Letters to the Editor
the NLSY. We evaluated the validity of these data in two
ways. First, we compared the reported data by year of birth,
a proxy for the length of time between the birth of the child
and the collection of data about the pregnancy (data about
children of the female NLSY respondents were first obtained in 1982, 3 years after the first round of the survey).
The reports of women whose infants were bom earlier in die
study period did not differ from those of women whose
babies were bom closer to the time of the NLSY data
collection.
In the absence of comparable data from another source,
our second approach was an evaluation of the reasonableness of the results. We found strong associations of maternal
height, weight gain (3), and age at menarche with birth
weight using the NLSY data, which, with the exception of
age at menarche (as described below), are consistent with
the results of previous research. In fact, the biologic variables explained a greater percentage of the variance in birth
weight man did the social environment or health behavior
variables.
Scholl et al. criticized the age at menarche data from the
NLSY because they were retrospectively collected, although they also used retrospectively collected data in their
studies (4, 5). Age at menarche is a significant event in a
girl's life, one that is not easily forgotten. Errors in recall
may occur, especially when women are asked to recall their
ages many years after the event; however, there is no
evidence that the timing of menarche is related to the
direction of recall errors (6, 7).
The age at menarche/birth weight relation we noted differs from the results of Scholl et al. (5). Later maturing
women had lower birth weights in our study. An early age
at menarche was related to an increased odds of low birth
weight in their study that was specific to small for gestational age babies. Their findings appear contrary to the
hypothesis of biologic immaturity, even though they argue
strongly about the importance of biologic immaturity for
adolescent pregnancy in their letter (1).
We suspect the reason for the different results is related to
differences in the two study samples. To control for chronologic age, Scholl et al. restricted their sample to births of
18-to 19-year-old women, whereas we sampled all first
pregnancies of women aged 14-25 years in 1979-1983,
and chronologic age was held constant in our analysis by
inclusion of the age variables in the regression model. By
imposing an age restriction for mother's age at birth, some
girls with later menarche were likely omitted from their
sample. Girls with later menarche differ in body type and
weight from early maturing girls (8, 9), which could explain
why they have smaller babies.
To reiterate our conclusions from the study (2), our
findings suggest that late menarche may have a negative
843
effect on pregnancy outcomes. Rather than the misinterpretation that biologic immaturity is not important, we concluded that the results of our analysis did not support the
biologic immaturity hypothesis as the reason that adolescents have smaller babies than women in their twenties. Our
evaluation of the data by year of birth and of the reasonableness of the results for height, weight gain, and age at
menarche suggests that errors in the measurement of these
variables are unlikely to be large. We stand by our conclusions that the reduced birth weights of adolescent mothers in
the NLSY sample are largely a result of their disadvantaged
social environment.
REFERENCES
1. Scholl TO, Hediger ML, Schall JI. Re: "Mechanisms for
maternal age differences in birth weight" (Letter). Am J
Epidemiol 1995; 143:843.
2. Strobino DM, Ensminger ME, Kim YJ, et al. Mechanisms for
maternal age differences in birth weight. Am J Epidemiol
1995;142:504-14.
3. Kleinman JC. Maternal weight gain during pregnancy: determinants and consequences. Department of Health and Human
Services, 1990. (Working paper series no. 21).
4. Scholl TO, Decker E, Karp RJ, et al. Early adolescent
pregnancy: a comparative study of pregnancy outcome in
young adolescents and mature women. J Adolesc Health Care
1984;5:167-71.
5. Scholl TO, Hediger ML, Vasilenko P m, et al. Effects of early
maturation of fetal growth. Ann Hum Biol 1989;16:335-45.
6. Damon A, Damon ST, Reed RB, et al. Age at menarche of
mothers and daughters, with a note on accuracy of recall. Hum
Biol 1969;41:161-75.
7. Livson N, McNeill D. The accuracy of recalled age of menarche. Hum Biol 1962;34:218-21.
8. Ellison PT. Morbidity, mortality and menarche. Hum Biol
1981;53:635-43.
9. Frisch RE. Fatness, menarche and female fertility. Perspect
BiolMed 1985;28:611-33.
Donna M. Strobino
Department of Maternal and Child Health
Margaret E. Ensminger
Department of Health Policy and
Management
Young J. Kim
Department of Population Dynamics
Joy Nanda
Department of Maternal and Child Health
School of Hygiene and Public Health
The Johns Hopkins University
624 North Broadway
Baltimore, MD 21205
RE: CONDOM EFFICACY AGAINST GONORRHEA AND NONGONOCOCCAL URETHRTTIS
The epidemic of human immunodeficiency virus (HIV)
has encouraged debate on the effectiveness of male condoms in preventing viral transmission. A variety of observational studies among couples with discordant infection
status have concluded that condoms are from 69 to 90
percent protective in typical "real world" settings (1, 2).
However, no study to date has reported on the true efficacy
of condoms per coital episode among discordant persons.
Am J Epidemiol
Vol. 143, No. 8, 1996
Data available from a clinical trial (3) conducted in 1975
provide a surrogate answer. In brief, male volunteers on a
large naval vessel were cultured for the presence of gonorrhea before shore leave. Upon returning to the ship, sexually
exposed members of the cohort were interviewed about
their sexual behavior and use of condoms. At this time, they
were also randomly assigned to either an antibiotic or a
placebo group. During the subsequent at-sea interval, a
844
Letters to the Editor
shipboard clinic monitored their gonorrhea status as well as
symptoms and signs of nongonococcal urethritis (NGU).
Our new tabulations differ slightly from those in the original
article because of the addition of NGU to the previously
reported cases.
Among 528 men in the placebo group, gonorrhea occurred in 50 and NGU in 21, for an incidence of 13.4
percent (table 1). However, no infections occurred in the 29
men who reported always using condoms during a total of
66 sexual exposures. Although the original article (3) stated
that the difference in gonorrhea between condom users and
nonusers was "not significant," our calculation including
NGU data and using a one-tailed Fisher's exact test showed
a p value of 0.02. Thus, reported use of condoms provided
significant protection against acquisition of gonorrhea or
NGU.
The strength of this study was its prospective determination of the condom status before the symptoms of infection
had occurred. Therefore, the exposure categories were ascertained independently from the outcome status, a difficult
situation to achieve among studies of sexual behavior and
transmission of sexually transmitted diseases. Although the
small number of condom users and the unknown infection
status of the sex partners limit the precision of additional
calculations, our analysis shows that condom use significantly protected the seaman from two of the most easily
transmitted sexually transmitted diseases.
TABLE 1. Rates of gonorrtiaa and nongonococcal urethritis
among male volunteers on a naval vessel, by use of
condoms*
Condom
use
Users
Nonusers
Total
No.
No.
Infected
Rate
29
499
528
0
71
71
O.Ot
14.2
13.4
* Rom Hooper et al. (3) and unpublished data,
t p < 0.05 by Fisher's one-tailed test.
When condoms are used correctly, consistently, and without breakage, they should be virtually 100 percent effective
in preventing infections transmitted from the cervix, vagina,
or rectal canal to the urethra and vice versa (e.g., gonorrhea,
chlamydial infection, trichomonal infection, and probably
human immunodeficiency virus and hepatitis virus infection). Moreover, when used consistently, condoms should
be partially effective in preventing infections of the external
genital epithelium, which is covered (e.g., syphilis, genital
herpes, human papillomavirus, and chancroid). From a population perspective, even for diese latter infections when
only partial prevention occurs, this can have major effects
on epidemic levels (4, 5).
REFERENCES
Weller SC. A meta-analysis of condom effectiveness in reducing sexually transmitted HTV. Soc Sci Med 1993;36:
1635-44.
Feldblum PJ, Morrison CS, Roddy RE, et al. The effectiveness
of barrier methods of contraception in preventing the spread of
HTV. AIDS 1995;9(Suppl A):585-93.
Hooper RR, Reynolds GH, Jones OG, et al. Cohort study of
venereal disease. I. The risk of gonorrhea transmission from
infected women to men. Am J Epidemiol 1978;108:136-44.
4. Cates W Jr, Hinman AR. AIDS and absolutism: the demand
for perfection in prevention. N Engl J Med 1992;327:492-4.
5. Anderson RM, May RM. Infectious diseases of humans: dynamics and control. Oxford, England: Oxford University
Press, 1991.
Willard Cates, Jr., M.D., M.P.H.
Corporate Director of Medical Affairs
Family Health International
Research Triangle Park, North Carolina
King K. Holmes, M.D., Ph.D.
Director, Center for AIDS and STD
Seattle, Washington
Editor's note: In accordance with Journal policy, the
original coauthors were asked if they wished to respond to
the letter by Drs. Cates and Holmes, but they chose not to
do so.
Am J Epidemiol
Vol. 143, No. 8, 1996