Let me make no bones about it. I’m a fan of Jimmy Moore. Why? It’s very simple. He helps a lot of people and he gets the word out from literally hundreds of others who help people too—both from his blog and podcast (I’ve been a 2-time guest myself). I’m not a perfect as enemy of the good kinda guy…and babies need a good drying off and cuddle after a bath.
I’d go so far as to say that in the early days (2007/8), for me, Jimmy’s podcast was the absolute most varied sources of information on an important health theme that I could find; which, in those days, was primarily focussed on the angelization of saturated fat and cholesterol in the diet as a means of counteracting the CW demonization of same.
Then he embraced Paleo. To me, that meant more, varied information. His podcast became even more interesting and complete. Others saw it differently, but I never gave a care to that. They’re just stoopid and short sighted, worried about what, I have no clue.
At the same time, I have never backed off from stating my disagreements with Jimmy. Done it a few times. Couldn’t take his chocolate cake/protein comparison, so there’s this: “Protein is the New Carbohydrate,” and Why to Ditch the Low-Carb Catechism (Sorry Jimmy). There’s maybe a couple of others—far ‘moore’ where I’ve defended him—but even Jimmy has noted that I never attack him personally. I never will. To me, his accomplishments far outweigh his errors, difficulties and troubles along the way.
I have my own glass house.
OK, so I think he just dismissed the issue of resistant starch out-of-hand, and probably because of the word “starch.” I began a Twitter exchange with him here.
@livinlowcarbman … This one too: bit.ly/18rTyXQ
You can just hit that first tweet link and scan forward for relevant tweets and replies over the next day or so. Some thought I was a bit tough on Jimmy, but they were ignorant of our long history. I respect Jimmy enough to not coddle him. I value his work enough to give it a shot in making him take this seriously.
Basically, what I got back from Jimmy was ‘yea, saw it, interesting, keep it up, etc.’ Dismissal—I know it when I see it. I went at him again, a few hours later.
@livinlowcarbman too many comments to draw attention too, but here’s one bit.ly/IQ3vEg
My story is similar to all of the others. Both the insulin sensitivity and dreams. I had a plate full of mashed potatoes last night for the first time in a long time. My BS never made it above 156. Unbelievable considering a cup of rice would normally send me well above 200. I too have very deep sleep and very vivid dreams. As a bonus I have now had 2 very lucid dreams. If you don’t know about lucid dreams they are a trip. Very fun (for me).
Turns out that really kicked it off. No need to copy it here. Just hit this link and you can see some of the tweet stream. To my point…Jimmy, to me, exposes the ignorance that has caused him, so far, to dismiss resistant starch. In one, he tweets that he ‘doesn’t have a resistant starch deficiency.’ Actually, no human does. It’s resistant to our digestion. It’s the trillions of gut bacteria numbering 10 times the cells in our body—and responsible for all sorts of metabolic, immunologic, inflammatory, auto-immune, hormonal processes and balancing acts of all—that have the deficiency. Moreover, per se and a priori, an Atikns modeled Low Carbohydrate Diet is the most nutrient deficient diet for our gut biome on the entire planet.
This point is inarguable, save perhaps for the Anorexic Diet, or the New Bulimic Discovery. They—our gut bugs—require resistant starches…not just fibers from leaves, flowers, and FODMAPS.
Here’s his tweet that exposed the fact that I was dealing, still, not with disagreement primarily (it’s derivative), but ignorance.
Moore wrong than a very wrong thing
Moreover, this exposes a very deep problem with the Low Carbohydrate advocates in the very general. Let’s flow with the logic.
- Low-carb has proven to be a great intervention for a lot of people generally, and even therapeutically. In realms of neurologic disorders (such a seizures, epilepsy, etc.) and even cancers, ketogenic diets show a low of upside potential. And everyone knows about the weight loss up to the point of stalling 20-40 pounds from goal.
- Atkins was a start, but it was entirely focussed initially on a macro, and not food quality. Hence, all the typical junk food—virtuous only in its lowness in a single evil (carbohydrate).
- Paleo and WAPF influences have had a profound impact on LCers in terms of food quality, and Jimmy has done his part in being nudged that way. Yea, I know: he ought just get all principled and not worry about his house, car, and other payment obligations while nobody sends him checks and only heckles, but I get it. “Idealists” never do. They’re the ones sitting on nice fat trust funds—not Jimmy.
- The gut biome is new science…still, and for a long time to come. Thinking back to 2007-11, metabolism was the whole enchilada. Now, we are discovering that macros are very ugly stepchildren, and that the trillions of critters in our gut constitute complex relationships we are only just now beginning to not begin to understand.
- They share in our food, which affects their antagonism and balance with each other, but they also have their own food. Resistant starch is one that’s exclusively for them. We don’t digest it.
- But resistant starch is largely only found in taboo foods for low carbers. They can supplement, eat tons of grams of RS from potato starch and it won’t even knock them out of ketosis, but it’s from taboo potatoes and other no-nos that violate a catechism of their own choosing.
- They have a serious dilemma. Already, I get the valid argument that supplementing potato starch is to supplement a processed food (it’s very minimally processed, but that’s a different subject). So, just as LCers embrace Real Food—except starchy ones—we come up with a processed supplement that does not affect their LC status at all.
- They are at once in the pickle of re-embarcing something processed, that comes from taboo potatoes or to make it even worse, having to consider dropping strict LC by adopting cooked & cooled rice, beans and potatoes—which are the highest modern dietary sources of resistant starch—though they’re always welcome to chow down on tree bark and cattail pollen, both high in RS, and prevalent in coprolite studies.
- Or, they get to close their eyes, put hands over their ears and yell lalalalala…
- Is that about it?
I got into this with Jimmy not for blog post fodder, though that’s fine and part of the process, but to admonish him to take a very close look. It is not at all that resistant starch is driving this. It’s that science concerning “the other 90% of us” is making us all very ignorant at best, exposing every stupidity, at even better. We simply know that resistant starch feeds the critters, and the evidence is that the beneficial ones feed preferentially and can themselves keep the bad ones in check.
Authorities are going to be kicked in the teeth for years, maybe decades to come over this. My prediction. …They were all looking at human metabolism, organic chemical reactions within a mere microcosm of the whole bio-ecosystem that includes 90% more cells, where they all have unknown chemical and hormonal influence, and where their makeup and balance, one-to-another, is very near incomprehensible.
I daresay that every new discovery and understanding concerning the infinitely complex relationships in our gut sets back our bro-science hubris years, perhaps decades.
I’m certainly humbled, but then I love to be wrong more than I love to be right.
…So next time some authority is waxing on about brain, muscle, organ, bone and other tissue cells and acting as though they have a complete picture, asks yourself if they have accounted for the other trillions of cells with receptors and that “poop” chemicals. Ask them further if they understand that every human is a snowflake, that every gut biome is different.
Then ask them how quickly humans can alter their mix of muscle cells and fibers; say, from slow twitch to fast twitch, etc? Once you get an answer, show them this:
In his latest research, conducted with a team of colleagues and published in Nature, David explored the ways and time frame in which diet might alter the community structure and activity of the microorganisms lingering within our intestinal tracts. This microbial presence is key to human health because it carries out digestive processes that our bodies cannot. […]
The scientists observed that the microbial activity taking place in participants’ guts mirrored differences between herbivorous and carnivorous mammals. For instance, the diet based exclusively on animal products contributed to the most dramatic changes in the bacterial community, inspiring growth of 22 species, among them bile-tolerant microorganisms (Alistipes, Bilophila wadsworthia, and Bacteroides). The animal-based diet also decreased the levels of Firmicutes, including Roseburia, Eubacterium rectale, and Ruminococcus bromii, which are necessary to metabolizing complex carbohydrates typically found in plants. Meanwhile, just three bacterial species came to prominence during the periods participants consumed only plant-based foods.
“In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles,” the authors wrote in their study.
What surprised the researchers most was the speed at which these changes could take place. “The relative abundance of various bacteria species looked like it shifted within a day after the food hit the gut,” David told NPR. Even more, the bacteria started to change their behavior after about three days on each diet. David added, “The kind of genes turned on in the microbes changed in both diets.”
I have the full text and it’s way too much to quote. So here’s the punchline(s).
Our findings that the human gut microbiome can rapidly switch between herbivorous and carnivorous functional profiles may reflect past selective pressures during human evolution. Consumption of animal foods by our ancestors was probably volatile, depending on season and stochastic foraging success, with readily available plant foods offering a fall-back source of calories and nutrients21. Microbial communities that could quickly, and appropriately, shift their functional repertoire in response to diet change would have subsequently enhanced human dietary flexibility. Examples of this flexibility may persist today in the form of the wide diversity of modern human diets11.
But, perhaps a truly omnivorous approach is called for, and I don’t just mean LowCarber leaves and flowers.
Finally, we found that microbiota changes on the animal-based diet could be linked to altered faecal bile acid profiles and the potential for human enteric disease. Recent mouse experiments have shown that high- fat diets lead to increased enteric deoxycholic concentrations (DCA); this secondary bile acid is the product of microbial metabolism and pro- motes liver cancer26. In our study, the animal-based diet significantly increased the levels of faecal DCA (Fig. 5a). Expression of bacterial genes encoding bile salt hydrolases, which are prerequisites for gut microbial production of DCA27, was also significantly higher on the animal-based diet (Fig. 5b). Elevated DCA levels, in turn, may have contributed to the microbial disturbances on the animal-based diet, as this bile acid can inhibit the growth of members of the Bacteroidetes and Firmicutes phyla28.
Mouse models have also provided evidence that inflammatory bowel disease can be caused by B. wadsworthia, a sulphite-reducing bacterium whose production of H2S is thought to inflame intestinal tissue6. Growth of B. wadsworthia is stimulated in mice by select bile acids secreted while consuming saturated fats from milk. Our study provides several lines of evidence confirming that B. wadsworthia growth in humans can also be promoted by a high-fat diet. First, we observed B. wadsworthia to be a major component of the bacterial cluster that increased most while on the animal-based diet (cluster 28; Fig. 2 and Supplementary Table 8). This Bilophila-containing cluster also showed significant positive correlations with both long-term dairy (P , 0.05; Spearman correlation) and baseline saturated fat intake (Supplementary Table 20), supporting the proposed link to milk-associated saturated fats . Second, the animal-based diet led to significantly increased faecal bile acid concentrations (Fig. 5c and Extended Data Fig. 9). Third, we observed significant increases in the abundance of microbial DNA and RNA encoding sulphite reductases on the animal-based diet (Fig. 5d, e). Together, these findings are consistent with the hypothesis that diet- induced changes to the gut microbiota may contribute to the development of inflammatory bowel disease. More broadly, our results emphasize that a more comprehensive understanding of diet-related diseases will benefit from elucidating links between nutritional, biliary and microbial dynamics.
Get that? Butyrate? Eat all the butter you like. It’s not how butyrate ought be formed. The abstract.
INTRODUCTION: Obesity is linked to type 2 diabetes and risk factors associated to the metabolic syndrome. Consumption of dietary fibres has been shown to have positive metabolic health effects, such as by increasing satiety, lowering blood glucose and cholesterol levels. These effects may be associated with short-chain fatty acids (SCFAs), particularly propionic and butyric acids, formed by microbial degradation of dietary fibres in colon, and by their capacity to reduce low-grade inflammation.
OBJECTIVE: To investigate whether dietary fibres, giving rise to different SCFAs, would affect metabolic risk markers in low-fat and high-fat diets using a model with conventional rats for 2, 4 and 6 weeks.
MATERIAL AND METHODS: Conventional rats were administered low-fat or high-fat diets, for 2, 4 or 6 weeks, supplemented with fermentable dietary fibres, giving rise to different SCFA patterns (pectin – acetic acid; guar gum – propionic acid; or a mixture – butyric acid). At the end of each experimental period, liver fat, cholesterol and triglycerides, serum and caecal SCFAs, plasma cholesterol, and inflammatory cytokines were analysed. The caecal microbiota was analysed after 6 weeks.
RESULTS AND DISCUSSION: Fermentable dietary fibre decreased weight gain, liver fat, cholesterol and triglyceride content, and changed the formation of SCFAs. The high-fat diet primarily reduced formation of SCFAs but, after a longer experimental period, the formation of propionic and acetic acids recovered. The concentration of succinic acid in the rats increased in high-fat diets with time, indicating harmful effect of high-fat consumption. The dietary fibre partly counteracted these harmful effects and reduced inflammation. Furthermore, the number of Bacteroides was higher with guar gum, while noticeably that of Akkermansia was highest with the fibre-free diet.
Ok yea, rat study. Not human. Right? Or, was it mostly a gut bacteria study, bacteria we both share? Eh? Eh?
Up for a quickie?
Transferring the gut microbes from a mouse with colon tumors to germ-free mice makes those mice prone to getting tumors as well, according to the results of a study published in mBio®, the online open-access journal of the American Society for Microbiology. The work has implications for human health because it indicates the risk of colorectal cancer may well have a microbial component.
I feel ignorant just when it was all figured out. How about you? How comforting to have it all figured out, but I find ignorance far more exciting. I’m just too curious for my own good and “Paleo” was getting so boring. Yep, nuthin’ wrong with fat, plenty of meat and such. But I find myself with a level of excitement I haven’t had for years. Can you tell?
…I’m reminded of Art De Vany, again. Somewhere along the line he talked about the vast variety of food that was probably consumed. Out of necessity, no doubt. So to me, the question arises: are our gut bugs an evolutionary result of an enormous variety of foods, animal and plant, including tubers, barks, pollen and other things?
…And I prefer this follow-on question to the more obvious one of “have we adapted to them as well”:
Are we dependent upon their wide flourishing, for more optimal health?
If the answer to that is yes, then it basically means that carnivory, low-carb, vegetarianism and veganism are all out the window. But it also means that omnivory must be taken very seriously. Fortunately, it’s not that hard. A good start might be to pick a half dozen different food cultures from around the world and either learn about, source and cook their foods or, if you live in an urban area, eat ethnic almost always when you go out.
…Which reminds me. I haven’t been to that Ethiopian place in a while, had all my food dumped on an injera to eat by hand.
Update: Jimmy has relented. He’s put up a fair and open minded post about resistant starch, opening the door for more of his readers to be exposed to its possibilities: What’s All The Fuss About Resistant Starch?