The Best Source of Resistant Starch

Resistant starch wasn’t discovered until 1982. Before that, we thought all starch could be digested by the digestive enzymes in our small intestine. Subsequent studies confirmed that there are indeed starches that resist digestion and end up in our large intestine, where they can feed our good bacteria, just like fiber does. Resistant starch is found naturally in many common foods, including grains, vegetables, beans, seeds, and some nuts, but in small quantities, just a few percent of the total. As I discuss in my video Getting Starch to Take the Path of Most Resistance, there are a few ways, though, to get some of the rest of the starch to join the resistance.

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, but the effect isn’t huge. The resistant starch goes from about 3 percent up to 4 percent. The best source of resistant starch is not from eating cold starches, but from eating beans, which start at 4 or 5 percent and go up from there.

If you mix cooked black beans with a “fresh fecal” sample, there’s so much fiber and resistant starch in the beans that the pH drops as good bacteria churn out beneficial short-chain fatty acids, which are associated both directly and indirectly with lower colon cancer risk. (See Stool pH and Colon Cancer.) The more of this poopy black bean mixture you smear on human colon cancer, the fewer cancer cells survive.

Better yet, we can eat berries with our meals that act as starch blockers. Raspberries, for example, completely inhibit the enzyme that we use to digest starch, leaving more for our friendly flora. So, putting raspberry jam on your toast, strawberries on your corn flakes, or making blueberry pancakes may allow your good bacteria to share in some of the breakfast bounty.

Another way to feed our good bacteria is to eat intact grains, beans, nuts, and seeds. In one study, researchers split people into two groups and had them eat the same food, but in one group, the seeds, grains, beans, and chickpeas were eaten more or less in a whole form, while they were ground up for the other group. For example, for breakfast, the whole-grain group got muesli, and the ground-grain group had the same muesli, but it was blended into a porridge. Similarly, beans were added to salads for the whole-grain group, whereas they were blended into hummus for the ground-grain group. Note that both groups were eating whole grains—not refined—that is, they were eating whole foods. In the ground-grain group, though, those whole grains, beans, and seeds were made into flour or blended up.

What happened? Those on the intact whole-grain diet “resulted in a doubling of the amount excreted compared to the usual diet and produced an additional and statistically significant increase in stool mass” compared with those on the ground whole-grain diet, even though they were eating the same food and the same amount of food. Why? On the whole-grain diet, there was so much more for our good bacteria to eat that they grew so well and appeared to bulk up the stool. Even though people chewed their food, “[l]arge amounts of apparently whole seeds were recovered from stools,” but on closer inspection, they weren’t whole at all. Our bacteria were having a smorgasbord. The little bits and pieces left after chewing transport all this wonderful starch straight down to our good bacteria. As a result, stool pH dropped as our bacteria were able to churn out so many of those short-chain fatty acids. Whole grains are great, but intact whole grains may be even better, allowing us to feed our good gut bacteria with the leftovers.

Once in our colon, resistant starches have been found to have the same benefits as fiber: softening and bulking stools, reducing colon cancer risk by decreasing pH, increasing short-chain fatty acid production, reducing products of protein fermentation (also known as products of putrefaction), and decreasing secondary bile products.

Well, if resistant starch is so great, why not just take resistant starch pills? It should come as no surprise that commercial preparations of resistant starch are now available and “food scientists have developed a number of RS-enriched products.” After all, some find it “difficult to recommend a high-fiber diet to the general public.” Wouldn’t be easier to just enrich some junk food? And, indeed, you now can buy pop tarts bragging they contain “resistant corn starch.”

Just taking resistant starch supplements does not work, however. There have been two trials so far trying to prevent cancer in people with genetic disorders that put them at extremely high risk, with virtually a 100-percent chance of getting cancer, and resistant starch supplements didn’t help. A similar result was found in another study. So, we’re either barking up the wrong tree, the development of hereditary colon cancer is somehow different than regular colon cancer, or you simply can’t emulate the effects of naturally occurring dietary fiber in plant-rich diets just by giving people some resistant starch supplements.

For resistant starch to work, it has to get all the way to the end of the colon, which is where most tumors form. But, if the bacteria higher up eat it all, then resistant starch may not be protective. So, we also may have to eat fiber to push it along. Thus, we either eat huge amounts of resistant starch—up near the level consumed in Africa, which is twice as much as were tried in the two cancer trials—or we consume foods rich in both resistant starch and fiber. In other words, “[f]rom a public health perspective, eating more of a variety of food rich in dietary fibre including wholegrains, vegetables, fruits, and pulses [such as chickpeas and lentils] is a preferable strategy for reducing cancer risk.”

What’s so great about resistant starch? See my video Resistant Starch and Colon Cancer.

I first broached the subject of intact grains in Are Green Smoothies Bad for You?.

Why should we care about what our gut flora eats? See Gut Dysbiosis: Starving Our Microbial Self.

Did I say putrefaction? See Putrefying Protein and “Toxifying” Enzymes.

Berries don’t just help block starch digestion, but sugar digestion as well. See If Fructose Is Bad, What About Fruit?.

The whole attitude that we can just stuff the effects into a pill is a perfect example of reductionism at work. See Reductionism and the Deficiency Mentality and Why is Nutrition So Commercialized? for more on this.

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:

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to “incapacitating pain that is a medical emergency.” Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it’s that common, though, is it just an inevitable consequence of aging? No, it’s a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn’t even merit mention in medical and surgical textbooks. The mystery wasn’t solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease—i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it’s easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That’s exactly what’s been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we’re talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That’s about one thousand times lower prevalence.

What, then, do we make of a new study concluding that a low-fiber diet was not associated with diverticulosis. I cover that in my video Does Fiber Really Prevent Diverticulosis?

For more on bowel health, see:

What if your doctor says you shouldn’t eat healthy foods like nuts and popcorn because of your diverticulosis? Share with them my Diverticulosis & Nuts video.

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:

Optimal Bowel Movement Position

Compared to rural African populations eating traditional plant-based diets, white South Africans and black and white Americans have more than 50 times more heart disease, 10 times more colon cancer, more than 50 times more gallstones and appendicitis, and more than 25 times the rates of “pressure diseases”—diverticulitis, hemorrhoids, varicose veins, and hiatal hernia.

As I discussed in my Should You Sit, Squat, or Lean During a Bowel Movement?, bowel movements should be effortless. When we have to strain at stool, the pressure may balloon out-pouchings from our colon, causing diverticulosis; inflate hemorrhoids around the anus; cause the valves in the veins of our legs to fail, causing varicose veins; and even force part of the stomach up through the diaphragm into our chest cavity, causing a hiatal hernia (as I covered previously). When this was first proposed by Dr. Denis Burkitt, he blamed these conditions on the straining caused by a lack of fiber in the diet. He did, however, acknowledge there were alternative explanations. For example, in rural Africa, they used a traditional squatting position when they defecated, which may have taken off some of the pressure.

For hundreds of thousands of years, everyone used the squatting position, which may help by straightening the “anorectal angle.” There’s actually a kink at almost a 90-degree angle right at the end of the rectum that helps keep us from pooping our pants when we’re just out walking around. That angle only slightly straightens out in a common sitting posture on the toilet. Maximal straightening out of this angle occurs in a squatting posture, potentially permitting smoother defecation. (I remember sitting in geometry class wondering when I’d ever use the stuff I was learning. Little did I know I would one day be calculating anorectal angles with it! Stay in school, kids 🙂

How did they figure this out? Researchers filled latex tubes with a radiopaque fluid, stuck them up some volunteers, and took X-rays with the hips flexed at various angles. They concluded that flexing the knees towards the chest like one does when squatting may straighten that angle and reduce the amount of pressure needed to empty the rectum. This idea wasn’t directly put to the test until 2002, when researchers used defecography (which are X-rays taken while the person is defecating) on subjects in sitting and squatting positions. Indeed, squatting increased the anorectal angle from around 90 degrees all the way up to about 140.

So should we all get one of those little stools for our stools, like the Squatty Potty that you put in front of your toilet to step on? No, they don’t seem to work. Researchers tried adding a footstool to decrease sitting height, but it didn’t seem to significantly affect the time it took to empty one’s bowels or decrease the difficulty of defecating. They tried even higher footstools, but people complained of extreme discomfort using them. Nothing seemed to compare with actual squatting, which may give the maximum advantage. However, in developed nations, it may not be convenient. But, we can achieve a similar effect by leaning forward as we sit, with our hands on or near the floor. The researchers advise all sufferers from constipation to adopt this forward-leaning position when defecating, as the weight of our torso pressing against the thighs may put an extra squeeze on our colons.

Instead of finding ways to add more pressure, why not get to the root of the problem? “The fundamental cause of straining is the effort required to pass unnaturally firm stools.” By manipulating the anorectal angle through squatting or leaning, we can more easily pass unnaturally firm stools. But why not just treat the cause and eat enough fiber-containing whole plant foods to create stools so large and soft that you could pass them effortlessly at any angle?

Famed cardiologist Dr. Joel Kahn once said that you know you know you’re eating a plant-based diet when “you take longer to pee than to poop.”

In all seriousness, even squatting does not significantly decrease the pressure gradient that may cause a hiatal hernia. It does not prevent the pressure transmission down into the legs that may cause varicose veins. And this is not just a cosmetic issue. Protracted straining can cause heart rhythm disturbances and reduction in blood flow to the heart and brain, resulting in defecation-related fainting and death. Just 15 seconds of straining can temporarily cut blood flow to the brain by 21% and blood flow to the heart by nearly one-half, thereby providing a mechanism for the well-known “bed pan death” syndrome. If you think you have to strain a lot while sitting, try having a bowel movement on your back. Bearing down for just a few seconds can send our blood pressure up to nearly 170 over 110, which may help account for the notorious frequency of sudden and unexpected deaths of patients while using bed pans in hospitals. Hopefully, if we eat healthy enough, we won’t end up in the hospital to begin with.

Wondering How Many Bowel Movements Should You Have Every Day? Watch the video to find out!

The “forcing part of your stomach up through the diaphragm into our chest cavity” phenomenon is covered in my video Diet and Hiatal Hernia. The “ballooning of out-pouchings from our colon” is called diverticulosis. There’s a video I did about 6 years ago (Diverticulosis & Nuts), but I have some new and improved ones available: Diverticulosis: When Our Most Common Gut Disorder Hardly Existed and Does Fiber Really Prevent Diverticulosis?

 More on that extraordinary African data here:

So excited to be able to slip in a plug for Dr. Kahn’s work. His brand of “interpreventional cardiology” can be found at

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: