A normally functioning menstrual cycle requires significant crosstalk between
hormones originating in ovarian and brain tissues. Reproductive hormone
dysregulation may cause abnormal function and sometimes infertility. The
inherent complexity in this endocrine system is a challenge to identifying
mechanisms of cycle disruption, particularly given the large number of unknown
parameters in existing mathematical models. We develop a new endocrine model to
limit model complexity and use simulated distributions of unknown parameters
for model analysis. By employing a comprehensive model evaluation, we identify
a collection of mechanisms that differentiate normal and abnormal phenotypes.
We also discover an intermediate phenotype--displaying relatively normal
hormone levels and cycle dynamics--that is grouped statistically with the
irregular phenotype. Results provide insight into how clinical symptoms
associated with ovulatory disruption may not be detected through hormone
measurements alone