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Adding Immunotherapy to Chemotherapy After Surgery Improves Survival in Colon Cancer

The AHA! Team — Mon, 04 Aug 2025 05:43:16 +0000

Mayo Clinic via News-Medical – Colon cancer is the third most prevalent form of cancer in the U.S., and while screening has helped detect and prevent colon cancer from spreading, major advancements in treating colon cancer have lagged. Now, new research led by Mayo Clinic Comprehensive Cancer Center found that adding immunotherapy to chemotherapy after surgery for patients with stage 3 (node-positive) colon cancer – and with a specific genetic makeup called deficient DNA mismatch repair (dMMR) – was associated with a 50% reduction in cancer recurrence and death compared to chemotherapy alone. Approximately 15% of people diagnosed with colon cancer exhibit dMMR and, to date, these tumors appear less sensitive to chemotherapy. The results of the multi-center study were presented during a plenary session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago. “The findings from our study represent a major advance in the adjuvant treatment of dMMR stage 3 colon cancer and will now change the treatment for this type of cancer,” says oncologist Frank Sinicrope, M.D., who led the study. “It’s extremely rewarding to be able to offer our patients a new treatment regimen that can reduce the risk of recurrence and improve their chances of survival.” Until now, the standard treatment after surgery for any stage 3 colon cancer has been chemotherapy. However, the researchers note that approximately 30% of patients experience cancer recurrence despite this treatment. The clinical trial enrolled 712 patients with dMMR stage 3 colon cancer that had been surgically removed and who had cancer cells in their lymph nodes. The immunotherapy given in this study was an immune checkpoint inhibitor, known as atezolizumab, which activates one’s immune system to attack and kill cancer cells, which are responsible for cancer recurrence and spread. The patients – who lived in the U.S. and Germany – received chemotherapy for six months along with immunotherapy and then continued with immunotherapy alone for another six months. Dr. Sinicrope and others previously studied patients with colon cancer whose cells are unable to repair errors during DNA replication that create a nucleotide mismatch, a condition called dMMR. They noted that these patients’ tumors showed a striking increase in inflammatory cells within the tumor, including those that express the target of immune checkpoint inhibitors. This sparked the idea of using immune checkpoint inhibitors to make the immune cells more effective in attacking and killing the cancer cells. Based on the data from this study, Dr. Sinicrope recommends this combination of immunotherapy and chemotherapy treatment to be the new standard treatment for stage 3 deficient mismatch repair colon cancer. The research team plans to approach the National Comprehensive Cancer Network, a nonprofit organization consisting of 33 leading cancer centers, including Mayo Clinic, with this recommendation. The study included patients with Lynch syndrome, the most common form of hereditary colon cancer, as these patients can have tumors that show deficient mismatch repair (dMMR). We’re changing the paradigm in colon cancer treatment. By using immunotherapy at earlier stages of disease, we are achieving meaningful benefits for our patients.” -Frank Sinicrope, M.D., Mayo Clinic Comprehensive Cancer Center Source: Mayo Clinic To read the original article click here.

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Study Shows New Links Between High Fat Diets and Colon Cancer

AHA Publisher — Fri, 18 Jun 2021 07:00:45 +0000

Arizona State University via EurekAlert – For decades, physicians and dieticians have urged people to limit their intake of high fat foods, citing links to poor health outcomes and some of the leading causes of death in the U.S., such as diabetes, heart disease and cancer. According to the Centers for Disease Control and Prevention, dietary components high in saturated fats such as red meat are thought to be risk factors for colon cancer. Diet is thought to strongly influence the risk of colorectal cancer, and changes in food habits might reduce up to 70% of this cancer burden. Other known epidemiological risk factors are family history, inflammatory bowel disease, smoking and type-2 diabetes. But out of all the risk factors that elevate colon cancer risk, diet is the one environmental and lifestyle factor that may be the easiest to control —simply by changing people’s behavior and eating habits—-if we knew the exact connections. “There’s epidemiological evidence for a strong link between obesity and increased tumor risk,” said School of Life Sciences assistant professor Miyeko Mana. “And in the intestine, the stem cells are the likely cell of origin for cancer. So, what is that connection? Well, diet is something that feeds into that cycle of obesity and colorectal cancer.” Now, a new ASU study led by Mana and her team has shown in greater detail than ever before of how high fat diets can trigger a molecular cascade of events that leads to intestinal and colon cancer. The study was published in the journal Cell Reports. Tales from the Crypts As foods are broken down and make their way through the gut, they interact with intestinal stem cells (ISC) that lie along the inside surfaces of the gut. These ISCs reside in a series of regularly folded valleys of the gut, called crypts. ISCs are thought to be the gateway that coordinates intestinal tumor formation when they adapt to high-fat diets, and elevate cancer risk. Within the ISCs are high-fat sensor molecules that sense and react to high-fat diets levels in the cells. “We were following up on mechanisms that might be required for stem cells to adapt to the high fat diet —and that’s where we came across the PPARs,” said Mana. These peroxisome proliferator-activated receptors (or PPARs) trigger a cellular program that elevates cancer risk, but the exact mechanisms were unclear because there are multiple types of PPARs, and complexities in teasing out their roles. “There is a family of 3 PPARs, named delta, alpha and gamma. At first, I thought just PPAR delta was involved, but in order to see if that gene is really responsible for the phenotype, you have to remove it.” Mana’s team was able to explore and unmask the role of individual PPAR delta and alpha using a mouse model that controlled their activity in the cell. In her team’s study, mice were given a long-term high fat or normal diet, and the activity of each PPAR was carefully monitored to study the effects on cancer risk. In their knockout study, they first removed the PPAR delta gene. “But when we removed it from the intestine, we still observed the phenotype. So, we wondered if maybe another PPAR was compensating and that’s where we thought about PPAR alpha. Both of those (PPAR delta and PPAR alpha) appear to be required for this high fat diet phenotype within the stem cells.” This was frustrating to Mana because she knew right away that developing a potential therapeutic to offset the PPARs just became a much taller task. “When you think about this therapeutically, if you are incorporating a lot of fat into your diet and you want to reduce your risk of colon cancer, targeting two different factors is more challenging then if you are targeting just one.” Looking Farther Downriver To further tease out the genetic complexity, Mana next turned her attention downstream of the PPARs. From their studies, and using new tools of the trade, they were able to slowly tease out the details—down to the level of doing molecular sequencing from individual cells from different areas of the small intestine and colon, mass spectrometry to measure the amounts of different metabolites, and radiolabeled isotopes of fuel sources to measure the carbon flow. Their first big clue came from the metabolic analysis. The high fat diet found in the ISC crypt cells they isolated increased the metabolism of fats, while at the same time, decreasing the breakdown of sugars. “So, we looked more downstream at what these two factors (PPARs) may target, and that was this mitochondrial protein, Cpt1a,” said Mana. “This is required for the import of long chain fatty acids (LCFAs) into mitochondria for use. The LCFAs are part of the high fat diet.” And when they performed the mouse knockout study of Cpt1a, they found they could stop tumor formation in its tracks. The loss of Cpt1a prevented both the expansion and proliferation of the ISCs in the crypts. “If you remove Cpt1a, you are spared this high fat diet phenotype in the intestinal stem cells,” said Mana. “So, you lower your risk of tumorigenesis at this point.” A New Model Emerges From their data, Mana’ team could trace the development of cancer, from diet all the way to tumor formation. First, fats are broken down to free fatty acids. The free fatty acids then stimulate sensors such as the PPARs and turn on genes that can break down the fatty acids. Next, the surplus free fatty acids are transported to the mitochondria, which can burn them up by oxidation to make more energy to feed the stem cells, which multiply, grow and regenerate gut tissue. But when the ISCs numbers are expanded, there is a greater likelihood that mutations can occur—just from random mutations and sheer numbers of cells—that lead to colon cancer. “The idea is that this larger pool of cells remain in the intestine and accumulate mutations, and that means they can be a source of mutated cells leading to transformation and tumor initiation,” said Mana. “We do think that is a likely possibility when there are conditions that expand your stem cell pool.” Mana’s group also found that feeding a high fat diet dramatically accelerated mortality in this model compared with the control condition, by accelerating tumorigenesis. “The levels of these fats that you can get through your diet are going to impact your stem cells, probably in a fairly direct way,” said Mana. “I think one of the surprising things we are finding in our studies is that fatty acids can have such a direct effect. But you can remove these PPARs, you can remove CPT1a, and the intestine is fine.” New Hopes With the new evidence from the study, the hope is to one day apply their work to human colon cancers. “These studies have all been in these mouse models to date,” said Mana. “One idea we started with was to understand the metabolic dependencies of the tumors that can arise in a natural or pharmacological context and then target these metabolic programs to the detriment of the tumor but not the normal tissue. We are making progress with the high fat diet model. Ultimately though, the goal is to eliminate or prevent colorectal cancer in humans.” To read the original article click here.

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Are Lectins in Food Good or Bad for You?

AHA Publisher — Mon, 22 Mar 2021 07:00:57 +0000

Michael Greger M.D. FACLM via NutritionFacts – Might lectins help explain why those who eat more beans and whole grains have less cancer? Lectins are to blame for the great “white kidney bean incident” of 2006 in Japan. One Saturday evening, a TV program introduced a new method to lose weight. The method was simple: toast some dry, raw, white kidney beans in a frying pan for three minutes, grind the beans into a powder, and then dust it onto rice. Within days, a thousand people fell ill, some with such severe diarrhea and vomiting they ended up in the hospital. Why? Lectin poisoning. Three minutes of dry heat is not enough to destroy the toxic lectins in kidney beans. If you don’t presoak them, you need to boil large kidney beans for a full hour to completely destroy all the lectins, though if you first soak them overnight 98 percent of the lectins are gone after boiling for just 15 minutes and all are gone by half an hour, as you can see at 0:44 in my video Are Lectins in Food Good or Bad for You?. And, indeed, when researchers tested the white beans, they found that toasting them for three minutes didn’t do a thing. It’s no wonder people got sick. But, 95 percent of the lectins were inactivated after boiling them for three minutes and completely inactivated after ten minutes of boiling. Evidently, “‘Do not eat raw beans’ is a traditional admonition in Japan to prevent intestinal problems”—and now we know why. While canning may completely eliminate lectins from most canned beans, some residual lectin activity may remain in canned kidney beans, though apparently not enough to result in toxicity. And, ironically, “How doses of lectins may be beneficial by stimulating gut function, limiting tumor growth, and ameliorating obesity.” What? I thought lectins were toxic. For as long as people have speculated dietary lectins are harmful, others have conjectured that they may be protective. “If this theory is correct, appropriate lectins by mouth should be of use in the prophylaxis [prevention] (and possibly treatment) of colon cancer.” Or, of course, we could just eat our beans. Interest in the purported antitumor effect of plant lectins started with the discovery in 1963 that lectins could distinguish between cancer cells and normal cells. Researchers at Massachusetts General Hospital found a substance in wheat germ—the lectin in whole wheat—that appeared to be “tumor cell specific,” clumping together the tumor cells, while the normal cells were left almost completely alone. In fact, it is so specific that you can take a stool sample from someone and, based on lectin binding to the colon lining cells that get sloughed off into the feces, effectively predict the presence of polyps and cancers. Subsequently, it was discovered that lectins couldn’t only distinguish between the two types of cells, but also extinguish the cancer cells, while largely leaving the normal cells alone. For example, that same white kidney bean lectin, as you can see at 2:53 in my video, was found to almost completely suppress the growth of human head and neck cancer cells, liver cancer cells, breast cancer cells, and cervical cancer cells (at least most of the way), within about three days—but that was in a petri dish. Those petri dish studies are largely the basis of the evidence for the antitumor activity of plant lectins. How do we even know dietary lectins are absorbed into our body? Colorectal cancer is one thing. The fact that lectins can kill off colon cancer cells in a petri dish may be applicable, since lectins we eat may come in direct contact with cancerous or precancerous cells in our colon, “providing a mechanism” by which bean consumption may help in “the prevention and treatment of colorectal cancer.” Even more exciting is the potential for effectively rehabilitating cancer cells. The “loss of differentiation and invasion are the histological hallmarks of malignant cells,” meaning that when a normal cell transforms into a cancer cell, it tends to lose its specialized function. Breast cancer cells become less breast-like, and colon cancer cells become less colon-like. What these researchers showed—for the first time—is that the lectin in fava beans could take colon cancer cells and turn them back into looking more like normal cells. As you can see at 4:13 in my video, before exposure to the fava bean lectins, the cancer cells were growing in amorphous clumps. But, after exposure to the fava bean lectins for two weeks, those same cancer cells started to go back to growing glandular structures like normal colon issue. Therefore, dietary lectins or putting them in a pill “may slow the progression of colon cancer,” potentially helping to explain why dietary consumption of beans, split peas, chickpeas, and lentils appears to reduce the risk of colorectal cancer based on 14 studies involving nearly two million participants. Okay, but what about cancers outside of the digestive tract? “Although lectin containing foods,” like beans and whole grains, “are frequently consumed cooked or otherwise processed, these treatments may not always inactivate the lectins…For example, lectins have been detected in roasted peanuts….” Peanuts are legumes, and we don’t tend to eat them boiled but just roasted or even raw. Are we able to absorb the lectins into our system? Yes. As you can see at 5:12 in my video, within an hour of consumption of raw or roasted peanuts, you can detect the peanut lectin in the bloodstream of most people. Same with tomatoes. Some of the non-toxic lectin in tomatoes also makes it down into our gut and into our blood. Wheat germ agglutinin, the wheat lectin known as WGA, doesn’t seem to make it into our bloodstream, though, even after apparently eating the equivalent amount of wheat germ in more than 80 slices of bread. And, if you ate something like pasta, the boiling in the cooking process might wipe out the lectin in the first place anyway. In terms of phytochemicals in the fight against cancer, lectins are able to “resist digestion resulting in high bioavailability,” potentially allowing “the cellular mechanisms of the host to utilize the full potential of the…dramatic anti-cancer benefits” lectins have to offer. But, these dramatic benefits have yet to be demonstrated in people. We do know, however, that population studies show “that the consumption of a plant-based diet is strongly associated with a reduced risk of developing certain types of cancer.” People eating a plant-based diet could just be eating fewer carcinogens, but plants do have all those active components that do seem to protect against the “initiation, promotion, or progression” of cancer. So, maybe lectins are one of those protective compounds. We know people who eat more beans and whole grains tend to get less cancer overall, but we’re just not sure exactly why. Now, you could say, “Who cares why?” Well, Big Pharma cares. You can’t make as much money on healthy foods as you can on “lectin based drugs.” This article has been modified. To read the original article click here. For more articles from Dr. Greger click here.

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The Role of Meat and Dairy Viruses in Cancer

AHA Publisher — Fri, 02 Oct 2020 07:00:44 +0000

Michael Greger M.D. FACLM via Nutrition Facts – “Nearly 20% of cancer cases arising worldwide can be linked to infectious agents, including viruses.” Seven viruses are now conclusively tied to human cancers, and, as new viruses enterinto human populations, the incidence and causes of cancer will likely change accordingly. The foundation of modern tumor virology was laid more than a century ago with the discovery of a cancer-causing chicken virus, for which a Nobel Prize was awarded. Another Nobel Prize went to the “medical doctor-turned-virologist” who discovered that the HPV virus was causing cervical cancer. In his acceptance speech, he mused that there may be a bovine polyoma virus—a multiple tumor virus in cattle—that could be playing a role in human colon cancer, lung cancer, and breast cancer, but no polyoma virus had ever been discovered in meat…until now. As I discuss in my video The Role of Burger Viruses in Cancer, polyomaviruses are a particular concern—not only because they are known to be carcinogenic, but also because they can survive cooking temperatures. Since a single burger these days can contain meat from “many dozens of animals,” researchers felt “this could present an ideal situation for virus-hunting…” Researchers from the National Cancer Institute purchased meat samples from three separate supermarkets and found three different polyomaviruses in ground beef, as you can see at 1:52 in my video. Now, just because three types of “polyomavirus species are commonly detectable in food-grade ground beef” doesn’t necessarily mean they are causing human disease. What made this Nobel laureate suspect them? Well, for one thing, some people got cancer right where they had been vaccinated for smallpox—a whole bunch of different cancers, in fact. The vaccine had been harvested from the skin of calves, so “it is possible” there could have been some cancer-causing cow virus. “Many people are exposed to potentially virus-contaminated meat and dairy products” through their diets, but those in the industry, “such as farm workers, butchers, veterinarians, and employees in dairies,” would be even more exposed. Do these groups have higher cancer incidence? Indeed, it now appears to be clear “that workers in the meat industry are at increased risk of developing and dying from cancer.” Another reason to suspect the involvement of some kind of bovine infectious factor in colorectal cancer is the fact that there appear to be relatively low rates of colorectal cancer in countries where not a lot of beef is eaten. And, when meat consumption suddenly increases, rates shoot up, as you can see at 3:15 in my video. “The only exception is Mongolia where they have low rates of colon cancer and eat a lot of red meat, but there they eat yak.” Maybe yaks don’t harbor the same viruses. Can’t you just avoid steak tartare? Even steak cooked “medium” may not reach internal temperatures above 70° Celsius, and it takes temperatures higher than that to inactivate some of these viruses, so we would expect viruses to survive both cooking and pasteurization. In fact, researchers followed up with a paper suggesting the consumption of dairy products may “represent one of the main risk factors for the development of breast cancer” in humans. The recent discovery of a larger number of presumably new viruses in the blood, meat, and milk of dairy cows should be investigated, since one might speculate that infectious “agents present in dairy products possess a higher affinity to mammary [breast] cells,” since they came from breast cells. The fact that people with lactose intolerance, who tend to avoid milk and dairy throughout their lives, have lower rates of breast and other cancers could be seen as supporting this concept. Though, there are certainly other reasons dairy may increase cancer risk, such as increasing levels of the cancer-promoting growth hormone IGF-1 or adversely affecting our gut microbiome. Or, for that matter, maybe the plant-based milks they’re drinking instead could be protective. That’s the problem with population studies: You can’t tease out cause and effect. It doesn’t matter how many viruses are found in retail beef, pork, and chicken, as you can see at 5:16 in my video, if we can’t connect the dots. Can’t we just look for the presence of these viruses within human tumors? Researchers have triedand did find some, but even if you don’t find any, that doesn’t necessarily mean viruses didn’t play a role. There’s a “viral hit-and-run” theory of cancer development that suggests that certain viruses can slip in and out of our DNA to initiate the cancer, but be long gone by the time the tumor matures. There’s still a lot of work to be done. But, if the link between bovine polyomaviruses and human disease pans out, the National Cancer Institute researchers envision the development of a high potency vaccine. So, just like the HPV vaccine may prevent cervical cancer from unsafe sex, perhaps one day, vaccines may prevent breast and colon cancer from unsafe sirloin. To read the original article click here. For more articles from Dr. Greger click here.

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Does Oral Bacteria Affect Colon Cancer?

AHA Publisher — Wed, 03 Jun 2020 07:00:48 +0000

Ratan-NM, M. Pharm. via News-Medical Net – The colon is a part of the digestive tract whose primary function is the absorption of water and nutrients from food. Colon cancer is a leading cause of mortality worldwide. Recent evidence suggests that microbiota alternations in the gut are directly associated with colon cancer – it is found that oral bacterium leads to the progression of cancer cells in the colon. Precancerous cells or early undetected cancer cells facilitate the growth and progression of oral bacteria. What Are the Causes of Colon Cancer? Colon cancer is caused by genetic mutations, which lead to the formation of polyps. Polyps are precancerous cells, and polyp’s formation is the first stage of development of colon cancer. Initially, colon cancers start with benign (noncancerous) lumps, which are known as adenomatous polyps. Genetic mutations develop up over some time – polyps may take around 20 years to develop into cancerous cells. However, external factors such as gut microbiota play a pivotal role in the progression of colon cancer and make it more aggressive. The micro-organisms present in the human digestive tract play a significant role in digestion and metabolism. But dysbiosis in mouth microbiota may trigger the formation of tumor cells and enhance the progression of cancer cells. The most common oral bacterium associated with colon cancer is Fusobacterium nucleatum (F. nucleatum), which accumulates with tooth decay. F. nucleatum is an anaerobic, gram-negative bacterium that is present in the digestive tract. The stable temperature and pH of the oral cavity promotes the growth of F. nucleatum, which accumulates in the periodontal plaque. A comparison of healthy individuals and patients with colon cancer showed that colon cancer patients have abundant F. nucleatum (oral bacterium) compared to healthy individuals. The presence of F. nucleatum in the gut promotes the growth of cancerous cells in the colon; however, these bacteria do not affect noncancerous cells. What Are the Signs and Symptoms of Colon Cancer? The most common symptom of colon cancer is abdominal distension without any weight gain. Abdominal pain is infrequent in the case of colon cancer. Frequency of bowel movements changes along with some weight loss. Vomiting and nausea of unknown cause are also common during colon cancer. How Do Oral Bacteria Cause Colon Cancer? F. nucleatum is present in the oral cavity, but it can enter the bloodstream. Through the bloodstream, it enters the colon and other parts of the digestive tract. F. nucleatum produces a molecule termed FadA adhesin, which turns on several genes in the colon and results in the formation of cancerous cells in the colon. FadA adhesin protein speeds up the formation and growth of cancerous cells in the colon. FadA adhesin protein has its effect only on cancerous cells. They do not affect the healthy cells in the colon. The probable reason for this is that healthy cells do not produce the proteins in response to FadA adhesion. F. nucleatum leads to the growth of cancer cells only in the case of a few individuals, and they do not affect all individuals. This is due to the different community nature of oral bacteria and the multifactorial etiology of cancer cells. Management of Oral Bacterium in Colon Cancer A significant reduction in the number of F. nucleatum can enhance the recovery process in patients with colon cancer. Hence, improved oral hygiene plays a crucial role in limiting the growth and spread of cancerous cells. A scientific approach to getting rid of colon cancer progression is through targeting the signaling pathway of oral bacteria. Disruption of the signaling path or suppression of FadA adhesin protein synthesis can significantly delay the speedy growth and spread of cancerous cells. Another approach to manage colon cancer is the use of probiotics. Administration of probiotics or prebiotics significantly reduces the composition and number of F. nucleatum. This also helps in controlling the progression of cancerous cells in the colon. Antibiotics, along with other antitumor drugs, are also given to patients with colon cancer. Antibiotics have shown promising results in the management of colon cancer by destroying the F. nucleatum. To read the original article click here.

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The Answer to a Colon Cancer Mystery

The AHA! Team — Sun, 18 Aug 2019 07:00:00 +0000

Michael Greger M.D. FACLM via Nutrition Facts – “[T]he method of cooking and eating the maize [corn] meal as a porridge results in an increase in resistant starch, which acts in the same way as fiber in the colon,” as a prebiotic, a food for our good bacteria to produce the same cancer-preventing, short-chain fatty acids. Colorectal cancer is the third most common cause of cancer death in the world. Thankfully, the good bacteria in our gut take the fiber we eat and make short-chain fatty acids, like butyrate, that protect us from cancer. We take care of them, and they take care of us. If we do nothing to colon cancer cells, they grow. That’s what cancer does. But if we expose the colon cancer cells to the concentration of butyrate our good bacteria make in our gut when we eat fiber, the growth is stopped in its tracks. If, however, the butyrate stops, if we eat healthy for only one day and then turn off the fiber the next, the cancer can resume its growth. So, ideally, we have to eat a lot of fiber-rich foods – meaning whole plant foods – every day. What about the populations, like those in modern sub-Saharan Africa, where they don’t eat a lot of fiber yet still rarely get colon cancer? Traditionally, they used to eat a lot of fiber, but now their diet is centered around highly refined corn meal, which is low in fiber – yet they still have low colon cancer rates. Why? This was explained by the fact that while they may be lacking protective factors like fiber, they are also lacking cancer-promoting factors like animal protein and fat. But are they really lacking protective factors? If you measure the pH of their stools, the black populations in South Africa have lower pH, which means more acidic stools, despite comparable fiber intakes. That’s a good thing and may account for the lower cancer rates. But, wait a second. Low colon pH is caused by short-chain fatty acids, which are produced by our good bacteria when they eat fiber, but they weren’t eating any more fiber, suggesting there was something else in addition to fiber in their diets that was feeding their flora. And, indeed, despite low fiber intake, the bacteria in their colon were still churning out short-chain fatty acids like crazy. But if their bacteria weren’t eating fiber, what were they eating? Resistant starch. “[T]he method of cooking and eating the maize [corn] meal as a porridge results in an increase in resistant starch, which acts in the same way as fiber in the colon,” as a prebiotic, a food for our good bacteria to produce the same cancer-preventing, short-chain fatty acids. As I discuss in my video Resistant Starch and Colon Cancer, “[r]esistant starch is any starch that is not digested and absorbed in the upper digestive tract [our small intestine] and, so, passes into the large bowel,” our colon, to feed our good bacteria. When you boil starches and then let them cool, some of the starch can recrystallize into a form resistant to our digestive enzymes. So, we can get resistant starch eating cooled starches, such as pasta salad, potato salad, or cold cornmeal porridge. “This may explain the striking differences in colon cancer rates.” Thus, they were feeding their good bacteria after all, but just with lots of starch rather than fiber. “Consequently, a high carbohydrate diet may act in the same way as a high fiber diet.” Because a small fraction of the carbs make it down to our colon, the more carbs we eat, the more butyrate our gut bacteria can produce. Indeed, countries where people eat the most starch have some of the lowest colon cancer rates, so fiber may not be the only protective factor. Only about 5 percent of starch may reach the colon, compared to 100 percent of the fiber, but we eat up to ten times more starch than fiber, so it can potentially play a significant role feeding our flora. So, the protection Africans enjoy from cancer may be two-fold: a diet high in resistant starch and low in animal products. Just eating more resistant starch isn’t enough. Meat contains or contributes to the production of presumed carcinogens, such as N-nitroso compounds. A study divided people into three groups: one was on a low-meat diet, the second was on a high-meat diet including beef, pork, and poultry, and the third group was on the same high-meat diet but with the addition of lots of resistant starch. The high-meat groups had three times more of these presumptive carcinogens and twice the ammonia in their stool than the low-meat group, and the addition of the resistant starch didn’t seem to help. This confirms that “exposure to these compounds is increased with meat intake,” and 90 percent are created in our bowel. So, it doesn’t matter if we get nitrite-free, uncured fresh meat; these nitrosamines are created from the meat as it sits in our colon. This “may help explain the higher incidence of large bowel cancer in meat-eating populations,” along with the increase in ammoniaâ€”neither of which could be helped by just adding resistant starch on top of the meat. “[T]he deleterious effects of animal products on colonic metabolism override the potentially beneficial effects of other protective nutrients.” So, we should do a combination of less meat and more whole plant foods, along with exercise, not only for our colon, but also for general health. This article has been modified. To read the original article click here. For more articles by Dr. Greger click here.

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