Category Archives: chocolate

Going Dutch on Dark Chocolate

During the production of dark chocolate, cacao beans are fermented, roasted, and processed into 3 components: chocolate liquorcocoa butter, and cocoa powder.  These are combined in various proportions to make unsweetened chocolate.  Sugar can be added to make dark chocolate, or milk & sugar added for milk chocolate.  White chocolate has no cocoa; it’s essentially cocoa butter, sugar, and milk.

ChocolateManufacturingChart

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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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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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Calories schmalories, alcohol, and chocolate

Some calories count, others don’t.  Some calories work in some people, but not others.  Does this sound like an irrefutable Law of Nature?  No, but it is a perfectly acceptable tenet of the Laws of Energy Balance (a construct of my design).

Do alcohol calories count?  Sometimes, but not this time:

The energy cost of the metabolism of drugs, including ethanol (Pirola & Lieber 1972)

This was a study on bona fide alcoholics who participated because they were promised treatment.  Metabolic ward.  FYI, one gram of alcohol burned in a calorimeter produces ~7.1 kilocalories; alcohol = 7.1 kcal/g.

Calories required to maintain body weight (ie, = total energy expenditure) was assessed the old-fashioned way: feeding them enough calories to maintain a stable body weight – they counted calories but relied on the bathroom scale to establish a baseline.  #TPMC.  After a week of weight stability, they ISOCALORICALLY exchanged carbohydrates for alcohol, and broke CICO.

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All my organs hurt and I think I’m going blind.

People, this is how you should eat.

There have been a lot of diet postings lately, and they are some of the healthiest diets you could imagine.  Please click the links to get the full versions, which include lifestyle tidbits, other pearls, and WHY.  And take notes.  I’ve just listed some of the foods here for the sake of brevity (and as an excuse to link to the diets).

Disclaimer: all of these diets fall somewhere on the “low carb” spectrum.  I don’t eat low carb because I have to*, I do so because it’s healthy, convenient for my lifestyle, and I rather like the foods.  *I say I don’t “have to” because I have no underlying health problems or carb-sensitive GI issues.  The people below are also far healthier than most (from what I can gather)… but if you are overweight &/or obesity-prone, or glucose-intolerant &/or diabetic, then you might want to consider following any of them.

Hyperlipid (Petro Dobromylskyj)The Optimal Diet
butter, egg yolks, cocoa, dark chocolate, macadamia nuts, sour cream, beef, green veggies.  His stats: BW stable, 28” waist, greying beard.  Peter will outlive us all.  And take over the world if he ever has the desire to do so.

Anna Fagan (Lifextension): Low Carb Paleo, probably keto
eggs, butter, avocado, cheese, shrooms, bacon, salmon, tea, coffee, nuts, sardines, lamb, pork, eggplant, cream  –> “high fat =/= fat.”  She’s currently off studying paleoanthropology somewhere in Turkey (?).

Jane Plain (ItsTheWooo): Ketogenic
cream, sour cream, nuts, butter, beef & fatty meats, pepperoni.  She, too, is rather fit.  The Scribble Pad = diet & lifestyle vs. psychoneuroendocrinology & metabolism (mixed with equal parts humor & gravitas).

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Eating in the Absence of Hunger

Hat tip to Jane Plain and her ongoing series on “The physiology of body fat regulation” for citing this study as it provides a rather interesting insight into the psychoendoneuropathophysiology of the obese condition.  Eating in the Absence of Hunger.  

Caloric compensation and eating in the absence of hunger in 5- to 12-y-old weight-discordant siblings (Kral et al., 2012)

They were all full or half, weight-discordant, same-sex siblings and each sibling pair had the same mother; same mitochondrial DNA, shared a womb, etc.

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Pocket Guide to Intermittent Fasting

Intermittent Fasting (IF) is all the rage these days, and there are a variety of different protocols out there, pioneered by people ranging from Ori Hofmekler (The Warrior Diet), Kate Harrison (The 5:2 Diet), Michael Mosley (The Fast Diet), Bert Herring (Fast-5), John Daugirdas (The QOD Diet), and Martin Berkhan (LeanGains), all the way to Jack Kruse (Epi-paleo Rx).  Chances are you’re probably unwittingly already doing one of them, at least intermittently.  The theoretical benefits are seemingly endless (albeit via few human trials), beyond the scope of my brain.

Tl;dr:

Non-IF: grazing; 6-8 meals per day.  Only significantly fasting duration occurs while asleep.
Normal-ish?: 3 squares.  Two 5-hour fasts, then fasting while asleep.
Eat Stop Eat or The 5/2 Bikini Diet: Eat only a small dinner 2 days/wk (600 kcal), eat normally other 5 days.
ADF: Alternate Day Fasting – 75% restriction on day 1; 25% surplus on day 2.
Leangains: Skip breakfast.
The Warrior Diet: Skip breakfast & lunch. (+1)
EOD: eat only Every Other Day.  36 hour fasts – from dinner on day 1 until breakfast on day 3.

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MOA of MCTs – black magic or something less?

MCTs provide a respectable boost in diet-induced thermogenesis (in some studies [eg, Kasai 2002  & Clegg 2012], but not others [Alexandrou 2007]), but I don’t think that’s what does it.

The alternative?  MCTs aren’t “linoleate.” (sorry for lack of suspense)

Alcohol + MCTs vs. corn oil (from Kirpich 2013):

Kirpich

Further, feed rats a diet rich in either coconut oil, olive oil, safflower oil, evening primrose oil, or menhaden oil… and eventually the fat stored in their bodies reflect those fats – eg, linoleate only accumulated in the tissues of those fed safflower & evening primrose oils (Yaqoob 1995) (expect similar results with soybean & corn oils).

Researchers constantly refer to MCTs & coconut oil as “saturated fats,” but I always thought the chain length should be recognized.  Perhaps.  But with regard to certain benefits (eg, hepatoprotection), perhaps not.

Cacao butter has a lot of stearate (a fully saturated 18-carbon fatty acid) but not much linoleate or MCTs.  This linoleate may very well be more of a detriment than stearate or MCTs are a benefit… (with regard to certain benefits [eg, hepatoprotection])Beef and chocolate

(Leslie Roberts, 1988) (she’s talking about stearate)

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Alcohol-proof your liver. SFAs.

it probably has other benefits, too. 

Tissue lipid turnover, adipose vs. liver.

Can the saturated fat & MCTs in dark chocolate & coconut oil protect liver against the ravages of alcohol?  Tonight?

The studies discussed in “The liver is evil but need not be punished.  SFAs”  entailed chronic alcohol feeding in combination with a high saturated fat/MCT diet – the animals were given a liquid diet of complete nutrition and a LOT of booze.   Not very applicable to humans, imo [hopefully].  Which brings up the question: how long does it take for coconut oil & dark chocolate to flex their hepato-protective muscles?

wine and dark chocolate

Fortunately, [if tissue fat composition is in fact the relevant protective factor], unlike adipose fat which hangs around for years (Beynen et al., 1980 & Katan et al., 1997), liver fat appears to turn over quite rapidly.

For example, a single shot of radiolabeled oleate is cleared out of the liver within a few days, whereas it lingers significantly longer in adipose of rats (Iritani et al., 2005).  And this is actually enhanced in rats fed a higher fat diet.fat-free diet

Similarly, a study on diet-induced changes in liver fat in humans showed that after only 3 days of low carb dieting, liver fat significantly declined in 5/10 patients, and in all of them by day 10 (Hollingsworth et al., 2006):liver fat time course

Shoutout to Mike Eades for directing me to this study.  Whatever happens after 3-10 days, I suspect, will reflect the new dietary pattern – you are what you eat?  :/

I don’t put too much stock in generic nutrition textbooks, but those data are rather close to estimates put forth by Frayn, Arner, and Yki-Jarvinen (2006, free full text):Frayn

Translation: while a single meal of dark chocolate and coconut oil may not acutely protect the liver from alcohol [tonight], a few days’ worth just might.

Others?

Red meat.   While the saturated fat content of red meat is expected to similarly bolster liver resistance to oxidative stress, another component – carnitine (of the recent TMAO infamy) – may also provide some benefit by enhancing liver fat turnover (Kepka et al., 2011 sorry no full text, so only in theory).  Taurine, also found in red meat, also prevents some alcohol-induced liver pathologies [in rats] (Kerai et al., 1998 & Pushpakiran et al., 2005).

Coffee, too (Gallus et al., 2002Tverdal et al., 2003; Klatsky et al., 2006; Lopez-Garcia et al., 2008Sugiyama et al., 2010).  Probably has more to do with prevention of lipid peroxidation via antioxidant polyphenols.  just sayin’     …compared to the SFA’ers, would those on a high PUFA diet benefit more from coffee in this regard?

The culprit isn’t red meat or TMAO, its cigarettes & sedentary obese HFCS PUFA empty calories – the bona fide confounding factors in most anti-nutrition propaganda.

 

calories proper

 

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