Asia napisala tak :

>>Nie chodzilo mi tez o autorytatywne stwierdznie co jest biale a co
czarne.Natomiast jesli Agnieszka prosi kilkakrotnie o krótkie wytlumacznie
na czym polega mechanizm dzialania czerwonego wina i czym rózni sie od
czegos tam to owe krótkie wyjasnienie ani nie zaszkodziloby
niczyjej wiedzy medycznej,ani stwierdzenie ze czarne jest czarne nie straciloby
nic na swojej aktualnosci.

Wiec raz jeszcze prosze, bardzo, o przeczytanie o której dyskusji
mówie i stwierdznie: potrafie/nie potrafie w paru slowach wytlumaczyc
Agnieszce na czym polega ów mechanizm.<<

Droga Asiu, rad bym Ci nieba przychylil. Ale wyjasnienie nie bedzie ani krotkie
ani proste.
Ale zacznijmy od poczatku (czytelnicy wybacza dlugosc ).

Otoz zacznijmy od prostej obserwacji populacji, opisanej w :

>>Lakartidningen 2001 May 23;98(21):2585-2588
[Beer, wine, spirits and mortality].
[Article in Danish]
Gronbaek MN, Sorensen TI, Johansen D, Becker U, Gottschau A, Schnohr P, Hein HO,
Jensen G.
Center for Epidemiologisk Grundforskning, Institut for Sygdomsforebyggelse,
Kommunehospitalet, Kobenhavn. m...@i...hosp.dk

A population based cohort study investigates the association between alcohol
intake and mortality from all causes, coronary heart disease and cancer. The
design is prospective with baseline assessment of intake of beer, wine and
spirits, smoking habits, educational level, physical activity, and body mass
index and a total of 257,859 person-years follow-up on mortality. A total of
4,833 participants died, of these 1,075 from coronary heart disease and 1,552 of
cancer. Compared with non-drinkers, light drinkers who avoided wine, had a
relative risk of death from all causes of 0.90 (0.82-0.99) and those who drank
wine had a relative risk of 0.66 (0.55-0.77). Heavy drinkers who avoided wine
were at higher risk of death from all causes than were heavy drinkers who
included wine in their alcohol intake. Wine drinkers had significantly lower
mortality from both coronary heart disease and cancer than did non-wine drinkers
(p = 0.007 and p = 0.004, respectively). In conclusion, wine intake may have a
beneficial effect on all cause mortality that is additive to that of alcohol.
This effect may be attributable to a reduction in death from both coronary heart
disease and cancer.<<

W skrocie wynika z niego, ze na badanej probce, osoby spozywajaca wodke albo
nie pijace alkoholu w ogole umieraja czesciej. Jak tylko zaczna pic wino to
umieraja mniej. Probka jest wcale solidna 257 tysiecy osobo-lat obserwacji. A
wiec wyniki badan maja duzy ciezar dowodowy (Jacek sie podnieca zwlaszcza
wynikami badan o malym ciezarze dowodowym, jak wiemy ).

Pytanie teraz, ktore obie stawiacie, pozostaje: a w jaki sposob sie to dzieje ?

A no sa , najprawdopodobniej dwa mechanizmy.

Pierwsza informacja przyszla z tak zwanego Framingham study. Nie wdajac sie w
szczegoly,

byla to wieloletnia obserwacja calej ludnosci sporego obszaru, wlasnie w
okolicy Framingham.

Badanie poziomow cholesterolu , notowanie tzw. koronary events ( angina,
zawaly) jak i

cerebro-vascular events .

Zaowocowalo to materialem pierwszej klasy, wlasnie ze wzgledu liczbe
obserwacji, jak i

dokladnosc badan, w tym laboratoryjnych. Z tego badania ukazala sie publikacja :

Circulation 2001 Jun 26;103(25):3051-3056
Genetic and environmental contributions to platelet aggregation: the Framingham
heart study.
O'Donnell CJ, Larson MG, Feng D, Sutherland PA, Lindpaintner K, Myers RH,
D'Agostino RA, Levy D, Tofler GH; Framingham Heart Study.
National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham,
Massachusetts, USA. c...@f...nhlbi.nih.gov

BACKGROUND: Platelet aggregation plays an important role in arterial thrombosis
in coronary heart disease, stroke, and peripheral arterial disease. However, the
contribution of genetic versus environmental influences on interindividual
variation in platelet aggregability is poorly characterized. METHODS AND
RESULTS: We studied the heritability of platelet aggregation responses in 2413
participants in the Framingham Heart Study. The threshold concentrations of
epinephrine and ADP required to produce biphasic platelet aggregation and
collagen lag time were determined. Mixed-model linear regression was used to
calculate correlation coefficients within sibships and within spouse pairs.
Variance and covariance component methods were used to estimate the proportion
of platelet aggregation attributable to measured covariates versus additive
genetic effects. After accounting for environmental covariates, the adjusted
sibling correlations for epinephrine, ADP, and collagen lag time were 0.24,
0.22, and 0.31, respectively (P=0.0001 for each). In contrast, adjusted
correlations for spouse-pairs were -0.01, 0.05, and -0.02, respectively (all
P>0.30). The estimated heritabilities were 0.48, 0.44, and 0.62, respectively.
Measured covariates accounted for only 4% to 7% of the overall variance in
platelet aggregation, and heritable factors accounted for 20% to 30%. The
platelet glycoprotein IIIa Pl(A2) polymorphism and the fibrinogen Hind III
beta-148 polymorphism contributed <1% to the overall variance. CONCLUSIONS: In
our large, population-based sample, heritable factors play a major role in
determining platelet aggregation, and measured covariates play a lesser role.
Future studies are warranted to identify the key genetic variants that regulate
platelet function and to lay the groundwork for rational pharmacogenetic
approaches.
PMID: 11425767 [PubMed - indexed for MEDLINE]

Okazuje sie wiec, ze nie tylko poziom cholesterolu ma wplyw na wystapienie ,
ale co wiecej - rowniez i zdolnosc plytek (tutaj opisana jako niezalezna od
leczenia) do tworzenia skrzepow.

Czy wiec mozna wplywac na plytki .Otoz okazuje sie, ze tak . Jak wiemy zaleca
sie osobom w pewnym wieku zazywanie malych dawek aspiryny. Bo wlasnie aspiryna
(oprocz wielu swoich zastosowan) obniza zdolnosc plytek do tworzenia skrzepow.

Czy inne srodki moga byc zastosowane ?

Okazuje sie , ze tak :

26: Circulation 2001 Jun 12;103(23):2792-2798
Select flavonoids and whole juice from purple grapes inhibit platelet function
and enhance nitric oxide release.
Freedman JE, Parker C 3rd, Li L, Perlman JA, Frei B, Ivanov V, Deak LR, Iafrati
MD, Folts JD.
Departments of Pharmacology and Medicine, Georgetown University Medical Center,
Washington, DC 20007, USA. f...@g...georgetown.edu

BACKGROUND: Moderate red wine consumption is inversely associated with coronary
ischemia, and both red wine and purple grape juice (PGJ) contain flavonoids with
antioxidant and antiplatelet properties believed to be protective against
cardiovascular events. Acute cardiac events are also associated with decreased
platelet-derived nitric oxide (NO) release. In this study, the effects of PGJ
and PGJ-derived flavonoids on platelet function and platelet NO production were
determined. METHODS AND RESULTS: Incubation of platelets with dilute PGJ led to
inhibition of aggregation, enhanced release of platelet-derived NO, and
decreased superoxide production. To confirm the in vivo relevance of these
findings, 20 healthy subjects consumed 7 mL. kg(-1). d(-1) of PGJ for 14 days.
Platelet aggregation was inhibited after PGJ supplementation, platelet-derived
NO production increased from 3.5+/-1.2 to 6.0+/-1.5 pmol/10(8) platelets, and
superoxide release decreased from 29.5+/-5.0 to 19.2+/-3.1 arbitrary units
(P<0.007 and P<0.05, respectively). alpha-Tocopherol levels increased
significantly after PGJ consumption (from 15.6+/-0.7 to 17.6+/-0.9 micromol/L;
P<0.009), and the plasma protein-independent antioxidant activity increased by
50.0% (P<0.05). Last, incubation of platelets with select flavonoid fractions
isolated from PGJ consistently attenuated superoxide levels but had variable
effects on whole-blood aggregation, platelet aggregation, and NO release.
CONCLUSIONS: Both in vitro incubation and oral supplementation with PGJ decrease
platelet aggregation, increase platelet-derived NO release, and decrease
superoxide production. These findings may be a result of antioxidant-sparing
and/or direct effects of select flavonoids found in PGJ. The suppression of
platelet-mediated thrombosis represents a potential mechanism for the beneficial
effects of purple grape products, independent of alcohol consumption, in
cardiovascular disease.


A wiec czerwony barwnik winogron ma dzialanie na plytki krwi, zmniejszajac
zdolnosc ich do tworzenia skrzepow.

Ale dlaczego wiec mowimy o winie ? Czy sam sok z winogron nie bylby
wystarczajacy ? Jaka jest rola alkoholu etylowego w tym ukladzie ?

Alcohol Clin Exp Res 2000 Sep;24(9):1456-1466
Alcohol inhibits the progression as well as the initiation of atherosclerotic
lesions in C57Bl/6 hyperlipidemic mice.
Emeson EE, Manaves V, Emeson BS, Chen L, Jovanovic I.
Department of Pathology, University of Illinois at Chicago, College of Medicine,
60612-7335, USA. e...@u...edu

BACKGROUND: Evidence that a moderate consumption of alcohol is associated with a
reduced incidence of and mortality due to coronary artery disease continues to
accumulate. Despite recent evidence that substances in red wine confer
resistance to coronary artery disease, it is clear that at least a substantial
proportion of the protective effect is due to the alcohol content of the
beverage. We have previously shown that the chronic ingestion of alcohol
incorporated into a total liquid diet during a 24-week period inhibits the
development of fatty streak lesions in hyperlipidemic C57Bl/6 mice. We have now
repeated this study and demonstrated that alcohol continues to markedly inhibit
atherogenesis during a 48-week period. METHODS: Mice were fed a high fat
atherogenic liquid diet with 0% or 6% alcohol or a high fat atherogenic pelleted
diet with 0% or 15% alcohol in their drinking water. After 24 and 48 weeks on
these diets, subgroups of mice were euthanized and the aortas were studied for
extent of atherosclerosis. Plasma lipid levels were also measured and flow
cytometry studies performed to characterize their T and B lymphocyte
populations. Additional groups of mice were given the high fat atherogenic diets
for 24 weeks to allow lesions to develop and were then treated with alcohol
diets to determine whether they inhibit the progression of the lesions. RESULTS:
The alcohol diets suppressed the development of atherosclerotic lesions at both
24 and 48 weeks in both the liquid and pelleted diet models. The addition of the
alcohol diets after allowing lesions to form for 24 weeks halted the further
progression of the lesions. The alcohol treatments also decreased the plasma
levels of total cholesterol and high density lipoprotein (HDL) cholesterol at
almost all time intervals. CONCLUSIONS: We conclude that alcohol not only
inhibits the initial development of atherosclerotic lesions but also inhibits
the progression of existing atherosclerotic lesions. The alcohol-mediated
decrease in HDL cholesterol in these experiments suggests that HDL plays little
or no role in amelioration of atherogenesis in this model.

PMID: 11003214 [PubMed - indexed for MEDLINE]

Czyli inaczej mowiac, na modelu zwierzecym udowodniono, ze alkohol zatrzymuje
powstania , a nawet zahamowanie, powstawania zmian typowych w miazdzycy
tetnic.

Czy to ma znaczenie dla czlowieka ?

Atherosclerosis 2000 Oct;152(2):503-510
Alcohol consumption and its relation to lipid-based cardiovascular risk factors
among middle-aged women: the role of HDL(3) cholesterol.
Sillanaukee P, Koivula T, Jokela H, Pitkajarvi T, Seppa K.
Departments of Clinical Chemistry and Psychiatry, University of Tampere, Medical
School and Tampere University Hospital, Tampere, Finland. finnish-immunotech.com

To study the association of alcohol consumption and lipid-based cardiovascular
risk factors among middle-age women, cross-sectional analysis among 274
middle-aged healthy women with different drinking habits and a follow-up
analysis of alcoholic women during abstinence was performed. Serum total
cholesterol, low and high-density lipoprotein cholesterol (LDL and HDL
cholesterol), triglycerides (TG), apolipoproteins A1 (Apo A1) and B (Apo B), and
HDL-cholesterol subfractions 2 (HDL(2)) and 3 (HDL(3)) were measured. All lipid
values except LDL cholesterol positively correlated with self-reported alcohol
consumption. When alcoholics were excluded the correlation was significant only
for HDL cholesterol, HDL(3), and Apo A1. The increasing trend of HDL
cholesterol, HDL(3) and Apo A1 were clearly seen first in women consuming >20-40
g/day of absolute alcohol. Alcohol consumption >40 g/day increased all lipid
values except LDL cholesterol. Abstinence for 2 weeks caused a significant
decrease in HDL(3) cholesterol, and an increase in LDL cholesterol and Apo B.
The results indicate that among middle-aged women the Apo A1 and HDL cholesterol
via its HDL(3) but not HDL(2) subfraction might play a role in the beneficial
coronary consequences associated with moderate alcohol consumption. However, the
increasing beneficial trend first appears when daily drinking exceeds 20 g/day.
PMID: 10998480 [PubMed - indexed for MEDLINE]

A wiec mamy dwa mechanizmy : oddzialywanie flavonoidow (barwnika czerwonego
wina) i oddzialywanie alkoholu etylowego. To ostatnie zmniejsza zawartosc tego
zlego cholesterolu (LDL), a podwyzsza tego dobrego (HDL) . Oba dzialania
skladnikow czerwonego wina ida w tym samym kierunku (zmniejszenie szans na
zawal lub udar mozgu).

Dlaczego wiec Jacek podnieca sie stwierdzeniami, iz ktos tam twierdzi
przeciwnie ?

A no po prostu dlatego, ze Jacek nie wie jak oceniac wartosc danego badania.
Jaka ono ma "sile dowodowa".

A poza tym tak jak pisalem, jedni pisza jedno, inni oceniaja to inaczej. Czas
pokaze, kto ma racje.

Jak na razie towarzystwa ubezpieczeniowe na zachodzie (USA/Kanada) daja wieksze
szanse na przezycie tym co pija jedna-dwie szklaneczki dziennie czerwonego
wina. I tak robia wszystkie towarzystwa ubezpieczeniowe. A jak to sie
sprawdza / A no jakos sie sprawdza. Ja zbieram korki od butelek, aby rodzina
mogla sie po mojej smierci wykazac.

Najprawdopodobniej alkohol wywiera dobroczynny wplyw poprzez jeszcze jeden
mechanizm, ale na razie pozwole sobie poprzestac na tym, co napisalem.

Dlaczego jednak sie mowi, ze kobiety winny pic mniej ? Czy one tez moga
korzystac z "benefits of drinking red wine" ?

A no popatrzmy na :

J Womens Health Gend Based Med 2000 Jul;9(6):607-616
Moderate alcohol consumption and changes in postprandial lipoproteins of
premenopausal and postmenopausal women: a diet-controlled, randomized
intervention study.
van der Gaag MS, Sierksma A, Schaafsma G, van Tol A, Geelhoed-Mieras T, Bakker
M, Hendriks HF.
Department of Nutritional Physiology, Organisation for Applied Scientific
Research (TNO) Nutrition and Food Research Institute, Zeist, The Netherlands.

Moderate alcohol consumption is associated with a reduced risk of coronary heart
disease. Earlier studies in men have shown that moderate alcohol consumption
affects lipoprotein metabolism and hemostasis. In this diet-controlled,
randomized, crossover trial, we investigated the effect on lipoprotein
metabolism of moderate consumption of red wine or red grape juice with evening
dinner for 3 weeks in premenopausal women using oral contraceptives and in
postmenopausal women. After 3 weeks, blood samples were collected 1 hour before
dinner up to 19 hours after starting dinner at 2-hour or 4-hour intervals.
Plasma triglyceride concentrations and very low density lipoprotein (VLDL)
triglyceride levels peaked 3 hours after dinner with wine in both premenopausal
and postmenopausal women. After wine consumption, the overall high-density
lipoprotein (HDL) cholesterol level was increased in postmenopausal women (mean
increase 0.17 mmol/L, or 12%, p = 0.03), and the plasma low-density lipoprotein
(LDL) cholesterol level was reduced in premenopausal women (mean reduction 0.35
mmol/L, or 12%, p = 0.01) as compared with grape juice consumption. The findings
suggest that postprandial lipoprotein metabolism after moderate alcohol
consumption differs between oral contraceptive-using premenopausal women and
postmenopausal women. The response of postmenopausal women to alcohol resembled
the response found in earlier studies in men.
PMID: 10957749 [PubMed - indexed for MEDLINE]

Zeby bylo smieszniej, jest u kobiet jeszcze jeden mechanizm (ja jestem
feminista, wiec mnie

to cieszy !) :

Alcohol 2000 Nov;22(3):123-127
Comment in:
Alcohol. 2000 Nov;22(3):121-2
Can alcohol promote aromatization of androgens to estrogens? A review.
Purohit V.

Division of Basic Research, Biomedical Research Branch, National Institute on
Alcohol Abuse and Alcoholism, National Institutes of Health, Suite 402, 6000
Executive Boulevard, Bethesda, MD 20892-7003, USA. v...@w...niaaa.nih.gov

Increased aromatization may be a mechanism for feminization of some male
alcoholics, as well as for the reported increases in plasma estrogen levels in
postmenopausal women subjected to moderate alcohol consumption. Alcohol
consumption-related increases in estrogen levels may in turn be partially
responsible for the associated decreased risk for coronary artery disease and
osteoporosis, as well as for increased risk for breast cancer. The purpose of
this review is to evaluate the literature to determine whether alcohol can
promote aromatization of androgens to estrogens. In male rats, chronic heavy
alcohol administration (36% of total calories=12-18 g/kg/day) led to increased
aromatization of androgen in the liver, but the results were equivocal for the
hypothalamus. In female rats, chronic heavy alcohol administration did not
promote aromatization in the hypothalamus exposed to alcohol in utero. In human
placental tissue, although ex vivo alcohol administration (less or more than 72
g/day) did not affect the rate of aromatization, in vitro incubation of
choriocarcinoma cells with 5-50 mM of alcohol increased estradiol secretion,
which could be due to increased aromatization. In in vitro human ovarian
granulosa cell studies, alcohol increased, had no effect on, or decreased
estradiol secretion, and in one study, 20 mM of alcohol significantly increased
aromatization of androstenedione to estrogens. These results may not be fully
relevant to normal human ovary because in both studies cells were heavily
luteinized by gonadotropins. A study of ovariectomized rats shows that only
heavy chronic alcohol intake (4.4 g/kg/day) for 10 weeks can increase plasma
estradiol levels and uterine weight, which could be due to increased
aromatization or delayed clearance of estradiol. In conclusion, chronic heavy
alcohol administration can result in aromatization of androgens in male rat
liver. It is not clear whether moderate alcohol intake can produce a similar
effect in the liver nor whether alcohol can potentiate aromatization of
androgens in other tissue or organs of male rats. In females, the available
information is not adequate to evaluate the effect of alcohol on aromatization.
Further studies are required in both genders to evaluate the ability of alcohol
(moderate vs. heavy dose) to promote aromatization of androgens to estrogens.
PMID: 11163119 [PubMed - indexed for MEDLINE]

Na polski jezyk oznacza to, ze heavy drinking zmienia profil hormonalny
mezczyzny na bardziej zblizony do kobiecego (zamienia testosteron na
estrogeny). Mnie to nie grozi, bo ja jestem niewrazliwy . Ale niektorym panom
rosna cyculki od alkoholu !

Przepraszam za cytaty w angieskim. Ale nie nadaje sie dobrze do tlumaczenia
tekstow z angielskiego na polski, bo nie robie tego na codzien. Zreszta w
pracy "mysle" po angielsku i mam klopoty z polska , medyczna, terminologia.

Chcialbym na zakonczenie podkreslic, ze informacje zawarte w tym tekscie nie sa
przeznaczone do tego aby zastapic porady wlasciwego lekarza. Przed
wprowadzeniem ich w zycie nalezy udac sie do lekarza !

Cytowane prace stanowia odzwierciedlenie pogladow ich autorow. Ja nie biore
odpowiedzialnosci za wymienione i zacytowane teksty. Nie we wszystkich
chorobach serca mozna spozywac alkohol. Alkohol zreszta sam jest przyczyna
wielu chorob serca. I nie tylko !!!

Mam nadzieje, ze zaspokoilem Twoja ciekawosc, pozdrawiam

dradam

PS. Przed dwoma laty przygotowalem kolekcje ponad 2000 miejsc na internecie
(WWW sites) oraz wykaz ponad 2000 list dyskusyjnych oraz BBS . KOlekcja ta
zostala wlaczona do stron listy LEKARZE, ktorej przekazalem wyniki mojego
zbierania. Kolekcja ta juz zajmuje sie inny kolega, ale jest ona nadal dostepna
dla publicznosci , co zalecam, bo zawiera ona spory dzial "dla pacjentow i ich
rodzin".

PS. Dalsze dane znajduja sie w zbiorze : Moderate Alcohol Consumption and
Cardiovascular Disease , edited by R.Paoletti, A,L. Klatsky, A.Poli oraz S.
Zakhari , wydane przez Kluwer Academic Publishers (adres do zamowien Kluwer
Academic Publishers , PO Box 17 3300 AA Dorthdrecht, The Netherlands ).

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