Abusing antibiotics could generate diabetes (study)

Abuse of antibiotics could generate diabetes because they generate an imbalance in the composition of bacterial flora in the intestine, which would impact other sectors of our body.

The warning extended to a good part of the medical community has beenThose medications.

The truth is that the risk already demonstrated that antibiotics lose their effectiveness, leaving doctors without tools to combat potentially mortal infections, new adverse effects related to their impact on the human organism are added.

The most recent is its denounced link with type 2 diabetes.

This disease, which is characterized by the organism's inability to use insulin to process food sugars and that can lead to the need to receive periodic doses of insulin, is in frank advance, as a result of the epidemic of obesity that affectscurrently to the western world.

However, excess body weight would not be the only risk factor.A recent American study suggests that excessive antibiotic use could increase the risk of diabetes, by altering intestinal flora.

"Although our study shows no causality, we believe that changing levels and diversity of intestinal bacteria could explain the link between antibiotics and the risk of diabetes," said Dr. Yu Xiao Yang, a researcher at the University of Pennsylvania.

Together with his colleagues, he analyzed medical information from one million people from the United Kingdom to find that those who had received at least two regimes of four types of antibiotics (peninchalins, cephalosporins, quinolones and macrolides) were more prone to contracting diabetes.

According to the analysis, of two to five penincilin regimes, they raise the risk of diabetes by 8 percent, but when it comes to people who received more than five regimes, the risk was 23 percent.

As for quinolones, two to five regimes increased the risk of diabetes by 15 percent, while more than five increased risk by 37 percent.

It has been suggested that intestinal bacteria influence the underlying mechanisms of obesity, insulin resistance and diabetes in both animal and human models.