Chapter 11: It’s About What’s In Your Gut


When I first read the research about how microbes in the gut impact obesity, I said aloud, “We’re in trouble.”  I was in my office, alone, but what I was reading was so impactful, such a huge game changer, I couldn’t help asking aloud, “Who’s in charge here?”

 This information is new and cutting edge as I write this. I’m sure that in the coming months and years, amazing discoveries will be made. Maybe what I’m sharing with you will be main stream by the time you read this, but right now, it’s a whole new game.

 When researchers first became serious about obesity, we focused on how the body processes foods and how those processes create fat and contribute to the metabolic syndrome. Next, we looked at how brain chemistry impacted our desire to eat. But no one thought to look at the other end. We knew that fiber in the gut slowed the absorption of carbohydrates, but we didn’t consider what else might be in our gut, and how those other things might affect our desire for food.  As usual, the evidence was already there; we just weren’t paying attention. The blindness caused by myths like the Seven Deadly Sins caused us to ignore what farmers had known for years. Antibiotics make us fat.

 That’s right, farmers noticed decades ago that if they treated young chickens with antibiotics, they would be fat later in life. It became a common practice. If you wanted to get your animals ready for market quickly, you exposed them to antibiotics early in life.

 It turns out that antibiotics alter the number and variety of microbes in the intestines. If you’ve ever been on an antibiotic regimen and then took probiotics afterward because of digestion issues, you know what I’m talking about. But when a human infant is exposed to antibiotics, their gut bacteria may be changed long term.

 We didn’t start looking at the relationship of microbes in the intestines and weight gain until 2009. Researchers from Arizona State University sequenced the bacterial genes in the feces of three people who just had gastric bypass surgery. They found that these three people had a lot of a certain bacteria that was almost missing in normal weight people.

 This finding led to an interesting study. Researchers gave obese mice a gastric bypass. The bypass created a bacterial environment that facilitated weight loss.  When they transplanted fecal bacteria from the bypass mice into other mice that had been bred to be microbe-free, these normal weight mice lost 5% of their weight. The researchers concluded that something was going on in the gut that sends messages to the brain and organs involved in the metabolic system.

 In a follow-up human study, researchers found that when obese volunteers went on a one year diet, they lost one-quarter of their body weight. Interestingly enough, their bacterial profiles changed to look more like thin-biology people.  In another study of twins with different weights, researchers found that the obese twin had less microbe diversity in their intestines than their skinnier sibling.

 So then researchers fed mutant and normal mice until they were all fat. They then did a gastric procedure that does not circumvent the small intestine. As you would expect, both types of mice lost weight within a week.

 But five weeks later, something interesting happened. The normal mice continued to keep the weight off, but the mutant mice gained all the weight back.

 What was different in the mutants? Certain bile-activated receptors were blocked. But what was also interesting was the normal mice had an abundance of a bacterium that is usually suppressed in people with diabetes.  What this suggests is that bile acid and bacteria communicate with organs in a manner that either prevents or causes diabetes, depending on the messages sent.

These findings were expanded by the observation that the bacterium Akkermansia muciniphila makes up three to five percent of the microbes in a normal human gut. But obese people and those with type-2 diabetes have much lower levels of this bacteria.

In addition, when mice were fed a high-fat diet, they had 100 times fewer of this microbe than mice eating a normal diet. When the now fat mice returned to a regular diet, levels of the bacterium returned to normal. When this occurred, the mice lost weight and became less insulin resistant.

Or how about this study, one that doesn’t involve fats. No, this one deals with artificial sweeteners; you know, those ones people use when they don’t want to gain weight. They think that since there are no calories, the “sugar-free” soda won’t make them fat. The ones listed as “diet.”

Well, when a thin mouse was fed artificial sweeteners, it gained weight. It became fat and diabetic. This shows the problem with all these artificial sweeteners and diet products, and how wrong the myth is that because they don’t have calories that they are healthy and good for your diet.  

But that wasn’t the point of the study. Researchers then took the fecal bacteria from the now fat and sick mice and put it into mice that were healthy and skinny. The results? By now you can guess that the skinny mouse got fat as well, even though it never ate the artificial sweeteners. 

So how far does it go? It turns out that microbes may even be affecting the type of foods you like. One study found that microbe-free mice had different taste receptors for fat on their tongues and in their intestines than normal mice. 

Similarly, food preferences may be contagious. Researchers found that oral and fecal microbes are similar between cohabiting people. The idea is that if one member of the household influences the consumption of a certain food, soon the other family members’ guts have microbes that also flourish with this food. The implication, of course, is that obesity may be contagious.

Microbial genes in your gut outnumber your own genes by 100 to 1. The 10 trillion or so microbial cells living in your gut have 100,000 genes, compared with the paltry 26,000 or so in the human genome. That means whole colonies are living in your GI track that have no genetic relationship with you.

 These microbes compete over nutrients and habitat. In a large field, where there are a number of competitors, the battles keep a type of equilibrium. But what happens when the field is stacked to benefit one group over another? When one type of microbe begins to dominate, it begins to call the shots in the intestines.

 Here’s where it gets interesting. Japanese tend to have a microbe that digests seaweed. African children raised on sorghum have unique microbes that digest cellulose. People who crave chocolate have different microbes than those who are indifferent to chocolate. We also know that certain types of microbes grow best on certain types of foods.

The microbes in our gut can also produce toxins that alter our moods. They can even hijack our vagus nerve which is one of the primary routes of communication between our bellies and our brains.

 When experimental mice were given certain bacteria, their stress cortisol levels went down. But when placed in a stressful situation (in their case, swimming in a bath with no escape), it was observed that they became pathologically persistent in their activities, swimming longer than the control mice, who were not given the bacteria.

The researchers wondered if there was a tie-in with the vagus nerve.  When they cut the vagus nerve of the experimental mice, the opposite behavior happened—they gave up and drowned.  This suggests that the microbes in our guts also manipulate our nervous system in complex behavioral ways.

 There are additional examples of microbes affecting their hosts’ moods. For instance, when researchers transferred microbes from anxious mice to microbe-free mice, the microbe-free mice became more timid. Similarly, when those anxious mice were given a fecal pellet from normal mice, they began to explore their surroundings again.

 Think of the pleasurable brain chemicals dopamine and serotonin.  These have intestinal sources. Certain inhabitants of your gut have been shown to boost dopamine levels 10 to 100 times.

 When you put all of this together, the implications are mind-boggling. From this chapter, you will probably be less likely to request antibiotics from your doctor for a minor ailment or a disease that is probably viral in origin.  If you do need to use antibiotics for health reasons, be sure and replace your normal microbiome by taking probiotics and fermented food products (such as yogurt, sauerkraut, and kimchi).

Much more research will be necessary before fecal transports are considered for the treatment of obesity.  In the meantime, we don’t want to be blaming people for battles that may be waging in their guts.