| 1. |
- Bentham, James, et al.
(författare)
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A century of trends in adult human height
- 2016
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Ingår i: eLIFE. - : eLife Sciences Publications Ltd. - 2050-084X. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Being taller is associated with enhanced longevity, and higher education and earnings. We reanalysed 1472 population-based studies, with measurement of height on more than 18.6 million participants to estimate mean height for people born between 1896 and 1996 in 200 countries. The largest gain in adult height over the past century has occurred in South Korean women and Iranian men, who became 20.2 cm (95% credible interval 17.5–22.7) and 16.5 cm (13.3– 19.7) taller, respectively. In contrast, there was little change in adult height in some sub-Saharan African countries and in South Asia over the century of analysis. The tallest people over these 100 years are men born in the Netherlands in the last quarter of 20th century, whose average heights surpassed 182.5 cm, and the shortest were women born in Guatemala in 1896 (140.3 cm; 135.8– 144.8). The height differential between the tallest and shortest populations was 19-20 cm a century ago, and has remained the same for women and increased for men a century later despite substantial changes in the ranking of countries.
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| 2. |
- Danaei, Goodarz, et al.
(författare)
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Effects of diabetes definition on global surveillance of diabetes prevalence and diagnosis: a pooled analysis of 96 population-based studies with 331288 participants
- 2015
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Ingår i: The Lancet Diabetes & Endocrinology. - 2213-8595 .- 2213-8587. ; 3:8, s. 624-637
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Tidskriftsartikel (refereegranskat)abstract
- Background Diabetes has been defined on the basis of different biomarkers, including fasting plasma glucose (FPG), 2-h plasma glucose in an oral glucose tolerance test (2hOGTT), and HbA(1c). We assessed the effect of different diagnostic definitions on both the population prevalence of diabetes and the classification of previously undiagnosed individuals as having diabetes versus not having diabetes in a pooled analysis of data from population-based health examination surveys in different regions. Methods We used data from 96 population-based health examination surveys that had measured at least two of the biomarkers used for defining diabetes. Diabetes was defined using HbA(1c) (HbA(1c) >= 6 . 5% or history of diabetes diagnosis or using insulin or oral hypoglycaemic drugs) compared with either FPG only or FPG-or-2hOGTT definitions (FPG >= 7 . 0 mmol/L or 2hOGTT >= 11 . 1 mmol/L or history of diabetes or using insulin or oral hypoglycaemic drugs). We calculated diabetes prevalence, taking into account complex survey design and survey sample weights. We compared the prevalences of diabetes using different definitions graphically and by regression analyses. We calculated sensitivity and specificity of diabetes diagnosis based on HbA1c compared with diagnosis based on glucose among previously undiagnosed individuals (ie, excluding those with history of diabetes or using insulin or oral hypoglycaemic drugs). We calculated sensitivity and specificity in each survey, and then pooled results using a random-effects model. We assessed the sources of heterogeneity of sensitivity by meta-regressions for study characteristics selected a priori. Findings Population prevalence of diabetes based on FPG- or-2hOGTT was correlated with prevalence based on FPG alone (r= 0 . 98), but was higher by 2-6 percentage points at different prevalence levels. Prevalence based on HbA(1c) was lower than prevalence based on FPG in 42 . 8% of age-sex-survey groups and higher in another 41 . 6%; in the other 15 . 6%, the two definitions provided similar prevalence estimates. The variation across studies in the relation between glucose-based and HbA(1c)-based prevalences was partly related to participants' age, followed by natural logarithm of per person gross domestic product, the year of survey, mean BMI, and whether the survey population was national, subnational, or from specific communities. Diabetes defined as HbA(1c) 6 . 5% or more had a pooled sensitivity of 52 . 8% (95% CI 51 . 3-54 . 3%) and a pooled specificity of 99 . 74% (99 . 71-99 . 78%) compared with FPG 7 . 0 mmol/L or more for diagnosing previously undiagnosed participants; sensitivity compared with diabetes defined based on FPG-or-2hOGTT was 30 . 5% (28 . 7-32 . 3%). None of the preselected study-level characteristics explained the heterogeneity in the sensitivity of HbA(1c) versus FPG. Interpretation Different biomarkers and definitions for diabetes can provide different estimates of population prevalence of diabetes, and differentially identify people without previous diagnosis as having diabetes. Using an HbA(1c)-based definition alone in health surveys will not identify a substantial proportion of previously undiagnosed people who would be considered as having diabetes using a glucose-based test.
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| 3. |
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| 4. |
- Holmgren, Anton, et al.
(författare)
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Detailed analyzes of the relation between childhood BMIand gain in height during puberty, separated into different Components
- 2016
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Ingår i: International Journal of Obesity. - 0307-0565 .- 1476-5497.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Background: We have previously found that childhood BMI is inversely related to pubertal height gain: overweight/obese children of both genders have less specific pubertal height gain. The QEPS-model (describing total growth in height as a combination of four mathematical functions), can be used for calculation of estimates of pubertal growth. Growth in height during puberty can be described as a combination of continuous ongoing growth, Q(ES), and a specific pubertal growth function, P. Objectives: To investigate the importance of when overweight/obesity starts during childhood in relation to subsequent growth in height during puberty; and to study the relationship between childhood BMI and pubertal growth functions from the QEPS-model in greater detail than previously presented. Material/Methods: The longitudinally followed GrowUpGothenburg 1990 birth cohort, with growth data from birth until adult height was analyzed, using the QEPS-model. Individual BMI-SDS values, from 3.5–8.0 years of age (n = 1901) were calculated for linear and subgroup analyses (normal /underweight, NwUw, overweight/obese, OwOb), based on the IOTF 2012 reference2. Relationships between childhood-BMI and total pubertal height gain were considered according to P-function and Q(ES)-function. Results: We found no significant difference in pubertal height gain depending on when in childhood the BMI-SDS peaked, in either sex. In general, the total pubertal growth in girls depended more on the continuous Q(ES)-function than P-function and this balance was shifted towards less P-function with higher BMI-SDS, especially for Ob girls (figure, left). NwUw boys had pubertal gain mostly from the P-function, for the Ow boys the pattern was more mixed and for Ob boys all had less P- than Q(ES)-function (figure, right). Conclusion: The results of the present study have shown that the reduced pubertal gain in height for OwOb children is not related to when during childhood the BMI peaked. For both genders, the pubertal gain shifted to less specific pubertal growth (P) and relatively more continuous growth (Q(ES)) with higher BMI-SDS.
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| 5. |
- Holmgren, Anton, et al.
(författare)
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Estimating secular changes in longitudinal growth patterns underlying adult height with the QEPS model: the Grow Up Gothenburg cohorts
- 2018
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Ingår i: Pediatric Research. - : Springer Science and Business Media LLC. - 0031-3998 .- 1530-0447. ; 84:1, s. 41-49
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Over the past 150 years, humans have become taller, and puberty has begun earlier. It is unclear if these changes are continuing in Sweden, and how longitudinal growth patterns are involved. We aimed to evaluate the underlying changes in growth patterns from birth to adulthood by QEPS estimates in two Swedish cohorts born in 1974 and 1990. METHODS: Growth characteristics of the longitudinal 1974 and 1990-birth cohorts (n = 4181) were compared using the QEPS model together with adult heights. RESULTS: There was more rapid fetal/infancy growth in girls/boys born in 1990 compared to 1974, as shown by a faster Etimescale and they were heavier at birth. The laterborn were taller also in childhood as shown by a higher Q-function. Girls born in 1990 had earlier and more pronounced growth during puberty than girls born in 1974. Individuals in the 1990 cohort attained greater adult heights than those in the 1974 cohort; 6 mm taller for females and 10 mm for males. CONCLUSION: A positive change in adult height was attributed to more growth during childhood in both sexes and during puberty for girls. The QEPS model proved to be effective detecting small changes of growth patterns, between two longitudinal growth cohorts born only 16 years apart.
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| 6. |
- Holmgren, Anton, et al.
(författare)
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Higher childhood BMI is associated with less pubertal gain
- 2015
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Ingår i: Obesity Facts (The European Journal of Obesity). - : S. Karger AG. - 1662-4025 .- 1662-4033.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Objective: Our objective was to investigate the impact of body mass index (BMI) in childhood on the pattern of growth during puberty. Methods: The longitudinally followed Grow up 1990 Gothenburg birth cohort, with growth data from birth until adult height was analyzed, using the QEPS growth model (describing total height as a combination of four mathematical functions; Quadratic -Q, Exponential -E, Pubertal -P and Stop –S, Fig 1.), for calculation of estimates for pubertal growth (1). Individual BMI-SDS values, from 3.5–8 years of age (n = 1908) were calculated for linear and subgroup analyses (low/normal- nw, overweight – ow, obese– ob), based on the IOTF 2012 reference. Results: Ow/ob children already at birth were heavier and grew faster in height in the pre pubertal period compared to nw, due to an increased Q function. Ow/ob children of both genders had 3.4–4.3 months earlier puberty, reduced growth during puberty, boys and girls had 3 cm and 2 cm, respectively, less pubertal gain from the specific pubertal growth function (P) compared to their nw peers. We saw a negative dose-response effect of childhood BMI on pubertal gain, across the whole BMI spectrum (Fig 2–3.). The adult height was not related to BMI in childhood. Conclusion: For the first time, the result of the present study has shown that; the higher the BMI is in childhood, the less is the pubertal gain. Higher childhood BMI was also associated with increased pre pubertal growth due to an increased Q-function and the resulting adult height was similar for ow/ob and nw children. Reference 1.Holmgren A et al.: Horm. res. in paed. 2013;80(suppl. 1):177.
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| 7. |
- Holmgren, Anton, et al.
(författare)
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Pubertal height gain is inversely related to peak BMI in childhood.
- 2017
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Ingår i: Pediatric research. - : Springer Science and Business Media LLC. - 1530-0447 .- 0031-3998. ; 81:3, s. 448-454
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundChildhood BMI may influence subsequent growth in height as well as the timing of puberty. The aim of the present study was to investigate associations between BMI in childhood and subsequent height gain/pubertal growth.MethodsLongitudinal growth data were used (GrowUp1990 Gothenburg cohort, n=1901). The QEPS growth-model was used to characterize height gain in relation to the highest BMISDS value between 3.5 and 8 years of age. Children were defined as overweight/obese (OwOb) or normal weight/underweight (NwUw), using the 2012 International Obesity Task Force criteria.ResultsA negative association between childhood BMISDS and pubertal height gain was observed. Already at birth, OwOb children were heavier than NwUw children, and had a greater height velocity during childhood. Onset of puberty was 3.5/3.0 months earlier in OwOb girls/boys, and they had 2.3/3.1cm less pubertal height gain from the QEPS-models specific P-function than NwUw children. Adult height was not related to childhood BMI.ConclusionWe found that pubertal height gain was inversely related to peak BMI in childhood. Higher childhood BMISDS was associated with more growth before onset of puberty, earlier puberty and less pubertal height gain, resulting in similar adult heights for OwOb and NwUw children.
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| 8. |
- Holmgren, Anton, et al.
(författare)
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The Pubertal Gain in Height is Inversely Related to BMI in Childhood
- 2015
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Ingår i: Hormone Research in Paediatrics. ; 84:Supplement 1, s. 268-69
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Background: Weight in childhood may influence the pubertal timing and pattern of growth. Objective: To investigate the impact of BMI in childhood on further growth, especially the specific pubertal pattern of growth. Method: The longitudinally followed GrowUpGothenburg1990 birth cohort, was analyzed using the QEPS growth model (Nierop et al. Horm Res in Ped.2013; 80(suppl 1):152–153) (describing total height as a combination of four mathematical functions; Quadratic – Q, Exponential – E, Pubertal – P and Stop – S). Individual BMISDS values, from 3.5–8 years of age were calculated for linear and subgroup analyses (low/normal – Lw/Nw, overweight/obese – Ow/Ob), based on the IOTF 2012 reference (Cole TJ, Lobstein T. Pediatric obesity. 2012; 7(4):284–94.). Results: Across the whole BMI range a negative dose-response effect of childhood BMI on pubertal gain (Pmax) was found. Already at birth Owob children were heavier, and they grew faster in height in the prepubertal period compared to Lw/Nw, as evidenced by an increased Q function. Owob children of both genders had earlier puberty (91–117 days), P = 0.0004, reduced growth during puberty, boys/girls 3.13/2.26 cm less pubertal gain P<0.0001, from the specific pubertal growth function (Pmax). The adult height was not related to BMI in childhood. Conclusion: The higher BMI in childhood, the faster the prepubertal growth, the earlier onset of puberty, the less pubertal gain. This was evident across the whole BMI-range, making weight status an important modifier of growth. Funding information: This work was supported by the Swedish Research Council (VR no 7509 and VR 2006-7777), VR/FORMAS/FORTE/VINNOVA (259-2012-38 and 2006-1624); EpiLife-TEENS research program, Pfizer AB, the Governmental Grants for University Hospital Research (ALF), the R&D Department, County of Halland, and the Foundation Växthuset for children.
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| 9. |
- Holmgren, Anton, et al.
(författare)
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The Specific Pubertal Height Gain is Higher in Boys as Well as in Children with Lower BMISDS
- 2016
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Ingår i: Hormone Research in Paediatrics. - 1663-2818 .- 1663-2826.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Background: Growth in height during puberty can be described by the QEPS-model as a combination of continuous basal growth, QES, and a specific pubertal growth function, P. Objective and hypotheses: To study the relationship between childhood BMISDS and the prepubertal gain and pubertal gain related to growth functions from the QEPS-model. Method: The longitudinally followed GrowUpGothenburg 1990 birth cohort, was analyzed, by the QEPS-model. Individual maximal BMISDS values, from 3.5–8.0 years of age (n=1901) were calculated for linear and subgroup analyses, underweight (blue cross), normal (blue open circles), overweight (red open circles), obese (red circles). Results: For girls (Figure left), total pubertal gain (Tpubgain) depended more on QESgain during puberty. For boys, total pubertal gain depended more on specific Pgain (Figure right). With higher BMISDS this balance was shifted towards less Pgain for both girls and boys. Before puberty, children with higher BMISDS were taller, expressed as higher QESgain, with a linear correlation over the whole BMI–range (P<0.001for both girls/ boys). Conclusion: During puberty, girls grew more due to the QES than the P functions, with opposite findings in boys. For both boys and girls, there were less Pgain and more QES- gain with higher childhood BMISDS. Before puberty, children with higher BMISDS were taller.
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| 10. |
- Zhou, Bin, et al.
(författare)
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Worldwide trends in diabetes since 1980: A pooled analysis of 751 population-based studies with 4.4 million participants
- 2016
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Ingår i: The Lancet. - : Elsevier B.V.. - 0140-6736 .- 1474-547X. ; 387:10027, s. 1513-1530
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Tidskriftsartikel (refereegranskat)abstract
- Background: One of the global targets for non-communicable diseases is to halt, by 2025, the rise in the age standardised adult prevalence of diabetes at its 2010 levels. We aimed to estimate worldwide trends in diabetes, how likely it is for countries to achieve the global target, and how changes in prevalence, together with population growth and ageing, are aff ecting the number of adults with diabetes.Methods: We pooled data from population-based studies that had collected data on diabetes through measurement of its biomarkers. We used a Bayesian hierarchical model to estimate trends in diabetes prevalence-defined as fasting plasma glucose of 7.0 mmol/L or higher, or history of diagnosis with diabetes, or use of insulin or oral hypoglycaemic drugs-in 200 countries and territories in 21 regions, by sex and from 1980 to 2014. We also calculated the posterior probability of meeting the global diabetes target if post-2000 trends continue.Findings: We used data from 751 studies including 4372000 adults from 146 of the 200 countries we make estimates for. Global age-standardised diabetes prevalence increased from 4.3% (95% credible interval 2.4-17.0) in 1980 to 9.0% (7.2-11.1) in 2014 in men, and from 5.0% (2.9-7.9) to 7.9% (6.4-9.7) in women. The number of adults with diabetes in the world increased from 108 million in 1980 to 422 million in 2014 (28.5% due to the rise in prevalence, 39.7% due to population growth and ageing, and 31.8% due to interaction of these two factors). Age-standardised adult diabetes prevalence in 2014 was lowest in northwestern Europe, and highest in Polynesia and Micronesia, at nearly 25%, followed by Melanesia and the Middle East and north Africa. Between 1980 and 2014 there was little change in age-standardised diabetes prevalence in adult women in continental western Europe, although crude prevalence rose because of ageing of the population. By contrast, age-standardised adult prevalence rose by 15 percentage points in men and women in Polynesia and Micronesia. In 2014, American Samoa had the highest national prevalence of diabetes (>30% in both sexes), with age-standardised adult prevalence also higher than 25% in some other islands in Polynesia and Micronesia. If post-2000 trends continue, the probability of meeting the global target of halting the rise in the prevalence of diabetes by 2025 at the 2010 level worldwide is lower than 1% for men and is 1% for women. Only nine countries for men and 29 countries for women, mostly in western Europe, have a 50% or higher probability of meeting the global target.Interpretation: Since 1980, age-standardised diabetes prevalence in adults has increased, or at best remained unchanged, in every country. Together with population growth and ageing, this rise has led to a near quadrupling of the number of adults with diabetes worldwide. The burden of diabetes, both in terms of prevalence and number of adults aff ected, has increased faster in low-income and middle-income countries than in high-income countries.
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