The Answer to a Colon Cancer Mystery

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? Traditionallly. 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 ammonia—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 is a follow-up to my video Is the Fiber Theory Wrong?.

What exactly is butyrate? See:

For videos on optimizing your gut flora, see:

Interested in more on preventing colon cancer? See:

If you’re eating healthfully, do you need a colonoscopy? Find out in Should We All Get Colonoscopies Starting at Age 50?.

When regular starches are cooked and then cooled, some of the starch recrystallizes into resistant starch. For this reason, pasta salad can be healthier than hot pasta, and potato salad can be healthier than a baked potato. Find out more in my video Getting Starch to Take the Path of Most Resistance.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

The Diet We Were Designed to Eat

There are three broad theories about evolution and food. One is that humans have become adapted to grains and other products of the agricultural revolution over the last 10,000 years. Two is the paleo view “that 10,000 years is a blink of an evolutionary eye, and that humans are adapted to paleolithic diets with a lot of lean meat,” but why stop there? The third theory is that the last 200,000 years “is a minute of the evolutionary year” when we were mostly Stone Age humans and represents just the last 1 percent of the roughly 20 million years we’ve been evolving since our common great ape ancestor. So, What Is the “Natural” Human Diet?

During our truly formative years, which one might say was the first 90 percent of our existence, our nutritional requirements reflected an ancestral past in which we ate mostly leaves, flowers, and fruits, with some bugs thrown in, thanks to wormy apples, to get our vitamin B12. “For this reason, another approach that might improve our understanding of the best dietary practices for modern humans is to focus attention not on the past but rather on the here and now; that is, on study of the foods eaten by the closest living relatives of modern humans,” given the bulk of our ancestral diets and “the lack of evidence supporting any notable diet-related changes in human nutrient requirements, metabolism, or digestive physiology” compared to our fellow great apes.

This could explain why fruits and vegetables are not only good for us but are vital to our survival. Indeed, we’re one of the few species so adapted to a plant-based diet that we could actually die from not eating fruits and vegetables, from the vitamin C-deficiency disease, scurvy. Most other animals simply make their own vitamin C, but why would our body waste all that effort when we evolved hanging out in the trees just eating fruits and veggies all day long?

Presumably, it’s not a coincidence that the few other mammals unable to synthesize their own vitamin C—including guinea pigs, some bunny rabbits, and fruit bats—are all, like us great apes, strongly herbivorous. Even during the Stone Age, data from rehydrated human fossilized feces tell us we may have been getting up to ten times more vitamin C and ten times more dietary fiber than we get today. The question is: Are these incredibly high-nutrient intakes simply an unavoidable by-product of eating whole, plant foods all the time, or might they actually be serving some important function, like antioxidant defense?

Plants create antioxidants to defend their own structures against free radicals. The human body must defend itself against the same types of pro-oxidants, so we too have evolved an array of amazing antioxidant enzymes, which are effective but not infallible. Free radicals can breach our defenses and cause damage that accumulates with age, leading to a variety of disease-causing and ultimately fatal changes. This is where plants may come in: “Plant-based, antioxidant-rich foods traditionally formed the major part of the human diet,” so we didn’t have to evolve that great of an antioxidant system. We could just let the plants in our diet pull some of the weight, like giving us vitamin C so we don’t have to be bothered to make it ourselves. Using plants as a crutch may well have relieved the pressure for further evolutionary development of our own defenses. That is we’ve become dependent on getting lots of plant foods in our diet, and when we don’t, we may suffer adverse health consequences.

Even during the Stone Age, this may not have been a problem. Only in recent history did we start giving up on whole plant foods. Even modern-day paleo and low-carb followers may be eating more vegetables than those on standard Western diets. There’s a perception that low-carbers are chowing down on the three Bs—beef, bacon, and butter—but that’s only a small minority. What they are eating more of is salad. Indeed, according to an online low-carb community, the number one thing they said they were eating more of was vegetables. Great! The problem isn’t people wanting to cut their carb intake by swapping junk food for vegetables. The concern is the shift to animal-sourced foods. “Greater adherence to [a low-carb diet] high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality post-MI,” or after a heart attack, meaning they cut their lives short.

If there’s one takeaway from our studies of ancestral diets, perhaps it’s that “diets based largely on plant foods promote health and longevity.”


For more on the paleo and low carb diets, see:

If you were fascinated by how we can take advantage of plant defense mechanisms, check out my videos Appropriating Plant Defenses and Xenohormesis: What Doesn’t Kill Plants May Make Us Stronger.

How many antioxidants should we shoot for? See:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

How to Lower Phthalate Exposure Through Diet

Phthalates are hormone-disrupting plastics chemicals linked to a number of adverse health effects, such as disturbing infant and child development, and, in adults, may affect reproductive health in men and endometriosis in women, and is associated with increased abdominal fat in both. “Given the increasing scientific evidence base linking phthalate exposure with harmful health outcomes, it is important to understand major sources of exposure,” which I discuss in my video What Diet Best Lowers Phthalate Exposure?.

What is the most major exposure source? Diet. If you have people stop eating for a few days, you get a significant drop in the amount of phthalates spilling out in their urine. One can only fast for so long, though. Thankfully, we can see similar drops just from eating a plant-based diet for a few days, which gives us a clue as to where most phthalates are found.

The highest levels are found in meats, fats, and dairy. Poultry consistently comes out as being the most contaminated across the board with some of the highest levels ever reported, though there are geographic exceptions. In the United Kingdom, for example, fish came out worse than poultry, and, in Belgium, nothing appears to beat out reindeer meat in terms of contamination. In the United States, though, it is poultry, and the finding that egg consumption is also significantly associated with phthalate levels “suggests that chickens themselves may be contaminated” and not just arise from the plastic they’re wrapped in at the store.

The same might not be true with dairy, however. Realizing that these chemicals may be harmful, researchers in Seattle took ten families and randomized them into a five-day complete dietary replacement with fresh organic foods without any packaging. Nothing touched plastic. Organic milk was delivered in glass, and even the crates used to carry the food were wooden instead of plastic. This was like a fasting study to see what role eliminating processed foods would have on lowering phthalate levels because not everyone wants to switch to a plant-based diet—or stop eating completely. In my video, I show a chart depicting where the families started at baseline before changing their diet and where they were a week after the experiment, once again back on their baseline diet. What happened in the middle? When eating fresh and organic food, their phthalate levels went up, “a dramatic and unexpected increase in one of the most toxic phthalates—and not just by a little: It was like a 2000 percent increase. So the researchers tested all the foods. One of the spices was off the chart, and so was the dairy. Most of the phthalates apparently don’t come from the cow, however; they come from the tubing. If you milk cows by hand (which even the Amish don’t do anymore) the levels of phthalates in the milk are low, but if the same cows are milked by machine, the milk picks up phthalates from the tubing. As such, the final levels may depend more on the tubing than on what the cows are fed.

We’re not sure where the chickens are getting contaminated with phthalates, though. While that study was done on adults, we learned more recently where our kids may be getting it. Researchers found pretty much the same thing: mostly meat, including poultry and fish. Again, poultry appeared to be the worst, while soy consumption was associated with significantly lower levels. But what kind of exposure are we talking about? Researchers calculated what may be typical exposures for infants, teens, and women. How do these data compare with current guidelines? The U.S. Environmental Protection Agency’s reference dose, which is like the maximum acceptable threshold, is 20 µg/kg-day, based on liver risk. Europe places their maximum daily intake for testicular toxicity at 50 µg/kg-day. So a typical infant diet exceeds the EPA’s safety level, “while a diet high in meat and dairy was over this threshold by approximately four times. For adolescents, a diet high in meat and dairy also exceeded the EPA’s reference dose.” Indeed, diets high in meat and dairy consumption resulted in a two-fold increase in exposure. And “[a]ll diets for all groups exceeded the allowable daily intakes (ADI) derived by the US Consumer Product Safety Commission” for problems with sperm production, while diets high in meat and dairy consumption may exceed the allowable intake for risk of reproductive birth defects as well.


For more information on dietary sources of phthalates, I encourage you to watch both Chicken Consumption and the Feminization of Male Genitalia and Lowering Dietary Antibiotic Intake. Diet isn’t the only way one can be exposed internally, though. See my video Avoiding Adult Exposure to Phthalates, which discusses the risk in both children’s and adult toys.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: