Category Archives: microbe

Project FermenTRP

People have been fermenting food for a long time, all over the world. Different cultures have different traditional fermenting techniques for various foods and beverages (eg, Bell et al., 2017). Many things, ranging from grapes, milk, and cabbages, even meat and fish. For all intents and purposes, it’s practically universally viewed as a beneficial and healthful practice …

for the ‘biome and beyond

#psychobiotics

 

Maybe it’s just because a robust ‘biome lowers the sugar content of your diet! LOL jk I’m sure it’s far more complex than that.

 

Also, the shelf-life of most ferments is forever, so when the zombie apocalypse happens, it’s a good skill to have.

 

Part 2. Project FermenTRP

I started down this rabbit hole because the TRP theory of muscle cramps is interesting. And, well, I got carried away LOL .

 

The idea of a “superfood” is kinda silly, but virtually all TRP agonists are found in so-called superfoods. Fermenting is cool, too, so I decided to combine the two because why not

 

[I know, I know, photography isn’t my specialty]

 

#torched

 

 

Torching habanero peppers does not lessen the burn. To be honest, I’d go with a WAY less hot pepper. And combine with other TRP activators. For synergy. Or something.

 

 

The TRP-theory, in brief:

An interesting theory on the treatment of muscle cramps

Herbs, spices, TRP receptors, and pain

TRP channels in the treatment of muscle pain & cramps

 

Here are some of the more common sources of TRP agonists in the literature:

Hot Peppers (capsaicin) (doesn’t have to be habanero) (DO NOT USE HABANERO)

Involvement of thermosensitive TRP channels in energy metabolism (Uchida et al., 2017)

Targeting nociceptive TRP channels to treat chronic pain: current state of the field (Moran and Szallasi, 2017)

 

Peppercorns (piperine)

Activation of TRPV1 and TRPA1 by black pepper components (Okumura et al., 2010)

 

Ginger (gingerols)

Effects of ginger and its pungent constituents on transient receptor potential channels (Kim et al., 2016)

 

Garlic (allicins & sulfides)

The pungency of garlic: activation of TRPA1 and TRPV1 in response to allicin (Macpherson et al., 2005)

Diallyl sulfides in garlic activate both TRPA1 and TRPV1 (Koizumi et al., 2009)

Intragastric administration of allyl isothiocyanaate increases carbohydrate oxidation via TRPV1 but not TRPA1 in mice (Mori et al., 2011)

 

Cinnamon (cinnamonaldehyde)

Effects of TRP channel agonist ingestion on metabolism and autonomic nervous system in a randomized clinical trial of healthy subjects (Michlig et al., 2016)

 

Mustard & Wasabi (isothiocyanates, I think)

The capsaicin receptor TRPV1 is a crucial mediator of the noxious effects of mustard oil (Everaerts et al., 2011)

Thermosensitive TRP channels and brain function (Tominaga, 2016)

 

Cloves (eugenol)

Oregano, thyme, and clove-derived flavors and skin sensitizers activate specific TRP channels (Xu et al., 2006)

 

There are many more, but those are just some of the ones that made it to part 3.

 

In brassica, speramus.

 

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calories proper

 

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Hey CICO, I’m playing by your rules.

Brief background: the notorious Ebbeling study of 2012 showed an apparent metabolic advantage of a ketogenic diet.  After losing some weight, participants were assigned to low fat (LF), low GI, or ketogenic diets.  As expected, energy expenditure (EE) declined in all groups after weight loss.

 

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Personalized Nutrition II

More on Zeevi et al. (2015) (this is a follow-up to part 1)

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

 

glucose and fructose

 

Bread:

 

bread

 

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):

 

 

banana and cookie

 

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…

 

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Sweet’n Low

I didn’t want to blog about the artificial sweetener study; to be honest, I didn’t even want to read it.  I just wanted to report: 1) how many Diet Cokes are we talking about; and 2) when are you going to die.

Artificial sweeteners induce glucose intolerance by altering the gut microbiota (Suez et al., 2014)

Non-caloric artificial sweeteners (NAS) = saccharin, sucralose, and aspartame. Saccharin worked the best (worst) in the mouse study, so they tested it in humans.  This was the part I found most relevant: seven healthy volunteers (5 men & 2 women, aged 28-36) who did not typically consume a lot of sweeteners were recruited and given 120 mg saccharin three times per day.  360 mg saccharin is ~10 packets of Sweet’n Low.

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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.

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