Dagmar l'Allemand

Ambulatory Health Information System for Obesity Prevention and Treatment (Pathmate) Tailored for Teenagers: A Preliminary Longitudinal Study

Background: The development of BMI in early childhood is dependent on socioeconomic factors. Our aim was to explore the impact of parental education level and family income for development of BMI from birth to 8 years age.Methods: 3018 children born in 1998–2006 from the IDEFICS study and register controls were included. Weight and height measurements from birth up to 8 years of age were obtained from the Child Health Services. Parental education and family disposable income, obtained from Statistics Sweden and the Medical Birth Register, were defined as high/low. Obesity was defined by WHO references. Confounders were sex and age of the child, parental origin, maternal smoking and maternal BMI.Results: At birth, the children’s mean BMI (SD) was lower in families of low vs. high income (13,74 (1,35) vs. 13,94 (1,36), p<0.0001). Results remained significant after adjusting for confounders. No differences in birth BMI were detected between children of low and high-educated parents (13,87 (1,37) vs. 13,83 (1,35), p=0.48). From 6 months onwards, children of low-educated parents showed higher mean BMI than children of high-educated. At 8 years, mean BMI in the low/high educated groups were 17.12 (2.44) and 16.38 (1.94), p<0.0001. Results remained significant after adjusting for confounders. Prevalence of obesity in the low and high-educated groups were 11% and 4,1%, p<0,0001. The difference in BMI at 8 years seen in the low/high income group disappeared after adjusting for confounders (17.5 vs. 17.6, p=0,63).Conclusion: Impact of family socioeconomic factors on children’s BMI differs by income and education. The effect of parental education becomes more evident by age up to 8 years of age. Interventions for healthy weight development must start very early in life.Background: Compelling evidence links obesity induced systemic inflammation to the development of chronic kidney disease (CKD). This systemic inflammation may result from exacerbated adipose inflammation. Besides the known detrimental effects of typical pro-inflammatory factors secreted by the adipose tissue (TNF-α, MCP-1 and IL-6) on the kidney, we hypothesize the enhanced obesity-induced secretion of serum amyloid A (SAA), an acute inflammatory protein, to play a key role in aggravating obesity-induced CKD. Methods: Groups of male C57Bl/6J mice (n = 99 in total) were fed a low (10% lard) or high (45% lard) fat diet for a maximum of 52 weeks. Mice were sacrificed after 24, 40 and 52 weeks. Whole blood samples, kidneys and adipose tissues were collected. The development of adipose and renal tissue inflammation was assessed on gene expression and protein level. Adipocytokine levels were measured in plasma samples. Results: A distinct inflammatory phenotype was observed in the adipose tissue of HFD mice prior to renal inflammation, which was associated with an early systemic elevation of TNF-α, leptin and SAA (1A-C). With aging, sclerotic lesions appeared in the kidney, the extent of which was severely aggravated by HFD feeding. Lesions exhibited typical amyloid characteristics (2A) and pathological severity positively correlated with bodyweight (2B). Interestingly, more SAA protein was detected in lesions of HFD mice. Conclusion: Our data suggest a causal link between obesity induced chronic inflammation and AA amyloidosis in C57Bl/6J mice. Though future studies are necessary to prove this causal link and to determine its relevance for the human situation, obesity may hence be considered a risk factor for the development and progression of renal AA amyloidosis in the course of CKD. (Figure Presented).Introduction: Existing treatment programs for obese children prove limited effectiveness and sustainability. Health Information System (HIS) enhanced interventions have the potential for higher accessibility and cost-effectiveness of multi-professional family-based obesity therapy. The aim was not only to modify the patient’s behavior but also to positively influence their family system. Methods: In cooperation with therapists, extremely obese children, their parents, computer scientists and information systems researcher, a mobile HIS was developed, consisting of a tablet PC with photo and patient’s privacy services, relaxation tools and the ability to measure speed of eating by electronic stop watch, emotional parameters by self-assessment manikin mood scale and physical activity by 3-axes accelerometer, Fitbit, combined with telephone interviews. Three groups of each six extremely obese children (BMI > 99.5, median BMI z-score 3.0, age 13.2 2.3 years) were assigned to therapy in either an (1) individual or (2) group setting with HIS, or (3) individual care without HIS. Physical activity, speed of eating and physical and emotional parameters were evaluated before and after 12 months of therapy. All patients and parents gave informed consent for adherence to therapy, monitoring and the use of tablet PC’s. Results: A total of 25% of extremely obese children with HIS and 60% without HIS decreased their BMI-SDS. Children using HIS did not reduce their obesity more than the control group without HIS, if parents did not support their children at home. Those children with parental support did use HIS for activity, mood and nutrition monitoring regularly. Conclusion: In extremely obese children, home support with HIS is only effective, when children are guided by their parents while using HIS. To select appropriate families for HIS home support, careful examination of the family system including their motivation and psychosocial factors is needed.Basel · Freiburg · Paris · London · New York · Chennai · New Delhi · Bangkok · Beijing · Shanghai · Tokyo · Kuala Lumpur · Singapore · Sydney

Does a Health Information Technology System developed by Children and their Parents improve Obesity Therapy

Background: The development of BMI in early childhood is dependent on socioeconomic factors. Our aim was to explore the impact of parental education level and family income for development of BMI from birth to 8 years age.Methods: 3018 children born in 1998–2006 from the IDEFICS study and register controls were included. Weight and height measurements from birth up to 8 years of age were obtained from the Child Health Services. Parental education and family disposable income, obtained from Statistics Sweden and the Medical Birth Register, were defined as high/low. Obesity was defined by WHO references. Confounders were sex and age of the child, parental origin, maternal smoking and maternal BMI.Results: At birth, the children’s mean BMI (SD) was lower in families of low vs. high income (13,74 (1,35) vs. 13,94 (1,36), p<0.0001). Results remained significant after adjusting for confounders. No differences in birth BMI were detected between children of low and high-educated parents (13,87 (1,37) vs. 13,83 (1,35), p=0.48). From 6 months onwards, children of low-educated parents showed higher mean BMI than children of high-educated. At 8 years, mean BMI in the low/high educated groups were 17.12 (2.44) and 16.38 (1.94), p<0.0001. Results remained significant after adjusting for confounders. Prevalence of obesity in the low and high-educated groups were 11% and 4,1%, p<0,0001. The difference in BMI at 8 years seen in the low/high income group disappeared after adjusting for confounders (17.5 vs. 17.6, p=0,63).Conclusion: Impact of family socioeconomic factors on children’s BMI differs by income and education. The effect of parental education becomes more evident by age up to 8 years of age. Interventions for healthy weight development must start very early in life.Background: Compelling evidence links obesity induced systemic inflammation to the development of chronic kidney disease (CKD). This systemic inflammation may result from exacerbated adipose inflammation. Besides the known detrimental effects of typical pro-inflammatory factors secreted by the adipose tissue (TNF-α, MCP-1 and IL-6) on the kidney, we hypothesize the enhanced obesity-induced secretion of serum amyloid A (SAA), an acute inflammatory protein, to play a key role in aggravating obesity-induced CKD. Methods: Groups of male C57Bl/6J mice (n = 99 in total) were fed a low (10% lard) or high (45% lard) fat diet for a maximum of 52 weeks. Mice were sacrificed after 24, 40 and 52 weeks. Whole blood samples, kidneys and adipose tissues were collected. The development of adipose and renal tissue inflammation was assessed on gene expression and protein level. Adipocytokine levels were measured in plasma samples. Results: A distinct inflammatory phenotype was observed in the adipose tissue of HFD mice prior to renal inflammation, which was associated with an early systemic elevation of TNF-α, leptin and SAA (1A-C). With aging, sclerotic lesions appeared in the kidney, the extent of which was severely aggravated by HFD feeding. Lesions exhibited typical amyloid characteristics (2A) and pathological severity positively correlated with bodyweight (2B). Interestingly, more SAA protein was detected in lesions of HFD mice. Conclusion: Our data suggest a causal link between obesity induced chronic inflammation and AA amyloidosis in C57Bl/6J mice. Though future studies are necessary to prove this causal link and to determine its relevance for the human situation, obesity may hence be considered a risk factor for the development and progression of renal AA amyloidosis in the course of CKD. (Figure Presented).Introduction: Existing treatment programs for obese children prove limited effectiveness and sustainability. Health Information System (HIS) enhanced interventions have the potential for higher accessibility and cost-effectiveness of multi-professional family-based obesity therapy. The aim was not only to modify the patient’s behavior but also to positively influence their family system. Methods: In cooperation with therapists, extremely obese children, their parents, computer scientists and information systems researcher, a mobile HIS was developed, consisting of a tablet PC with photo and patient’s privacy services, relaxation tools and the ability to measure speed of eating by electronic stop watch, emotional parameters by self-assessment manikin mood scale and physical activity by 3-axes accelerometer, Fitbit, combined with telephone interviews. Three groups of each six extremely obese children (BMI > 99.5, median BMI z-score 3.0, age 13.2 2.3 years) were assigned to therapy in either an (1) individual or (2) group setting with HIS, or (3) individual care without HIS. Physical activity, speed of eating and physical and emotional parameters were evaluated before and after 12 months of therapy. All patients and parents gave informed consent for adherence to therapy, monitoring and the use of tablet PC’s. Results: A total of 25% of extremely obese children with HIS and 60% without HIS decreased their BMI-SDS. Children using HIS did not reduce their obesity more than the control group without HIS, if parents did not support their children at home. Those children with parental support did use HIS for activity, mood and nutrition monitoring regularly. Conclusion: In extremely obese children, home support with HIS is only effective, when children are guided by their parents while using HIS. To select appropriate families for HIS home support, careful examination of the family system including their motivation and psychosocial factors is needed.Basel · Freiburg · Paris · London · New York · Chennai · New Delhi · Bangkok · Beijing · Shanghai · Tokyo · Kuala Lumpur · Singapore · Sydney