The link between Gut Bacteria and Obesity

Worldwide, obesity and metabolic syndromes like insulin resistance and type 2 diabetes have become major problems. Recent research has shown that altered microbiota composition in the gut plays an important role in these conditions.

The microbiome in the gut

The human colon contains over 100 trillion bacteria. However, recent advancements in DNA extraction, DNA culturing and sequencing technology have shown that the four most dominant families (or species in taxonomy) in humans are Bacteroidetes and Firmicutes as well as Actinobacteria, Proteobacteria, and Proteobacteria.

Over 1000 bacteria species co-exist within these four families, including lactobacilli and clostridia.

Other living organisms in the human stomach include Fungi, like Candida spp., and Archaea. Archea may have been mentioned in articles on Small Intestinal Bacterial Overgrowth, SIBO. This condition is often associated with Fructose Malabsorption.

Evolution has brought together the best combination of bacteria to create a healthy environment for all living things.

These bacteria consume our undigested food, make nutrients, regulate our immune system, and then extract the calories used for energy. Colonic bacteria have also been shown that regulates our rate of glucose absorption. This is how your blood sugar levels fluctuate.

There is no question that microbial diversity is crucial to our health. The Human Microbiome Project’s research has shown that the loss of diverse bacterial species in the western intestine is one of the major causes of many modern diseases, including allergies, asthma, Crohn’s disease, Crohn’s disease, and obesity.

However, diversity is not the only thing affecting our gut health. It is also important to consider the ratio of different species. Large fluctuations in the bacterial population numbers can be caused by diet, antibiotic use and aging. This can lead to various unpleasant symptoms, including brain fog, chronic bloating, and constipation.

Recent research has shown that the ratio between Bacteroidetes (the family I mentioned) and Firmicutes is the cause of modern obesity in children and adults.

The Fat Microbes

Recent research has shown that a higher intake of Firmicutes than Bacteroidetes can increase the calories we eat. The bottom line is that if you have high levels of Firmicutes, you will gain weight no matter how hard you exercise or what diet you follow.

Emory University School of Medicine’s research found that mice unable to distinguish good from bad bacteria developed insulin resistance and high blood pressure. They also experienced weight gain, elevated blood cholesterol, obesity, and fatty liver.

Researchers wanted to find out why this was so. Because of their dysfunctional immune system, the mice had an abnormally high gut microbiota. They were more likely to have more Firmicutes than Bacteroidetes. This change in the microbial ratio allowed mice to extract more calories from their food and increased their appetite.

The mice did not gain weight when their calorie intake was reduced, but they still showed blood markers of insulin resistance. This is a risk factor for developing heart disease.

Insulin resistance and a dysregulated gut microbe

Insulin resistance causes your cells to become starved. They no longer respond to the signal that they need nutrients. Insulin resistance can be described as a key that doesn’t fit into your cell’s keyhole. This is exactly what happens to people with diabetes who starve to death because their cells stop receiving food.

Your brain tells you your cells require energy so that you may feel hungry all the while. Your blood sugar levels rise, causing more glucose to flood your bloodstream. This causes your pancreas and liver to produce more insulin. Your pancreas will eventually run out of steam and stop producing enough insulin. This can lead to type 2 diabetes.

Your body stores the extra glucose in fat cells around your middle, leading to insulin resistance.

Inflammatory bowel disease (IBS) was also more likely in mice from the above study. This is not surprising. This is not surprising. Insulin resistance can trigger inflammation. Chronic inflammation causes your gut to leak, leading to allergies, asthma, and auto-immune disease.

However, correlation can be very different than causation in science. Although they had found a correlation between obesity and changes in the microbiota of obese mice, this was not enough to prove that the bacteria ratio had caused them to become obese. The next experiment was.

Coprophilic mice eat each others’ feces. When placed together, the researchers found that obese mice also had an increased appetite, metabolic syndrome, and weight gain. The germ-free mice developed a faulty microbiota from eating their fat friends’ poo. (Feces contain our intestinal flora). This caused a link between obesity and high Firmicutes.

Human research

Further human research was conducted to confirm the link between obesity and altered microbiota.

An analysis of 79 subjects (both adults and children) showed that the percentages of Firmicutes were higher in obese people than in those with normal weight.

Also, the study found that subjects with higher Firmicutes levels had higher levels of hsCRP. This blood marker for systemic inflammation has been linked to increased cardiovascular risk.

Another prospective cross-sectional study, looking at fecal analyses of 26 overweight/obese and 27 lean children, found that obese children had a higher Firmicutes-to-Bacteroidetes ratio than lean children.

Study of twins and the microbiome

The most important study that established the connection between obesity, insulin resistance, and changes in the bacterial ratio was the 2013 research of Vanessa K. Ridaura (a Washington University graduate student).

Ridaura recruited four identical twins. Each pair was composed of a lean twin and an obese twin. Similar genes but different microbiomes.

The twins’ feces were then transferred to some germ-free mice. The obese twins’ transplanted feces made the mice obese. The transplanted mice from the slim twins kept them lean.

Ridaura did more than give this amazing result. She also housed the mice with other lean mice who had been given the “obese” transplant. What happened?

This time, the mice weren’t obese. Why? Research has shown that our microbiome fluctuates as we share it. Ridaura’s experiment showed that a subset of Bacteroidetes, Bacteroides, passed from obese mice to those with the obese microbiome.

Even more amazing is that this result depended on high-fiber diets feeding mice. The fiber-fed the good bacteria and kept them high in numbers. This keeps the ‘obese bacteria away.

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