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Vierailija

Se lausutaan HOLESTERINI, painotus ensimmäisessä i:ssä (ei kuitenkaan niin älytöntä venytystä, että tarvittaisiin 2 samaa kirjainta).

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Vierailija

Olen itse aina kuvitellut että lausutaan kuten kirjoitetaankin, mutta joka kerta kun mainostetaan sitä madaltavaa tuotetta, tai puhutaan julkisuudessa aiheesta jostain muusta syystä, tavalliset tallaajat, tutkijat ja asiantuntijat puhuvat kolestroolista.

Vierailija

Vierailija kirjoitti:
Arvaa!

Minusta kuulostaa siltä, että suurin osa ihmisistä lausuu sen noin. Mutta en tiedä, mihin suomen kieliopin sääntöön tuollainen virheellinen lausuminen perustuu?

Vierailija

Olen itse yrittänyt lausua sen juuri niinkuin se kirjoitetaan "kolesteroli", mutta olen välillä tuntenut itseni ääliöksi kun muut lausuvat sen kolestrooliksi.

Vierailija

Mielestäni siinä on ”puolitoista” oo:ta. Eli välimuoto lyhyen ja pitkän o:n väliltä. Samoin sanassa sekunti on puolitoista t:tä

Vierailija

Vierailija kirjoitti:
Kolesteroliarvon tuijottaminen on turhaa kun sen hapettuminen voidaan estää antioksidanteilla.

Linkit : https://pubmed.ncbi.nlm.nih.gov/12600905/https://pubmed.ncbi.nlm.nih.gov...

Vitamin E Combined With Selenium Inhibits Atherosclerosis in Hypercholesterolemic Rabbits Independently of Effects on Plasma Cholesterol Concentrations
Dawn C. Schwenke and Stephen R. Behr
Originally published24 Aug 1998https://doi.org/10.1161/01.RES.83.4.366Circulation Research. 1998;83:366–377
Abstract
Abstract—Several antioxidants inhibit atherosclerosis. This study investigated the hypothesis that combining vitamin E, a lipophilic antioxidant, with vitamin C, a hydrophilic antioxidant, and/or selenium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effectively than vitamin E alone. We also considered whether regional variation in inhibition of atherosclerosis by antioxidants would be associated with regional variation in aortic lipophilic antioxidants. Rabbits were fed an atherogenic diet (control) or an atherogenic diet supplemented with vitamin E, vitamins E and C, vitamin E+selenium, vitamins E and C+selenium, or probucol (positive control). Supplements were as follows: vitamin E, 146 IU/d; vitamin C, 791 mg/d; selenium, 22 μg/d; or probucol, 406 mg/d. Vitamin C did not influence atherosclerosis. After 22 weeks of treatment, rank order of aortic atherosclerosis was control>vitamin E (with or without vitamin C)>vitamin E+selenium (with or without vitamin C)>probucol. Antioxidant treatment reduced aortic cholesterol concentrations 21% to 56%, 29% to 86%, and 19% to 75% for the aortic arch, descending thoracic aorta, and abdominal aorta, respectively (P<0.025 to P<0.0003 by ANOVA), with slightly greatly reductions for areas of atherosclerotic lesions. Some treatments reduced plasma cholesterol concentrations, but none altered the distribution of cholesterol among lipoproteins. Corrected for differences in plasma cholesterol concentrations, aortic cholesterol concentrations were reduced up to 72% (P<0.02) by the antioxidant treatments, with equal reductions by vitamin E+selenium and by probucol. Aortic α-tocopherol standardized by aortic cholesterol as a measure of aortic lipids was lower in the abdominal aorta than in the aortic arch of rabbits not given α-tocopherol and increased relatively more in the abdominal aorta than in the aortic arch with α-tocopherol supplementation. The results of this study suggest that vitamin E+selenium inhibited atherosclerosis as effectively as an equally hypocholesterolemic dose of probucol by a mechanism(s) that is in part independent of effects on plasma and lipoprotein cholesterol concentrations. The tendency for greater efficacy of antioxidant treatments in the abdominal aorta than aortic arch may relate to the lower concentrations of α-tocopherol in the abdominal aorta of unsupplemented rabbits.

Vierailija

Vierailija kirjoitti:
Vierailija kirjoitti:
Kolesteroliarvon tuijottaminen on turhaa kun sen hapettuminen voidaan estää antioksidanteilla.

Linkit : https://pubmed.ncbi.nlm.nih.gov/12600905/https://pubmed.ncbi.nlm.nih.gov...

Vitamin E Combined With Selenium Inhibits Atherosclerosis in Hypercholesterolemic Rabbits Independently of Effects on Plasma Cholesterol Concentrations
Dawn C. Schwenke and Stephen R. Behr
Originally published24 Aug 1998https://doi.org/10.1161/01.RES.83.4.366Circulation Research. 1998;83:366–377
Abstract
Abstract—Several antioxidants inhibit atherosclerosis. This study investigated the hypothesis that combining vitamin E, a lipophilic antioxidant, with vitamin C, a hydrophilic antioxidant, and/or selenium, a cofactor of peroxidases that detoxify lipid peroxides, would inhibit atherosclerosis more effectively than vitamin E alone. We also considered whether regional variation in inhibition of atherosclerosis by antioxidants would be associated with regional variation in aortic lipophilic antioxidants. Rabbits were fed an atherogenic diet (control) or an atherogenic diet supplemented with vitamin E, vitamins E and C, vitamin E+selenium, vitamins E and C+selenium, or probucol (positive control). Supplements were as follows: vitamin E, 146 IU/d; vitamin C, 791 mg/d; selenium, 22 μg/d; or probucol, 406 mg/d. Vitamin C did not influence atherosclerosis. After 22 weeks of treatment, rank order of aortic atherosclerosis was control>vitamin E (with or without vitamin C)>vitamin E+selenium (with or without vitamin C)>probucol. Antioxidant treatment reduced aortic cholesterol concentrations 21% to 56%, 29% to 86%, and 19% to 75% for the aortic arch, descending thoracic aorta, and abdominal aorta, respectively (P<0.025 to P<0.0003 by ANOVA), with slightly greatly reductions for areas of atherosclerotic lesions. Some treatments reduced plasma cholesterol concentrations, but none altered the distribution of cholesterol among lipoproteins. Corrected for differences in plasma cholesterol concentrations, aortic cholesterol concentrations were reduced up to 72% (P<0.02) by the antioxidant treatments, with equal reductions by vitamin E+selenium and by probucol. Aortic α-tocopherol standardized by aortic cholesterol as a measure of aortic lipids was lower in the abdominal aorta than in the aortic arch of rabbits not given α-tocopherol and increased relatively more in the abdominal aorta than in the aortic arch with α-tocopherol supplementation. The results of this study suggest that vitamin E+selenium inhibited atherosclerosis as effectively as an equally hypocholesterolemic dose of probucol by a mechanism(s) that is in part independent of effects on plasma and lipoprotein cholesterol concentrations. The tendency for greater efficacy of antioxidant treatments in the abdominal aorta than aortic arch may relate to the lower concentrations of α-tocopherol in the abdominal aorta of unsupplemented rabbits.

Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study
Riitta M Salonen et al. Circulation. 2003.
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Abstract
Background: Self-selected supplementation of vitamin E has been associated with reduced coronary events and atherosclerotic progression, but the evidence from clinical trials is controversial. In the first 3 years of the ASAP trial, the supplementation with 136 IU of vitamin E plus 250 mg of slow-release vitamin C twice daily slowed down the progression of carotid atherosclerosis in men but not women. This article examines the 6-year effect of supplementation on common carotid artery (CCA) intima-media thickness (IMT).

Methods and results: The subjects were 520 smoking and nonsmoking men and postmenopausal women aged 45 to 69 years with serum cholesterol > or =5.0 mmol/L (193 mg/dL), 440 (84.6%) of whom completed the study. Atherosclerotic progression was assessed ultrasonographically. In covariance analysis in both sexes, supplementation reduced the main study outcome, the slope of mean CCA-IMT, by 26% (95% CI, 5 to 46, P=0.014), in men by 33% (95% CI, 4 to 62, P=0.024) and in women by 14% (not significant). In both sexes combined, the average annual increase of the mean CCA-IMT was 0.014 mm in the unsupplemented and 0.010 mm in the supplemented group (25% treatment effect, 95% CI, 2 to 49, P=0.034). In men, this treatment effect was 37% (95 CI, 4 to 69, P=0.028). The effect was larger in subjects with either low baseline plasma vitamin C levels or CCA plaques. Vitamin E had no effect on HDL cholesterol.

Conclusions: These data replicate our 3-year findings confirming that the supplementation with combination of vitamin E and slow-release vitamin C slows down atherosclerotic progression in hypercholesterolemic persons.

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* Tämä kenttä pitää täyttää jotta oikeat käyttäjät erottuvat boteista.
 

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