East Meets West

Faulty HDL, Lifestyle Linked to Asians’ Risk of Heart Disease

South Asian immigrants in America have a higher risk of heart disease than any other American population.

The trouble, MCG researchers suspect, is a combination of dysfunctional highdensity lipoprotein (the socalled “good” cholesterol) and a Westernized lifestyle.

“Research shows that while only 9 percent of whites develop coronary artery disease, between 18 and 25 percent of South Asian immigrants eventually develop it,” said Dr. Sunita Dodani, an MCG epidemiologist, cardiologist and assistant dean for research in the School of Nursing. “Interestingly, South Asians who live in their homelands have normal rates of the disease.”

In most South Asians, dysfunctional HDL, first identified by the historic Framingham Heart Study, is likely caused by a mutation of ApoA1, the gene that codes the major protein component of HDL, Dr. Dodani said.

“HDL can only protect people from heart disease if it’s functional,” she explained. “The dysfunctional HDL and external risk factors like stress from moving and new jobs and highfat diets make for a deadly combination.”

Dr. Dodani, a South Asian immigrant herself, and collaborators at MCG and the University of California at Los Angeles have been studying 29 Augusta immigrants, seeking a connection between the gene mutation and dysfunctional HDL.

Blood samples were sent to UCLA to determine whether each subject had dysfunctional HDL. DNA sequencing helped researchers target ApoA1 mutations, and a portable carotid Doppler machine measured the thickness of carotid arteries.

“Recent research has shown that thickening of the carotid arteries is directly related to thickening of the coronary arteries,” said Dr. Dodani. “The Doppler machine is less invasive than angiography (injecting a contrast medium into a patient) and can just as easily detect the disease in the early stages.”

Dr. Dodani and her colleagues suspected that subjects with thickened carotid arteries would have dysfunctional HDL and a polymorphism of the ApoA1 gene. This is the first time researchers have examined a possible correlation between the gene polymorphisms, dysfunctional HDL and arterial thickness.

Interestingly, 40 percent of the study population had arterial thickness and, among that group, 17 percent had high blood pressure and more than 30 percent had high cholesterol. Half the study population also had dysfunctional HDL. DNA analysis of those blood samples also found six different mutations of ApoA1.

“This is a strong indicator that these novel polymorphisms, which haven’t been found in any previous studies, are linked to dysfunctional HDL,” Dr. Dodani said. “These findings support our theory that the disease in South Asians is most likely caused by a combination of dysfunctional HDL, a stressful lifestyle and highfat diets.

That could explain the high rates in immigrants and not those who stay in their homelands.”

Dr. Dodani has applied for National Institutes of Health funding to enlarge the study and eventually include other populations for comparison. “Then we will be able to figure out what’s next,” she said. “If the cause is a combination of this gene mutation and other factors, are there preventive strategies that we can employ? Should cholesterollowering drugs be started earlier in certain populations? Those are questions we hope to eventually answer.”

Jennifer Hilliard