Tag Archives: microbiota

Gut microbiome & short-chain fatty acids: resistant starch vs. prebiotics

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).

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On resistant starch and blood glucose control

For overall health and well-being, fermented foods like sauerkraut and kefir are great.  Especially when following a low carbohydrate diet which is generally low in the types of foods which feed the gut microbiome.

For those with gastrointestinal problems, the gut microbiota is probably involved.  Whether it is bacterial overgrowth or dysbiosis, gut bugs are usually the culprit.  Treatment options vary widely, ranging from global extermination with vinegar & a low fibre diet (as per Jane Plain), or remodeling the microbiome with a prebiotic like galactooligosaccharides.   Probiotics like bifidobacteria can help, too, if they’re administered with either prebiotics or fermented foods (they need something to nourish them in transit).  Dark chocolate is also an excellent vessel.  Resistant starch is another option, although the question remains as to whether or not this is compatible with a low carbohydrate diet.

Resistant starch has been around for a while, and when I was in school it received about 10 minutes of attention during the fibre lecture.  But Jimmy Moore and Richard Nikolay have been talking about it a lot lately so I decided to freshen up on the topic.  In brief, it can be therapeutic for GI issues, but some studies have shown mixed effects on glucose & insulin metabolism.  The former is virtually unarguable, but I found the latter interesting.  And the impact of resistant starch on ketosis is included as well.

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Impact of a low-carbohydrate, high-fat diet on gut microbiota.

NPR recently reported on a study where the participants ate either a meat-based, fiber-free ketogenic diet or a vegetarian diet and had their gut microflora analyzed.  The low carb diet was much higher in fat, and as such, increased the prevalence of a microbe involved in fat digestion.  “Bilophila.”  The article focused on this one and cited a 2012 study where Bilophila was associated with intestinal inflammation… however, the ketogenic diet increased the levels of Bacteroides and decreased Firmicutes.  These are the two that brought the whole gut microbe-obesity connection into the spotlight.  The microbiome in obese mice is characterized by low Bacteriodetes and high Firmicutes. Fecal transplants from obese mice to lean mice causes them to gain weight.  Little is known about Bilophila relative to Bacteriodetes & Firmicutes, and I suspect the focus was on Bilophila because the authors wanted something negative to say about a meat-based, fiber-free ketogenic diet, and that 2012 mouse study suggested Bilophila could be their answer.

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Ketosis: anti-brain fog. Neurotransmitters, dietary protein, and the gut microbiome.

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.

ketosis

 

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.keto metabolism

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.

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Guts ‘n GOS, Op. 142

Part 1.  Guts

Nice review article about the great diversity of carbohydrate-modified diets used in the treatment of gastroin-testiness.

Short-chain carbohydrates and functional gastrointestinal disorders (Shepherd, Lomer, and Gibson 2013)

this handy table:
handy table

the full version (click to enlarge, print, and use as a cheat sheet):full table

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Non-sequiter nutrition IV. in vino veritas

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).

NADH inhibits gluconeogenesis (Krebs et al., 1969); as such, alcohol lowers blood glucose, regardless of whether if it’s pinot, cabernet, or straight moonshine (Harold  R. Murdock, 1971).

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Almonds: nutrition’s coolest drupe, Op. 89

(it’s a “drupe,” not a nut.  [Thank you Wikipedia.])

Should almonds be upgraded from “snack” to food?  Should almond flour be used in place of some or all white flour?  Yes and yes, IMHO.

In 2007, Josse and colleagues did a quick-and-dirty study on almonds and glucose tolerance.  They fed a group of volunteers 50 grams of carbs from white bread and either 0, 30, 60, or 90 grams of almonds and then measured blood glucose over the following two hours.  “Quick” because they probably had almonds and bread in the refrigerator, and glucometers in their desk drawers; “dirty” because there were a lot of uncontrolled variables; for example: fiber, protein, and fat content of the test meals differed wildly:In a proper study, they might have tried to feed everyone the same amount of fiber, protein, and fat, because each of these is known to affect blood glucose.  In any case, the result was pretty cool:

Whole almonds dose-dependently blunted the blood glucose response to the test meal.  Conclusion: almonds = anti-hyperglycemic.  But almonds are complex lil’ things; they’re made of protein, fat, fiber, and a lot of nutrients; so what’s responsible for all the anti-hyperglycemic effect?  this post is not simply an academic pursuit; indeed, almond flour and almond oil are commercially available, affordable, widely used, and are comprised of different fractions of the almond.  So Mori and colleagues decided to study.

Acute and second-meal effects of almond form in impaired glucose tolerant adults: a randomized crossover trial.  (Mori et al., 2011)

In this excessively high quality study, the effect of 4 different types of almond preparations on glucose tolerance was assessed.

What was tested (in a FIVE-WAY crossover study):
WA = whole almonds
AB = almond butter
AF = defatted almond flour (remember this stuff? lacks all the bifidogenicity of regular almond flour )
AO = almond oil
V = vehicle: negative control.

Basically, the participants were fed a breakfast of OJ and Cream of Wheat with the equivalent of 33 almonds (42.5 grams) for a total of 75 grams of carbs, and blood glucose was measured over the next 2 hours.

Notable nutritional differences between the almond preparations:  they all contain a similar fat content except for the defatted almond flour; whole almonds and almond butter have 2-3 times more fiber than almond flour and almond oil; almond oil has half the protein as all the others.

In brief, no almond preparation affected insulin or free fatty acids.

Whole almonds, almond butter, and almond oil, on the other hand, all blunted the glycemic response.  Defatted almond flour, which only really differs in its lack of almond fat, did not.  Thus, according to last post, almond fat is a potent bifidogen (i.e., good for gut bacteria); and now we see it’s also responsible for the anti-hyperglycemic effect of almonds.  These two effects are probably unrelated, however, as any effect on gut bacteria will take significantly longer than a few hours as the almond fat hasn’t even reached the large intestine by then… (the anti-hyperglycemic effect is evident within 2 hours; the bifidogenic effect noted by Mandalari was 8-24 hours).

OK, almond fat slows the absorption of glucose, so what? this is not exciting… it’s common among most fats- “dietary fat reduces the glycemic index of food.”  But this has a greater implication: one could alternatively conclude that almond flour’s lack of fiber was at fault, as dietary fiber is also known to slow glucose absorption.  However, almond oil, which has even less fiber than defatted almond flour, was also anti-hyperglycemic.  So it’s not the fiber (… perhaps because almond fiber is predominantly insoluble).

With regard to all-things-almonds: almond fat, not almond fiber, is anti-hyperglycemic and bifidogenic (what can’t it do?).

Almond fat: +2

Solution: whole almonds (with meals?), almond oil (with whatever), and regular [non-defatted] almond flour (for baking?).  WRT the latter, get all the benefits, a boost for the gut microbiota, and significantly fewer carbs than with white flour (while actually attenuating the glycemic impact of said white flour).

An argument for almond flour: most baked goods are made with white flour.  These foods are predominantly empty calories, the bane of human health and well-being.  Substituting almond flour for white flour is one way to decrease the emptiness of those calories, and thus of life itself (it’s gluten-free too).

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The day almonds became interesting.

Non-sequiter nutrition: Atwater’s almonds, et al., Op. 87

Almonds have been considered a super-food for as long as I can remember.  And in accord with my level of interest in super-foods, I’ve never cared.  Today, however, almonds became interesting. One small serving of almonds (1 ounce or 28 grams) provide ~171 kilocalories (alternatively, 100 calorie packs have, well, 100 kilocalories).  This measurement of a food’s energy content takes into account the amount of heat produced when it is electrocuted in a bomb calorimeter as well as its digestibility.  The importance of taking both of those things into consideration?  Marshmallows and tree bark produce a lot of heat when they burn.  Unlike marshmallows, however, a tree bark smoothie wouldn’t give us any energy because we can’t digest wood.  This is further complicated because digestibility of a food consumed by itself can differ when it’s eaten with a meal.

Usually, and unlike carbs and protein, the digestibility of fat is impeccably high and unvarying.  Almond oil, however, might be an exception in more ways than one.

Discrepancy between the Atwater factor predicted and empirically measured energy values of almonds in human diets (Novotny et al., 2012)

This was a ridiculously complicated study designed to determine the calories in almonds.  It was a three-way crossover with 18-day feedings of 0, 42, or 84 grams of almonds per day (0, 1.5, or 3 ounces per day).  The researchers gave the volunteers ALL of their food for the entire study, and in exchange, the volunteers gave the researchers the byproducts (urine, feces) for the second half of each feeding period.  This is already an expensive and extremely  labor-intensive study, but I think they were trying to do more than just quantify the calories in almonds; I think they were trying to stick-it-to-the-man.

N.B. the almonds were eaten with normal meals.  The diet was normal.  There are no tricks up my or the researcher’s sleeves.  And I’m honestly fascinated by Table 2.

1.5 servings of almonds (42 grams) had a phenomenal effect on food digestibility.  And 3 servings doubled the amount of non-absorbed calories.  In the beginning of the post I noted that a serving of almonds had 171 kilocalories.  But a serving of almonds increases the non-absorbed kilocalories by about 50.  So does this mean we should re-assign a serving of almonds to 121 kcal?

Yes, the authors decided; and I agree.  And I think this sticks-it-to-the-man.  Perhaps this is the source of almond weight loss lore (?)… imagine the fastidious dieter who weighs out 3 servings of almonds for their daily snack, accounts for the 513 kilocalories in their food diary (but is really only getting 357 kilocalories), and they lose weight…  and those 100 calorie packs only have 68 calories.  Ha!

OK, but just out of curiosity which calories aren’t absorbed?  Are almond calories poorly absorbed, or do almonds block the absorption of other nutrients?

From Table 3, it’s probably fat.  Combined with earlier findings from Ellis, it’s probably almond fat that was trapped inside delicious and crunchy cell walls (Ellis et al., 2004).

In brief, Ellis measured almond fat after three treatments:

1)      Mechanically crushing the almonds

2)      Chewing the almonds (and measuring spit-out almond fat)

3)      Eating the almonds (… and measuring accessible fecal almond fat)

The first two methods didn’t release a lot of almond fat, but the third did, by a little.  As opposed to crushing or chewing, after actual digestion, gut microbes degrade the crunchy cell walls to release the almond fat contained therein.  Unfortunately, however, fat absorption is very inefficient in the large intestine (where this is all happening), which is why the almond fat is either fermented or excreted.

So at this point we’ve got more fat, but also more carbs and fiber from the almond cellular structures making their way into the large intestine (on a high almond diet)… what do the resident microbes have to say about all of this?

A lot, according to a series of studies by Mandalari and his robotic gut simulator  (Mandalari et al., 2008).

Unless you are seriously constipated, the bacterial changes after 24 hours of fermentation are irrelevant.  Looking at 8 hours, which is probably more physiologically relevant, gives us this:FOS, fructooligosaccharides; FG, finely ground almonds; DG, defatted finely ground almonds.

Table 2 (above) is, in a word, perplexing.  Whether or not Mandalari set out to stick-it-to-the-man, he sure did (unless that is just a thing with almonds [?]).  Similar to FOS, almonds had a relatively potent bifidogenic effect.  This is not surprising because of almond’s high fiber content.  What was surprising, however, was that this is completely absent in defatted almonds.  The fiber is the same in almonds and defatted almonds, therefore there is something uniquely magical about almond fat and the long series of unfortunate unlikely events that must occur in order for the bifidogenic effects of almonds to manifest.

The unlikely events: the almond fat must first be protected during chewing and digestion, otherwise it would be absorbed in the small intestine, before it made it all the way to the more “microbial” large intestine.  This is accomplished by almond’s robust cell walls.  Almond fat needs to be released in the large intestine; this requires microbes and is therefore less likely to occur in the small intestine (where microbes are less abundant; if there were more microbes in the small intestine, the almond fat would be released and absorbed before it made it into the large intestine).  The almond fat needs to be not absorbed in the large intestine so it can exert its bifidogenic effect; this happens because the large intestine is inherently poor at fat absorption.  Everything must be exactly in place (kind-of-like in M. Night Shyamalan’s “Signs”): almond’s cellular structure, the intestine’s region-specific digestive enzymes, microbial geography, differential fat absorption capacity, etc., etc.  It’s like an astrological event that occurs once every million years.

***

Back to the Novotny (Atwater) study for a moment.  48 grams (1.5 servings) of almonds only provide about 5 grams of fiber, but it increased stool weight by almost half.  Fiber is known to increase “regularity,” but the effect of almonds is pharmacologically disproportionate to it’s fiber content.

According to a review by Ahmad (2010), almond oil improves bowel transit time and reduces the symptoms of irritable bowel syndrome.  Not whole almonds.  Not almond fiber.  Almond oil.  And injecting it might even cure IBS (don’t try this at home; Sasaki et al., 2004).

Is it time for a paradigm switch?  Will almond oil open the door for other fats to be researched for bona fide prebiotic properties, akin to inulin and GOS?

Indeed, almonds became interesting today.

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