Can You Outrun Your Genes?
A 68-year-old man presents to his cardiologist’s office for chest discomfort while training for a marathon. He is very active and has run one or two marathons each year. He does not have high blood pressure, diabetes or elevated cholesterol levels. He is not obese and does not smoke. However, his father had a heart attack at age 40 and a brother had a heart attack and heart surgery in his 40’s. He underwent an exercise stress test followed by a heart catheterization, which showed severe blockage in his heart arteries. He then had coronary artery bypass surgery. At his follow up visit after his bypass, he asks, “Why did this happen to me? I have done everything right for so long”.
What factors contribute to the development of heart artery disease? Is it our genes, how we are built? Or is it our lifestyle? It’s the age-old question of nature versus nurture. It has been known for years that heart artery disease runs in families. This is especially true for families with members who had heart attacks at young ages (generally less than 50 years old). It has also been known for years that certain lifestyles contribute to heart artery disease. Smoking, obesity, diet, and a sedentary lifestyle have all been associated with the development of blockage in the heart arteries. It is also known that lifestyle modification can control or even reverse heart artery disease. In the 1990’s Dr. Dean Ornish developed an intensive lifestyle modification program focusing on a plant based diet, smoking cessation, moderate exercise and stress management. He found that lifestyle changes were as good as heart procedures (angioplasty or bypass surgery) in reducing chest pain without increasing heart attacks or deaths. So, which is more important, genes or lifestyle?
A recent study involving 55,000 participants sought to define the interplay between genes and lifestyle on the development of heart artery disease. Based on DNA analysis, the participants were placed into two categories, high genetic risk for heart disease or low genetic risk. Similarly, the participants were placed into two lifestyle categories, a favorable lifestyle (at least three of four healthy lifestyle factors) or an unfavorable lifestyle (no or one healthy lifestyle factor). The healthy lifestyle factors were: no smoking, no obesity, regular physical activity and a healthy diet. The researchers found that genetic risk and lifestyle factors independently contribute to heart artery disease. In other words, having a high genetic risk or an unfavorable lifestyle is equally risky in developing heart disease. Both nature and nurture matter. The researchers also found that genes were not the final determinant in heart disease. In the high genetic risk category, those who followed a favorable lifestyle had a nearly 50% reduction in risk of heart disease compared to those who followed an unfavorable lifestyle. Therefore, following a favorable lifestyle can reduce genetic risk.
The long distance running of our 68-year-old man could not keep him from meeting the cardiac surgeon; his family history eventually caught up to him. However, if he had not been as active and had followed an unfavorable lifestyle, he very likely would have manifested heart artery disease at a much earlier age, similar to his father and brother. By following a favorable lifestyle, he had delayed the progression of his heart disease, likely by about twenty years. So, clearly you cannot out run your genes. On the other hand, your genes don’t necessarily determine the fate of your heart. If you have a strong family history of early heart attacks, don’t give up, sit on the couch and not take care of yourself. Lifestyle changes make a difference, although they are not easy. Following a favorable lifestyle is an every day, all the time, year after year commitment. It is, however, worth it, especially for those at the highest genetic risk for heart disease.
Steve Georgeson, the author of this article, is a cardiologist who works at Medicor Cardiology.
View this article on the TAPinto website here.