Researchers have theorized that the evolutionary pressure from pathogenic gut bacteria has led to the link between SFAs and a prophylactic inflammation: our bodies ramp up a defense response to SFAs because these fats feed harmful bacteria. In contrast, monounsaturated fats (MUFAs) and polyunsaturated fats (PUFAs) are actually antimicrobial.
However, it appears that pathogenic species are not being stimulated directly by dietary fats, but rather by cholesterol in our own bile. This makes sense, because most fats should be absorbed before they reach the large colon, but bile is one of the largest inputs to our large intestines. If this is true, than dietary fats are not the culprit so much as our own bodies' reaction to SFAs.
"Multiple studies have shown that a high fat diet produces low-grade inflammation, which in turn promotes metabolic disease such as diabetes. Interestingly, the low-grade inflammation correlates with circulating levels of a plasma endotoxin known as lipopolysaccharide (LPS). LPS is the primary structural component of the outer membrane of Gram-negative bacteria. Importantly, LPS only originate in the gut."
He concludes that intestinal permeability and the translocation of inflammatory toxins occurs only in the absence of Bifidobacteria, a type of beneficial bacteria found in mother's milk and fermented dairy products. Importantly, stimulation of these species with fiber prebiotics like FOS and inulin has been shown to block inflammation from saturated fats. Indeed, higher dietary intake of fiber has been repeatedly associated with lower markers of inflammation.
Take home message: always eat enough fiber with higher-fat meals.
Even so, the association between saturated fat intake and inflammation has been repeated numerous times. For example, one study of obese women on a high-fat low-carb diet noted 25% increase in C-reactive protein (CRP, a marker of inflammation) compared to a 43 decrease on a low-fat high-carb diet. But when I searched for studies confirming this, I found a 2008 study from the University of Aukland, New Zealand, found that in healthy men, a single high-fat (71% of calories) meal did not lead to changes in tumor necrosis factor-α (TNF-α), and CRP. Also, a 2004 study looking at the acute effect of a high-fat (50% of calories) meal in young healthy men noted no significant changes in CRP.
Jeff Leach at the Human Food Project lays out an interesting theory to explain these divergent results:
Jeff Leach at the Human Food Project lays out an interesting theory to explain these divergent results:
"Multiple studies have shown that a high fat diet produces low-grade inflammation, which in turn promotes metabolic disease such as diabetes. Interestingly, the low-grade inflammation correlates with circulating levels of a plasma endotoxin known as lipopolysaccharide (LPS). LPS is the primary structural component of the outer membrane of Gram-negative bacteria. Importantly, LPS only originate in the gut."
He concludes that intestinal permeability and the translocation of inflammatory toxins occurs only in the absence of Bifidobacteria, a type of beneficial bacteria found in mother's milk and fermented dairy products. Importantly, stimulation of these species with fiber prebiotics like FOS and inulin has been shown to block inflammation from saturated fats. Indeed, higher dietary intake of fiber has been repeatedly associated with lower markers of inflammation.
Take home message: always eat enough fiber with higher-fat meals.
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