Just in case there are still doubts out there about just how detrimental PUFA is to our health, here is a study showing that just one of PUFA’s “normal” metabolites (i.e. enzymatically derived, instead of through peroxidation) is sufficient to elevate lipolysis, and that effect alone is enough to cause fibrosis, obesity and ultimately diabetes. Obviously, since fibrosis is also induced, the study suggests that this PUFA metabolite (through the COX enzyme) – prostaglandin E2 (PGE2), to be precise – can lead to organ failure and cancer as fibrosis is an obligate step on the road to those end-states. The study tries to play dumb and says the findings should lead to the development of new therapies, but it fails to mention the “elephant in the room” – aspirin. The latter is perhaps the oldest COX inhibitor in existence and it inhibits the synthesis of PGE2 more than anything else. Oh, and if that was not enough, aspirin also has anti-lipolytic effects, so it should have anti-obesity, anti-fibrotic and anti-diabetic effects independently of PGE2, since many other factors can drive excessive lipolysis including acute/chronic stress, low-carb diets, fasting, intense exercise, etc.
“…Bioactive lipid prostaglandin (PG)E2, produced in adipose tissue, was demonstrated for the first time in the world to promote lipolysis and fibrosis via its receptor EP4 and lead to ectopic fat deposition in the liver, resulting in lifestyle-related diseases such as diabetes. The results of this research project should lead to new preventive and treatment methods for lifestyle-related diseases. This program was implemented with the support of the Advanced Research & Development Programs for Medical Innovation (AMED-CREST) by AMED.”