|Mahabir, Somdat - NIH, NCI|
|Johnson, Laura - NIH, NCI|
|Frenkel, Krystyna - NEW YORK UNIVERSITY|
|Dorgan, Joanne - FOX CHASE CANCER CTR|
|Campbell, William - NIH, NCI|
|Hartman, Terryl - PENN STATE UNIV|
|Albanes, Demetrius - NIH, NCI|
|Taylor, Philip - NIH, NCI|
Submitted to: European Journal of Cancer Prevention
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 20, 2004
Publication Date: August 20, 2005
Citation: Mahabir, S., Baer, D.J., Johnson, L.L., Frenkel, K., Dorgan, J.F., Campbell, W., Hartman, T.J., Clevidence, B.A., Albanes, D., Judd, J.T., Taylor, P.R. 2005. No association between alcohol supplementation and autoantibodies to dna damage in postmenpausal women in a controlled feeding study. European Journal of Cancer Prevention 14: 427-429. Interpretive Summary: Oxidative damage to DNA is one proposed mechanism by which alcohol may increase risk for certain cancers. One marker of DNA damage is 5-hydroxymethyl-2-deoxyuridine (5-HMdU). The presence of 5-HMdU in DNA increases the production of specific IgM-class autoantibodies (aAbs). Thus, the concentration of these antibodies may be a marker of oxidative DNA damage and a biological response to that damage. To determine if moderate alcohol consumption increases DNA damage, we measured 5-HMdu in the blood of fifty-one postmenopausal women who participated in a controlled feeding study. The women consumed a placebo beverage (no alcohol), one drink/day or 2 drinks/day for 8 weeks each. There was no change in this marker after consuming 1 or 2 drinks/day compared to the control beverage. While this is only one of many markers of DNA oxidative damage, it appears that moderate alcohol consumption may have little impact on this particular marker of DNA damage. These findings are important to physicians, allied health professional, and individuals concerned about the relationship between risk for cancer and its relationship to diet.
Technical Abstract: The formation of 5-hydroxymethyl-2-deoxyuridine (5-HMdU), an oxidized DNA base derivative, results from attacks by reactive oxygen species. It appears that the presence of 5-HMdU in DNA stimulates the production of specific IgM-class autoantibodies (aAbs). Thus, the titers of these antibodies may constitute a marker of oxidative DNA damage and a biological response to that damage. In a controlled feeding study (n=51), we tested the hypothesis that eight weeks of moderate (15 g ethanol/ day or 30 g ethanol/ day) alcohol consumption versus a placebo increases serum 5-HMdU aAbs concentrations in healthy postmenopausal women. After consuming 15 g per day of alcohol resulted in a non-significant 1.8% increase compared to 0 g per day of alcohol, while 30 g per day alcohol increased 5-HMdU aAbs a non-significant 0.8% (95% CI = -3.0% to 4.7%). No significant linear trend was observed (p=0.70). We found no effect of alcohol consumption on levels of oxidative DNA damage measured by serum 5-HMdU aAbs. Thus, it appears that alcohol consumption may have little impact on this particular marker of DNA damage, and that the increased risk of some cancers which are associated with alcohol intake may be related to other mechanisms.