PC choline to stabilize membranes

LucH

PC choline as a missing link to stabilize or improve membrane integrity (AA cascade) which leads to inflammation.
Situation
How can we limit the absorption of PUFAs when consuming 6 to 10 g of omega-6, while our needs are only 1 to 2%? This is not about the standard American diet, which often contains 20% of PUFAs from lipids (corn and soy). It's a rhetorical question.
Thus, for 2,000 kcal, 1 to 2% corresponds to between 20 and 40 kcal, or approximately between 2 and 4.5 g of PUFAs. Ultimately, we cannot simply "burn bad fats" the day after consuming them. They remain in the body and influence inflammatory markers for years. Indeed, even though we preferentially burn fatty acids stored in adipocytes (C16:0), ultimately, 19 to 24% of the fatty acids stored in adipose tissue are in this form. Studies show that saturated and monounsaturated fatty acids (such as C16) or oleic acid (C9) are preferred substrates for beta-oxidation, compared to polyunsaturated fatty acids. (1-3) This is why a small amount of "bad" fats is more harmful in the long run than a large amount of "good" fats. I know this, even though I try to guide my intake. Bad because it's very unstable and often consumed in excess. I often say that we are surrounded by omega-6s in conventional diets if we're not careful…
I also know that the omega-3/omega-6 ratio is much more important than the quantity, to a certain extent, but if we ingest, say, 10g of omega-6, we store the rest in adipose tissue until we are subjected to stress or injury (AA cascade).
Tactics
Therefore, we will not simply act after the fact, trying to calm pro-inflammatory prostaglandins (PGE-2) with phytonutrients such as curcumin, white willow (salicin), or EPA. We will attempt to act downstream rather than upstream, by trying to strengthen the integrity of the body's internal environment, namely its membranes.

Sources and References

Fatty acid preference for beta-oxidation in mitochondria of murine cultured astrocytes
https://doi.org/10.1111/gtc.13144
Calculation of triglyceride composition in human adipose tissue
doi: 10.1194/jlr.D800010-JLR200 J Lipid Res. 2008.
Human adipose tissue is composed largely of triglycerides. Seven fatty acids predominate as follows (number of carbons:number of double bonds, typical abundance): myristic (14:0, 3%), palmitic (16:0, 19–24%), palmitoleic (16:1, 6–7%), stearic (18:0, 3–6%), oleic (18:1, 45–50%), linoleic (18:2, 13–15%), and linolenic (18:3, 1–2%) (22, 23). These fatty acids account for well over 90% of the fatty acids in human adipose tissue.
Beta-Oxidation: Palmitic Acid as a Source of ATP (preferably stored form in adipocytes)
https://www.metwarebio.com/palmitic-acid-health-diet-metabolism/#:~:text=In adipose (fat) tissue%2C,to be used as fuel.
Palmitic acid is also a critical component of phospholipids, which are the main structural molecules that make up cell membranes.
Figure: Membranes protected by Vitamin E, beta-carotene, astaxanthin and Vitamin C

LucH

Lipid Protection
We already know that vitamin E (tocopherol mix, with gamma-tocotrienols), beta-carotene (via diet), and astaxanthin are frequently cited for counteracting ROS (reactive oxygen species scavenger effect). And more generally, an intake of vitamin C, magnesium, zinc, and selenium (GPx enzyme) is also recommended.
Last but not least, it is essential to maintain the lipid bilayer composed of phosphatidylcholine (PC).

Magnesium acts as a moderator (inhibitor) of PLA2. PLA2 is the enzyme that releases arachidonic acid (a pro-inflammatory precursor) from cell membranes (AA cascade).
Mg2⁺ stabilizes the phospholipid bilayers, reduces the activation of calcium-dependent PLA₂, and decreases eicosanoid production. 350-420 mg/day of elemental magnesium.
=> Magnesium bisglycinate. 2.5 g/day, divided into 2 or 3 doses. To reach 450 mg. More, in case of stress (after the event; do not anticipate stress in case of "upset"; otherwise, it is not appropriate).
Selenium, to ensure that the GPx4 enzyme can repair any lipid oxidation that occurs. (GPx4 = glutathione peroxidase 4). GPx4 specifically degrades lipid hydroperoxides in membranes, thus maintaining redox homeostasis.
100 mcg 2 to 3 times/week. More frequently if inflammation is present. Double the dose if detoxifying ML.
Note: More is not better. Actual needs are met. An overdose can cause fatigue and systemic problems, as the residues lead to an overload of the liver and kidneys (neutralization and elimination).
Tocos Mix (with Gamma): To act as a bodyguard for fat-soluble molecules. 400 IU tocos mix (with gamma tocotrienols) 2 to 3 times per week. Or 20-25 mg per day.
Note: More is not better, here too.
Zinc: Zinc stabilizes membranes by protecting thiols, inhibits lipid peroxidation induced by NADPH oxidase, indirectly limiting the arachidonic acid cascade. 10-15 mg/day.
Key refs:
• Prasad, Am J Clin Nutr, 2009 – zinc, oxidative stress, inflammation
• Ho et al., Free Radic Biol Med, 2008 – Zn and membrane oxidative stability
Mechanistically: ↓ membrane peroxidation → ↓ PLA₂ activation → ↓ free AA → ↓ PGE₂, independent of COX inhibition.
Stearic acid: Consider adding a source of stearic acid (such as cocoa butter) to "solidify" the membranes (balance between fluidity and structure).

Phosphatidylcholine (PC)
Function of PC Choline
Phosphatidylcholine (PC) is the main structural phospholipid of membranes, generally constituting 40 to 60% of the phospholipid composition, with a particularly high concentration in the outer (exoplasmic) membrane. Its fundamental role is to maintain the structural integrity, fluidity, and functionality of membranes, acting as a molecular buffer that allows the membrane to fold without rupturing.
=> Integrity, fluidity, maintenance (repair), protection (surfactant, hydrophobic agent)
PC vs. Choline
Although choline is the essential nutrient, the phosphatidylcholine (PC) form is more effective for direct membrane repair because it is already integrated into a phospholipid structure. Choline bitartrate could be only about 30% bioavailable (metabolized in the intestine into trimethylamine (TMA) by the microbiota, depending on the dose).

PC choline as a missing link in stabilizing or improving membrane integrity (AA cascade) that leads to inflammation
Phosphatidylcholine (PC), often called PC choline, plays a crucial role as a "missing link" in stabilizing and improving the integrity of cell membranes, notably by regulating the arachidonic acid (AA) cascade that leads to inflammation.
Here's how PC acts as a stabilizing element in this context:
1. PC as a Reservoir and Membrane Stabilizer
• Major Composition: PC is the most abundant phospholipid in mammalian cell membranes (40–50% of the total). It is essential for membrane fluidity, structure, and permeability.
• Membrane Repair: PC provides structural building blocks that maintain membrane integrity. A PC deficiency can weaken the membrane, making it more susceptible to degradation.
• Arachidonic Acid (AA) Control: Arachidonic acid (AA), a precursor of inflammation, is stored in the membrane, often bound to phosphatidylcholine (AA-PC). Ensuring sufficient PC levels stabilizes membranes, preventing excessive AA release.
2. PC and the Arachidonic Acid (AA) Cascade
• The Release Link: During inflammation or injury, the enzyme phospholipase A2 (PLA2) hydrolyzes PC to release arachidonic acid, which is then converted into inflammatory mediators (prostaglandins, leukotrienes).
• Modulation of the Cascade: PC acts as a buffer. If the membrane is rich in healthy PC, it can better manage lipid remodeling. Conversely, degradation of membrane PC activates the AA cascade, leading to pain and inflammatory responses (e.g., neuropathic pain).
• Effect of Lysophosphatidylcholine (LPC): When PC is degraded by PLA2, it forms lysophosphatidylcholine (LPC). It has been shown that LPC can act as a "brake" on membrane merger, thereby regulating the final stages of AA release.
3. Impact on Integrity and Resilience
• Homeoviscous Adaptation: PC helps maintain optimal membrane fluidity ("homeoviscous adaptation") in the face of stress.
• Neuronal Protection: In neurons, AA-PC is concentrated along the axon, and its integrity is associated with actin dynamics and tactile sensitivity.
• PC Synthesis: The CDP-choline pathway is the primary pathway for synthesizing PC, which is essential for membrane stabilization.
In summary, PC choline is not just a passive component, but an active player which, by stabilizing the membrane structure, modulates the speed and intensity of the arachidonic acid cascade, thus acting as a key regulator of inflammation and cellular integrity.

Sources & References
https://mirzoune-ciboulette.forumactif.org/t2172-pc-choline-pour-stabiliser-les-membranes#30616

Which form and where to buy PC choline.

bio3nergetic

I think mitolipin from georgi is the only saturated PC I know of that is accessible.

LucH

@bio3nergetic said in PC choline to stabilize membranes:

I think mitolipin from georgi is the only saturated PC

Probably yes. It's stearic and palmitic support, at 39.99 $ + 16 $ for costs abroad.
When I can get mine in 420 mg softgels or from eggs, guess the next step
*) Natural factors 420 mg 90 gel. 12.64 € => 0.14 € /gél. *
Gelatin, glycerin
*) Thorne 420 mg 60 gel. 26.74 € => 0.45 €
Gelatin (bovin), glycerin

alfredoolivas

@bio3nergetic It doesn't matter. Your body will break down the PC into lysophosphatidylcholine + free fatty acids.
Back in the body, your body will a join the lysophosphatidylcholine with circulating fatty acids. When the enter the cell, it breakds down back into lysophosphatidylcholine, and rejoins with fatty acids in the cell back into PC.So as long, as you eat saturated fat with the PC, then basically, you will be receiving saturated PC.

It's not a scam by Haidut, because he is selling what it says on the label, but it's useless when compared to alternetive forms of PC, which are sold for much much cheaper.

bio3nergetic

@alfredoolivas said in PC choline to stabilize membranes:

Your body will break down the PC into lysophosphatidylcholine + free fatty acids.
Back in the body, your body will a join the lysophosphatidylcholine with circulating fatty acids. When the enter the cell, it breakds down back into lysophosphatidylcholine, and rejoins with fatty acids in the cell back into PC.So as long, as you eat saturated fat with the PC, then basically, you will be receiving saturated PC.

This doesn't seem to make enough sense for me. The fact there is a kind of lipolysis makes the fact even more crucial that there be a saturated PC. If the original PC contains PUFAs like linoleic acid (18:2), those PUFAs are released into circulation and can be incorporated into tissues, including mitochondrial and cellular membranes, where they increase oxidative stress and inflammation.
Even if lysoPC is re-acylated with saturated fats, some PUFA has already entered the system, and it’s not excreted immediately. Crucially, the enzyme LPCAT3 responsible for re-acylation, strongly prefers polyunsaturated fatty acyl-CoAs, especially arachidonic acid. Although, I tend to use different language in describing that, as more or less a hijacking than anything else.

This means that even in a high-saturated-fat context, the body prioritizes incorporating PUFAs into PC when available. And although metabolcally and typically, saturated fats are preferential fuel over PUFA, in the case of the building PC, PUFA wins, hence why I prefer the term hijack. So if dietary PC contains PUFAs, they’re more likely to be retained and recycled, not replaced.

Studies show that LPCAT3 knockout mice have reduced PUFA content in PC and are protected from diet-induced fatty liver! This was a indirect evidence incidentally, because the researchers were looking at total overall PC from high fat diet as related to disease progression. But guess what, the high fat diet is your typical formula: 25 grams Soybean Oil and almost 300 grams pig lard. This confirming that this enzyme drives PUFA incorporation into membranes. The takeaway being it is doubly important we use saturated PC.

High-fat diet-induced upregulation of exosomal phosphatidylcholine contributes to insulin resistance
Anil Kumar, et al