Women who take over-the-counter medicines for headaches and inflammation boost their chances of developing high blood pressure, a long-term epidemiological study suggests. Among the drugs are acetaminophen and ibuprofen, but not aspirin, researchers report in the Oct. 28 Archives of Internal Medicine.
Scientists analyzed medical and lifestyle data from questionnaires filled out by 80,020 female nurses aged 31 to 50. The surveys, completed by women in 15 states in 1995 and again in 1997, revealed how often the women used these analgesics and whether they had been diagnosed with high blood pressure during that time.
About half the women took aspirin at least once a month, and three-fourths used acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, that often.
Women taking acetaminophen or NSAIDs in any amount had about a one-sixth greater incidence of high blood pressure than did women who didn’t take any of the analgesics. Moreover, compared with the no-analgesics group, women who took acetaminophen or NSAIDs at least 22 days per month had roughly twice the rate of high blood pressure, and women who took aspirin, whether seldom or frequently, were no more likely to have high blood pressure, the researchers found.
Acetaminophen is sold as Tylenol; ibuprofen, as Advil or Motrin. Both drugs are also marketed generically.
To eliminate any differences among the women that might skew the results, the scientists took into account age, weight, and other physical and lifestyle factors, says study coauthor Gary C. Curhan, an epidemiologist and nephrologist at Harvard Medical School in Boston.
It’s possible that women taking acetaminophen and NSAIDs have more aches and pains and therefore visit doctors more often than women not taking analgesics, he says. Such women might get their blood pressure checked more frequently and hence be diagnosed with hypertension more often. However, such “detection bias” seems unlikely here, Curhan says, because the women routinely taking aspirin, another analgesic, presumably would fall into the same group. Yet they were no more likely to have hypertension than women not taking the pain relievers.
Any biological link between having high blood pressure and taking pain relievers remains obscure, Curhan says. But there are points at which the phenomena cross paths. For example, natural hormonelike compounds called prostaglandins influence blood pressure, inflammation, and muscle contraction. NSAIDs inhibit prostaglandin production in the body, which is how the drugs reduce inflammation. Acetaminophen apparently does so in the brain (SN: 9/21/02, p. 180: Acetaminophen in Action: Effect on an enzyme may stop pain, lower fever).
Even so, precisely how the drugs’ influence on prostaglandins–or other compounds in the body–might increase blood pressure has yet to be determined, Curhan says.
Mahendr S. Kochar, an internist at the Medical College of Wisconsin in Milwaukee, agrees.
“This work is provocative,” he says. It raises a question about connections between high blood pressure and NSAIDs and acetaminophen, “but I don’t think it answers it.” To do that, researchers need to conduct a blood pressure study in which some participants get placebos instead of acetaminophen or NSAIDs, Kochar says, and that might help establish a cause and effect.
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