Low-Dose Atropine (0.01%–0.05%) Combined with Defocus Lenses: The LAMP Protocol

Historically, atropine was believed to stop myopia by paralyzing ciliary muscle accommodation. Today, research has definitively proven that atropine works through a non-accommodative biochemical pathway, acting as a non-selective antagonist on M1 and M4 muscarinic acetylcholine receptors located in the retina and sclera.

By blocking these receptors, atropine directly upregulates glycosaminoglycan synthesis and prevents collagen fibril dissolution in the posterior scleral shell, physically preventing the eye from stretching.

The landmark LAMP (Low-Concentration Atropine for Myopia Progression) study published in Ophthalmology evaluated 438 children across multiple years:

• 0.01% Atropine: Produced modest myopia control (approx. 27% reduction in axial elongation).
• 0.025% Atropine: Demonstrated significantly stronger efficacy (approx. 50% reduction).
• 0.05% Atropine: Achieved the optimal balance—reducing spherical equivalent progression by 67% and axial elongation by 51% with minimal pupillary dilation ($< 1\ \text{mm}$) and negligible accommodation loss.

While atropine stiffens the sclera biochemically, defocus lenses (DIMS or H.A.L.T.) provide optical myopic defocus cues on the peripheral retina. Because they target two completely separate physiological pathways, their combined therapeutic effect is additive—achieving over 80% total myopia arrest in aggressive progressors.

Because atropine causes mild pupil dilation ($0.5\text{--}1.0\ \text{mm}$), patients require spectacles equipped with ELLASUV UV400 and high-efficiency anti-glare coatings to protect the light-sensitized crystalline lens and retina.