Brown · Journal of diabetes science and technology 2015 · prospective longitudinal observational study · n=12

Fluctuations of Hyperglycemia and Insulin Sensitivity Are Linked to Menstrual Cycle Phases in Women With T1D.

Cited 76 times in the scientific literature.

Level 4 - case-series / case-control

Small prospective observational study evaluating within-subject repeated measures without an external control group.

PubMed 26468135 · doi:10.1177/1932296815608400 · record verified 2026-08-29

What was done

Twelve women with type 1 diabetes on continuous subcutaneous insulin infusion and continuous glucose monitoring were followed prospectively across 3 consecutive menstrual cycles (33 of 36 cycles confirmed ovulatory using ovulation prediction kits and laboratory confirmation). Glycemic risk was evaluated using the Low and High Blood Glucose Indices (LBGI and HBGI), and insulin sensitivity was estimated via Kalman filtering from meal and insulin data. Changes across menstrual cycle phases were assessed using repeated-measures ANOVA.

What was found

In 12 subjects (mean age 33.1 ± 7.0 years, BMI 25.7 ± 2.9 kg/m², A1c 6.8 ± 0.7%): - Hyperglycemia risk (HBGI) varied significantly across the cycle (P = .023), increasing during periovulation and early luteal phases before returning to baseline. - Insulin sensitivity was significantly depressed during the luteal phase compared to the early follicular phase (P ≤ .05). - Hypoglycemia risk (LBGI) was stable in the follicular phase and decreased non-significantly thereafter. - Total daily insulin, carbohydrates, and calories showed no significant fluctuations across the cycle.

Why it matters

This study provides evidence that menstrual cycle phases predictably influence insulin sensitivity and hyperglycemia risk in women with type 1 diabetes, which could inform adaptive closed-loop insulin delivery algorithms.

Limits

The sample size was very small (n = 12), and participants had well-controlled diabetes (mean A1c 6.8%), limiting generalizability. Insulin sensitivity was mathematically estimated from meal and insulin data rather than measured directly via hyperinsulinemic clamp.

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