Do Carb-Heavy Eaters Get Diabetes?

I was reading something about people who have lived on high carbohydrate diets for years-most are not obese , and are actually quite healthy. White potatoes are some of the highest glycemic foods around-yet the Irish lived off them, quite successfully.
So my question: doe people like the Peruvians, Bolivians, Irish, etc. (who subsist mainly on potatoes) have any unusual incidence of diabetes? A potato diet would be boring as hell-but could it actually be healthy?

No, a high carb diet does not necessarily lead to diabetes. But a high carb diet is detrimental to a diabetic person. What you are questioning goes way back and much has been learned since then. For instance, when I was a child the disease was commonly called sugar diabetics and it was thought that (at least to layman) that it was caused by eating too much sugar. We now know better.

Of course if you are pre-diabetic and are eating a high carb diet it may hasten the onset of full diabetes, but that is only if you are per-disposed to getting the disease in the first place.

Also, while a lot of what they ate was potatoes, that doesn’t mean they ate a lot of potatoes, relative to their activity level

A lot fo people are, however. Not that many people manage to get to old age with a trim waistline and a fully active lifestyle, so it definitely becomes a risk factor.

Diabetes mellitus is called “sugar diabetes” not because it was thought to be caused by eating too much sugar, but too much glucose is in the blood, not being taken up by the liver and muscles. There is another type of diabetes, diabetes insipid, which is a different problem.

From what I know about the mechanisms of diabetes (there are several) I doubt that’s true, but what can happen is that developing a constant urge for carbs when you didn’t use to have it can be a sign of diabetes setting in: your cells are not getting the sugar they need, so they keep asking for it, so you crave sugar, but because the process chain is broken your cells are not getting the sugar they need…

Yep, they used to call the other kind water diabetes.

Recent research however does show that the level of added sugars in the diet correlates with increased diabetes mellitus risk for any given genetic predisposition or bmi. The study was over hyped with calling sugar toxic but the finding of increased risk as an independent factor seemed valid.

Too much sugar makes you fat.

Too much fat is associated with diabetes mellitus.

In between the two are a number of other factors including your genes.

Again CP, it is true that adiposity is an independent risk factor for DM, as is genetic predisposition, and also added sugar intake appears to an independent risk factor beyond its impact on adiposity.

Yes, here’s the study you’re referring to:

Note that the effects revealed by the study were quite small. It found that consuming the equivalent of one can of soda per day increased your risk of developing Type 2 diabetes by just 1.1%.

Did the study look at activity level? One significant difference between the carb-heavy diet of an Irish peasant and that of a modern cube-dweller is that the peasant is likely engaging in a high level of physical activity on a very regular basis. Glucose gets metabolized very quickly under those circumstances. So it seems logical to me that both a sedentary modern eating 1500 calories of mostly carbs a day and a very active peasant eating 2300 calories of mostly carbs a day might have the same BMI, but very different metabolic patterns.

Apparently not. The statistics published by this researcher indicate that diabetes is far less prevalent in heavy-potato-eating cultures (Peru, Bolivia and Chile) than it is in the United States (backed up with sources).

Further, according to the same researcher says, “Potatoes appear not to cause fat gain, and in fact frequently cause fat loss and improve metabolic health in people who are overweight.”

Also, here’s an MD who treats metabolic and cardiovascular diseases who says ”Starchy foods (rice, corn, potatoes, beans, etc. cause the body’s own insulin to become more powerful; insulin sensitivity is increased” (he backs up that statement with footnoted sources).

Here’s a dietitian who says “there is no real credible evidence at all that potatoes, when consumed close to their natural state and cooked conservatively by baking, boiling, and/or steaming, etc, . . . will cause diabetes or are associated with an increased risk.” He also backs up his statement with sources.

Finally, I don’t know how trustworthy the source is (“Diabetes Health” magazine), but according to this article, modern Peruvians are eschewing potatoes in favor of more American fare and it’s affecting their health.

Yes Manda Jo, they controlled for activity level. Of course the possibility exists that they did not control well enough or another unrecognized confounder exists. Hence we can only claim it “appears” …

“The potato diet” has gotten a bit trendy in some circles. One cool thing about potatoes is that unheated leftover spuds have lots of resistant starch … Which feeds gut bacteria thought to be beneficial, and produces short chain fatty acids (SCFAs) that are thought to have a host of beneficial effects. FWIW.

In fact, cells do get enough sugar even in the setting of uncontrolled diabetes. Let me elaborate.

It is important to note that sugar can get into cells by two mechanisms. One of these is through the action of insulin (at least for those cells that have “working” receptors for insulin).

The second mechanism, though, is independent of insulin. This non-insulin mediated glucose uptake occurs in all cells of the body and is in direct proportion to the glucose level in the bloodstream. So, if the sugar is twice the normal level, then twice as much of it will get into cells compared to the amount getting when the glucose level is normal. If the glucose level is five times normal, then five times as much gets in, etc. Again, this ‘glucose-concentration-dependent’ entry of glucose into cells (more formally called non-insulin mediated glucose uptake or NIMGU) is independent of insulin action.

You could even rationalize the process by noting that as insulin action fails, the body’s cells would starve for glucose if there was no other mechanism to get glucose into cells. However, as insulin action fails, the blood glucose level rises and, thus, via the mechanism described above, this ensures that glucose continues to get into cells, basically offsetting the effect of lack of insulin action to get glucose into cells.

I’ve read from reliable sources that there is another method: exercise. When you exercise, glucose is driven into the cells without the aid of insulin receptors. I do know, however, some diabetics who do exercise, but apparently exercise reduces the amount of insulin needed.

Indeed, exercise is a prime driver of non-insulin mediated glucose uptake into muscle. This is an example of the NIMGU that I mentioned above.

Exercise also, by several mechanisms, improves insulin sensitivity. More detail than you could ever want here, but it turns out that those insulin-independent mechanisms reviewed in that 1997 article may actually not be so completely independent. The years have shown that it gets very complicated - at least to my read.

It is truly a complicated issue. I should have been more forthright when I said that exercise increases non-insulin mediated glucose uptake (NIMGU). In fact, it’s been known for many years that at least a small amount of insulin must be present and acting for exercise to lead to increased glucose flux into muscle, and thus to lower blood glucose. For example, under conditions of extreme insulin deficiency, exercise winds up raising blood glucose levels (and can even precipitate or accelerate the development of DKA).

In other words, exercise increases NIMGU only in the presence of insulin which is not the same saying it increases NIMGU per se.

I missed the edit window but had wanted to say that the effect of exercise to reduce insulin resistance and improve insulin sensitivity is a function of the time elapsed since the last bout of exercise. So, even someone who had achieved a great reduction in their insulin resistance by virtue of exercise, will find that their insulin resistance returns to earlier levels if they postpone their next bout of exercise for too long.

The bottom line is that exercise-induced improvement in insulin sensitivity is an acute phenomenon and is not due to long term muscle (or cardiovascular) fitness or strength. The same degree of improvement in insulin resistance will follow from one hour of exercise as it does after one year of exercise.