[Risk of binge eating disorder (BED) in nutrition and dietetics consultations and its relationship with eating pattern]. / Riesgo de trastorno por atracones (TPA) en las consultas de nutrición y dietética y su relación con el patrón alimentario.

Introduction: Introduction: evidence has shown a relationship between obesity and binge eating disorder (BED) as well as differences in dietary pattern. The objective was to establish the risk of BED in nutrition and dietetics consultations (N&D) and its relationship with dietary pattern. Methods: a cross-sectional study in 113 people who attended the N&D clinic to lose weight. They completed the BES questionnaire, a food consumption frequency questionnaire, and anthropometric measurements were taken. A descriptive analysis of the variables was performed, and an attempt was made to establish a relationship between the different explanatory variables and risk of BED. Results: 35.3 % of subjects were at risk for BED. The variables that showed significant differences for risk of BED were sex (p = 0.047), BMI (p < 0.001), previous diagnosis of eating disorder (p = 0.002), cabrohydrate intake higher than recommendations (p < 0.001), and protein intake lower or equal than recommendations (p < 0.001). In the adjusted logistic regression model the variables finally included were BMI, OR = 1.2 (95 % CI, 0.8-1.4, p = 0.02), cabrohydrate intake higher than recommendations, OR = 1.4 (95 % CI, 0.1-2.8, p = 0.02), and protein intake lower or equal than recommendations, OR = 1.2 (95 % CI, 0.4-4.1, p = 0.04). Conclusion: the risk of BED in overweight patients who come to consult for weight loss is high. There is a relationship between this risk and dietary pattern. Other similar studies are required.

Introducción: Introducción: la evidencia ha mostrado relación entre la obesidad y el trastorno por atracones (TPA) y diferencias en el patrón dietético. El objetivo fue establecer el riesgo de TPA en las consultas de nutrición y dietética (NyD) y su relación con el patrón dietético. Métodos: estudio transversal sobre 113 personas que acudieron a consulta de NyD para perder peso. Se seleccionaron aquellas que acudían a su primera consulta. Cumplimentaron el cuestionario Binge Eating Scale (BES), un cuestionario de frecuencia de consumo de alimentos, y se tomaron medidas antropométricas. Se realizó el análisis descriptivo de las variables y se trató de establecer una asociación entre las diferentes variables explicativas con el riesgo de TPA. Resultados: el 35,3 % de los individuos presentaron riesgo de TPA. Las variables que mostraron diferencias significativas para el riesgo de TPA fueron el sexo (p = 0,047), el IMC (p < 0,001), el diagnóstico previo de TCA (p = 0,002), la ingesta de carbohidratos superior a las recomendaciones (p < 0,001) y la ingesta de proteínas igual o inferior a las recomendaciones (p < 0,001). En el modelo de regresión logística ajustado, las variables incluidas finalmente fueron: IMC, OR = 1,2 (IC 95 %: 0,8-1,4; p = 0,02); ingesta de carbohidratos superior a las recomendaciones, OR = 1,4 (IC 95 %: 0,1-2,8; p = 0,02); e ingesta de proteínas igual o inferior a las recomendaciones, OR = 1,2 (IC 95 %: 0,4-4,1; p = 0,04). Conclusión: el riesgo de TPA en los pacientes con sobrepeso que acuden a consulta para pérdida de peso es elevado. Existe relación entre este riesgo y el patrón dietético. Es necesario realizar otros trabajos similares..

Riesgo de trastorno por atracones (TPA) en las consultas de nutrición y dietética y su relación con el patrón alimentario / Risk of binge eating disorder (BED) in Nutrition and dietetics consultations and its relationship with eating pattern

Introducción: la evidencia ha mostrado relación entre la obesidad y el trastorno por atracones (TPA) y diferencias en el patrón dietético. El objetivo fue establecer el riesgo de TPA en las consultas de nutrición y dietética (NyD) y su relación con el patrón dietético. Métodos: estudio transversal sobre 113 personas que acudieron a consulta de NyD para perder peso. Se seleccionaron aquellas que acudían a su primera consulta. Cumplimentaron el cuestionario Binge Eating Scale (BES), un cuestionario de frecuencia de consumo de alimentos, y se tomaron medidas antropométricas. Se realizó el análisis descriptivo de las variables y se trató de establecer una asociación entre las diferentes variables explicativas con el riesgo de TPA. Resultados: el 35,3 % de los individuos presentaron riesgo de TPA. Las variables que mostraron diferencias significativas para el riesgo de TPA fueron el sexo (p = 0,047), el IMC (p < 0,001), el diagnóstico previo de TCA (p = 0,002), la ingesta de carbohidratos superior a las recomendaciones (p < 0,001) y la ingesta de proteínas igual o inferior a las recomendaciones (p < 0,001). En el modelo de regresión logística ajustado, las variables incluidas finalmente fueron: IMC, OR = 1,2 (IC 95 %: 0,8-1,4; p = 0,02); ingesta de carbohidratos superior a las recomendaciones, OR = 1,4 (IC 95 %: 0,1-2,8; p = 0,02); e ingesta de proteínas igual o inferior a las recomendaciones, OR = 1,2 (IC 95 %: 0,4-4,1; p = 0,04). Conclusión: el riesgo de TPA en los pacientes con sobrepeso que acuden a consulta para pérdida de peso es elevado. Existe relación entre este riesgo y el patrón dietético. Es necesario realizar otros trabajos similares. (AU)

Introduction: evidence has shown a relationship between obesity and binge eating disorder (BED) as well as differences in dietary pattern. The objective was to establish the risk of BED in NUTRITION and dietetics consultations (N&D) and its relationship with dietary pattern. Methods: a cross-sectional study in 113 people who attended the N&D clinic to lose weight. They completed the BES questionnaire, a food consumption frequency questionnaire, and anthropometric measurements were taken. A descriptive analysis of the variables was performed, and an attempt was made to establish a relationship between the different explanatory variables and risk of BED. Results: 35.3 % of subjects were at risk for BED. The variables that showed significant differences for risk of BED were sex (p = 0.047), BMI (p < 0.001), previous diagnosis of eating disorder (p = 0.002), cabrohydrate intake higher than recommendations (p < 0.001), and protein intake lower or equal than recommendations (p < 0.001). In the adjusted logistic regression model the variables finally included were BMI, OR = 1.2 (95 % CI, 0.8-1.4, p = 0.02), cabrohydrate intake higher than recommendations, OR = 1.4 (95 % CI, 0.1-2.8, p = 0.02), and protein intake lower or equal than recommendations, OR = 1.2 (95 % CI, 0.4-4.1, p = 0.04). Conclusion: the risk of BED in overweight patients who come to consult for weight loss is high. There is a relationship between this risk and dietary pattern. Other similar studies are required. (AU)

Ethnicity Strongly Influences Body Fat Distribution Determining Serum Adipokine Profile and Metabolic Derangement in Childhood Obesity.

Background: Body fat content and distribution in childhood is influenced by sex and puberty, but interethnic differences in the percentage and distribution of body fat also exist. The abdominal visceral/subcutaneous fat ratio has been the main feature of body fat distribution found to associate with the serum adipokine profile and metabolic derangement in adulthood obesity. This has also been assumed for childhood obesity despite the known singularities of this disease in the pediatric age in comparison to adults. Objective: We aimed to investigate the effect of ethnicity, together with sex and pubertal status, on body fat content and distribution, serum adipokine profile, metabolic impairment and liver steatosis in children and adolescents with obesity. Patients and Methods: One hundred and fifty children with obesity (50% Caucasians/50% Latinos; 50% males/50% females) were studied. Body fat content and distribution were studied by whole body DXA-scan and abdominal magnetic resonance, and their relationships with liver steatosis (as determined by ultrasonography), glycemia, insulinemia, lipid metabolism, uric acid, total and HMW-adiponectin, leptin, leptin-receptor, and sex steroid levels were explored. Results: Latino patients had more severe truncal obesity (higher trunk/lower limb fat ratio, odds ratio 10.00; p < 0.05) and higher prevalence of liver steatosis than Caucasians regardless of sex or pubertal status, but there were no difference in the visceral/subcutaneous abdominal fat ratio, except for pubertal females. A higher trunk/lower limb fat ratio, but not the visceral/subcutaneous abdominal fat ratio, was associated with adipokine profile impairment (higher free leptin index and lower adiponectin levels), insulin resistance and dyslipidemia, and was further enhanced when liver steatosis was present (p < 0.05). A higher abdominal visceral/subcutaneous fat ratio was observed in prepubertal children (p < 0.01), except for Latino females, whereas predominant subcutaneous fat deposition was observed in adolescents. Conclusion: Ethnicity is one of the main determinants of increased trunk body fat accumulation in Latino children with obesity, which is best estimated by the trunk/lower limb fat ratio and related to the development of metabolic derangement and liver steatosis.

Repuesta de los autores: Importancia de los factores socioeconómicos en estudios de obesidad / Authors Reply: The importance of socioeconomic factors in obesity studies

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Sex, puberty, and ethnicity have a strong influence on growth and metabolic comorbidities in children and adolescents with obesity: Report on 1300 patients (the Madrid Cohort).

BACKGROUND: The capacity to correctly assess insulin resistance and its role in further obesity-associated metabolic derangement in children is under debate, and its determinants remain largely unknown. OBJECTIVE: We investigated the association of the insulin secretion profile with other metabolic derangements and anthropometric features in children and adolescents with obesity, exploring the role of ethnicity. PATIENTS AND METHODS: Growth and metabolic features, including fasting insulin levels and insulin secretory profile in an oral glucose tolerance test (OGTT), were analyzed according to ethnicity in 1300 patients with obesity (75.8% Caucasians/19.0% Latinos). RESULTS: Height and bone age were influenced by sex, ethnicity, and insulinemia. Latino patients had higher insulin (P < .001), but similar glycemia both prepubertally and postpubertally, compared with Caucasians. Type 2 diabetes was uncommon (0.1%). Impaired glucose tolerance was associated to higher age, BMI, uric acid, and triglyceride levels (all P < .05), as was fasting hyperinsulinism. Impaired fasting glucose or HbA1c 5.7% to 6.4% showed no association with further metabolic derangement. A delayed insulin peak in the OGTT was associated to more severe metabolic disturbances. CONCLUSIONS: Obesity-associated hyperglycemia is unusual in our environment whereas fasting and late postprandial hyperinsulinemia are highly prevalent, with this being influenced by race and closely related with lipid metabolism impairment.

Influencia de la antropometría neonatal sobre las comorbilidades del paciente obeso / Influence of neonatal anthropometry on the comorbidities of the obese patient

Introducción: Los recién nacidos pequeños para su edad gestacional (PEG) presentan mayor riesgo de sufrir diversas enfermedades, tales como talla baja, obesidad infantil y sus comorbilidades metabólicas. Pacientes y métodos: Estudio de 883 pacientes obesos (47% niñas/53% niños; edad: 10,33 ± 3,32 años, IMC: +3,93 ± 1,42 SDS) con seguimiento prospectivo (5 años) del crecimiento para registro de talla adulta (n = 104). Se compararon al diagnóstico según hubiesen presentado antropometría neonatal adecuada (AEG; n = 810) o PEG (n = 73), las siguientes variables: edad en primera consulta, talla estandarizada (Z-score) respecto a talla diana, edad ósea, predicción de talla adulta, IMC estandarizado (Z-score), glucemia, insulinemia, HOMA, colesterol total, HDL, LDL, triglicéridos, 25-OH-vitamina D, área bajo la curva (AUC) de glucemia/insulinemia en el TTOG, cocientes LDL/HDL y CT/HDL y niveles de IGF-I e IGFBP-3. Resultados: Los pacientes nacidos PEG presentaban (a igualdad de edad, IMC-SDS, distribución étnica y puberal) una afectación más intensa del metabolismo lipídico (triglicéridos e índice triglicéridos/HDL superiores, ambos p<0,05) e hidrocarbonado (mayores niveles de glucemia, AUC de glucosa e insulina, HOMA, HbA1c y menor WBISI, todos p < 0,05), así como menores niveles circulantes de vitamina D (p < 0,05). Asimismo, presentaban un peor pronóstico de talla adulta con respecto a su talla diana (p < 0,01), pese a mostrar un grado similar de aceleración de la maduración esquelética y niveles comparables de IGF-I e IGFBP-3 que los AEG. Conclusiones: El antecedente de antropometría neonatal PEG se asocia a una mayor frecuencia e intensidad de alteraciones metabólicas y a un peor pronóstico de talla adulta en los niños y adolescentes obesos

Introduction: Small for gestational age (SGA) newborns show an increased risk of several diseases such as short stature, childhood obesity, and metabolic comorbidities. Patients and methods: The study included 883 obese patients (47% females/53% males; mean age: 10.33 ± 3.32 years, BMI: + 3.93 ± 1.42 SD), with prospective follow-up (5 years) of growth, recording adult height when achieved (n=104). Comparisons at diagnosis, according to their neonatal anthropometry; adequate for gestational age (AGA; n=810) vs. SGA (n=73), were performed for the following features: age at their first visit, standardised height for target height (Z-score), bone age, adult height prediction, BMI (Z-score), glycaemia, insulinaemia, HOMA, total cholesterol, HDL, LDL, triglycerides, 25-OH-vitamin D, area under the curve (AUC) for glucose and insulin in the OGTT, LDL/HDL and triglyceride/HDL ratio, insulin-like growth factor (IGF-I) and IGF-binding protein 3 (IGFBP-3) serum levels. Results: Despite similar BMI-SDS, ethnic, and pubertal distribution in both groups, patients with SGA showed more severe changes in lipid profile (triglyceride and triglyceride/HDL ratio, both P<.05) and carbohydrate metabolism (higher glycaemia, glucose and insulin AUCs, HOMA, HbA1c and lower whole-body insulin sensitivity index (WBISI), all P<.05) and lower 25-OH vitamin D levels (P<.05). They also showed a poorer adult height prediction (adjusted for target height) (P<.01), despite a similar degree of advance in skeletal maturation and similar IGF-I and IGFBP-3 levels than AGA patients. Conclusions: The background of SGA neonatal anthropometry is associated with a higher prevalence and severity of metabolic comorbidities and to a poorer adult height prediction in obese children and adolescents

La obesidad parental se asocia con la gravedad de la obesidad infantil y de sus comorbilidades / Parental obesity is associated with the severity of childhood obesity and its comorbidities

Introducción: La influencia de la obesidad parental sobre la de los hijos y sus comorbilidades, aunque asumida, está insuficientemente caracterizada. Pacientes y métodos: Estudio retrospectivo de 800 pacientes obesos (45,2% niñas; edad: 10,35 ± 3,40 años, índice de masa corporal [IMC]: + 4,22 ± 1,68 standard deviation score[SDS]). Se realizaron comparaciones entre grupos según la presencia de obesidad en ningún (n = 347) o algún progenitor (n = 453), diferenciando entre presencia de obesidad en el padre (n = 185), la madre (n = 151) o ambos progenitores (n=117). Variables consideradas: edad al inicio de la obesidad y en primera consulta, peso neonatal (PRN), IMC-SDS, glucemia, insulinemia, índice homeostatic model assessment (HOMA), colesterol total (CT), HDL, LDL, triglicéridos, 25-OH-vitamina D, área bajo la curva (AUC) de insulinemia en el test de tolerancia oral a la glucosa (TTOG), whole body insulin sensitivity index (WBISI), cocientes LDL/HDL y CT/HDL y reducción ponderal en los 12 primeros meses de seguimiento. Resultados: No hubo diferencias la distribución por sexo, etnia y pubertad entre grupos. Aquellos pacientes con algún progenitor obeso presentaron mayor PRN-SDS e IMC-SDS (p < 0,01), mayor afectación del metabolismo hidrocarbonado (insulinemia, AUC-insulina, HOMA, HbA1c [p < 0,01] y menor WBISI [p < 0,05]) que aquellos sin ningún progenitor obeso. Entre aquellos con un único progenitor obeso, se observó mayor PRN-SDS, insulinemia y HOMA y menor 25-OH-vitamina D (p < 0,05) cuando el antecedente era materno. Existía mayor prevalencia de síndrome metabólico cuando ambos progenitores eran obesos (chi2 = 5,96, p < 0,05). De todos ellos, 132 disminuyeron el IMC ≥ 1,5 SDS y/o el peso ≥10%, sin influencia del antecedente de obesidad parental. Conclusiones: La obesidad en algún progenitor determina mayor gravedad de la obesidad y de las alteraciones del metabolismo hidrocarbonado en sus hijos; acentuándose cuando la obesidad es materna o de ambos progenitores, pero sin influir en la posibilidad de éxito terapéutico

Introduction: The influence of parental obesity on their obese offsprings is acknowledged but insufficiently characterised. Patients and methods: Retrospective study of 800 obese patients (45.2% girls; age: 10.35 ± 3.40 years, body mass index [BMI]: + 4.22 ± 1.68 standard deviation score [SDS]). Group comparison according to the presence of obesity in none (n = 347) or any of the parents (n = 453), and then whether the obese parent was the father (n = 185), the mother (n = 151), or both parents (n = 117) were performed. The parameters analysed were: Age at the onset of the obesity and at their first visit, birth weight (BW), BMI-SDS, blood glucose, insulin level, homeostatic model assessment (HOMA) index, total cholesterol (TC), HDL, LDL, triglycerides, 25-OH-vitamin-D, area under the curve (AUC) for insulin in the oral glucose tolerance test (OGTT), whole body insulin sensitivity index (WBISI), LDL/HDL and TC/HDL ratios, and weight loss after 12 month follow-up. Results: No differences were observed between groups as regarding gender, ethnic background, or pubertal stage. Patients with one obese parent showed higher BW-SDS and BMI-SDS (P < .01), more severe impairment of carbohydrate metabolism (blood insulin, insulin-AUC, HOMA, HbA1c [P < .01] and lower WBISI [P < .05]) than those with no obese parent. Among those patients with a single obese parent, higher BW-SDS, insulin, HOMA, and lower 25-OH-vitamin D (P < .05) was observed when obesity was present in the mother. There was a higher prevalence of metabolic syndrome when both parents were obese (chi2 = 5.96, P < .05). A total of 132 patients reduced their BMI by ≥ 1.5 SDS, or their weight by ≥ 10%, with no influence of the background of parental obesity. Conclusions: Obesity in any parent determines a higher severity of their offspring obesity and metabolic comorbidities, more importantly when obesity is present in the mother or in both parents, but without interference in the options of therapeutic success

[Influence of neonatal anthropometry on the comorbidities of the obese patient]. / Influencia de la antropometría neonatal sobre las comorbilidades del paciente obeso.

INTRODUCTION: Small for gestational age (SGA) newborns show an increased risk of several diseases such as short stature, childhood obesity, and metabolic comorbidities. PATIENTS AND METHODS: The study included 883 obese patients (47% females/53% males; mean age: 10.33±3.32 years, BMI:+3.93±1.42 SD), with prospective follow-up (5 years) of growth, recording adult height when achieved (n=104). Comparisons at diagnosis, according to their neonatal anthropometry; adequate for gestational age (AGA; n=810) vs. SGA (n=73), were performed for the following features: age at their first visit, standardised height for target height (Z-score), bone age, adult height prediction, BMI (Z-score), glycaemia, insulinaemia, HOMA, total cholesterol, HDL, LDL, triglycerides, 25-OH-vitamin D, area under the curve (AUC) for glucose and insulin in the OGTT, LDL/HDL and triglyceride/HDL ratio, insulin-like growth factor (IGF-I) and IGF-binding protein 3 (IGFBP-3) serum levels. RESULTS: Despite similar BMI-SDS, ethnic, and pubertal distribution in both groups, patients with SGA showed more severe changes in lipid profile (triglyceride and triglyceride/HDL ratio, both P<.05) and carbohydrate metabolism (higher glycaemia, glucose and insulin AUCs, HOMA, HbA1c and lower whole-body insulin sensitivity index (WBISI), all P<.05) and lower 25-OH vitamin D levels (P<.05). They also showed a poorer adult height prediction (adjusted for target height) (P<.01), despite a similar degree of advance in skeletal maturation and similar IGF-I and IGFBP-3 levels than AGA patients. CONCLUSIONS: The background of SGA neonatal anthropometry is associated with a higher prevalence and severity of metabolic comorbidities and to a poorer adult height prediction in obese children and adolescents.

[Parental obesity is associated with the severity of childhood obesity and its comorbidities]. / La obesidad parental se asocia con la gravedad de la obesidad infantil y de sus comorbilidades.

INTRODUCTION: The influence of parental obesity on their obese offsprings is acknowledged but insufficiently characterised. PATIENTS AND METHODS: Retrospective study of 800 obese patients (45.2% girls; age: 10.35±3.40 years, body mass index [BMI]:+4.22±1.68 standard deviation score [SDS]). Group comparison according to the presence of obesity in none (n=347) or any of the parents (n=453), and then whether the obese parent was the father (n=185), the mother (n=151), or both parents (n=117) were performed. The parameters analysed were: Age at the onset of the obesity and at their first visit, birth weight (BW), BMI-SDS, blood glucose, insulin level, homeostatic model assessment (HOMA) index, total cholesterol (TC), HDL, LDL, triglycerides, 25-OH-vitamin-D, area under the curve (AUC) for insulin in the oral glucose tolerance test (OGTT), whole body insulin sensitivity index (WBISI), LDL/HDL and TC/HDL ratios, and weight loss after 12 month follow-up. RESULTS: No differences were observed between groups as regarding gender, ethnic background, or pubertal stage. Patients with one obese parent showed higher BW-SDS and BMI-SDS (P<.01), more severe impairment of carbohydrate metabolism (blood insulin, insulin-AUC, HOMA, HbA1c [P<.01] and lower WBISI [P<.05]) than those with no obese parent. Among those patients with a single obese parent, higher BW-SDS, insulin, HOMA, and lower 25-OH-vitamin D (P<.05) was observed when obesity was present in the mother. There was a higher prevalence of metabolic syndrome when both parents were obese (χ2=5.96, P<.05). A total of 132 patients reduced their BMI by ≥1.5SDS, or their weight by ≥10%, with no influence of the background of parental obesity. CONCLUSIONS: Obesity in any parent determines a higher severity of their offspring obesity and metabolic comorbidities, more importantly when obesity is present in the mother or in both parents, but without interference in the options of therapeutic success.