The growing knowledge in research communities concerning the symbiotic relationship we have with our bacterial organism population is increasingly reflecting that which we have been discussing for many years – namely the use of antibiotics (and many of our current lifestyle habits) is not a benign event in terms of microbiome outcomes. It seems that even short pulses of widely used antibiotics (amoxicillin and tylosin in this paper) can lead to long-term development changes in mouse pups, including increased body mass and bone growth and changes to the gut microbiota, according to a study published in Nature Communications.[1]
Long understood as an aid in farm animal growth, the continuous low dose of antibiotics fattens stock more quickly, could this be translatable to others mammals including humans in the use of short infrequent exposures to antibiotics rather than low dose long term exposure was one of the underlying proposals for this study?
Perhaps the most translatable component for this experiment can be in the recognition that altering the composition and ratio of bacteria and most likely viruses in the gut in developing mammals has a number of impacts on their health and wellbeing. Some of these may be beneficial and others may be problematic. Antibiotic treatment in adults for example has been linked to recent weight gain and increased risk of type 2 diabetes, especially after multiple courses or sustained exposure.
The referenced study used 2 different antibiotics, each had differing impacts on compositional changes, exacerbated by a high fat diet – something we see in adult populations of humans as well. Of note the researchers reported that changes in body mass, bone size and mineral density occurred predictably suggesting that antibiotics affect early life development. They also noted that this pulsed use of antibiotics would change various gene expression related processes in the liver for up to 120 days after last antibiotic treatment further indicating that antibiotics contribute to changes in metabolic signalling.
Pulsed antibiotic treatment affected the metabolism of young mice. Although differences were observed and the overall magnitude was small, both the beta-lactam (amoxicillin) and the macrolide (tylosin) significantly affected early growth, lean muscle mass, bone development and hepatic gene expression.
What implications could this present for human health, or is it already happening?
In less than 100 years, the leading diseases and causes of death have already shifted dramatically away from infectious diseases and heavily towards what are referred to as noncommunicable diseases (NCDs), not just in developed countries, but around the globe. NCDs now occupy the title as the ‘number one killer’ worldwide, accounting for a disturbing 63 percent of all mortalities.[2] There is no question that environmental variables, including exposure to cigarette smoke, dietary factors (of which there are many positive and negative elements), and chemicals such as heavy metals, pesticides, endocrine disruptors, or particular drugs, increase one’s risk of developing an NCD. Psychosocial stressors and economic pressures also play a role. But any assumption that the ongoing NCD epidemic is due solely to external factors would be missing a key part of the story: the human microbiome. In reality, the NCD epidemic is as much about the ways we have altered our microbiomes in recent decades, and continue to confer generational transfer of risks related to loss of bacterial diversity as it is about our changing external environment.
References
[1] Y.R. Nobel et al. “Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment,” Nature Communications, 30 June 2015
[2] D.E. Bloom et al., “The global economic burden of noncommunicable diseases,” Geneva, World Economic Forum, 2011. View Full Report
