Rather than leveraging science & technology along with data driven personalisation to understand the path that drives an individual to develop a disease & finding therapeutics/nutrition to eliminate the pro-inflammatory molecules before the disease occur, we are still focussed on managing the existing disease we already have.
One case in point is pointless promotion & endorsement of anti-obesity drugs, also referred to as GLP-1 Receptor Agonists. There are multiple molecular mechanisms which can make this drug just a piece of chemical without any anti-inflammatory benefits(1).
It is not out of context to mention that certain gut microbes active & expressing right genes can lead to production of beneficial acetate that secretes GLP-1- the hormones responsible for regulating satiety.
The effectiveness of these GLP-1 drugs depends upon their interaction with gut microbes. Certain gut microbes such as Bacteroides dorei and Roseburia inulinivorans if active & expressing right genes have positive correction with glycemic reduction while some other bugs such as Prevotella copri if expressing virulence genes have negative correlation(2).
In addition to this specific gut microbe Enterococcus faecalis if expressing virulence factor protease GelE could degrade GLP-1 leading to obesity & type 2 diabetes. Therefore subscribing to GLP-1 would only give side effects, nothing else.
Besides, there are multiple other mechanisms at play that could cause obesity. One of the most important gas produced inside our body every millisecond -Nitric Oxide has a role to play in insulin signalling & it has been found that people suffering from obesity have underexpression of Nitric Oxide Synthase(NOS) attributed to overexpression of tumor necrosis factor-α( triggered by secretion of gut derived metabolite LPS which causes adiposity). Taking GLP-1 drugs is pointless if the source code of obesity is not identified(3).
There are multiple other factors that could cause uncoupling of NOS from endothelial cells- one the major one being oxidation of Tetrahydrobiopterin (BH4 to BH2). In fact, this is said to cause vascular dysfunction during obesity & type 2 diabetes state. This could further be augmented if oral microbiome is imbalanced & not producing nitric oxide via Nitrate- Nitrite- NO Pathway.
Subscribing to these GLP-1 drugs without understanding the gut microbial ability to make it effective & /or not decoding the root cause of obesity is shot in the dark.
Check out our recently concluded talk on what could render GLP-1 drug ineffective.
Citations below:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8793908/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7021470/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112002
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8833664/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2268073/