We are what we eat

July 14, 2016

We are what we eat

A new genetic study supports the hypothesis that microbiome, a collective of the microorganism genetic heritage that is hosted in our intestine, is strongly influenced by diet and lifestyle. Microorganism cells that live in the human body, especially the intestine, are up to ten times more numerous than other cells. The set of genes of these host microorganisms, so-called microbiome, has a significant influence on human health. One of the results of the research is that in the intestines of those who live in industrialized countries, especially in the Western world, microbiome is less varied than that of the hunter-gatherer populations. The reason for this difference is as yet still unexplained. Latest studies suggest that diet is the most important factor for determining the composition of human microbiome: we are what we eat and microbiome quite faithfully reflects our lifestyle.

Each individual has an “unique” microbiota for age, geographic area, diet, ethnicity, etc.. Numerous events can significantly alter the intestinal microbiota of an individual: dietary changes, infections, antibiotic therapy, etc., but the intestinal microbiota is “resilient.” When, for various reasons, the microbiota is not restored, a “dysbiosis” may be determined, whose consequences can be manifold. It is hypothesized that precisely the alteration of intestinal microbiota may lead to chronic and immunological diseases, colon cancer, gastric ulcer, cardiovascular diseases, intestinal pathologies and especially obesity. Some studies have concluded that the complex interactions between environment, microbiota and host genetics determine the metabolic phenotype and that the microbiota influences the development of obesity, inflammation and insulin resistance. Numerous research, in fact, have shown the association between the prevalence of certain bacteria and BMI, DM2 and obesity, because microbiota can increase energy extraction from food, change the host’s metabolic pathways, causing low-grade chronic inflammation, increase insulin resistance, affecting the secretion of intestinal hormones (incretins) and intestinal motility. Moving from a mainly vegetable and low-fat diet to one rich in fat and sugar, the intestinal flora changes dramatically even within 24 hours, with the proliferation of microorganisms that facilitate the assimilation of these substances and favors the onset of obesity.