Antibiotic-associated diarrhea occurs in 5-35% of all antibiotic therapies
Antibiotic-associated diarrhea occurs in 5-35% of all antibiotic therapies

A very well-known case of an imbalanced ecosystem in our bodies is the antibiotics-associated diarrhea. First, the gut’s ecosystem is impaired by the unspecific antibiotics and thus the gut loses many important tools it needs for healthy digestion, along with the necessary weapons to fight pathogenic bacteria. The exposed areas which crop up on the intestinal walls are now the perfect place for pathogenic bacteria to colonize. One of the most abundant and dangerous ones is called Clostridium difficile. C. difficile damages the mucosa and induces inflammation of the colon through the release of two potent toxins.


The microbiome influences our appetite
The microbiome influences our appetite

The microbial composition of our gut influences our appetite and the ability to deposit fat.

The bacteria residing in our stomach, namely Helicobacter pylori, tell us when we´re hungry or full. Besides regulating the acidity in the stomach, this bug causes a decrease in the hormone ghrelin, which is involved in appetite regulation. The absence of this bacterium in the stomach causes elevated ghrelin secretion, leading to an even bigger appetite. Unfortunately, H. pylori has had a bad reputation throughout the last decades as a causative agent for peptic ulcers in susceptible people; it has therefore almost been eradicated from our stomachs through the use of antibiotics. For example, two or three generations ago in the U.S., 80%  of Americans harbored this bug; now less than 6% of American children are host to it, which may be one explanation for the increase in child obesity in the United States. At the same time, a formerly very rare form of oesophagus cancer increased ten-fold.

The composition of our microbiota in the intestines determine the amount of calories we can use from the food we eat. In former times, when food was a scarce good, people with a microbiome that was able to deposit more fat from the food had a greater chance of survival. Now that food is available at any time, these microbiomes induce obesity. Two people eating the same amount of food can either become obese or stay slim, depending on how their microbiomes utilize the carbohydrate source.

On the other hand, the kind of food we eat also influences the gut microbiome. When looking at people living in countries such as Japan, where more plant-derived carbohydrates are consumed, we find more bacteria capable of breaking down these plant carbohydrates in the gut. Also, the consumption of high-fat products reduces the total volume of the intestinal microbiome volume and induces the growth of bacteria that support a rapid fat deposition.

Gastrointestinal cancers

Heterocyclic amines, present in grilled meat can result in cancer.
Heterocyclic amines, present in grilled meat can result in cancer.

Your microbiome can also correlate with gastrointestinal cancers. It's not your microbiome which is inducing the cancer, it is the food you eat that induces the wrong bacteria to feel at home in your intestines. The Western-style diet in particular (a great deal of meat and fat coupled with a low intake of vegetables) favors the bacteria that produce specific enzymes and bile acids. These special enzymes can turn harmless compounds into carcinogens, such as heterocyclic amines, which you eat with grilled meat. After having transformed them into an electrophilic derivative, it can damage your DNA and thus result in cancer. So, an apple a day…

Inflammatory bowel disease

One disease which shows how dependent bacterial species are on one another is inflammatory bowel disease (IBD). IBD is a chronic, relapsing inflammation of the gastrointestinal (GI) tract, leading to mucosal damage. Normally in healthy individuals the GI tract is dominated by microbes of the divisions Firmicutes and Bacteroides. In IBD patients these bacteria are not dominant. The lowered number of Firmicutes in turn leads to a reduced abundance of Clostridium (of the IXa and IV groups), which normally lowers the level of pro-inflammatory cytokines by the release of butyrate. Additionally, the bacterium Bacteroides fragilis which is also reduced in IBD patients, boosts regulatory T cells, and thus stops the pro-inflammatory T cells from becoming too aggressive. Taken together, bacteria which are usually there to keep the immune system in check, are missing, thus the immune system is hyperactive and reacts against its own cells.

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