When animals are fed diets different from what they evolved to eat, they develop metabolic and cardiovascular diseases that do not occur in their natural wild environments.
Mechanism
Synthesis from 2 studies
When animals eat food their bodies weren’t designed for, the good bacteria in their gut get replaced by harmful ones that release toxins. These toxins damage the liver, kidneys, and pancreas, leak into the blood, and cause inflammation that makes the heart thicken and blood sugar rise. The body...
Most probable mechanism
When animals eat food that’s very different from what their bodies evolved to digest, the bacteria in their gut change in harmful ways. Some bad bacteria grow too much and produce toxins that damage the kidneys and liver, while also making it harder for the body to control blood sugar and fat. At the same time, good bacteria that help protect the gut lining and reduce inflammation die off, letting harmful substances leak into the bloodstream. This triggers widespread inflammation, stresses the heart and liver, and causes the body to store more fat and produce too much glucose, leading to diabetes, fatty liver, and heart enlargement.
Consumption of non-native, high-fat, high-sugar diets alters the composition of the gut microbiome, enriching pro-inflammatory bacterial taxa and reducing microbial diversity
Enriched bacterial species produce metabolites such as uremic toxins, acyl-carnitines, and allantoic acid that accumulate in circulation and impair kidney function by reducing tubular reabsorption and inhibiting nitric oxide production
Elevated plasma compounds such as CMPF induce oxidative stress in pancreatic beta cells, reducing insulin secretion and promoting insulin resistance
Disruption of bile acid conjugation increases hepatic lipid accumulation and impairs lipid export, leading to steatosis, inflammation, and fibrosis in the liver
Mitochondrial dysfunction in liver and muscle cells suppresses the tricarboxylic acid cycle, reducing energy production and forcing the body to generate glucose through alternative pathways that elevate blood sugar
Loss of beneficial bacteria reduces production of protective metabolites like conjugated linoleic acids and indole-3-propionate, weakening the intestinal barrier and allowing bacterial endotoxins to enter the bloodstream
Circulating endotoxins trigger chronic low-grade inflammation that activates stress pathways, elevates cortisol, and promotes adipose tissue expansion
Chronic inflammation and metabolic stress suppress proteins critical for maintaining heart muscle structure and signaling, leading to abnormal thickening of the heart walls and reduced contractile efficiency
Evidence from Studies
Supporting (2)
Community contributions welcome
Diet, obesity, and the gut microbiome as determinants modulating metabolic outcomes in a non-human primate model
Contradicting (0)
Community contributions welcome
Gold Standard Evidence Needed
According to GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this specific claim, ordered from strongest to weakest evidence.