As I write this, New Year’s resolutions are being made. By the time you read this, many of them will likely be forgotten. One resolution, for the profession in general and for we as individuals, can be to recognize and treat early age-related macular degeneration (AMD).

As refractive specialists, we see patients regularly who interpret their problems as solvable by refraction. We have seen recently that subtle symptoms, such as reduced reading speed in the case of glaucoma (Burton et al, 2015; Smith et al, 2014; Ramulu et al, 2013; Cerulli et al, 2014), or difficulties in low-light conditions in the case of early AMD (Yazdanie et al, 2017; Laíns et al, Sep. 2017; Laíns et al, Apr. 2017; Tahir et al, 2017, and others. Full list available at .) represent early indicators of these vision-threatening conditions.

In addition, the prevalence of these two disorders has been reported as greater than previously thought in the case of glaucoma (Waisbourd et al, 2016) and overlooked in the case of early AMD (Neely et al, 2017). Eyecare practitioners have the unique position and responsibility to make early diagnoses based on subtle symptoms masquerading as refractively corrective problems.

Early AMD Clues

An emerging sentinel for consequential AMD is impaired dark adaptation (DA) (Owsley et al, Feb. 2016; Owsley et al, 2014). Querying patients when suspicious of subclinical AMD can lead to definitive quantitation of prolonged DA. The pathophysiological basis for this phenomenon is subclinical deposits (basal laminar and linear deposits) at the level of Bruch’s membrane prior to the development of clinically detectable drusen (Owsley et al, Apr. 2016; Owsley et al, Feb, 2016). The mechanism is obstructed nutritional transport from the choriocapillaris to the outer retina. This is significant when considering the specific underdiagnosis of early AMD (Neely et al, 2017). In this report, both clinical examination and fundus-photo evaluation by clinicians overlooked approximately one-quarter of patients diagnosed with early AMD on further review by trained readers (not clinicians).

Intervene ASAP

Because of the significant and growing problem that AMD represents, the earliest diagnosis, as with glaucoma, demands the earliest interventions. Some may argue that the Age-Related Eye Disease Study (AREDS) and the Age-Related Eye Disease Study 2 (AREDS2) showed only a reduced progression in patients who had been diagnosed with moderate-to-advanced AMD (AREDS Research Group, 2001; AREDS2 Research Group et al, 2013). The train had already left the station, so to speak. And, the cascade of vision loss in AMD is thought to be inevitable (Ferris et al, 2013).

But, what if impaired DA could identify reliably subclinical indicators of AMD? Some would say that the proven interventions apply only to the parameters of AREDS participants (over 50 years old, moderate-to-advanced AMD in at least one eye), with the expectation of slowing the progression to vision loss. In fact, there is some controversy over the individual outcomes and the wholesale recommendation of the AREDS2 formula (Evans and Lawrenson, 2017).

However, there is evidence for a prophylactic role for AREDS and AREDS components for early AMD (Ho et al, 2011; Gong et al, 2017; García-Layana et al, 2017). In addition, minimization of alterable lifestyle risk factors can be employed as well (Joachim et al, 2017; Jabbarpoor Bonyadi et al, 2017; Gopinath et al, 2015). Supplemental carotenoids, for example, can minimize the result of reduced transport across a compromised Bruch’s membrane.

Realizing the predicted impact to individuals and society (Rein et al, 2009; West, 2000), with newer diagnostic protocols available, let’s resolve to identify the earliest changes and intervene for these candidates for vision loss. CLS

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