Important Questions about PUFA: Testing, Exercise and Glucorinidation

[PeatyTheFool]

Hello everyone!

This is my first post so please be gentle.. I've been lurking these forums for a year now and have used many peaty principles to heal most of my issues! PUFA depletion and vitamin E in particular have been really powerful. I started a thread because I feel that there are some aspects of PUFA which are not well explained or maybe just mentioned with no evidence or very little explanation. So I have a few questions here that hopefully could also maybe improve PUFA depletion protocols in the future.

I'll go through every aspect of dietary PUFA: accumulation/testing, consumption, elimination.

Testing
1. So far, what I've understood is that the best measure for PUFA accumulation is the percentage of PUFAs in adipose tissue. Since, most people aren't gonna cut up a piece of their fat to measure their omega 6 this probably isn't a reasonable test for most people. (Please correct me if wrong)
Omega 3 Blood Test: This test for the omega 3 levels in red blood cells, but also tests for plasma linoleic acid levels. Is this useful? Does the linoleic acid level in blood over time give a good indication of PUFA stores or not really?
3. Intraocular Pressure: How accurate is this? Is is affected by other factors and what?
4. Serum Iodine?

I feel like having good testing for PUFA would be sooo useful for running experiments and being able to track improvements and what not..

Consumption/Absorption
Okay so, after consumption, as PUFA gets digested:
1. Gut Bacteria CLA and Hydrogenation: How much of a role does gut bacteria play in metabolising linoleic acid? Are trans-fats produced through gut metabolism safe or even beneficial? It seems that our gut bacteria can even fully hydrogenate linoleic acid to some degree just like ruminants. Is vitamin E required in this process? Can this be exploited to reduce the amount of PUFAS we actually accumulate in our bodies?
2. Is there some compound that would somehow allow PUFAs to pass through the digestive canal without getting absorbed? A bit unlikely I know, but just curious.

Elimination
1. Glucuronidation: First of all, does this actually happen with linoleic acid? What exactly is it? I haven't been able to find much in regards to this online, are there any sources for this? What is the exact pathway? Is this process limited by anything ? I've seen someone mention oleic acid increasing glucoronidation by 8 fold, but I don't see any real discussion on this topic. It seems like it should be something EXTREMELY important. If the body does indeed dispose of PUFAs via glucoronidation and there is a way to increase the rate of it it would be REALLY important to understand!
2. Using PUFA for energy: I've seen mixed ideas on this. In some threads, the body holds on to PUFA and prioritizes burning SFA, in others its the opposite, what's the consensus here? This is also really important to understand because if the body does prioritize burning off PUFA then low intensity activity could be a very good approach towards PUFA depletion.

Looking forward to hearing your answers! Thank you!

 

[WombOfFuturity]

Quick glucuronidation rundown:

What exactly is it?

One of the essential protective functions that decline with aging is the liver's ability to detoxify chemicals, by combining them with glucuronic acid, making them water soluble so that they can be excreted in the urine. The liver (and also the intestine and stomach) efficiently process DHA by glucuronidation (Little, et al., 2002). Oleic acid, one of the fats that we synthesize ourselves, increases (about 8-fold) the activity of the glucuronidation process (Krcmery and Zakim, 1993; Okamura, et al., 2006). However, this system is inhibited by the PUFA, arachidonic acid (Yamashita, et al., 1997), and also by linoleic acid (Tsoutsikos, et al., 2004), in one of the processes that contribute to the accumulation of PUFA with aging.

Fats, functions and malfunctions.

does [glucuronidation] actually happen with linoleic acid?

...several members of UGT1A and UGT2B families are capable of converting LA and AA metabolites into glucuronide derivatives, which is considered an irreversible step to inactivation and elimination of endogenous substances from the body.

Glucuronidation of arachidonic and linoleic acid metabolites by human UDP-glucuronosyltransferases - PubMed

Is this process limited by anything ?

Anything that can impede thyroid or liver function will tend to limit glucuronidation.