Patients with type 1 diabetes (T1D) have different ocular biometry than normal eyes, according to researchers. Although prior studies suggested that diabetic eyes show “accelerated aging,” a research team who published in Advances in Ophthalmology Practice and Research say they have developed a paraxial eye model that describes growth and change in diabetic eyes as fundamentally different from normal eyes.

Until now, no such model has illustrated how individuals with diabetes differ in refractive error, corneal curvature radii, and internal measurements. Researchers  used these and other biometric measurements of 72 patients with T1D to create the model.

The population sample (mean age 41.5±12.4 years) were recruited chiefly at Queensland University of Technology for the LANDMark study. Cohort data was compared with healthy eyes of the Atchison aging emmetropic eye model.


Continue Reading

Results of linear regression analysis show almost no influence of HbA1c on biometric measurements. Parameters of anterior corneal radius of curvature (RoC), central corneal thickness, and spherical equivalent refraction were constant. Three factors were impacted by the time since diabetes onset, though — anterior and posterior lens RoC, and anterior chamber depth (ACD). Finally, 3 measurements depended on current age along with time since onset — axial length (AL), lens thickness, and posterior corneal RoC.

The model’s data reveals that, when taking out the element of age of onset, both ACD and lens thickness proceed along a similar course in T1D and healthy eyes, but at an increased rate. Anterior lens RoC and lens equivalent index traced a pattern not unlike emmetropic eyes, as well — also to a higher degree.

However, researchers found 2 other parameters that demonstrated trends that are not the same as a normal aging eye model. Healthy eyes had a slow, steady reduction in lens power of -0.0425 D per year, but diabetic eyes exhibited no significant change. Further, vitreous chamber depth of normal eyes experienced a drop of -0.013 mm per year, although diabetic eyes’ decreased by -0.021 mm per year. “This rate was half the [lens thickness] increase (+0.043 mm/yr), while the other half of the lens increase matched the decrease in ACD (–0.022 mm/yr),” according to the study. 

For the factors of ACD, lens thickness, lens RoC, and vitreous chamber depth; developing diabetes earlier in life caused growth changes sooner. AL, posterior corneal RoC, and lens power were constant with current age, subject to age at onset. The investigation notes that even though diabetic eyes do not display age-related lens power decreases, concurrent changes in equivalent lens index may explain this “lens paradox.” Diabetic eyes appear to present a distinctive refractive evolution compared with normal eyes of any age. Also, earlier childhood diabetic lens changes that happen slowly may let them adapt, potentially resulting in higher lens powers and shorter AL.

Since the sample included participants with well-controlled blood sugar, no disease-related eye disorders, and a narrow scope of refractions, data may not represent patients with retinopathy — a limitation of the study. However, this analysis builds the basis for a paraxial eye model, and presents new knowledge demonstrating “too many discrepancies with normal growth to support the idea that the influence of diabetes may simply be considered as accelerated aging.”

Reference

Rozema JJ, Khan A, Atchison DA. Modeling ocular ageing in adults with well-controlled type 1 diabetes. Advances in Ophthalmology Practice and Research. Available online on April 12, 2022. doi:10.1016/j.aopr.2022.100048