If you’re healthy, no major complaints, then you probably won’t benefit from tweaking your ‘biome. Ymmv. But if you’re gonna do it anyway, here are some tips (mostly my opinions).
If you’re healthy, no major complaints, then you probably won’t benefit from tweaking your ‘biome. Ymmv. But if you’re gonna do it anyway, here are some tips (mostly my opinions).
Warning: this post isn’t #Paleo Certified™. It’s more about convenience, choosing the lesser evil.
Quest Nutrition led the charge in low carb, high protein, fibre-rich bars. “Fibre-rich” is really the key in allowing a bona fide “low carb” bar with shelf-stability and decent texture. Sugar alcohols have also been used in some, but due to the high incidence of maltitol-induced GI discomfort, ymmv. But in general, you need one or the other to provide bulk and keep it together (except Epic Bars, which use black magic).
For the most part, the new bars have basically copied Quest’s formula with some new flavors.
Disclaimer #1: I’m a whole foods guy. Not really #Paleo™, but when it comes to people’s actual lifestyles, I recognize convenience is a huge factor… and selecting the lesser evil is frequently the best option — eg, you can store a couple LC protein bars in your office, car, etc.; not so much with hard-boiled eggs or other protein-rich foods… and these options are WAY better than many other snacks or “fast-foods” out there.
Disclaimer #2: yeah, I keep a few of these bars in my office, just in case…
Quest recently switched from isomaltosaccharides to soluble corn fibre (SCF), which will likely impact GI effects. YMMV! Isomaltosaccharides are cool, but I’m not prepared to say they’re superior to SCF for everyone, in every #context (personally, for the ‘biome, I prefer brassicas, alliums, the gristly bits, galactooligosaccharides, et al.).
[it’d awesome if Bi2Muno would collaborate with one of these companies]
In these n00bs to the protein bar market, some of the biggest differentiating factors are cost, net carbs, ratio of fibre to sugar alcohols, flavor profiles, etc.
With no further ado, here are the newcomers:
[or just skip to the chart at the bottom]
I like this study a lot, or at least the fundamentals… or new tools that it might bring to the table. Like, we know sleep and physical activity are important, and we know all calories aren’t created equal. This study is the next level, showing there are even big differences in specific carb-rich foods depending on who’s eating them.
And more interestingly, if I’m interpreting the results of the intervention study correctly (which may not be the case), gut microbial responses to specific foods were very individualized… and predictable!
But first, the main part of the study — standardized meals (after overnight fast): 50g carbs from glucose, white bread, bread and butter, bread and dark chocolate, and fructose. All repeated at least once (except fructose). Everyone responded pretty similarly to fructose (little to no blood glucose spike), but a wide range of responses to glucose.
PPGR = PostPrandial Glucose Response
The range of PPGR to bread was ~15 to 79!
Again, here are some of the findings I found most interesting (besides the huge range in glycemic response to bread):
Participant #468 has a consistently higher response to glucose than to white bread. Participant #663 is the opposite. And participant #445 is still winning.
I truly wonder if there’s a gut microbe (or something) that’s involved here…
There are multiple distinct flavors of diabetes/obesity, as evidenced by the fact that some people have: 1) impaired glucose tolerance (but normal fasting glucose); 2) others have impaired fasting glucose (but normal glucose tolerance); and 3) others have both. This means there isn’t a linear relationship between these phenomena*. There are also: 4) obese patients with normal glucose metabolism; and 5) lean patients with type 2 diabetes.
*I think the great Dr. Kraft may have missed some of the nuances here.
There is not 100% overlap among these, suggesting [confirming] distinct diabetes/obesity phenotypes (and probably causes & best treatments).
“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.
Nuts are good calories.
I’m not a big fan of the omega-6 fatty acid linoleate, but that’s largely in the context of processed foods and confectioneries, where it’s more than likely no longer in it’s native form (Dc9,1218:2n6)… but in the context of unprocessed whole foods (eg, nuts), a little n6 is fine imo.
What are good calories? They’re nutrient-dense and don’t generally lead to overeating… like the opposite of soda and junk food. Nuts are low carb and many are highly ketogenic (eg, Brazils, macadamias, and pecans are ~90%fat). Mr. Ramsey may even approve of macadamias because they have virtually zero PUFAs.
BONUS: magnesium, copper, selenium, many trace minerals and micronutrients, etc., etc.
I’m not saying you should crack open a can of Deluxe Mixed Nuts and sit down with nothing to do other than NOM NOM NOM ALL THE NUTZ. I’m talking about a few nuts with a meal. Possibly earlier in the day (coinciding with LIGHT); nuts are tryptophan-rich and this may improve melatonin onset -> good for circadian rhythms:
In this study, the participants were instructed to eat a serving of almonds (~43g, ~245 kcal) daily for four weeks, at different times of the day (with breakfast, midmorning snack, lunch, or afternoon snack).
Regardless of when the almonds were consumed, the calories were practically completely compensated for. The participants unwittingly ate less other stuff. And in 3 out of 4 of the conditions, the almonds were so satiating that the participants actually ended up eating fewer overall calories.
That, in a nutshell, is what I call “good calories,” and I don’t think it’s too far from Taubes’ original definition… especially because it was accompanied with [modest] reductions in body fat (NS). To be clear, they were instructed to eat more (in the form of almonds), but ended up eating less, BECAUSE ALMONDS. This wasn’t a cross-sectional study, so no healthy user bias or other obvious confounders.
Further, the participants clearly weren’t obesity resistant. They were overweight, obese, or lean with a strong family history of type 2 diabetes. Sam Feltham would’ve been excluded.
This is not an isolated finding: another study showed a dose-dependent response to almonds: 28g or 42g consumed in the morning resulted in a compensatory reduction of hunger and total energy intake at lunch and dinner (Hull et al., 2014). This wouldn’t happen with soda or junk food.
Another study tested ~350 kcal almonds daily for 10 weeks and concluded: “Ten weeks of daily almond consumption did not cause a change in body weight. This was predominantly due to compensation for the energy contained in the almonds through reduced food intake from other sources” (Hollis and Mattes, 2007).
Almonds vs. complex carbs? Almonds, FTW.
1 Brazil nut daily: “After 6 months, improvements in verbal fluency and constructional praxis (two measures of cognitive performance) were significantly greater on the supplemented group when compared with the control group.” ONE FRIGGIN’ NUT!
Pistachios improve metabolic and vascular parameters (Kasliwal et al., 2015).
Meta-analysis (not an intervention study): nut consumption is associated with lower risk of all-cause mortality (Grosso et al., 2015). Yeah yeah yeah, I know, correlation =/= causation. Whatever.
Nuts are good calories. That’s all I’m saying.
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).
So we have three studies on purified “gluten,” asking if it’s the gluten, FODMAPs, or something else in wheaty food that is problematic.
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:
Baseline = low gluten diet
Run-in = low gluten and low FODMAPs
Here’s the fly in the ointment:
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…
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.
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.”
“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.
Affiliate links: still looking for a pair of hot blue blockers? Carbonshade and TrueDark are offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERE. If you have no idea what I’m talking about, read this then this.
If you want the benefits of ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else.
Join Earn.com with this link. Get paid to answer questions!
From what I gather, it’s been difficult to pinpoint the role of plants in the diet of our ancestors for a variety of reasons. For example, evidence of plants on cooking tools and dental remains is suggestive but doesn’t disprove the possibility that said evidence came from preparing the plants for some other purpose (eg, tools, weapons, or medicine), or that the stomach contents of an herbivore was ingested (which gets partial credit).
That said, after reviewing a few studies on the topic (see below), it’s safe to say that plants were eaten, probably frequently, and the types & quantities varied seasonally & geographically. Collectively, the data suggest we aren’t carnivores.
@CaloriesProper I do wonder why there is so much debate around this? Ancient humans ate plants and animals. The end.
— Jamie Scott (@_Jamie_Scott) July 2, 2014
…you had to have something to hold you over until the next fish fell prey to your deadly hunting spear…
From Times LIVE: “Does junk food make you lazy?”
“A diet rich in processed foods and fat – and the extra weight that comes along with it – may actually cause fatigue, a lack of motivation and decreased performance, according to a recent study involving lab rats… excessive consumption of processed and fat-rich foods affects our motivation as well as our overall health.”
(this is categorically false as both diets used in the study being discussed were very low in fat.)
And from Psych Central: “Rat study shows junk food can make you lazy”
The theory itself isn’t too far-fetched: a crap diet can cause weight gain and reduced energy expenditure, or a tendency to minimize any kind of physical activity… instead of: “’laziness’ causes obesity.” And whether or not it’s true, unlike what some would have you believe, this wasn’t the study to prove it.
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.
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.
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.
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).
Collagen (tendons, ligaments, skin, cartilage, bones, etc.)
Rabbit bone, hair, and skin (Chicken McNuggets?)
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:
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.”
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:
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:
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.
Affiliate discounts: if you’re still looking for a pair of hot blue blockers, Carbonshade is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERE. If you have no idea what I’m talking about, read this then this.
For full access to all articles (or if you just like what I do and want to support it), head over to Patreon! Three bucks a month and there are many other options. It’s ad-free and you can cancel if it sucks ????
— Gerard Pinzone (@GerardPinzone) March 26, 2014