In adult women asthma severity has been associated with phase in menstrual cycle1, reported early menarche2 and pregnancy3. Incident asthma has been associated with the use of hormone replacement therapy4 and with the use of the oral contraceptive (abstract only) with effects being more marked in lean women . These observations suggest that exposure to female sex hormones is important in asthma but the hormonal profile that would explain these associations is far from clear5. Studying children, particularly but not exclusively girls, through puberty may improve our understanding of the disease.

There are few large cohort studies with detailed information on asthma phenotype (eg;symptoms, atopic status and lung function), pubertal stage and other relevant physiological (eg: waist hip ratio; fasting blood sugar) and lifestyle/environmental factors (eg exercise). To date only the Tucson cohort has examined in depth the association of asthma with puberty but these analyses are insufficiently powered to fully disentangle the effects of obesity, age of puberty and differences between boys and girls. In the 1200 children studied analyses have suggested that there is a strong association of new asthma onset6 with increase in BMI - particularly in girls with early menarche - and that there is greater persistence of asthma symptoms through adolescence in those who are obese and in those with early puberty -associations observed in both boys and girls7 and which are independent of each other.

While it is widely thought that the association of asthma with early puberty may reflect a direct effect of hormones on asthma, an alternative hypotheses is that it reflects an underlying association of asthma with the metabolic syndrome. Epidemiological evidence for this is an association of asthma and some atopic markers with menstrual symptoms suggestive of polycystic ovarian syndrome (a feature of metabolic syndrome) 8 and studies suggesting an association of markers of insulin resistance with abnormal lung function9;10

The proposed collaboration would aim to:

1) Describe gender differences in asthma onset and asthma persistence from ages 8 to 15 years

2) Assess the association of age of puberty with asthma onset, asthma persistence, atopy and lung function

3) Develop from these testable hypotheses to explain observed associations. This would lead to a grant application for personnel and possibly further physiological/serological measures (including questionnaire based/physiological measures for the next follow-up). The application would most likely be to Asthma UK where asthma in adolescence has been identified as a priority area for research.