Part 2 of my series on the N=2 will be up early next week. In the meantime, here’s a study, with full text.
M Denise Robertson, Alex S Bickerton, A Louise Dennis, Hubert Vidal, and Keith N Frayn
From the Introduction:
“…Insoluble fibers, such as resistant starch (RS), are nonviscous and thus have no effect on glucose absorption, yet they have been shown in short-term human studies (8) to increase insulin sensitivity. Despite epidemiologic evidence linking insoluble fiber intake to a reduced incidence of type 2 diabetes (9-11), the metabolic link between chronic RS ingestion and insulin sensitivity has yet to be proven in humans.
“One possible mechanism by which dietary RS intake might modulate insulin sensitivity is through alterations in fatty acid flux. Fatty acid metabolism is a key feature in determining tissue insulin sensitivity. Abnormalities in fatty acid storage and lipolysis in insulin-sensitive tissues with increased flux from adipose to nonadipose tissues such as skeletal muscle may be a critical event in the development of insulin resistance (12). The direct effect of RS consumption on fatty acid flux is unknown beyond studies that have measured fasting triacylglycerol and cholesterol concentrations after RS intervention (7). In isolation, short-chain fatty acids (SCFAs), which are produced during colonic fermentation of RS, inhibit adipose tissue lipolysis (13), but an in vivo effect of dietary RS intake has yet to be shown.
“We showed previously that short-term (24 h) high doses of RS (60 g/d) significantly elevate postprandial insulin sensitivity, with lower circulating concentrations of both NEFAs and SCFAs (8). In the present study, we assessed the effect of a more sustainable dose of RS of 30 g/d for 4 wk to allow the assessment of longer-term metabolic adaptation to RS. By using an integrative approach to this nutritional question, we have assessed adaptation to RS intake at the gene-tissue and whole-body levels in humans.”
A few of the charts show pretty stark differences between intervention and placebo. I’ll pick Ghrelin, but you can simply check the paper to see all the other interesting things.
“Mean (±SEM) plasma ghrelin concentrations after a meal tolerance test (dashed line) in healthy subjects after a 4-wk intervention of 30 g resistant starch (RS)/d (○) compared with placebo (•). n = 10. Repeated-measures ANOVA showed a significant effect of the RS intervention (P = 0.027).”
Now, from the Discussion section:
“An interesting observation was the increase in the circulating concentration of total ghrelin after RS supplementation. This result is counterintuitive from what we know about the satiating effects of RS (35, 36) and the appetite-stimulating effects of ghrelin (37). Perhaps the systemic concentration of ghrelin is more relevant in determining its peripheral actions, independent of those induced within the hypothalamus. Elevations in plasma ghrelin have been linked to increased insulin sensitivity in numerous studies (38-40), although debate still exists as to the mechanism. It is hypothesized that the hyperinsulinemia of insulin resistance down-regulates ghrelin release and thus that elevated ghrelin is merely a consequence of the low insulin concentrations. In the present study, fasting ghrelin concentrations were significantly elevated with no significant change in fasting insulin concentrations, and thus it is doubtful that this mechanism is in place. Ghrelin has been shown to inhibit lipolysis, stimulate lipogenesis, and stimulate the expression of peroxisome proliferator activated receptor γ in vitro (41), which potentially influence insulin sensitivity in vivo. The lack of a change in fatty acid uptake into muscle in our study implies that any insulin-sensitizing effects of ghrelin are independent of those induced in adipose tissue. Ghrelin may have direct insulin-sensitizing effects on skeletal muscle. Muscle expresses the putative ghrelin receptor GHS-R1b (42), although a function for this receptor remains to be described. It is perhaps more likely that the skeletal muscle ghrelin receptor is a protein independent of either GHS-R1a or 1b (43), such as the fatty acid translocase protein CD36/FAT, as has been shown in cardiac muscle (44). If elevated plasma ghrelin concentrations are partly responsible for the insulin-sensitizing effects of RS, then the link between fermentation in the colon and ghrelin production from the stomach warrants further investigation.”
…As if life wasn’t complicated enough. You gotta love counterintuitive results like this, though (far higher Ghrelin—”the hunger hormone”—the supposed Yang to Leptin’s Yin—in the face of observed increased satiation under RS supplementation). Just goes to show that while a lot of people know a lot of pieces to the whole puzzle, nobody has even come close to putting the million piece puzzle all together.
More from the Discussion section:
“…In an earlier short-term study (60 g RS for 24 h), we found RS intake to increase insulin sensitivity at the whole-body level and to increase hepatic insulin clearance, a finding that was corroborated in the present study when RS was included in the diet at more physiologic levels (30 g RS/d for 4 wk). We have now shown insulin sensitization at the whole-body level assessed by both the hyperinsulinemic-euglycemic clamp and the MTT methods. In addition, we showed a reduction in adipose tissue lipolysis and an increase in the insulin sensitivity of skeletal muscle glucose clearance. These effects of RS may be due to changes in the peripheral metabolism of SCFAs or in the secretion of ghrelin.”
“In conclusion, RS intake increases insulin sensitivity in non-insulin-resistant subjects by changing both adipose tissue and skeletal muscle metabolism. This is potentially due to elevations in the systemic concentrations of both ghrelin and SCFAs. RS intake at this dose (30 g/d) was well tolerated and thus could have beneficial effects for the treatment of insulin-resistant persons or those with type 2 diabetes. This would require further investigation.”
In my own Conclusion, let’s jump back up to the Results section:
“There was no significant difference in reported food intake between the 2 supplementation periods and no subsequent change in either body weight or BMI. There was a small but significant increase in lean body mass (P = 0.003) averaging 1.1 kg (0.6–1.6 kg) over the 4-wk period of RS supplementation”
Translation: if weight or BMI didn’t change, but lean mass increased to the tune of 2.2 pounds over 4 weeks, then body fat had to have decreased. Now, run that out to several years worth of supplementing resistant starch. A few tablespoons of cheap Bob’s Red Mill Potato Starch just might be your slow, body comp improvement Ace in the Hole.
Leave it to the guy at SupVersity to be on the trail: Fast Absorbed High Molecular Weight Resistant Starches Make a Comeback in Diabetic Formula: Are RS-4 (WM-HDP) Based Products An Ideal Meal Replacement for Diabetics?
He’s talking about more expensive, engineered stuff. Just use the Bob’s Red Mill Potato Starch or get some plantain flour; or tapioca starch will do the trick, too. I like to mix & match, plus eat leftovers cold, including properly prepared beans.
Trust me: this is only going to get worse and worse for LC Starchophobes, who make no critical distinction based on their religious reading of a 6-letter word. …Until they come clean and begin to display some honesty, which I predict will happen, eventually. However, they will have to admit they have been wrong for decades about a lot, which they have been. They should also admit that they’ve been huck-huck obstinate, arrogant and dismissive about it, too. This stuff has been out there for a long time. Completely dismissed, because of a word: STARCH!!!
And so, the reputations of LC advocates have basically taken a big hit with me now, especially in light of out-of-hand dismissals, which I suspect were simply just-so attempts to discount any relevance and benefit, in order to smear good science in favor of catechism and doctrine. I always call it how I see it, and that’s how I see it. Very difficult for me to trust that they are truly looking at stuff with open hearts, minds, and eyes.
But I’m a sucker for redemption, so let’s get on with it.