Twin study suggests genetic link between major depression and heart disease risk
21/10/2009
Last Updated: 2009-10-16 18:02:57 -0400 (Reuters Health)
NEW YORK (Reuters Health) - A new study in twins points to a common genetic root for major depressive disorder and microvascular dysfunction that could help explain the association between depression and heart disease.
"Our results suggest that, similar to traditional risk factors, major depressive disorder is associated with perfusion abnormalities compatible with microvascular dysfunction," Dr. Viola Vaccarino of Emory University School of Medicine in Atlanta and her colleagues write.
Oxidative stress, inflammation, and immune system activation are all likely associated with microvascular disease, they add, and have also all been linked to major depression.
"Our data indicate that the influence of major depressive disorder on coronary heart disease risk is at least in part heritable and that genetically predisposed individuals could be at risk for both major depressive disorder and (heart disease)," the researchers add.
In fact, they found, coronary flow rate was significantly lower in dizygotic twins with a history of major depression compared to their fraternal twins without major depression, but there was no significant flow rate difference between monozygotic twins discordant for the disorder.
The study, reported in the October 12 Archives of Internal Medicine, involved 53 twin pairs discordant for a lifetime history of major depression and a control group of 183 twin pairs with no history of major depression and no relationship to the experimental group. Myocardial blood flow before and after adenosine stress was determined with positron emission tomography.
Among the 53 twin pairs discordant for major depressive disorder, 25 were dizygotic and 28 were monozygotic. Of the 183 depression-free control twin pairs, 76 were dizygotic and 107 were monozygotic.
Depression was in remission in most subjects, with only four meeting diagnostic criteria for a major depressive episode.
While resting myocardial blood flow wasn't different in any of the twin pairs, dizygotic twins with major depression had a 14% lower coronary flow rate response to adenosine challenge compared to their brothers without depression. This difference wasn't seen in the monozygotic pairs discordant for major depression. Adjusting for myocardial perfusion defects had no effect on the results, nor did adjustment for Framingham risk score.
In 35 twin pairs, the depressed twin had scored 10 or higher on the Beck Depression Inventory-II. In these pairs, the difference in coronary flow rate between the 20 dizygotic twins was 17.6%, with again no difference between the monozygotic twin pairs. As the difference in depression score between the dizygotic twin pairs rose, the difference in flow rate increased as well.
"These results have substantial implications for our understanding of the link between major depressive disorder and coronary heart disease risk," the investigators write.
They add, "Our results also provide a clue to the inconsistencies in previous literature concerning the association between major depressive disorder and coronary heart disease. If genetically predisposed individuals with (major depression) are those at highest risk, the genetic admixture of the population may be the reason for the inconsistent findings."
Arch Intern Med 2009;169:1668-1676.