My thesis is that if it is, it’s not because of anything Grace Liu of Animal Pharm is feverishly posting, in five parts so far. The time for vitriol and snark is over; so this time, it’s just the facts, ma’am, and you can judge for yourselves.
…I mean, really. If she’d just say, “I don’t recommend PS, I think there are better prebiotics,” then fine. I’d still think it plays a role, but whatever. Chocolate. Vanilla. But this endless cycle of “proof” that “PS is destroying gutz!!!” is quite ridiculous, smelling a lot more like a campaign to discredit those of us who’ve been advocating it than honest, science-based inquiry. Since I’m seeing little in the way of this “doctor’s” conclusions being challenged, I guess it’s time to do so semi-formally.
This addresses just the first part of the last of her posts on the topic: High Dose Potato Starch Can Make You Fatter, Insulin Resistant By Lowering GLP-1 AND ESPECIALLY If You Are Missing Bifidobacteria longum and Akkermansia mucinophila, aka SAD Microbial Fingerprint (Part V) NSFW (December 24, 2014).
First off, she cites Bodinham, 2014 and Table 1. Her take:
The drop in the gut hormone GLP1 was quite significant and was one of the few parameters that met statistically significance in this study.
Optimal gut health is supposed to yield better fat burning, leanness and metabolic improvements, no? Not high dosage RS2 it appears. Why? [emphasis added]
Then she lists everything from Table 1 as “proof” that RS2 is bad vis-a-vis gut health or downstream consequences. The problem is, almost everything on that table is labelled NS, meaning not statistically significant. The few things that are not labelled NS, she misinterprets as BAD!!!
For instance: “OMG GLP-1 decreased!” But what does Bodinham actually say?
Fasting GLP1 concentrations were significantly lower (P=0.049) following HAM-RS2 compared with placebo; however, there was a significantly greater meal GLP1 excursion with HAM-RS2 than with the placebo (P=0.009; Fig. 1C). [emphasis added]
Indeed, GLP1, a well-defined incretin, was found to be elevated postprandially after HAM-RS2 intake, again a finding which was not found in our previous published work in those without diabetes (23) but has been reported in studies of RS in animal models (24). Interestingly, there was no effect of this elevated GLP1 on postprandial insulin levels and so any effect on postprandial glucose disposal may have been through insulin-independent mechanisms. GLP1 has been shown to directly increase muscle glucose uptake in rodent models (25), with the GLP1 receptor recently localized to human skeletal muscle (26). GLP1 acutely raises nitric oxide (NO) levels and so acute changes in both microvascular recruitment (27) and endothelial function (28) at the level of the muscle are believed to be involved in this effect. In the current study, glucose uptake across forearm muscle measured directly using A-V sampling was increased following HAM-RS2 intake and against a background of elevated GLP1 (Fig. 1) [emphasis added]
So, while fasting levels were lower, the after-meal effect was higher. GLP-1 has a half-life of 1-5 minutes in the blood. The lowered fasting GLP-1 is probably a good thing, but seen simply as a curiosity by Bodinham. To make a lesser point, her series is about potato starch, not HAM (high amylose maize RS2).
And just as an aside—a lesson in dishonest manipulation—here’s the line item on pancreatic fat she makes a big—32.5% INCREASED, WTF!?!?!—deal of:
Beyond the fact that the non-significant findings overlap in potential +/-, if you wanted to manipulate someone, would you tell them they were driving 13 in a 10 zone, or that they were breaking the speed limit by over 32%!
But here’s the real kicker…this Bodinham 2014 study was conducted on “well-controlled T2 diabetics.”
In conclusion, this is the first RS feeding study in human T2DM where the metabolic effects of RS (rather than a manipulation of dietary glycemic index/glycemic load (37)) have been investigated. HAM-RS2 intake improved meal glucose tolerance in patients with existing good diabetic-control due to a mechanism which appears to involve increased muscle uptake of FAs and increased S-IMCL. However, as a caveat, changes in both ectopic TG distribution and plasma TG were found, the clinical significance of which is unknown. Further work is now warranted to elucidate the molecular mechanisms within muscle tissue attributable to HAM-RS2, which would be vital in terms of recommending diet/exercise interventions to maximize the benefits for muscle glucose uptake. A larger scale intervention should now be undertaken in patients using high-fiber foods, with less well-controlled diabetes and over a longer time frame before a change to the evidenced-based dietary guidelines could be proposed. [emphasis added]
Bodinham is saying he thinks that RS2 has further improved T2D in these subjects —just like we’ve been saying here for 2 years in over 100 posts—not destroyed them in any way…but there were a few metabolic changes they were not expecting to see. These were not normal, healthy, people…they all had diabetes and were either taking meds (15 out of 17 participants) or being controlled through diet and exercise (2/17):
All participants had well-controlled diabetes (mean HbA1c levels of 46.6 (s.e.m. 2) mmol/mol at screening) and were diet and exercise controlled (2/17), taking metformin (13/17) or metformin and pioglitazone (2/17), were weight stable, and excluded if they had a history of gastrointestinal, cardiovascular, or other endocrine diseases.
OK. Then she invokes an older study, same dude, Bodinham 2012. She does the same thing: takes Table 1 and makes all of the NS items sound like a death sentence. Unfortunately for her, the only thing on Table 1 that was really significant was a reduction in fasting glucose. She explains this is really—trust her—a bad thing. Yes, you’ll read that right:
Fasting glucose THIS TIME decreased BUT that is because all the spikes in post-prandial insulin is shoving all the glucose into adipose cells now and making them fatty which is clear by the increased TG and higher insulin-related consequences: higher systolic and diastolic blood pressures. wtf. I bet it lowered GLP1 where it is already low and lame in overweight and T2 diabetes subjects. [double emphasis added]
What did Bodinham say?
This study was designed to further explore the effects of HAM-RS2 on insulin secretion. To our knowledge this is the first study to demonstrate a significant improvement in first-phase insulin secretion following short-term supplementation with dietary fibre in the form of resistant starch (HAM-RS2). This work adds to our group’s previous findings of a positive effect of HAM-RS2 on insulin sensitivity. [emphasis added]
Let’s take another look at her GLP-1 “theory.” In this 2012 study just cited, Bodinham said:
However, whilst there are data from rodent studies showing increases in GLP-1 following RS intake – data confirming this effect in humans are lacking, and indeed, one study in humans has shown that it may take a year of increased fibre intake (increase of 20 g/day) to increase GLP-1 secretion.
But just 2 years later, in 2014, he did show that RS2 raised postprandial GLP-1 in the human T2D subjects. So, all of this GLP-1 “proof” is completely wrong, and seems intentionally misleading.
Indeed, GLP1, a well-defined incretin, was found to be elevated postprandially after HAM-RS2 intake, again a finding which was not found in our previous published work in those without diabetes… (Bodinham, 2014) [emphasis added]
Yet, here’s what she says says:
What is GLP1?
I love GLP-1.
It helps us to burn and remodel fat. “Glucagon-like peptide 1 (GLP-1), a gut-derived peptide, has been reported to have profound effects on metabolism and to reduce insulin resistance (Yang et al 2013).” High protein diets raise GLP-1 and satiating PYY gut hormones to cause nice fat burning. It appears that high dosage raw starches causes a downward trend of this fat-burning molecule. Ruh-OH. This time it does not depend on either the pre-existing gut or what human gut symbions are missing. It happens in healthy human subjects in several trials so far. [emphasis added]
So, she uses a guy’s study to try and “prove” what’s not proved, implying it’s relevant to healthy people; is going to make them fat, when it actually involved diabetic people and improved their status on balance. Then, she finally acknowledges the diabetic point, but only to make a false distinction in healthy people, claiming results that don’t actually exist.
OK, I think I’ve wasted enough time on this. Really, the whole post is a mess. The links don’t jive with what she’s saying. She’s just making stuff up, as in the foregoing. I suspect that a similar close examination of her Parts 1-4 are going to yield similar poison fruit. And, if you have a good memory, you might even remember when she wrote this in her own comments:
(Akkermansia is good for us 😉 lol unless overgrown in defective barriers
Unfortunately, so very many just read post titles, skim—maybe check a few sycophant comments—and chalk it up to another “excellent post” by the “Gut Goddess” Fake Doctor. In contrast, there are over 130 posts here on RS and GutGeneral, over 10,000 comments, over two years. The positive anecdotes of N=1,000+ are legion.
I can only conclude that she wants to stop or inhibit that for her own selfish gain, because she has statistically insignificant relevance to do with any shred of it. She’s made no long-term meaningful contributions—often inhibiting—but rather, only tried to dishonestly garner an unearned limelight.
Finally, she’s spent five posts on a straw man, because except for diabetics and those who insist on remaining VLC, high dose potato starch was never touted as the be-all-cure-all. Not even from the very first post on RS. I’ve addressed this before.
Now, this simply serves as something linkable next time someone asks me to address her idiotic posts that they don’t want to take the time to examine closely themselves.