Category Archives: fiber

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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Good calories

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:

 

nuts and melatonin

 

 

Appetitive, dietary, and health effects of almonds consumed with meals or as snacks: a randomized controlled trial (Tan and Mattes, 2013)

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!

 

http://www.dreamstime.com/-image11630100

 

Walnuts protect against alcohol-induced liver damage (in rats) (Bati et al., 2015) and may improve brain health (in humans) (Poulose et al., 2014).

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.

 

Tl;dr: buy these and one of these, not this.

 

 

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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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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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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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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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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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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Protein bar round-up, take II.

The meaning of ingredients, just the facts.

My official statement:  protein bars are not superior to high protein foods like steak or eggs; they’re just incredibly convenient.  For exercisers, it is much easier to snack on a protein bar than a Tupperware bowl full of chicken (on your way TO the gym, that is).  They shouldn’t be relied upon for providing substantial nutrition because, well, they don’t.

That said, while perusing the various categories of protein bars at Bodybuilding.com, I found some big differences between the “best sellers,” “newest,” and “highest rated.”  So which should you buy: what everyone else is buying (best sellers)? the new kids on the block (newest)? or the favorite (highest rated)?

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Coconut flour is a protein & fiber powerhouse, Op. 90

and similar to almond flour, it’s gluten-free and anti-hyperglycemic (i.e., the opposite of white flour).

Glycaemic index of different coconut-flour products in normal and diabetic subjects (Trinidad et al., 2003)

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

Moving on,
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.

calories proper

 

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