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:

Proof that Lifelong Cholesterol Reduction Prevents Heart Disease

“It is well accepted that coronary atherosclerosis is a chronic progressive disease that begins early in life and slowly progresses over several decades” before symptoms arise. However, the average age in cholesterol-lowering drug trials is 63; therefore, people have already been exposed to a lifetime of circulating LDL cholesterol. It’s no wonder pharmaceutical therapies typically reduce cardiovascular disease risk by only 20 to 30 percent.

We know LDL, the so-called bad cholesterol, plays “a central role” in the “initiation, development, and progression” of our number-one killer. In fact, more than 100 prospective studies involving more than a million people have demonstrated that those with higher LDL levels are at higher risk.

“It seems reasonable to assume, therefore, that if lowering LCL-C [cholesterol] levels beginning later in life can slow the progression of advanced atherosclerotic plaques…then keeping LDL-C levels low, beginning much earlier in life” might prevent our arteries from getting clogged in the first place. A reasonable assumption, certainly—but let’s not just assume.

“It would be…unethical to set up a controlled clinical trial in which young adults with elevated serum cholesterol levels were treated or not treated over their lifetime”—just as we couldn’t ethically set up a study in which half the young adults are made to start smoking to see if smoking really does cause lung cancer. That’s where observational studies come in. We can follow people who already smoke and compare their disease rates to those who don’t.

It was aroud 40 years ago when the president of the American Heart Association tried to argue we should all stop smoking even though there were no randomized controlled trials. You can see a copy of the “Presidential Address” entitled “The Case for Prevention of Coronary Heart Disease” to the AHA’s 47th Scientific Sessions at 1:34 in my video. Those who smoke have a higher risk of heart attack, and the more we smoke the higher the risk. After we stop smoking, our risk drops. The same can be said for high cholesterol.

Young men 18 through 39 years of age were followed for up to 34 years, and their cholesterol levels, even when they were young, predicted long-term risk of heart disease and death. Men in their 20s and 30s who have a total cholesterol just under 200 have a “substantially longer estimated life expectancy”—around 4 to 9 years longer—than those with levels over 240.

“Evidence from observational studies, however, [is] vulnerable to confounding” factors. Eating a diet that is plant-based enough to lower cholesterol below average, for example, may add years to our lives regardless of what our cholesterol actually is. Ideally, we’d have a long-term, randomized, controlled trial.

Nature may have actually set one up for us. Each of us, at conception, gets a random assortment of genes from our mother and our father, and some of those genes may affect our cholesterol levels. Just like there are rare genetic mutations that result in unusually high cholesterol levels, there are rare genetic mutations that lead to unusually low cholesterol levels, “provid[ing] an ideal system in which to assess the consequences of low LDL cholesterol levels independently of other factors that may modify disease progression,” such as confounding diet and lifestyle factors.

Starting at 3:14 in my video, you can see what I mean. About 1 in 40 African Americans have a mutation that drops their LDL cholesterol from around 130 down toward more optimal levels. Now, this group didn’t eat healthy to get achieve that drop. It’s just in their genes. More than half had high blood pressure and there were a lot of smokers and diabetics in the group, yet those with genetically low LDL levels still had a significant reduction in the incidence of coronary heart disease even in the presence of all those other risk factors. How significant? How much less heart disease? A remarkable 88 percent of heart disease was simply gone.

The astounding finding was that the risk of heart disease in these individuals was reduced by more than 80 percent, whereas the same 20- to 40-point decrease in LDL from drugs only reduces risk around 30 percent. Makes sense, though, because the folks with the mutation had low levels their entire life. They didn’t simply start taking a pill when they were 60.

“The magnitude of the effect of long-term exposure to lower LDL-C [cholesterol] concentrations observed in each of these studies represents a threefold greater reduction in the risk of CHD,” or coronary heart disease, compared to drug treatment started later in life. (As an aside, for all of my fellow research nerds, check out that p value shown in my video at the 4:30 mark. You’d have to do arourd a quintillion studies to get that kind of result by chance!)

“Therefore, a primary prevention strategy that promotes keeping LDL [cholesterol] levels as low as possible, beginning as early in life as possible, and sustaining those low levels of LDL [cholesterol] throughout the whole of one’s lifetime has the potential to dramatically reduce the risk of CHD,” coronary heart disease.

If you don’t know your cholesterol level, you should get it checked—maybe even starting in childhood. See my video Should All Children Have Their Cholesterol Checked? to learn more.

What if you do get tested and your doctor tells you not to worry because your cholesterol’s “normal”? Having a “normal” cholesterol level in the society where it’s normal to drop dead of a heart attack (the number-one killer of men and women) is not really such a good thing. See my video When Low-Risk Means High-Risk.

Check out Optimal Cholesterol Level and What’s the Optimal Cholesterol Level? to find out where you should be.

What if your doctor tells you your LDL is large and fluffy? See my video Does Cholesterol Size Matter?.

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:

All Children Should Have Their Cholesterol Checked Between Ages 9 and 11

Coronary artery disease does not magically appear. The disease begins “during early childhood and progress[es] unrecognized for several decades to its often final and unexpected endpoint of chest pain, disability, or premature death.”

As I discuss in my video Should All Children Have Their Cholesterol Checked?, “we need to remind ourselves that atherosclerosis begins in childhood as fatty streaks” in the arteries, which “are the precursors of the advanced lesions that ultimately” kill us. By the time we’re in our 20s, 20 percent of the inner surface of the artery coming off the heart is covered in fatty streaks, as you can see at 0:58 in my video. Fifty years ago, pathologists began raising the question of whether heart disease is best handled by cardiologists or by pediatricians.

“By their 30s, many young adults already have advanced coronary atherosclerosis,” so, in reality, intervention during our 30s and beyond “is actually secondary prevention, because advanced atherosclerosis is likely already present.” Indeed, intervention is just trying to mediate the ravages of the disease rather than prevent the disease itself.

What’s more, we are exporting the problem around the world. A study of young, thin, apparently healthy individuals found 97 percent of their collected arteries had atherosclerosis, which you can see at 4:52 in my video. So, even in developing countries like Brazil, where they’ve acquired our eating habits, we’re seeing an epidemic of heart disease and sudden death.

“Moreover, the risk factors that correlate with the extent of such early lesions are the same risk factors that correlate with myocardial infarction [or, heart attacks] later in life.” In other words, it’s the same disease but in the early stages. So, pathologists, the ones doing the autopsies on all these young people and seeing all this coronary artery disease, “began urging many years ago that preventive measures should be instituted earlier in life.”

We’ve known that fatty streaks exist in young children for more than a century, but it wasn’t until 1994 that a task force convened by the government came up with a “radical” idea: “The strategic key, and the greatest opportunity in preventing [cardiovascular disease] CVD, is to prevent the development of CVD risk in the first place.”

In my video Heart Disease Starts in Childhood, I noted that fatty streaks, the first stage of atherosclerosis, were found in the arteries of nearly 100 percent of kids by age ten who were raised on the standard American diet. In recognition of this fact, the latest Academy of Pediatrics’ recommendation is for all kids to get their cholesterol tested starting between the ages of 9 and 11.

Of course, this has drug companies salivating at the thought of slipping statins into Happy Meals, but “long-term drug intervention is costly and may be associated with adverse effects.” So, the conversation is about lifestyle modification.

In my video How Many Meet the Simple Seven?, I revealed the breathtaking statistic that only about 1 in 2,000 U.S. adults met the seven American Heart Association criteria for a heart-healthy lifestyle. What about American teenagers? Of the 4,673 adolescents aged 12 to 19 who were studied, zero made the cut. Not one teen “exhibited ideal levels of all 7 cardiovascular health behaviors and health factors.”

Most teen boys and girls don’t smoke, and most aren’t overweight. What was the main sticking point? Almost no one ate a healthy diet. Indeed, less than 1 percent of young men and women met a minimum of healthy diet criteria.

This sorry state of affairs is what’s behind a “controversial valuation that the current generation of US children and adolescents may be one of the first generations to be less healthy and have shorter life expectancy than their parents.”

If you think atherosclerosis by age ten is bad, check out my video Heart Disease May Start in the Womb.

Adverse effects with cholesterol-lowering drugs? See Statin Muscle Toxicity. I don’t think most people realize—doctors and patients alike—realize how relatively ineffective these drugs are. Watch, for example, The Actual Benefit of Diet vs. Drugs.

Cholesterol can do more than just build up and block off our arteries. In fact, Cholesterol Crystals May Tear Through Our Artery Lining.

What’s the Optimal Cholesterol Level? Does Cholesterol Size Matter? Watch the videos to find out.

Let’s take a step back, though. What about all the “cholesterol skeptics”? Check out How Do We Know That Cholesterol Causes Heart Disease?.

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: