In four prospective cohort studies, obese adults who were overweight or obese in childhood had increased rates of cardiovascular risk factors. Those who were overweight or obese as children but not ...as adults had risks similar to the risks among those who were never obese.
During the past three decades, the prevalences of overweight and obesity in the pediatric population have increased substantially.
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Childhood obesity is a predictor of an increased rate of death, owing primarily to an increased risk of cardiovascular disease.
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–
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Forecasts suggest that the “obesity epidemic” may reverse the current trend of the declining rate of death from cardiovascular causes,
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leading to a shorter lifespan for today's children.
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There is substantial evidence that the association between obesity and cardiovascular disease is explained by the adverse cardiovascular risk-factor profile that is frequently seen in obese adults. This profile includes increased rates of . . .
Abstract
Aims
The relationship between life-course body mass index (BMI) trajectories and adult risk for cardiovascular disease (CVD) is poorly described. In a longitudinal cohort, we describe BMI ...trajectories from early childhood to adulthood and investigate their association with CVD risk factors Type 2 diabetes mellitus (T2DM), high-risk lipid levels, hypertension, and high carotid intima-media thickness (cIMT) in adulthood (34–49 years).
Methods and results
Six discrete long-term BMI trajectories were identified using latent class growth mixture modelling among 2631 Cardiovascular Risk in Young Finns Study participants (6–49 years): stable normal (55.2%), resolving (1.6%), progressively overweight (33.4%), progressively obese (4.2%), rapidly overweight/obese (4.3%), and persistent increasing overweight/obese (1.2%). Trajectories of worsening or persisting obesity were generally associated with increased risk of CVD outcomes in adulthood (24–49 years) all risk ratios (RRs) >15, P < 0.05 compared with the stable normal group. Although residual risk for adult T2DM could not be confirmed RR = 2.6, 95% confidence interval (CI) = 0.14–8.23, participants who resolved their elevated child BMI had similar risk for dyslipidaemia and hypertension as those never obese or overweight (all RRs close to 1). However, they had significantly higher risk for increased cIMT (RR = 3.37, 95% CI = 1.80–6.39).
Conclusion
The long-term BMI trajectories that reach or persist at high levels associate with CVD risk factors in adulthood. Stabilizing BMI in obese adults and resolving elevated child BMI by adulthood might limit and reduce adverse cardiometabolic profiles. However, efforts to prevent child obesity might be most effective to reduce the risk for adult atherosclerosis.
Childhood obesity: Current and novel approaches Sabin, Matthew A., MRCPCH (UK), FRACP, PhD; Kiess, Wieland, MD
Best Practice & Research Clinical Endocrinology & Metabolism,
06/2015, Letnik:
29, Številka:
3
Journal Article
Recenzirano
The prevalence of childhood obesity has increased over the last fifty years by approximately 5% per decade, and approximately a quarter of all children are now either overweight or obese. These ...children have a significantly increased risk of many future health problems including adult obesity, type 2 diabetes and heart disease. Despite this relentless increase, common-sense approaches aimed at prevention and treatment have failed to solve the problem. Current approaches at prevention have faced major challenges with some progress in implementing smaller scale programs and social marketing, but little action on broad public policy approaches which often appears unpalatable to society or individual governments. Meanwhile, treatment approaches have mainly focused on lifestyle change, and novel approaches are urgently needed. Prevention needs to shift to improving maternal health prior to conception, with more research focussed on the impact of early years in programming offspring to future overweight/obesity. Likewise, treatment paradigms need to move from simply thinking that obesity can be solved by readdressing diet and activity levels. Novel approaches are needed which take into consideration the complex physiology which regulates early childhood growth and the development of obesity in susceptible individuals.
Profound knowledge about child growth, development, health, and disease in contemporary children and adolescents is still rare. Epidemiological studies together with new powerful research ...technologies present exciting opportunities to the elucidation of risk factor-outcome associations with potentially major consequences for prevention, diagnosis and treatment.
To conduct a unique prospective longitudinal cohort study in order to assess how environmental, metabolic and genetic factors affect growth, development and health from fetal life to adulthood.
The 'Leipzig Research Centre for Civilization Diseases (LIFE) Child Study' focuses on two main research objectives: (1) monitoring of normal growth, development and health; (2) non-communicable diseases such as childhood obesity and its co-morbidities, atopy and mental health problems. Detailed assessments will be conducted alongside long-term storage of biological samples in 2,000 pregnant women and more than 10,000 children and their families.
Close coordination and engagement of a multidisciplinary team in the LIFE Child study successfully established procedures and systems for balancing many competing study and ethical needs. Full participant recruitment and complete data collection started in July 2011. Early data indicate a high acceptance rate of the study program, successful recruitment strategies and the establishment of a representative cohort for the population of Leipzig. A series of subprojects are ongoing, and analyses and publications are on their way.
This paper addresses key elements in the design and implementation of the new prospective longitudinal cohort study LIFE Child. Given the recognized need for long-term data on adverse effects on health and protective factors, our study data collection should provide magnificent opportunities to examine complex interactions that govern the emergence of non-communicable diseases.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background
There is paucity of knowledge concerning the specific age in youth when the associations of metabolic syndrome (MetS) begin to be operative. Thus, we investigated the relation of age to ...the associations of childhood MetS with adult MetS, type 2 diabetes mellitus and high carotid intima‐media thickness.
Methods and Results
Five thousand eight‐hundred three participants were analyzed in 4 cohort studies (Cardiovascular Risk in Young Finns, Bogalusa Heart Study, Princeton Lipid Research Study, Insulin Study). International cutoffs and previously used 75th percentile cutoffs were used for children to define MetS and its components. Mean follow‐up period was 22.3 years. Logistic regression was used to calculate risk ratios and 95% confidence intervals. Childhood MetS and overweight were associated with over 2.4‐fold risk for adult MetS from the age of 5 years onward. Risk for type 2 diabetes mellitus was increased from the age of 8 (risk ratio, 2.6–4.1; 95% confidence interval, 1.35–6.76 and 1.12–7.24, respectively) onward for the 2 childhood MetS criteria based on international cut‐off values and for childhood overweight. Risk for high carotid intima‐media thickness was significant at ages 11 to 18 years in relation to childhood MetS or overweight (risk ratio, 2.44–4.22; 95% confidence interval, 1.55–3.55 and 2.55–5.66, respectively). Continuous childhood MetS score was associated with adult MetS from the age of 5, with type 2 diabetes mellitus from the age of 14 and with high carotid intima‐media thickness from the age of 11 years onward.
Conclusions
Adult MetS was predicted by MetS in childhood beginning at age 5. However, adult type 2 diabetes mellitus and subclinical atherosclerosis were not predicted by childhood data until after age 8. Body mass index measurement alone at the same age points provided similar findings.
Obesity, a chronic inflammatory disease, is the most prevalent modifiable risk factor for cardiovascular disease. The mechanisms underlying inflammation in obesity are incompletely understood. Recent ...developments have challenged the dogma of immunological memory occurring exclusively in the adaptive immune system and show that the innate immune system has potential to be reprogrammed. This innate immune memory (trained immunity) is characterized by epigenetic and metabolic reprogramming of myeloid cells following endogenous or exogenous stimulation, resulting in enhanced inflammation to subsequent stimuli. Trained immunity phenotypes have now been reported for other immune and non-immune cells. Here, we provide a novel perspective on the putative role of trained immunity in mediating the adverse cardiovascular effects of obesity and highlight potential translational pathways.
Obesity, a chronic inflammatory disorder, is the most prevalent modifiable risk factor for cardiovascular disease throughout the life-course; long-term outcomes following lifestyle interventions have generally been disappointing.Inhibition of inflammation has been shown to decrease cardiovascular risk in patients with a residual inflammatory risk.Recent studies have demonstrated that the innate immune system can adopt a long-term memory (trained immunity) after a previous encounter with a stimulus, resulting in an increased response upon secondary stimulation. Monocytes from patients with atherosclerosis have a trained immune phenotype.In obesity, a state of dyslipidemia, endotoxemia, and increased plasma cytokines and adipokines is likely to induce trained immunity.Non-immune cells can also be trained, indicating a possible role for adipocyte memory in chronic inflammation.
Identifying early life risk factors remains key to the prevention of nonalcoholic fatty liver (hereinafter "fatty liver") in adulthood. However, the longitudinal association of childhood passive ...smoking with adult fatty liver is not studied. We examined the association of childhood and adulthood passive smoking with fatty liver in midlife.
This was a 31-year prospective cohort study of 1,315 participants. Information on childhood passive smoking (parental smoking) was collected in 1980 (aged 3-18 years) and 1983 and adulthood passive smoking in 2001, 2007, and 2011. Fatty liver was determined by ultrasound in 2011 (aged 34-49 years).
The prevalence of fatty liver was 16.3%. Both childhood and adulthood passive smoking were associated with higher risk of fatty liver, adjusting for potential confounders such as age, sex, childhood socioeconomic status, and adulthood physical activity and alcohol consumption (relative risk = 1.41, 95% confidence interval: 1.01-1.97 for childhood; 1.35, 1.01-1.82 for adulthood). Individuals with persistent exposure to passive smoking between childhood and adulthood had the highest risk (relative risk = 1.99, 95% confidence interval: 1.14-3.45) compared with those without passive smoking in either childhood or adulthood.
Passive smoking in both child and adult lives are associated with increased risk of adult fatty liver, suggesting that the prevention of passive smoking should start as early as possible and maintain throughout lifetime.
Hypertension may be predicted from childhood risk factors. Repeated observations of abnormal blood pressure in childhood may enhance prediction of hypertension and subclinical atherosclerosis in ...adulthood compared with a single observation. Participants (1927, 54% women) from the Cardiovascular Risk in Young Finns Study had systolic and diastolic blood pressure measurements performed when aged 3 to 24 years. Childhood/youth abnormal blood pressure was defined as above 90th or 95th percentile. After a 21- to 31-year follow-up, at the age of 30 to 45 years, hypertension (>140/90 mm Hg or antihypertensive medication) prevalence was found to be 19%. Carotid intima-media thickness was examined, and high-risk intima-media was defined as intima-media thickness >90th percentile or carotid plaques. Prediction of adulthood hypertension and high-risk intima-media was compared between one observation of abnormal blood pressure in childhood/youth and multiple observations by improved Pearson correlation coefficients and area under the receiver operating curve. When compared with a single measurement, 2 childhood/youth observations improved the correlation for adult systolic (r=0.44 versus 0.35, P<0.001) and diastolic (r=0.35 versus 0.17, P<0.001) blood pressure. In addition, 2 abnormal childhood/youth blood pressure observations increased the prediction of hypertension in adulthood (0.63 for 2 versus 0.60 for 1 observation, P=0.003). When compared with 2 measurements, third observation did not provide any significant improvement for correlation or prediction (P always >0.05). A higher number of childhood/youth observations of abnormal blood pressure did not enhance prediction of adult high-risk intima-media thickness. Compared with a single measurement, the prediction of adult hypertension was enhanced by 2 observations of abnormal blood pressure in childhood/youth.
Objective To assess the effect on spermatogenesis of adding recombinant follicle-stimulating hormone (FSH) to human chorionic gonadotropin (hCG) treatment protocols for adolescent/young adult males ...with hypogonadotropic hypogonadism (HH). Design Observational descriptive study. Setting Outpatient clinics. Patient(s) Nineteen males with hypogonadotropic hypogonadism, aged 14.5 to 31.0 years. Intervention(s) Treatment with either hCG treatment alone (n = 9; group 1) or in combination with recombinant FSH (n = 10; group 2), over 6 to 9 months. Main Outcome Measure(s) Combined testicular volume (CTV) and testosterone, inhibin B, semen/urine analysis at 6 to 9 months. Result(s) There were no differences between the two groups in baseline variables or changes in CTV with treatment. Despite this, evidence of spermatogenesis was present in all group 2 patients by 9 months (range 0.2 to 15 × 106 /mL) compared with three of nine patients in group 1 (range 0 to <1 × 106 /mL). Whole group and subgroup analyses did not demonstrate any statistically significant correlations between age at onset of treatment and either CTV or sperm count. Conclusion(s) The addition of recombinant FSH to hCG treatment protocols in adolescent/young adult HH males results in normal testicular growth and may hasten induction of spermatogenesis.
To examine how overweight and obesity at specific ages and overall BMI growth patterns throughout childhood predict cardiometabolic phenotypes at 11 to 12 years.
In a population-based sample of 5107 ...infants, BMI was measured every 2 years between ages 2 to 3 and 10 to 11 years. We identified 5 BMI trajectories using growth curve models. At ages 11 to 12 years, 1811 children completed assessments for metabolic syndrome risk scores, carotid-femoral pulse wave velocity, and carotid intima-media thickness. Multivariable regression models were used to estimate associations, adjusted for potential confounders (eg, age, sex, smoking exposure, and small for gestational age).
Overweight and obesity from early childhood onward were strongly associated with higher cardiometabolic risk at 11 to 12 years of age. At age 6 to 7 years, compared with those with a healthy weight, children with overweight had higher metabolic syndrome risk scores by 0.23 SD units (95% confidence interval 0.05 to 0.41) and with obesity by 0.76 SD units (0.51-1.01), with associations almost doubling by age 10 to 11 years. Obese (but not overweight) children had higher outcome pulse wave velocity (0.64-0.73 SD units) from ages 6 to 7 years and slightly higher outcome carotid intima-media thickness (0.20-0.30 SD units) at all ages. Cumulative exposure to high BMI from 2 to 3 years of age carried the greatest cardiometabolic risk, with a gradient of risk across trajectories.
High early-childhood BMI is already silently associated with the development of cardiometabolic risk by 11 to 12 years, highlighting the urgent need for effective action to reduce overweight and obesity in early childhood.
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