Why is there an obesity epidemic?

I learned something new this morning. The ratio of people who are overweight or obese has been steadily rising for over 50 years. This is not a phenonema limited to North America. It is a pandemic affecting 1/3 of the world's population. It isn't affecting just humans though. A similar pattern of metabolic disease or fatty liver disease has also been seen in dolphins!

Ask yourself a question. Why is this happening across humans worldwide but also across mammalian species? Is it a chemical in the environment or is the a organic reason for this. This video discusses one of the solutions to the obesithy issue: supplementation of C15 fatty acid. C15 fatty acids are found in dairy products and ruminant meat. It can also be found in fatty fish such as sardines, mackeral and salmon. Obviously there are not many dolphins milking dairy cows so this is the likely source of C15 for dolphins.

There is an interesting side-note to this story. While C15 fatty acid helps in reducing fatty liver disease, C16 has the opposite affect. Since the ratio of C16 to C15 is over 400 to 1 in fish sources and over 40 to 1 in dairy sources, sometimes eating those sources can have a reverse effect. I can exacerbate fatty liver disease and Type 2 Diabetes. This raises the quesstion WHY?!

Are there diseases that are common between Dolphins and Humans. Surprisingly, dolphins and humans can both develop stomach ulcers. The bacteria that causes ulcers in dolphins - Helicobacter cetorum is closely related to Helicobacter Pylori - the bacteria responsible for ulcers in humans. The story doesn't end there. Supplementation with C15 is treating a symptom. It is necessary to dive deeper to understand what H Pylori is doing.

As fatty acids are used and metabolized, they lose two Carbon atoms. C15 become C13, C11, etc. until it reaches C3 Fatty acid. According to Grok AI. NAFLD is Non-alcoholic Fatty liver disease.

Animal Studies: Research in rodent models of NAFLD has shown that propionate supplementation reduces liver fat content, improves insulin sensitivity, and lowers inflammatory markers.

H Pylori increases the multiple routes. Once again Grok describes the following:

H. pylori infection promotes insulin resistance, a key driver of NAFLD, by increasing pro-inflammatory cytokines (e.g., TNF-α, IL-6) and altering adipokine levels (e.g., reduced adiponectin, increased leptin). Insulin resistance enhances hepatic lipogenesis and fat accumulation, contributing to steatosis.

In conclusion, while supplementing the diet with C15 fatty acids will treat a symptom of fatty liver disease we need to investigate and cure the root cause.