| 1. |
- Mishra, A, et al.
(författare)
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Diminishing benefits of urban living for children and adolescents' growth and development
- 2023
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 615:7954, s. 874-883
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Tidskriftsartikel (refereegranskat)abstract
- Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified.
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| 2. |
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| 3. |
- Bramsved, Rebecka, 1982, et al.
(författare)
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Birth Weight, Childhood and Young Adult Overweight, and the Risk of Coronary Heart Disease in Men.
- 2024
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Ingår i: Arteriosclerosis, thrombosis, and vascular biology. - 1524-4636. ; 44:1, s. 314-321
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Tidskriftsartikel (refereegranskat)abstract
- Low birth weight is a known risk factor for adult coronary heart disease (CHD), but the additional effect of weight development during childhood and early adult life has not been studied.We included 35659 men born 1945 to 1961 from the population-based BMI Epidemiology Study Gothenburg, with data available on birthweight, BMI in childhood (8 years), and BMI in young adulthood (20 years). Information on CHD diagnoses was retrieved from national registers. We used Cox proportional hazards regression to estimate hazard ratios and 95% CIs for the risk of early and late CHD (before and after 58.4 years of age, respectively).During follow-up, a total of 3380 cases of CHD (fatal and nonfatal) were registered. Birth weight was inversely associated with the risk of both early (hazard ratio, 0.88 per SD increase [95% CI, 0.84-0.92]) and late (hazard ratio, 0.94 per SD increase [95% CI, 0.90-0.98]) CHD, independently of BMI at 8 years and BMI change during puberty. In a model including birth weight (below or above the median) together with overweight at 8 and 20 years, only birth weight and young adult overweight, but not overweight in childhood, were significantly associated with the risk of CHD. A birth weight below the median, followed by overweight at 20 years of age was associated with a more than doubled risk of early CHD (hazard ratio, 2.29 [95% CI, 1.86-2.81]), compared with the reference (birth weight above the median and normal weight at 20 years of age). This excess risk was even more pronounced for a birthweight below 2.5 kg.We demonstrate that low birth weight and young adult overweight are important developmental markers of risk for adult CHD. These findings motivate a life course perspective for prevention and risk assessment of adult CHD.
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| 4. |
- Bygdell, Maria, et al.
(författare)
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A secular trend of increasing pubertal BMI change among Swedish adolescents
- 2022
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Ingår i: International Journal of Obesity. - : Springer Science and Business Media LLC. - 0307-0565 .- 1476-5497. ; 46, s. 444-446
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Tidskriftsartikel (refereegranskat)abstract
- Pubertal BMI change is an independent risk marker of cardiovascular mortality/morbidity. Previous studies demonstrated a secular trend of increased childhood BMI but it is unknown if there is a concomitant secular trend regarding pubertal BMI change. The aim of this study was to describe the trend in pubertal BMI change. We collected heights and weights before and after puberty from school health records and military conscript records for boys born every five years during 1946-1991 (n = 3650, total cohort) and calculated pubertal BMI change (young adult BMI at 20 years of age minus childhood BMI at 8 years of age) for all study participants. A secular trend of increasing pubertal BMI change during the study period was observed. The increase in pubertal BMI change (0.27 kg/m(2) per decade [0.22; 0.32]) explained 54% of the secular trend of increasing young adult BMI (0.50 kg/m(2) per decade [0.43; 0.57]). We made the novel observation that there is a secular trend of increasing pubertal BMI change. We propose that the secular trend of increasing pubertal BMI change might contribute more than the secular trend of increasing childhood BMI to the adverse cardiovascular health consequences associated with the ongoing obesity epidemic.
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| 5. |
- Bygdell, Maria, et al.
(författare)
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Birth weight and young adult body mass index for predicting the risk of developing adult heart failure in men.
- 2022
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Ingår i: European journal of preventive cardiology. - : Oxford University Press (OUP). - 2047-4881 .- 2047-4873. ; 29:6, s. 971-978
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Tidskriftsartikel (refereegranskat)abstract
- Hospitalizations for heart failure among young adults and middle-aged individuals have increased. The aims of the present study were to evaluate the association between birth weight and risk of adult heart failure and the importance of change from low birth weight to overweight/obesity at young adulthood.We used the population-based body mass index (BMI) Epidemiology Study cohort Gothenburg (n=35659) with birth weight and young adult BMI (20years) available from child healthcare records, school health records, and military conscription register for men born 1945-1961. The cohort includes all children who finished school, which was mandatory, in Gothenburg, Sweden. Information on heart failure diagnosis was retrieved from the National Patient Register and the Cause of Death Register (n=415). In cox regression analyses, there was an inverse association between birth weight and risk of heart failure [hazard ratio (HR) 0.83 per standard deviation (SD), 95% confidence interval (CI) 0.76-0.90], and a direct association for young adult BMI (HR 1.48 per SD, 95% CI 1.36-1.61). Of note, individuals with birth weight in the lowest tertile, who were overweight/obese in young adulthood had a five-fold risk of heart failure (HR 4.95, 95% CI 3.36-7.31) compared with individuals in the middle birth weight tertile who were normal weight at 20years.Birth weight was inversely associated with the risk of hospitalization due to heart failure. The combination of low birth weight and overweight/obesity in young adulthood results in excess risk of heart failure beyond that of low birth weight or young adult overweight/obesity separately. These findings indicate the need of a life course perspective in heart failure prevention and risk assessment.
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| 6. |
- 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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| 7. |
- Bygdell, Maria, et al.
(författare)
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Prevalence of overweight and obesity from 5 to 19 years of age in Gothenburg, Sweden
- 2021
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Ingår i: Acta Paediatrica. - : Wiley. - 0803-5253 .- 1651-2227. ; 110:12, s. 3349-3355
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Tidskriftsartikel (refereegranskat)abstract
- Aim The aim of this study was to present prevalence data for overweight and obesity across school age in a large, recent, population-based cohort of children in Gothenburg, Sweden. Methods We included 66,807 children (48.5% girls) aged 5-18.9 years who had their height and weight measured in school health care 2015-2018. The BMI values were categorised according to the age-dependent cut-offs for overweight and obesity from the International Obesity Task Force (IOTF). Results Overall, the prevalence of overweight and obesity for girls and boys was 18.1% and 18.0%, respectively. We observed increasing proportions of overweight (girls 11.5-17.1% and boys 8.4-17.4%) and obesity (girls 3.0-4.2% and boys 2.7-6.1%) with increasing age (p < 0.001 for trend in both sexes). Moreover, girls had higher prevalence of overweight during ages 5.0 to 8.9 years compared with boys (p < 0.001), while boys had higher prevalence of obesity 15.0-18.9 years compared with girls (p < 0.001). Conclusion In conclusion, we demonstrate increasing prevalence of overweight and obesity across the entire school age range, as well as differences in prevalences between boys and girls, in a population-based sample of 67,000 children in Gothenburg city, Sweden. Continuous monitoring of schoolchildren, together with effective preventive measures, is crucial to curb the obesity epidemic and its consequences.
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| 8. |
- 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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| 9. |
- Bygdell, Maria, et al.
(författare)
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The rise and the recent decline of childhood obesity in Swedish boys: the BEST cohort.
- 2017
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Ingår i: International journal of obesity (2005). - : Springer Science and Business Media LLC. - 1476-5497 .- 0307-0565. ; 41:5, s. 807-812
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Tidskriftsartikel (refereegranskat)abstract
- Childhood obesity increases the risk for adult obesity and diseases. The aim of this study was to investigate secular changes of childhood body mass index (BMI), overweight and obesity in boys born during 1946-2006, using the population-based BMI Epidemiology STudy (BEST) cohort in Gothenburg, Sweden.We collected height and weight from archived school health records for boys born every 5 years 1946-2006 (birth cohort 1946 n=1584, each birth cohort 1951-2006 n=425). Childhood BMI at 8 years of age was obtained for all the participants.Childhood BMI increased 0.18kgm(-2) (95% confidence interval: 0.16-0.20) per decade increase in birth year, during 1946-2006. The increase was significant from birth year 1971, peaked 1991 and was then followed by a stabilization or tendency to a reduction. Next, we aimed to thoroughly explore the trend after birth year 1991 and therefore expanded birth cohorts 1991 (n=1566), 2001 (n=6478) and 2006 (n=6515). Importantly, decreases in mean BMI (P<0.01), prevalences of overweight (P<0.01) and obesity (P<0.05) were observed after birth year 1991. For boys born in Sweden and with parents born in Sweden, a substantial reduction in the prevalences of overweight (-28.6%, P<0.001) and obesity (-44.3%, P<0.001) were observed between birth year 1991 and birth year 2006.This long-term study captures both the rise and the recent decline of childhood obesity. As childhood obesity is strongly associated with subsequent adult obesity, we anticipate a similar reduction in adult obesity during the coming decades in Swedish men.
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| 10. |
- Börjesson, Anna E, et al.
(författare)
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Roles of transactivating functions 1 and 2 of estrogen receptor-alpha in bone.
- 2011
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 108:15, s. 6288-6293
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Tidskriftsartikel (refereegranskat)abstract
- The bone-sparing effect of estrogen is primarily mediated via estrogen receptor-α (ERα), which stimulates target gene transcription through two activation functions (AFs), AF-1 in the N-terminal and AF-2 in the ligand binding domain. To evaluate the role of ERα AF-1 and ERα AF-2 for the effects of estrogen in bone in vivo, we analyzed mouse models lacking the entire ERα protein (ERα(-/-)), ERα AF-1 (ERαAF-1(0)), or ERα AF-2 (ERαAF-2(0)). Estradiol (E2) treatment increased the amount of both trabecular and cortical bone in ovariectomized (OVX) WT mice. Neither the trabecular nor the cortical bone responded to E2 treatment in OVX ERα(-/-) or OVX ERαAF-2(0) mice. OVX ERαAF-1(0) mice displayed a normal E2 response in cortical bone but no E2 response in trabecular bone. Although E2 treatment increased the uterine and liver weights and reduced the thymus weight in OVX WT mice, no effect was seen on these parameters in OVX ERα(-/-) or OVX ERαAF-2(0) mice. The effect of E2 in OVX ERαAF-1(0) mice was tissue-dependent, with no or weak E2 response on thymus and uterine weights but a normal response on liver weight. In conclusion, ERα AF-2 is required for the estrogenic effects on all parameters evaluated, whereas the role of ERα AF-1 is tissue-specific, with a crucial role in trabecular bone and uterus but not cortical bone. Selective ER modulators stimulating ERα with minimal activation of ERα AF-1 could retain beneficial actions in cortical bone, constituting 80% of the skeleton, while minimizing effects on reproductive organs.
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