There were only two options.
The first was for Tim & I to have our little gig in posts and comments and giggle in emails and keep it cloistered, or just put it out there and see what happens. Obviously we chose the latter. Since it’s gone Plaeoviral, there’s problems.
- Wow, I ate that 30oz porterhouse and I don’t feel so good.
- Wow, a quart of heavy cream per day and I’ve gained weight. Who knew?
- I broke my leg the other day, and it was only a week since I started Paleo/LC.
- I started low carb a week ago and I can’t stop peeing.
- I started low carb a week ago and I’ve lost at least 5 pounds. This is a miracle.
I would have expected Fred Hahn to be better than this, given that LC is a 2-week induction and weeks beyond that, with admonitions every step of the way. But PS is obviously a magic bullet, or it’s shit. Yep, feeding 3 billion year old gut bugs that number 100 trillion with a proven substrate studied over 30 years in numbers of studies that dwarf paleo and low carb studies combined is dismissible in a week, because Fred Farted, and gained 2 pounds, weight he’d scoff at with any LCer, on either side.
Shame, but it is what it is:
Hell, I’m in since April (8 months) and even now doing more experiments with dosing, timing, fasting, etc. I’ve come to control flatulence in curious ways (bolus dosing 2-3 days, zero 2-3 days). I’m a chronic GERD sufferer since a teenager and this has made it better in time. But what does that matter? Low Carb essentially comes from a perch of knowing everything.
“We have no [resistant] starch deficiency.” So saith the Lord; so say we all.
Or, is Fred’s dismissal just an attempt to dismiss PS quickly, because it undercuts the mutherfuck out of LC dogma (the discovery of the import of the gut biome renders all previous pronouncements on metabolism as rather ancient) and puts them in short pants on a bunch of levels? You decide.
Side note: if you do insist on an LC diet qua “healthy lifestyle,” potato starch is ironically your potential salvation. You’re fucking welcome.
Recent stuff that makes a laughing stock of LC ignorance. I get this stuff every fucking day and any full text is but keystrokes away.
~ Microbiota-Generated Metabolites Promote Metabolic Benefits via Gut-Brain Neural Circuits. Published last week.
- Propionate directly initiates portal-brain neural communication
- Butyrate and propionate induce intestinal gluconeogenesis via different mechanisms
- Intestinal gluconeogenesis provides a causal link for benefits of dietary fiber
- Propionate and butyrate positively influence the host metabolism
Eat all the dietary fat you want, but all that above, you need to eat fiber and resistant starch to get, because that’s the way it is. They make it for you.
How many recall back in the early days, the most common Paleo/LC fancy term was gluconeogenesis? It was like, “huck, huck huck; I don’t need no stinkin’ carbs, and I don’t have a starch deficiency; i got gluconeonozgenesezez.”
Now, hear me clearly: they have a new kind of gluconeogenesis to account for and if you do not hold every LC guru to account for this and demand that they explicitly account for it, then you are part of the problem. Study summary.
Soluble dietary fibers promote metabolic benefits on body weight and glucose control, but underlying mechanisms are poorly understood. Recent evidence indicates that intestinal gluconeogenesis (IGN) has beneficial effects on glucose and energy homeostasis. Here, we show that the short-chain fatty acids (SCFAs) propionate and butyrate, which are generated by fermentation of soluble fiber by the gut microbiota, activate IGN via complementary mechanisms. Butyrate activates IGN gene expression through a cAMP-dependent mechanism, while propionate, itself a substrate of IGN, activates IGN gene expression via a gut-brain neural circuit involving the fatty acid receptor FFAR3. The metabolic benefits on body weight and glucose control induced by SCFAs or dietary fiber in normal mice are absent in mice deficient for IGN, despite similar modifications in gut microbiota composition. Thus, the regulation of IGN is necessary for the metabolic benefits associated with SCFAs and soluble fiber. [emphasis added]
I’ll probably get to some other interesting stuff in the study one of these days, unless a low carber, starving of glucose and enamored of all things neo and genesis in the realm, beats me to it. I’m sitting here, holding my breath because I know I’m going to see this on an LC blog any minute now.
~ GPR109a: The Missing Link between Microbiome and Good Health? Published last week.
A complex partnership between the host and the vast intestinal microbial ecosystem serves numerous biological activities including nutrition, immunity, and barrier function. In this issue of Immunity, Singh et al. (2014) demonstrate that microbial-derived butyrate mediated its protective activity against inflammation and colorectal cancer through GPR109a signaling.
Don’t look, low carbers. You need not apply because you don’t need to worry about it. And I’ll tell you why.
Now listen. This means something. Not a single one of your LC gurus has the slightest clue about this (and likely not to this day). They have never told you, never even suggested that it might be of concern. It’s all about carbohydrate, the food of so many who are not you.
That’s forgivable, because this at least is new. Therefore, you should expect them to be telling you that maybe LC might not be the cat’s meow any time, now. I’m holding my breath, again.
Yes, you can shift your gut microbiome (dramatically) with diet in a very, very short period of time. Below is my microbial composition – at the phylum level – after shifting my diet. In short, while maintaining a high fat / protein diet, I simply dropped out the plants and fiber. This, in theory, resulted in less fermentation in my colon which shifted to the pH to be more alkaline. Under these conditions, the genus Bacteroides within the phylum Bacteroidetes, was able to bloom as strains of Bacteroides are pH sensitive and don’t grow as well in acidic conditions created by the productions of short chain fatty acids and organic acids during fermentation of fiber/resistant starch (and fermentation of host-derived substrates. Take home message (IMO): acidity good, blooms of Bacteroides (which is driving the spike in the phylum Bacteroidetes in right-hand side pie), not so good.
He elaborated in a post I highlighted the other day, one that no LC gurus pointed you to because it makes them look, um, primitive.
Commensal gut microflora and dietary fiber protect against colonic inflammation and colon cancer through unknown targets. Butyrate, a bacterial product from fermentation of dietary fiber in the colon, has been implicated in this process. GPR109A (encoded by Niacr1) is a receptor for butyrate in the colon. GPR109A is also a receptor for niacin, which is also produced by gut microbiota and suppresses intestinal inflammation. Here we showed that Gpr109a signaling promoted anti-inflammatory properties in colonic macrophages and dendritic cells and enabled them to induce differentiation of Treg cells and IL-10-producing T cells. Moreover, Gpr109a was essential for butyrate-mediated induction of IL-18 in colonic epithelium. Consequently, Niacr1−/− mice were susceptible to development of colonic inflammation and colon cancer. Niacin, a pharmacological Gpr109a agonist, suppressed colitis and colon cancer in a Gpr109a-dependent manner. Thus, Gpr10a has an essential role in mediating the beneficial effects of gut microbiota and dietary fiber in colon.
~ Diabetes is predominantly an intestinal disease. Published three months ago.
This one bears some extensive fucking quoting.
Diabetes mellitus (DM) is a chronic, progressive, medically incurable disease and is poorly controlled in a vast majority, in spite of tremendous advancements in pharmacotherapy. Altered gut microbiome can predict diabetes. There is strong and consistent evidence regarding role of the gut and many gut hormones like incretins in energy and glucose homeostasis. Incretin group of agents including glucagon-like peptide (GLP-1) receptor agonists and dipeptidyl peptidase IV (DPP-IV) inhibitors are efficacious therapeutic agents in diabetes treatment. A growing body of evidence, however, appears to indicate that type 2 DM (T2DM) may be an operable intestinal illness—a novel revolutionary concept about an old disease. This may facilitate research that can better clarify our understanding of the etiology of the disease and provide a new opportunity to develop new and more effective therapies. Future research should focus on an approach to bypass the bypass, that is, to replace the gastric bypass by equally effective but less invasive treatments for majority of diabetics. [emphasis added]
Did you catch that reference? Well, I’m sure you’ve learned on all your LC forums and diabetes forums that type II is cured in the recovery room after gastric bypass surgery.
Oh, wait. I know: they’re cured in anticipation of a lower carbohydrate intake!
The connection between gut microbiota and energy homeostasis and low-grade inflammation contribute to dysregulation of normal glucose tolerance. In animals models, altered gut microbiota led to development of obesity, insulin resistance, and diabetes by altered fatty acid metabolism in adipose tissue and liver, modulation of gut peptide YY and glucagon-like peptide (GLP)-1 secretion, activation of the lipopolysaccharide toll-like receptor-4 axis, and modulation of intestinal barrier integrity by GLP-2. Gut bacteria were recently proposed to contribute to differences in body weight, insulin sensitivity, glucose metabolism, and other cardiometabolic risk. A recent study by Karlsson et al., found that the gut microbiome with abundance of particular bacterial species in the gut could differentiate diabetic vs normal glucose tolerant individuals with a degree of accuracy similar to that of traditional predictive models. The bacterial species most predictive of T2D was not consistent across different ethnic groups. In mice with substantial changes in their gut microbiome were unable to make fatty acid synthase (FAS) in the intestine developed chronic inflammation in the gut, a powerful predictor of diabetes. People with diabetes also have defects in FAS.
The gut is the most exciting endocrine organ in the body with important neuroendocrine role of the gut in energy homeostasis, a finding consistent with evidence that many gut hormones are involved in glucose homeostasis. Incretins are hormones released from the gut into the bloodstream in response to ingestion of nutrients in the food, and modulate the insulin and glucagon secretory response to food. The incretin effect accounts for at least 50% of the total insulin secreted after oral glucose. Incretin hormones are insulinotropic, that is, they induce insulin secretion at usual physiological concentrations seen in the plasma after food ingestion. [emphasis added]
IT’S THE CARBS!!!!!!!!!!!!!!!!!
IT’S JUST THE CARBS!!!!!!!!!!!!!!
I DONT HAVE A STARCH DEFICIENCY!!!!!!!!!!!!!!!
Or, it’s complicated, and bringing one’s self to task (like I have, over months) involves asking questions.
- Have we accounted for the gut biome of 100 trillion chemical plants?
- How many drugs on the market have accounted for the 100 trillion chemical plants in our gut, and is this what the list of “potential side effects” that would read longer in any commercial than the commercial if read in a normal voice?
- Granting paleo and Low Carb their due, which I do, have they accounted for these 100 trillion chemical plants?
- And if not, it’s OK, because what’s important is who now does take account. Feel free to place a bet on which one will, and which one will struggle to ignore it.
In conclusion, here’s a comment I wrote this morning, and ended up being the motivation to do this post.
That’s interesting. In over 50 posts on RS with thousands of comments, hundreds of positive anecdotes with the principle one being both improved fasting BG as well as lowered spikes, and all I say is:
You might want to give this a try.
Then, some wench comes along, tells us a 3rd party single anecdote and tells you:
This is not for you.
“Wenchypoo” said via a 3rd party anecdote that someone they know got a higher A1C reading after taking PS (plus, with emphasis as though it helps her report, doing some other stuff).
But hell, it’s nothing. Fred, a gym guy, gained 2 pounds in a week. Bet that never happens in gyms, either way. I’ll bet there’s no protocols in gym settings where one looks to see what the diet was, hydration, etc., and what might have changed. And certainly, full results have to be in by a week’s time, just like anything ever done in a gym.
I think someone else said somewhere that somebody got a nosebleed. That one at least makes sense, because obviously, anything adverse that happens to you after the introduction of potato starch, regardless of anything else, it’s the potato starch. Even though: it’s really just food. Here’s Dr. Josh M, PharmD from that link:
We need more studies to be sure, but this is simply food. Not some exotic root extract or untested laboratory compound. This is real food and the easiest way to supplement it is with Bob’s Red Mill Potato Starch. This may be a critical component of the human diet that processed foods leave out.
…I’ve been at this for eight months with as much as 10T potato starch in a day, chased with beans…and only mix it up and eff with it even more, all while I kinda laf at breathless comments: ‘how much should i take?.’ I dunno, man. How many bites should you eat?
Recently, I’ve even incorporated a 100% paleo food: wild, raw honey.
More on that, later. But don’t listen to me. I’m sure all your Low Carb Gurus are going to be taking all of this up any minute, now.
Thankfully, self experimenters are coming out of the woodwork and some even taking up blogging about it. Michael’s link came to me at just the right time.
I’m shocked at the results so far, and yes they are totally anecdotal. Let’s just say that 2013 was not the year of my digestive system. As a result of my diet completely going off the rails, my digestive system really paid the price. Without going into too much detail of my bathroom activities, let’s just say they were often and not-firm. To make matters worse, I came down with the Shigella bacteria after a trip to Mexico in November. Things were very loose and liquid for an extended period of time. Sorry to gross you out.
I’ve been taking potato starch now for 7 days, and as of about 3 days ago, my digestive system feels like a brand new car. I now have a single bowel movement per day, and it’s the kind of movement that you would see in a text book. I can’t remember any point in my life where I have had such a standard excrement.
Well, there’s the downside to potato starch if you must, and I will side with you. Instead of just talking shit, like I do, people want to talk about their shit.