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\r\n \r\n The sampling seems small, but the theory seems strong to me. I wonder if l-carnatine could be preventive as well. Anyway, here\'s info for anyone who may have or may have to experience such operations or heart attacks.
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\nResults of systematic review of 13 controlled studies reported in Mayo Clinic Proceedings
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\nRochester, MN, April 12, 2013 � L-carnitine significantly improves cardiac health in patients after a heart attack, say a multicenter team of investigators in a study published today in Mayo Clinic Proceedings. Their findings, based on analysis of key controlled trials, associate L-carnitine with significant reduction in death from all causes and a highly significant reduction in ventricular arrhythmias and anginal attacks following a heart attack, compared with placebo or control.
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\nHeart disease is the leading cause of death in the United States. Although many of the therapies developed in recent decades have markedly improved life expectancy, adverse cardiovascular events such as ventricular arrhythmias and angina attacks still occur frequently after an acute myocardial infarction (heart attack).
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\nIt is known that during ischemic events L-carnitine levels are depleted. Investigators sought to determine the effects of targeting cardiac metabolic pathways using L-carnitine to improve free fatty acid levels and glucose oxidation in these patients. By performing a systematic review and meta-analysis of the available studies published over several decades, they looked at the role of L-carnitine compared with placebo or control in patients experiencing an acute myocardial infarction.
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\nL-carnitine is a trimethylamine which occurs in high amounts in red meat and is found in certain other foods, and is also widely available as an over-the-counter nutritional supplement which is claimed to improve energy, weight loss, and athletic performance. Its potential role in treating heart disease was first reported in the late 1970s.
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\nA comprehensive literature search yielded 153 studies, 13, published from 1989-2007, were deemed eligible. All the trials were comparison trials of L-carnitine compared with placebo or control in the setting of acute myocardial infarction.
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\nThis systematic review of the 13 controlled trials in 3,629 patients, involving 250 deaths, 220 cases of new heart failure, and 38 recurrent heart attacks, found that L-carnitine was associated with:
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\n Significant 27% reduction in all-cause mortality (number needed to treat 38)
\n Highly significant 65% reduction in ventricular arrhythmias (number needed to treat 4)
\n Significant 40% reduction in the development of angina (number needed to treat 3)
\n Reduction in infarct size
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\nThere were numerically fewer myocardial reinfarctions and heart failure cases associated with L-carnitine, but this did not reach statistical significance.
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\nFirst author James J. DiNicolantonio, PharmD, Wegmans Pharmacy, Ithaca, NY, observes, "Although therapies for acute coronary syndrome (ACS), including percutaneous coronary intervention, dual antiplatelet therapy, b-blockers (BBs), statins, angiotensin-converting enzyme inhibitors (ACEIs), omega-3 fatty acids, and cardiac rehabilitation, have markedly improved clinical outcomes, adverse cardiovascular (CV) events still occur too frequently after ACS. One promising therapy for improving cardiac health involves using L-carnitine to improve free fatty acid levels and glucose oxidation."
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\n"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," says DiNicolantonio.
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\nL-carnitine is proven to be safe and is readily available over the counter. The investigators agree that the overall results of this meta-analysis support the potential use of L-carnitine in acute myocardial infarction and possibly in secondary coronary prevention and treatment, including angina. They advocate for a larger randomized, multicenter trial to be performed to confirm these results in the modern era of routine revascularization and other intensive medical therapies following acute myocardial infarction. But, says DiNicolantonio, "L-carnitine therapy can already be considered in selected patients with high-risk or persistent angina after acute myocardial infarction who cannot tolerate treatment with ACE inhibitors or beta blockers, considering its low cost and excellent safety profile."
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\nThese findings may seem to contradict those reported in a study published earlier this month in Nature Medicine by Robert A. Koeth and others (Koeth, R. A. et al. Nature Med. https://dx.doi.org/10.1038/nm.3145), which demonstrated that metabolism by intestinal microbiota of dietary L-carnitine produced trimethylamine N-oxide (TMAO) and accelerated atherosclerosis in mice. They also noted that omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine, and suggested a possible direct link between L-carnitine, gut bacteria, TMAO, and atherosclerosis and risk of ischemic heart disease.
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\n"The Nature Medicine paper is of interest," agrees senior investigator Carl J. Lavie, M.D.,FACC,FACP,FCCP, Medical Director of the Cardiac Rehabilitation and Prevention Center at the John Ochsner Heart and Vascular Institute at the University of Queensland School of Medicine in New Orleans, "but the main study reported there was in animals, and unlike our study, lacks hard outcomes." He also notes that "there are various forms of \'carnitine\' and our relatively large meta-analysis specifically tested L-carnitine on hard outcomes in humans who had already experienced acute myocardial infarction."\r\n
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\r\n \r\n\r\nDefault\r\n\r\n New Study Reckons L-Carnitine Can be Implicated in INCREASING Coronary Heart Disease\r\n
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\r\n \r\n Quite a few assumptions in this research which claims a certain strain of gut bacteria can turn carnitine in red meat, energy drinks and dietary supplements into an increase in CVD.
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\nhttps://www.theheart.org/article/1526279.do
\n(Read the comments as well as the article)
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\nNo printed article available yet only PUBMED abstract on the study:
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\nhttps://www.ncbi.nlm.nih.gov/pubmed/2...?dopt=Abstract
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\nLecethin it is also claimed turns into the same harmful bacteria.
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\nhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086762/\r\n
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\r\n \r\n Contradicting studies. I hope to see more research. On the one side, l-carnitine is reducing the bad parts of the CVD incidents. On the other, is l-carnitine the villain?\r\n
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\r\n \r\n From Mark Sisson;
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\n"I’ve been asked to comment on the latest media deluge to suggest that red meat is again the primary cause of atherosclerosis, heart disease, and your impending doom. At least this time they’re targeting something other than cholesterol: this time it’s carnitine."
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\r\n \r\n Carnitine is found in red meat, mostly, as well as dairy, tempeh, and some other meats, and it performs a number of important roles in the human body, foremost of which is the transportation of fatty acids into the mitochondria for breakdown into useable energy. It’s so important to basic function that we make endogenous carnitine by synthesizing it from the amino acids lysine and methionine. Vegans and vegetarians, who tend to run deficient in carnitine, benefit greatly from supplementation (or a nice steak). It’s even been used to reduce atherosclerosis (albeit in rabbits), improve arterial function, and help heart failure patients recover. Carnitine is not some evil compound.
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\n Oh, the study. Let’s get into it. It consisted of several sections, actually.\r\n \r\n
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Read more
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\r\n \r\n An excellent, in-depth article here blowing huge, gaping holes in the red meat theory. The scientific evidence just isn\'t there.
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\r\nhttps://articles.mercola.com/sites/ar...paign=20130417\r\n
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\r\n \r\n Oh no! I\'m so tired of this. Now eggs get pounded down again. This time it is lecithin, which is chemically related to carnitine.
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\nThis is from the NY Times
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\r\n \r\n For the second time in a matter of weeks, a group of researchers reported a link between the food people eat and bacteria in the intestines that can increase the risk of heart attacks.
\n Two weeks ago, the investigators reported that carnitine, a compound found in red meat, can increase heart disease risk because of the actions of intestinal bacteria. This time they reported that the same thing happens with lecithin, which is abundant in egg yolks.
\n The lecithin study, published Wednesday in The New England Journal of Medicine, is part of a growing appreciation of the role the body�s bacteria play in health and disease. With heart disease, investigators have long focused on the role of diet and heart disease, but expanding the scrutiny to bacteria adds a new dimension.
\n Heart disease perhaps involves microbes in our gut,� said the study�s lead researcher, Dr. Stanley Hazen, chairman of the department of cellular and molecular medicine at the Cleveland Clinic Lerner Research Institute.
\n In the case of eggs, the chain of events starts when the body digests lecithin, breaking it into its constituent parts, including the chemical choline. Intestinal bacteria metabolize choline and release a substance that the liver converts to a chemical known as TMAO, for trimethylamine N-oxide. High levels of TMAO in the blood are linked to increased risk of heart attack and stroke.
\n To show the effect of eggs on TMAO, Dr. Hazen asked volunteers to eat two hard-boiled eggs. They ended up with more TMAO in their blood. But if they first took an antibiotic to wipe out intestinal bacteria, eggs did not have that effect.
\n To see the effects of TMAO on cardiovascular risk, the investigators studied 4,000 people who had been seen at the Cleveland Clinic. The more TMAO in their blood, the more likely they were to have a heart attack or stroke in the ensuing three years.
\n Carnitine � the red meat chemical � and lecithin are chemically related, Dr. Hazen said. As with lecithin, when carnitine is digested, choline is released and can be acted on by intestinal bacteria.
\n The results of the new studies, though, do not directly prove that reducing TMAO protects against heart disease. That would require large studies following people who lowered their TMAO levels, which should be possible with a vegetarian or high-fiber diet.
\n Dr. Hazen said that people who are worried about heart attacks may want to consider reducing lecithin and choline in their diet, which would require eating less of foods high in fat and cholesterol. Dr. Hazen said it also may be wise to avoid supplements or vitamins with added choline.
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\r\n Originally Posted by jfh\r\n View Post\r\n
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Oh no! I\'m so tired of this. Now eggs get pounded down again. This time it is lecithin, which is chemically related to carnitine.
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\nThis is from the NY Times
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\nMusical nutrition, huh?
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\nAnother portly fellow who wants to profess nutrition. As a cardiac researcher, he should know how weight correlates with coronary health.\r\n
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jfh will become famous soon enoughjfh will become famous soon enough
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\r\n \r\n But don\'t worry. Big pharma will make pills that will stop the liver from producing this TMAO. Then people can replace their anti-cholesterol pills with the new one.\r\n
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Default l-Carnitine improves results following heart attack

The sampling seems small, but the theory seems strong to me. I wonder if l-carnatine could be preventive as well. Anyway, here's info for anyone who may have or may have to experience such operations or heart attacks.

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Results of systematic review of 13 controlled studies reported in Mayo Clinic Proceedings

Rochester, MN, April 12, 2013 � L-carnitine significantly improves cardiac health in patients after a heart attack, say a multicenter team of investigators in a study published today in Mayo Clinic Proceedings. Their findings, based on analysis of key controlled trials, associate L-carnitine with significant reduction in death from all causes and a highly significant reduction in ventricular arrhythmias and anginal attacks following a heart attack, compared with placebo or control.

Heart disease is the leading cause of death in the United States. Although many of the therapies developed in recent decades have markedly improved life expectancy, adverse cardiovascular events such as ventricular arrhythmias and angina attacks still occur frequently after an acute myocardial infarction (heart attack).

It is known that during ischemic events L-carnitine levels are depleted. Investigators sought to determine the effects of targeting cardiac metabolic pathways using L-carnitine to improve free fatty acid levels and glucose oxidation in these patients. By performing a systematic review and meta-analysis of the available studies published over several decades, they looked at the role of L-carnitine compared with placebo or control in patients experiencing an acute myocardial infarction.

L-carnitine is a trimethylamine which occurs in high amounts in red meat and is found in certain other foods, and is also widely available as an over-the-counter nutritional supplement which is claimed to improve energy, weight loss, and athletic performance. Its potential role in treating heart disease was first reported in the late 1970s.

A comprehensive literature search yielded 153 studies, 13, published from 1989-2007, were deemed eligible. All the trials were comparison trials of L-carnitine compared with placebo or control in the setting of acute myocardial infarction.

This systematic review of the 13 controlled trials in 3,629 patients, involving 250 deaths, 220 cases of new heart failure, and 38 recurrent heart attacks, found that L-carnitine was associated with:

Significant 27% reduction in all-cause mortality (number needed to treat 38)
Highly significant 65% reduction in ventricular arrhythmias (number needed to treat 4)
Significant 40% reduction in the development of angina (number needed to treat 3)
Reduction in infarct size

There were numerically fewer myocardial reinfarctions and heart failure cases associated with L-carnitine, but this did not reach statistical significance.

First author James J. DiNicolantonio, PharmD, Wegmans Pharmacy, Ithaca, NY, observes, "Although therapies for acute coronary syndrome (ACS), including percutaneous coronary intervention, dual antiplatelet therapy, b-blockers (BBs), statins, angiotensin-converting enzyme inhibitors (ACEIs), omega-3 fatty acids, and cardiac rehabilitation, have markedly improved clinical outcomes, adverse cardiovascular (CV) events still occur too frequently after ACS. One promising therapy for improving cardiac health involves using L-carnitine to improve free fatty acid levels and glucose oxidation."

"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," says DiNicolantonio.

L-carnitine is proven to be safe and is readily available over the counter. The investigators agree that the overall results of this meta-analysis support the potential use of L-carnitine in acute myocardial infarction and possibly in secondary coronary prevention and treatment, including angina. They advocate for a larger randomized, multicenter trial to be performed to confirm these results in the modern era of routine revascularization and other intensive medical therapies following acute myocardial infarction. But, says DiNicolantonio, "L-carnitine therapy can already be considered in selected patients with high-risk or persistent angina after acute myocardial infarction who cannot tolerate treatment with ACE inhibitors or beta blockers, considering its low cost and excellent safety profile."

These findings may seem to contradict those reported in a study published earlier this month in Nature Medicine by Robert A. Koeth and others (Koeth, R. A. et al. Nature Med. https://dx.doi.org/10.1038/nm.3145), which demonstrated that metabolism by intestinal microbiota of dietary L-carnitine produced trimethylamine N-oxide (TMAO) and accelerated atherosclerosis in mice. They also noted that omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine, and suggested a possible direct link between L-carnitine, gut bacteria, TMAO, and atherosclerosis and risk of ischemic heart disease.

"The Nature Medicine paper is of interest," agrees senior investigator Carl J. Lavie, M.D.,FACC,FACP,FCCP, Medical Director of the Cardiac Rehabilitation and Prevention Center at the John Ochsner Heart and Vascular Institute at the University of Queensland School of Medicine in New Orleans, "but the main study reported there was in animals, and unlike our study, lacks hard outcomes." He also notes that "there are various forms of 'carnitine' and our relatively large meta-analysis specifically tested L-carnitine on hard outcomes in humans who had already experienced acute myocardial infarction."
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