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Puberty/testosterone/ Increases Malaria Resistance in Boys
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- Subject: Puberty/testosterone/ Increases Malaria Resistance in Boys
- From: ttweed@wildrockies.org (Tony Tweedale)
- Date: Sun, 5 Dec 1999 20:08:32 -0700 (MST)
- Delivered-To: dioxin-l@venice.essential.org
Puberty Increases Malaria Resistance in Boys
WASHINGTON, Dec 02 (Reuters Health) - In boys, puberty
increases resistance to malaria caused by Plasmodium
falciparum, in parallel with increases in testosterone and
dehydroepiandrosterone sulfate (DHEAS).
The findings were presented earlier this week at the 48th
annual meeting of the American Society of Tropical Medicine
and Hygiene here.
Dr. Jonathan D. Kurtis from the University of Pennsylvania in
Philadelphia, Pennsylvania, and his team evaluated the impact
of age and pubertal development on the reappearance of
malaria parasites in young males, aged 12 to 35 years, during
two consecutive malaria seasons in western Kenya.
"Age significantly predicted pretreatment disease absence and
posttreatment malaria resistance, as well as the time to
reinfection," Dr. Kurtis said. "However, this age prediction was
confined to the pubertal age stratum...12 to 15."
"Resistance to parasitemia during the second season was
significantly associated with increased gonadal development,
as measured by Tanner staging, and hormonal measures,
including both DHEAS and testosterone levels," he said.
In multivariate models, increased testosterone and DHEAS
were independently associated with resistance to
parasitemia, after adjusting for age. "Males aged 15 to 20
years with high DHEAS levels had 45% lower mean parasite
densities than similar men with lower DHEAS levels, while
males with high testosterone levels experienced parasitemia
51% less often," he said.
The relationships did not hold for the youngest boys, Dr. Kurtis
reported, suggesting that some minimum level of exposure to
the parasite might be required for resistance to develop.
Although DHEAS and testosterone are recognized immune
modulators, Dr. Kurtis said, epidemiologic data do not support
a protective role, in that similar-aged nonpregnant females
have a lower incidence of malaria than males. He suggested
that the hormones may simply serve as indicators of other
developmental factors.
"Nevertheless," Dr. Kurtis concluded, "the data indicate that
developmental changes during puberty contribute to male
resistance to P. falciparum, independent of cumulative
exposure to malaria."
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