Rectal biopsies taken before and after eating meat determine the potentially DNA-damaging dose of heme.
Is Heme Iron the Reason Meat Is Carcinogenic?
4.8/5 - (98 votes)
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
US Patent No. 9,700,067 was Impossible Food’s dream of improving plant-based meat substitutes to better replicate the aromas and flavors of meat by using plant-based heme. Okay, but what about the heme-induced formation of nitroso compounds? When we eat lots of meat, you can pick up more and more nitroso compounds in people’s poop, a small fraction of which may be due directly to the heme. The toxicological significance of this remains to be established, since only some nitroso compounds are of concern. But should the nitroso compounds formed in the intestine as a result of heme consumption be shown to be mutagenic or carcinogenic, this might help explain the association between red meat consumption and colorectal cancer. But you don’t know, until you put it to the test.
“DNA damage is considered an essential component of the [development] of colonic cancer;” so, researchers looked at “fecal water genotoxicity.” You’ve heard of green tea and black tea? This is more like brown tea, basically like a filtered fecal smoothie. That’s definitely one where you want to double-check the blender lid is on tight.
But what they found was that the DNA-damaging effects of the fecal water was independent of the amount of nitroso compounds they found. Now the lack of correlation between the apparent total nitroso compound concentrations and DNA damage could be due to much lower levels of nitroso compounds found in fecal water compared to the feces themselves. I mean, just looking at the fecal water, the nitroso compounds are the same across meat groups, but the real poop had the real scoop.
Ideally, though, we’d like to know what’s happening in the human colon. So, researchers took biopsies before and after a week that included a few daily servings of beef and veal. Not only did they see more than a “twofold increase in fecal water genotoxicity,” that correlated with pro-carcinogenic gene expression changes in the before-and-after biopsy specimens after just one week.
Still, there has only been “circumstantial evidence that the [N-nitroso compounds] formed in the large bowel after eating [meat]….may be important genotoxins”—until now, or at least until this study. A significant increase in nitroso compounds, significantly correlated with a significant increase in DNA damage characteristic of N-nitroso genotoxicity. You can visualize the DNA damage in rectal biopsies—the brown staining on the right—after a month of three beef and lamb servings a day. The researchers suggest dietary heme as a reasonable explanation, but the lowest dose of heme showing evidence of direct DNA damage, in this case from freshly-resected colon tissue, was 10 micromoles. I contacted Impossible, and they said that’s equivalent to three times the concentration of heme found in their burgers. After completing this deep dive, therefore, it’s not clear to me that heme at typical dietary doses causes harm, and even less clear that heme is a culprit in the meat and cancer connection. If it’s not the heme, though, what is it?
Well, there are “reasons to suspect involvement of bovine infectious factors in colorectal cancer.” There are heat-resistant tumor-causing viruses that could survive meat cooked medium or rare. A specific class of infectious agents that have been isolated from both cows and around human colon cancer tissue, not to mention the brains of MS victims. “What do breast and colorectal cancers and multiple sclerosis have in common?” Several potentially infectious factors from cattle blood and milk, but that’s a whole video topic in and of itself.
Less speculatively, it could just be the saturated and trans fats, or sulfur-containing amino acids concentrated in the meat interacting with our gut microbes, resulting in oxidative stress and inflammation that drives the cancer. If you compare the gut bacteria in stools from cancer patients to healthy subjects, a high meat-to-fruit-and-veggie ratio “appears to associate with outgrowth of bacteria that might contribute to a more hostile gut environment.” A hunt for “global microbial signatures that are specific for colorectal cancer” suggested a “metabolic link between cancer-associated gut microbes and a fat- and meat-rich diet.”
Maybe it’s from the meat putrefying in your colon. Putrefaction inside the human gastrointestinal tract pertains to decomposition of undigested proteins in the gut. Some of the products of this putrefaction process, like ammonia, putrescine, and uremic toxins like cresol, indole, and phenol have been implicated in the development of colorectal cancer. But cut out the meat, and levels of some of these compounds may fall by more than half, perhaps because they cultivated fewer putrefying bacteria.
Bad bacteria also produce secondary bile acids, which are associated with both cancer risk and cancer progression as a potential promoter of colorectal tumor enlargement, in part by damaging the intestinal lining––causing a leaky gut. Put people on a diet packed with animal foods, and you get a massive increase in the bacterial production within days, whereas if you cut out meat, you can go the other way. Even just eating more plant-based––swapping out the standard American diet for healthier fare––remarkably reduced secondary bile acids by 70 percent within just two weeks.
There also may be a “strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat.” Maybe that’s the link between what our gut bugs are doing with meat and risk of colorectal cancer. Maybe because of the inflammation caused by TMAO, but if could also be the oxidative stress, or DNA damage, or protein disruption.
Or what about the nonhuman sialic acid known as Neu5Gc that is incorporated into the tissues of meat consumers, and elicits an inflammatory immune reaction. And antibody levels against this foreign compound found in meat are associated with colorectal cancer risk. One could go on and on.
The bottom line health-wise is that while nutrition experts are understandably concerned you’re going to be ordering that Impossible Whopper with fries and a Coke, hey—it’s better than getting fries and a Coke with a regular Whopper.
Please consider volunteering to help out on the site.
- Fraser R. Methods and compositions for affecting the flavor and aroma profile of consumables. July 11, 2017.
- Kuhnle GG, Story GW, Reda T, et al. Diet-induced endogenous formation of nitroso compounds in the GI tract. Free Radic Biol Med. 2007;43(7):1040-7.
- Bingham SA, Hughes R, Cross AJ. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response. J Nutr. 2002 Nov;132(11 Suppl):3522S-5S.
- Rowland IR, Granli T, Bøckman OC, Key PE, Massey RC. Endogenous N-nitrosation in man assessed by measurement of apparent total N-nitroso compounds in faeces. Carcinogenesis. 1991;12(8):1395-1401.
- Cross AJ, Pollock JR, Bingham SA. Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat. Cancer Res. 2003;63(10):2358-60.
- Cross AJ, Greetham HL, Pollock JR, Rowland IR, Bingham SA. Variability in fecal water genotoxicity, determined using the Comet assay, is independent of endogenous N-nitroso compound formation attributed to red meat consumption. Environ Mol Mutagen. 2006;47(3):179-84.
- Gratz SW, Wallace RJ, El-Nezami HS. Recent Perspectives on the Relations between Fecal Mutagenicity, Genotoxicity, and Diet. Front Pharmacol. 2011;2:4.
- Pearson JR, Gill CI, Rowland IR. Diet, fecal water, and colon cancer--development of a biomarker. Nutr Rev. 2009;67(9):509-26.
- Hebels DG, Sveje KM, de Kok MC, et al. Red meat intake-induced increases in fecal water genotoxicity correlate with pro-carcinogenic gene expression changes in the human colon. Food Chem Toxicol. 2012;50(2):95-103.
- Lewin MH, Bailey N, Bandaletova T, et al. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk. Cancer Res. 2006;66(3):1859-65.
- Le Leu RK, Winter JM, Christophersen CT, et al. Butyrylated starch intake can prevent red meat-induced O6-methyl-2-deoxyguanosine adducts in human rectal tissue: a randomised clinical trial. Br J Nutr. 2015;114(2):220-30.
- Glei M, Klenow S, Sauer J, Wegewitz U, Richter K, Pool-Zobel BL. Hemoglobin and hemin induce DNA damage in human colon tumor cells HT29 clone 19A and in primary human colonocytes. Mutat Res. 2006;594(1-2):162-71.
- zur Hausen H. Red meat consumption and cancer: reasons to suspect involvement of bovine infectious factors in colorectal cancer. Int J Cancer. 2012;130(11):2475-83.
- de Villiers EM, Gunst K, Chakraborty D, Ernst C, Bund T, Zur Hausen H. A specific class of infectious agents isolated from bovine serum and dairy products and peritumoral colon cancer tissue. Emerg Microbes Infect. 2019;8(1):1205-18.
- Whitley C, Gunst K, Müller H, Funk M, Zur Hausen H, de Villiers EM. Novel replication-competent circular DNA molecules from healthy cattle serum and milk and multiple sclerosis-affected human brain tissue. Genome Announc. 2014;2(4):e00849-14.
- zur Hausen H. Risk factors: What do breast and CRC cancers and MS have in common? Nat Rev Clin Oncol. 2015;12(10):569-70.
- Song M, Garrett WS, Chan AT. Nutrients, foods, and colorectal cancer prevention. Gastroenterology. 2015;148(6):1244-60.e16.
- Feng Q, Liang S, Jia H, et al. Gut microbiome development along the colorectal adenoma-carcinoma sequence. Nat Commun. 2015;6:6528.
- Wirbel J, Pyl PT, Kartal E, et al. Meta-analysis of fecal metagenomes reveals global microbial signatures that are specific for colorectal cancer. Nat Med. 2019;25(4):679-89.
- Kaur H, Das C, Mande SS. In Silico Analysis of Putrefaction Pathways in Bacteria and Its Implication in Colorectal Cancer. Front Microbiol. 2017;8:2166.
- Patel KP, Luo FJ, Plummer NS, Hostetter TH, Meyer TW. The production of p-cresol sulfate and indoxyl sulfate in vegetarians versus omnivores. Clin J Am Soc Nephrol. 2012;7(6):982-8.
- O'Keefe SJ, Li JV, Lahti L, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nat Commun. 2015;6:6342.
- Kawano A, Ishikawa H, Kamano T, et al. Significance of fecal deoxycholic acid concentration for colorectal tumor enlargement. Asian Pac J Cancer Prev. 2010;11(6):1541-6.
- Liu L, Dong W, Wang S, et al. Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis. Food Funct. 2018;9(11):5588-97.
- David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature. 2014;505(7484):559-63.
- Allinger UG, Johansson GK, Gustafsson JA, Rafter JJ. Shift from a mixed to a lactovegetarian diet: influence on acidic lipids in fecal water - a potential risk factor for colon cancer. Am J Clin Nutr. 1989;50(5):992-6.
- Xu R, Wang Q, Li L. A genome-wide systems analysis reveals strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat. BMC Genomics. 2015;16 Suppl 7(Suppl 7):S4.
- Chan CWH, Law BMH, Waye MMY, Chan JYW, So WKW, Chow KM. Trimethylamine-N-oxide as One Hypothetical Link for the Relationship between Intestinal Microbiota and Cancer - Where We Are and Where Shall We Go?. J Cancer. 2019;10(23):5874-82.
- Jeyakumar A, Dissabandara L, Gopalan V. A critical overview on the biological and molecular features of red and processed meat in colorectal carcinogenesis. J Gastroenterol. 2017;52(4):407-18.
- Samraj AN, Bertrand KA, Luben R, et al. Polyclonal human antibodies against glycans bearing red meat-derived non-human sialic acid N-glycolylneuraminic acid are stable, reproducible, complex and vary between individuals: Total antibody levels are associated with colorectal cancer risk. PLoS One. 2018;13(6):e0197464.
- Hu FB, Otis BO, McCarthy G. Can Plant-Based Meat Alternatives Be Part of a Healthy and Sustainable Diet? JAMA. 2019;1-3.
Video production by Glass Entertainment
Motion graphics by Avocado Video
- animal products
- beef
- black tea
- breast cancer
- cancer
- carcinogens
- colon cancer
- colorectal cancer
- DNA damage
- fake meat
- fiber
- green tea
- gut flora
- hamburgers
- heme iron
- iron
- meat
- meat substitutes
- microbiome
- multiple sclerosis
- Neu5Gc
- oxidative stress
- plant protein
- Plant-Based Diets
- saturated fat
- soy
- TMAO
- trans fats
- vegans
- vegetarians
- veggie burgers
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
US Patent No. 9,700,067 was Impossible Food’s dream of improving plant-based meat substitutes to better replicate the aromas and flavors of meat by using plant-based heme. Okay, but what about the heme-induced formation of nitroso compounds? When we eat lots of meat, you can pick up more and more nitroso compounds in people’s poop, a small fraction of which may be due directly to the heme. The toxicological significance of this remains to be established, since only some nitroso compounds are of concern. But should the nitroso compounds formed in the intestine as a result of heme consumption be shown to be mutagenic or carcinogenic, this might help explain the association between red meat consumption and colorectal cancer. But you don’t know, until you put it to the test.
“DNA damage is considered an essential component of the [development] of colonic cancer;” so, researchers looked at “fecal water genotoxicity.” You’ve heard of green tea and black tea? This is more like brown tea, basically like a filtered fecal smoothie. That’s definitely one where you want to double-check the blender lid is on tight.
But what they found was that the DNA-damaging effects of the fecal water was independent of the amount of nitroso compounds they found. Now the lack of correlation between the apparent total nitroso compound concentrations and DNA damage could be due to much lower levels of nitroso compounds found in fecal water compared to the feces themselves. I mean, just looking at the fecal water, the nitroso compounds are the same across meat groups, but the real poop had the real scoop.
Ideally, though, we’d like to know what’s happening in the human colon. So, researchers took biopsies before and after a week that included a few daily servings of beef and veal. Not only did they see more than a “twofold increase in fecal water genotoxicity,” that correlated with pro-carcinogenic gene expression changes in the before-and-after biopsy specimens after just one week.
Still, there has only been “circumstantial evidence that the [N-nitroso compounds] formed in the large bowel after eating [meat]….may be important genotoxins”—until now, or at least until this study. A significant increase in nitroso compounds, significantly correlated with a significant increase in DNA damage characteristic of N-nitroso genotoxicity. You can visualize the DNA damage in rectal biopsies—the brown staining on the right—after a month of three beef and lamb servings a day. The researchers suggest dietary heme as a reasonable explanation, but the lowest dose of heme showing evidence of direct DNA damage, in this case from freshly-resected colon tissue, was 10 micromoles. I contacted Impossible, and they said that’s equivalent to three times the concentration of heme found in their burgers. After completing this deep dive, therefore, it’s not clear to me that heme at typical dietary doses causes harm, and even less clear that heme is a culprit in the meat and cancer connection. If it’s not the heme, though, what is it?
Well, there are “reasons to suspect involvement of bovine infectious factors in colorectal cancer.” There are heat-resistant tumor-causing viruses that could survive meat cooked medium or rare. A specific class of infectious agents that have been isolated from both cows and around human colon cancer tissue, not to mention the brains of MS victims. “What do breast and colorectal cancers and multiple sclerosis have in common?” Several potentially infectious factors from cattle blood and milk, but that’s a whole video topic in and of itself.
Less speculatively, it could just be the saturated and trans fats, or sulfur-containing amino acids concentrated in the meat interacting with our gut microbes, resulting in oxidative stress and inflammation that drives the cancer. If you compare the gut bacteria in stools from cancer patients to healthy subjects, a high meat-to-fruit-and-veggie ratio “appears to associate with outgrowth of bacteria that might contribute to a more hostile gut environment.” A hunt for “global microbial signatures that are specific for colorectal cancer” suggested a “metabolic link between cancer-associated gut microbes and a fat- and meat-rich diet.”
Maybe it’s from the meat putrefying in your colon. Putrefaction inside the human gastrointestinal tract pertains to decomposition of undigested proteins in the gut. Some of the products of this putrefaction process, like ammonia, putrescine, and uremic toxins like cresol, indole, and phenol have been implicated in the development of colorectal cancer. But cut out the meat, and levels of some of these compounds may fall by more than half, perhaps because they cultivated fewer putrefying bacteria.
Bad bacteria also produce secondary bile acids, which are associated with both cancer risk and cancer progression as a potential promoter of colorectal tumor enlargement, in part by damaging the intestinal lining––causing a leaky gut. Put people on a diet packed with animal foods, and you get a massive increase in the bacterial production within days, whereas if you cut out meat, you can go the other way. Even just eating more plant-based––swapping out the standard American diet for healthier fare––remarkably reduced secondary bile acids by 70 percent within just two weeks.
There also may be a “strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat.” Maybe that’s the link between what our gut bugs are doing with meat and risk of colorectal cancer. Maybe because of the inflammation caused by TMAO, but if could also be the oxidative stress, or DNA damage, or protein disruption.
Or what about the nonhuman sialic acid known as Neu5Gc that is incorporated into the tissues of meat consumers, and elicits an inflammatory immune reaction. And antibody levels against this foreign compound found in meat are associated with colorectal cancer risk. One could go on and on.
The bottom line health-wise is that while nutrition experts are understandably concerned you’re going to be ordering that Impossible Whopper with fries and a Coke, hey—it’s better than getting fries and a Coke with a regular Whopper.
Please consider volunteering to help out on the site.
- Fraser R. Methods and compositions for affecting the flavor and aroma profile of consumables. July 11, 2017.
- Kuhnle GG, Story GW, Reda T, et al. Diet-induced endogenous formation of nitroso compounds in the GI tract. Free Radic Biol Med. 2007;43(7):1040-7.
- Bingham SA, Hughes R, Cross AJ. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response. J Nutr. 2002 Nov;132(11 Suppl):3522S-5S.
- Rowland IR, Granli T, Bøckman OC, Key PE, Massey RC. Endogenous N-nitrosation in man assessed by measurement of apparent total N-nitroso compounds in faeces. Carcinogenesis. 1991;12(8):1395-1401.
- Cross AJ, Pollock JR, Bingham SA. Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat. Cancer Res. 2003;63(10):2358-60.
- Cross AJ, Greetham HL, Pollock JR, Rowland IR, Bingham SA. Variability in fecal water genotoxicity, determined using the Comet assay, is independent of endogenous N-nitroso compound formation attributed to red meat consumption. Environ Mol Mutagen. 2006;47(3):179-84.
- Gratz SW, Wallace RJ, El-Nezami HS. Recent Perspectives on the Relations between Fecal Mutagenicity, Genotoxicity, and Diet. Front Pharmacol. 2011;2:4.
- Pearson JR, Gill CI, Rowland IR. Diet, fecal water, and colon cancer--development of a biomarker. Nutr Rev. 2009;67(9):509-26.
- Hebels DG, Sveje KM, de Kok MC, et al. Red meat intake-induced increases in fecal water genotoxicity correlate with pro-carcinogenic gene expression changes in the human colon. Food Chem Toxicol. 2012;50(2):95-103.
- Lewin MH, Bailey N, Bandaletova T, et al. Red meat enhances the colonic formation of the DNA adduct O6-carboxymethyl guanine: implications for colorectal cancer risk. Cancer Res. 2006;66(3):1859-65.
- Le Leu RK, Winter JM, Christophersen CT, et al. Butyrylated starch intake can prevent red meat-induced O6-methyl-2-deoxyguanosine adducts in human rectal tissue: a randomised clinical trial. Br J Nutr. 2015;114(2):220-30.
- Glei M, Klenow S, Sauer J, Wegewitz U, Richter K, Pool-Zobel BL. Hemoglobin and hemin induce DNA damage in human colon tumor cells HT29 clone 19A and in primary human colonocytes. Mutat Res. 2006;594(1-2):162-71.
- zur Hausen H. Red meat consumption and cancer: reasons to suspect involvement of bovine infectious factors in colorectal cancer. Int J Cancer. 2012;130(11):2475-83.
- de Villiers EM, Gunst K, Chakraborty D, Ernst C, Bund T, Zur Hausen H. A specific class of infectious agents isolated from bovine serum and dairy products and peritumoral colon cancer tissue. Emerg Microbes Infect. 2019;8(1):1205-18.
- Whitley C, Gunst K, Müller H, Funk M, Zur Hausen H, de Villiers EM. Novel replication-competent circular DNA molecules from healthy cattle serum and milk and multiple sclerosis-affected human brain tissue. Genome Announc. 2014;2(4):e00849-14.
- zur Hausen H. Risk factors: What do breast and CRC cancers and MS have in common? Nat Rev Clin Oncol. 2015;12(10):569-70.
- Song M, Garrett WS, Chan AT. Nutrients, foods, and colorectal cancer prevention. Gastroenterology. 2015;148(6):1244-60.e16.
- Feng Q, Liang S, Jia H, et al. Gut microbiome development along the colorectal adenoma-carcinoma sequence. Nat Commun. 2015;6:6528.
- Wirbel J, Pyl PT, Kartal E, et al. Meta-analysis of fecal metagenomes reveals global microbial signatures that are specific for colorectal cancer. Nat Med. 2019;25(4):679-89.
- Kaur H, Das C, Mande SS. In Silico Analysis of Putrefaction Pathways in Bacteria and Its Implication in Colorectal Cancer. Front Microbiol. 2017;8:2166.
- Patel KP, Luo FJ, Plummer NS, Hostetter TH, Meyer TW. The production of p-cresol sulfate and indoxyl sulfate in vegetarians versus omnivores. Clin J Am Soc Nephrol. 2012;7(6):982-8.
- O'Keefe SJ, Li JV, Lahti L, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nat Commun. 2015;6:6342.
- Kawano A, Ishikawa H, Kamano T, et al. Significance of fecal deoxycholic acid concentration for colorectal tumor enlargement. Asian Pac J Cancer Prev. 2010;11(6):1541-6.
- Liu L, Dong W, Wang S, et al. Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis. Food Funct. 2018;9(11):5588-97.
- David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature. 2014;505(7484):559-63.
- Allinger UG, Johansson GK, Gustafsson JA, Rafter JJ. Shift from a mixed to a lactovegetarian diet: influence on acidic lipids in fecal water - a potential risk factor for colon cancer. Am J Clin Nutr. 1989;50(5):992-6.
- Xu R, Wang Q, Li L. A genome-wide systems analysis reveals strong link between colorectal cancer and trimethylamine N-oxide (TMAO), a gut microbial metabolite of dietary meat and fat. BMC Genomics. 2015;16 Suppl 7(Suppl 7):S4.
- Chan CWH, Law BMH, Waye MMY, Chan JYW, So WKW, Chow KM. Trimethylamine-N-oxide as One Hypothetical Link for the Relationship between Intestinal Microbiota and Cancer - Where We Are and Where Shall We Go?. J Cancer. 2019;10(23):5874-82.
- Jeyakumar A, Dissabandara L, Gopalan V. A critical overview on the biological and molecular features of red and processed meat in colorectal carcinogenesis. J Gastroenterol. 2017;52(4):407-18.
- Samraj AN, Bertrand KA, Luben R, et al. Polyclonal human antibodies against glycans bearing red meat-derived non-human sialic acid N-glycolylneuraminic acid are stable, reproducible, complex and vary between individuals: Total antibody levels are associated with colorectal cancer risk. PLoS One. 2018;13(6):e0197464.
- Hu FB, Otis BO, McCarthy G. Can Plant-Based Meat Alternatives Be Part of a Healthy and Sustainable Diet? JAMA. 2019;1-3.
Video production by Glass Entertainment
Motion graphics by Avocado Video
- animal products
- beef
- black tea
- breast cancer
- cancer
- carcinogens
- colon cancer
- colorectal cancer
- DNA damage
- fake meat
- fiber
- green tea
- gut flora
- hamburgers
- heme iron
- iron
- meat
- meat substitutes
- microbiome
- multiple sclerosis
- Neu5Gc
- oxidative stress
- plant protein
- Plant-Based Diets
- saturated fat
- soy
- TMAO
- trans fats
- vegans
- vegetarians
- veggie burgers
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Title
Is Heme Iron the Reason Meat Is Carcinogenic?
LicenseCreative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
Content URLDoctor's Note
This is the final installment in a nine-video series on plant-based meats, which includes:
- The Environmental Impacts of Plant-Based Meat Substitutes
- Are Beyond Meat and the Impossible Burger Healthful?
- Are Pea and Soy Protein Isolates Harmful?
- Plant-Based Meat Substitutes Put to the Test
- The Health Effects of Mycoprotein (Quorn) Products BCAAs in Meat
- What About the Heme in Impossible Burgers?
- Does Heme Iron Cause Cancer?
- Heme-Induced N-Nitroso Compounds and Fat Oxidation
If you want all nine of the videos in the plant-based meat series in one place, you can get them right now in a digital download from my webinar a few months ago.
If you haven’t yet, you can subscribe to my videos for free by clicking here. Read our important information about translations here.
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