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Articles by M. B Schulze
Total Records ( 2 ) for M. B Schulze
  B Buijsse , E. J Feskens , M. B Schulze , D Palli , G Tognon , J Halkjaer , A Tjonneland , M. U Jakobsen , D. L van der A , T. I Sorensen and H. Boeing

Background: High fruit and vegetable intakes may limit weight gain, particularly in susceptible persons, such as those who stop smoking.

Objective: The objective was to assess the association of fruit and vegetable intake with subsequent weight change in a large-scale prospective study.

Design: The data used were from 89,432 men and women from 5 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). The association between fruit and vegetable intake and weight change after a mean follow-up of 6.5 y was assessed by linear regression. Polytomous logistic regression was used to evaluate whether fruit and vegetable intake relates to weight gain, weight loss, or both.

Results: Per 100-g intake of fruit and vegetables, weight change was –14 g/y (95% CI: –19, –9 g/y). In those who stopped smoking during follow-up, this value was –37 g/y (95% CI: –58, –15 g/y; P for interaction < 0.0001). When weight gain and loss were analyzed separately per 100-g intake of fruit and vegetables in a combined model, the odds ratios (95% CIs) were 0.97 (0.95, 0.98) for weight gain ≥0.5 and <1 kg/y, 0.94 (0.92, 0.96) for weight gain ≥1 kg/y, and 0.97 (0.95, 0.99) for weight loss ≥0.5 kg/y. In those who stopped smoking during follow-up, the odds ratios (95% CIs) were 0.93 (0.88, 0.99), 0.87 (0.81, 0.92), and 0.97 (0.88, 1.07), respectively (P for interaction < 0.0001).

Conclusions: Fruit and vegetable intake relates significantly, albeit weakly inversely, to weight change. For persons who stop smoking, high fruit and vegetable intakes may be recommended to reduce the risk of weight gain.

  E Fisher , N Stefan , K Saar , D Drogan , M. B Schulze , A Fritsche , H. G Joost , H. U Haring , N Hubner , H Boeing and C. Weikert

Background— Elevated circulating levels of fetuin-A in blood have been associated with increased risk of cardiovascular disease. The goal of our study was to prospectively investigate the potential causal nature of the association between fetuin-A levels and myocardial infarction (MI) and ischemic stroke by applying a Mendelian randomization approach.

Methods and Results— Five tagging single-nucleotide polymorphisms (rs2248690, rs2070633, rs2070635, rs4917, and rs6787344) capturing the common genetic variation of the fetuin-A coding gene 2-Heremans-Schmid glycoprotein (AHSG) were genotyped in a case-cohort comprising 214 MI cases, 154 ischemic stroke cases, and 2152 persons who remained free of cardiovascular disease events in the European Prospective Investigation into Cancer and Nutrition-Potsdam study. One single-nucleotide polymorphism (rs6787344) was discarded because of Hardy-Weinberg disequilibrium. All AHSG tagging single-nucleotide polymorphisms were associated with fetuin-A plasma levels (P<0.0001). AHSG rs4917 C>T showed the strongest association, explaining 21.2% of the phenotypic variance independent of potential confounding factors (+35.5 µg/mL increase per C-allele, P=2x10–121). Furthermore, the rs4917 C-allele showed a significant association with MI (adjusted hazard rate ratio [RR] 1.34, 95% CI 1.05 to 1.70, P=0.02). Based on this association, the expected RR for MI corresponding to 1 SD in fetuin-A was 1.54 and, thus, strikingly matches the previously observed association between fetuin-A plasma levels and MI risk (RR 1.59).

Conclusions— These data provide evidence for the causal nature of the recently reported association between fetuin-A plasma levels and MI risk, thereby suggesting an involvement of fetuin-A in the pathogenesis of cardiovascular disease.

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