"Your heart disease is 'genetic'"

At 53, Sam had been through the wringer with heart disease.

He suffered his first heart attack at age 50. Since then, he's undergone four heart catheterizations, received 5 stents, and, most recently, a bypass operation. He wanted to know whether there was a better way.

After hearing Sam's story, I asked him, "Did your doctors suggest to you why you had heart disease?"

Sam, a non-smoker with no diabetes who had taken a cholesterol drug throughout the entire process, replied, "Well, they said it was genetic, since my father went through the same thing in his early 50s. He died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are many ways to inherit causes that lead to coronary heart disease: genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify - and correct. They are not chromosomal markers, but end products of genetic patterns. (Although the world of chromosomal markers for heart disease is getting underway, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can result from a combination of poor lifestyle magnifying a genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern), while ApoE2 people are exceptionally sensitive to carbohydrates, develop dramatic increased triglycerides, and are diabetes-prone with even the most minimal weight gain.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do (particularly if associated with small LDL and other markers of increased risk).