Our bacterial lodgers need attention too!
Writer: Lucy Masdin
Editor: Sophie Chan
Artist: Jamie Hau
Obesity is a pandemic, taking over the planet at an alarming rate. The World Health Organisation (WHO) suggests that by 2030, 20% of the adult population will be obese. In other words, 1 in 5 adults would be at risk from a multitude of chronic diseases. No doubt, eating McDonalds every day will help you put on the pounds. However, researchers are straying away from the oversimplified narrative of ‘EAT LESS’ and are delving deeper into the whys and hows of obesity, uncovering that the gut microbiome may be playing a large role.
One of the pioneering points of research in the field, compared the microbiome of obese and lean people, which led to the proposal that a shifted ratio of bacterial families (specifically Bacteroidetes: Firmicutes) could be of significance. The Human Microbiome Project then linked a specific species of bacteria (Christensenella minuta) to weight-loss, given its increased presence in leaner people, reinforced by its weight-loss effects after introducing it into mice. Much of the literature suggests that leaner people’s microbiome contain bacteria which are more efficient at breaking down carbohydrates.
Another study, compared the faecal composition of children in Italy, living on a largely westernised diet, with children in Burkina Faso, with a diet more similar to early settlers’. Italian children were found to be completely lacking in two genera of bacteria, indicating that changing the diet changed what was able to live in the gut. It’s all pointing to the fact that we are responsible for changing our gut microbiome, potentially to the detriment of our health.
The danger with fixating on key bacteria having an explicit role in obesity then implies simplicity of the microbiome. Should the microbiome be considered as a human organ in its own right, having its own web of complex and delicate interactions that have an impact on various metabolic processes in the body? We understand the genome is not as simple as just a set list of genes independently having one distinct effect, so why do we do this for the microbiome? Little is understood about precisely what certain bacteria are doing to make us healthier, but these early findings are proof enough that this is a growing area of research.
However, another issue that scientists must account for is, how vastly different the bacterial colonisers of different organs are. While, the easiest way to assess the microbiome is through our faeces, this may not provide the most representative picture, but stomach and intestinal samples are more difficult to obtain.
Faecal transplants are emerging as an important subject, not only in monitoring the effects of microbiome changes, but also as a potential therapeutic procedure. Sterile mice receiving faecal bacteria from obese women accumulated body fat and developed metabolic complications. This was a key finding, as it infers that directly changing the microbiome could change the host metabolic phenotype.
An alternative view emphasises the gut microbiome’s role in appetite control and whether bacterial metabolites are stimulating signalling pathways. For example, Acetobacter and Lactobacillus bacteria were found to suppress flies’ appetite for protein and increase it for sugar. A more critical evaluation of how the microbiome interacts with hosts may shed light on how to focus on long-term solutions for weight-loss control, as many current strategies are difficult to maintain with patients often resorting to costly bariatric surgeries.
Perhaps we should start cherishing our microbiome, or else it might fight back with obesity!