12 January - 20 June 2016

High red meat consumption increases chemicals associated with heart disease

A study published in European Heart Journal has examined whether chronic (4 week) ingestion of an iso-caloric diet containing protein derived predominately from either red meat, white meat or non-meat sources affect levels of TMAO, many of its nutrient precursors and both their overall metabolism and renal execution rates in vivo.

High levels of gut microbiota-generated metabolite, trimethylamine N-oxide (TMAO) has been associated with heart disease.  High blood levels have also been found to be linked to cardiovascular disease development and heart attack, stroke and even death. TMAO is a dietary by-product that is formed by gut bacteria during digestion and is derived in part from nutrients that are abundant in red meat. A study published in European Heart Journal has examined whether chronic (4 week) ingestion of an iso-caloric diet containing protein derived predominately from either red meat, white meat or non-meat sources affect levels of TMAO, many of its nutrient precursors and both their overall metabolism and renal execution rates in vivo. 

The study by Wang et al. recruited 113 healthy men and women, who were omnivores, with normal renal function and with a median age of 45 years. The participants were instructed to consume a 2 week diet which they state reflected a typical American diet containing 49% carbohydrate, 14% protein and 37% fat.  They were then provided with a three experimental diets of either red meat (equivalent of about 8oz of steak daily), white meat or non-meat in random order for 4 weeks separated by a 2-7 week washout period.  Whilst all diets contained the same amount of calories, half of the participants were also placed on high fat versions of the three diets. At the end of each diet period, blood and urine sample were collected and analysed for TMAO and other metabolites including various choline and carnitine nutrients precursors.

Wang et al. found that when the participants consumed the red meat diet, blood levels of TMAO increased by “approximately three-fold compared with the white meat or non-meat diets, with some subjects showing over a 10-fold increase.”  When the participants changed diets from the red meat diet to either the white meat or non-meat diets, the study authors report that there was “a marked reduction in fasting plasma TMAO levels”. No differences were observed in results when the participants consumed either a high or low saturated fat diet.  Those who had a higher level of TMAO following the baseline diet, were reported to be more susceptible to “larger elevation of TMAO during consumption of the red meat diet.” Following ingestion of red meat, the amount of TMAO excreted, was significantly reduced compared to the white meat or non-meat diets.  Whilst the amount of carnitine, ϒ-butyrobetaine and crotonobetaine increased significantly.

The authors concluded their study by reiterating that their findings show that a diet high in red meat compared to white or non-meat results in substantial increases in fasting plasma and urine TMAO levels.  They continue by stating that red meat diet raises systemic TAMO levels by 3 different mechanisms: enhanced nutrient density of dietary TMA precursors, increased microbial TMA/TMA production from carnitine, but not choline and reduced renal TAMO excretion.  Discontinuation of red meat reduced plasma TMAO levels within 4 weeks. 

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