Dead Lift – Using 90% of your 1RM for the math, complete:
KB Swings (go heavier than normal)
Is Red Meat A Fish Story?
First let me address the problems with the original paper. As several critics were quick to point out (and as I should have reported originally), a key assumption of the original paper– that eating red meat can in fact cause atherosclerosis– has never been demonstrated with scientific rigor and is actually the subject of intense controversy. I asked Stanley Hazen, the senior author of the Nature Medicine paper, about this. He admitted that “in truth, we did not examine this,” though he pointed to several lines of evidence linking carnitine to heart disease.
Second, the Nature Medicine paper did not mention a key fact that could dramatically change one’s interpretation of the research. The Nature Medicine paper claims that red meat leads to atherosclerosis through the conversion of carnitine to TMAO. But the paper didn’t mention that fish– which almost everyone thinks of as being heart healthy– often have very high levels of TMAO. I asked Hazen about this and whether he had measured TMAO levels in fish. He didn’t say whether he had measured TMAO in fish, but agreed that “some forms of fish that have very high levels of TMAO,” such as deep sea fish in Arctic waters, which use TMAO as anti-freeze and “and have extraordinarily high TMAO” levels. Surface fish, like trout, “tend to have very low TMAO,” he said.
I agree strongly with Hazen’s takeaway message about this: ”NOTHING is always black and white – all things are nuanced. So not all fish are the same – not all meat is the same (lamb has a lot higher carnitine level compared to beef,” and chicken, he said, has ten time less TMAO than that. “Cardiovascular disease,” he concluded, “is a complex multifactoral process – this is one facet of the story – a new facet – one not yet known before.”
Could Carnitine Be Good For You?
A new paper published today offers an entirely different view of carnitine.Published in Mayo Clinic Proceedings, the new paper is a metaanalysis of 13 previous studies looking at the effect of L-carnitine (the biologically active isomer of carnitine) when given immediately after a heart attack. After combining data from all the smaller studies, the researchers found that MI patients who received L-carnitine instead of placebo or other control had a significant reduction in all-cause mortality, ventricular arrhythmias, and recurrent angina.
“The potential mechanisms responsible for the observed beneficial impact of L-carnitine in acute myocardial infarction are likely multifactorial and may, in part, be conferred through the ability of L-carnitine to improve mitochondrial energy metabolism in the heart by facilitating the transport of long-chain fatty acids from the cytosol to the mitochondrial matrix, where b-oxidation occurs, removing toxic fatty acid intermediates, reducing ischemia induced by long-chain fatty acid concentrations, and replenishing depleted carnitine concentrations seen in ischemic, infarcted, and failing myocardium,” said first author James DiNicolantonio.
I asked Hazen about the new study that appeared at first glance to contradict the direction of his own study. He noted– quite correctly– that any metaanalysis should be interpreted with caution, but he did not dispute the finding. However, he noted an important difference between the studies that could reconcile their apparent differences. The meta-analysis, he notes, looked at L-carnitine in the acute setting of a heart attack, and found that “brief ” supplementation may be beneficial. Hazen’s study, by contrast, suggests “chronic exposure to dietary carnitine, whether from food or supplement, may not be a healthy thing for the vasculature over the long run.”
It is hard to argue with Hazen’s conclusion: “both findings argue for more studies being needed to tease out the role, if any, and the safety, of chronic carnitine supplementation.” This sort of conclusion may not get big headlines or network TV coverage, but it has its own virtue.