Why We Should Eat Less Red Meat
By James J. Kenney PhD, FACN
It can be difficult to know whether we should continue eating processed and unprocessed red meat.
We may hear that it is healthy to consume as much as we’ve always eaten and then hear that we should eat less red meat and even limit it to once a week.
Conflicting Information About Red Meat Consumption
The 2015-2020 United States Dietary Guidelines for Americans (USDG) recommended limiting consumption of red meat. The USDG suggested that both processed and unprocessed meat be limited to approximately 1 weekly serving (1). However, a recent article in the October 2019 Annals of Internal Medicine evaluated four systematic reviews. These reviews focused on both observational studies and clinical trials. They addressed the health effects associated with red meat and processed meat consumption. One systematic review addressed people's health-related values and preferences regarding meat consumption.
The expert panel of 14 US and international nutrition experts came to a very different conclusion than prior reviews. This expert panel stated: “…. adults continue current unprocessed red meat consumption. Similarly, the panel suggests adults continue current processed meat consumption.” The panel did note these recommendations were based on “weak evidence” (2). Not surprisingly, that conclusion was widely reported to the general public.
The article has drawn sharp criticisms from other researchers and many clinicians. They say that the methodology used to grade the existing research misrepresents the vast data that shows red meat’s many known and suspected adverse metabolic effects and health outcomes. This includes heart disease, some cancers, and type 2 diabetes. Nonetheless, the meat industry is helping to spread this “good news” for those who enjoy processed and unprocessed red meat.
Red Meat and Heart Disease
Certainly, this review of reviews does little to eliminate the well-established and suspected potentially-detrimental adverse metabolic effects of consuming red meats -- especially those high in fat and processed. Red meats are generally high in saturated fat and cholesterol. We have long known that increasing the consumption of both saturated fat and/or cholesterol in the diet elevates LDL-C and non HDL-C in the blood(3). And no one doubts that higher LDL-C and non HDL-C levels promote more coronary artery disease (CAD)(4).
For example, a large prospective study from nine European countries (European Heart Journal Trial) followed middle-aged and older subjects for 12.6 years and showed that heart attacks are strongly associated with eating mammal meat and processed meats(5). Many previous studies have shown that a more vegetarian diet is associated with reduced heart attack risk(6). For more than 70 years, scientists have blamed dietary saturated fat and cholesterol intake as responsible for causing heart attacks, but there is growing evidence that red meats may promote heart disease in other ways too.
TMAO and the Metabolic Effects of Red Meat
TriMethylAmine oxide (TMAO) is another possible metabolite increased by a steady diet of red meat. People who switch from eating red meat to eating primarily chicken and plants see their blood levels of TMAO drop markedly along with the concentrations of the colon bacteria that make TMA(7).
Here is how that process works. Foods that contain choline or L-carnitine are converted to a gas called trimethylamine (TMA) by gut bacteria. This gas is absorbed into the bloodstream and passes to the liver, where an enzyme converts TMA to TMAO.
Choline and carnitine are found in large amounts in red meat and are also found in poultry, fish, dairy, and egg yolks, but in far lower amounts in plants. However, red meat raises blood levels of TMAO much higher than does poultry, and it also changes the bacteria in your colon to the ones that make more TMA. The European Heart Journal Trial suggested that elevated blood levels of TMAO may increase risk of heart attacks in several ways:
TMAO and Chicken, Fish, Dairy
Fatty dairy products and egg yolks are high in saturated fat and cholesterol. Egg yolks and fatty dairy products also contain choline. Fish can contain carnitine and choline that raise blood levels of TMAO. Some cold deep-water fish also contain TMAO, which they appear to use as an anti-freeze. However, eating fish is generally not associated with an increased risk for heart attacks(9). This could be because the omega-3 fatty acids in deep-water fish may help to reduce inflammation and clotting that increase heart attack risk, thus countering or blunting the adverse metabolic effects of TMAO.
Reducing TMAO Levels
Last May 22nd, the Journal of the American Medical Association contained a detailed article by Jennifer Abbasi. She wrote: "Researchers at Stanford University are already studying the effects of plant-based meat alternatives on TMAO levels in a clinical trial. But short of going full-on herbivore, people can substantially reduce TMAO levels within as little as a month by eliminating or reducing red meat, according to the European Heart Journal Trial that compared protein sources."
Red Meat May Cause Overly Active Immune System
It appears that eating red meat turns on your immune system just as germs do, and if you eat red meat regularly, your immune system may stay overly active all the time. This can lead to chronic inflammation.
Back in 1982, Professor Ajit Varki of the University of California San Diego discovered a sugar-protein complex molecule (called Neu5Gc) that appears in the tissues of almost every mammal except humans (10). Two to three million years ago, our pre-human ancestors had a single genetic mutation in their CMAH gene that apparently helped protect them from a deadly form of malaria in Africa. Apes, gorillas, chimpanzees, and other human progenitors were dying from a type of malaria called Plasmodium reichenowi. Then along came a pre-human ancestor with a CMAH gene mutation. Instead of making a cell surface sugar-protein complex called Neu5Gc, this mutation resulted in another molecule called Neu5Ac (11).
As a result, that pre-human ancestor did not die from malaria like other apes, monkeys and gorillas, so his or her children lived and proliferated. The result is that today all humans have Neu5Ac instead of Neu5Gc. Chimpanzees share more than 99 percent of their genes with modern humans, but the CMAH gene is one of the areas of difference. As often happens in nature, the malaria parasite then modified its own genetic makeup into a variant called Plasmodium falciparum, which can infect humans, but not chimpanzees, so today humans can be infected only with Plasmodium falciparum while chimpanzees and other great apes can be infected only with Plasmodium reichenowi.
Since no other mammal developed this genetic mutation, only humans make Neu5Ac and so have an immune system that reacts to Neu5Gc.
When people eat mammal meat their immune system is triggered in much the same way as when it responds to infecting microbes. Your immune system tries to kill what it mistakes as invading germs. The same cells and chemicals that attack and kill germs can damage arteries, making it easier for more cholesterol to be delivered to the artery wall.
Chronic inflammation may also destabilize cholesterol-rich atherosclerotic plaques that can rupture and lead to a heart attack. People who have the most markers of an overactive immune system and inflammation are the ones most likely to suffer, and die from, heart attacks(12). Researchers have identified a gene (CMAH) that produces the potentially harmful component in red meats(13).
Heart disease causes about one-third of the deaths in North America. Well-established risk factors for heart attacks include high blood cholesterol, high blood sugar, high blood pressure, obesity, smoking, and lack of exercise. There are, however, about 15 percent of people who suffer heart attacks and yet do not have elevated levels of any of these risk factors(14).
Other mammals can suffer heart attacks when they have these risk factors (often caused by human lifestyle habits), but they seldom suffer heart attacks if they do not have any of these risk factors as some people do(15). When mice were genetically modified to have the same CMAH gene mutation, these CMAH gene-modified mice suffered double the risk of atherosclerosis compared to unmodified mice when fed red meat. Like humans, they also experience an increased risk for inflammation, heart attacks, strokes, diabetes, and some types of cancers.
Reasons to Eat Less Red Meat
Continuing research adds more evidence as to why a steady diet of red meat may promote serious ills over the long term. Processed and red meat intake has been linked to increased risk for diabetes, some types of cancers, and other diseases. Certainly, we need more research to establish precisely how eating red meat appears to promote chronic inflammation and other adverse metabolic effects that promote disease.
When added to the fact that red meat is high in saturated fat and cholesterol, this new data suggests that most people would likely be better off in the long run if they eat less red meat and especially fatty processed red meat intake. There seems to be adequate data showing that people who regularly eat red meat are indeed more likely to have an increased risk for heart attacks, strokes, diabetes, and cancers(16). However, there is not enough data at this time to conclude that even eating small amounts of red meat on occasion is dangerous to one’s health.
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1. U.S. Department of Health and Human Services 2015-2020 Dietary Guidelines for Americans. Washington, DC, U.S. Department of Health and Human Services. December 2015.
5. Circulation, April 22, 2019
6. Am J of Clin Nutr, July 1, 2014;100(suppl 1):320S–328S
7. Eur Heart J, Feb 14, 2019;40(7):583–594
8. Cell, March 24, 2016;165(1):111-124.
9. Microbial Ecology in Health and Disease, May 19, 2017:28(1)
10. Proc Nat Acad of Sciences, Sept 29, 2003
11. Proc Natl Acad Sci USA, Sept 6, 2005;102(36): 12819–12824
12. J of Nutr, May 22, 2019
13. Genome Biol Evol, Jan 1, 2018;10(1):207-219
14. CDC, NCHS, Underlying Cause of Death, 1999-2013
15. Evol Appl, 2009 Feb; 2(1): 101–112
16. Genome Biol Evol, Jan 1, 2018;10(1):207-219