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:

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: