BACKGROUND: There is increasing evidence that a major part of the tumour-promoting action of alcohol is mediated via its first, toxic and carcinogenic metabolite acetaldehyde. MATERIALS & METHODS: The double blinded randomized control trial was designed for 82 male volunteers aged 20-29 years. Exclusion criteria were individual under antibiotic therapy, smokers, mutant Aldehyde Dehydrogenase deficient subject or any other systemic disease. Subjects were randomized in experimental (alcohol + soft drink) and control group (soft drink) from each pair of equal body weighted volunteers. The amount of alcohol consumed was calculated to be equivalent to 0.7 g alcohol/kilogram of body weight. Samples of breath for Acetaldehyde concentration (AC) were captured with the aid of a highly reproducible fuel cell gas-sampling device (PST-M1; Lions Laboratories, Cardiff, Wales). In Statistical analysis, mean AC was compared among both groups at different interval using paired t-test and Analysis of variance. RESULTS:Mean acetaldehyde level was recorded higher ([Formula: see text]) among interventional group which can be produced from ethanol during metabolism or by oro-pharyngeal microbes. After 15 minutes of drink, the AC was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group. There was significant increase in AC after 1 hour ([Formula: see text]) which was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group. CONCLUSION: Although acetaldehyde is metabolite of alcohol, its organ specific production with risk for oro-pharyngeal and pulmonary carcinogenesis makes alcohol an independent risk factor of carcinogenesis. How to cite this article: Dagli RJ, Kulkarni S, Duraiswamy P, Dagli NR, Khara NV, Khara BN. Is Alcohol an independent risk factor for Oro-Pharyngeal and Pulmonary Carcinogenesis - An Acetaldehyde concentrations based Double Blinded Randomized Control Trial. J Int Oral Health 2013; 5(4):62-67.
RCT Entities:
BACKGROUND: There is increasing evidence that a major part of the tumour-promoting action of alcohol is mediated via its first, toxic and carcinogenic metabolite acetaldehyde. MATERIALS & METHODS: The double blinded randomized control trial was designed for 82 male volunteers aged 20-29 years. Exclusion criteria were individual under antibiotic therapy, smokers, mutant Aldehyde Dehydrogenase deficient subject or any other systemic disease. Subjects were randomized in experimental (alcohol + soft drink) and control group (soft drink) from each pair of equal body weighted volunteers. The amount of alcohol consumed was calculated to be equivalent to 0.7 g alcohol/kilogram of body weight. Samples of breath for Acetaldehyde concentration (AC) were captured with the aid of a highly reproducible fuel cell gas-sampling device (PST-M1; Lions Laboratories, Cardiff, Wales). In Statistical analysis, mean AC was compared among both groups at different interval using paired t-test and Analysis of variance. RESULTS: Mean acetaldehyde level was recorded higher ([Formula: see text]) among interventional group which can be produced from ethanol during metabolism or by oro-pharyngeal microbes. After 15 minutes of drink, the AC was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group. There was significant increase in AC after 1 hour ([Formula: see text]) which was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group. CONCLUSION: Although acetaldehyde is metabolite of alcohol, its organ specific production with risk for oro-pharyngeal and pulmonary carcinogenesis makes alcohol an independent risk factor of carcinogenesis. How to cite this article: Dagli RJ, Kulkarni S, Duraiswamy P, Dagli NR, Khara NV, Khara BN. Is Alcohol an independent risk factor for Oro-Pharyngeal and Pulmonary Carcinogenesis - An Acetaldehyde concentrations based Double Blinded Randomized Control Trial. J Int Oral Health 2013; 5(4):62-67.
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Authors: A Yokoyama; T Muramatsu; T Ohmori; T Yokoyama; K Okuyama; H Takahashi; Y Hasegawa; S Higuchi; K Maruyama; K Shirakura; H Ishii Journal: Carcinogenesis Date: 1998-08 Impact factor: 4.944