95 replies to this topic

[Dorian Grey]

Thank you for this Michael...  I've been taking PPC Lecithin (polyenylphosphatidylcholine) for over half a decade.  Brand names PhosChol and HepatoPro.  I don't know if this qualifies as a "clean" product, but it is advertised as the most highly refined lecithin product available.  

 

http://www.phoschol....about_phoschol/

 

I'd be interested in knowing if anyone had any more info or opinions on this (PPC).  

[Michael]

Thank you for this Michael...  I've been taking PPC Lecithin (polyenylphosphatidylcholine) for over half a decade.  Brand names PhosChol and HepatoPro.  I don't know if this qualifies as a "clean" product, but it is advertised as the most highly refined lecithin product available.  
 
http://www.phoschol....about_phoschol/

 
As far as I can see (here, here, here under "Advanced Technology for Choline Delivery", and at your link in the section "The Gold Standard"), PPC is "refined" to enrich its content of phosphatidylcholine per se over other mixed phospholipids and phosphatide (normal "phosphatidylcholine" supplements are enriched from lecithin to provide 30-35% PC (1200 mg softgel delivering 420 mg PC, usually), and PPC is 94–96% of polyunsaturated PC, about half of which is dilinoleoylphosphatidylcholine, followed by 23-24% palmitoyl-linoleoylphosphatidylcholine. This should give some small advantage by giving less junk to oxidize or feed bacteria, but I don't expect much, particularly since it's encapsulated in a softgel (vs. lecithin granules, which are more exposed to oxygen, more readily contaminated by bacteria, and have a much lower %PC in turn). Not worth the extra $ in my view: both the NutraSal PhosChol and LEF HepatoPro provide 900 mg pure PC, vs. 420 mg in normal PC supplements, but cost many, many times more for a small and hypothetical advantage on the TMA(O) front.

Edited by Michael, 28 September 2014 - 06:22 PM.

[krillin]

What have we decided about alpha-GPC? In rats only low amounts leave via urine or feces - most gets metabolized and the carbon is exhaled as CO2. That could mean that it mostly gets absorbed before reaching the bacteria.

 

Eur J Drug Metab Pharmacokinet. 1993 Apr-Jun;18(2):173-80.

Absorption, tissue distribution and excretion of radiolabelled compounds in rats after administration of [14C]-L-alpha-glycerylphosphorylcholine.

Abbiati G, Fossati T, Lachmann G, Bergamaschi M, Castiglioni C. 

Abstract 

The kinetics and metabolism of L-alpha-glycerylphosphoryl-choline (alpha-GPC) were investigated in male and female rats after i.v. (10 mg/kg) and oral doses (100-300 mg/kg). alpha-GPC was labelled with [14C]-glycerol ([14G]-GPC) or [14C]-choline ([14C]-GPC). Different kinetic and metabolic profiles were observed after i.v. and oral administration. It is assumed that alpha-GPC is hydrolyzed by phosphodiesterases in the gut mucosa. The different labelled metabolites have different kinetic properties of absorption, distribution and clearance, leading to different blood concentration-time curves of total radioactivity. Both labelled compounds gave a wide distribution of radioactivity, particularly concentrated in the liver, kidney, lung and spleen compared to blood. Brain concentrations of [14C]-GPC were comparable to ([14G]-GPC) or lower than ([14C]-GPC) total blood radioactivity. The metabolite profile in the perfused brain showed a small amount of choline and two unknown metabolites, probably the same as in blood. In addition, choline was incorporated into brain phospholipids in increasing amounts within 24 h of dosing. In all cases renal and fecal excretion of radioactivity was low and comparable for [14G]-GPC and [14C]-GPC. Mostly the administered radioactivity was exhaled as 14CO2, this degradation being faster and more pronounced for the glycerol-labelled metabolites than for the choline-labelled metabolites for both routes of administration. In all cases the results were the same for male and female rats. 

PMID: 8243501

[Kevnzworld]

II think that the controversy re: PPC is overrated . The study that krillin posted regarding A-GPC doesn't confirm that, but suggests that, given the low level that was secreted in fecal matter....

Edited by Kevnzworld, 29 September 2014 - 07:04 AM.

[albedo]

Let us also not forget some genotypes related to our choline dietary requirement.....

 

Here looking at rs2236225 or variant 1958A on MTHFD1 shows an increase need of choline vs.people w/o this allele. Looks like men with one or two 1958A alleles need to get about twice as much choline from food as people without this allele:

Genetic variation of folate-mediated one-carbon transfer pathway predicts susceptibility to choline deficiency in humans

 

Here the carriers of two copies of rs7946 variants V175M on PEMT are also about 2x more likely to have NAFLD (nonalcoholic fatty liver disease) than non carriers:

Polymorphism of the PEMT gene and susceptibility to nonalcoholic fatty liver disease (NAFLD).

 

Here also looking at PEMT and rs12325817 increases the probability that carriers might show choline deficiency with a low-choline diet:

Nutritional Genomics: Defining the Dietary Requirement and Effects of Choline

[jwilcox25]

All:
 
A few additional things on this subject: [...]
 
The pop sci article, and the headline & abstract of the report, focus on phosphatidylcholine (which is the form in lecithin and food), but the issue is that a small percentage of dietary or supplemental phosphatidylcholine (PC) can be degraded into free choline, which in turn is metabolized into trimethylamine (TMA) and trimethylamine N-oxide (TMAO). Unsurprisingly, then, taking dietary supplements composed of free choline have been shown in human studies (I've checked the references ((1,3) below)) to spike TMA levels much higher than phosphatidylcholine itself.

There is very little free choline in the diet, and despite this new study, previous reports show that very little naturally-occurring, food-bound PC is converted to choline in a way that leads to formation of TMA/TMAO

...the study in Nature seems to suggest that even in the range present in the population at large, where nearly all choline will come from dietary PC rather than free or PC-bound choline supplements, even the higher end of that much narrower range is enough to increase risk of CVD.

 
I don't understand why PC is better than free choline supplementation.  If the beneficial effects of PC are due to free choline (eg cognitive), wouldn't a lower dose of free choline (resulting in plasma choline concentration equal to the amount resulting from PC supplementation) have the same risk / benefit trade-off as PC?  Or is PC metabolized into free choline in target tissues like the brain in appreciable amounts (as opposed to liver metabolism -> plasma -> target tissue)?

Edited by Michael, 23 April 2017 - 04:19 PM.
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