 These findings of inflammatory compounds in animal foods and fermented foods therefore suggest that apparently unspoiled foodstuffs may nevertheless contain at some point in their preparation or processing a sufficient microbial load to release endotoxin receptor stimulants into their growth environment. This notion is supported by many previous studies showing that certain commonly consumed foodstuffs can contain a high bacterial load before cooking, such as fresh hamburger, which has often been shown to contain approximately 100 million bacteria per quarter-pounder. Notably, however, the purpose of the present study was not to examine the microbial quality of each foodstuff since the pathogen-associated molecular pattern biological activity is retained independently of bacterial viability or cooking, meaning the bacteria can be dead. The bacteria can be cooked, but their endotoxins are still there. You can boil meat for two hours straight, dip it in an acid bath, like our stomach, and expose it to digestive enzymes. Bacterial endotoxins were found to survive both cooking and our body's best attempts at acid and enzyme digestion. This led them to speculate that the occasional ingestion of meals high in bacterial endotoxins could promote transient mild systemic inflammatory episodes that predispose subjects to the development of atherosclerosis and insulin resistance, which can lead to diabetes. The animal fat may play a profound role in the pathogenesis of this after-meal inflammation by increasing the absorption of the endotoxins. That's where the animal fat comes in, since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the bloodstream. So animal fat may play a role in boosting endotoxin absorption, but the primary reason all those studies show increased inflammation from animal foods, but not from most plant foods, may be the load of dead bacteria in animal products, which release endotoxins that are absorbed into our system, leading to the endotoxic inflammation we see after meat, egg, and dairy consumption as well. So now that we know what's going on, what do we do? From a 2012 follow-up, well, the most obvious solution to this metabolic endotoxemia appears to be to reduce saturated fat intake, which in the US is mostly from cheese and chicken. But the researchers fear the Western diet is not conducive to this mode of action. It's difficult for patients to comply with this request.