cholesteral reducing white wine grape?

[Bucko]

No, Redman is right. However, smoking exerts its main effects on LDL from all of my readings. LDL must be in an oxidized form to do its nasty stuff with atheromas/cholesterol plaques. Because smoking is associated with increased lipid peroxidation, it activates more LDL, thus increasing risk of cardiovascular disease.

Here is one abstract:

Effects of alpha-tocopherol on superoxide production and plasma intercellular adhesion molecule-1 and antibodies to oxidized LDL in chronic smokers.

Free Radic Biol Med 2001 May 15;30(10):1122-9 (ISSN: 0891-5849)

van Tits LJ; de Waart F; Hak-Lemmers HL; van Heijst P; de Graaf J; Demacker PN; Stalenhoef AF
Department of Medicine, Division of General Internal Medicine, University Medical Center Nijmegen, Nijmegen, The Netherlands. B.vantits@aig.azn.nl.

Antioxidants have been postulated to exert beneficial effects in atherosclerosis. Atherosclerosis is associated with raised plasma levels of soluble intercellular adhesion molecule-1 (sICAM-1) and autoantibodies against oxidized low-density lipoprotein (oxLDL). It is not known whether antioxidants affect these plasma factors in chronic smokers. In a randomized double-blind placebo-controlled study involving 128 male normolipidemic chronic smokers the effect of a 2-year alpha-tocopherol treatment (400 IU dL-alpha-tocopherol daily) on plasma levels of sICAM-1 and autoantibodies against oxLDL was evaluated. In addition, we monitored production of superoxide by leukocytes ex vivo. It was found that compared to nonsmokers (n = 33) plasma levels of IgG but not IgM autoantibodies against oxLDL and concentrations of sICAM-1 in smokers were significantly elevated (30 and 42%, respectively). After supplementation with alpha-tocopherol concentration of TBARS in plasma and in vitro oxidizability of LDL had decreased, but autoantibodies and sICAM-1 had not changed. Production of superoxide was not different between alpha-tocopherol- and placebo-treated smokers. It is concluded that in chronic smokers, long-term treatment with alpha-tocopherol does not normalize the raised levels of sICAM-1 and autoantibodies against oxLDL, both risk factors for initiation or progression of cardiovascular disease, despite a decrease in in vitro oxidizability of LDL.

Here is an abstract that does show some effects of smoking and lowered HDL:

The interrelationship among tobacco consumption, high-density lipoprotein cholesterol and leukocyte counts.

J Cardiovasc Risk 1997 Aug;4(4):279-81 (ISSN: 1350-6277)

Celada MM; Reguero JR; Cubero GI
Servicio de Cardiologia, Hospital Universitario Central de Asturias, Oviedo, Spain.

BACKGROUND: Tobacco consumption is a major cardiovascular risk factor that has been related to changes in lipoprotein levels and in the leukocyte count. OBJECTIVE: To investigate the interrelationship among leukocytes, high-density lipoprotein (HDL) cholesterol levels and tobacco consumption. METHODS: In total 1022 healthy male miners aged 40.5+/-8 years (mean+/-SD) were evaluated consecutively during the period 1993-1994. We evaluated the smoking history of all of the subjects by means of a structured questionnaire. After the subject had fasted for 12 h we extracted blood samples by venepuncture. Plasma concentrations of HDL were determined enzymatically (by the CHOD-PAP method) and the leukocyte count was determined with an automatic analyser. Statistical analysis was performed using analysis of variance for the mean differences and the Pearson and stepwise tests to determine correlations. RESULTS: The leukocyte count was significantly lower (8.014+/-2.327/mm3, P < 0.05) in those subjects with levels of HDL cholesterol equal to or greater than 0.9 mmol/l in comparison with that in those with HDL cholesterol levels lower than 0.9 mmol/l (8.450+/-2.375/mm3). Leukocyte counts were correlated directly to tobacco consumption (r= 0.3119, P < 0.01) and inversely to H DL cholesterol levels (r = -0.1513, P < 0.01). HDL cholesterol levels were lower in smokers (1.15+/-0.31 mmol/l) and these differences were significant with respect to the levels in non-smokers (1.22+/-0.30 mmol/l, P<0.05) but not with respect to those in former smokers (1.21+/-0.39 mmol/l). The leukocyte count was significantly greater in smokers (8.963+/-2.428/mm3, P<0.05) than it was in former smokers (7.041+/-1.698/mm3) and in non-smokers (6.793+/-1.599/mm3). CONCLUSIONS: The results of this study indicate that tobacco consumption is associated with lower HDL cholesterol levels and higher leukocyte counts. Leukocyte counts correlate positively to tobacco consumption and inversely to HDL cholesterol levels. Subjects with HDL cholesterol levels lower than 0.9 mmol/l present with leukocyte counts higher than those found in those with HDL cholesterol values equal to or greater than 0.9 mmol/l.

All of that said, my original statement is still true -- smoking is a risk factor independent of cholesterol.