To the Editor The article titled "Effect of Dietary Supplementation With Lutein, Zeaxanthin, and ω-3 on Macular Pigment: A Randomized Clinical Trial," by Korobelnik et al 1 has drawn conclusions that may not follow readily from the data. In specific, the finding that macular pigment (MP) does not increase in response to supplemental lutein among firstgeneration offspring of patients with neovascular age-related macular degeneration (AMD) might not be correct.In this study, 2 techniques were used to measure MP. 1 The first technique, the use of a MPD-Visucam (Carl Zeiss Meditec), has been independently discredited by multiple investigators on multiple occasions. 2,3 The investigators also used the Heidelberg Retina Angiograph to measure MP, an instrument which, to our knowledge, has not been validated and for which there are no published concordance data with readings taken with validated instruments. To measure MP with this device, the image must cover an expanse of retina that includes an anatomic site where MP is known to be optically present and an anatomic site where MP is known to be optically absent (a reference point). Measurements of MP are then calculated from the difference of the readings recorded centrally and those recorded at the reference point, in much the same way that one measures the height of a mountain against sea level and not from a point that is someway up a mountain path. Unfortunately, the reported method lacks a valid reference point; rather, it uses 6°, where MP is optically plentiful. Furthermore, MP is known to increase at 6°of eccentricity in response to supplementation, and so in this case the rising mountain peak was measured against a likewise rising mountain path, masking actual increases in MP. 4 Moreover, if 50% genetic risk for AMD precluded macular response to supplemental lutein (ie, the average genetic risk of the study cohort), surely those with 100% genetic risk (ie, patients with AMD) would also not respond to supplemental lutein? Yet we know from more than 20 peer-reviewed publications, 5 each using validated technology to measure MP, that maculae with AMD do exhibit increases in MP in response to supplemental lutein. Finally, the study did not have a profile-matched control group (ie, participants without a family history of AMD). This limitation would impede a clinically meaningful comment on the macular response to supplemental lutein in the cohort of interest.In summary, we would question the interpretation of the results of their study. We would welcome hearing how the authors would interpret their results in light of these comments.