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Träfflista för sökning "WFRF:(Sonestedt Emily) ;pers:(Hedblad Bo)"

Search: WFRF:(Sonestedt Emily) > Hedblad Bo

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1.
  • Drake, Isabel, et al. (author)
  • Development of a diet quality index assessing adherence to the Swedish nutrition recommendations and dietary guidelines in the Malmö Diet and Cancer cohort.
  • 2011
  • In: Public Health Nutrition. - 1475-2727. ; 14, s. 835-845
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To develop a diet quality index (DQI) that assesses adherence to the Swedish nutrition recommendations (SNR) and the Swedish dietary guidelines (SDG). DESIGN: A cross-sectional study within the Malmö Diet and Cancer (MDC) cohort. A diet history method collected dietary data, a structured questionnaire lifestyle and socio-economic information, and anthropometric data were collected by direct measurements. The index (DQI-SNR) included six components: SFA, PUFA, fish and shellfish, dietary fibre, fruit and vegetables, and sucrose. SETTING: Malmö, Sweden. SUBJECTS: Men (n 4525) and women (n 8491) of the MDC cohort enrolled from September 1994 to October 1996. RESULTS: For participants with high DQI-SNR scores, nutrient and food intakes were close to recommendations. However, most of the study population exceeded the recommended intake for SFA (98 %) and few reached recommended intakes for dietary fibre (24 %), fruit and vegetables (32 %), vitamin D (18 %) and folate (2 %). A high DQI-SNR score was positively associated with age, physical activity, not smoking, past food habit change, education and socio-economic status. Individuals with high scores were more likely to have a diabetes diagnosis or experienced a cardiovascular event. CONCLUSIONS: Results suggest that the DQI-SNR is a useful tool for assessing adherence to the SNR 2005 and the SDG in the MDC cohort. No index has previously been developed with the aim of evaluating adherence to the current dietary recommendations in Sweden. Further validation of the DQI-SNR, and evaluation of its utility, is needed.
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2.
  • Drake, Isabel, et al. (author)
  • Scoring models of a diet quality index and the predictive capability of mortality in a population-based cohort of Swedish men and women.
  • 2012
  • In: Public Health Nutrition. - 1475-2727. ; :May 29, s. 1-11
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To examine how different scoring models for a diet quality index influence associations with mortality outcomes. DESIGN: A study within the Malmö Diet and Cancer cohort. Food and nutrient intakes were estimated using a diet history method. The index included six components: SFA, PUFA, fish and shellfish, fibre, fruit and vegetables, and sucrose. Component scores were assigned using predefined (based on dietary recommendations) and population-based cut-offs (based on median or quintile intakes). Multivariate Cox regression was used to model associations between index scores (low, medium, high) and all-cause and cause-specific mortality by sex. SETTING: Malmö, the third largest city in Sweden. SUBJECTS: Men (n 6940) and women (n 10 186) aged 44-73 years. During a mean follow-up of 14·2 years, 2450 deaths occurred, 1221 from cancer and 709 from CVD. RESULTS: The predictive capability of the index for mortality outcomes varied with type of scoring model and by sex. Stronger associations were seen among men using predefined cut-offs. In contrast, the quintile-based scoring model showed greater predictability for mortality outcomes among women. The scoring model using median-based cut-offs showed low predictability for mortality among both men and women. CONCLUSIONS: The scoring model used for dietary indices may have a significant impact on observed associations with disease outcomes. The rationale for selection of scoring model should be included in studies investigating the association between dietary indices and disease. Adherence to the current dietary recommendations was in the present study associated with decreased risk of all-cause and cause-specific mortality, particularly among men.
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3.
  • Hellstrand, Sophie, et al. (author)
  • Genetic susceptibility to dyslipidemia and incidence of cardiovascular disease depending on a diet quality index in the Malmö diet and cancer cohort
  • 2016
  • In: Genes & Nutrition. - : Springer Science and Business Media LLC. - 1555-8932 .- 1865-3499. ; 11:1
  • Journal article (peer-reviewed)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.
  • Hellstrand, Sophie, et al. (author)
  • Genetic Variation in FADS Has Little Effect on the Association between Dietary PUFA Intake and Cardiovascular Disease.
  • 2014
  • In: Journal of Nutrition. - : Elsevier BV. - 1541-6100 .- 0022-3166. ; 144:9, s. 1356-1363
  • Journal article (peer-reviewed)abstract
    • The unclear link between intake of polyunsaturated fatty acids (PUFAs) and risk of cardiovascular disease (CVD) could depend on genetic differences between individuals. Minor alleles of single-nucleotide polymorphisms (SNPs) in the ∆5 fatty acid desaturase (FADS) 1 gene were associated with lower blood concentrations of long-chain ω-3 (n-3) and ω-6 (n-6) PUFAs, indicating an associated loss of function effect. We examined whether the SNP rs174546 in FADS1 modifies the association between PUFA intakes and CVD risk. We included 24,032 participants (62% women, aged 44-74 y) from the Malmö Diet and Cancer cohort without prevalent CVD and diabetes. During a mean follow-up of 14 y, 2648 CVD cases were identified. Diet was assessed by a modified diet history method. Borderline interaction was observed between the α-linolenic acid (ALA) (18:3n-3)-to-linoleic acid (LA) (18:2n-6) intake ratio and FADS genotype on CVD incidence (P = 0.06). The ALA-to-LA intake ratio was inversely associated with CVD risk only among participants homozygous for the minor T-allele (HR for quintile 5 vs. quintile 1 = 0.72; 95% CI: 0.50, 1.04; P-trend = 0.049). When excluding participants reporting unstable food habits in the past (35%), the interaction between the ALA-to-LA intake ratio and FADS genotype on CVD incidence was strengthened and statistically significant (P = 0.04). Additionally, we observed a significant interaction between ALA and FADS genotype on ischemic stroke incidence (P = 0.03). ALA was inversely associated with ischemic stroke only among TT genotype carriers (HR for quintile 5 vs. quintile 1 = 0.50; 95% CI: 0.27, 0.94; P-trend = 0.02). In this large cohort, we found some weak, but not convincing, evidence of effect modification by genetic variation in FADS on the associations between PUFA intakes and CVD risk. For the 11% of the population homozygous for the minor T-allele of rs174546 that associates with lower ∆5 FADS activity, high ALA intake and ALA-to-LA intake ratio may be preferable in the prevention of CVD and ischemic stroke.
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5.
  • Hellstrand, Sophie, et al. (author)
  • Intake levels of dietary long-chain PUFAs modify the association between genetic variation in FADS and LDL-C
  • 2012
  • In: Journal of Lipid Research. - 1539-7262. ; 53:6, s. 1183-1189
  • Journal article (peer-reviewed)abstract
    • Polymorphisms of the FA desaturase (FADS) gene cluster have been associated with LDL, HDL, and triglyceride concentrations. Because FADS converts alpha-linolenic acid (ALA) and linoleic acid into PUFAs, we investigated the interaction between different PUFA intakes and the FADS polymorphism rs174547 (T>C) on fasting blood lipid and lipoprotein concentrations. We included 4,635 individuals (60% females, 45-68 years) from the Swedish population-based Malmo Diet and Cancer cohort. Dietary intakes were assessed by a modified diet history method including 7-day registration of cooked meals. The C-allele of rs174547 was associated with lower LDL concentration (P = 0.03). We observed significant interaction between rs174547 and long-chain omega-3 PUFA intakes on LDL (P = 0.01); the C-allele was only associated with lower LDL among individuals in the lowest tertile of long-chain omega-3 PUFA intakes (P < 0.001). In addition, significant interaction was observed between rs174547 and the ratio of ALA and linoleic FA intakes on HDL (P = 0.03). However, no significant associations between the C-allele and HDL were detected within the intake tertiles of the ratio. Our findings suggest that dietary intake levels of different PUFAs modify the associated effect of genetic variation in FADS on LDL and HDL.-Hellstrand, S., E. Sonestedt, U. Ericson, B. Gullberg, E. Wirfalt, B. Hedblad, and M. Orho-Melander. Intake levels of dietary PUFAs modify the association between genetic variation in FADS and LDL-C. J. Lipid Res. 2012. 53: 1183-1189.
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7.
  • Hlebowicz, Joanna, et al. (author)
  • Food patterns, inflammation markers and incidence of cardiovascular disease: the Malmö Diet and Cancer study.
  • 2011
  • In: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 270, s. 365-376
  • Journal article (peer-reviewed)abstract
    • Objectives: To examine the associations between food patterns constructed using cluster analysis and markers of systemic and vascular inflammation, and incident cardiovascular disease (CVD) after 13 years of follow-up. Design: Population-based, prospective cohort study. Setting and subjects: Cluster analysis identified six food patterns from 43 food group variables among 4999 subjects, aged 45-68 years, who participated in the Malmö Diet and Cancer cardiovascular programme between 1991 and 1994. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2) ), C-reactive protein concentration and white blood cell (WBC) count were measured using blood samples at baseline. Incidence of CVD (coronary events and ischaemic stroke) was monitored over 13 years of follow-up. Results: The fibre-rich bread pattern was associated with favourable effects on WBC count in women, and the low-fat and high-fibre pattern with favourable effects on Lp-PLA(2) mass in women, and on Lp-PLA(2) activity in men. However, the milk fat and sweets and cakes patterns were both associated with adverse effects; the former on WBC count in women and on Lp-PLA(2) mass in men, and the latter on WBC count and Lp-PLA(2) mass in women. The milk fat and sweets and cakes patterns were associated with increased CVD risk in women. Conclusions: The results of this study support the present Nordic dietary recommendations indicating that diets rich in high-fibre, low-fat and low-sugar foods are favourably associated with markers of inflammation and, potentially, with CVD risk.
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8.
  • Rukh, Gull, et al. (author)
  • Genetic susceptibility to obesity and diet intakes: association and interaction analyses in the Malmö Diet and Cancer Study.
  • 2013
  • In: Genes & Nutrition. - : Springer Science and Business Media LLC. - 1555-8932 .- 1865-3499. ; 8:6, s. 535-547
  • Journal article (peer-reviewed)abstract
    • Gene-environment interactions need to be studied to better understand the obesity. We aimed at determining whether genetic susceptibility to obesity associates with diet intake levels and whether diet intakes modify the genetic susceptibility. In 29,480 subjects of the population-based Malmö Diet and Cancer Study (MDCS), we first assessed association between 16 genome-wide association studies identified obesity-related single-nucleotide polymorphisms (SNPs) with body mass index (BMI) and associated traits. We then conducted association analyses between a genetic risk score (GRS) comprising of 13 replicated SNPs and the individual SNPs, and relative dietary intakes of fat, carbohydrates, protein, fiber and total energy intake, as well as interaction analyses on BMI and associated traits among 26,107 nondiabetic MDCS participants. GRS associated strongly with increased BMI (P = 3.6 × 10(-34)), fat mass (P = 6.3 × 10(-28)) and fat-free mass (P = 1.3 × 10(-24)). Higher GRS associated with lower total energy intake (P = 0.001) and higher intake of fiber (P = 2.3 × 10(-4)). No significant interactions were observed between GRS and the studied dietary intakes on BMI or related traits. Of the individual SNPs, after correcting for multiple comparisons, NEGR1 rs2815752 associated with diet intakes and BDNF rs4923461 showed interaction with protein intake on BMI. In conclusion, our study does not provide evidence for a major role for macronutrient-, fiber- or total energy intake levels in modifying genetic susceptibility to obesity measured as GRS. However, our data suggest that the number of risk alleles as well as some of the individual obesity loci may have a role in regulation of food and energy intake and that some individual loci may interact with diet.
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9.
  • Sonestedt, Emily, et al. (author)
  • Association between fat intake, physical activity and mortality depending on genetic variation in FTO.
  • 2011
  • In: International Journal of Obesity. - : Springer Science and Business Media LLC. - 1476-5497 .- 0307-0565. ; 35, s. 1041-1049
  • Journal article (peer-reviewed)abstract
    • Objective:We wanted to explore if FTO genotype interacts with fat intake, or leisure-time physical activity, on fat mass, lean mass and mortality.Subjects and methods:Among 22 799 individuals (44-74 years) in the population-based Malmö diet and cancer cohort that were genotyped for rs9939609 in FTO and had information on dietary intake (from a modified diet history method) and no history of diabetes, cancer or cardiovascular disease, 2255 deaths (including 1100 cancer and 674 cardiovascular deaths) occurred during 12.0 years of follow-up. Leisure-time physical activity was determined from a list of 17 different physical activities in a questionnaire. Body composition was measured using bioelectric impedance method.Results:FTO genotype associated strongly with both fat mass and lean mass (P(trend)<1 × 10(-16) for both) but we found only significant interactions with fat intake, or physical activity, on fat mass (P(interaction)=0.01 and 0.004). No significant interaction between FTO genotype and fat intake (P(interaction)=0.72), or leisure-time physical activity (P(interaction)=0.07), on total mortality were observed. However, we observed a significant interaction between leisure-time physical activity and FTO genotype on cardiovascular mortality (P(interaction)=0.03). The highest vs lowest quintile of physical activity was associated with 46% (95% confidence interval, 17-64%) reduced cardiovascular mortality among TT-carriers (P(trend)=0.004), and 11% reduced cardiovascular mortality among A-allele carriers (P(trend)=0.68).Conclusion:Our results indicate that FTO genotype associates with both fat mass and lean mass, but the level of fat intake and physical activity only modify the association with fat mass. In addition, FTO genotype may modify the association between physical activity and cardiovascular mortality.International Journal of Obesity advance online publication, 21 December 2010; doi:10.1038/ijo.2010.263.
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