Epidemiological survey for the prevalence of overweight and abdominal obesity in Greek adolescents

This study was designed to provide estimates of overweight (OW), obesity (OB), and abdominal OB (AO) in a representative sample of adolescents throughout the whole of Greece. A total of 14,456 adolescents aged 13-19 years (6,677 boys and 7,779 girls) had direct measurements (height, weight, waist circumference (WC)) taken at school during 2003. The overall prevalence of OW including OB in the population studied was 29.4% in boys and 16.7% in girls. OB prevalence was also higher in boys than in girls (6.1% vs. 2.7%), whereas prevalence of AO was higher in girls than in boys (21.7% vs. 13.5%). Rates of OW, OB, and AO were significantly more prevalent in the Greek than in the foreign male population (immigrants). OW% in adolescent girls was independently associated with smoking and alcohol consumption. The prevalence of OW and OB in Greek adolescents is high, particularly in boys, comparable with that reported for most Mediterranean European countries. AO, mainly in adolescent girls, also appears high. Preventive and treatment strategies are urgently needed to combat this OB epidemic in Greece.     

Accelerated Growth in Early Life and Obesity in Preschool Chilean Children

In Chile, childhood obesity rates are high. The purpose of this article is to compare BMI growth characteristics of normal (N), overweight (OW), and obese (OB) 5‐year olds from 0 to 5 years and explore the influence of some prenatal factors on these patterns of growth. The study was done on a retrospective cohort of 1,089 5‐year olds with birth weight >2,500 g. Weight and height were obtained from records at nine occasions (0–36 months); at 52 and 60 months, we measured them. At 60 months, children were classified as N, OW, and OB. At each age, BMI and z‐score of BMI (BMI Z) differences were compared among groups. The influence of birth weight, pre‐pregnancy BMI, and prenatal variables (weight gain, smoking, and presence of diabetes and preeclampsia) on BMI Z differences between N and OB was also explored. Adiposity rebound (AR) was not observed for the N, although for the OW, it occurred ～52 months and for the OB at ～24 months. BMI Z differences between N and OB were significant from birth, but were greatest between 6–12 and 36–52 months. Additional adjustment by birth weight, pre‐pregnancy BMI, and prenatal variables decreased the BMI Z differences for the first 24 months with virtually no effect after this age. Accelerated growth in OB children from post‐transition countries occurs immediately after birth, much earlier than the AR. The influence of prenatal factors on adiposity acquisition may extend at most until 2 years of life, although BMI gains thereafter are more related to postnatal variables.     

Social influences are associated with BMI and weight loss intentions in young adults

Christakis and colleagues have shown that health behaviors cluster in social networks and suggest social norms may account for the clustering. This study examined: (i) whether obesity clusters among young adults and whether social norms do in fact account for the clustering, and (ii) among overweight/obese (OW/OB) young adults, whether number of social contacts trying to lose weight is associated with weight loss intentions and whether social norms for weight loss account for this effect. Normal weight (NW) and OW/OB young adults (N = 288; 66% female; 75% white) completed measures assessing number of OW social contacts and social norms for obesity. OW/OB young adults also indicated number of OW social contacts currently trying to lose weight, social norms for weight loss, and weight loss intentions. Compared to NW, OW/OB young adults were more likely to have OW romantic partners and best friends and had more OW casual friends and family members (Ps < 0.05), but social norms for obesity did not differ between groups, and social norms did not mediate the relationship between OW social contacts and participants' weight status. However, among OW/OB young adults, having more social contacts trying to lose weight was associated with greater intention to lose weight (r = 0.20, P = 0.02) and social norms for weight loss fully mediated this effect (P < 0.01). This study is the first to show that social contacts and normative beliefs influence weight status and intentions for weight control in young adults. Findings underscore the importance of targeting social influence in the treatment and prevention of obesity in this high-risk age group.     

Body mass index, prevalence of overweight and obesity in Lithuanian children and adolescents, 1985-2002

The study provides the body mass index (BMI), the prevalence of overweight (OW) and obesity (OB) in Lithuanian children and adolescents, 1985-2002. In the 2000-2002 more than 9000 schoolchildren of 7-18 years old were investigated in the 5 biggest towns and surrounding settlements of Lithuania. These data were compared with the 1985 data. The prevalence of OW and OB was estimated using the International Obesity Task Force (IOTF) cut-off points. The prevalence of OW in Lithuanian children and adolescents was higher among younger schoolchildren in comparison with older adolescents. OW was lower among the older girls in comparison with the older boys: 4.60%-11.50%/4.80%0-13.62% in the 7-13 years girls/boys, versus 1.50%-6.60%/3.90%-9.50% in the 14-18 years old girls/boys. The prevalence of OW among younger Lithuanian adolescents did not change significantly in the last 15 years, but it slightly decreased in older boys and demonstrably diminished in older adolescent girls. In generally, the prevalence of OW among Lithuanian adolescents is low in comparison with the prevalence of OW in children from the other countries.     

Expression of the Bitter Taste Receptor,T2R38, in Enteroendocrine Cells of the Colonic Mucosa of Overweight/Obese vs. Lean Subjects

Bitter taste receptors (T2Rs) are expressed in the mammalian gastrointestinal mucosa. In the mouse colon, T2R138 is localized to enteroendocrine cells and is upregulated by long-term high fat diet that induces obesity. The aims of this study were to test whether T2R38 expression is altered in overweight/obese (OW/OB) compared to normal weight (NW) subjects and characterize the cell types expressing T2R38, the human counterpart of mouse T2R138, in human colon. Colonic mucosal biopsies were obtained during colonoscopy from 35 healthy subjects (20 OW/OB and 15 NW) and processed for quantitative RT-PCR and immunohistochemistry using antibodies to T2R38, chromogranin A (CgA), glucagon like peptide-1 (GLP-1), cholecystokinin (CCK), or peptide YY (PYY). T2R38 mRNA levels in the colonic mucosa of OW/OB were increased (> 2 fold) compared to NW subjects but did not reach statistical significance (P = 0.06). However, the number of T2R38 immunoreactive (IR) cells was significantly increased in OW/OB vs. NW subjects (P = 0.01) and was significantly correlated with BMI values (r = 0.7557; P = 0.001). In both OW/OB and NW individuals, all T2R38-IR cells contained CgA-IR supporting they are enteroendocrine. In both groups, T2R38-IR colocalized with CCK-, GLP1- or PYY-IR. The overall CgA-IR cell population was comparable in OW/OB and NW individuals. This study shows that T2R38 is expressed in distinct populations of enteroendocrine cells in the human colonic mucosa and supports T2R38 upregulation in OW/OB subjects. T2R38 might mediate host functional responses to increased energy balance and intraluminal changes occurring in obesity, which could involve peptide release from enteroendocrine cells.     

Trends in body mass index, prevalence of overweight and obesity in preschool Lithuanian children, 1986-2006

The study provides the body mass index (BMI), the prevalence of overweight and obesity in preschool Lithuanian children, 1986-2006. In the 2003-2006 more than 1000 preschool 3-6 year old children from Vilnius (the capital of Lithuania) were investigated according to the standard anthropometric methods. The prevalence of overweight (OW) and obesity (OB) was estimated according to the cut-off points recommended by the International Obesity Task Force (IOTF). Recent data were compared with the data of preschool children from the 1986 Vilnius study and with the data from the other countries. The BMI of preschool children did not change significantly during the last 20 years, except for the statistically significant BMI increment in 6 years old girls. The prevalence of OB among preschool Lithuanian children was low (0.8%-3.7% in boys, and 0-1.9% in girls) and did not change significantly during 1986-2006. The prevalence of OW was higher in preschool girls (10.7%-18.2%) in comparison with preschool boys (6.5%-12.4%). The significant increment of the prevalence of OW was observed among the 6-year-old girls from the 2006 study in comparison with the 1986 study. The possible socio-economic reasons of the defined trend in the BMI and prevalence of OW and OB among preschool Lithuanian children are discussed in the paper.     

Interactive Effects of Early Exclusive Breastfeeding and Pre-Pregnancy Maternal Weight Status on Young Children’s BMI – A Chinese Birth Cohort

Objectives

To assess if the maternal pre-pregnancy weight status (MPWS) alters the association of early infant feeding pattern (at one and third months) with infant body mass index (BMI) in the first two years of life.

Methods

A cohort of 2,220 neonates were recruited in a community-based study conducted in China. Body weight and length were measured at birth, at age one and two, with BMI calculated accordingly. The BMI z-scores (BMI-Z) were computed according to the World Health Organization Growth Standard (2006). Feeding patterns were classified as exclusive breastfeeding (EBF), mixed feeding (MF), and formula feeding (FF). General linear models (GLM) were employed to estimate main and interaction effects of EBF and MPWS on children’s BMI-Z.

Results

No main effect of MPWS was found on child BMI-Z at ages one and two, nor the feeding patterns. An interaction between MPWS and feeding patterns was detected (p<0.05). For children who were formula fed during the first month, those who were born to overweight/obesity (OW/OB) mothers had a significantly greater BMI-Z at ages one and two, compared with those with underweight/normal weight (UW/NW) mothers. FF children had greater BMI-Z at ages one and two compared with their EBF and MF counterparts, when they were born to OW/OB mothers.

Conclusions

Maternal pre-pregnancy weight control and early initiation of EBF for children are essential for healthy development in children’s BMI, hence the prevention of early life obesity.     

Cardiovascular risk in 26,008 European overweight children as established by a multicenter database

Objective: Although the obesity epidemic is progressing in European children too, there is no consensus on the population‐specific prevalence of comorbidities or efficient diagnostic strategies. Therefore, weight‐related risk factors, their interrelationship, and association with biological parameters were assessed in a large group of overweight (OW) children, documented by an electronic database. Methods and Procedures: Data of 26,008 children (age 12.6 ± 2.9 years, 56% females) presented for OW (BMI > 90th percentile) or obesity (>97th percentile) in 98 specialized centers were evaluated using a simple software (Adipositas Patienten Verlaufsbeobachtung (APV)) for standardized longitudinal documentation. After local anonymization, data were transmitted for central analysis including multiple logistic regression. Results: A total of 5.9% of the children were normal weight, 41% obese (OB), and 37% extremely OB (>99.5th percentile, XXL; 41% of the girls). In 50%, at least one risk factor and in 11% a cluster of two were found, comprising increased blood pressure (BP): 35.4%, dyslipidemia: 32% (total cholesterol: 14.1%, low‐density lipoprotein (LDL)‐cholesterol: 15.8%, high‐density lipoprotein (HDL)‐cholesterol: 11.1%, triglycerides: 14.3%), impaired glucose tolerance (IGtT): 6.5% and suspicion of diabetes: 0.7%. The degree of OW was inversely associated with HDL‐cholesterol and directly with clustered risk factors, impaired glucose metabolism, increased BP and triglycerides (odds ratios (ORs) XXL vs. normal = 6.15, >10, 4.3, 3.0 and 2.5, respectively), but not with LDL‐cholesterol. Discussion: In a very large cohort of young Europeans risk factors for cardiovascular (CV) diseases are frequently found, related to the degree of OW and tend to cluster, thus a comprehensive screening is justified in all OW or OB children. Electronic patient documentation is feasible in a large obesity care network.     

Weight loss and improved gross motor coordination in children as a result of multidisciplinary residential obesity treatment

This study evaluated the short‐term effectiveness of a multidisciplinary residential obesity treatment program by describing changes in body weight, related measures, and gross motor co‐ordination. Secondarily, it was examined to what extent the amount of relative weight loss achieved by overweight and obese (OW/OB) participants explained the projected improvement in gross motor co‐ordination. Thirty‐six OW/OB children (aged 10.5 ± 1.4 years, 12 girls and 24 boys) were recruited at the Zeepreventorium VZW (De Haan, Belgium), where they followed a specific program consisting of moderate dietary restriction, psychological support, and physical activity. For reference purposes, an additional group of 36 age‐ and gender‐matched healthy‐weight (HW) children was included in the study. Anthropometric measures were recorded and gross motor co‐ordination was assessed using the Körperkoordinationstest für Kinder (KTK) on two occasions with an interval of 4 months. Regardless of the test moment, OW/OB participants displayed significantly poorer KTK performances (P < 0.001). However, treatment was found to be efficacious in decreasing body weight (Δ 17.9 ± 3.1%, P < 0.001) and generating a significant progress in gross motor co‐ordination performance, with a greater increase in KTK score(s) from baseline to re‐test as compared to HW peers (P < 0.01). Within the OW/OB group, the amount of relative weight loss explained 26.9% of the variance in improvement in overall KTK performance. Therefore, multidisciplinary residential treatment and concomitant weight loss can be considered an important means to upgrade OW/OB children's level of gross motor co‐ordination, which in turn may promote physical activity participation.     

Genetic variant of AMD1 is associated with obesity in urban Indian children

Background

Hyperhomocysteinemia is regarded as a risk factor for cardiovascular diseases, diabetes and obesity. Manifestation of these chronic metabolic disorders starts in early life marked by increase in body mass index (BMI). We hypothesized that perturbations in homocysteine metabolism in early life could be a link between childhood obesity and adult metabolic disorders. Thus here we investigated association of common variants from homocysteine metabolism pathway genes with obesity in 3,168 urban Indian children.

Methodology/Principal Findings

We genotyped 90 common variants from 18 genes in 1,325 children comprising of 862 normal-weight (NW) and 463 over-weight/obese (OW/OB) children in stage 1. The top signal obtained was replicated in an independent sample set of 1843 children (1,399 NW and 444 OW/OB) in stage 2. Stage 1 association analysis revealed association between seven variants and childhood obesity at P<0.05, but association of only rs2796749 in AMD1 [OR = 1.41, P = 1.5×10^-4] remained significant after multiple testing correction. Association of rs2796749 with childhood obesity was validated in stage 2 [OR = 1.28, P = 4.2×10^-3] and meta-analysis [OR = 1.35, P = 1.9×10^-6]. AMD1 variant rs2796749 was also associated with quantitative measures of adiposity and plasma leptin levels that was also replicated and corroborated in combined analysis.

Conclusions/Significance

Our study provides first evidence for the association of AMD1 variant with obesity and plasma leptin levels in children. Further studies to confirm this association, its functional significance and mechanism of action need to be undertaken.     

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.     

Circulating oxidized LDL and inflammation in extreme pediatric obesity

Oxidative stress and inflammation have not been well-characterized in extreme pediatric obesity. We compared levels of circulating oxidized low-density lipoprotein (oxLDL), C-reactive protein (CRP), and interleukin-6 (IL-6) in extremely obese (EO) children to normal weight (NW) and overweight/obese (OW/OB) children. OxLDL, CRP, IL-6, BMI, blood pressure, and fasting glucose, insulin, and lipids were obtained in 225 children and adolescents (age 13.5 ± 2.5 years; boys 55%). Participants were classified into three groups based on gender- and age-specific BMI percentile: NW (<85th, n = 127), OW/OB (85th- <1.2 times the 95th percentile, n = 64) and EO (≥1.2 times the 95th percentile or BMI ≥35 kg/m(2), n = 34). Measures were compared across groups using analysis of covariance, adjusted for gender, age, and race. Blood pressure, insulin, and lipids worsened across BMI groups (all P < 0.0001). OxLDL (NW: 40.8 ± 9.0 U/l, OW/OB: 45.7 ± 12.1 U/l, EO: 63.5 ± 13.8 U/l) and CRP (NW: 0.5 ± 1.0 mg/l, OW/OB: 1.4 ± 2.9 mg/l, EO: 5.6 ± 4.9 mg/l) increased significantly across BMI groups (all groups differed with P < 0.01). IL-6 was significantly higher in EO (2.0 ± 0.9 pg/ml) compared to OW/OB (1.3 ± 1.2 pg/ml, P < 0.001) and NW (1.1 ± 1.0 pg/ml, P < 0.0001) but was not different between NW and OW/OB. Extreme pediatric obesity, compared to milder forms of adiposity and NW, is associated with higher levels of oxidative stress and inflammation, suggesting that markers of early cardiovascular disease and type 2 diabetes mellitus are already present in this young population.     

Thyroid hormone dysregulation in intrauterine growth retardation associated with maternal malnutrition and/or anemia.

Data on the effect of maternal malnutrition and/or anemia on thyroid hormone regulation in human fetuses are scarce, and would be of great importance in examining the relevance of Barker's hypothesis, which proposes adaptation of fetuses to undernutrition leading to permanent metabolic and endocrine changes that form the basis of adult diseases. To examine the quantitative variations in thyroid hormone profile of neonates born to malnourished and/or anemic mothers, we quantitated the T3, T4, rT3 and TSH levels in cord blood of neonates and maternal blood of their corresponding mothers that are malnourished and/or anemic. Further, we classified neonates born to each of these groups of mothers into Small for Gestational Age (SGA) or Appropriate for Gestational Age (AGA) based on the intrauterine growth curve for our population, and examined the thyroid hormone profile in these neonates. Our results show that firstly, the effects of malnutrition or anemia on thyroid hormone profile are distinct, secondly, significantly higher levels of cord blood T4 and correspondingly lower levels of T3 and rT3 are observed in the neonates born to anemic and malnourished mothers and thirdly, decreases in cord blood T3 levels were observed in Small for Gestational Age neonates born to anemic mothers. These observations lead us to speculate that alterations in the pituitary-thyroid function result in beneficial adaptations to the hostile intrauterine environment in malnutrition related growth retardation and anemia.     

Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition

The discovery of a link between in utero experience and later metabolic and cardiovascular disease is one of the most important advances in epidemiology research of recent years. There is now increasing evidence that alterations in the fetal environment have long-term consequences on metabolic and endocrine pathophysiology in adult life. This process has been termed "fetal programming," and we have shown that undernutrition of the mother during gestation leads to obesity, hypertension, hyperphagia, hyperinsulinemia, and hyperleptinemia in offspring. Using this model of maternal undernutrition throughout pregnancy, we investigated whether prenatal influences may lead to alterations in postnatal locomotor behavior, independent of postnatal nutrition. Virgin Wistar rats were time mated and randomly assigned to receive food either ad libitum (ad libitum group) or at 30% of ad libitum intake (undernourished group). Offspring from UN mothers were significantly smaller at birth than AD offspring. At weaning, offspring were assigned to one of two diets [control or hypercaloric (30% fat)]. At ages of 35 days, 145 days, and 420 days, voluntary locomotor activity was assessed. At all ages studied, offspring from undernourished mothers were significantly less active than offspring born of normal birth weight for all parameters measured, independent of postnatal nutrition. Sedentary behavior in programmed offspring was exacerbated by postnatal hypercaloric nutrition. This work is the first to clearly separate prenatal from postnatal effects and shows that lifestyle choices themselves may have a prenatal origin. We have shown that predispositions to obesity, altered eating behavior, and sedentary activity are linked and occur independently of postnatal hypercaloric nutrition. Moreover, the prenatal influence may be permanent as offspring of undernourished mothers were still significantly less active compared with normal offspring at an advanced adult age, even in the presence of a healthy diet throughout postnatal life.     

Different levels of overnutrition and weight gain during pregnancy have differential effects on fetal growth and organ development

Background

Nearly 50% of U.S. women of child-bearing age are overweight or obese, conditions linked to offspring obesity and diabetes.

Methods

Utilizing the sheep, females were fed a highly palatable diet at two levels of overfeeding designed to induce different levels of maternal body weight increase and adiposity at conception, and from conception to midgestation. Fetal growth and organ development were then evaluated at midgestation in response to these two different levels of overfeeding. Ewes were fed to achieve: 1) normal weight gain (control, C), 2) overweight (125% of National Research Council [NRC] recommendations, OW125) or 3) obesity (150% of NRC recommendations, OB150) beginning 10 wks prior to breeding and through midgestation. Body fat % and insulin sensitivity were assessed at three points during the study: 1) diet initiation, 2) conception and 3) mid-gestation. Ewes were necropsied and fetuses recovered at mid-gestation (day 78).

Results

OB150 ewes had a higher % body fat than OW125 ewes prior to breeding (P = 0.03), but not at mid-gestation (P = 0.37). Insulin sensitivity decreased from diet initiation to mid-gestation (P = 0.04), and acute insulin response to glucose tended to be greater in OB150 ewes than C ewes (P = 0.09) and was greater than in OW125 ewes (P = 0.02). Fetal crown-rump length, thoracic and abdominal girths, and fetal perirenal fat were increased in the OW125 and OB150 versus C ewes at mid-gestation. However, only fetal heart, pancreas, and liver weights, as well as lipid content of fetal liver, were increased (P < 0.05) in OB150 ewes versus both C and OW125 ewes at midgestation.

Conclusions

These data demonstrate that different levels of overfeeding, resulting in differing levels of maternal weight gain and adiposity prior to and during pregnancy, lead to differential effects on fetal overgrowth and organ development.     

The Obesity Epidemic: Metabolic Imprinting on Genetically Susceptible Neural Circuits

The apparent obesity epidemic in the industrialized world is not explained completely by increased food intake or decreased energy expenditure. Once obesity develops in genetically predisposed individuals, their obese body weight is avidly defended against chronic caloric restriction. In animals genetically predisposed toward obesity, there are multiple abnormalities of neural function that prime them to become obese when dietary caloric density and quantity are raised. Once obesity is fully developed, these abnormalities largely disappear. This suggests that obesity might be the normal state for such individuals. Formation of new neural circuits involved in energy homeostasis might underlie the near permanence of the obese body weight. Such neural plasticity can occur during both nervous system development and in adult life. Maternal diabetes, obesity, and undernutrition have all been associated with obesity in the offspring of such mothers, especially in genetically predisposed individuals. Altered brain neural circuitry and function often accompanies such obesity. This enhanced obesity may then be passed on to subsequent generations in a feed‐forward, upward spiral of increasing body weight across generations. Such findings suggest a form of “metabolic imprinting” upon genetically predisposed neural circuits involved in energy homeostasis. Centrally acting drugs used for obesity treatment lower the defended body weight and alter the function of neural pathways involved in energy homeostasis. But they generally have no permanent effect on body weight or neural function. Thus, early identification of obesity‐prone mothers, infants, and adults and treatment of early obesity may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals.     

Evidence of a Double Burden of Malnutrition in Urban Poor Settings in Nairobi,Kenya

Background

Many low- and middle-income countries are undergoing a nutrition transition associated with rapid social and economic transitions. We explore the coexistence of over and under- nutrition at the neighborhood and household level, in an urban poor setting in Nairobi, Kenya.

Methods

Data were collected in 2010 on a cohort of children aged under five years born between 2006 and 2010. Anthropometric measurements of the children and their mothers were taken. Additionally, dietary intake, physical activity, and anthropometric measurements were collected from a stratified random sample of adults aged 18 years and older through a separate cross-sectional study conducted between 2008 and 2009 in the same setting. Proportions of stunting, underweight, wasting and overweight/obesity were dettermined in children, while proportions of underweight and overweight/obesity were determined in adults.

Results

Of the 3335 children included in the analyses with a total of 6750 visits, 46% (51% boys, 40% girls) were stunted, 11% (13% boys, 9% girls) were underweight, 2.5% (3% boys, 2% girls) were wasted, while 9% of boys and girls were overweight/obese respectively. Among their mothers, 7.5% were underweight while 32% were overweight/obese. A large proportion (43% and 37%%) of overweight and obese mothers respectively had stunted children. Among the 5190 adults included in the analyses, 9% (6% female, 11% male) were underweight, and 22% (35% female, 13% male) were overweight/obese.

Conclusion

The findings confirm an existing double burden of malnutrition in this setting, characterized by a high prevalence of undernutrition particularly stunting early in life, with high levels of overweight/obesity in adulthood, particularly among women. In the context of a rapid increase in urban population, particularly in urban poor settings, this calls for urgent action. Multisectoral action may work best given the complex nature of prevailing circumstances in urban poor settings. Further research is needed to understand the pathways to this coexistence, and to test feasibility and effectiveness of context-specific interventions to curb associated health risks.     

Maternal perinatal undernutrition impairs chromaffin cells proliferation in the postnatal rat.

Numerous data show that malnutrition during early life programs chronic diseases in adulthood. Many of these disorders may result from alterations in the development of neuroendocrine systems, such as the hypothalamo-pituitary-adrenal axis and the sympathoadrenal system. We have previously reported that maternal 50% food restriction during late pregnancy and lactation reduces adrenal weight and impairs chromaffin cell differentiation in male rats at weaning. In addition, maternal undernutrition modifies the expression of several genes involved in proliferation and apoptosis. This study therefore investigated the impact of maternal food restriction on adrenal cell growth in the late postnatal rat. Histological analysis showed that the number of proliferating chromaffin cells assessed by nuclear labelling with BrdU was reduced by 45%, whereas the level of apoptosis visualised by caspase-3 immunoreactivity was increased by 340% in adrenal medulla of offspring from undernourished mothers. In contrast, maternal food restriction did not affect proliferation and apoptosis in cortical cells of rats. These developmental changes were associated with overexpression of TGFbeta2. These data show that perinatal undernutrition impairs the balance between chromaffin cell proliferation and apoptosis. These modifications may lead to "malprogramming" of adrenal medulla development, which could contribute to the pathogenesis of chronic diseases in adulthood.     

The reduction of Calpain-10 expression is associated with risk polymorphisms in obese children

Excessive weight gain and obesity are major public health concerns. Childhood obesity is growing at an alarming rate. Polymorphisms in the Calpain-10 gene and the reduced expression of this gene in muscle cells and adipocytes have been associated with an increased risk of type 2 diabetes mellitus in several populations. In the present study, we explored the contribution of Calpain-10 in the development of metabolic impairment in childhood. We evaluated the presence of risk polymorphisms in the CAPN10 gene (SNP-44, SNP-43, InDel-19 and SNP-63) and the associated changes in the Calpain-10 mRNA levels in a pediatric population. A total of 161 Mexican children between 4 and 18 years old were included in this study. This population was classified into three groups according to international growth references: healthy weight (HW), overweight (OW) and obese (OB). Association studies of the anthropometric data, clinical values, genotyping and expression assays showed a decrease in the Calpain-10 mRNA and protein expression in the OW and OB groups with respect to the HW group. This decrease in the Calpain-10 mRNA expression was more evident in individuals homozygous for SNP-44 (T/T) and InDel-19 (3/3), alone (p < 0.001 and p = 0.015, respectively) or in combination (p = 0.017). These polymorphisms were also associated with elevated BMI, weight percentiles, z-scores, waist circumferences, fasting glucose levels and beta cell functions in the OW and OB groups (p < 0.05). Moreover, our results indicate a statistically significant decrease in the expression of the 75-kDa Calpain-10 isoform in the OW+OB group. The presence of polymorphisms and alterations in the expression of the CAPN10 gene at early ages might result in metabolic impairment in adulthood and should be further investigated.     

Decreased energy levels can cause and sustain obesity

Obesity has reached epidemic proportions and has become one of the major health problems in developed countries. Current theories consider obesity a result of overeating and sedentary life style and most efforts to treat or prevent weight gain concentrate on exercise and food intake. This approach does not improve the situation as may be seen from the steep increase in the prevalence of obesity. This encouraged us to reanalyse existing information and look for biochemical basis of obesity. Our approach was to ignore current theories and concentrate on experimental data which are described in scientific journals and are available from several databases. We developed and applied a Knowledge Discovery in Databases procedure to analyse metabolic data. We began with the contradictory information: in obesity, more calories are consumed than used up, suggesting that obese people should have excess energy. On the other side, obese people experience fatigue and decreased physical endurance that indicates diminished energy supply in the body. The result of our work is a chain of metabolic events leading to obesity. The crucial event is the inhibition of the TCA cycle at the step of aconitase. It disturbs energy metabolism and results in ATP deficiency with simultaneous fat accumulation. Further steps in obesity development are the consequences of diminished energy supply: inhibition of beta-oxidation, leptin resistance, increase in appetite and food intake and a decrease in physical activity. Thus, our theory shows that obesity does not have to be caused by overeating and sedentary life-style but may be the result of the "obese" change in metabolism which is forcing people to overeat and save energy to sustain metabolic functions of cells. This "obese" change is caused by environmental factors that activate chronic low-grade inflammatory process in the body linking obesity with the environment of developed countries.