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>> Subject: Re: Lecithin raises HDL cholesterol
>> From: "Juhana Harju" shantigiri@despammed.com
[quoted text clipped - 23 lines]
>
> http://tinyurl.com/599of
They are not the same.
http://www.degussa-foodingredients.de/foodingredients/html/e/health/eng/kh/l6.1.htm
http://www.biochem.arizona.edu/classes/bioc801/tutorial/Lec34T.ppt
http://www.herbalgram.org/iherb/expandedcommissione/he090.asp
"Description
Soy lecithin consists of the phospholipids extracted from the seeds of Glycine
max (L.) Merrill [Fam. Fabaceae] and its preparations in effective dosage. Soy
lecithin contains (3-sn-phosphatidyl)choline, phosphatidylethanolamine, and
phosphatidylinositol.
Chemistry and Pharmacology
The main constituents are a natural mixture of phosphatides, mainly
phosphatidylcholine (20-31.6%), phosphatidylethanolamine and
phosphatidylinositol, in combination with fatty acids, carbohydrates, and other
substances (DAB, 1998; Der Marderosian, 1999; Der Marderosian et al., 1988; FCC
III, 1981; CFR 21, 1998). Soybean lecithin contains 11.7% palmitic, 4% stearic,
8.6% palmitoleic, 9.8% oleic, 55.0% linoleic, 4.0% linolenic, and 5.5% C20 to
C22 acids (Budavari, 1996; Der Marderosian, 1999). Pharmacopeial grade soy
lecithin must contain a minimum 20% and maximum 31.6% phosphatidyl choline,
calculated on the dried substance. Its iodine number value must be between 76
and 85, its acid value maximum 35, and peroxide value maximum 10 (DAB, 1998)."
http://www.whatislife.com/reader2/Metabolism/pathway/phospholipid.html
"1,2-diglyceride is a precursor for both phosphatidylcholine (C00157, lecithin)
and phosphatidylethanolamine (C00350) by combining the diacylglycerol with an
activated choline (ethanolamine) group using the nucleoside CTP to form
CDP-choline (C00307) and CDP-ethanolamine (C00570), respectively. Choline is
activated by phosphorylation using ATP to phosphorylcholine and
phosphorylcholine in turn is formed to CDP-choline by CTP releasing
pyrophosphate as byproduct.
These committed reactions are analogous to the activation of glucose-1-P to
UDP-glucose for glycogen synthesis. Phosphatidylethanolamine can also serve as
precursor for phosphatidylcholine by transfer of three activated choline groups
In addition, phosphatidylserine is derived from phosphatidylethanolamine by
exchanging the ethanolamine headgroup for serine.
Two minor phospholipids are phosphatidylglycerol (PG) and (PI). They are derived
from phosphatidic acid instead of 1,2-diglyceride. Phosphatidic acid is
activated by activation using CTP to form the high energy compound
CDP-diglyceride (C00269). The cytosine unit is replaced by either inositol to
form phosphatidylinositol (PI) and CMP, or glycerol-3-phosphate to form
phosphatidylglycerol (PG) and CMP and Pi. Both PG and PI are negatively charged
phospholipids because of the single negative charge contributed by the phosphate
ester linkage."
So it is clear that phosphatidylinositol is a *specific form* of lecithin. The
point is whether a mixture of phospholipids would have the same the same effect
on cholesterol as phosphatidylinositol or not.

Signature
Juhana
doe - 14 Dec 2004 21:41 GMT
>Subject: Re: Lecithin raises HDL cholesterol
>From: "Juhana Harju" shantigiri@despammed.com
>So it is clear that phosphatidylinositol is a *specific form* of lecithin.
>The
>point is whether a mixture of phospholipids would have the same the same
>effect
>on cholesterol as phosphatidylinositol or not.
It does .. in .. rabbits ..
Br J Exp Pathol 1985 Feb;66(1):35-46
Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol
and lecithin.
Hunt CE, Duncan LA
Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel
diet containing 14% hydrogenated coconut oil and 0.06% cholesterol
(approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the
same ingredients but with no coconut oil or cholesterol. Rabbits fed
atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months)
and plasma lipoprotein (LP) distribution shifted from a pattern in which
high-density lipoproteins (HDL) predominated to one in which very-low-density
lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d
less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP
distribution returned to normal in rabbits fed atherogenic diet for 18 months
followed by atherogenic diet plus 3% soya lecithin for an additional 4 months.
Rabbits fed atherogenic diet for 18 months had extensive, usually full
circumference fibromuscular plaques in main branches of coronary arteries and
all portions of aorta which compromised lumen area by almost 50%. These lesions
were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked
foam cells and cholesterol clefts, were less cellular with a distinct fibrous
surface and occupied less space. Animals fed basal diet did not develop
hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of
plasma LP shifted slightly in favour of increased low-density lipoproteins
(LDL) and decreased HDL compared with rabbits fed standard commercial diet.
Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam
cell lesions in proximal aorta. Liver injury including fatty change,
cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus,
rabbits fed appropriate diets low in cholesterol accumulate
cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta
and main branches of coronary arteries which are similar to those in man. Also,
in this experimental model, dietary lecithin promotes a return to normal of the
LP distribution profile and removal of lipid from established atherosclerotic
plaque.
PMID: 3970829, UI: 85122459
Who loves ya.
Tom
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