| 51. |
- Burgaz, Ann, et al.
(författare)
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Associations of diet, supplement use, and ultraviolet B radiation exposure with vitamin D status in Swedish women during winter
- 2007
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 86:5, s. 1399-1404
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Vitamin D is produced endogenously after sun exposure but can also be obtained from natural food sources, food fortification, and dietary supplements. OBJECTIVE: We aimed to determine the vitamin D status of women (61-86 y old) living in central Sweden (latitude 60 degrees ) during winter and its relation with vitamin D intake and exposure to ultraviolet B radiation. DESIGN: In a cross-sectional study, we assessed the vitamin D status (serum 25-hydroxyvitamin D [25(OH)D]) of 116 women by using an enzyme immunoassay. The women completed questionnaires covering food habits, use of dietary supplements, and sun-related behavior. RESULTS: In a multiple linear regression model, the main determinants of serum 25(OH)D concentrations (x +/- SD: 69 +/- 23 mmol/L) were dietary vitamin D (6.0 +/- 1.8 mug/d), travel to a sunny location during winter within the previous 6 mo (26%), and the use of dietary supplements (16%). There was no association between serum 25(OH)D status during the winter and age, time spent outdoors, the use of sunscreen, or skin type. Serum 25(OH)D concentrations increased by 25.5 nmol/L with 2-3 servings (130 g/wk) fatty fish/wk, by 6.2 nmol/L with the daily intake of 300 g vitamin D-fortified reduced-fat dairy products, by 11.0 nmol/L with regular use of vitamin D supplements, and by 14.5 nmol/L with a sun vacation during winter. Among nonsupplement users without a wintertime sun vacation, 2-3 servings fatty fish/wk increased serum vitamin D concentrations by 45%. CONCLUSION: Fatty fish, vitamin D-fortified reduced-fat dairy products, regular supplement use, and taking a sun vacation are important predictors for serum concentrations of 25(OH)D during winter at a latitude of 60 degrees .
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| 52. |
- Byberg, Liisa, et al.
(författare)
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Cancer death is related to high palmitoleic acid in serum and to polymorphisms in the SCD-1 gene in healthy Swedish men
- 2014
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 99:3, s. 551-558
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:A high proportion of monounsaturated fatty acids (MUFAs) or a high ratio of MUFAs to saturated fatty acids in plasma, reflecting a high activity of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1), has been shown to be related to cancer death and incidence in some studies.OBJECTIVES:The objective was to study whether the serum cholesteryl ester proportion of palmitoleic acid [16:1n-7 (16:1ω-3)] and the ratio of palmitoleic to palmitic acid (16:1n-7/16:0), as an estimation of the activity of SCD-1, are related to cancer death and to investigate whether polymorphisms in the SCD-1 gene are related to cancer mortality.DESIGN:A community-based cohort of 50-y-old men was followed for a maximum of >40 y. Survival analysis was used to relate fatty acid composition in serum, analyzed at baseline by gas-liquid chromatography (n = 1981), and single nucleotide polymorphisms in the SCD-1 gene (n = 986) to cancer death. A 7-d dietary record was completed at age 70 y (n = 880).RESULTS:The proportions of 16:1n-7 and the ratio of 16:1n-7 to 16:0 were associated with cancer mortality during follow-up in a comparison of the highest with the lowest quartile of 16:1n-7 (adjusted HR: 1.37; 95% CI: 1.04, 1.82). Inherited variance of the SCD-1 gene seemed to be related to cancer death, especially among men with a low proportion of PUFA in the diet in a comparison of the highest with the lowest weighted genetic risk score (HR: 2.14; 95% CI: 1.13, 4.04).CONCLUSION:The findings are compatible with the hypothesis that there is an association between endogenously synthesized MUFAs and cancer death.
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| 53. |
- Byberg, Liisa, et al.
(författare)
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Reply to WB Grant
- 2017
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 106:2, s. 700-701
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 54. |
- Byberg, Liisa, et al.
(författare)
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Reply to Y Mao and H Yu.
- 2017
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 106:2, s. 698-699
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 55. |
- 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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| 56. |
- 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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| 57. |
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| 58. |
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| 59. |
- Callahan, Emily A., et al.
(författare)
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Assessing the safety of bioactive ingredients in infant formula that affect the immune system : recommendations from an expert panel
- 2022
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Ingår i: American Journal of Clinical Nutrition. - : Oxford University Press. - 0002-9165 .- 1938-3207. ; 115:2, s. 570-587
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Tidskriftsartikel (refereegranskat)abstract
- Bioactive ingredients for infant formula have been sought to reduce disparities in health outcomes between breastfed and formula-fed infants. Traditional food safety methodologies have limited ability to assess some bioactive ingredients. It is difficult to assess the effects of nutrition on the infant immune system because of coincident developmental adaptations to birth, establishment of the microbiome and introduction to solid foods, and perinatal environmental factors. An expert panel was convened to review information on immune system development published since the 2004 Institute of Medicine report on evaluating the safety of new infant formula ingredients and to recommend measurements that demonstrate the safety of bioactive ingredients intended for that use. Panel members participated in a 2-d virtual symposium in November 2020 and in follow-up discussions throughout early 2021. Key topics included identification of immune system endpoints from nutritional intervention studies, effects of human milk feeding and human milk substances on infant health outcomes, ontologic development of the infant immune system, and microbial influences on tolerance. The panel explored how "nonnormal" conditions such as preterm birth, allergy, and genetic disorders could help define developmental immune markers for healthy term infants. With consideration of breastfed infants as a reference, ensuring proper control groups, and attention to numerous potential confounders, the panel recommended a set of standard clinical endpoints including growth, response to vaccination, infection and other adverse effects related to inflammation, and allergy and atopic diseases. It compiled a set of candidate markers to characterize stereotypical patterns of immune system development during infancy, but absence of reference ranges, variability in methods and populations, and unreliability of individual markers to predict disease prevented the panel from including many markers as safety endpoints. The panel's findings and recommendations are applicable for industry, regulatory, and academic settings, and will inform safety assessments for immunomodulatory ingredients in foods besides infant formula.
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| 60. |
- Carlsson-Kanyama, Annika, et al.
(författare)
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Potential contributions of food consumption patterns to climate change
- 2009
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Ingår i: American Journal of Clinical Nutrition. - 0002-9165 .- 1938-3207. ; 89:5, s. S1704-S1709
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Tidskriftsartikel (refereegranskat)abstract
- Anthropogenic warming is caused mainly by emissions of greenhouse gases (GHGs), such as carbon dioxide, methane, and nitrous oxide, with agriculture as a main contributor for the latter 2 gases. Other parts of the food system contribute carbon dioxide emissions that emanate from the use of fossil fuels in transportation, processing, retailing, storage, and preparation. Food items differ substantially when GHG emissions are calculated from farm to table. A recent study of approximate to 20 items sold in Sweden showed a span of 0.4 to 30 kg CO2 equivalents/kg edible product. For protein-rich food, such as legumes, meat, fish, cheese, and eggs, the difference is a factor of 30 with the lowest emissions per kilogram for legumes, poultry, and eggs and the highest for beef, cheese, and pork. Large emissions for ruminants are explained mainly by methane emissions from enteric fermentation. For vegetables and fruits, emissions usually are <= 2.5 kg CO2 equivalents/kg product, even if there is a high degree of processing and substantial transportation. Products transported by plane are an exception because emissions may be as large as for certain meats. Emissions from foods rich in carbohydrates, such as potatoes, pasta, and wheat, are <1.1 kg/kg edible food. We suggest that changes in the diet toward more plant-based foods, toward meat from animals with little enteric fermentation, and toward foods processed in an energy-efficient manner offer an interesting and little explored area for mitigating climate change.
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