Effect of alcohol consumption on serum concentration of 25-hydroxyvitamin D3, retinol, and retinol-binding protein

Bjørneboe, G E; Johnsen, Jon; Bjørneboe, Anders; Rousseau, Brigitte; Pedersen, Jan I.; Norum, Kaare R.; Mørland, Jörg; Drevon, C. A.

doi:10.1093/ajcn/44.5.678

Cited by 45 publications

(25 citation statements)

References 28 publications

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“…Heavy consumption of ethanol reduced the plasma level of ·-tocopherol as well [12]. The serum concentration of ·-tocopherol was 30% lower in the alcoholics [13]; in another study it was reduced by 37% as compared to controls [11].…”

Section: Discussionmentioning

confidence: 83%

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Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

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Alcohol-induced oxidative stress is linked to the metabolism of ethanol. Three metabolic pathways of ethanol have been described in the human body so far. They involve the following enzymes: alcohol dehydrogenase, microsomal ethanol oxidation system (MEOS) and catalase. Each of these pathways could produce free radicals which affect the antioxidant system. Ethanol per se, hyperlactacidemia and elevated NADH increase xanthine oxidase activity, which results in the production of superoxide. Lipid peroxidation and superoxide production correlate with the amount of cytochrome P450 2E1. MEOS aggravates the oxidative stress directly as well as indirectly by impairing the defense systems. Hydroxyethyl radicals are probably involved in the alkylation of hepatic proteins. Nitric oxide (NO) is one of the key factors contributing to the vessel wall homeostasis, an important mediator of the vascular tone and neuronal transduction, and has cytotoxic effects. Stable metabolites – nitrites and nitrates – were increased in alcoholics (34.3 ± 2.6 vs. 22.7 ± 1.2 µmol/l, p < 0.001). High NO concentration could be discussed for its excitotoxicity and may be linked to cytotoxicity in neurons, glia and myelin. Formation of NO has been linked to an increased preference for and tolerance to alcohol in recent studies. Increased NO biosynthesis also via inducible NO synthase (NOS, chronic stimulation) may contribute to platelet and endothelial dysfunctions. Comparison of chronically ethanol-fed rats and controls demonstrates that exposure to ethanol causes a decrease in NADPH diaphorase activity (neuronal NOS) in neurons and fibers of the cerebellar cortex and superior colliculus (stratum griseum superficiale and intermedium) in rats. These changes in the highly organized structure contribute to the motor disturbances, which are associated with alcohol abuse. Antiphospholipid antibodies (APA) in alcoholic patients seem to reflect membrane lesions, impairment of immunological reactivity, liver disease progression, and they correlate significantly with the disease severity. The low-density lipoprotein (LDL) oxidation is supposed to be one of the most important pathogenic mechanisms of atherogenesis, and antibodies against oxidized LDL (oxLDL) are some kind of epiphenomenon of this process. We studied IgG oxLDL and four APA (anticardiolipin, antiphosphatidylserine, antiphosphatidylethanolamine and antiphosphatidylcholine antibodies). The IgG oxLDL (406.4 ± 52.5 vs. 499.9 ± 52.5 mU/ml) was not affected in alcoholic patients, but oxLDL was higher (71.6 ± 4.1 vs. 44.2 ± 2.7 µmol/l, p < 0.001). The prevalence of studied APA in alcoholics with mildly affected liver function was higher than in controls, but not significantly. On the contrary, changes of autoantibodies to IgG oxLDL revealed a wide range of IgG oxLDL titers in a healthy population. These parameters do not appear to be very promising for the evaluation of the risk of atherosclerosis. Free radicals increase the oxidative modification of LDL. This is one of the most important mechanism...

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Section: Discussionmentioning

confidence: 83%

“…Selenium and ·-tocopherol levels were decreased in all patients with skeletal muscle myopathy, whereas patients with normal muscle biopsies showed adequate antioxidant status [40]. Heavy consumption of ethanol reduced the plasma levels of ·-tocopherol and selenium [12].…”

Section: Discussionmentioning

confidence: 94%

Oxidative Stress, Metabolism of Ethanol and Alcohol-Related Diseases

Zima

Fialová

Mestek

et al. 2001

Journal of Biomedical Science

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“…32]. Diminished serum con centration of 25-hydroxyvitamin Dy has been reported among alcoholics [33,34], and may contribute to the high frequency of os teomalacia in alcoholics. Clinical studies concerning the possible effect of ethanol on serum concentration of a-tocopherol are scarce, but reduced serum levels of a-tocoph erol have been reported in alcoholics with hepatitis and cirrhosis [21,22], Our dietary survey revealed a signifi cantly reduced intake of a-tocopherol among the alcoholics as compared to the controls.…”

Section: Discussionmentioning

confidence: 99%

Diminished Serum Concentration of Vitamin E in Alcoholics

Bjørneboe¹,

Johnsen²,

Bjørneboe³

et al. 1988

Ann Nutr Metab

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The effect of heavy alcohol consumption on serum concentrations of vitamin E (α-tocopherol) and selenium was studied in 13 alcoholics and 19 control subjects. Ethanol intake during the year previous to the study was in the range from 22 to 354 g/day and from 0 to 16 g/day among the alcoholics and controls, respectively. Of the 13 alcoholics, 6 had a serum concentration of α-tocopherol below the lower limit of reference (14 µmol/l) and mean serum concentration of α-tocopherol was reduced by 37% as compared to controls (p < 0.002). Estimated dietary intake of α-tocopherol during the year previous to the study was approximately 40% lower for the alcoholics (p < 0.05). During hard-drinking periods the alcoholics had a markedly reduced intake of α-tocopherol as compared to moderate-drinking and abstinent periods. Mean serum concentration of selenium was significantly reduced in the alcoholics (1.2 ± 0.3 µmol/l) as compared to the controls (1.6 ± 0.2 µmol/l) (p < 0.002). The reduced serum levels of α-tocopherol and selenium may influence the maintenance of normal cell structure and function, and contribute to development of diseases frequently observed in alcoholics.

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“…136,137 Smoking is also associated with lower PTH levels, 138 blunted 1,25-(OH)2D-PTH axis and impairment of calcium absorption. 139 Excessive alcohol consumption is linked to lower 25-(OH)D concentrations, 140 but moderate intake is consistently reported to relate to better VitD status. 30,67,131,141,142 Strengths of our study include the large number of subjects for whom 25-(OH)D measurements were available and the wide age distribution, which lead us to consider our cohort as being representative of the general population of a Mediterranean island.…”

Section: 55mentioning

confidence: 99%