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Träfflista för sökning "WFRF:(Schulz Christina Alexandra) ;pers:(Hellstrand Sophie)"

Sökning: WFRF:(Schulz Christina Alexandra) > Hellstrand Sophie

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1.
  • Ericson, Ulrika, et al. (författare)
  • Dietary and genetic risk scores and incidence of type 2 diabetes
  • 2018
  • Ingår i: Genes and Nutrition. - : Springer Science and Business Media LLC. - 1555-8932 .- 1865-3499. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Both lifestyle and genetic predisposition determine the development of type 2 diabetes (T2D), and studies have indicated interactions between specific dietary components and individual genetic variants. However, it is unclear whether the importance of overall dietary habits, including T2D-related food intakes, differs depending on genetic predisposition to T2D. We examined interaction between a genetic risk score for T2D, constructed from 48 single nucleotide polymorphisms identified in genome-wide association studies, and a diet risk score of four foods consistently associated with T2D in epidemiological studies (processed meat, sugar-sweetened beverages, whole grain and coffee). In total, 25,069 individuals aged 45-74 years with genotype information and without prevalent diabetes from the Malmö Diet and Cancer cohort (1991-1996) were included. Diet data were collected with a modified diet history method. Results: During 17-year follow-up, 3588 incident T2D cases were identified. Both the diet risk score (HR in the highest risk category 1.40; 95% CI 1.26, 1.58; P trend=6×10-10) and the genetic risk score (HR in the highest tertile of the genetic risk score 1.67; 95% CI 1.54, 1.81; P trend=7×10-35) were associated with increased incidence of T2D. No significant interaction between the genetic risk score and the diet risk score (P=0.83) or its food components was observed. The highest risk was seen among the 6% of the individuals with both high genetic and dietary risk scores (HR 2.49; 95% CI 2.06, 3.01). Conclusions: The findings thus show that both genetic heredity and dietary habits previously associated with T2D add to the risk of T2D, but they seem to act in an independent fashion, with the consequence that all individuals, whether at high or low genetic risk, would benefit from favourable food choices.
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2.
  • Ericson, Ulrika, et al. (författare)
  • Food sources of fat may clarify the inconsistent role of dietary fat intake for incidence of type 2 diabetes.
  • 2015
  • Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 101:5, s. 1065-1080
  • Tidskriftsartikel (refereegranskat)abstract
    • Dietary fats could affect glucose metabolism and obesity development and, thereby, may have a crucial role in the cause of type 2 diabetes (T2D). Studies indicated that replacing saturated with unsaturated fats might be favorable, and plant foods might be a better choice than animal foods. Nevertheless, epidemiologic studies suggested that dairy foods are protective.
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3.
  • Hellstrand, Sophie, et al. (författare)
  • Genetic susceptibility to dyslipidemia and incidence of cardiovascular disease depending on a diet quality index in the Malmö diet and cancer cohort
  • 2016
  • Ingår i: Genes & Nutrition. - : Springer Science and Business Media LLC. - 1555-8932 .- 1865-3499. ; 11:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: By taking diet quality into account, we may clarify the relationship between genetically elevated triglycerides (TG) and low-density lipoprotein-cholesterol (LDL-C), and better understand the inconsistent results regarding genetically elevated high-density lipoprotein-cholesterol (HDL-C), and cardiovascular disease (CVD) risk. Methods: We included 24,799 participants (62 % women, age 44-74 years) from the Malmö Diet and Cancer cohort. During a mean follow-up time of 15 years, 3068 incident CVD cases (1814 coronary and 1254 ischemic stroke) were identified. Genetic risk scores (GRSs) were constructed by combining 80 validated genetic variants associated with higher TG and LDL-C or lower HDL-C. The participants’ dietary intake, assessed by a modified diet history method, was ranked according to a diet quality index that included six dietary components: saturated fat, polyunsaturated fat, fish, fiber, fruit and vegetables, and sucrose. Results: The GRSLDL-C (P=5×10-6) and GRSHDL-C (P = 0.02) but not GRSTG (P = 0.08) were significantly associated with CVD risk. No significant interaction between the GRSs and diet quality was observed on CVD risk (P > 0.39). A high compared to a low diet quality attenuated the association between GRSLDL-C and the risk of incident ischemic stroke (P interaction = 0.01). Conclusion: We found some evidence of an interaction between diet quality and GRSLDL-C on ischemic stroke.
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4.
  • Sonestedt, Emily, et al. (författare)
  • Diet quality and change in blood lipids during 16 years of follow-up and their interaction with genetic risk for dyslipidemia
  • 2016
  • Ingår i: Nutrients. - : MDPI AG. - 2072-6643. ; 8:5
  • Tidskriftsartikel (refereegranskat)abstract
    • A high diet quality according to the Swedish nutrition recommendations is associated with a reduced risk of cardiovascular disease in the population-based Malmö Diet and Cancer cohort. To further clarify this protective association, we examined the association between high diet quality and change in triglycerides, high density lipoprotein-cholesterol (HDL-C), and low density lipoprotein-cholesterol (LDL-C) after 16 years of follow-up in 3152 individuals (61% women; 46–68 years at baseline). In addition, we examined if genetic risk scores composed of 80 lipid-associated genetic variants modify these associations. A diet quality index based on intakes of saturated fat, polyunsaturated fat, sucrose, fiber, fruit and vegetables, and fish was constructed. A high diet quality was associated with lower risk of developing high triglycerides (p = 0.02) and high LDL-C (p = 0.03) during follow-up compared with a low diet quality. We found an association between diet quality and long-term change in HDL-C only among those with lower genetic risk for low HDL-C as opposed to those with higher genetic risk (p-interaction = 0.04). Among those with lower genetic risk for low HDL-C, low diet quality was associated with decreased HDL-C during follow-up (p = 0.05). In conclusion, individuals with high adherence to the Swedish nutrition recommendation had lower risk of developing high triglycerides and LDL-C during 16 years of follow-up.
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