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:

How the Egg Industry Tried to Bury the TMAO Risk

“Metabolomics is a term used to describe the measurement of multiple small-molecule metabolites in biological specimens, including bodily fluids,” with the goal of “[i]dentifying the molecular signatures.” For example, if we compared the metabolic profile of those with severe heart disease to those with clean arteries, we might be able to come up with a cheap, simple, and noninvasive way to screen people. If heart patients happened to have something in their blood that healthy people didn’t, we could test for that. What’s more, perhaps it would even help us understand the mechanisms of disease. “To refer to metabolomics as a new field is injustice to ancient doctors who used ants to diagnose the patients of diabetes” (because the ants could detect the sugar in the diabetics’ urine).

The first modern foray discovered hundreds of substances in a single breath, thanks to the development of computer technology that made it possible to handle large amounts of information—and that was in 1971, when a computer took up nearly an entire room. “[N]ew metabolomics technologies [have] allowed researchers to measure hundreds or even thousands of metabolites at a time,” which is good since more than 25,000 compounds may be entering our body through our diet alone.

Researchers can use computers to turn metabolic data into maps that allow them to try to piece together connections. You can see sample data and a map at 1:28 in my video Egg Industry Response to Choline and TMAO. Metabolomics is where the story of TMAO started. “Everyone knows that a ‘bad diet’ can lead to heart disease. But which dietary components are the most harmful?” Researchers at the Cleveland Clinic “screened blood from patients who had experienced a heart attack or stroke and compared the results with those from blood of people who had not.”

Using an array of different technology, the researchers identified a compound called TMAO, which stands for trimethylamine N-oxide. The more TMAO people had in their blood, the greater the odds they had heart disease and the worse their heart disease was.

Where does TMAO come from? At 2:19 in my video, you can see a graphic showing that our liver turns TMA into TMAO—but where does TMA come from? Certain bacteria in our gut turn the choline in our diet into TMA. Where is the highest concentration of choline found? Eggs, milk, and meats, including poultry and fish. So, when we eat these foods, our gut bacteria may make TMA, which is absorbed into our system and oxidized by our liver into TMAO, which may then increase our risk of heart attack, stroke, and death.

However, simply because people with heart disease tend to have higher TMAO levels at a snapshot in time doesn’t mean having high TMAO levels necessarily leads to bad outcomes. We’d really want to follow people over time, which is what researchers did next. Four thousand people were followed for three years, and, as you can see in the graph at 3:10 in my video, those with the highest TMAO levels went on to have significantly more heart attacks, strokes, or death.

Let’s back up for a moment. If high TMAO levels come from eating lots of meat, dairy, and eggs, then maybe the only reason people with high TMAO levels have lots of heart attacks is that they’re eating lots of meat, dairy, and eggs. Perhaps having high TMAO levels is just a marker of a diet high in “red meat, eggs, milk, and chicken”—a diet that’s killing people by raising cholesterol levels, for example, and has nothing to do with TMAO at all. Conversely, the reason a low TMAO level seems so protective may just be that it’s indicative of a more plant-based diet.

One reason we think TMAO is directly responsible is that TMAO levels predict the risk of heart attacks, strokes, or death “independently of traditional cardiovascular risk factors.” Put another way, regardless of whether or not you had high cholesterol or low cholesterol, or high blood pressure or low blood pressure, having high TMAO levels appeared to be bad news. This has since been replicated in other studies. Participants were found to have up to nine times the odds of heart disease at high TMAO blood levels even after “controll[ing] for meat, fish, and cholesterol (surrogate for egg) intake.”

What about the rest of the sequence, though? How can we be certain that our gut bacteria can take the choline we eat and turn it into trimethylamine in the first place? It’s easy. Just administer a simple dietary choline challenge by giving participants some eggs.

Within about an hour of eating two hard-boiled eggs, there is a bump of TMAO in the blood, as you can see at 4:51 in my video. What if the subjects are then given antibiotics to wipe out their gut flora? After the antibiotics, nothing happens after they eat more eggs. In fact, their TMAO levels are down at zero. This shows that our gut bacteria play a critical role. But, if we wait a month and give their guts some time to recover from the antibiotics, TMAO levels creep back up.

These findings did not thrill the egg industry. Imagine working for the American Egg Board and being tasked with designing a study to show there is no effect of eating nearly an egg a day. How could a study be rigged to show no difference? If we look at the effect of an egg meal (see 5:32 in my video), we see it gives a bump in TMAO levels. However, our kidneys are so good at getting rid of TMAO, by hours four, six, and eight, we’re back to baseline. So, the way to rig the study is just make sure the subjects hadn’t eaten those eggs in the last 12 hours. Then, you can show “no effect,” get your study published in the Journal of the Academy of Nutrition and Dietetics, and collect your paycheck.


Unfortunately, this appears to be part for the course for the egg industry. For more on their suspect activities, see:

For more on the TMAO story, 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:

How to Increase Gut Bacterial Richness

We live in an “obesogenic environment,” with cheap junk food everywhere, thanks in part to subsidies going to the “‘food industrial complex,’ which manufactures obesogenic foods that foster addiction…The root causes…[may] make obesity difficult to escape,” but a lot of people do. If it were simply the external environment, why isn’t everyone obese?

“Some individuals seem to be more susceptible to the obesogenic environment…than others,” which suggests a genetic component, supported by studies of twins and adopted kids, but the genes that have been identified so far account for only 6 to 11 percent of the genetic variation in body mass index between individuals. Perhaps variation in our “other genome”—that is, all the different microbes that inhabit our body, known as the microbiome—may be playing a role. We have a hundred times more bacterial genes inside us than human genes.

As I discuss in my video Gut Microbiome: Strike It Rich with Whole Grains, a study found that people tend to fall into one of two groups: those who have lots of different types of bacteria in their gut (high “gut bacterial richness”) and those with relatively few types. Those with low bacterial richness had more overall body fat, insulin resistance, which is the cause of type 2 diabetes, high triglycerides, and higher levels of inflammatory markers, like C-reactive protein, compared to those with high bacterial richness. Not only did people with lower bacterial richness start out heavier, but the obese individuals with lower bacterial richness also gained more weight over time.

The question then becomes: Can a dietary intervention have any impact “A number of studies have associated increased microbial richness…with diets higher in fruits, vegetables, and fiber.”

Just giving fiber-type supplements doesn’t seem to boost richness, however, but the “compositional complexity” of a whole food, like whole grains, “could potentially support a wider scope of bacterial taxa,” types of bacteria, “thereby leading to an increase in diversity.” Human studies to investigate the effects of whole grains had been neglected, though…until now.

Subjects were given whole-grain barley, brown rice, or a mixture of both for a month, and all three caused an increase in bacterial community diversity. Therefore, it may take a broad range of substrates to increase bacterial diversity, and this can be achieved by eating whole plant foods.

Moreover, the alterations of gut bacteria in the study coincided with a drop in systemic inflammation in the body. We used to think that the way fiber in whole grains helped us was by gelling in our small intestine right off of our stomach, slowing the rate at which sugars were absorbed and blunting the spike in blood sugars one might get from refined carbs. We now know, however, that fiber is broken down in our colon by our friendly flora, which release all sorts of beneficial substances into our bloodstream that can have anti-inflammatory effects, as well. So, perhaps what’s happening in our large intestine helps explain the protective effects of whole grain foods against type 2 diabetes.

Interestingly, the combination of both barley and brown rice worked better than either grain alone, suggesting a synergistic effect. This may help explain “the discrepancy of the health effects of whole grains obtained in epidemiological [population-based] and interventional studies.”

Observational studies “strongly suggest” that those who consume three or more servings of whole grains a day tend to have a lower body mass index, less belly fat, and less tendency to gain weight, but recent clinical trials, where researchers randomized subjects to eat white bread rolls versus whole-wheat rolls, failed to provide evidence of a beneficial effect on body weight. Of course, whole grains are so superior nutritionally that they should continue to be encouraged. However, the “[i]nterventional trials might have failed to show [weight] benefits because they focused on a limited selection of whole grains, while in epidemiological trials [or the population studies], subjects are likely to consume a diverse set of whole grains which might have synergistic activities.”


Until recently, we knew very little about how powerfully our gut bacteria can affect our health. Catch up on the latest science with these related videos:

When it comes to rice, even white rice can be better than many choices, but brown rice is better and pigmented rice is probably the best. See my videos Kempner Rice Diet: Whipping Us Into Shape and Is It Worth Switching from White Rice to Brown? for more.

But what about the arsenic in rice? Learn more:

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: