Genes and Heart Disease

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.

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.