PKlopp - A lot of water under the bridge since I wrote the original post. I am even MORE convinced now that everyone needs RS in their diet--whether they take me up on it is of no consequence to me, but I like to keep pointing out current research and letting people make up their own minds. If I ever saw anything that said RS was not recommended, like this from Eades this week, I will post it. But I have yet to see anything that says RS is a bad idea for people, except in the case of GERD sufferers. In the comments from the 'anti-RS' article I just linked, Dr. Eades says:
This is because Dr. Eades was looking at RS in the context of people with gut dysbiosis--not looking at healthy people who want better guts. However, also this week, Dr BG wrote this great piece on RS and gut microbes. where she says:Also, I don’t know enough about resistant starch to make an intelligent comment. And I have no experience with it, personal or otherwise, in the sense your talking about. It seems that I may have written a post on resistant starch years ago, but I don’t believe I was thinking about it then in the way it’s thought of today.
And, I know you love to pick apart studies, but the one you picked apart above concluded this:Diet absolutely shifts bacterial communities in the gut ecology -- simple sugars lowers the good, raises the bad. More fiber and RS both raise the good (in Bacteroidetes -- Prevotella, etc), lowers the bad (in Firmicutes -- virulent strains of clostridas, E. coli's, enterococci, streps). This is borne out in pig, children and human studies. Flint et al do a great review here which includes a raffinose study (fiber from legumes) that enriched and ↑ F. prausnitzii, Bifidobacterium spp. Like many of the good gut flora, Bifidobacter tightens up the intestinal tight junctions as super tight as a nun's **ss, which is enteroproctive and immunoprotective again gastroenteritis, intestinal permeability and necrotizing enterocolitis in trials. Guess what? Magnesium deficiency compromises Bifidobacter and intestinal permeability (or which came first?). Bifido appears to enjoy magnesium. In rodent studies fed a mag-deficient diet, intestinal permeability and quantitative changes to cecal bifidobacteria were associated.
The study kind of defined a bell curve for the dose. Their 5% dose of RS equates to about 10g/day and the 10% dose is 20g/day. Paul Jaminet commented on this study and uses the 10g/day figure repeatedly in his book. Do you have any idea how hard it is to get 10g/day of RS? 1 green banana, 1 cup of cooked/cooled/reheated rice, 1 cup of legumes, not that hard--but you have to actively seek it out. The normal LC Paleo diet with a Big Ass Salad does not provide anywhere near 10g/day unless one really likes eating green bananas every day.This study is the first to identify that addition of 5.4% RS to a single meal can cause a significant increase in total and meal fat oxidation in healthy individuals relative to a 0% RS diet over the postprandial/postabsorptive period (24 h). This discovery was verified using two different methods, indirect calorimetry and the oxidation of [14C]-triolein to 14CO2, to measure in vivo fat oxidation. This increase in fat oxidation was accompanied by a concomitant decrease in carbohydrate oxidation and fat storage, although these parameters did not reach statistical significance. Further, the magnitude of the increase in fat oxidation indicates that this effect is biologically relevant and could be important for preventing fat accumulation in the long term by effecting total fat balance under chronic feeding conditions. Finally, this study revealed that there may be a maximal effect of RS addition to the diet and that the addition of RS over this threshold confers no metabolic benefit or change from a 0% RS meal.
I went to Google Scholar the other day. Searched for Resistant Starch and filtered the results to 2013...care to guess how many new entries from this year? I didn't count, but there were about 20 pages worth. The newest line of study in RS centers on propianate.
In a study titled "Propionate as a health-promoting microbial metabolite in the human gut"
They say of RS:
Another area of new study is centered around 'Regulatory T cells' (Tregs) that are critical for regulating intestinal inflammation.Resistant starch consists of a large number of glucose units linked together by a-(1,4) or a-(1,6) glycosidic
bonds and is resistant to amylase degradation.Depending on the origin of the starch, it is fermented to butyrate48 or
propionate.49 In particular, resistant starch from rice is associated with increased propionate production. Fermentation
of this compound in different proportions was investigated in rats by Cheng and Lai.49 Hepatic triglyceride and total cholesterol concentrations in rats fed rice starch (630 g/kg feed) were found to be significantly lower (1.5 fold) than in the control group without starch. This was in parallel with a significant increase in serum propionate concentration.
In a paper called "The Microbial Metabolites, Short-Chain Fatty Acids, Regulate Colonic Treg Cell Homeostasis" the authors say:
Another paper, titled "Feed Your Tregs More Fiber" says:Gut microbiota–host immune misadaptation has been implicated in the rising incidence of inflammatory bowel disease, other inflammatory diseases, and obesity (22). The Western dietary pattern, specifically reduced ingestion of plantbased fibers and resistant starch, may be a critical factor that links the gut microbiome to disease (23). Although the gut microbiota composition is divergent across individuals, functional gene profiles are quite similar (24, 25), and alterations to common gut microbial metabolic pathways may affect the production of symbiotic factors, such as SCFAs, which regulate intestinal adaptive immune responses and promote health.
So, the zombie apocalypse continues...you got a lot of slaying to do if you want to convince me that RS is an unimportant piece of the puzzle.How can intestinal bacterial communities be exploited to infl uence immune responses
that benefit the host? One approach is to feed specific “substrates” to the host that would
preferentially expand beneficial bacteria—so-called prebiotics.