For men, the incidence rate for self-reported STIs was 2.0 per 100 person-years from first coitus to age twenty-one, 3.2 between age 21 to 26, and 2.0 between age 26 to 32. For women the rates over these time periods were 4.4, 3.0, and 1.4 per 100 person-years, respectively (Table 3).
The incidence rates for all self-reported STIs by number of sexual partners over these age periods are shown in Figure 1. Risk increased with number of partners, for both genders and most age periods. Within each stratum of number of partners save 0 to 1, the incidence rates for men peaked in the age period 21 to 26. For women with fewer than 10 sexual partners, there was a similar though much less marked peak in the age period 21 to 26, with rates across the 3 age periods similar to those for men. However, for women with 10 or more partners, the incidence rates were dramatically high for the youngest age period from first coitus to 21, decreasing slightly between 21 to 26 years, and dropping markedly by the age period 26 to 32.
Table 3 also displays the relationships between STI incidence and age period for men and women separately. Men in the age period 21 to 26 years had a statistically significantly higher incidence of all STIs compared with the younger age period (up to age 21) which increased after adjustment for number of partners to IRR = 1.9, 95% CI 1.3–2.8. Incidence rates dropped in the oldest age period (between ages 26 to 32) and were similar to those in the age period up to age 21; adjustment did not alter these findings (IRR = 1.1, 95% CI 0.70–1.9). Conversely for women, incidence rates decreased over time, with significantly lower rates in the age period 21 to 26 compared with first coitus to 21, though this difference was no longer significant after adjustment for number of sexual partners and condom use in the last 12 months (IRR = 0.79, 95% CI 0.56–1.1). Incidence rates decreased significantly further in the age period 26 to 32 years compared with the youngest period; this marked difference persisted after adjustment (IRR = 0.39, 95% CI 0.27–0.57). The general patterns for bacterial and viral STIs over these times were similar.
Table 4 displays the relationships between incidence of STIs and gender in 3 different age periods. There is evidence of a gender difference in STI incidence in the youngest age period (first coitus to 21), but not in the older age periods. In the age period up to age 21 years, incidence rates for all STIs were more than twice as high for women compared with men, a difference which was strengthened after adjustment for number of sexual partners (IRR = 2.6, 95% CI 1.8–4.0). No differences were found before or after adjustment in the older periods. This pattern held for bacterial and viral infections.
To investigate whether the patterns by gender and age could be explained by differences in opportunistic screening for STIs, we examined reasons for seeking health care (Table 5). Very few of the men’s diagnoses in the 2 youngest periods were made when “attending a health professional for another reason” (ie, could have been made by an opportunistic test). In contrast, for women this was the case for 22.5% of the infections diagnosed up to age 21. This partly explains the gender difference in the youngest age period. Nevertheless, women still had higher rates than men for the period first coitus to 21 (IRR = 2.0, 95% CI 1.3–3.1), then similar rates for the period 21 to 26 (IRR = 0.81, 95% CI 0.56–1.2) and the period 26 to 32 (IRR = 0.75, 95% CI 0.46–1.2). The patterns by age for men and women also remained the same when opportunistically diagnosed infections were removed from the analysis. For women, compared with the age period first coitus to 21 the rates decreased for the age period 21 to 26 (IRR = 0.90, 95% CI 0.62–1.3) and further for 26 to 32 (IRR = 0.45, 95% CI 0.29–0.69). For men, compared with the period first coitus to 21 the rates peaked for the age period 21 to 26 (IRR = 1.8, 95% CI 1.2–2.7) then dropped between 26 and 32 (IRR = 0.96, 95% CI 0.58–1.6).
We have shown, using data collected at 3 ages in a birth cohort, that adolescent women have significantly higher incidence rates of self-reported STIs than adolescent men. This difference remains after taking into account the number of partners and excluding diagnoses which may have been opportunistically detected. After adolescence, adjusted incidence rates increased significantly for men up to ages 21 to 26 and then fell, whereas for women, rates fell significantly throughout. Incidence of STIs increased with number of sexual partners, except for women in the age period 26 to 32 years. In this population, the commonest STIs were chlamydia, genital warts, and genital herpes.
A major strength of this study is that it is of a population-based birth cohort, so it is possible to examine age effects within the same people. Moreover, patterns by age between men and women can be compared directly. The cohort has a remarkably high retention rate, so participation bias is minimised. This is especially true in comparison with most studies of sexual behavior and self-reported STI where response rates are often in the region of 65% or less, and in which such bias is possible.13 Finally, detailed information on timing of first sexual intercourse and number of partners allowed adjustment for these aspects of sexual behavior. The results should be generalizable to industrialized countries with similar common STIs, as the cohort is in most respects representative of the New Zealand population. Although a comparison between this cohort and a national survey of sexual behavior showed that cohort members were more likely to report multiple sexual partners at age 18, this is likely to reflect the higher response rate and the methods of data collection which facilitated disclosure in our study.14 Furthermore, the occurrence of STIs up to age 21 was similar to US rates for a similar age and time period.15
One important limitation is that the data are based on self-reported diagnoses by a clinician. Self-report depends on access to diagnostic facilities for symptomatic cases (or their contacts) and to screening for asymptomatic cases. The accuracy of self-report is hard to gauge and it has been suggested that women may confuse cervical smear abnormalities with STI diagnoses.16 Although access to diagnostic facilities is good in New Zealand, access to screening has been variable and will have changed over time. Confusion with cytologic abnormalities is also likely to relate only to screen detected disease. Hence, most reliance can be placed on the results that exclude cases identified by opportunistic testing. Reassuringly these showed the same pattern as the overall results. Furthermore, most surveillance systems for STIs rely on diagnoses by clinicians and population surveys often rely on self-report. Both these data sources also have further limitations in examining patterns by gender and age, in particular that they are not able to account for generational differences.
A further limitation is that data on condom use and partner risk was incomplete and did not cover the whole period in which STI information was sought. Moreover, only limited information on patterns of sexual mixing was available. Hence, some residual confounding by aspects of sexual behavior is inevitable. The complexities of context, partners’ infection status, and the interdependency among sexual behaviors call for cautious interpretation of comparisons of STI rates.17 We have considered explanations for the observed differences with this caveat in mind.
Whether a person acquires an STI depends on biologic, behavioral, and epidemiologic factors. Further, whether the STI is recognized depends on the occurrence of symptoms, and whether testing is carried out in response to symptoms or undertaken on asymptomatic individuals. To interpret the incidence of self-reported STIs by gender and age requires consideration of all these factors related to acquisition and recognition.
Comparing women with men in the youngest age period, the much higher STI rate for women, after accounting for differences in testing and sexual behavior, implies either greater biologic susceptibility, greater prevalence of infection in sexual contacts, or a greater proportion of symptomatic infection for women. Current evidence suggests the latter is implausible.1 Greater biologic susceptibility may be because of the amount or vulnerability of the epithelial surface exposed (including cervical ectopy in adolescents) and the duration of exposure. This is the usual explanation for the higher efficiency of transmission from men to women in diseases that cause discharge, and hence for higher rates in women.1 Susceptibility may also be because of the body’s immunologic response. A further explanation, that there might be a greater prevalence of disease in sexual contacts of young women compared to men, was explored by adjusting for relative sexual experience of last partner, and for concurrent partnerships. These did not appreciably affect the incidence rate ratios over and above adjustment for number of sexual partners. From this evidence, biologic factors may be the most important determinants of the comparatively high rates of STIs among young women though an effect of prevalence of disease in sexual contacts cannot be ruled out because of the limitations of adjustment for confounding.
Comparing women and men in the older age periods, the similar rates of diagnosed STIs (adjusted for sexual behavior) were surprising, given the plausible biologic reasons for women’s greater susceptibility (apart from cervical ectopy). These similar rates were related to different ages of peak risk for men and women: for men, risk peaked at 21 to 26 years and then declined, whereas for women risk declined throughout. The decline in risk, after adjustment for sexual behavior, could represent residual confounding especially in relation to partners’ risk, but it could also suggest a decline in susceptibility.
The remarkably low rates for women between 26 to 32 years, and especially for those with 10 or more partners, was investigated further. They applied to both bacterial and viral infection. For genital herpes infections it is possible that the lower incidence at older ages for women could be because of previous infections (only first symptomatic infections were counted) or because of an increase in unrecognized infections. Our earlier analysis of serologically diagnosed herpes simplex virus 2 had shown that incident infections continued to increase with age.18 When we restricted our analysis to women who had reported no previous herpes infection, incidence rates of symptomatic disease still dropped with age (data not shown). On the other hand, comparison of self-reported herpes infections with serological diagnoses showed that, for women, the proportion that were clinically recognized dropped with age, though not significantly (data not shown). Hence, the decline in clinical herpes infections with age may be because of an increase in asymptomatic or unrecognized infections.
For bacterial STIs among women in the oldest age period (that were almost exclusively chlamydia), the most intriguing possibility for the lower incidence at older ages is that such women had greater exposure through more previous sexual partners, and had developed immunity to chlamydial infection. Prevalence of chlamydial infection in women has been shown to decrease with increasing age (though this analysis did not account for changes in partner numbers); and among sex workers the incidence of infection is significantly raised in adolescents compared with older women.19,20 A study of the natural history of chlamydial infection found that, at 4 years follow-up, 94% of women had cleared the infection.21 Rekart and Brunham have recently reviewed such evidence in seeking to understand the reason for increasing incidence of chlamydial infection in Canada.22 They propose that chlamydial infection which is not treated early leads to protective immunity, whereas early treatment may prevent its development, though the evidence for this explanation is contested.23,24
To explore whether older women with more partners might have protective immunity, we examined the previous sexual history of women aged 26 to 32. Women who reported 10 or more partners in that time period were significantly more likely to have had 10 or more sexual partners up to age 26 (82%), than those who reported fewer partners (40%), P <0.001. The proportions for men were similar (P <0.001). Thus our data, showing that older women who report more sexual partners were more likely to have had multiple partners in the past, and less likely to report a recent diagnosis of chlamydia, are consistent with previous infection which is not treated early leading to natural immunity.23 In New Zealand there has been no organized screening program for chlamydia so early treatment for asymptomatic infection will have been relatively uncommon. The fact that the same pattern was not seen for men, despite similar sexual histories, could be because of a different immune response by men, or to acquisition of immunity at a later age (not yet evident in our sample) as the peak risk for bacterial infections was older for men than for women. Further investigation of protective immunity to chlamydia and its effect on disease occurrence in both men and women is warranted.
In conclusion, the findings point to the period up to age 21 being a time of special risk for common STIs for women and of lower risk for men, confirming clinic-based surveillance data. In addition, the findings from age 21 to 32 point to changes in risk of STIs with age which are not accounted for by behavioral risk factors. It is not possible to determine definitively whether these differences represent unaccounted differences in sexual behavior, changes in the proportion with symptomatic disease, or changes in susceptibility.
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