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ADHD Medications Don't Pose Cancer Risk

Study found 2 popular drugs do not cause genetic damage that can lead to disease

FRIDAY, Nov. 21 (HealthDay News) -- Two popular medications for treating attention-deficit hyperactivity disorder (ADHD) do not cause genetic damage linked to an increased risk for developing cancer, a new study says.

The study, done by researchers at Duke University Medical Center and the National Institutes of Health, counters a previous one that reported biomarkers associated with an increased cancer risk were present in the blood of children taking the ADHD drug methylphenidate.

"The new findings should help alleviate some of the concerns that were raised by the previous study," study co-author Scott Kollins, director of Duke's ADHD program, said in a university news release. "However, we need to continue to study the long-term effects of these medications and expand our analyses to include older patient populations."

The new study, which looked at methylphenidate (Ritalin LA and Concerta) and amphetamine (Adderall and Adderall XR), used a larger study sample and conditions that apply to a wider cross-section of children with ADHD than the initial study did, he said.

"We looked at three common markers associated with damaged chromosomes and did not find increased genetic abnormalities in children taking either medication, regardless of a variety of factors, such as age, sex, body weight, height, race or ADHD subtype," Kollins said.

About 2 million children have ADHD, a condition commonly characterized by inattention, hyperactivity and impulsivity. Methylphenidates and amphetamines have been used to treat the condition for decades, with millions of prescriptions written for them in the United States every year.

The study was published in the November online issue of the Journal of the American Academy of Child & Adolescent Psychiatry.

More information

The U.S. National Institute of Mental Health has more about ADHD.

-- Kevin McKeever

SOURCE: Duke University Medical Center, news release, Nov. 19, 2008

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