OBJECTIVE The nature of the independent relationship between polycystic ovary syndrome (PCOS) and type 2 diabetes remains unclear. Few studies have aimed to clarify this relationship independent of obesity in longitudinal population-based cohorts. RESEARCH DESIGN AND METHODS We used the Australian Longitudinal Study on Women’s Health (ALSWH) (2000–2015) database to estimate nationwide incidence rates and predictors of type 2 diabetes among women aged 18–42 using person-time and survival analysis. RESULTS Over a follow-up of 1,919 person-years (PYs), 186 women developed type 2 diabetes. The incidence rate was 4.19/1,000 and 1.02/1,000 PYs (P < 0.001) in PCOS and control subjects. On subgroup analyses across healthy-weight, overweight, and obese categories of women, the incidence rates for type 2 diabetes were 3.21, 4.67, and 8.80, whereas incidence rate ratios were 4.68, 3.52, and 2.36 (P < 0.005) in PCOS versus age-matched control subjects. PCOS was one of the most influential predictors for type 2 diabetes in the entire cohort (hazard ratio 3.23, 95% CI 2.07–5.05, P < 0.001) adjusting for BMI, education, area of residence, and family history of type 2 diabetes. CONCLUSIONS Women with PCOS are at an increased risk of type 2 diabetes, irrespective of age and BMI. The incidence of type 2 diabetes increases substantially with increasing obesity; yet, PCOS adds a greater relative risk in lean women. Based on the overall moderate absolute clinical risk demonstrated here, guideline recommendations suggest type 2 diabetes screening every 1–3 years in all women with PCOS, across BMI categories and age ranges, with frequency influenced by additional type 2 diabetes risk factors.

Background: Polycystic ovary syndrome (PCOS) is challenging to diagnose. While the 2003 Rotterdam criteria are widely used for adults, the 2018 international PCOS guideline recommended updated Rotterdam criteria with both hyperandrogenism and oligo-anovulation for adolescents based on evidence-informed expert consensus. This study compared the prevalence of PCOS using updated and original Rotterdam criteria in community-based adolescents and explored long-term body mass index (BMI) trajectories across different diagnostic phenotypes. Methods: Overall, 227 postmenarchal adolescent females from the prospective cohort Raine Study undertook comprehensive PCOS assessment at age 14–16 years. Detailed anthropometric measurements were collected from birth until age 22 years. Cross-sectional and longitudinal BMI were analyzed using t tests and generalized estimating equations. Results: PCOS was diagnosed in 66 (29.1%) participants using original criteria versus 37 (16.3%) participants using updated Rotterdam criteria. Using updated criteria, participants with PCOS had higher BMI than participants without PCOS from prepubertal. Only the phenotype meeting the updated criteria was significantly associated with higher long-term BMI gain whereas other PCOS phenotypes had similar BMI trajectories to participants without PCOS (p < 0.001). Conclusions: The use of the 2018 updated Rotterdam criteria reduces over-diagnosis of PCOS in adolescents and identifies those at the greatest risk of long-term weight gain, a key contributor to disease severity and long-term health implications. The BMI trajectories of females with PCOS on updated criteria diverge prepubertally compared to those without PCOS. This work supports targeting adolescents diagnosed with PCOS on the 2018 updated criteria for early lifestyle interventions to prevent long-term health complications.

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting 8%–13% of reproductive‐aged women. The aetiology of the syndrome is complex, with genetic susceptibility, androgen exposure in early life and adiposity related dysfunction leading to perturbance in hypothalamic–ovarian function. PCOS clinical features are heterogeneous, with manifestations arising even in early adolescence, developing into multisystem reproductive, metabolic and psychological manifestations in adulthood. In this review, we will discuss challenges in the diagnosis of PCOS and understanding of the natural history of PCOS.

Human placental lactogen (hPL) is a placental hormone which appears to have key metabolic functions in pregnancy. Preclinical studies have putatively linked hPL to maternal and fetal outcomes, yet—despite human observational data spanning several decades—evidence on the role and importance of this hormone remains disparate and conflicting. We aimed to explore (via systematic review and meta-analysis) the relationship between hPL levels, maternal pre-existing and gestational metabolic conditions, and fetal growth. MEDLINE via OVID, CINAHL plus, and Embase were searched from inception through 9 May 2022. Eligible studies included women who were pregnant or up to 12 months post-partum, and reported at least one endogenous maternal serum hPL level during pregnancy in relation to pre-specified metabolic outcomes. Two independent reviewers extracted data. Meta-analysis was conducted where possible; for other outcomes narrative synthesis was performed. 35 studies met eligibility criteria. No relationship was noted between hPL and gestational diabetes status. In type 1 diabetes mellitus, hPL levels appeared lower in early pregnancy (possibly reflecting delayed placental development) and higher in late pregnancy (possibly reflecting increased placental mass). Limited data were found in other pre-existing metabolic conditions. Levels of hPL appear to be positively related to placental mass and infant birthweight in pregnancies affected by maternal diabetes. The relationship between hPL, a purported pregnancy metabolic hormone, and maternal metabolism in human pregnancy is complex and remains unclear. This antenatal biomarker may offer value, but future studies in well-defined contemporary populations are required.