Anders86
Member
- Joined
- Feb 7, 2017
- Messages
- 355
Uridine is already formed in humans from breakdown of oral CDP-choline. You only need extra uridine (oral - not sublingual - with food and carbs) if you take Alpha-GPC, egg yolks, choline bitartrate or choline citrate and you don't consume milk (source of orotate - uridine precursor) or you have the genetic flaw that prevents uridine production through the orotate pathway (unlikely you have this).
Too much, too high uridine too long can probably cause harm - extremely underresearched substance - so am cautious about it. High blood uridine mimics fasting conditions, although so far (2016) this is basically just correlation.
Traditionally Kennedy pathway - in liver, anyway - is limited by CTP:phosphocholine cytidylyltransferase which is limited by endogenous orotate/Uridine/UMP production, but in other circumstances other variables enter such as DAG abundance.
The main point of my posts was just to point out that PEMT is probably responsible for export of polyunsaturated phospholipids from the liver, while the less stress-related Kennedy pathway should tend to produce Ray Peat approved phospholipids. There is a whole other dimension when it comes to tissue- and organ-specific phospholipid synthesis outside liver.
You probably know of the Mr.Happy stack? Seems like most got mixed results. But I wouldnt be surprised if Mr.Happy is still going strong.