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admin · #14 (**permalink**) 11-15-2010, 07:22 AM

Compound N is a very special highly pure derivative of PC called PPC (Polyenylphosphatidylcholine) containing up to 52% DLPC (Dilinoleoylphosphatidylcholin e) which researchers have confirmed is the active compound responsible for all if not most of PPC's benefits.

In many countries it is a drug called Lipostabil or Essentiale used for various serious liver conditions and has been in clinical use for decades.
In the US it goes by PhosChol or simply PPC for short. There are little if any research showing any benefits of lecithin or regular PC in large part due to displacement by other phospholipids much like taking a bunch of other fats with CLA will reduce it's effectiveness or like eating a pound of eggs to get AA but also getting a bunch of other fats and cholesterol as well.

In over fifty years of use, and in thousands of animal and clinical studies, PPC has been proven safe and reliable.

Over 30 million daily doses of PhosChol have been sold worldwide, and according to a rough estimation a total of 350 million daily doses of PPC (used in a similar European product) were sold in Germany between 1954 and 2000 and approximately 600 million daily doses globally.

There are no studies showing any of other phospholipids (phosphatidyl inositol, phosphatidylethanolamine, and phosphatidic acid) present in lecithin are responsible for any of PPC's benefits aside from perhaps some being converted into PC in small amounts through methylation.

Most importantly is PPC (of which 52% is DLPC) replaces regular PC in cell membranes which is a main factor in it's benefits.

2.4 Pharmacokinetics
The phospholipids reaching the organism by the way of EPL differ from endogenous phosphatidylcholines by their fatty acid pattern. 1,2-
dilinoleoylphosphatidylcholine , the main active ingredient, is usually not present in the body. Therefore, in pharmacokinetic investigations radioactively labelled 1,2-dilinoleoylphosphatidylcholine was used, which can be obtained by synthetic or semisynthetic ways. In order to find an answer to the questions of distribution and excretion, different isotopes (32P, 3H, 14C) and sometimes multiple labels, at various molecular components were applied.

Examination of lipoproteins revealed that the specific activity of polyenylphosphatidylcholine in HDL was 2 to 6 times higher than in apo-Bcontaining
lipoproteins, and up to 20 times that of red blood cells or total blood. Thus, in man, EPL is also incorporated preferentially into the HDL fraction. According to Zierenberg et al. (766, 768) "essential" phospholipids are exchanged for phospholipids of membranes and lipoproteins.

3.2 Membrane Fluidity and EPL
The main active ingredient in EPL is 1,2-dilinoleoylphosphatidyicholine , which is present to about 52 % of the applied mixture of phosphatidylcholine
molecules (128). 1,2-dilinoleoylphosphatidylcholine is not physiologically present in the human body. Endogenous phospholipids are substituted by
"essential" phospholipids, especially by the 1,2-dilinoleoylphosphatidylcholine , which are incorporated in all membrane-containing fractions
(404, 405).

This means that the phosphatidylcholine molecules in the membranes with a saturated fatty acid at position 1 (718) are partly exchanged against those with
a linoleic acid or a linolenic acid at this position; additionally, the amount of phosphatidylchoIine molecules with a linoleic acid at position 2 is increased
(524). In total the number of double-bonds in the group of phosphatidylcholine molecules in the membrane increases. One of the important consequences of such a substitution of body-own phospholipids by these highly unsaturated phosphatidylcholines is a change of
membrane fluidity.

3.7 EPL, Carrier of Polyunsaturated Fatty Acid and of Choline
Due to its high amount of polyunsaturated fatty acids (especially linoleic acid and linolenic acid in the phosphatidylcholine molecules (404)) EPL is a
splendid supplier of eicosanoid precursors (318, 443, 484, 520, 755). Due to the substitution of body-own phospholipids in the membrane against EPL,
the pool of these precursors is increased, which the organism uses on demand (486).

The Japanese research team of K. Shirai et al. (650) used dipalmitoylphosphatidylcholine (DPPC) and polyenylphosphatidylcholine (EPL; Lipostabil) vesicles to investigate the intensity of the release of 3Hcholesterol from macro****es isolated from the peritoneum of rats. Due to their lower microviscosity and their greater fluidity, the capacity of polyenylphosphatidylcholine vesicles to remove cholesterol from the macro****es after 2 and 6 hours of incubation was clearly superior to DPPC vesicles.

- Polyenylphosphatidylcholine micelles/liposomes are more efficient than other PC-particles as to forming complexes with cholesterol. The plasma clearance of these PC-particles, which is usually fast, appears to be slowed down when binding to apo A1 or apo HDL.

According to G.Assmann et al. (28) who investigated different phosphatidylcholines, including dilinoleoylphosphatidylcholine (tab. 36), the mechanisms of LCAT activation remain to be established. In their opinion the formation of an LCAT/substrate complex and hence cholesterol esterification are faciliated by an increased fluidity of the PC substrate due to unsaturated fatty acid chains in the 1- and 2-position of the molecule, as present in 1,2-dilinoleoylphosphatidylcholine . <%Tab. 38: Presentation of the relative reaction rate of purified LCAT with phosphatidylcholine substrates which contain identical fatty acids in 1- and 2- position The highest transacylation rates were seen with 1,2- dilinoleoylphosphatidylcholine ..

Different forms of PC make a difference.

Composition:

Highly purified Essential Phospholipids (EPL) or Polyunsaturated Phosphatidylcholine / Polyenylphosphatidylcholine (PPC) (active principle: diglyceride esters of cholinephosphoric acid of natural origin, with excess of unsaturated fatty acids, predominantly linoleic acid [approximately 70%] with 1,2- dilinoleoylphosphatidylcholine [(DLPC) up to 52%], linolenic acid and oleic acid).

Approximately 15 kg of soya beans are required to obtain a daily dose of PPC 1.8 grams

About 3.18 kg equals a TB of lecithin granules.

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Clin Toxicol (Phila). 2007 Aug 30;:1-10
Multivitamins and phospholipids complex (PPC) protects the hepatic cells from androgenic-anabolic-steroids-induced toxicity.

Pagonis TA, Koukoulis GN, Hadjichristodoulou CS, Toli PN, Angelopoulos NV. Department of Endocrinology, Thessaly University Medical School, Larissa, Greece.

Introduction. Androgenic-anabolic-steroids (AAS)-induced hepatotoxicity typically occurs with C-17 alkylated oral agents abused by exercising individuals at clinically recommended doses. Injectable compounds appear to have the same risk for hepatotoxicity, but are applied in doses three to six times higher than clinically recommended. AAS users occasionally try to avoid the well-known hepatotoxic effects associated with the abuse of a multitude of AAS agents, by using the pharmaceutical agent compound N a phospholipid/vitamin preparation. Primary Objective. The investigation of the actual hepatoprotective effect of compound N against AAS-induced toxicity. Methodology. This was an observational cohort study of 320 athletes; 160 were AAS users and the other 160 were not abusing any substances. Of the 160 users, 44 were using AAS and compound N (group A), and 116 were using solely AAS (group . The 160 athletes abstaining from substances abuse acted as controls (group C). All athletes were tested for alterations in serum levels of hepatic enzymes. Enzyme levels before the study's onset and after the end of the 8-week AAS regimes were compared among the three groups, in order to delineate the hepatoprotective effect of compound N. Results. Prior to our research all groups showed normal values in all enzymes except creatine kinase (CK). After the 8-week period, CK levels were slightly lower in group A, but without variation in Groups B and C; gamma-Glutamyl Transferase (gammaGT) levels remained normal. Groups A and C had no elevations in any of the enzymes, except CK, while in group B all enzymes' values were elevated above the normal range. The only factor differentiating AAS users in group A from those in group B was the use of compound N, thus the results being suggestive of the compound's detoxification effect. The severity of AAS abuse was positively associated with the degree of changes (Delta values) in all measured enzymes except gammaGT and CK. Conclusions. Previous suggestions that serum hepatic enzyme elevations in exercising AAS abusers are connected to muscle fiber damage rather than the abuse itself, are contradicted by our results. Since all AAS abusing athletes were prone to exhibit elevations in enzymes' values, the mean values of group A were to be similar to those observed in group B, exceeding normal values. The group hepatic enzyme values of group B were significantly higher than the group C (control). Notably, group A did not have any statistically significant difference in the hepatic enzyme values compared to group C. The effect of exercise on these enzymes' elevations was ruled out by the comparability of training regimens and AAS toxicity was correlated to the severity of AAS abuse.

Basically bodybuilders on steroids using the liver drug PPC protected and normalized liver damage/stress caused by steroids. While you could try taking an unresearched PC complex in the hopes of getting a similar effect to save a few bucks you really don't want to mess around with your liver when a proven inexpensive well studied and gov approved drug PPC is available.