Marshall Price wrote:
Taka wrote:
The effect is mediated by the "good" AA metabolite PGI2 which has
vasodilatative properties (side effect is face flushing):
http://www.loweringhighcholesterol.org/Niacin,_A_Miracle_Vitamin,_Beats_Bad_Cholesterol..html
"Niacin's actions for reducing the risk factors for heart disease
arise out of the fact that, niacin has a strong effect on your body's
production of hormone-like chemicals, called prostaglandins, such as
PGI2 that are vital to numerous body functions, and niacin increases
their production.
PGI2 is critical to blood platelet aggregation, and without
sufficient PGI2, your blood has a tendency to clot. So, the greater
the chances of tendency to clot, the greater the risk of vascular
occlusion, a risk factor for heart disease,do you see.
Niacin inreases the production of PGI2, and therefore prevents the
possible tendency of blood to clot."
Lancet. 1979 May 26;1 (8126):1111-4 86835 (P,S,E,B) Cited:1 Successful
therapy of advanced arteriosclerosis obliterans with prostacyclin.
[My paper] A Szczeklik, R Nizankowski, S Skawinski, J Szczeklik, P
Gluszko, R J Gryglewski
Five patients with advanced arteriosclerosis obliterans of the lower
extremities, as evidenced by resting pain, ischaemic ulcers, and focal
necrosis, received intra-arterial infusions of prostacyclin at doses
of 5--10 ng/kg/min for 72 h. Within 2 days of termination of the
infusion, pain at rest had disappeared in all patients. In three of
the five, the necrosis had completely regressed and the ischaemic
ulcers healed within 2 months. The other two patients showed
considerable improvement. Prostacyclin therapy was not associated with
changes in the radiographic appearance of the major blood-vessels.
However, muscle blood-flow, as measured by xenon-133 clearance, was
significantly increased both during prostacyclin infusion and for the
6 weeks of measurement after its termination.
Prostaglandins. 1981 May ;21 (5):827-32 6803307 (P,S,E,B) Cited:1
Increased platelet activity after termination of prostacyclin infusion
into man.
[My paper] A Dembinska-Kiec, A Zmuda, L Grodzinska, K Bieron, M
Basista, A Kedzior, E Kostka-Trabka, E Telesz, T Zelazny
Infusion of PGI2 at a dose of 5 or 10 ng/kg/min during 72 hours into
patients with peripheral vascular disease was followed by increased
susceptibility of platelets to proaggregatory action of ADP and
collagen but not that of arachidonate. The above effects were observed
24 hours after termination of infusion of PGI2. A tendency to an
increased formation of TXA2 in PRP aggregated by arachidonate was also
noticed. Infusion of PGI2 at a dose of 2 mg/kg/min during 72 hours
into the patients caused the decreased platelet aggregability to ADP
and arachidonate but not to collagen, and a decreased tendency to
production of TXA2 in PRP aggregated by arachidonate. The existence of
a "rebound effect" in platelets after a long term PGI2 therapy is
suggested.
http://www.jstor.org/pss/2395630
http://acta.uta.fi/english/teos.phtml?3615
" 1. All the test compounds modulated eicosanoid synthesis in vitro.
Nicotine stereoisomers and cotinine stimulated PGE2, but inhibited
LTB4, LTE4 and TXB2 synthesis in vitro. The results imply that
nicotine stereoisomers and cotinine stimulate COX, but inhibit 5-LO
and TX-synthase. Nicotinic acid stimulated PGE2, TXB2 and LTE4
synthesis in vitro. In vitro pyridoxine and at high concentrations
pyridoxal-5'-phosphate stimulated PGE2 and TXB2 production, but had no
effect on LTE4 synthesis.
2. Nicotinic acid stimulated but pyridoxine inhibited PGE2, TXB2, and
LTE4 synthesis ex vivo. Nicotinic acid increased systemic TX and LTE4
synthesis, and tended to enhance systemic PGI2 production. Pyridoxine
treatment decreased TX and LTE4 production in vivo, but increased
production of PGI2. The increased TX and LTE4 synthesis caused by
nicotinic acid is potentially unfavorable, while the inhibition of LT
synthesis and the increase in PGI2 production caused by pyridoxine
might be beneficial.
3. Both ex vivo and systemic (in vivo) eicosanoid synthesis was higher
in smokers than in non-smoking controls, which may contribute to the
harmful cardiovascular effects of smoking. Cessation of smoking
without nicotine substitution decreased eicosanoid synthesis; the
decreases in TX and leukotriene synthesis may contribute to the
decreased risk of cardiovascular diseases and to the improvement of
lower respiratory tract inflammatory changes after smoking cessation."
Good AA metabolites can negate the bad AA metabolites or we can get
rid of them all and don't have to worry ...
Taka
Are you going to trust somebody who writes like this?
-----
How Niacin , A Miracle Vitamin,Lowers Your Cholesterol Naturally
The worst offender, ldl cholesterol relies on vldl for it's production,
and niacin lowers vldl to begin with, therefore the ldl levels in your
blood automatically drop.
By the way, niacin and nicotinic acid are infact inter-changeable terms
for exactly the same B-complex miracle vitamin.
Niacin is metabolised by your body and the result is niacinamide.
-----
...and gets everything confused like that?
Hoffer and Osmond knew about this in the sixties. Just look for
references to "niacin" with "cholesterol" on the orthomolecular.org site.
Every doctor who's read up on blood lipids, atherosclerosis, or
vitamins knows about it -- and isn't likely to get all the facts confused
or rave about "miracles" and "natural" and "good" versus "bad"
metabolites.
Everybody in this newsgroup ought to know about it anyway, but for
goodness sake, go to a decent source!
I'm ashamed of the way I reacted to your post, Taka. Sorry.
--
Marshall Price of Miami
Known to Yahoo as d021317c
