| 1. |
|
|
| 2. |
- Beghin, L, et al.
(författare)
-
Nutritional and pubertal status influences accuracy of self-reported weight and height in adolescents: the HELENA Study
- 2013
-
Ingår i: Annals of nutrition & metabolism. - : S. Karger AG. - 1421-9697 .- 0250-6807. ; 62:3, s. 189-200
-
Tidskriftsartikel (refereegranskat)abstract
- <b><i>Background and Aims:</i></b> The aim of this study was to assess factors that have an effect on the accuracy of self-reported weight and height in adolescents. <b><i>Methods:</i></b> Weight and height of 3,865 European adolescents aged 12.5 to 17.5 years were self-reported via specific questionnaire. Then real weight and height were measured using accurate equipment and standardized protocols. Differences (D) between self-reported and measured weight and height were calculated, and factors that could have influenced the accuracy of self-reported weight and height were assessed. Data were analyzed using ANOVA, Student's t test and multivariate regression. <b><i>Results:</i></b> Adolescents underestimated their weight (D = -0.81 kg; n = 2,968) and overestimated their height (D = +0.74 cm; n = 3,308). Obese girls underestimated their weight (D = -4.70 kg) and overestimated their height (D = +0.22 cm) to a greater extent (p < 0.05) than obese boys (D = -3.13 kg and +0.14 cm for weight and height, respectively). Underestimation of weight (D = -1.25 kg) and overestimation of height (D = +0.15 cm) were only significant for girls who had finished puberty (Tanner stage 5). Socioeconomic status, nutritional knowledge, physical fitness, physical activity level, food choice and preference, and healthy eating behaviour had no significant influence on the accuracy of self-reported weight and height. <b><i>Conclusion:</i></b> Our data confirms that self-reports of weight and height made by adolescents are inaccurate and demonstrate that inaccuracy is strongly influenced by nutritional status, pubertal status and gender.
|
|
| 3. |
- Bäckhed, Fredrik, 1973
(författare)
-
Programming of host metabolism by the gut microbiota.
- 2011
-
Ingår i: Annals of nutrition & metabolism. - : S. Karger AG. - 1421-9697 .- 0250-6807. ; 58 Suppl 2:Suppl 2, s. 44-52
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The human gut harbors a vast ensemble of bacteria that has co-evolved with the human host and performs several important functions that affect our physiology and metabolism. The human gut is sterile at birth and is subsequently colonized with bacteria from the mother and the environment. The complexity of the gut microbiota is increased during childhood, and adult humans contain 150-fold more bacterial genes than human genes. Recent advances in next-generation sequencing technology and mechanistic testing in gnotobiotic mice have identified the gut microbiota as an environmental factor that contributes to obesity. Germ-free mice are protected against developing diet-induced obesity and the underlying mechanisms whereby the gut microbiota contributes to host metabolism are beginning to be clarified. The obese phenotype is associated with increased microbial fermentation and energy extraction; however, other microbially modulated mechanisms contribute to disease progression as well. The gut microbiota has profound effects on host gene expression in the enterohepatic system, including genes involved in immunity and metabolism. For example, the gut microbiota affects expression of secreted proteins in the gut, which modulate lipid metabolism in peripheral organs. In addition, the gut microbiota is also a source of proinflammatory molecules that augment adipose inflammation and macrophage recruitment by signaling through the innate immune system. TLRs (Toll-like receptors) are integral parts of the innate immune system and are expressed by both macrophages and epithelial cells. Activation of TLRs in macrophages dramatically impairs glucose homeostasis, whereas TLRs in the gut may alter the gut microbial composition that may have profound effects on host metabolism. Accordingly, reprogramming the gut microbiota, or its function, in early life may have beneficial effects on host metabolism later in life.
|
|
| 4. |
|
|
| 5. |
- Christensen, S., et al.
(författare)
-
Meal-Q - a new meal-based FFQ on the web
- 2011
-
Ingår i: Annals of Nutrition and Metabolism. - : KARGER. - 0250-6807 .- 1421-9697. ; 58, s. 414-414
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
- Domellöf, Magnus
(författare)
-
Iron requirements in infancy
- 2011
-
Ingår i: Annals of Nutrition and Metabolism. - Basel : Karger. - 0250-6807 .- 1421-9697. ; 59:1, s. 59-63
-
Tidskriftsartikel (refereegranskat)abstract
- Iron deficiency anemia is the most common micronutrient deficiency worldwide and infants constitute a risk group due to their high iron requirements. Iron is critical for brain development, and case control studies have shown a consistent association between iron deficiency anemia in infancy and poor neurodevelopment, suggesting that it is important to prevent iron deficiency anemia in infants. However, it is also important to avoid excessive iron intakes which may have adverse effects on growth. Due to redistribution of iron from hemoglobin to iron stores, healthy, term, normal birth weight infants are virtually self-sufficient with regard to iron during the first 6 months of life. After that age, iron becomes a critical nutrient. The estimated daily iron requirements at the age of 6-12 months (0.9-1.3 mg/kg body weight) are higher than during any other period of life. Exclusively breast-fed infants normally do not need additional iron until 6 months of life. Formula-fed infants should receive iron-fortified formula. Low birth weight infants should receive additional iron supplements from an early age. From 6 months of age, all infants should receive a sufficient intake of iron-rich (complementary) foods, which may be meat products or iron-fortified foods. The estimations of iron requirements in infants have a weak evidence base and current European and American recommendations for infants differ significantly. To further clarify iron requirements in infants, there is clearly a need for randomized, controlled trials assessing the effects of different iron intake on anemia, neurodevelopment, and other health outcomes.
|
|
| 9. |
|
|
| 10. |
|
|
