Returned to this question by a current thread on fat people surviving longer on a desert island, particularly:
http://boards.straightdope.com/sdmb/showpost.php?p=16949591&postcount=11
I’ve heard different answers and can’t remember the reasons given.
ETA: That’s some pretty fine quotin’, if I do say so myself.
ETA2: Must remember to start thread in ATMB about why the heck it’s so hard to do nested quotes here.
ETA3. It’s by WhyNot.
No, it isn’t. Some Type 1 diabetics are adult-onset, although in adults, the onset is usually much less dramatic than in children or teenagers; in children, it can come on in a matter of hours, whereas adults can develop symptoms over days or even weeks.
There’s one subtype that some people have dubbed “Type 1 1/2” because it’s not related to obesity, and people who have it use a combination of oral antidiabetic drugs and insulin for optimal control. I’ve seen it in people as young as their early 20s, and this woman was actually underweight.
Gestational diabetes, which can indicate a predisposition to Type 2 diabetes later in life, is not related to obesity as much as it is to maternal age. The older the woman, the more likely she is to have it, although teenage mothers are not exempt from it. It usually goes away when the baby is born.
My mother was diagnosed as Type 2 when she was in her 60s. She was petite and somewhat underweight.
My spouse is considered Type II. He was diagnosed after a bout of pancreatitis that destroyed a good piece of his pancreas. What’s left apparently works just fine, there’s just not enough of it to entirely do the intended job. No one is sure why he came down with the condition - he entirely lacks the two biggest risk factors: alcoholism and gallstones. Nor is he obese. The only explanation is “sometimes it happens and we don’t know why”.
My wife is Type 1, which used to be called juvenile diabetes. For Type 2 / Adult-Onset, it is predominantly caused by obesity but that’s not the only cause, as others have already said. Genetics and gender can contribute to the cause of Type 2, and even a lack of sleep and its effect on metabolism.
From Type 2 diabetes - Wikipedia
… and …
An asthmatic Doper recently mentioned inhaled corticosteroids were causing diabetic symptoms. The further discussion seemed to indicate that these results can be permanent with continued use.
This is very very similar to me. I had a bout of pancreatitis (again, no known cause - possibly genetic) about a decade ago, and it apparently kept up on a slow, asymptomatic burn until my pancreas had almost completely shriveled up and died. In my case, though, I’m much more like type I, because my pancreas is essentially completely gone and not making anything.
My doctor said that technically, I’m not considered type I or type II. To be “real” type I, you need to have the autoimmunity that is what usually causes it.
So, anyway, I am a case of adult-onset diabetes that is not type II or linked to obesity.
You might be interested in this past thread.
12% of newly diagnosed diabetics have a “normal” BMI at diagnosis. They have a distinctly worse prognosis than those who are overweight or obese at diagnosis, a situation sometimes referred to as “the obesity paradox.”
As has already been amply said, but I’ll back up with more anecdotal evidence: No, DMII is not always linked to obesity, but if you’re a betting man, that’s the way to bet.
I wasn’t aware that the prognosis was poorer, but it doesn’t surprise me much. It seems that my normal or underweight by BMI patients with DMII (I’ve had five, out of a couple hundred patients with DMII) have a lot more difficulty with blood sugar control, even when they eat “right.” And they just cannot seem to “cheat” like the obese patients can - even a little splurging sends their sugars wonky, and they report a greater number and more bothersome symptoms of hypoglycemia at higher numbers than obese patients, and also a greater number and more bothersome symptoms of hyperglycemia at lower numbers. So it’s harder for them to stay in their safe window, *and *that window is smaller. Major suckage. Major *anecdotal *suckage, I hasten to reinterate. I don’t know if studies have looked at or borne out my “narrowed window” hypothesis.
On the other hand, at least most of them can get their own shoes on to protect their feet, and can look at their feet to pay attention to and keep an eye on any cuts or nicks they get. The obese patients often have trouble physically reaching their feet for diabetic foot exams, and that’s bad for keeping all your limbs. 
On top of that, the disease process can often be reversed if an obese person loses enough weight (although how often does that happen? Essentially never). A person who’s of normal or under-weight doesn’t have that option.
My mom was diagnosed with Type II when she was in her mid 40s and she told me it was because her pancreas had been producing too much insulin and then suddenly stopped. I have no idea, I was around 17 then and didn’t do much research on it. Is something like that possible? I could try looking that up. She’s not obese, but does have fat in her abdominal area which is know is considered to be worse than having a more even distribution of fat.
Suddenly? No. But inexorably, yes.
You describe her as what are clearly one segment of those referenced in my post above - metabolically obese normal weight (MONW); overlapping with thin outside fat inside/skinny fat - BMI may be fine, percent body fat even possibly (although often not) but the where they have their fat is intra-abdominal including in the liver. That pattern is associated with increased and increasing insulin resistance. Consequently the pancreas has to produce more and more insulin to keep blood sugar in range and eventually it can’t keep up and at some point after that begins to burn out. Maybe she progressed from “can’t keep up” to “burn out” pretty quickly.
It is not clear that all MONW have central fat with normal BMI but clearly it is at least a common pattern.
Unless I missed it, why again is fat around the belly different than fat around your butt/thighs, say, different as far as your endocrine system cares?
I was diagnosed with Type 1 at age 38, and the doctor who eventually diagnosed me told me she’d diagnosed people in their 80s with Type 1. So no, it’s not always linked to obesity.
Also relevant: although I was a regular exerciser, ate fewer carbs and more vegetables than they told me a diabetic should, and had a BMI of around 24, I was first diagnosed as Type 2. I’ve also talked to more than a few fit, thin Type 2s. It happens.
Are you/they sure they’re Type 2? I ended up having to go to Joslin Diabetes to get my proper diagnosis. What I dealt with in the 6 month prior to that was very much like you describe: I was on Lantus (long acting insulin, for those who don’t know. 1 shot a day). and Metformin, yet still could not eat more than about 10 carbs at a time without having a major spike in blood sugar that took forever to get down. It was even worse pre-Lantus. I had a strong feeling I’d been misdiagnosed, so managed it by just not eating carbs until I could get to a specialist.
Anyway, the point I was trying to make is that once I got to Joslin, they told me they saw lots & lots of people who were diagnosed incorrectly. Most docs don’t see ketones and immediately say “Type 2”, but it’s more subtle than that, according to the Endos at Joslin.
Here’s an excerpt from the Wikipedia article on abdominal obesity:
By the way, if you do a Google image search for “obesity” and “diabetes risk,” you will see pictures which show a pretty strong relationship between obesity and diabetes. And which seem to bear out what Whynot said about the odds.
It may even be that subcutaneous fat, at least the superficial componant of it (SSAT), compared to the deeper subcutaneous componant (DSAT) is protective, resulting in total subcutaneous fat as neutral. Apparently subcutaneous fat outside the fascia superficialis is specifically associated with lower risks. The person with washboard abs is not the ideal from the health perspective.
Who knows if the compounds that the Wiki article are the whole story or not? I’d doubt it. What we can say is that we have to think of fat tissue as part of, a huge part of, the endocrine system. And different adipose tissue behaves differently in that role. Different portions of adipose tissue respond differently to different stimuli (foods, exercise, etc.), produce different stuff, so on.
Everything you say here is amazing and ignorance fought.
Also, just to be clear–to myself also, because I was starting to forget–the “fit/not fit” thing we’re talking about is the predispositive case. Getting fit, ie exercising, hasn’t nearly so many open questions.
Ummm, right?
Not sure if I understand the question but there is no question that regular exercise makes DM easier to control and helps delay or even prevent it by several means -
Within a period of time it increases insulin sensitivity (and needs to be kept up regularly to do that).
Over time it changes body composition, increasing fat free mass and preferentially decreasing visceral abdomninal fat.
It lowers the risk of a host of potential complications and comorbidities of diabetes.
Odds are a combination of both aerobic and resistance exercise is most effective in treating, delaying and preventing T2DM. Details here.
A recent BMJ article put it into some perspective:
NYT had a nice summary of it.
(Bolding mine.)
You gotta exercise. Gotta gotta gotta. Don’t worry about the scale as the goal. The exercise itself is key to control your diabetes, as important as medicine is.
Well, $360 ago I signed up for monthly membership at a gym after the most recent time the riot act was read to me by my endocrinologist. It would have been simpler, and I would have gotten more exercise, to walk past it once a month and tear up a $50 and four $10s.
His office just called, coincidentally. Time to face the music again.