| 1. |
- Aasheim,, et al.
(författare)
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Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch.
- 2009
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 90:1, s. 15-22
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Bariatric surgery is widely performed to induce weight loss. OBJECTIVE: The objective was to examine changes in vitamin status after 2 bariatric surgical techniques. DESIGN: A randomized controlled trial was conducted in 2 Scandinavian hospitals. The subjects were 60 superobese patients [body mass index (BMI; in kg/m(2)): 50-60]. The surgical interventions were either laparoscopic Roux-en-Y gastric bypass or laparoscopic biliopancreatic diversion with duodenal switch. All patients received multivitamins, iron, calcium, and vitamin D supplements. Gastric bypass patients also received a vitamin B-12 substitute. The patients were examined before surgery and 6 wk, 6 mo, and 1 y after surgery. RESULTS: Of 60 surgically treated patients, 59 completed the follow-up. After surgery, duodenal switch patients had lower mean vitamin A and 25-hydroxyvitamin D concentrations and a steeper decline in thiamine concentrations than did the gastric bypass patients. Other vitamins (riboflavin, vitamin B-6, vitamin C, and vitamin E adjusted for serum lipids) did not change differently in the surgical groups, and concentrations were either stable or increased. Furthermore, duodenal switch patients had lower hemoglobin and total cholesterol concentrations and a lower BMI (mean reduction: 41% compared with 30%) than did gastric bypass patients 1 y after surgery. Additional dietary supplement use was more frequent among duodenal switch patients (55%) than among gastric bypass patients (26%). CONCLUSIONS: Compared with gastric bypass, duodenal switch may be associated with a greater risk of vitamin A and D deficiencies in the first year after surgery and of thiamine deficiency in the initial months after surgery. Patients who undergo these 2 surgical interventions may require different monitoring and supplementation regimens in the first year after surgery. This trial was registered at clinicaltrials.gov as NCT00327912.
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| 2. |
- Baker, Jennifer L, et al.
(författare)
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Breastfeeding reduces postpartum weight retention
- 2009
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 88:6, s. 1543-51
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Weight gained during pregnancy and not lost postpartum may contribute to obesity in women of childbearing age. OBJECTIVE: We aimed to determine whether breastfeeding reduces postpartum weight retention (PPWR) in a population among which full breastfeeding is common and breastfeeding duration is long. DESIGN: We selected women from the Danish National Birth Cohort who ever breastfed (>98%), and we conducted the interviews at 6 (n = 36 030) and 18 (n = 26 846) mo postpartum. We used regression analyses to investigate whether breastfeeding (scored to account for duration and intensity) reduced PPWR at 6 and 18 mo after adjustment for maternal prepregnancy body mass index (BMI) and gestational weight gain (GWG). RESULTS: GWG was positively (P < 0.0001) associated with PPWR at both 6 and 18 mo postpartum. Breastfeeding was negatively associated with PPWR in all women but those in the heaviest category of prepregnancy BMI at 6 (P < 0.0001) and 18 (P < 0.05) mo postpartum. When modeled together with adjustment for possible confounding, these associations were marginally attenuated. We calculated that, if women exclusively breastfed for 6 mo as recommended, PPWR could be eliminated by that time in women with GWG values of approximately 12 kg, and that the possibility of major weight gain (>or=5 kg) could be reduced in all but the heaviest women. CONCLUSION: Breastfeeding was associated with lower PPWR in all categories of prepregnancy BMI. These results suggest that, when combined with GWG values of approximately 12 kg, breastfeeding as recommended could eliminate weight retention by 6 mo postpartum in many women.
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| 3. |
- Berg, Christina, 1963, et al.
(författare)
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Food patterns and cardiovascular disease risk factors: the Swedish INTERGENE research program.
- 2008
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 88:2, s. 289-97
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Analyzing the impact of the intake of many foods simultaneously provides additional knowledge about analyses of nutrients and might make it easier to implement recommendations for the public. OBJECTIVE: The objective was to examine food patterns in a Swedish population and determine how they are related to metabolic risk factors for cardiovascular disease. DESIGN: The study is based on data from the INTERGENE population study of women and men aged 25-74 y in western Sweden. Dietary patterns were identified with cluster analysis of 93 food frequencies reported by 3452 participants. Associations with features of the metabolic syndrome, including blood lipids, blood pressure, and anthropometric measures, were analyzed. RESULTS: Five distinct food patterns were identified, of which one was interpreted as a "healthy" reference pattern. This healthy cluster was distinguished by more frequent consumption of high-fiber and low-fat foods and lower consumption of products rich in fat and sugar. The 4 other clusters differed significantly from the reference cluster with respect to prevalence of cardiovascular disease risk factors and the metabolic syndrome. For example, body mass index and waist-to-hip ratio were significantly higher in a cluster characterized by high consumption of energy-dense drinks and white bread and low consumption of fruit and vegetables (P < 0.0001 and P = 0.004, respectively). CONCLUSIONS: It is possible to distinguish food patterns that are related to obesity and obesity-related cardiovascular disease risk factors in contrast with a more healthy pattern conforming with current dietary guidelines. Thus, the results indicate no reason for questioning the current recommendations.
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| 4. |
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| 5. |
- Bygdell, Maria, et al.
(författare)
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Childhood BMI is inversely associated with pubertal timing in normal-weight but not overweight boys.
- 2018
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 108:6, s. 1259-1263
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Tidskriftsartikel (refereegranskat)abstract
- An inverse association between childhood body mass index (BMI; in kg/m2) and pubertal timing is well established for girls. Among boys, studies are scarce and the results inconclusive.We aimed to determine the association between childhood BMI and age at peak height velocity (PHV) in boys.We collected height and weight measurements between 6.5 and 22 y of age for boys born 1945-1961 (original cohort; n=31,971; mean±SD childhood BMI: 15.74±1.41; age at PHV: 14.06±1.11 y) and 1981-1996 (replication cohort; n=1465; childhood BMI: 16.47±2.06; age at PHV: 13.71±1.08 y) attending schools in Gothenburg, Sweden, and examined at mandatory military conscription. Age at PHV was obtained from curve-fitting of measured heights with the use of a modified Infancy-Childhood-Puberty model.In the original cohort, childhood BMI was inversely associated with age at PHV (P<0.001) and a significant quadratic term for childhood BMI (P<0.001) indicated the nonlinearity of this association. Via piecewise linear regression, we identified a threshold for the association at a childhood BMI of 18.42. A significant inverse association was observed below (β:-0.17 y/BMI unit; 95% CI: -0.18, -0.16 y/BMI unit) but not above (β:0.02 y/BMI unit; 95% CI: -0.03, 0.06 y/BMI unit) this childhood BMI threshold. For every unit increase in childhood BMI, age at PHV was ∼2 mo earlier up to the childhood BMI threshold. Similar results were observed in the replication cohort, demonstrating a significant inverse association below (β:-0.16; 95% CI: -0.21, -0.11) but not above (β:-0.03; 95% CI: -0.11, 0.05) the childhood BMI threshold. The identified threshold was close to the cutoffs for overweight at 8 y of age, and childhood BMI was inversely associated with age at PHV below but not above the overweight cutoffs.The present findings establish an inverse association between childhood BMI and pubertal timing in normal-weight but not overweight boys.
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| 6. |
- Bygdell, Maria, et al.
(författare)
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Revisiting the critical weight hypothesis for regulation of pubertal timing in boys.
- 2021
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 113:1
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Tidskriftsartikel (refereegranskat)abstract
- Recent findings indicate that there is a body weight-sensing homeostatic regulation of body weight in postpubertal rodents and humans. It is possible that body weight sensing also might be involved in the regulation of pubertal timing. Although an early small study suggested that there is a critical body weight for pubertal timing in girls, most studies have focused on BMI and reported an inverse association between BMI and pubertal timing.In the present longitudinal well-powered cohort study, we revisited the critical weight hypothesis and tested if prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys.We included men born during 1945-1961 (old cohort; n=31,971) and men born during 1981-1996 (recent cohort; n=1465) in the large BMI Epidemiology Study (BEST) Gothenburg (combined BEST cohort n=33,436). Men with information on prepubertal body weight and BMI at 8 y of age and age at peak height velocity (PHV; an objective measure of pubertal timing) were included.Body weight explained more of the variance in age at PHV than BMI in both the old cohort and the recent cohort (combined cohort, body weight 6.3%, BMI 3.6%). Both body weight (β: -0.24 SD/SD increase in weight; 95% CI: -0.25, -0.23) and BMI (β: -0.18 SD/SD increase in BMI, 95% CI: -0.19, -0.17) were inversely associated with age at PHV but the association for body weight was significantly more pronounced than the association for BMI (P<0.001).In conclusion, prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. We propose that body weight sensing constitutes a feedback mechanism to regulate pubertal timing.
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| 7. |
- Emaus, Marleen J., et al.
(författare)
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Vegetable and fruit consumption and the risk of hormone receptor-defined breast cancer in the EPIC cohort
- 2016
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 103:1, s. 168-177
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Tidskriftsartikel (refereegranskat)abstract
- Background: The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased steroid hormone receptor–negative breast cancer risk.Objective: This study aimed to investigate the association between vegetable and fruit intake and steroid hormone receptor–defined breast cancer risk.Design: A total of 335,054 female participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were included in this study (mean ± SD age: 50.8 ± 9.8 y). Vegetable and fruit intake was measured by country-specific questionnaires filled out at recruitment between 1992 and 2000 with the use of standardized procedures. Cox proportional hazards models were stratified by age at recruitment and study center and were adjusted for breast cancer risk factors.Results: After a median follow-up of 11.5 y (IQR: 10.1–12.3 y), 10,197 incident invasive breast cancers were diagnosed [3479 estrogen and progesterone receptor positive (ER+PR+); 1021 ER and PR negative (ER−PR−)]. Compared with the lowest quintile, the highest quintile of vegetable intake was associated with a lower risk of overall breast cancer (HRquintile 5–quintile 1: 0.87; 95% CI: 0.80, 0.94). Although the inverse association was most apparent for ER−PR− breast cancer (ER−PR−: HRquintile 5–quintile 1: 0.74; 95% CI: 0.57, 0.96; P-trend = 0.03; ER+PR+: HRquintile 5–quintile 1: 0.91; 95% CI: 0.79, 1.05; P-trend = 0.14), the test for heterogeneity by hormone receptor status was not significant (P-heterogeneity = 0.09). Fruit intake was not significantly associated with total and hormone receptor–defined breast cancer risk.Conclusion: This study supports evidence that a high vegetable intake is associated with lower (mainly hormone receptor–negative) breast cancer risk.
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| 8. |
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| 9. |
- Fu, Z. J., et al.
(författare)
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Dietary omega-3 polyunsaturated fatty acids decrease retinal neovascularization by adipose-endoplasmic reticulum stress reduction to increase adiponectin
- 2015
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 101:4, s. 879-888
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Tidskriftsartikel (refereegranskat)abstract
- Background: Retinopathy of prematurity (ROP) is a vision-threatening disease in premature infants. Serum adiponectin (APN) concentrations positively correlate with postnatal growth and gestational age, important risk factors for ROP development. Dietary omega-3 (n-3) long-chain polyunsaturated fatty acids (omega-3 LCPUFAs) suppress ROP and oxygen-induced retinopathy (OIR) in a mouse model of human ROP, but the mechanism is not fully understood. Objective: We examined the role of APN in ROP development and whether circulating APN concentrations are increased by dietary omega-3 LCPUFAs to mediate the protective effect in ROP. Design: Serum APN concentrations were correlated with ROP development and serum omega-3 LCPUFA concentrations in preterm infants. Mouse OIR was then used to determine whether omega-3 LCPUFA supplementation increases serum APN concentrations, which then suppress retinopathy. Results: We found that in preterm infants, low serum APN concentrations positively correlate with ROP, and serum APN concentrations positively correlate with serum omega-3 LCPUFA concentrations. In mouse OIR, serum total APN and bioactive high-molecular-weight APN concentrations are increased by omega-3 LCPUFA feed. White adipose tissue, where APN is produced and assembled in the endoplasmic reticulum, is the major source of serum APN. In mouse OIR, adipose endoplasmic reticulum stress is increased, and APN production is suppressed. omega-3 LCPUFA feed in mice increases APN production by reducing adipose endoplasmic reticulum stress markers. Dietary omega-3 LCPUFA suppression of neovascularization is reduced from 70% to 10% with APN deficiency. APN receptors localize in the retina, particularly to pathologic neovessels. Conclusion: Our findings suggest that increasing APN by omega-3 LCPUFA supplementation in total parental nutrition for preterm infants may suppress ROP.
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