Diabetes and Heart Disease: Do Certain Genes Increase Risk of Heart Disease?

Gretchen Becker Health Guide
  • Every day, it seems, there's another gloomy news story saying that "diabetics" are more apt to acquire other medical problems, or drugs that help other people don't help "diabetics," or foods that are OK for other people to eat aren't OK for "diabetics."

    Lately, for example, we've been told that people with diabetes are more likely to get Alzheimer's disease, low-dose aspirin that helps prevent heart attacks doesn't work in people with diabetes, and although it's now considered healthy for most people to eat eggs, people with diabetes should still avoid them.

    If you read just the headlines you're apt to want to throw in the towel and stop taking care of yourself. It seems almost hopeless.

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    But the thing is, these stories, and often the research papers they're based on, never bother to define what they mean by "diabetics." Do they mean anyone who has been diagnosed with diabetes? Type 1? Type 2? People with poor control? People with good control? People with diabetes regardless of control?

    What are they talking about, anyway?

    A recent study by Boston-area researchers is a good illustration of this. They started out by saying that diabetes increases the risk of a "major cardiovascular event" by a factor of 2 to 4 compared with people without diabetes.


    Then they described their study of some genes involved in predicting heart disease. It had previously been discovered that mutations in a gene on a particular region of chromosome 9 greatly increased the risk of heart disease. In the general population, people who had the defective gene were more likely to have coronary artery disease: their risk was approximately 1.25 to 1.5 times greater, depending on whether they had one or two copies of the gene.

    But the researchers found that among people with type 2 diabetes who had the defective gene, the risk was increased even more. People with diabetes who had one copy of the defective gene had their risk increased by a factor of approximately 1.5, and people with two copies of the defective gene had approximately 2.4 times the risk of type 2s without the gene.

    Sounds like more gloomy news. But wait! There's more!

    It turns out that it's not just having the defective genes that increases the risk. The A1c level is important too. People with type 2 who had two copies of the defective genes but whose A1c levels were under 7.6 had approximately twice the risk of developing heart disease, but those who had two copies of the defective gene and A1c levels over 7.6 had 4 times the risk of type 2s without the gene.

    Those with only one copy of the defective gene or only increased A1c levels had increased risks, but they were not statistically significant.

    When they looked at the average A1c levels going back for up to 7 years, the results were even more striking. Those with two copies of the defective gene had an insignificant increased risk, but those with average A1cs greater than 7.9 had an almost 8 times greater risk.

    The results from another analysis of data from the Joslin Diabetes Center looking at long-term (about 10 years) blood glucose (BG) control and mortality was also striking. Those who had two copies of the defective gene and A1cs over 8.9 had twice the number of deaths than those with lower A1cs. And those with two copies of the gene but lower A1cs did not have higher mortality rates than those without the defective gene.

  • (This study, which went back into older Joslin records, used higher cutoffs because the trend in previous years had been to allow higher A1c levels than today.)

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    In other words, patients with the genetic defect and poorly controlled BG levels had increased mortality rates. But just having the genetic defect did not increase mortality. It was only a combination of having the genetic defect and also having long-term high BG levels that caused the increased risk of death within the 10-year period. [We all have a 100% risk of death, although as someone wisely pointed out, the evidence is purely annecdotal.]

    This could be true of the other dire predictions for people with diabetes. The increased risk for Alzheimer's disease, for example, might be the result of high BG levels rather than the underlying disease itself.

    Most researchers assume that having diabetes is synonymous with having high BG levels. Often it is. But it doesn't need to be. And although we can't reverse the fact that we have diabetes, we can help to control our BG levels.

    The A1c cutoff levels used in these studies were fairly high according to the standards of many people. Even the ADA says A1cs should be under 7. Endocrinologists prefer the A1c to be under 6.5. Many patients aim for A1cs in the normal range, under 6. And Richard K. Bernstein, the type 1 guru of the low-carb diet for people with diabetes, wants his patients to achieve A1cs in the 4s.


    Diet and exercise definitely help. Many people find that low-carb diets result in plummeting BG levels without drugs. If these aren't enough, we need to insist that our doctors prescribe medication that will help. Insulin is often the simplest therapy, with the fewest long-term side effects. And for those without good drug coverage, even an expensive basal insulin is cheaper than three or four expensive new diabetes drugs.

    There are many people with diabetes who have A1c levels of 8 or 9 or even higher; this is simply not acceptable. Of course not everyone has the deleterious genes described in this study. But there are undoubtedly other factors that, like this gene, can harm us when we let our BG levels get too high.

    It's not easy. But controlling our BG levels is worth the work. It's not simply having diabetes that causes complications. It's having high BG levels.





Published On: January 27, 2009