Sudden infant death syndrome (SIDS) may sometimes have a genetic component, a team of German researchers reports.

DNA analysis from a small group of infants who succumbed to SIDS revealed that many of the male children carried a particular enzyme mutation that may have impaired their ability to breath properly. This was not the case for female SIDS patients.

Study author Dr. Michael Klintschar, director of the Institute for Legal Medicine at Medical University Hannover in Germany, said his team tried to build upon previous research suggesting that "abnormalities in the brain stem, the part of the brain that regulates breathing and other basic functions, lead to SIDS."

"The reasons for these abnormalities are unclear," he noted, "but some scientists believe that the genes inherited by the parents might be one of several factors."

Klintschar and his colleagues found indications that SIDS risk might be higher among male infants who carry a mutation of an enzyme -- called MAOA -- that appears to impede key neurotransmitter function.

"Babies that have this variant inherited might have an impaired breathing regulation," he said. "But the risk conveyed by this gene variant is relatively small compared to other factors, like sleeping position (or exposure to) smoking. Moreover, the findings have to be replicated in another population sample."

The study appears online and in the March issue of Pediatrics.

The authors noted that SIDS is one of the great mysteries in pediatric medicine, with efforts to pin down the root cause for the sudden loss of children under the age of 1 year falling short of a definitive answer.

The new study focused on 156 white infants (99 boys and 57 girls) who were born in the Lower Saxony region of Germany and died while sleeping.

The deaths took place between the second and the 51st week of life, and all remained "unexplained" despite full autopsies, clinical history reviews and analyses of the circumstances of death.

DNA samples were taken from all the deceased, as well as from another 260 male adults between the ages of 18 and 30.

The result: MAOA mutations were more commonly found among male SIDS children than among their healthy male counterparts. This did not hold true with female SIDS children.

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Gene may be culprit in SIDS for boys

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