By David Liu, PHD

Thursday Oct 11, 2012 (foodconsumer.org) -- Research suggests branched chain amino acids, leucine, isoleucine and valine, can help treat human diseases. Now a study in Metabolism suggests that a high leucine diet (HLD) can mitigate cardiac injury and boost survival odds for patients who have experienced myocardial infarction or heart attack.

Myocardial infarction is a major killer in the United States, and maybe many other developed countries as well.  The study led by W.G. Witham and colleagues showed after myocardial infarction, mice using a high leucine diet for 28 days improved cardiac structure, function and survival odds.

For the study, 11 to 12 week old male mice were subjected to experimental myocardial infarction or sham procedure and then received either a regular diet with 1.5% leucine or a high leucine diet with 5% leucine for 28 days.

The mice were sacrified and historical parameters were measured including hypertrophy, fibrosis and apoptosis."  Measured were also "inflammation, hypertrophic gene expression, signal transduction, and glucose, palmitate and leucine metabolism" in 3.5-day old hearts.

The high leucine diet did not cause any undesired outcomes in sham mice or the mice that had not suffered myocardial  infarction, except that leucine levels increased and glucose oxidation decreased.

However, in mice that had experienced myocardial infarction,  the high leucine diet significantly improved cardiac structure, function, and survival.  And at 3.5 days after myocardial infarction, the high leucine diet already increased cardiac hypertrophic signaling and reduced inflammation. 

In mice that experienced myocardial infarction, the regular diet did not decrease cardiac leucine oxidation whereas the high leucine diet significantly did so.

Additionally, along with these changes in metabolism, a significant increase was also observed in cardiac ATP content in the mice on high leucine diet. 

Finally, at both 3.5 and 28 days after myocardial infarction, the high leucine diet increased "compensatory hypertrophy, and attenuated cardiac fibrosis and apoptosis."

The researchers concluded "An HLD increases compensatory hypertrophy, attenuates fibrosis and apoptosis, and positively modulates oxidative metabolism to improve cardiac structure, function, and survival post-MI (myocardial infarction)."