Updating Our Microbiome Software and Hardware

Good bacteria, those living in symbiosis with us, are nourished by fruits, vegetables, grains, and beans, whereas bad bacteria, those in dysbiosis with us and possibly contributing to disease, are fed by meat, junk food and fast food, seafood, dairy, and eggs, as you can see at 0:12 in my video Microbiome: We Are What They Eat. Typical Western diets can “decimate” our good gut flora.

We live with trillions of symbionts, good bacteria that live in symbiosis with us. We help them, and they help us. A month on a plant-based diet results in an increase in the population of the good guys and a decrease in the bad, the so-called pathobionts, the disease-causing bugs. “Given the disappearance of pathobionts from the intestine, one would expect to observe a reduction in intestinal inflammation in subjects.” So, researchers measured stool concentrations of lipocalin-2, “which is a sensitive biomarker of intestinal inflammation.” As you can see at 1:13 in my video, within a month of eating healthfully, it had “declined significantly…suggesting that promotion of microbial homeostasis”—or balance—“by an SVD [strict vegetarian diet] resulted in reduced intestinal inflammation.” What’s more, this rebalancing may have played a role “in improved metabolic and immunological parameters,” that is, in immune system parameters.

In contrast, on an “animal-based diet,” you get growth of disease-associated species like Bilophila wadsworthia, associated with inflammatory bowel disease, and Alistipes putredinis, found in abscesses and appendicitis, and a decrease in fiber-eating bacteria. When we eat fiber, the fiber-munching bacteria multiply, and we get more anti-inflammatory, anti-cancer short-chain fatty acids. When we eat less fiber, our fiber-eating bacteria starve away.

They are what we eat.

Eat a lot of phytates, and our gut flora get really good at breaking down phytates. We assumed this was just because we were naturally selecting for those populations of bacteria able to do that, but it turns out our diet can teach old bugs new tricks. There’s one type of fiber in nori seaweed that our gut bacteria can’t normally breakdown, but the bacteria in the ocean that eat seaweed have the enzyme to do so. When it was discovered that that enzyme was present in the guts of Japanese people, it presented a mystery. Sure, sushi is eaten raw, so some seaweed bacteria may have made it to their colons, but how could some marine bacteria thrive in the human gut? It didn’t need to. It transferred the nori-eating enzyme to our own gut bacteria.

“Consequently, the consumption of food with associated environmental bacteria is the most likely mechanism that promoted this CAZyme [enzyme] update into the human gut microbe”—almost like a software update. We have the same hardware, the same gut bacteria, but the bacteria just updated their software to enable them to chew on something new.

Hardware can change, too. A study titled “The way to a man’s heart is through his gut microbiota” was so named because the researchers were talking about TMAO, trimethylamine N-oxide. As you can see at 3:33 in my video, certain gut flora can take carnitine from the red meat we eat or the choline concentrated in dairy, seafood, and eggs, and convert it into a toxic compound, which may lead to an increase in our risk of heart attack, stroke, and death.

This explains why those eating more plant-based diets have lower blood concentrations of TMAO. However, they also produce less of the toxin even if you feed them a steak. You don’t see the same “conversion of dietary L-carnitine to TMAO…suggesting an adoptive response of the gut microbiota in omnivores.” They are what we feed them.

As you can see at 4:17 in my video, if you give people cyclamate, a synthetic artificial sweetener, most of their bacteria don’t know what to do with it. But, if you feed it to people for ten days and select for the few bacteria that were hip to the new synthetic chemical, eventually three quarters of the cyclamate consumed is metabolized by the bacteria into another new compound called cyclohexylamine. Stop eating it, however, and those bacteria die back. Unfortunately, cyclohexylamine may be toxic and so was banned by the FDA in 1969. In a vintage Kool-Aid ad from 1969, Pre-Sweetened Kool-Aid was taken “off your grocer’s shelves,” but Regular Kool-Aid “has no cyclamates” and “is completely safe for your entire family.”

But, if you just ate cyclamate once in a while, it wouldn’t turn into cyclohexylamine because you wouldn’t have fed and fostered the gut flora specialized to do so. The same thing happens with TMAO. Those who just eat red meat, eggs, or seafood once in a while would presumably make very little of the toxin because they hadn’t been cultivating the bacteria that produce it.

Here’s the link to my video on TMAO: Carnitine, Choline, Cancer, and Cholesterol: The TMAO Connection. For an update on TMAO, see How Our Gut Bacteria Can Use Eggs to Accelerate Cancer, Egg Industry Response to Choline and TMAO, and How to Reduce Your TMAO Levels.

Interested in more on keeping our gut bugs happy? 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 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: