I understand that overweight and diabetes are strongly correlated. And I think that extra weight can cause a person’s body to be less sensitive to its own insulin. That would seem to be a causative factor, but is there a direct causal link between overweight and diabetes? And how is “overweight” defined in this case?
Way it was explained to me was:
Pancreas pushes out insulin as needed by body when sugar comes in.
Insulin needs to travel through body.
Fat in stomach stops insulin reaching needed areas.
Pancreas has to pump out more insulin to compensate.
Pancreas gets overworked and starts to ‘die’ ie produce less insulin.
Eventually cant produce enough insulin - diabetes.
Losing weight means pancreas works less, so lasts longer - delay diabetes or reduce effects of lower pancreas output.
Cant say how much is ‘overweight’, but there are standard waist sizes that are considered risk factors. And thats why waist size is a bigger risk than your overall fat as thats the fat creating a barrier.
Otara
I don’t know the connection. I do know that a larger waist results in a higher diabetes risk. I believe a waist of 40" or higher gives 12x the type II diabetes risk of someone with a waist of 34" or less.
However because (aside from surgery) we really don’t know how to make people lose significant amounts of weight and keep it off I don’t know if those numbers apply to people who were originally fat and became thin. ie, would someone who had a waist of 46" and lost weight and developed a waist of 32" (a loss of roughly 70 pounds) have a 92% lower risk of type II diabetes over the course of the next 10-20 years? I don’t know. Are obesity and type II diabetes both symptoms of the same metabolic issues, or does obesity cause diabetes, or something else.
I also know that obesity surgery can clear up type II diabetes within hours or days. So if a person weighs 400 pounds, has surgery and weighs 395 pounds 2 days later their diabetes may have already cleared up. So severely obese people who get obesity surgery can see their blood sugars normalize before any significant weight loss occurs.
this is going to be one of those threads where everyone who posts in it fancies themselves a physiologist, right?
The explanation I gave is what I was given during my diabetes course 2 months ago ( as in education for people at risk ie me, not as a professional).
I am not a physiologist, and I may have misremembered, but it did explain to me why they focus on waist as a risk factor so much rather than fat levels alone.
Otara
Why would it do that? The insulin is in the bloodstream, the fat is inside the cells of adipose tissue. (I presume by “stomach” you mean the belly area. Having fat in you actual stomach has nothing particularly to do with obesity.)
IANA physiologist but I do have type II diabetes that was caused by being overweight (currently controlled by diet and exercise). So it is something I’ve done a bit of research on since it does affect me directly.
The way it was explained to me is that if you are overweight, fat can clog up the insulin receptors in your cells. In response to this, the cells in your pancreas have to work harder to produce more insulin to overcome all of the clogged insulin receptors. Over time, the extra strain on the cells in your pancreas can damage them, and these cells don’t grow back. Once they are gone, they are gone.
If you catch it in time, you can reduce your weight through diet and exercise, and if the cells in your pancreas haven’t been damaged too badly, you can basically be “cured” and don’t have to go on medication. However, the cells in your pancreas have been permanently damaged by this point, and I know our resident QtM likes to call it “managed” rather than “cured”. If you do too much damage to your pancreas, then you are on meds (and possibly insulin) for the rest of your life.
Forgot to answer this part.
Overweight is when the fat clogs up the insulin cells to the point where it overworks your pancreas and causes damage. Some people just naturally have fewer insulin receptors and are therefore more prone to this type of thing, where other people have more insulin receptors and can tolerate being more overweight before they start overworking their pancreas. So there’s no simple hard and fast definition of “overweight” in this case. It depends on the person.
I dont know. I suspect this was given at a ‘atoms are made up of’ explanation level, where the reality is more complex.
Otara
Several levels of explanations.
The first level of explanation is focused on downregulation of peripheral insulin receptors as result of long term exposure to excess energy, so much so that fat cells get to where they no longer sucks it up so effectively.
But of course the real situation is much more interesting and complicated than that.
Fat also contributes to inflammation (via both free fatty acids and a variety of other inflammatory molecules) which also has a major role in insulin resistance (including in brain tissue which in turn regulates metabolism and appetite). Certain foods, in particular the mainstay high simple carb/high fat foods prevalent in the American diet, are very potent at triggering that inflammation as well. Also obesity is correlated with less muscle mass and less exercise, whereas more muscle exercising more results in greater insulin sensitivity.
The bit with central (abdominal) obesity being particularly correlated with diabetes risk may be both because its inflammatory products have more of a direct shot at the liver and pancreas causing direct damage, and because that visceral fat is different, secreting products that more directly impair insulin function.
Overweight and obesity are clinical terms based on BMI. Some believe that percent body fat or waist hip ratio would be more useful, but that is a debate, not a GQ.
It must also be added that degrees of susceptibility to Type 2 diabetes also exist, based on genetic factors, on prenatal nutritional factors, on early life nutritional factors, and on multi-generational epigenetic factors. Some can tolerate a degree of overweight without triggering much in the way of insulin resistance, others will become insulin resistant with no overweight at all, and some of the same factors that predispose to Type diabetes also predispose to central obesity. In short, obesity is a major contributing factor to Type 2 diabetes but the causality chain is not completely linear.
I hope that helps more than confuses.
IME
About 7 or 8 years ago I hurt my back, for about 4 years I was incapacitated, I gained a lot of weight, I reckon I weighed about 19stone (260+ lbs), because I’m ~6ft I didn’t look obese although I was classed as medically obese, my waist measurement was always the smallest of my three measurements.
I went to the doctor in terror of Type II Diabetes, had bloods taken and was told I was in the clear.
Three years later, my back is okay, I’ve been exercising, have lost a load of weight and have gone on holiday. While I’m on holiday I feel ill (lightheaded) after 4 days I go to a doctor, he checks me over, can’t find anything wrong, does a blood test. Results come back, he is completely unconcerned and suggests I might want to have that re-done when I get home.
I come home, take the test results to the locum who is standing in for my own GP, she doesn’t seem overly bothered at the numbers on the sheet and mentions my iron levels are slightly raised, but since I’m here she takes bloods. 48 hours later I’m asked to come down tomorrow morning fasting.
Next day I’m told I have Diabetes, the doctor is in near hysterics, gives me a script for meds and tells me to start taking them immediately and come back every day for the next week. A week later she increases the dosage of my meds.
I speak to the practice dietician - she’s obviously expecting me to have a dreadful diet/exercise regime. I tell her I’m carer to my Mother, and give her a list of what I eat a day. My late father had a bad heart and we have eaten a low fat diet for over 20 years, and my exercise regime was better than average. None of my immediate family have Diabetes. She couldn’t understand why I’d been told I had Diabetes and suggested I go back to the GP and ask for further testing.
MY GP took more blood and said I was diabetic. I reminded her of the bloods from a few years ago that were normal (no pre-diabetes signs) when I was grossly overweight. She dismisses it as one of those things. I ask about the bloods from when I was on holiday, and she can’t find the results in my records, but looks at my notes and there’s nothing in there [that the locum wrote] about my blood sugars being too high…
I’ve been told by a worker at the Carers group that I attend, that the lightheadedness I’d felt when I was on holiday was probably my stress hormones going mad as I wasn’t stressing at the time, and that the high mmol (20+) on the morning that I’d been fasting could have been the stress of coming home and my mother screaming abuse at me non stop for having gone off gallivanting while she had to rot in a home :rolleyes:
I was tested for Diabetes in my teens when I took ill. All tests were negative.
All I know is that a gastric bypass, especially a mini gastric bypass, cures diabetes almost overnight.The important thing to note is that the surgery cures diabetes e*ven before any significant weight is lost. *
The mechanics are not very well understood yet, but IMHO it points towards one possible cause of diabetes being correlated with something that also correlates with obesity. In other words: it’s complicated.
I remember a radio interview about diabetes once with the inventors of the 30-second workout.
Sounds like a joke, and it was introduced with the “silly” angle, but the interview was quite serious after that. These were a bunch of university researchers; their theory was that people who were fat, consumed a significant amount of carbs and did very little exercise were prone to diabetes.
The problem was that the cells stored as much energy as they possibly could (as ATP?), from the sugar in the bloodstream. Eventually, the cells cannot store any more. However, the person continues to have high blood sugar from their diet, and the pancreas continues to pump out insulin as a reaction to that, trying to get the sugar to go into the cells. Eventually, the cells “learn” to ignore insulin.
(Then, in response to increasing levels of blood sugar, the body produces more and more insulin until in the later stages the pancreas burns out and you may stop producing insulin…)
Their test was to take a high-risk person, put them on an exercise bike, and pedal as hard as they could for 30 seconds. In the first 30 seconds, you burn up most of the stored energy (ATP) in your muscles. The thigh muscles are pretty much the biggest muscles in the body, so draining themat least once or twice a week meant that those muscles, at least, would not forget how to “reload” with sugar using insulin.
The experiment showed promising results, but it was long-term. They had to track a sizable sample and see if this regimen reduced the proportion who became diabetic, and their results were beginning to show that it did.
The suggestion was that regular serious exercise was the best way to prevent type II diabetes. Also mentioned was that once this process began, it was not reversible. Diet and exercise could keep blood-sugar within tolerances, but the cells did not seem to relearn forgotten insulin sensitivity.
It’s multifactorial as I’m sure you know. Here’s a much abbreviated, incomplete, semi-physiological overview:
Obesity, that is, abdominal obesity, leads to insulin resistance. As has been stated insulin resistance means the pancreas must put out more insulin. Eventually it becomes “exhausted”.
But, there is another important, probably causal, factor regarding obesity. Specifically, the more abdominal fat someone has, the higher will be that person’s level of free fatty acids (FFA). That happens as a result of the spontaneous breakdown of stored abdominal fat into its constituent parts, i.e. into FFAs and glycerol. This is simply a consequence of the chemical equilibrium between FFA + glycerol <==> fat. In other words it is not 100% over to the ‘fat side’. Basically, FFAs leak out of fat. Now, that in turn means that the more (abdominal) fat you have (i.e. the “fatter” or more obese that someone is), the more FFA will leak out of it (by ‘mass action’). And, insulin resistance (or insulin lack) causes even more FFA to leak out (i.e. insulin normally shifts reaction to the ‘fat’ side).
What is the effect of high levels of FFAs? Three-fold (at least). High FFAs cause more insulin resistance (or at least prevent the muscles from using glucose as they should - see Randle cycle). And high levels of FFAs impair the pancreas’s ability to make insulin. The potential for a vicious cycle leading to less and less insulin, while there is more and more insulin resistance, is pretty clear. As an extra ‘insult’, high FFAs also signal the liver to make more glucose. It’s important to note, as well, that any degree of high blood sugar (however caused) will also lead to more insulin resistance and less insulin secretion by the pancreas. Bingo.
Dr. Gauss - thank you.
How sure are we about that?
I understood* that this study was reported by the same surgeon who was doing the surgeries, and that so far no other study has been able to confirm those results. So at this point it would be preliminary, at best.
- from my vast medical knowledge, which comes from listening to a half-hour NPR program about this.
It shouldn’t be surprising that glucose levels are lowered almost immediately following gastric bypass surgery (which is not the same as ‘curing’ diabetes). Whenever there is dramatic and sudden caloric restriction (however achieved, including good old “diet”), the liver stops making excessive glucose which is a key contributor to the elevated glucose levels of diabetes.
In terms of the benefit of such surgery, it really does seem to work (in good hands). This eight-year old paper showed an over 75 percent resolution of diabetes following the operation (and over 85 percent significantly improved).
More recently, and in my opinion, more importantly, this recent paper showed bariatric surgery not only helps the diabetes, but leads to about a fifty percent reduction in heart attacks and strokes.