Summary: In a 12-month study of adolescents with poorly controlled type 1 diabetes, bone density was below reference values, but changes in glycaemic control and a measured advanced glycation end-product did not correlate with bone outcomes, whereas a rise in IGF-1 was associated with bone density accrual.
PICO Summary
| Element | Detail |
|---|---|
| Population | 37 adolescents with poorly controlled type 1 diabetes (mean HbA1c 9.9%, mean age 14.3); 12-month longitudinal study within an RCT, Finland. |
| Intervention | Assessment of glycaemic control (HbA1c, CGM, glycaemic load), IGF-1, and the AGE methylglyoxal-hydro-imidazolone (MG-HI) against DXA bone measures. |
| Comparison | Correlation/regression across the cohort over 12 months. |
| Outcome | Bone mineral density z-scores at spine, proximal femur, and total body were about 0.5 SD below reference (p=0.005–0.04). Over 12 months the only significant BMD change was an increase at the proximal femur in girls. An increase in IGF-1 was associated with BMD accrual, while changes in HbA1c, time in range, or MG-HI were not. No vertebral fractures were found. |
Expert Commentary
This is a careful mechanistic study that complicates a tidy assumption, and its honesty is its strength. It confirms what we suspect, that adolescents with poorly controlled type 1 diabetes have lower bone density, roughly half a standard deviation below reference at multiple sites, during the very years when peak bone mass should be accruing. But the intuitive culprit did not hold up: neither changes in HbA1c or time in range nor the measured advanced glycation end-product correlated with bone outcomes, which argues against a simple glucose-to-bone causal chain over this timeframe. What did track with bone density accrual was IGF-1, pointing toward the growth-hormone axis as a more proximate driver of skeletal health in this group. The limitations are clear: only 37 adolescents, a single AGE measured, DXA rather than higher-resolution bone imaging that can assess microarchitecture, and twelve months may simply be too short to capture glycaemia’s slower skeletal effects. Can I use this with my patients? Conceptually. It reminds me to consider bone health in adolescents with long-standing poor control while being honest that tightening glucose alone may not quickly repair density, and that the IGF-1 signal and better imaging deserve follow-up before firm clinical guidance.
References
Pulkkinen MA, Varimo T, Toiviainen-Salo S, et al. Skeletal health in adolescents with poorly controlled type 1 diabetes: results from a randomized controlled trial. BMJ Open Diabetes Res Care. 2025;13(5):e005134. doi:10.1136/bmjdrc-2025-005134