Childhood obesity : behind the doors of the epidemic

Childhood obesity is reaching alarming proportions and is currently one of the most important public health problems. It is associated with significant physical and psychosocial health consequences, both in the short and long term. In this thesis we looked below the tip of the childhood obesity iceberg, and dived into a few important issues encountered in daily clinical practice. Within this scope a range of studies was carried out. We investigated the health-related quality of life in children and adolescents at the start of hospital-based obesity treatment, studied the expression of adiponectin and leptin receptors on circulating immune cells in obese children pre- and post-lifestyle intervention compared to normal weight control children, and evaluated ambulatory blood pressure measurement patterns in a population of overweight and obese children and adolescents. Additionally, the effects of the multidisciplinary, multicomponent, family-based childhood obesity treatment programmes in Hospital Gelderse Vallei were investigated, specifically comparing overweight or obese (young) children and adolescents. Furthermore, a systematic review and meta-analysis was performed summarising the existing knowledge on programmes and initiatives aimed at long-term maintenance of a healthy or reduced weight in children and adolescents following initial treatment of overweight. Finally, several overarching theoretical, practical, and methodological issues derived from this thesis were discussed, followed by implications for clinical practice and directions for future research.</p

Quality of life of children and adolescents with clinical obesity, perspectives of children and parents

Background/objectives: Childhood obesity can have important psychological impacts. The objective of this study was to evaluate the Health Related Quality of Life (HRQoL) of children and adolescents with overweight and obesity. The participants were referred to an outpatient hospital-based obesity treatment. Additionally, we investigated the differences between parent- and self-reported HRQoL. Subjects/methods: Children and adolescents aged 3−18 years with overweight or obesity, referred by their general practitioner or youth health care physician to the pediatric outpatient clinic of Hospital Gelderse Vallei (Ede, the Netherlands) for multidisciplinary obesity treatment, were enrolled in this cross-sectional study (n = 119). Interventions/methods: Parent-proxy reported HRQoL was assessed using the Child Health Questionnaire Parental Form 50 (CHQ-PF50, n = 119) and the Infant Toddler Quality of Life Questionnaire 97 (ITQOL-97). Adolescents completed CHQ Child Form 87 (CHQ-CF87, n = 45) and Impact of Weight on Quality of Life-Kids (IWQOL-Kids, n = 38) to assess self-reported HRQoL. Results: The mean age of the children was 9.6 years (SD 4.3). Both parent-proxy reports and child self-reports showed lower HRQoL in children with a higher degree of obesity, especially in the physical domains of HRQoL (p < 0.05). Child self-reported scores were significantly lower than parent-proxy scores on the subscales ‘bodily pain/discomfort’ and ‘general health perceptions’, and significantly higher on ‘behavior’ and ‘family cohesion’ (p < 0.05). Conclusions: Childhood obesity has a negative effect on HRQoL, especially on the physical aspects. The discordance between parent and child reports underscores the importance of using a combination of parent-proxy and child self-reports to assess HRQoL

Office blood pressure versus ambulatory blood pressure measurement in childhood obesity

Abstract Background The prevalence of obesity-related co-morbidities is rising parallel to the childhood obesity epidemic. High blood pressure (BP), as one of these co-morbidities, is detected nowadays at increasingly younger ages. The diagnosis of elevated BP and hypertension, especially in the childhood population, presents a challenge to clinicians. The added value of ambulatory blood pressure measurement (ABPM) in relation to office blood pressure (OBP) measurements in obese children is unclear. Furthermore, it is unknown how many overweight and obese children have an abnormal ABPM pattern. In this study we evaluated ABPM patterns in a population of overweight and obese children and adolescents, and compared these patterns with regular OBP measurements. Methods In this cross-sectional study in overweight or obese children and adolescents aged 4–17 years who were referred to secondary pediatric obesity care in a large general hospital in The Netherlands, OBP was measured during a regular outpatient clinic visit. Additionally, all participants underwent a 24-hour ABPM on a regular week-day. Outcome measures were OBP, mean ambulatory SBP and DBP, BP load (percentage of readings above the ambulatory 95th blood pressure percentiles), ambulatory BP pattern (normal BP, white-coat hypertension, elevated BP, masked hypertension, ambulatory hypertension), and BP dipping. Results We included 82 children aged 4–17 years. They had a mean BMI Z-score of 3.3 (standard deviation 0.6). Using ABPM, 54.9% of the children were normotensive (95% confidence interval 44.1–65.2), 26.8% had elevated BP, 9.8% ambulatory hypertension, 3.7% masked hypertension, and 4.9% white-coat hypertension. An isolated night-time BP load > 25% was detected in almost a quarter of the children. 40% of the participants lacked physiologic nocturnal systolic BP dipping. In the group of children with normal OBP, 22.2% turned out to have either elevated BP or masked hypertension on ABPM. Conclusions In this study a high prevalence of abnormal ABPM patterns in overweight or obese children and adolescents was detected. Additionally, OBP poorly correlated with the child’s actual ABPM pattern. Herewith, we emphasized the usefulness of ABPM as an important diagnostic tool in this population

Differential adipokine receptor expression on circulating leukocyte subsets in lean and obese children

Background: Childhood obesity prevalence has increased worldwide and is an important risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD). The production of inflammatory adipokines by obese adipose tissue contributes to the development of T2D and CVD. While levels of circulating adipokines such as adiponectin and leptin have been established in obese children and adults, the expression of adiponectin and leptin receptors on circulating immune cells can modulate adipokine signalling, but has not been studied so far. Here, we aim to establish the expression of adiponectin and leptin receptors on circulating immune cells in obese children pre and post-lifestyle intervention compared to normal weight control children. Methods: 13 obese children before and after a 1-year lifestyle intervention were compared with an age and sex-matched normal weight control group of 15 children. Next to routine clinical and biochemical parameters, circulating adipokines were measured, and flow cytometric analysis of adiponectin receptor 1 and 2 (AdipoR1, AdipoR2) and leptin receptor expression on peripheral blood mononuclear cell subsets was performed. Results: Obese children exhibited typical clinical and biochemical characteristics compared to controls, including a higher BMI-SD, blood pressure and circulating leptin levels, combined with a lower insulin sensitivity index (QUICKI). The 1-year lifestyle intervention resulted in stabilization of their BMI-SD. Overall, circulating leukocyte subsets showed distinct adipokine receptor expression profiles. While monocytes expressed high levels of all adipokine receptors, NK and iNKT cells predominantly expressed AdipoR2, and B-lymphocytes and CD4+ and CD8+ T-lymphocyte subsets expressed AdipoR2 as well as leptin receptor. Strikingly though, leukocyte subset numbers and adipokine receptor expression profiles were largely similar in obese children and controls. Obese children showed higher naïve B-cell numbers, and pre-intervention also higher numbers of immature transition B-cells and intermediate CD14++CD16+ monocytes combined with lower total monocyte numbers, compared to controls. Furthermore, adiponectin receptor 1 expression on nonclassical CD14+CD16++ monocytes was consistently upregulated in obese children pre-intervention, compared to controls. However, none of the differences in leukocyte subset numbers and adipokine receptor expression profiles between obese children and controls remained significant after multiple testing correction. Conclusions: First, the distinct adipokine receptor profiles of circulating leukocyte subsets may partly explain the differential impact of adipokines on leukocyte subsets. Second, the similarities in adipokine receptor expression profiles between obese children and normal weight controls suggest that adipokine signaling in childhood obesity is primarily modulated by circulating adipokine levels, instead of adipokine receptor expression

Differential adipokine receptor expression on circulating leukocyte subsets in lean and obese children

Background: Childhood obesity prevalence has increased worldwide and is an important risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD). The production of inflammatory adipokines by obese adipose tissue contributes to the development of T2D and CVD. While levels of circulating adipokines such as adiponectin and leptin have been established in obese children and adults, the expression of adiponectin and leptin receptors on circulating immune cells can modulate adipokine signalling, but has not been studied so far. Here, we aim to establish the expression of adiponectin and leptin receptors on circulating immune cells in obese children pre and post-lifestyle intervention compared to normal weight control children. Methods: 13 obese children before and after a 1-year lifestyle intervention were compared with an age and sex-matched normal weight control group of 15 children. Next to routine clinical and biochemical parameters, circulating adipokines were measured, and flow cytometric analysis of adiponectin receptor 1 and 2 (AdipoR1, AdipoR2) and leptin receptor expression on peripheral blood mononuclear cell subsets was performed. Results: Obese children exhibited typical clinical and biochemical characteristics compared to controls, including a higher BMI-SD, blood pressure and circulating leptin levels, combined with a lower insulin sensitivity index (QUICKI). The 1-year lifestyle intervention resulted in stabilization of their BMI-SD. Overall, circulating leukocyte subsets showed distinct adipokine receptor expression profiles. While monocytes expressed high levels of all adipokine receptors, NK and iNKT cells predominantly expressed AdipoR2, and B-lymphocytes and CD4+ and CD8+ T-lymphocyte subsets expressed AdipoR2 as well as leptin receptor. Strikingly though, leukocyte subset numbers and adipokine receptor expression profiles were largely similar in obese children and controls. Obese children showed higher naïve B-cell numbers, and pre-intervention also higher numbers of immature transition B-cells and intermediate CD14++CD16+ monocytes combined with lower total monocyte numbers, compared to controls. Furthermore, adiponectin receptor 1 expression on nonclassical CD14+CD16++ monocytes was consistently upregulated in obese children pre-intervention, compared to controls. However, none of the differences in leukocyte subset numbers and adipokine receptor expression profiles between obese children and controls remained significant after multiple testing correction. Conclusions: First, the distinct adipokine receptor profiles of circulating leukocyte subsets may partly explain the differential impact of adipokines on leukocyte subsets. Second, the similarities in adipokine receptor expression profiles between obese children and normal weight controls suggest that adipokine signaling in childhood obesity is primarily modulated by circulating adipokine levels, instead of adipokine receptor expression

Patient characteristics.

<p>Patient characteristics.</p

Leukocyte subset numbers.

<p>Leukocyte subset numbers.</p

Adiponectin receptor 1 expression.

<p>Adiponectin receptor 1 expression.</p

Adiponectin receptor 2 expression.

<p>Adiponectin receptor 2 expression.</p