Type II diabetes predicts a 7 year shorter life, due to cardiovascular disease. No one knows why. It also destroys small blood vessels, leading to blindness and loss of feeling in the extremities (thence falls or infections). This is called microvascular damage and is fairly well-understood as the direct result of blood sugar. The cardiovascular disease is called macrovascular damage to imply it is similar, but it’s really a smokescreen.
Timmons cites two studies of diet and exercise improving blood sugar but failing to improve heart disease. One is a small Finnish study. The other is a big American study, Lookahead, but it hasn’t published yet; items 88 and 89 in its bibliography sound relevant. As background, there are two large past studies that have conflicting results on whether improving diabetes (mainly via drugs) improves CVD. 15 years ago, the UKPDS study compared aiming for 7% A1c is better than aiming for 8%. It reduced CVD, though not as much as it reduced microvascular outcomes. So 7% became the new baseline and follow-up studies were started that are only just reporting. A couple of years ago, the ACCORD trial finished comparing aiming for 6% to 7%. It found the more aggressive treatment had worse mortality (and worse CVD, though not statistically significantly). The Accord study had lower A1c targets in both arms than UKPDS, but I think it only achieved the same levels, probably because its patients were older and had more advanced diabetes.
One hypothesis that people throw around is that if you are too aggressive with drugs, you cause hypoglycemic events (too low blood sugar), and these are correlated with CVD. But if you lower blood sugar by diet and exercise, you don’t expect to cause hypoglycemic events, so there was some hope that this would improve CVD, despite the Accord study. But the recent studies falsify this loophole. (Also, I think it failed to explain the detailed Accord data.)
Still, the UKDPS suggests that for some people reduced blood sugar improves CVD. Maybe microvascular problems are due to very high levels of blood sugar, at the tail end of diabetes, while CVD is due to long exposure to lower blood sugar. Perhaps for the Accord patients it was too late, but starting earlier with the UKDPS patients worked.
Added: In other words, blood sugar might just be a symptom, not a direct cause of heart disease (but definitely a direct cause of diabetic morbidity). This is not too surprising, since the mechanism isn’t understood. Experiments in the past had mixed results. What’s new is lifestyle experiments, in contrast to drug experiments. It is surprising that they are worse, but type of patients probably matters.
One hypothesis that people throw around is that if you are too aggressive with drugs, you cause hypoglycemic events (too low blood sugar), and these are correlated with CVD.
I just want to point out that this is entirely dependent on what kind of medication you take, it’s practically impossible (I have never heard of it at least) to have a hypoglycemic event without insulin being a part of your cocktail.
Diabetes and Heart Disease.
Type II diabetes predicts a 7 year shorter life, due to cardiovascular disease. No one knows why. It also destroys small blood vessels, leading to blindness and loss of feeling in the extremities (thence falls or infections). This is called microvascular damage and is fairly well-understood as the direct result of blood sugar. The cardiovascular disease is called macrovascular damage to imply it is similar, but it’s really a smokescreen.
Timmons cites two studies of diet and exercise improving blood sugar but failing to improve heart disease. One is a small Finnish study. The other is a big American study, Lookahead, but it hasn’t published yet; items 88 and 89 in its bibliography sound relevant. As background, there are two large past studies that have conflicting results on whether improving diabetes (mainly via drugs) improves CVD. 15 years ago, the UKPDS study compared aiming for 7% A1c is better than aiming for 8%. It reduced CVD, though not as much as it reduced microvascular outcomes. So 7% became the new baseline and follow-up studies were started that are only just reporting. A couple of years ago, the ACCORD trial finished comparing aiming for 6% to 7%. It found the more aggressive treatment had worse mortality (and worse CVD, though not statistically significantly). The Accord study had lower A1c targets in both arms than UKPDS, but I think it only achieved the same levels, probably because its patients were older and had more advanced diabetes.
One hypothesis that people throw around is that if you are too aggressive with drugs, you cause hypoglycemic events (too low blood sugar), and these are correlated with CVD. But if you lower blood sugar by diet and exercise, you don’t expect to cause hypoglycemic events, so there was some hope that this would improve CVD, despite the Accord study. But the recent studies falsify this loophole. (Also, I think it failed to explain the detailed Accord data.)
Still, the UKDPS suggests that for some people reduced blood sugar improves CVD. Maybe microvascular problems are due to very high levels of blood sugar, at the tail end of diabetes, while CVD is due to long exposure to lower blood sugar. Perhaps for the Accord patients it was too late, but starting earlier with the UKDPS patients worked.
Added: In other words, blood sugar might just be a symptom, not a direct cause of heart disease (but definitely a direct cause of diabetic morbidity). This is not too surprising, since the mechanism isn’t understood. Experiments in the past had mixed results. What’s new is lifestyle experiments, in contrast to drug experiments. It is surprising that they are worse, but type of patients probably matters.
Upvoted.
I just want to point out that this is entirely dependent on what kind of medication you take, it’s practically impossible (I have never heard of it at least) to have a hypoglycemic event without insulin being a part of your cocktail.
Yes, insulin is a prerequisite for a hypoglycemic event. But once on insulin, most drugs increase the rate of events.