Cholesterol and fat have been synonymous with coronary artery disease or “heart disease” for the past several decades through heavy research and commercialization. Cholesterol lowering medications, such as simvastatin, are one the world’s most widely prescribed drugs. However, even through our efforts to lower cholesterol by the way of medications, the prevalence of coronary atherosclerosis, and its subsequent consequence of heart attacks, continue to climb at epidemic rates. I experience seeing many patients on cholesterol lowering drugs with worsening chest pain and atherosclerotic disease despite their cholesterol numbers meeting widely used recommended guidelines.
According to much research that is coming out, the affect of meat on heart disease goes beyond just the fat content of the food. One of these major links between meat and heart disease is a chemical compound known as trimethylamine N-oxide (TMAO). TMAO is found in sea animals to stabilize protein by counteracting urea due to heavy pressured environments these animals are found in. TMAO is the cause of the oder of rotting seafood. However, though the chemical seem to be beneficial in sea animals, it has a different affect when they are present in mammals, such has humans.
So what is TMAO?
TMAO is a chemical compound that is produced by the liver with help from gut bacteria. Your body harbors millions of symbiotic bacteria on the skin, in your mouth, stomach, and intestine just to name a few places. Through dietary means, you acquire important nutrients with similar chemical structures, or are interrelated through various biochemical pathways, such as L-Carnitine, choline, phosphatidylcholine, etc. These nutrients are metabolized, or broken down/converted, to another substance called TMA. TMA then gets absorbed and transported to the liver where it is converted to TMAO.
In studies done with both rats and humans, subjects fed with a high choline content experienced increase in blood TMAO levels and significant increased risk of atherosclerosis compared to subjects receiving a diet low in choline. In addition, in a study done with rats, when gut bacteria was eradicated with antibiotics, there was a subsequent lower level of blood TMAO and decreased risk of atherosclerosis.
The link of TMAO to atherosclerosis is currently being studied and the exact mechanism is not entirely known. However, current evidence link TMAO in suppressing reverse cholesterol transport, macrophage dysfunction, and inflammation, all which causes atherosclerosis and coronary artery disease. Most likely, the effect of TMAO involves all of these mechanisms as well as many others we may never completely understand.
How does this affect your health?
As stated previously, carnitine is also increase your risk of atherosclerosis and “heart disease.” Dietary carnitine is also converted to TMA and then to TMAO, just like choline. A study published by nature in 2013 by Nature Medicine, human subjects with high levels of L-Carnitine had increased risk via TMAO mechanisms.
Carnitine is an essential chemical compound that is required by the body to convert fatty acids to energy in the cells’ mitochondria. It is found heavily in red meat (~95 mg in 100g of steak) and much lower in most plant based food (~0.195 mg in 100 g of asparagus). So because Carnitine is important in energy production, we need more of it, right? That is certainly what energy drink makers do as they supplement their beverages with carnitine. This is simply not true as carnitine is produced by the body using a common amino acid called lysine, which can be found in plant-based food, especially beans.
Therefore, this huge discrepancy in carnitine load between plant and meat largely explains why people who eat meat have a much higher prevalence rate of heart attacks than vegetarians. Also, because dietary carnitine is converted by gut bacteria to TMA, there is lower chance of the carnitine to be absorbed by the intestine to be used in the body. On the other hand, eating a plant base diet with lots of beans allows the body to absorb the lysine and convert it to carnitine appropriately and in the right amount that the body currently requires.
Many drug companies and researchers are going jump at this evolving research such as producing antibiotics to eradicate the bacteria in our gut that promote TMA conversion. Unfortunately, this short-sighted approach is dangerous as it can create antibiotic resistant, dangerous bacteria as well as the hundreds of side effects associated with medications. The answer to coronary artery disease is simply not found in pills, rather it lies in our daily habits such as eating a diet full of plant based food that is nurturing for our hearts rather than destructive.
“Dig your well before you are thirsty” – Indian proverb
Wang Z et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011 (472) 57-63
Loscalzo, J. Gut microbiota, the genome, and diet in atherogenesis. New England Journal of Medicine 2013: 368(17) 1647-1649
Tang W et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. New England Journal of Medicine 2013: 368(17) 1575-1584
Koeth R et al. Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature Medicine 2013 (19) 576-585