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Research · 04 of 06

Three years of CGM in type 1 diabetes: the groups you expect to do worst are not the ones who fail to improve

Set glycaemic targets from the patient's own CGM trajectory, not from their age or CKD label — those groups improved without more hypoglycaemia.

Design
multicentre longitudinal observational study using linear mixed-effects models
Population
1,028 adults with type 1 diabetes contributing 3,441 CGM profiles over three years
Primary outcome
longitudinal change in time in range 70-180 mg/dL, time below range and glycaemic variability by subgroup
Effect
improvement in time in range for CKD (beta = 0.228; P = 0.002) and highest TyG tertile (beta = 0.083; P = 0.001); attenuated by severe beta-cell failure (beta = -0.119; P = 0.025); older vs younger comparable (beta = 0.110; P = 0.102) with time below range 1.7% vs 3.5% (P < 0.001)

A multicentre study followed 1,028 adults with type 1 diabetes contributing 3,441 continuous glucose monitoring profiles over three years, stratified by age, chronic kidney disease, beta-cell function, BMI and triglyceride-glucose tertile. At baseline the expected pattern held: older age, CKD, severe beta-cell failure, higher BMI and the highest TyG tertile all spent more time above 180 mg/dL.

The trajectories diverged from that expectation. Older adults improved time in range comparably to younger ones and held a lower time below 70 mg/dL throughout. The CKD group improved time in range significantly without more hypoglycaemia. It was severe beta-cell failure — not age, not kidney disease — that attenuated both the gain in time in range and the reduction in time below range.

The authors' own emphasis is on the spread: CGM metrics varied widely within every subgroup. A label such as 'older' or 'CKD' predicts the baseline but not the direction of travel, which is an argument for setting targets from a patient's own CGM trajectory rather than from their risk category.

In practice that means the reflex of loosening targets for an older patient or one with CKD deserves a look at their actual data first.

  • Before relaxing a target for age or CKD, look at that patient's own time below range over the last three months
  • Residual beta-cell function is the variable most worth knowing when improvement stalls despite good engagement
  • Track time below 70 mg/dL as a separate outcome, not as a footnote to time in range
  • Review CGM trajectory across visits rather than judging from a single 14-day report
  • Where beta-cell failure is severe, set expectations about the ceiling on improvement early rather than after repeated intensification

Don't overread it

This was observational follow-up, not a trial — it cannot show that any intervention produced the improvement seen in the older and CKD groups.

The statistics, in plain English

The beta coefficients are from linear mixed-effects models and describe the difference in rate of change per subgroup, not an absolute difference in time in range — so beta = 0.228 for CKD means that group improved faster, not that they gained 0.23 percentage points. The older-adult comparison, beta = 0.110 with P = 0.102, is a non-significant result: it supports 'no detectable difference from younger adults', which is the point being made, but a non-significant difference is not proof of equivalence. The wide within-subgroup variation the authors report is the reason a group-level average should not be read onto an individual patient.

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