Analgesic use in relation to sex hormone and prolactin concentrations in premenopausal women
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Common analgesics (aspirin, non-aspirin NSAIDs, and acetaminophen) may be associated with hormone-related cancers, possibly via effects on sex hormone and prolactin concentrations.
Between 1996 and 1999, 29,611 participants in the Nurses’ Health Study II (NHSII) provided blood samples; 18,521 provided samples timed in the early follicular and mid-luteal phases of the menstrual cycle, the remainder provided untimed samples. We assessed the cross-sectional relationship between analgesic use and plasma sex hormone and prolactin concentrations among 2,034 premenopausal women, 32–54 years old, who served as controls in nested case–control studies, or participated in a within-person hormone reproducibility study in the NHSII; this included 1,700 timed and 334 untimed samples. Estrogens and progesterone were measured in timed samples; androgens and prolactin were measured in timed and untimed samples.
In multivariable models, non-aspirin NSAIDs were positively associated with follicular free estradiol [13.5 % higher, use ≥4 days/week vs. nonusers (p = 0.04; p trend = 0.11)]; results for follicular total estradiol were similar (13.2 % higher, p = 0.06; p trend = 0.11). Acetaminophen use was inversely associated with prolactin (11.8 % lower, use 2 days/week vs. nonusers, p = 0.01, p trend = 0.04). Acetaminophen was also inversely associated with free testosterone (7.1 % lower, use 2 days/week vs. nonusers, p = 0.04; p trend = 0.04). No other associations were observed with the other hormones, or with aspirin use.
There were no clear patterns between analgesic use and sex hormones in premenopausal women. Acetaminophen use may be modestly associated with prolactin and free testosterone. Our results do not support that analgesic use influences cancer risk through alterations in premenopausal circulating sex hormones or prolactin.
KeywordsAnalgesics NSAID Aspirin Sex hormone Prolactin Premenopausal
Funding for this project came from the NIH R01 CA67262 and R01 CA50385 as well as NIH/NCRR CTSA Grant Number UL1 RR024150. RT Fortner is supported in part by T32 CA09001.
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