Tag Archives: inulin

Non-celiac gluten sensitivity

Gluten is protein, not carbs.  A gluten-free diet is frequently low-carb, because most dietary gluten comes in the form of bread (and wheaty foods).  But believe it or not, bread is an incredibly complex food… many different proteins, carbohydrates, and nutrients that could be problematic for some people (more on this later).

Gluten is not a FODMAP, but most gluten-containing foods are.  Gluten is actually very rich in the amino acid glutamine.  Gluten, not bread.

So we have three studies on purified “gluten,” asking if it’s the gluten, FODMAPs, or something else in wheaty food that is problematic.

Study #1. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of FODMAPs (Biesiekierski et al., 2013)

Strong study design; patient population was people who thought they were gluten sensitive (but definitely not celiac).

This is the study which led journalists to claim non-celiac gluten sensitivity doesn’t exist, and it’s really sensitivity to FODMAPs, in part, because of this:

 

 

low FODMAPs and gluten free

 

 

Baseline = low gluten diet
Run-in = low gluten and low FODMAPs

 

Here’s the fly in the ointment:

 

symptoms returned in all participants

 

After the run-in period, subjects still followed their gluten-free diets but also received either 16g relatively pure gluten/d (High gluten), 2g gluten + 14g whey protein (Low gluten), or 16g whey protein (placebo).  GI symptoms returned in all participants.  So, low FODMAPs worked for about a week, but then symptoms returned regardless of whether they were eating gluten or not.  In other words, neither low FODMAPs nor low/no gluten worked very well in this study.

But this study may have introduced a brilliant new confounder: food intake was strictly controlled — the experimental diets were different from their normal diets.  Restricting gluten and FODMAPs may have provided some transient benefit, but if the new experimental diet introduced something else that caused problems, then that may explain the gradual return of symptoms…

bollixed?

 

 

Study #2. Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: a Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial (Di Sabatino et al., 2015)

It was another high quality study design: “Randomized, Double-Blind, Placebo-Controlled, Cross-Over.”  And it was addressing a basic question: do people who strongly suspect they have non-celiac gluten sensitivity (NCGS) really have NCGS?  Alternatively, is NCGS real?

Intervention was strong:

1) 4.375 grams of gluten or placebo (rice starch) daily for a week.  This is roughly equivalent to two slices of bread (note: this is way more than enough gluten to destroy the intestines of a patient with bona fide celiac disease).

2) important: they defined the what they would classify as NCGS prior to starting the trial.  A priori.

61 patients strongly suspected of NCGS started the trial, and one withdrew due to gluten-related symptoms in both the gluten and placebo groups.

 

Results:  regardless of whether they were assigned to gluten or placebo FIRST (prior to the crossover), most patients reported gluten-related symptoms.  More importantly, 3 of the 59 patients exhibited significantly worse symptoms on gluten relative to placebo according to the endpoint they defined prior starting the trial.  In one sense, this could be interpreted to mean 5% of people who strongly believe they have NCGS actually have NCGS.

 

gluten sensitive patients

 

Two patients reacted just as selectively strongly to the placebo as the three “real” NCGS patients did to gluten.  Rice-starch sensitivity?

 

See here for a more detailed description of the statistics involved in this study.  I’m willing to accept the “5%” rate, despite the strength of the placebo-responders, whereas the author of that blog post is not.  That’s fair, imo.

And here is another article which questions the legitimacy of NCGS based on this study.  I don’t think that’s totally fair.

And Raphael’s post, where he humorously concludes: “[Gluten-free] does not include advice to sport a gas mask when walking past bakeries.”

 

 

Study #3. Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity (Hollon et al., 2015)

 

 

gluten increases intestinal permeability

 

 

“Delta TEER” is basically the amount of intestinal permeability in intestinal explants exposed to media + gluten (experimental condition) minus those exposed to plain media (control condition).  A better control condition, imo, would’ve been something like they did above: substitute gluten with another protein like whey protein.

 

NC: healthy people
RCD: celiac patients in remission
ACD: celiac patients with active disease
GS: non-celiac gluten sensitivity

 

Active celiac samples responded significantly worse than those in remission, which is good as it functions as a positive control for the experimental protocol.

 

However, gluten sensitive samples responded significantly worse than celiac remission samples; actually, they responded just as badly as celiac samples with active disease.  Celiac disease is supposed to be a million times worse than non-celiac gluten sensitivity… and statistically speaking, even permeability the normal samples declined as much as NCGS samples.

 

This led some to conclude that gluten is bad for EVERYONE.  I’d say it means the assay is bollixed.  Occam’s razor?

 

 

My advice: don’t be anti-science, but don’t use bad science to justify diet choices.  We simply need better studies on non-celiac gluten sensitivity and FODMAPs.

If bread doesn’t work for you, don’t eat bread.  You’re not missing much.

 

calories proper

 

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Animal fibre

Fruits and veggies, fermented or otherwise, aren’t the only source of prebiotics in your diet.  Eat a whole sardine and some of the ligaments, tendons, bones, and cartilage will surely escape digestion to reach the distal intestine where they will be fermented by the resident microbes.  

sardines

Salmon skin and the collagen in its flesh, the tendons that hold rib meat to the bone, and maybe even some of the ligaments between chicken bones.  All of these are potential prebiotics or “animal fibres.”  And it may explain why fermented sausages are such good vessels for probiotics.


 
“Animal prebiotic” may be a more appropriate term because the food matrix is quite different from that of non-digestible plant polysaccharides.  And while I doubt those following carnivorous diets are dining exclusively on steak, these studies suggest it might be particularly important to eat a variety of animal products (as well as greens, nuts, dark chocolate, fermented foods, etc.) in order to optimize gut health.

almonds

These studies are about the prebiotics in a cheetah’s diet.  Cheetah’s are carnivores, and as such, they dine on rabbits, not rabbit food.

cheetah

As somewhat of a proof of concept study, Depauw and colleagues tried fermenting a variety of relatively non-digestible animal parts with cheetah fecal microbes (2012).  Many of the substrates are things that are likely present in our diet (whether we know it or not).

Cartilage

Collagen (tendons, ligaments, skin, cartilage, bones, etc.)

Glucosamine-chondroitin (cartilage)

Glucosamine (chitin from shrimp exoskeleton? exo bars made with cricket flour?)

Rabbit bone, hair, and skin (Chicken McNuggets?)

Depauw ferments

The positive control, fructooligosaccharides (FOS), was clearly the most fermentable substrate; however, glucosamine and chondroitin weren’t too far behind.  Chicken cartilage and collagen were also well above the negative control (cellulose).  Rabbit skin, hair, and bone weren’t particularly good substrates.

As to fermentation products, collagen, glucosamine, and chondroitin were actually on par with FOS in terms of butyrate production:

Depauw SCFAs

Glycosaminoglycans (glucosamine and chondroitin) are found in cartilage and connective tissues (ligaments and tendons) and may have been mediating some of these effects as they’re some of the carbiest parts of animal products.  Duck Dodgers wrote about this in a guest post at FTA and in the comments of Norm Robillard’s article (probably elsewhere, too); very interesting stuff.

The authors also mentioned that the different fermentation rates in the first few hours suggests an adaptive component (some took a while to get going), or that certain substrates induced the proliferation of specific microbes.  “Animal prebiotics.”

Depauw close up

This is particularly noticeable for FOS (solid line), which is a plant fibre that wouldn’t really be present at high levels in a cheetah’s diet, so the microbes necessary to ferment it were probably not very abundant (initially).  Chicken cartilage (long dashes), on the other hand, started immediately rapidly fermenting, perhaps because this is more abundant in the cheetah’s diet.


 
Depauw took this a step further and fed cheetahs either exclusively beef or whole rabbit for a month (2013). Presumably, the beef had much less animal fibre than whole rabbit.  When they initially examined fecal short chain fatty acids, there were no major differences between the groups:

SCFAs per gram

However, if you take into consideration that the whole rabbit-fed cheetahs produced over 50% more crap than meat-fed cheetahs, then some other differences become apparent.  For example, the concentration of total SCFAs is actually greater in the feces from whole rabbit-fed cheetahs:

updated table

edit: la Frite pointed out that the table in the original manuscript is incorrect; the total SCFA numbers are reversed. The excel table above is corrected.

Further, the mere fact that there was 50% more fecal mass per day pretty much confirms way more animal fibre in whole rabbits.  And while neither of these studies were accompanied by microbial analysis, a more recent study on cheetahs fed primarily meat, “randomly interspersed with unsupplemented whole rabbits,” showed low levels of Bacteroidetes and Bifidobacteria, two potentially health-promoting groups of microbes (Becker et al., 2014).  I suspect this may have been at least partially due to a relative lack of animal fibre, compared to the Depauw’s exclusive whole rabbit diet.

Human digestive physiology and gut microbes are certainly far different from that of a cheetah, but maybe we too receive some prebiotic benefits from these animal fibres… just something to think about next time you’re eating sardines or pork ribs.

calories proper

 

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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

Continue reading

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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).

Continue reading

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Protein bar takedown, part III (or V)

No more pretense or cute backstory; I just like reviewing ingredient profiles of protein bars.  It’s a hobby of mine:
Candy in disguise, Op. 73 (circa April 2012)
Decepticon Promicor (soluble corn fiber), Op. 81 (June 2012)
Candy in disguise II, Op. 87 (July 2012)
Protein bar round-up, take II (September 2012)

See?

This is a review of Netrition’s “highest rated” bars.  Important notes about this category: these are not necessarily “new” protein bars, or even the bars everyone buy (“best sellers”).  They are the bars everyone who votes like the most.  They’re not the healthiest either… but some come close.   Continue reading

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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.

calories proper

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Gluten vs. gut bacteria, Op. 78

Whether it is being used to treat Celiac disease, autism, or Paleo-deficiency,  a gluten-free diet (GFD) is probably the most inconvenient diet.  There’s no health risk imposed by recreational gluten avoidance; actually, it might even be healthier.

For example, cereal fibre (aka whole grains) provides the majority of gluten in the Western diet.  I have not been shy about my stance on cereal fibre in the past.  In the seminal DART study (Burr et al., 1989 Lancet), people who were instructed to eat more cereal fibre had a higher mortality rate.  There are definitely many nuances and specifics, etc., yada yada yada, but this finding should be your mind’s pantheon for all-things-gluten.

gravitas

One example of how my brain organizes information:   gluten-free diets include GFCF (duh), Paleo, and Atkins.  The low FODMAPs diet is indirectly gluten-free because cereals and grains are excluded.  N.B. these are all healthy diets… I repeat: GFCF, Paleo, Atkins, and low FODMAPs are all healthy diets.  But don’t take my word for it, Miley Cyrus and Kim Kardashian are also gluten-free (so it MUST be true; there’s no hiding from the Glutenista!).  No grain, no pain!

A downside?  One possible side effect of gluten avoidance is potentially detrimental alterations in gut bacteria.  For example, de Palma and colleagues (2009) showed that a strict GFD significantly reduced bifidobacteria (one of the good guys) in healthy adults.  A GFD is the only clinically effective treatment for Celiac disease, but my gut tells me (no pun intended) that the beneficial effects are not due to reduced bifidobacteria… I’m waiting for a study where a GFD is supplemented with bifidobacteria and inulin/GOS to test this.

On the bright side, the anti-bifido effect of gluten avoidance is not universal.  De Cagno and colleagues (2009) showed that children with Celiac disease have less bifidobacteria in their gut and this is reversed by a GFD (phew!).

gluten - hiding in plain sight... everywhere

Crackpot theory of the week:  could inulin/GOS increase gluten tolerance?  He and colleagues (2008) gave lactose-intolerant patients supplemental bifidobacteria in the form of capsules (1.8×10^9  cfu B. longum) and yogurt (3×10^10 cfu B. animalis) which significantly improved their lactose tolerance (it nearly cured them).  In this study, yogurt provided the prebiotics necessary to ensure survival of the supplemental bifidobacteria.  I imagine inulin or GOS
would’ve had a more profound effect.

Celiac disease, lactose-intolerance, IBS, and veganism are all associated with reduced bifidobacteria and could theoretically benefit from inulin/GOS supplementation.  You could try a diet high in onions, garlic, and breast milk, but cost, availability, and potential for halitosis favor the supplemental route  (finally found a source of high quality GOS).   And it sure as hell beats eating shit.

calories proper

Gluten-free food pyramid

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