ease the minds of clinicians concerned about increased cravings in patients undergoing calorie restriction interventions.
Substantial weight loss is possible across a range of treatment modalities, but long-term sustenance of lost weight is much more challenging, and weight regain is typical1–3. In a meta-analysis of 29 long-term weight loss studies, more than half of the lost weight was regained within two years, and by five years more than 80% of lost weight was regained (Figure 1)4. Indeed, previous failed attempts at achieving durable weight loss may have contributed to the recent decrease in the percentage of people with obesity who are trying to lose weight5 and many now believe that weight loss is a futile endeavor.
Appetite changes likely play a more important role than slowing metabolism in explaining the weight loss plateau since the feedback circuit controlling long-term calorie intake has greater overall strength than the feedback circuit controlling calorie expenditure. Specifically, it has been estimated that for each kilogram of lost weight, calorie expenditure decreases by about 20–30 kcal/d whereas appetite increases by about 100 kcal/d above the baseline level prior to weight loss31. Despite these predictable physiologic phenomena, the typical response of the patient is to blame themselves as lazy or lacking in willpower, sentiments that are often reinforced by healthcare providers, as in the example of Robert, above.
>their bodies endocrine system gets pretty messed up and their bodies will basically request 3500 calories per day
And what if they don't eat that much? They die or what?
You risk alienating people by focussing on BMI though. Weight has been moralized in the US (being fat is seen as a moral failing). People do not easily accept advice that is given through a moral lens.
The data shows that there is a better measure than BMI which doesn't carry all the stigma, so why not use that one?
> 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.
My understanding is the argument is not whether to use someone's fatness as a measure of health if there's a much better, specific metric besides being fat (ie. resting insulin levels) to prescribe exercise and diet over.
I don't think it'll reduce stigma or whatever of fat people, but I do agree that if someone is fat but their insulin is normal maybe a doctor can pay attention to something else like if they came in for an allergy test or something they may not need the diet/exercise spiel. Similarly if someone's thin but their insulin is crazy its time to talk diet/exercise.
There is a rare, rare, rare chance you can some weird diseases that mess up insulin sensitivity, so you can be skinny and have issues. Those are rare and not solved by diet and exercise.
Otherwise if your insulin is high, you need to diet and exercise. Measuring blood insulin is a lab procedure - you go to a collection lab, you get jabbed, they mail it for testing.
Measuring BMI requires stepping on a scale and knowing how tall you are.
> Measuring BMI requires stepping on a scale and knowing how tall you are.
There are contradicting posts in this very thread that say high BMI and obesity aren't necessarily the same thing, because apparently you can be tall and be only mildly into lifting and suddenly you have a high BMI. If that's the case [I'm not a lifter] then it makes total sense to me to track resting blood glucose, not obesity, because it's simply the more accurate measurement.
> because apparently you can be tall and be only mildly into lifting and suddenly you have a high BMI.
Very unlikely. BMI is a standardized model. Unless you are dramatically out of the parameters (you're 7'2" or you are an olympic lifter) it is pretty accurate.
You can also use calipers in that case - you need someone to help you because you can't reach it yourself but it's very fast and accurate.
Again, insulin testing is expensive, invasive and time consuming. You might get insulin tested once a year.
I'm merely pointing out that it's apparently not as simple as stepping on a scale because no one can get their heads straight about high BMI's causation to begin with or what to do about it.
It just seems much simpler to me to take an actually accurate test once a year and prescribe purely based on the accurate testing. That way we also get skinnyfat people.
Imagine if once a year, your boss sat you down and went "Hey, you did a terrible job this year. No promotion."
You might ask him why he didn't give you any feedback earlier so you could have fixed the issue. "Oh, well I only give feedback once a year since it is hard to do".
You need regular (weekly, biweekly) feedback on your diet.
This seems like a textbook example of the model 11 "bad control" from <http://causality.cs.ucla.edu/blog/index.php/category/back-do...>. X is BMI, Y is mortality, and Z is fasting insulin and blood sugar. Basically, if X causes Z and Z causes Y, then controlling for Z hides the relationship between X and Y.
Does it hide, or does it actually clarify the relationship if after you do that BMI is negatively correlated to mortality at the same fasting insulin and level of c-reactive protein?
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.
The percentage of people with normal BMIs and type 2 diabetes or prediabetes is so small that is irrelevant from a mass health perspective.
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.
> The percentage of people with normal BMIs and type 2 diabetes or prediabetes is so small that is irrelevant from a mass health perspective.
Then my father is irrelevant, being diagnosed with prediabetes at 6', 165lb.
So is it really irrelevant numerically, or is that hyperbole? Does your irrelevance include millions of people?
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edit:
> There is no evidence that obese BMIs are negatively correlated to mortality, only the opposite.
TFA mentions that it is negatively correlated when you control for two things that are positively correlated with BMI. So, while the study doesn't say that high BMI reduces mortality (it in fact observes the opposite), nobody claimed it did.
But in finding the negative BMI correlation when controlled for insulin, it does make a very good case that
> 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.
are largely irrelevant to the mortality of the obese relative to the thin, and inflammation and insulin resistance are decisive.
> Then my father is irrelevant, being diagnosed with prediabetes at 6', 165lb.
BMI is a population-level metric, and population-level analyses of health risks, from an epidemiological perspective to inform healthcare providers and public health officials of risks, frankly, don't care about your father.
Yes, it's irrelevant numerically, and it's irrelevant numerically because there's little evidence that any significant portion of the population (much less millions of people) falls into this category, whereas we are one of the fattest countries on Earth, which has absolutely no need to minimize or downplay the health effects of that.
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Edit (ugh):
> TFA mentions that it is negatively correlated when you control for two things that are positively correlated with BMI.
Kinda the point is that TFA is mathematical gaming which doesn't yield any actionable results for healthcare providers.
> So, while the study doesn't say that high BMI reduces mortality (it in fact observes the opposite), nobody claimed it did.
You did, a bit:
> It also means that if we can control people's reactions to sugar, their weight becomes irrelevant (or possibly even protective.)
There is a range in which increased BMI provides increased survivability from catastrophic events, since the body has energy reserves and some protection from trauma, but then it drops off a cliff. It's not going to be "irrelevant" for health outcomes, much less protective very far outside of the overweight range.
> are largely irrelevant to the mortality of the obese relative to the thin, and inflammation and insulin resistance are decisive.
Yeah, ok. I guess a bunch of things which every significant health organization on Earth calls out as leading causes of mortality and linked to obesity are actually due to inflammation and insulin resistance, which must also have an effect on how hard it is to push a tube into an obese patient's throat, to find a vein to get a line in, the amount of pressure their weight exerts on their lungs, the amount of medication it takes to keep them anesthetized, how much fat accumulates in their liver, plaque buildup inside arterial walls, etc. Definitely just inflammation.
"The increase in mortality that has been attributed to higher BMI is more likely due to hyperinsulinemia and inflammation rather than obesity."
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.
And... one big factor in inflammation is our modern lack of sun exposure (infrared).
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.
If someone is in sufficiently acute danger that a hospital bed is under discussion, I suspect that the manner of lighting and any putative benefits thereof is a relatively small concern.
Look at the research. Inflammation is naturally removed from mitochondria with the use of naturally occuring infrared light. (I know it sound far fetched and hippie)
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.
Is this more or less saying there's no definitive link between obesity and mortality risk?
Not really, their conclusion is simply worded in a highly misleading way. They say the increase in mortality is due to hyperinsulinemia and inflammation, however both of those are caused at least in part by obesity.
> both of those are caused at least in part by obesity
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.
Of course you can have inflammation without being obese, no one here is arguing for that. The point is it's very rare to find someone who is obese without inflammation. In other words, A implies B does not mean B implies A.
> very rare
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.
For whatever reason you seem to be building a lot of strawmen here. No one prior to you was talking about 100%. Similarly for shifting the onus, you can pick up most any study on obesity and inflammation. Not liking medical facts does not make them go away.
Sorry. Maybe I lost sight of the context of your original reply.
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. :)
This is not the way to react when asked for evidence of your claim. Instead of talking about 100%, subtract "very rare" from 100%, and supply evidence for that. It's difficult not to like "medical facts" when none have been offered.
If I am reading it correctly, if you can maintain good fasting blood sugar - yes. However, that is a big “if”, because those are related.
I’m not very well versed in this terminology, what does a “good fasting blood sugar” mean? Does that mean that generally speaking, your blood sugar remains relatively stable / low? Eg a person eating mostly meat and no sugar?
It means that you aren't insulin resistant and it actually does its job.
Ya, I'd like to understand this too. How do you manage this? And do obese people generally have this problem (hence the correlation, but not causation)?
Since obesity is often caused by a poor diet/lack of exercise maybe that causes obesity and also causes insulin resistance, not that poor diet/lack of exercise causes obesity causes insulin resistance. So you can be fat off salad and be ok and also be thin off canned chili and not ok.
There aren't people who are fat from salads, except for the loosest definition of the word.
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.
Well said. I was almost T2D then lost >100 pounds with strict keto going from terrible BMI to ideal and my N=1 experience fully supports your explanation.
I'd be curious for a follow up study to measure if thin people with high fasting blood sugar can be predicted to have the same mortality as fat people. The confirmation of skinnyfat, basically.
Is there any evidence that "skinnyfat" people have high fasting insulin levels?
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.
Not really - it's just saying that the definitive link is almost entirely caused by hyperinsulinemia and inflammation, and if you control for them, there's no other causality. Hyperinsulinemia and inflammation are massive metabolic problems, controlling for them is effectively like controlling for lung cancer in a study of smoker. Like, sure, people aren't choking to death on cigarettes.
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.
That's what the conclusions appear to be saying:
> 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.
But isn’t the obesity causing the higher fasting insulin?
Isn’t high BMI interchangeable with obesity in most studies?
As a side note, BMI is a terrible measure of obesity for outliers. I have several first hand experiences where the BMI indicates obese or even morbidly obese, while the DEXA scan would show fat in single digits.
> BMI is a terrible measure of obesity for outliers
That's basically tautological. Outliers are outliers because they don't fit the model.
BMI is a terrible measure in general, not just for outliers. It doesn't normalize well to fairly obvious factors. You could arguably get a better reading just by looking at someone and visually estimating how fat they are.
Waist measurement is a stronger measure but still flawed.
Yea, ask many athletes at the US military academies about this. All of the football players basically had to have a waiver for BMI for the military standards or had to get taped (body dimensions measured) to do a more-complex calculation to determine a more accurate fat content. They also had to make standards in off-season, so the big linemen were constantly eating before the season to put on weight, then working hard at the end of the season to lose it.
What does this mean for us T2D types that need the insulin? Are we just fucked?
it's saying that high BMI as a cause of premature death is likely just a proxy for high fasting insulin and inflammation and is not _by itself_ life shortening.
for folks like yourself with T2D, noting changes. Keep on keeping on (i.e. follow current medical advice)
> it's saying that high BMI as a cause of premature death is likely just a proxy for high fasting insulin and inflammation and is not _by itself_ life shortening.
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).
All valid points, thanks :)
Well shit, my BMI is 35. And I've got a pair of stents in my ticker. OTOH I'm doing crossfit 3x/week. And can dead lift over 300# so I feel like I'm getting better. ALso, I'm built like a fireplug, so probably not fat as just big. BMI is a shitty measure.
What is your actual body fat content? And I mean by a real test like a DEXA scan, not calipers.
whoops, didnt see this. No real test done. My scale (that i haven't jumped on in forever) says like 35% at the last "scan".
Those scales use electrical resistance as a procy measure of water density, a proxy of muscle to fat ratio. It's a tenuous link and isn't all that accurate. If you can afford the $100, go get a DEX scan.
TLDR this is only about obese people, don't bother reading if you have healthy BMI, heck median BMI of participants was 27, way beyond healthy since overweight starts at 25 and I would say even that is very generous
~20.3 here
Using the primary cohort, time to mortality was regressed on all three exposures of interest: BMI, fasting insulin, and CRP. A number of parametrizations of these three exposures were explored. The models with the best fit used linear and quadratic terms for BMI, a linear term for fasting insulin, and the natural logarithm of CRP.
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.
"Please don't post shallow dismissals, especially of other people's work. A good critical comment teaches us something."
"Don't be snarky."