PubMed · 2640539
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P Pichot. 1989. [Current facts about depression].. https://pubmed.ncbi.nlm.nih.gov/2640539/
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BACKGROUND: Experimental and epidemiologic investigations suggest that alpha-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and beta-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received beta-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of beta-carotene and vitamin A. PURPOSE: We examined the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. METHODS: A total of 29,133 men aged 50-69 years who smoked five or more cigarettes daily were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), alpha-tocopherol and beta-carotene, or a placebo daily for 5-8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of alpha-tocopherol and beta-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. RESULTS: No overall effect was observed for lung cancer from alpha-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87-1.13; P = .86, logrank test). beta-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02-1.33; P = .02, logrank test). The beta-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07-1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76-1.23) and in those with a higher alcohol intake (> or = 11 g of ethanol/day [just under one drink per day]; RR = 1.35; 95% CI = 1.01-1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85-1.24). CONCLUSIONS: Supplementation with alpha-tocopherol or beta-carotene does not prevent lung cancer in older men who smoke. beta-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. IMPLICATIONS: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose beta-carotene supplementation.
To determine whether changes in androgen receptor (AR) expression are associated with trophic actions of androgens, we have examined the laryngeal motor nucleus (N. IX-X) of Xenopus laevis 1 and 5 months after section of the laryngeal nerve. In situ hybridization was used to recognize cells expressing mRNA for the Xenopus AR and bromodeoxyuridine to assess cell proliferation. In addition, the total number of cells was determined in untreated and dihydrotestosterone (DHT)-treated animals after 5 months of axotomy. After 1 month of axotomy, the number of AR mRNA-expressing cells in N. IX-X is 1.8-fold higher than in the intact side. Androgen upregulates expression of AR mRNA in N. IX-X on both the intact and the axotomized sides, suggesting that the increase is independent of contact with muscle. Neither the axotomy- nor the androgen-induced increase in number of cells expressing AR mRNA is attributable to cell proliferation. Five months after axotomy, both the total number of cells and the number of AR mRNA-expressing cells are severely decreased in the axotomized N. IX-X. DHT treatment mitigates the cell loss in N. IX-X induced by prolonged axotomy; the effect includes maintenance of AR mRNA-expressing cells. Gonadally intact males have more cells in the axotomized N. IX-X than castrated animals, suggesting that androgen acts at physiological levels as a trophic hormone. Axotomy-induced upregulation of AR expression may facilitate the trophic actions of androgens.