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Background and Objectives: Personalized nutritional counseling about calcium intake during office encounters requires rapid estimation of calcium intake. We compared the accuracy of physician estimates to a validated calcium intake measure and characterized women whose intakes were incorrectly deemed inadequate by physicians., Methods: As part of a controlled trial of brief, office-based calcium intake counseling of women, family physicians estimated calcium intake from patients' self-reported intake of dairy food/beverage intake and from their supplement use. We compared estimates to the Short Calcium Questionnaire (SCQ), a validated 7-day dietary recall measure completed by patients. Sensitivity/specificity of physician-estimated calcium intake was estimated by comparison with the SCQ., Results: For 97 women, SCQ rated 32 (33%) as inadequate, 55 (57%) as adequate, and 10 (10%) as excessive. When compared to SCQ, the sensitivity of physician-estimated calcium intake inadequacy was 97% (95% confidence interval [CI]: 94%-100%), specificity was 51% (95% CI: 41%-61%), and positive predictive value was 49% (95% CI: 39%-59%). Women with underestimated intakes were more likely to report a family history of osteoporosis and take a daily multivitamin. The major source of physician underestimation of calcium intake was underestimate of dairy product contribution., Conclusions: More accurate estimates of dairy-based calcium intake will lead to greater specificity in identifying inadequate calcium intake.

Purpose: [corrected] To confirm whether specific polymorphisms in intron 8 (IVS8) of the OPA1 gene are found more commonly in patients with normal tension glaucoma (NTG) compared to normal controls., Methods: This is a cohort study of 61 patients with NTG, 49 known healthy controls and 119 individuals from the general population. The DNA sequence was determined at the +4 and +32 positions of IVS8 of the OPA1 gene. Hardy-Weinberg equilibrium was confirmed in our population by comparing the allele frequencies in two additional genes, TP53 and TYRP1. Genotypes for the NTG and control groups were compared for statistically significant differences., Results: There were no differences in the OPA1 genotypes of the NTG and control groups at the +4 location, as had been suggested in a previous study, but a significant difference was observed at the +32 location of IVS8. The CC genotype was found in 28% of NTG patients compared to 13% of controls (p=0.006). The TC genotype was more prevalent in the control population (p=0.02) but this difference did not reach statistical significance when the Bonferroni adjustment was made for multiple analyses., Conclusions: We have refined the previously reported association between OPA1 sequence changes and NTG by identifying a specific CC genotype at position +32 in IVS8 of the OPA1 gene that acts as a marker for NTG. At the current time, NTG is frequently diagnosed late when loss of neurons has already caused significant and irreversible peripheral field loss. If a test could be designed to identify those people at risk of developing NTG, then careful screening might detect earlier signs of disease allowing commencement of treatment before significant field loss has occurred.