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:

Is Type 1 Diabetes Triggered by the Bovine Insulin in Milk?

The tight correlation among countries between the incidence of type 1 diabetes in children and cow’s milk consumption didn’t account for Iceland. Indeed, studies correlating dairy intake in children and adolescents with the incidence of type 1 diabetes deliberately excluded the Icelandic data. Why? Is it because of genetics? Perhaps, yes and no. The people of Iceland are similar genetically to other Nordic countries, but their cows are not. As I discuss in my video Does Bovine Insulin in Milk Trigger Type 1 Diabetes?, there are two main types of the cow milk protein casein: A1 and A2. Icelandic cattle, who “have been isolated from interbreeding with other cattle breeds for over 1,100 years,” are unusual in that they produce mostly A2 milk, which may explain the lower incidence of type 1 diabetes in Iceland.

Unlike A2 casein, A1 casein breaks down into casomorphin, which has opioid properties that may alter immune function, perhaps increasing susceptibility to infections that may themselves trigger type 1 diabetes. That’s what’s in the milk from the classic black-and-white patterned Holstein cows, who make up about 95 percent of the U.S. dairy herd and much of the global herd—A1 casein. This issue has even caused dairy boards to begin taking out patents on methods for selecting “nondiabetogenic” milk to avoid triggering of Type 1 diabetes. Indeed, looking only at A1 casein consumption certainly restores that tight linear relationship between milk intake and type 1 diabetes and you can see at 1:47 in the video.

These so-called ecological, or country-by-country, studies, however, primarily serve to suggest possibilities that then need to be put to the test. For example, a study was designed where hundreds of siblings of type 1 diabetics were followed for about ten years and found that those who drank a lot of milk did have about five times the risk of coming down with the disease, too. By the mid-1990s, more than a dozen such studies were done.

Overall, researchers found that early cow’s milk exposure appears to increase the risk of type 1 diabetes by about 50 percent. Those data were enough for the American Academy of Pediatrics to decide that “cow’s milk protein may be an important factor” in the initiation of the process that destroys our insulin-producing cells. The organization went on to say that the avoidance of cow’s milk protein may reduce or delay the onset of type 1 diabetes. As such, the American Academy of Pediatrics emphasizes that breast milk is best and, for those at higher risk of the disease, strongly encourages the avoidance of products containing cow’s milk protein that is intact, as opposed to hydrolyzed formula where the milk proteins are broken up into tiny pieces.

Typically, hydrolyzed formula is given to children with dairy allergies and could potentially make it less risky, but we don’t know until we put it to the test. Based on the population studies and meta-analyses of antibody studies, which suggested that “cow’s milk may serve as a trigger of Type 1 diabetes,” a pilot study was initiated the following year. Researchers wanted to see if babies at high genetic risk for the disease would be less likely to develop antibodies that would then attack their own pancreas if they drank hydrolyzed casein—that is, casein that was chopped up. The hydrolyzed formula did seem to reduce the appearance of at least one autoimmune antibody, but not two or more, which is much more predictive of the development of the disease.

Nevertheless, that was enough for the investigators to embark on the ambitious Trial to Reduce Incidence of Diabetes in Genetically at Risk, also known as the TRIGR study. This multinational, randomized prospective trial involved randomizing thousands of newborns across 15 countries. In 2010, preliminary data suggested the hydrolyzed formula may have helped, but they didn’t quite reach statistical significance, approximately meaning there was greater than a 1 in 20 chance the findings could have just been a fluke. Indeed, when the final autoimmune antibody results were published, the special hydrolyzed formula didn’t seem to help at all.

The researchers only looked at a special group of children, though—ones who were at high genetic risk with diabetes running in the family—whereas the great majority of children who get type 1 diabetes do not have any afflicted close relative. Perhaps most importantly, however, as the researchers themselves emphasized, their study wasn’t designed to test whether cow’s milk is or is not a trigger for the disease. Instead, it aimed to analyze the potential effects of the hydrolyzed casein formula. Maybe it’s not the casein, though. Maybe it’s the bovine insulin.

Insulin autoantibodies—antibodies our body produces to attack our own insulin—often appear as the first sign in prediabetic children. “Because cow’s milk contains bovine insulin,” around the same time researchers were looking into casein, another team “followed the development of insulin-binding antibodies in children fed with cow’s milk formula.” They found significantly more antibodies to bovine insulin in the cow’s milk formula group compared to the exclusively breastfed group, who may have only been exposed to cow proteins through their mom’s breast milk (if their mothers consumed dairy). Furthermore, the bovine antibodies cross-reacted with human insulin, potentially being that caught-in-the-crossfire cause triggering at least some cases of type 1 diabetes.

Of course, we can’t know for sure until we put it to the test. Researchers ran another randomized, double-blind trial, but, this time, tried a cow’s milk formula from which the bovine insulin had been removed. And, indeed, without the bovine insulin exposure, the children built up significantly fewer autoimmune antibodies. What we don’t know yet is whether this will translate into fewer cases of diabetes.


You may also want to check out:

For more on the concerns with cow’s milk exposure in infancy and childhood, see:

I’ve developed a six-part series on the role of gluten-free, casein-free diets in the treatment of autism:

What’s The Best Baby Formula? Breast milk!

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 Phytoestrogens Can have Anti-Estrogenic Effects

When the Women’s Health Initiative study found that menopausal women taking hormone replacement therapy suffered “higher rates of breast cancer, cardiovascular disease, and overall harm,” a call was made for safer alternatives. Yes, the Women’s Health Initiative found that estrogen does have positive effects, such as reducing menopausal symptoms, improving bone health, and reducing hip fracture risk, but negative effects were also found, such as increasing the blood clots in the heart, brain, and lungs, as well as breast cancer.

Ideally, to get the best of both worlds, we’d need what’s called a selective estrogen receptor modulator—something with pro-estrogenic effects in some tissues like bone but at the same time anti-estrogenic effects in other tissues like the breast. Drug companies are trying to make these, but phytoestrogens, which are natural compounds in plants, appear to function as natural selective estrogen receptor modulators. An example is genistein, which is found in soybeans, which happen to be structurally similar to estrogen. How could something that looks like estrogen act as an anti-estrogen?

The original theory for how soy phytoestrogens control breast cancer growth is that they compete with our own estrogens for binding to the estrogen receptor. As more and more soy compounds are dripped onto breast cancer cells in a petri dish, less and less actual estrogen is able to bind to them. So, the estrogen-blocking ability of phytoestrogens can help explain their anti-estrogenic effects. How do we then explain their pro-estrogenic effects on other tissues like bone? How can soy have it both ways?

The mystery was solved when it was discovered there are two different types of estrogen receptors in the body and the way in which a target cell responds depends on which type of estrogen receptor they have. The existence of this newly discovered estrogen receptor, named “estrogen receptor beta…to distinguish it from the ‘classical’ estrogen receptor alpha,” may be the “key to understanding the health-protective potential of soy” phytoestrogens. And, unlike our body’s own estrogen, soy phytoestrogens preferentially bind to the beta receptors.

For instance, within eight hours or so of eating about a cup of cooked whole soybeans, genistein levels in the blood reach about 20 to 50 nanomoles. That’s how much is circulating throughout our body, bathing our cells. About half is bound up to proteins in the blood, so the effective concentration is about half the 20 to 50 nanomoles. What does that mean for estrogen receptor activation?

In my video Who Shouldn’t Eat Soy?, I feature a graph explaining the mysterious health benefits of soy foods. Around the effective levels we would get from eating a cup of soybeans, there is very little alpha activation, but lots of beta activation. What do we find when we look at where each of these receptors are located in the human body? The way estrogen pills increase the risk of fatal blood clots is by causing the liver to dump out extra clotting factors. But guess what? The human liver contains only alpha estrogen receptors, not beta receptors. So, perhaps eating 30 cups or so of soybeans a day could be a problem, but, at the kinds of concentrations we would get with just normal soy consumption, it’s no wonder this is a problem with drug estrogens but not soy phytoestrogens.

The effects on the uterus also appear to be mediated solely by alpha receptors, which is presumably why no negative impact has been seen with soy. So, while estrogen-containing drugs may increase the risk of endometrial cancer up to ten-fold, phytoestrogen-containing foods are associated with significantly less endometrial cancer. In fact, protective effects are found for these types of gynecological cancers in general: Women who ate the most soy had 30 percent less endometrial cancer and appeared to cut their ovarian cancer risk nearly in half. 

Soy phytoestrogens don’t appear to have any effect on the lining of the uterus and can still dramatically improve some of the 11 most common menopausal symptoms (as compiled by the Kupperman Index).

In terms of bone health, human bone cells carry beta estrogen receptors, so we might expect soy phytoestrogens to be protective. And, indeed, they do seem to “significantly increase bone mineral density,” which is consistent with population data suggesting that “[h]igh consumption of soy products is associated with increased bone mass…” But can soy phytoestrogens prevent bone loss over time?

In a two-year study, soymilk was compared to a transdermal progesterone cream. The control group lost significant bone mineral density in their spine over the two years, but the progesterone group lost significantly less than that. The group drinking two glasses of soymilk a day, however, actually ended up even better than when they started.

In what is probably the most robust study to date, researchers compared the soy phytoestrogen genistein to a more traditional hormone replacement therapy (HRT) regimen. Over one year, in the spine and hip bones, the placebo group lost bone density, while it was gained in both the soy phytoestrogen and HRT estrogen groups. The “study clearly shows that genistein prevents bone loss…and enhances new bone formation…in turn producing a net gain of bone mass.”

The main reason we care about bone mass is that we want to prevent fractures. Is soy food consumption associated with lower fracture risk? Yes. In fact, a significantly lower risk of bone fracture is associated with just a single serving of soy a day, the equivalent of 5 to 7 grams of soy protein or 20 to 30 milligrams of phytoestrogens, which is about a cup of soymilk or, even better, a serving of a whole soy food like tempeh, edamame, or the beans themselves. We don’t have fracture data on soy supplements, though. “If we seek to derive the types of health benefits we presume Asian populations get from eating whole and traditional soy foods,” maybe we should look to eating those rather than taking unproven protein powders or pills.

Is there anyone who should avoid soy? Yes, if you have a soy allergy. That isn’t very common, though. A national survey found that only about 1 in 2,000 people report a soy allergy, which is 40 times less than the most common allergen, dairy milk, and about 10 times less than all the other common allergens, such as fish, eggs, shellfish, nuts, wheat, or peanuts.


What if you’re at high risk for breast cancer? See BRCA Breast Cancer Genes and Soy

What if you already have breast cancer? See:

What if you have fibroids? See Should Women with Fibroids Avoid Soy?.

What about hot flashes? See Soy Phytoestrogens for Menopause Hot Flashes.

What about genetically modified soy? See GMO Soy and Breast Cancer.

Not all phytoestrogens are beneficial, though. See What Are the Effects of the Hops Phytoestrogen in Beer? and The Most Potent Phytoestrogen Is in Beer.

How deleterious is hormone replacement therapy? See How Did Doctors Not Know About the Risks of Hormone Therapy?.

Synthetic estrogens used in animal agriculture are also a concern. For more on this, see Zeranol Use in Meat and Breast Cancer.

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: