How to Foster a Healthy Gut Flora

What’s more important: probiotics or prebiotics? And where can we best get them?

“Virtually every day we are all confronted with the activity of our intestine, and it is no surprise that at least some of us have developed a fascination for our intestinal condition and its relation to health and disease.”

“Over the last years the intestinal microbiota [our gut flora] has been identified as a fascinating ‘new organ’” with all sorts of functions. Well, if the bacteria in our gut make up an entire, separate organ inside our body, what about doing an organ transplant? I discuss this in my video How to Become a Fecal Transplant Super Donor.

What would happen if you transferred intestinal bacteria from lean donors into obese subjects? Researchers figured that rebalancing the obesity-causing bacteria with an infusion of gut bacteria from a lean donor might help. They had wanted the study to be placebo-controlled, which, for drugs is easy, because the control subjects can just be given a sugar pill. But, when you’re inserting a tube down people’s throats and transplanting feces, what do you use as the placebo—or poocebo, if you will? Both the donors and the subjects brought in fresh stools, and the subjects were randomized to either get a donor’s stool or their own collected feces. So, the placebo was simply getting their own stool back.

What happened? As you can see at 1:32 in my video, the insulin sensitivity of the skinny donors was up around 50, which is a good thing. High insulin sensitivity means a low level of insulin resistance, which is the cause of both type 2 diabetes and prediabetes. The obese subjects started out around 20 and, after an infusion of their own feces, stayed around 20. The group of obese donors getting the skinny fecal infusion similarly started out low but then shot up near to where the slim folks were.

It’s interesting that not all lean donors’ stools conveyed the same effect on insulin sensitivity. Some donors, the so-called super-fecal donors, had very significant effects, whereas others had little or no effect, as you can see at 2:02 in my video. It turns out this super-donor effect is most probably conveyed by the amounts of short-chain fatty acid-producing intestinal bacteria in their feces. These are the food bacteria that thrive off of the fiber we eat. The short-chain fatty acids produced by fiber-eating bacteria may contribute to the release of gut hormones that may be the cause of this beneficial, improved insulin sensitivity.

“The use of fecal transplantation has recently attracted considerable attention because of its success in treatments as well as its capacity to provide cause–effect relations,” that is, cause-and-effect evidence that the bacteria we have in our gut can affect our metabolism. Within a few months, however, the bacterial composition returned back to baseline, so the effects on the obese subjects were temporary.

We can get similar benefits by just feeding what few good gut bacteria we may already have. If you have a house full of rabbits and feed them pork rinds, all the bunnies will die. Yes, you can repopulate your house by infusing new bunnies, but if you keep feeding them pork rinds, they’ll eventually die off as well. Instead, even if you start off with just a few rabbits but if you feed them what they’re meant to eat, they’ll grow and multiply, and your house will soon be full of fiber-eating bunnies. Fecal transplants and probiotics are only temporary fixes if we keep putting the wrong fuel into our guts. But, by eating prebiotics, such as fiber, which means “increasing whole plant food consumption,” we may select for—and foster the growth of—our own good bacteria.

However, such effects may abate once the high-fiber intake ceases. Therefore, our dietary habits should include a continuous consumption of large quantities of high-fiber foods to improve our health. Otherwise, we may be starving our microbial selves.


The microbiome is one of the most exciting research areas in medicine these days. For more information, see, for example:

For more on health sources of prebiotics, check out:

In health,

Michael Greger, M.D.

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

How to Boost the Fat Burning Hormone FIAF

Although recent increases in the availability of junk food and decreases “in institutionally driven physical activity” have created an obesity-permissive environment, several other factors may contribute. We know, for example, that the use of antibiotics is linked to obesity, so our gut flora may play a role. I discuss this in my video Is Obesity Infectious?.

Recently, specific bacterial species were identified. Eight species seemed protective against weight gain, and they are all producers of a short-chain fatty acid called butyrate.

Early on, we thought there might be some intestinal bacteria that were able to extract additional calories from what we eat, but the relationship between our gut flora and obesity has proven to be more complex, as you can see at 0:49 in my video. Our gut flora may affect how we metabolize fat, for example, such as through the hormone FIAF—fasting-induced adipose factor.

While we’re fasting, our body has to stop storing fat and instead start to burn it off. FIAF is one of the hormones that signals our body to do this, which could be useful for someone who is obese, and may be one way our gut flora manages our weight. Some bacteria repress this hormone, thereby increasing fat storage. In contrast, when we feed fiber to our fiber-eating bacteria, those that secrete short-chain fatty acids like butyrate are able to upregulate this hormone in all human cell lines so far tested.

“Currently, when an individual fails to lose weight…the only other option is surgery,” but “[a]s the mechanisms of the microbiota’s [gut flora’s] role in weight regulation are elucidated, one can envision transplanting intestinal contents from a thin individual into an obese individual.” Such so-called fecal transplants may suffer from “repulsive esthetics,” though. It turns out there may be easier ways to share.

We’ve known that people who live together share a greater similarity in gut bacteria than people living apart. This could be because co-habitants inadvertently swap bacteria back and forth, or possibly because they eat similar diets, living in the same house. We didn’t know…until now. Not only do co-habiting family members share bacteria with one another—they also share with their dogs, who are probably eating a different diet than they are. You may be interested in the charts at 2:22 in my video.

In fact, it’s been “suggest[ed] that homes harbor a distinct microbial fingerprint that can be predicted by their occupants.” Just by swabbing the doorknobs, you can tell which family lives in which house, as shown at 2:35 in my video. And, when a family moves into a new home, “the microbial community in the new house rapidly converged” or shifted toward that of the old house, “suggesting rapid colonization by the family’s microbiota.” Experimental evidence suggests that individuals raised in a household of lean people may be protected against obesity—no fecal transplant necessary. (Indeed, people may be sharing gut bacteria from kitchen stools instead.)

Moreover, as we know, people living together share more bacteria than those living apart, but when a dog is added to the mix, the people’s bacteria get even closer, as you can see at 3:11 in my video. Dogs can act like a bridge to pass bacteria back and forth between people. Curiously, owning cats doesn’t seem to have the same effect. Maybe cats don’t tend to drink out of the toilet bowl as much as dogs do?

Exposure to pet bacteria may actually be beneficial. It’s “intriguing to consider that who we cohabit with, including companion animals, may alter our physiological properties by influencing the consortia of microbial symbionts [or bacteria] that we harbor in and on our various body habitats.” This may be why “[r]ecent studies link early exposure to pets to decreased prevalence of allergies, respiratory conditions, and other immune disorders” as kids grow older. In my video Are Cats or Dogs More Protective for Children’s Health?, I talk about studies in which dog exposure early in life may decrease respiratory infections, especially ear infections. Children with dogs “were significantly healthier,” but we didn’t know why. Indeed, we didn’t know the mechanism until, perhaps, now—with the first study tying together the protection from respiratory disease through pet exposure to differences in gut bacteria. None of the studied infants in homes with pets suffered from wheezy bronchitis within the first two years of life, whereas 15 percent of the pet-deprived infants had. And, when comparing stool samples, this correlated with differences in gut bacteria depending on the presence of pets in the home.

There was a famous study of 12,000 people that found that a “person’s chances of becoming obese increased by 57%…if he or she had a friend who became obese,” suggesting social ties have a big effect. However, given the evidence implicating the role of gut bacteria in obesity, this “raises up the possibility that cravings and associated obesity might not just be socially contagious”—that is, because, for instance, you all go out together and eat the same fattening food—“but rather truly infectious, like a cold.”


Viruses may also play a role in obesity. How? See Infectobesity: Adenovirus 36 and Childhood Obesity. An Obesity-Causing Chicken Virus may help explain the link found between poultry consumption and weight gain, and you may also be interested in Chicken Big: Poultry and Obesity.

The important question: Can Morbid Obesity Be Reversed Through Diet? Find out in my video, and also check out Coconut Oil and Abdominal Fat.

For more on the amazing inner world in our guts, 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 presentations:

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: