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| 2. |
- Drake, Isabel, et al.
(författare)
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TCF7L2 type 2 diabetes risk variant, lifestyle factors, and incidence of prostate cancer.
- 2014
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Ingår i: The Prostate. - : Wiley. - 0270-4137. ; 74:12, s. 1161-1170
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Tidskriftsartikel (refereegranskat)abstract
- Variation in transcription factor 7-like 2 (TCF7L2), the strongest genetic risk factor for type 2 diabetes (T2D), may play a role in prostate cancer (PCa) depending on lifestyle factors. The aims of this study were to determine if TCF7L2 rs7903146 is associated with risk of PCa and if the association is modified by lifestyle factors independently of T2D status.
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| 3. |
- Drake, Isabel, et al.
(författare)
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Type 2 diabetes, adiposity and cancer morbidity and mortality risk taking into account competing risk of noncancer deaths in a prospective cohort setting
- 2017
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136. ; 141:6, s. 1170-1180
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Tidskriftsartikel (refereegranskat)abstract
- Type 2 diabetes (T2D) and adiposity associate with increased risk of several cancers, but the impact of competing risk of noncancer deaths on these associations is not known. We prospectively examined participants in the Malmö Diet and Cancer Study aged 44–73 years with no history of cancer at baseline (n = 26,953, 43% men). T2D was ascertained at baseline and during follow-up, and body mass index (BMI) and waist circumference (WC) at baseline. Multivariable cause-specific hazard ratios (HR) and subdistribution hazard ratios (sHR), taking into account noncancer deaths, were estimated using Cox- and competing risk regression. During follow-up (mean 17 years), 7,061 incident cancers (3,220 obesity-related cancer types) and 2,848 cancer deaths occurred. BMI and WC were associated with increased risk of obesity-related cancer incidence and cancer mortality. In T2D subjects, risk of obesity-related cancer was elevated among men (HR = 1.31, 95% CI: 1.12–1.54; sHR = 1.29, 95% CI: 1.10–1.52), and cancer mortality among both men and women (HR = 1.34, 95% CI: 1.20–1.49; sHR = 1.30, 95% CI: 1.16–1.45). There was no elevated actual risk of cancer death in T2D patients with long disease duration (sHR = 1.00, 95% CI: 0.83–1.20). There was a significant additive effect of T2D and adiposity on risk of obesity-related cancer and cancer mortality. In conclusion, detection bias may partially explain the increased risk of cancer morbidity among T2D patients. Both excess risk of competing events among patients with T2D and depletion of susceptibles due to earlier cancer detection will lower the actual risk of cancer, particularly with longer diabetes duration and at older ages.
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| 4. |
- Ericson, Ulrika, et al.
(författare)
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Food patterns in relation to weight change and incidence of type 2 diabetes, coronary events and stroke in the Malmö Diet and Cancer cohort
- 2019
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Ingår i: European Journal of Nutrition. - : Springer Science and Business Media LLC. - 1436-6207 .- 1436-6215. ; 58:5, s. 1801-1814
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: We examined if data-driven food-patterns associate with weight change, incidence of type 2 diabetes (T2D), coronary events (CE) and stroke. Methods: The study included 20,487 individuals (61% women) from the Malmö Diet and Cancer cohort, 45–74 years, without diabetes and CVD at baseline (1991–1996) and who did not report dietary changes. Diet was measured with a modified diet history method. During 15 years follow-up, 2206 T2D, 1571 CE and 1332 stroke cases were identified. Data on weight change after 16.7 years were available in 2627 individuals. Results: From principal component analysis, we identified six food-patterns which were similar in women and men. The first pattern, explaining 7% of the variance, was characterized by high intake of fibre-rich bread, breakfast cereals, fruits, vegetables, fish and low-fat yoghurt, and by low intake of low-fibre bread. This health conscious pattern was associated with lower T2D risk (HR comparing highest quintile with lowest: 0.75; 95% CI 0.61–0.92, 0.82; 95% CI 0.68–1.00 in women and men, respectively, P trends = 0.003, 0.01) and CE (HR 0.77; 95% CI 0.58–1.02, HR 0.83; 95% CI 0.68–1.01, P trends = 0.05, 0.07), and in men also with lower risk of ischemic stroke (HR 0.69; 95% CI 0.54–0.88; P trend = 0.001) and less pronounced weight gain (0.93 kg/10 years, P trend = 0.03). A low-fat product pattern was associated with increased T2D risk in gender combined analyses (P trend = 0.03) and a pattern characterized by dressing and vegetables with lower CE risk in men (P trend = 0.02). Conclusions: Our main finding was that a dietary pattern indicating health conscious food choices was associated with lower risk of cardiometabolic diseases in both genders.
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| 5. |
- Ericson, Ulrika, et al.
(författare)
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Food sources of fat may clarify the inconsistent role of dietary fat intake for incidence of type 2 diabetes.
- 2015
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 101:5, s. 1065-1080
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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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| 6. |
- Ericson, Ulrika, et al.
(författare)
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High intakes of protein and processed meat associate with increased incidence of type 2 diabetes.
- 2013
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Ingår i: British Journal of Nutrition. - 1475-2662. ; 109:6, s. 1143-1153
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Tidskriftsartikel (refereegranskat)abstract
- Diets high in protein have shown positive effects on short-term weight reduction and glycaemic control. However, the understanding of how dietary macronutrient composition relates to long-term risk of type 2 diabetes is limited. The aim of the present study was to examine intakes of macronutrients, fibre and protein sources in relation to incident type 2 diabetes. In total, 27 140 individuals, aged 45-74 years, from the population-based Malmö Diet and Cancer cohort, were included. Dietary data were collected with a modified diet history method, including registration of cooked meals. During 12 years of follow-up, 1709 incident type 2 diabetes cases were identified. High protein intake was associated with increased risk of type 2 diabetes (hazard ratio (HR) 1·27 for highest compared with lowest quintile; 95 % CI 1·08, 1·49; P for trend = 0·01). When protein consumption increased by 5 % of energy at the expense of carbohydrates (HR 1·20; 95 % CI 1·09, 1·33) or fat (HR 1·21; 95 % CI 1·09, 1·33), increased diabetes risk was observed. Intakes in the highest quintiles of processed meat (HR 1·16; 95 % CI 1·00, 1·36; P for trend = 0·01) and eggs (HR 1·21; 95 % CI 1·04, 1·41; P for trend = 0·02) were associated with increased risk. Intake of fibre-rich bread and cereals was inversely associated with type 2 diabetes (HR 0·84; 95 % CI 0·73, 0·98; P for trend = 0·004). In conclusion, results from the present large population-based prospective study indicate that high protein intake is associated with increased risk of type 2 diabetes. Replacing protein with carbohydrates may be favourable, especially if fibre-rich breads and cereals are chosen as carbohydrate sources.
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| 7. |
- Ericson, Ulrika, et al.
(författare)
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Sex-specific interactions between the IRS1 polymorphism and intakes of carbohydrates and fat on incident type 2 diabetes.
- 2012
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165.
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The minor T allele of rs2943641 near the gene encoding for insulin receptor substrate 1 (IRS1) has been associated with decreased risk of type 2 diabetes (T2D) and adiposity in genome-wide association studies. Dietary intake can influence the regulation of IRS1, and studies have indicated sex-specific associations between IRS1 and adiposity. OBJECTIVE: The objective was to examine the interaction between IRS1 rs2943641 and macronutrient intakes on incident T2D and percentage body fat in the Malmö Diet and Cancer cohort. DESIGN: The study included 15,227 women and 9614 men aged 45-74 y without prevalent diabetes. Dietary data were collected with a modified diet history method. During 12 y follow-up, 1567 incident T2D cases were identified. RESULTS: The T allele was associated with lower incidence of T2D (P-trend = 0.003) and, in men, with higher percentage body fat (P-trend = 0.00002). We observed 3-way interactions between sex, rs2943641, and carbohydrate intake (P = 0.01) as well as between sex, rs2943641, and fat intake (P = 0.01) on incident T2D. Among women, the T allele was associated with decreased risk only in the lower tertiles of carbohydrate intake (P-trend = 0.01, P-interaction = 0.01). In contrast, among men, the T allele was associated with decreased risk in the lowest tertile of fat intake (P-trend = 0.01, P-interaction = 0.02). No interaction was observed between macronutrient intakes and rs2943641 on percentage body fat. CONCLUSIONS: Our results indicate that IRS1 rs2943641 interacts with carbohydrate and fat intakes on incident T2D in a sex-specific fashion. A protective association between the rs2943641 T allele and T2D was restricted to women with low carbohydrate intake and to men with low fat intake.
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| 8. |
- Hellstrand, Sophie, et al.
(författare)
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Genetic susceptibility to dyslipidemia and incidence of cardiovascular disease depending on a diet quality index in the Malmö diet and cancer cohort
- 2016
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Ingår i: Genes & Nutrition. - : Springer Science and Business Media LLC. - 1555-8932 .- 1865-3499. ; 11:1
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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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| 9. |
- Hellstrand, Sophie, et al.
(författare)
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Genetic Variation in FADS Has Little Effect on the Association between Dietary PUFA Intake and Cardiovascular Disease.
- 2014
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Ingår i: Journal of Nutrition. - : Elsevier BV. - 1541-6100 .- 0022-3166. ; 144:9, s. 1356-1363
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Tidskriftsartikel (refereegranskat)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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| 10. |
- Hellstrand, Sophie, et al.
(författare)
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Intake levels of dietary long-chain PUFAs modify the association between genetic variation in FADS and LDL-C
- 2012
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Ingår i: Journal of Lipid Research. - 1539-7262. ; 53:6, s. 1183-1189
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Tidskriftsartikel (refereegranskat)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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