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Articles by B Rosner
Total Records ( 2 ) for B Rosner
  E. E Devore , F. J van Rooij , A Hofman , B Rosner , M. J Stampfer and M. M. Breteler
 

Background: Greater fish and omega-3 (n–3) polyunsaturated fatty acid (PUFA) intake may reduce dementia risk; however, previous studies have reported conflicting results, which were largely based on short-term follow-up.

Objective: The objective was to study the dietary consumption of fish and omega-3 PUFAs in relation to long-term dementia risk.

Design: We studied 5395 participants aged ≥55 y in the Rotterdam Study who were free of dementia and reported dietary information at baseline. We used age- and sex-adjusted Cox proportional hazard and multivariate-adjusted models to evaluate the relative risk of dementia and Alzheimer disease (AD) across categories of typical fish intake (none, low, and high) and fish type consumed (none, lean, and fatty). We also evaluated dementia and AD risk across tertiles of omega-3 PUFA intake, specifically, total long-chain omega-3 fatty acids: eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), -linolenic acid, and EPA and DHA individually.

Results: During an average follow-up of 9.6 y, dementia developed in 465 participants (365 with a diagnosis of AD). In multivariate-adjusted models, total fish intake was unrelated to dementia risk (P for trend = 0.7). Compared with participants who typically ate no fish, those with a high fish intake had a similar dementia risk (hazard ratio: 0.95; 95% CI: 0.76, 1.19), as did those who typically ate fatty fish (hazard ratio: 0.98; 95% CI: 0.77, 1.24). Dietary intakes of omega-3 PUFAs were also not associated with dementia risk, and the results were similar when we considered AD specifically.

Conclusion: In this Dutch cohort, who had a moderate consumption of fish and omega-3 PUFAs, these dietary factors do not appear to be associated with long-term dementia risk.

  E. L Berson , B Rosner , M. A Sandberg , C Weigel DiFranco , R. J Brockhurst , K. C Hayes , E. J Johnson , E. J Anderson , C. A Johnson , A. R Gaudio , W. C Willett and E. J. Schaefer
 

Objective  To determine whether lutein supplementation will slow visual function decline in patients with retinitis pigmentosa receiving vitamin A.

Design  Randomized, controlled, double-masked trial of 225 nonsmoking patients, aged 18 to 60 years, evaluated over a 4-year interval. Patients received 12 mg of lutein or a control tablet daily. All were given 15 000 IU/d of vitamin A palmitate. Randomization took into account genetic type and baseline serum lutein level.

Main Outcome Measures  The primary outcome was the total point score for the Humphrey Field Analyzer (HFA) 30-2 program; prespecified secondary outcomes were the total point scores for the 60-4 program and for the 30-2 and 60-4 programs combined, 30-Hz electroretinogram amplitude, and Early Treatment Diabetic Retinopathy Study acuity.

Results  No significant difference in rate of decline was found between the lutein plus vitamin A and control plus vitamin A groups over a 4-year interval for the HFA 30-2 program. For the HFA 60-4 program, a decrease in mean rate of sensitivity loss was observed in the lutein plus vitamin A group (P = .05). Mean decline with the 60-4 program was slower among those with the highest serum lutein level or with the highest increase in macular pigment optical density at follow-up (P = .01 and P = .006, respectively). Those with the highest increase in macular pigment optical density also had the slowest decline in HFA 30-2 and 60-4 combined field sensitivity (P = .005). No significant toxic effects of lutein supplementation were observed.

Conclusion  Lutein supplementation of 12 mg/d slowed loss of midperipheral visual field on average among nonsmoking adults with retinitis pigmentosa taking vitamin A.

Application to Clinical Practice  Data are presented that support use of 12 mg/d of lutein to slow visual field loss among nonsmoking adults with retinitis pigmentosa taking vitamin A.

Trial Registration  ClinicalTrials.gov Identifier: NCT00346333

 
 
 
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