Table C-1Summary of results from human studies on breast cancer

StudyModelStudy DesignMechanism ExaminedAmount and Duration of Ethanol and/or Acetaldehyde ExposureResultsConclusions as Reported by Study Authors
Hartman et al. 20057653 postmenopausal womenCase controlIncrease levels of biomarkers of oxidative stressControlled diet plus each of three treatments (15 or 30 g alcohol per day or no-alcohol placebo beverage), during three 8-week periods in random orderAfter adjusting for body mass index (all models) and total serum cholesterol (tocopherol and isoprostane models), there was a 4.6% decrease (p = 0.02) in α-tocopherol and a 4.9% increase (p = 0.07) in isoprostane levels when women consumed 30 g alcohol/day (p = 0.06 and 0.05 for overall effect of alcohol on a-tocopherol and isoprostanes, respectively).Moderate alcohol consumption increases some biomarkers of oxidative stress in postmenopausal women.
Dorgan et al. 200185
Same as 311
51 healthy postmenopausal women not using hormone replacement therapyThree-period crossover designElevated serum levels of estradiol, estrone, estrone sulfate, testosterone, androstenedione, progesterone, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), and androstenediol15 g or 30 g of alcohol per day or an alcohol-free placebo beverage through a three 8-week dietary period. Alcohol was supplied as 95% ethanol in 12 oz orange juice. Each dietary period was preceded by a 2- to 5-week washout period when participants did not consume any alcohol.15 g of alcohol/day resulted in an increase of 7.5% (95% confidence interval [CI]: −0.3 to 15.9%; p = 0.06) of estrone sulfate. 30 g of alcohol/day resulted in an increase of 10.7% (95% CI: 2.7 to 19.3%; p = 0.009) estrone sulfate
15 g of alcohol/day resulted in an increase of 5.1% (95% CI: 1.4 to 9.0%; p = 0.008) DHEAS. 30 g of alcohol/day resulted in an increase of 7.5% (95% CI: 3.7 to 11.5%; p <0.001) DHEAS
Results suggest a possible mechanism by which consumption of one or two alcoholic drinks per day by postmenopausal women could increase their risk of breast cancer.
Ginsburg et al. 19968812 postmenopausal women receiving oral estrogen (estradiol, 1 mg/day) and progestin (medroxy-progesterone acetate) replacement therapy were compared with 12 postmenopausal women who were not using estrogen replacement therapy (ERT).Randomized, double-blind, placebo-controlled crossover studyEffects of alcohol ingestion on estrogens in postmenopausal womenPineapple juice and 40% ethanol at a dose of 2.2 mL/kg of body weight (0.7 g/kg of body weight) in a total volume of 300 mL over 15 minutesWithin 50 minutes of alcohol ingestion in postmenopausal women on ERT, there was a 3-fold increase in estradiol levels from 297 to 973 pmol/L (p <0.001)
No changes in estradiol following alcohol ingestion in postmenopausal women not on ERT
Acute alcohol ingestion may lead to significant and sustained elevations in circulating estradiol.
Ginsburg et al. 19958714 menopausal women using transdermal estradiolTwo randomized crossover studiesEffect of acute ethanol ingestion on prolactin in menopausal women using estradiol replacementEthanol (1 mL/kg, 95% ethanol) over 20 minutesAlcohol when compared to isocaloric carbohydrate drink ingestion resulted in increased serum prolactin levels in both study 1 (p <0.03) and study 2 (p <0.001)There was an increase in serum prolactin levels.
Reichman et al. 19938634 premenopausal women with a history of regular menstrual cycleRandomized, diet-controlled crossover interventionThe effects of alcohol consumption on plasma and urinary hormone (DHEA, estrogens) concentrations in premenopausal women30 g of ethanol daily for three menstrual cycles and no alcohol for the other threePlasma DHEAS levels increased by 7.0% (p = 0.05) in the follicular phase
Plasma estrone levels increased by 21.2% (p = 0.01) in the peri-ovulatory phase
Plasma estradiol increased by 27.5% (p = 0.01), urinary estradiol increased by 31.9% (p = 0.009) in the peri-ovulatory phase
At the luteal phase, urinary estrone increased by 15.2% (p = 0.05), estradiol levels increased by 21.6% (p = 0.02), and estriol levels increased by 29.1% (p = 0.03)
Results suggest a possible mechanism between alcohol consumption and risk of breast cancer.

From: Appendix C, Evidence Tables

Cover of Alcohol Consumption and Cancer Risk
Alcohol Consumption and Cancer Risk: Understanding Possible Causal Mechanisms for Breast and Colorectal Cancers.
Evidence Reports/Technology Assessments, No. 197.
Oyesanmi O, Snyder D, Sullivan N, et al.

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