Category Archives: Grains

Saturated fat, cholesterol, and carbohydrates

“You catch more flies with honey…”

^^^good policy in general, but especially for debating in the realm of nutritional sciences.

 

A short while back, Nina Teicholz discussed low carb ketogenic diets and plant-based diets with John Mackey.  Although I disagree with the dichotomy (keto vs. plant-based), it’s well-worth a watch:

 

 

Three topics that could not be avoided in such a discussion: saturated fat, cholesterol, and carbohydrates.

 

 

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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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OmniCarb

Why Low Carb?

OmniCarb (Sacks et al., 2014)

Study design & results in a nutshell:

5 weeks, low(ish) vs. high carb (40 vs. 58%) with the calorie difference split between protein (23 vs. 16%) and fat (37 vs. 27%).  In other words, the low(ish) carb diet was higher in protein and fat.  And there was 2 versions of each diet —  a high and low glycemic index.  Lots of crossing over; all in all, weak intervention but decent study design & execution.

Aaaand nothing drastic happened.  Goal was insulin sensitivity, not weight loss.

 

glucose and insulin

 

Important points:

1) The participants were relatively healthy at baseline.  Anyone on meds was excluded.  Average BMI 32.  Mostly educated non-smokers.  This population is expected to respond reasonably well to any diet (wrt body weight… see next point).

2) “Calorie intake was adjusted to maintain initial body weight.”

^^^this really knocks the wind out of low carb. One of the big benefits of cutting carbs is spontaneous appetite suppression –- two points here: 1) this effect is most prominent in obese IR; and 2) it is more relevant to weight loss.  By not targeting insulin resistant and/or type 2 diabetics, and feeding specifically to prevent weight loss, I ask you this: Why Low Carb?

3) the biggest difference between the two diets was carbs (45% higher in low[ish] fat group), but the biggest difference from baseline, was protein in the LC group (53% increase).  In other words, the Low Carb group had their carbs decreased from 50 to 40% of calories. *meh*

4) Body composition wasn’t assessed; so even if LCHP induced nutrient partitioning and improved body comp, we wouldn’t know it.

5) Everyone was eating cereal or oatmeal for breakfast, bread with most meals, and pasta or rice for dinner.  What did you expect?  Really?

REALLY?

Prior posts in what seems to be developing into a series of rants:
2 New Diet Studies
CICO and rant 

 

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CICO and rant

“Wait… what?  nutrient partitioning?”

Calories In, Calories Out should not be interpreted as “eat less, move more,” but rather kept in its more meaningless form of: “if you eat less than you expend, you’ll lose weight.”  At least then, it’s correct… meaningless, but correct.  Eating less and moving more is no guarantee of fat loss, in part, because total energy expenditure isn’t constant and there’s that whole thing with nutrient partitioning.

For obese insulin resistant folks, this is Low Carb’s strong suit: it causes “eat less, move more”spontaneously.

For some obese insulin sensitive patients, for whatever reason, their adherence and success is greater with Low Fat.  You might say, “yeah, but those suckers had to count calories.”  To that, I’d counter with: “it doesn’t matter, THEY WERE MORE SUCCESSFUL COUNTING CALORIES ON LOW FAT THAN NOT COUNTING ON LOW CARB.”  The spontaneous reduction in appetite obviously didn’t cut it.  Do not be in denial of these cases.

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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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Mediterranean Diet Fail – Nutrition Disinformation, Part I.

Do not get your hopes up, do not pass GO!  do not collect $200.  The Mediterranean Diet.  Fail.

Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (Estruch et al., 2013)

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.

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Paleotard, meet potatotard, Op. 132

(credit to Dylan and Woo, respectively, for introducing me to those terms)

Empty calories – the potato

While it has a decent amino acid profile, with only 3 grams of protein it’d take a diabetic amount of potatoes to fulfill your daily protein.  By “diabetic,” I mean about a thousand grams of starch.  potatoes are just as glycemic as white bread.

potato

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Fish oil. Pills or directly from the source? Opus 118.

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,

Association between fish consumption, long chain omega 3 fatty acids, and risk of cerebrovascular disease: systematic review and meta-analysis (Chowdhury et al., 2012)

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).

divide and conquer

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Corn. A riddle, wrapped in a mystery, inside an enigma.

Utterly.  Shocked.  is how I feel gazing upon the ingredients listed on one particular popular snack food.  And it isn’t one of those fancy gourmet all-natural whole food snacks, it is a classic that is probably in the kitchen of every child-wielding household.

Corn, corn oil, and salt.  And salt doesn’t even count, so it might just as well have said corn and corn oil, which could be summarized as “corn.”  Ladies and gentlemen, I present to you, the reigning champion of snack food sorcery, the red-headed stepchild (no offense) of international superpower PepsiCo… Fritos.  Using only corn, the wizards of Frito-Lay are turning this:into this:

and that’s without the use of trans fat, gluten, artificial additives, dairy, msg, onions, or soy.  They’re Kosher too.

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