| 1. |
- Astrup, Arne, et al.
(författare)
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The role of reducing intakes of saturated fat in the prevention of cardiovascular disease : where does the evidence stand in 2010?
- 2011
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 93:4, s. 684-688
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Tidskriftsartikel (refereegranskat)abstract
- Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of >= 2-3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical end-points could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
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| 2. |
- Barres, R, et al.
(författare)
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DNA methylation in metabolic disorders
- 2011
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 93:4, s. 897S-900S
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Tidskriftsartikel (refereegranskat)
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| 3. |
- Bellavia, Andrea, et al.
(författare)
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Differences in survival associated with processed and with nonprocessed red meat consumption
- 2014
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Ingår i: American Journal of Clinical Nutrition. - : OXFORD UNIV PRESS. - 0002-9165 .- 1938-3207. ; 100:3, s. 924-929
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Tidskriftsartikel (refereegranskat)abstract
- Background: High red meat consumption is associated with an increased mortality risk. This association is partly explained by the negative effect of processed meat consumption, which is widely established. The role of nonprocessed meat is unclear. Objective: The objective was to examine the combined association of processed and nonprocessed meat consumption with survival in a Swedish large prospective cohort. Design: In a population-based cohort of 74,645 Swedish men (40,089) and women (34,556), red meat consumption was assessed through a self-administered questionnaire. We estimated differences in survival [15th percentile differences (PDs), differences in the time by which the first 15% of the cohort died] according to levels of total red meat and combined levels of processed and nonprocessed red meat consumption. Results: During 15 y of follow-up (January 1998 to December 2012), we documented 16,683 deaths (6948 women; 9735 men). Compared with no consumption, consumption of red meat >100 g/d was progressively associated with shorter survival-up to 2 y for participants consuming an average of 300 g/d (15th PD: -21 mo; 95% CI: -31, -10). Compared with no consumption, high consumption of processed red meat (100 g/d) was associated with shorter survival (15th PD: -9 mo; 95% CI: -16, -2). High and moderate intakes of nonprocessed red meat were associated with shorter survival only when accompanied by a high intake of processed red meat. Conclusions: We found that high total red meat consumption was associated with progressively shorter survival, largely because of the consumption of processed red meat. Consumption of nonprocessed red meat alone was not associated with shorter survival. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.
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| 4. |
- Bellavia, Andrea, et al.
(författare)
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Fruit and vegetable consumption and all-cause mortality : a dose-response analysis.
- 2013
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 98:2, s. 454-459
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The association between fruit and vegetable (FV) consumption and overall mortality has seldom been investigated in large cohort studies. Findings from the few available studies are inconsistent.OBJECTIVE: The objective was to examine the dose-response relation between FV consumption and mortality, in terms of both time and rate, in a large prospective cohort of Swedish men and women.DESIGN: FV consumption was assessed through a self-administrated questionnaire in a population-based cohort of 71,706 participants (38,221 men and 33,485 women) aged 45-83 y. We performed a dose-response analysis to evaluate 10th survival percentile differences (PDs) by using Laplace regression and estimated HRs by using Cox regression.RESULTS: During 13 y of follow-up, 11,439 deaths (6803 men and 4636 women) occurred in the cohort. In comparison with 5 servings FV/d, a lower consumption was progressively associated with shorter survival and higher mortality rates. Those who never consumed FV lived 3 y shorter (PD: -37 mo; 95% CI: -58, -16 mo) and had a 53% higher mortality rate (HR: 1.53; 95% CI: 1.19, 1.99) than did those who consumed 5 servings FV/d. Consideration of fruit and vegetables separately showed that those who never consumed fruit lived 19 mo shorter (PD: -19 mo; 95% CI: -29, -10 mo) than did those who ate 1 fruit/d. Participants who consumed 3 vegetables/d lived 32 mo longer than did those who never consumed vegetables (PD: 32 mo; 96% CI: 13, 51 mo).CONCLUSION: FV consumption <5 servings/d is associated with progressively shorter survival and higher mortality rates. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.
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| 5. |
- Benedict, Christian, et al.
(författare)
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Acute sleep deprivation reduces energy expenditure in healthy men
- 2011
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 93:6, s. 1229-1236
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundEpidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown.ObjectiveWe examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans.DesignAccording to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session.ResultsIn comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by approximate to 5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected.ConclusionOur findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.
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| 6. |
- Berglund, Staffan, 1975-, et al.
(författare)
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Effects of iron supplementation on serum hepcidin and serum erythropoietin in low-birth-weight infants
- 2011
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Ingår i: American Journal of Clinical Nutrition. - : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 94:6, s. 1553-1561
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The iron-regulatory hormone hepcidin has not been studied in infants, who experience large physiologic changes in iron status. OBJECTIVE: The objective was to study hepcidin and erythropoietin and their correlation with iron status in iron-replete and iron-deficient low-birth-weight (LBW) infants-a group at particular risk of iron deficiency (ID). DESIGN: We randomly assigned 285 otherwise healthy LBW infants to receive, from 6 wk to 6 mo of age, 3 doses of iron supplements: 0 (placebo), 1, or 2 mg/kg daily. Hepcidin, erythropoietin, hemoglobin, and variables of iron status were analyzed. RESULTS: Serum hepcidin did not change over time in the placebo group, despite a rapid decrease in serum ferritin. In iron-supplemented infants, hepcidin increased significantly, reaching a mean (±SD) concentration of 19.2 ± 2.5 ng/mL in the 2-mg/kg group compared with 13.0 ± 2.6 ng/mL in the placebo group at age 6 mo (P < 0.001). The difference was even larger between iron-deficient and iron-replete infants. Hepcidin was independently positively correlated with ferritin at all ages and was negatively correlated with the transferrin receptor concentration at age 6 wk and with transferrin at age 6 mo. Erythropoietin was initially similar between groups but decreased significantly in iron-supplemented infants. In addition to being negatively correlated with hemoglobin, it was also independently negatively correlated with indicators of iron status. CONCLUSIONS: Hepcidin is closely associated with iron status and may be a useful indicator of iron stores and ID in infants. Erythropoietin is negatively correlated with iron status, which suggests a feedback mechanism that needs further study. This trial is registered at clinicaltrials.gov as NCT00558454.
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| 7. |
- Bertz, Fredrik, et al.
(författare)
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Diet and exercise weight-loss trial in lactating overweight and obese women
- 2012
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165. ; 96:4, s. 698-705
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Tidskriftsartikel (refereegranskat)abstract
- Background: Current evidence suggests a combined treatment of postpartum weight loss of diet and exercise. However, to our knowledge, neither their separate and interactive effects nor long-term outcomes have been evaluated. Objective: We evaluated whether a 12-wk dietary behavior modification (D) treatment to decrease energy intake, physical exercise behavior modification (E) treatment to implement moderate aerobic exercise, or combined dietary and physical exercise behavior modification (DE) treatment compared with control (usual care) (C) reduces body weight in lactating women measured at the end of treatment and at a 1-y follow-up 9 mo after treatment termination. Design: At 10-14 wk postpartum, 68 lactating Swedish women with a prepregnancy BMI (in kg/m(2)) of 25-35 were randomly assigned to D, E, DE, or C groups. Measurements were made at baseline, after the intervention, and again at a 1-y follow-up 9 mo later. A 2 x 2 factorial approach was used to analyze main and interaction effects of treatments. Results: Weight changes after the intervention and 1-y follow-up were -8.3 +/- 4.2 and -10.2 +/- 5.7 kg, respectively, in the D group; -2.4 +/- 3.2 and -2.7 +/- 5.9 kg, respectively, in the E group; -6.9 +/- 3.0 and -7.3 +/- 6.3 kg, respectively, in the DE group; and -0.8 +/- 3.0 and -0.9 +/- 6.6 kg, respectively, in the C group. The main effects of D treatment, but not of E treatment, on weight were significant at both times (P < 0.001). Conclusions: Dietary treatment provided clinically relevant weight loss in lactating postpartum women, which was sustained at 9 mo after treatment. The combined treatment did not yield significant weight or body-composition changes beyond those of dietary treatment alone. This trial was registered at clinicaltrials.gov as NCT01343238. Am J Clin Nutr 2012;96:698-705.
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| 8. |
- Bjermo, Helena, et al.
(författare)
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Effects of n-6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity : a randomized controlled trial
- 2012
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 95:5, s. 1003-1012
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Replacing SFAs with vegetable PUFAs has cardiometabolic benefits, but the effects on liver fat are unknown. Increased dietary n-6 PUFAs have, however, also been proposed to promote inflammation-a yet unproven theory. OBJECTIVE: We investigated the effects of PUFAs on liver fat, systemic inflammation, and metabolic disorders. DESIGN: We randomly assigned 67 abdominally obese subjects (15% had type 2 diabetes) to a 10-wk isocaloric diet high in vegetable n-6 PUFA (PUFA diet) or SFA mainly from butter (SFA diet), without altering the macronutrient intake. Liver fat was assessed by MRI and magnetic resonance proton (1H) spectroscopy (MRS). Proprotein convertase subtilisin/kexin type-9 (PCSK9, a hepatic LDL-receptor regulator), inflammation, and adipose tissue expression of inflammatory and lipogenic genes were determined. RESULTS: A total of 61 subjects completed the study. Body weight modestly increased but was not different between groups. Liver fat was lower during the PUFA diet than during the SFA diet [between-group difference in relative change from baseline; 16% (MRI; P < 0.001), 34% (MRS; P = 0.02)]. PCSK9 (P = 0.001), TNF receptor-2 (P < 0.01), and IL-1 receptor antagonist (P = 0.02) concentrations were lower during the PUFA diet, whereas insulin (P = 0.06) tended to be higher during the SFA diet. In compliant subjects (defined as change in serum linoleic acid), insulin, total/HDL-cholesterol ratio, LDL cholesterol, and triglycerides were lower during the PUFA diet than during the SFA diet (P < 0.05). Adipose tissue gene expression was unchanged. CONCLUSIONS: Compared with SFA intake, n-6 PUFAs reduce liver fat and modestly improve metabolic status, without weight loss. A high n-6 PUFA intake does not cause any signs of inflammation or oxidative stress. Downregulation of PCSK9 could be a novel mechanism behind the cholesterol-lowering effects of PUFAs.
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| 9. |
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| 10. |
- Braem, Marieke G. M., et al.
(författare)
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Coffee and tea consumption and the risk of ovarian cancer : a prospective cohort study and updated meta-analysis
- 2012
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Ingår i: American Journal of Clinical Nutrition. - Bethesda : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 95:5, s. 1172-1181
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Tidskriftsartikel (refereegranskat)abstract
- Background: In 2007 the World Cancer Research Fund Report concluded that there was limited and inconsistent evidence for an effect of coffee and tea consumption on the risk of epithelial ovarian cancer (EOC). Objective: In the European Prospective Investigation into Cancer and Nutrition (EPIC), we aimed to investigate whether coffee intakes, tea intakes, or both are associated with the risk of EOC. Design: All women participating in the EPIC (n = 330,849) were included in this study. Data on coffee and tea consumption were collected through validated food-frequency questionnaires at baseline. HRs and 95% CIs were estimated by using Cox proportional hazards models. Furthermore, we performed an updated meta-analysis of all previous prospective studies until April 2011 by comparing the highest and lowest coffee- and tea-consumption categories as well as by using dose-response random-effects meta-regression analyses. Results: During a median follow-up of 11.7 y, 1244 women developed EOC. No association was observed between the risk of EOC and coffee consumption [HR: 1.05 (95% CI: 0.75, 1.46) for the top quintile compared with no intake] or tea consumption [HR: 1.07 (95% Cl: 0.78, 1.45) for the top quintile compared with no intake]. This lack of association between coffee and tea intake and EOC risk was confirmed by the results of our meta-analysis. Conclusion: Epidemiologic studies do not provide sufficient evidence to support an association between coffee and tea consumption and risk of ovarian cancer. Am J Clin Nutr 2012;95:1172-81.
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