Category Archives: liver

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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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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