Another “controversial” study, which adds even more evidence to the hypothesis that low-carb diets (and by extension, probably fasting as well) are not that good for our health. Unfortunately, I cannot get access to the full study, but even just the abstract is pretty damning. Namely, ketogenic diet created systemic inflammation, which resulted in impaired gut barrier. It is likely the combination of both those effects that aggravated colitis in the animal model used. Interestingly enough, ketogenic diet decreased levels of saturated fats (SFA), which was probably due to the fact that most commercial high-fat diets available for rodent studies contain predominantly PUFA as lipids. Even though the study does not mention it, the impaired gut barrier is probably the worst effect, since it increases endotoxin/LPS absorption into the blood, which likely created the systemic inflammatory state. Thus, while the study focused only on colitis, this systemic endotoxemia likely resulted in negative effects on many other organs/tissues, with long-term effects far surpassing the relatively localized issue of colitis. In other words, if low-carb diets create systemic endotoxemia and inflammation, one could reasonably say that such diets are probably a causative factor in virtually all chronic conditions known to medicine, since medicine has started to recognize the role of the gut barrier and endotoxin in cardiovascular disease (CVD), obesity, insulin resistance, diabetes (both type I & II), cancer, Alzheimer Disease (AD), Parkinson Disease (PD), depression, psychosis, dementia, etc, etc. Unfortunately, the study findings suggest that the recent push by public health officials to reduce the presence of carbohydrates in the food supply, at the expense of fats, will likely exacerbate public health, instead of improving it.
https://pubmed.ncbi.nlm.nih.gov/34542110/
“…Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease with a high incidence. Multiple factors including dietary composition contribute to its occurrence. Recently, ketogenic diet which consists of a high proportion of fat and low carbohydrates has gained great popularity. Our study is aimed to explore the effect of ketogenic diet on IBD and its potential mechanisms. C57BL/6 mice were given a ketogenic diet or a control diet for a month and IBD was induced by 2% DSS in drinking water in the last week. Gut histology, inflammatory cytokines and chemokines, gut microbiota and metabolism were assessed. Ketogenic diet substantially worsened colitis, in terms of higher body weight loss, DAI scores and histological scores as well as colon length shortening. Levels of serum and colon inflammatory cytokines and chemokines (IL-1α, IL-6, TNF-α, IL-17, GM-CSF and IL-10) were significantly up-regulated in mice treated with ketogenic diet and DSS. Increased intestinal permeability and decreased expressions of intestinal epithelial barrier associated genes were observed due to ketogenic diet administration. Pretreatment with ketogenic diet alters the bacterial abundance, increasing pathogenic taxa such as Proteobacteria, Enterobacteriaceae, Helicobactor and Escherichia-Shigella and decreasing potential beneficial taxa such as Erysipelotrichaceae. Ketogenic diet also modified gut metabolism, increasing metabolites in the bile secretion such as ouabain, taurochenodeoxycholic acid, quinine, cholic acid and glycocholic acid, and decreasing metabolites associated with the biosynthesis of saturated fatty acids including stearic acid, arachidic acid, erucic acid, and docosanoic acid. These results suggest that ketogenic diet aggravates DSS-induced colitis in mice by increasing intestinal and systemic inflammation, and disrupting the intestinal barrier, which results from modulated gut microbiota and metabolism.”
