Posted by Trotter on December 27, 2012, at 17:15:41
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by larryhoover on December 27, 2012, at 16:59:24
> The studies I first referenced make clear that the inflammatory markers are not caused by high fat intake, but arise from refined carbs. Recent work has broken the confound.
>This review highlights the inflammatory and insulin-antagonizing effects of saturated fatty acids (SFA), which contribute to the development of metabolic syndrome.
Several studies have demonstrated potential health benefits of substituting SFA with unsaturated FA, particularly oleic acid and (n-3) FA. Thus, reducing consumption of foods rich in SFA and increasing consumption of whole grains, fruits, vegetables, lean meats and poultry, fish, low-fat dairy products, and oils containing oleic acid or (n-3) FA is likely to reduce the incidence of metabolic disease.
http://www.ncbi.nlm.nih.gov/pubmed/19056664
"Conventionally raised specific-pathogen free (CONV) and germ-free (GF) mice were given HF or low fat (LF) diet for 216 weeks. Body weight and adiposity were measured. In CONV but not GF mice, HF diet induced increases in body weight and adiposity."
"Bacteria and HF diet interact to promote proinflammatory changes in the small intestine, which precede weight gain and obesity and show strong and significant associations with progression of obesity and development of insulin resistance. To our knowledge, this is the first evidence that intestinal inflammation is an early consequence of HF diet which may contribute to obesity and associated insulin resistance. Interventions which limit intestinal inflammation induced by HF diet and bacteria may protect against obesity and insulin resistance."
"Clearly the bowel bacteria have a role to play in increasing inflammation with a high fat diet. The implication is that it is the high fat diets affect on the bacteria that causes inflammation and subsequent depression, not the high fat diet itself. If I can maintain bifidobacteria numbers I may be able to avoid any inflammation from a high fat diet."
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012191
C57BL/6J and TLR4-deficient C57BL/10ScNJ mice were maintained on a low-fat (10 kcal % fat) diet (LFD) or a highfat (60 kcal % fat) diet (HFD) for 8 weeks.
HFD induced macrophage infiltration and inflammation in the adipose tissue, as well as an increase in the circulating proinflammatory cytokines. Furthermore, HFD induced colonic inflammation, including the increased expression of proinflammatory cytokines, the induction of Toll-like receptor 4 (TLR4), iNOS, COX-2, and the activation of NF-κB in the colon.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047713
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