Bifidobacteria undoubtedly like resistant starch (RS). They bind and hold on tight, an effect mediated by cell surface proteins. Big thanks to Tim Steele for passing along many of the studies cited here. One of said studies showed that treatment of bifidobacteria with proteases abolished the RS binding; but even dead critters would bind if their cell surface proteins were intact (Crittenden et al., 2007).
I suspect fermented foods have this all figured out. The microbes in sauerkraut are going to be embedded in & all around the cabbage polysaccharides; likely protected from digestive enzymes (to a degree) and holding on tight.
Something similar has been shown for galactooligosaccharides (GOS) (Shoaf et al., 2006). In this study, GOS, but not a variety of other fibres, inhibited the binding of pathogenic gut microbes to intestinal epithelial cells.
These mechanisms are likely not mutually exclusive, and both seem like they could benefit the host (us).
Treatment for dietary protein-induced brain fog: dark chocolate with 3% GOS and 10% MCTs. Who’s in?
#IntermediaryMetabolism (bear with me here)
Ketosis from liver’s perspective: increased fatty acid influx & [partial] oxidation causes acetyl-CoA levels to rise dramatically. Concomitantly, gluconeogenesis redirects oxaloacetate (OAA) away from combining with acetyl-CoA via TCA cycle citrate synthesis and toward gluconeogenesis. Since the acetyl-CoA doesn’t have much OAA with which to couple, it does itself to make acetoacetate. Ergo, ketosis, and fortunately liver lacks ketolytic apparatus.
Brain is singing a different tune. Ketones provide ample acetyl-CoA and are efficiently metabolized in the TCA cycle. Ketolysis is not ketogenesis in reverse, else liver would consume ketones.
Teleologically speaking (and I don’t really know what that word means), ketones are meant to spare glucose for the brain by replacing glucose as a fuel for peripheral tissues like skeletal muscle and displacing some brain glucose utilization. The former is vital as one of the few sources of “new” glucose is skeletal muscle amino acids, and they would be exhausted in a short amount of time if skeletal muscle kept burning glucose –> incompatible with survival. Getting some of that fuel from fatty acids, ie, ketones, is just way better. Thus, the “glucose sparing effect of fat-derived fuel.” And by “glucose,” I mean “muscle;” and by “fat-derived fuel,” I mean “ketones.” There are numerous intracellular signaling events and biochemical pathways pwned, but that’s the gist of it.
This is one of the biggest diet studies we’ve seen in a while, and no doubt it was a very good one. It very effectively put the Mediterranean Diet to the test.
I felt compelled to write about this study out of fear for the nutrition disinformation that it would likely inspire. The Mediterranean Diet is associated with all good things, happiness, red wine and olive oil; whereas the Atkins Diet is associated with artery clogging bacon-wrapped hot dogs and a fat guy who died of a heart attack. Nutrition disinformation.
If you ran a diet study with 3 intervention groups for 5 years, and by the end of the study everybody (in all 3 groups) was on more prescription medications, would you conclude any of the diets were “healthy?” If so, then we should work on your definition of “healthy.”
Study details: big study, lasted roughly 5 years, and the diet intervention was pristine. Mediterranean diet plus extra virgin olive oil (EVOO) vs. Mediterranean diet plus nuts vs. low fat control. They even used biomarkers to confirm olive oil and nut intake (hydroxytyrosol and linoleate, respectively). Compliance was good.
The French Paradox is neither a paradox nor French, really. Red wine isn’t saving the French from a saturated-fat induced heart attack epidemic…. Not to take anything away from red wine, however, as the metabolic effects of red wine (and alcohol in general) are rather interesting.
Background info: alcohol (ethanol) metabolism produces NADH (stick with me here, this article doesn’t get all technical on you I promise).
As a proponent of consuming fatty fish (sardines, salmon, etc.), I was interested to read the new fish oil study; as an opponent of meta-analyses, however, not so much. A meta-analysis is a type of study whereby the researcher thinks of something they want to prove, then cherry picks studies that best support their point. Or perhaps I’m just biased. Nonetheless,
In brief, regarding whole fish consumption, 3 servings per week reduced stroke risk by 6% and 5 servings by 12%. Surprisingly, there was no effect of fish oil pills that contained ~1.8 grams of long chain omega 3 fatty acids. What this study lacks is any information about the dose of EPA and DHA (the major bioactive fatty acids in fatty fish); and with 38 studies analyzed, I’m not about to try to figure it out (sorry team)… a serving of fish can have anywhere from 0 to 1 gram of EPA and DHA; 1.8 grams of long chain omega 3 fatty acids can have anywhere from 0 to 1.8 grams of EPA and DHA. Therefore, I’ll resort to reviewing two of my favorite fish studies of all time: DART and GISSI. For a more detailed review of fish oils and these studies, check out The poor, misunderstood calorie (chapter 9).
In this CROSSOVER study, different doses of coconut flour were incorporated into common test foods to see how they impacted the blood glucose response to said test foods. The total carbohydrate load of each food was 50 grams and to make a long story short, coconut flour dose-dependently reduced the glycemic index.
There’s a lot happening in that figure, but basically the foods with the least coconut flour (e.g., white bread) elicited far greater increases in blood glucose than foods with the most coconut flour (e.g., coconut flour brownies). Mechanistically, this is most likely due to coconut flour’s fiber and/or fat content (both of which slow down glucose absorption and both of which are markedly higher in coconut flour compared than white flour).
Coconut flour: anti-hyperglycemic
the lipid component of coconut flour, coconut oil, is kind-of-amazing in itself.
1) Coconut oil is a perfectly suitable substitute for butter if you’re following a casein-free diet (e.g., GFCF). You don’t need to be a molecular gastronomer or food scientist to try it; refined coconut oil can be used just like butter (“virgin” coconut oil, on the other hand, retains a strong coconut flavor).
2) Coconut oil is rich in the magical ketogenic medium chain fatty acids (e.g., C12 laurate) and to over-simplify a series of very elegant studies on diet and diabetes (detailed in Diet, diabetes, and death [oh my] [highly recommended reading if you’re into fatty acids, etc.]), coconut oil is remarkably protective against diabetic pathophysiology; a property not shared with lard, corn oil, or shortening.
Indirect confirmation of the presence of ketogenic medium chain fatty acids in coconut oil can be seen in this study by Romestaig. Rats fed a diet rich in coconut oil ate more calories but gained less weight than rats fed a high butter or low fat diet:
Coconut oil-fed rats (solid black circles) ate more than the butter group but weighed less. Coconut oil-fed rats ate WAY more than the low fat group but weighed just as much. Nice, huh? Getting back to the point, this is virtually identical to what happens on bona fide ketogenic diets (see Episode 2 of the ketosis series and Ketosis, III), where carbohydrates are kept below 5% of calories (which is phenomenally low, 25 grams on a 2000 kcal diet).
Coconut flour: anti-hyperglycemic Coconut oil: ketogenic
Coconut protein ? … calorie for calorie, coconut flour has more protein than most other flours.
In recent study on diabetic rats, Salil showed that coconut protein completely protected against alloxan-induced diabetes (this study was published in 2011; unlike the earlier studies referenced above, researchers are no longer allowed to give fatal doses of alloxan to rats and count the days until they die. Nowadays they just look at the surrogate marker blood glucose [it goes up very high in diabetes]). Alloxan is a pancreatic toxin which destroys insulin-producing beta cells.
Group 1 (open bar) = controls group. Group II (black bar) = fed coconut protein. Group III (vertical stripes) = diabetic. Group IV (diagonal stripes) = diabetic and fed coconut protein. A diet high in coconut protein made these rats invincible to alloxan… just like coconut oil. Coincidence? (to be continued)
Coconut oil and coconut protein are both present in coconut flour. While it’s not as expensive as almond flour, coconut flour is still pricier than regular white flour. But people love their baked goods, pastas, and breads. If there is ever going to be a way for these foods exit the realm of “empty calories,” the first step is abandoning white flour. Maybe your muffins won’t be so big and fluffy, but neither will your ass.
I heard a comedian say he wished exercise was like high school; once you get your diploma, that’s it. You never need to do high school again. Unfortunately, the same isn’t true with artificial nutrition. the mad food scientists are at it again.
Enter: Soluble corn fiber (SCF), mass produced by MegatronPromitor
Over a decade ago, Atkins released low carb bars. Well, they weren’t actually low carb per se, they were low sugar. This was accomplished by replacing sugar with glycerol (a sugar alcohol) and polydextrose (a pseudo-fiber). While their bars are made from cheap ingredients and low quality protein, sugar alcohols and pseudo-fibers are certainly better than sugar.
More recently, the field took a considerable philosophical leap forward and starting using real fiber, good fiber. Inulin appeared in some Atkins bars, VPX Zero Impact, and the original Quest bars. Quest has since switched to another good fiber, isomalto-oligosaccharides. Unfortunately no one is using GOS, yet, but they will … mark my words (that’s a prediction, or stock tip… not a threat).
But now the field has taken a turn and we have another artificial ingredient, a pseudo-fiber, with which to deal. “Soluble corn fiber (SCF)” first appeared in Splenda Fiber packets and then in Promax LS bars.
If you’re like me, you’re asking yourself: what is this stuff? Is it real fiber? Is it like the super fibers inulin and GOS? Hello Pubmed
Divide and conquer
Stewart (2010) compared SCF to 3 other fibers and maltodextrin, 12 g/d x 2 weeks =
Pullulan, a rather potent fiber, is not well-tolerated. Resistant starch (an insoluble fiber), soluble fiber dextrin, and SCF were all OK. The gut microbiota seemed to have no preference, as short chain fatty acid production was similar in all groups (perhaps 12 grams is subthreshold?). Similarly, health biomarkers, hunger levels, and body weight were unaffected.
Boler (2010) compared a commercially available SCF preparation to polydextrose, 21 grams per day for 21 days in 21 healthy men (cute.)
NFC, no fiber control; PDX, polydextrose; SCF, soluble corn fiber
In this study, however, SCF didn’t do so well. It caused gas and reflux. Perhaps this wasn’t observed in Stewart’s study because of the lower dose (12 vs. 21 grams). Furthermore, polydextrose reduced while SCF increased short chain fatty acid production, both of which resulting in a higher acetate:butyrate ratio. So unlike 12 grams of any of Stewart’s fibers (including SCF), the gut microbiota seems to respond to 21 grams of SCF. And they pooped more (both fiber groups).
This same group reported a more detailed analysis of the gut microbiota which unfortunately did NOT exactly confirm their earlier finding (Hooda et al., 2012):
Data presentation is different in the two publications, and if both are true, then SCF selectively increases a few specific strains of bifidobacteria but reduces many others (enough to increase the total amount but decrease the variety). The functional implications of this are unclear (to me).
In the meantime, SCF appears to be at most an OK pseudo-fiber substitute. Megatron Promitor is not likely to test it against the super fibers (e.g., inulin, GOS, etc.) any time soon, so we won’t know if it’s an advance or simply a side-step. Such is life.