Low birth weight and small for gestational age are associated with complications of childhood and adolescence obesity: systematic review and meta-analysis

In recent decades, the incidence of type 2 diabetes (T2D) has increased dramatically in children and adolescents, posing a real public health problem. Beyond unhealthy diets and sedentary lifestyles, growing evidence suggests that some perinatal factors, such as low birth weight (LBW), are associated with higher risk of T2D in adulthood. In this regard, it remains unclear whether the increased risk is already present in childhood and adolescence. We conducted a systematic review and meta-analysis to clarify the association of LBW or being small for gestational age (SGA) with insulin resistance in childhood and adolescence. The systematic review resulted in 28 individual studies, and those with the same outcome were included within two random-effects meta-analyses. Compared with children or adolescents born with adequate size for gestational age, those SGA had 2.33-fold higher risk of T2D (95% confidence interval [CI]: 1.05–5.17). Furthermore, LBW and being SGA were associated with 0.20 higher mean homeostasis model assessment of insulin resistance (HOMA-IR) values (95% CI: 0.02–0.38). Given the high prevalence of preterm babies, from a population perspective, these results may be of great importance as they point to the existence of a potentially vulnerable subgroup of children and adolescents that could benefit from screening tests and early preventive strategies

Correlation between serum advanced glycation end products and dietary intake of advanced glycation end products estimated from home cooking and food frequency questionnaires

Abstract Background & aims: To our knowledge the association between dietary advanced glycation end-products (dAGEs) and cardiometabolic disease is limited. Our aim was to examine the association between dAGEs and serum concentration of carboxymethyl-lysine (CML) or soluble receptor advanced glycation end-products (sRAGEs), and to assess the difference on dAGEs and circulating AGEs according to lifestyle and biochemical measures. Methods and results: 52 overweight or obese adults diagnosed with type 2 diabetes were included in this cross-sectional analysis. dAGEs were estimated from a Food Frequency Questionnaire (FFQ) or from a FFQ þ Home Cooking Frequency Questionnaire (HCFQ). Serum concentrations of CML and sRAGEs were measured by ELISA. Correlation tests were used to analyze the association between dAGEs derived from the FFQ or FFQ þ HCFQ and concentrations of CML or sRAGEs. Demographic characteristics, lifestyle factors and biochemical measures were analyzed according to sRAGEs and dAGEs using student t-test and ANCOVA. A significant inverse association was found between serum sRAGEs and dAGEs estimated using the FFQ þ HCFQ (r Z 0.36, p Z 0.010), whereas no association was found for dAGEs derived from the FFQ alone. No association was observed between CML and dAGEs. dAGEs intake estimated from the FFQ þ HCFQ was significantly higher among younger and male participants, and in those with higher BMI, higher Hb1Ac levels, longer time with type 2 diabetes, lower adherence to Mediterranean diet, and higher use of culinary techniques that generate more AGEs (all p values p < 0.05). Conclusions: These results show knowledge on culinary techniques is relevant to derive the association between dAGEs intake and cardiometabolic risk factors

Influence of fat intake and BMI on the association of rs1799983 NOS3 polymorphism with blood pressure levels in an Iberian population

Introduction Hypertension contributes to the burden of heart disease, stroke, kidney failure and premature mortality [1]. In fact, hypertension complications account for 9.4 million deaths worldwide every year [2]. Key risk factors include age, race, endocrine and metabolic disorders, lifestyle behaviors and genetics, among others [1]. In this context, familial and twin studies have estimated the heritable component of Blood Pressure (BP) to be about 30%-60% [3]. Moreover, Genome Wide Association Studies (GWAS) have identified a large number of polymorphisms associated with BP or hypertension, which are located in or near genes involved in the renin-angiotensin-aldosterone system, related to enzymes and receptors of the mineral-and glucocorticoid pathways and associated with proteins implicated in the structure and/or regulation of vascular tone [4].Among them, the Nitric Oxide Synthase (NOS3) gene is regarded as one of the putative candidate gene for BP regulation and hypertension, since it is involved in the production of Nitric Oxide (NO) which has vasodilator effects (i.e. inhibiting vascular smooth muscle contraction) [5]. Indeed, it has been observed in an animal model that the disruption of NOS3 gene led to hypertension, while in humans the inhibition of NOS3 elevated BP [5, 6]. Between NOS3 genetic variants, the rs1799983 is the most recognized polymorphism related not only to BP and hypertension, but also to coronary artery and vascular diseases, myocardial infarction, metabolic syndrome and type 2 diabetes [7]. Unfortunately, the results of studies seeking associations of rs1799983 and BP or hypertension have not always been consistent in different populations, which might be due to gene-environmental risk factors interactions [8]. However, to our knowledge, there are few reports on the modulation of environmental factors such as excess body weight or diet, two risk factors widely associated with increased BP levels and hypertension, on the association between rs1799983 and BP or hypertension [9, 10]. Therefore, the aims of the present research were to examine the potential association between the rs1799983 NOS3 genetic variant and BP levels and hypertension, and to investigate the possible influence of non-genetic risk factors on that association

Parity implications for anthropometrical variables, lifestyle behaviors and dietary habits in pregnant women

Altogether the results presented in this thesis clearly show that dietary and genetic factors could modulate susceptibility to obesity and its metabolic disorders. Notably, individuals with a high genetic predisposition to obesity, defined by a GRS based on 16 obesity and lipid metabolism related polymorphisms, showed higher adiposity measures and obesity risk than those individuals with a low genetic predisposition. Although scientific evidence suggests the heritability component of obesity, in the present study we observed that genetic factors explain a small percentage of BMI variation as has been found by other authors. However, when we include in the regression model phenotypic features such as age, physical activity and energy intake the percentage of BMI explanation increased. These results confirm that obesity should be treated as a multifactorial disease in which a large number of phenotypic and genotypic factors are involved. Furthermore, our research work also contributes to better understand not only the role of genetics on body weight loss but also how the diet could modify the association between a polymorphism and body weight regulation. Specifically, for the first time we reported the interaction between the ADCY3 rs10182181 genetic variant and dietary macronutrient distribution on changes in anthropometric and body composition measurements. In addition, the MTNR1B rs101830963 genetic variant interacted with dietary fat intake in response to a hypocaloric diet in terms of body composition and lipid metabolism traits. On the other hand, the fat/carbohydrate intake modified the association between the PPM1K rs1440581 variant and changes in insulin and insulin resistance traits after a dietary intervention to induced weight loss. Finally, the association between the NOS3 rs1799983 polymorphism and DBP and risk of hypertension was modified by MUFA and PUFA intake, and BMI, respectively. Nutrigenetics emerges as a good option to further investigate the interindividual susceptibility to metabolic disorders and the response to dietary interventions, and therefore provide personalized nutrition based on the genetic make-up for preventing and treating obesity and its related comorbidities

Changes in Anxiety and Depression Traits Induced by Energy Restriction: Predictive Value of the Baseline Status

Current evidence proposes diet quality as a modifiable risk factor for mental or emotional impairments. However, additional studies are required to investigate the effect of dietary patterns and weight loss on improving psychological symptoms. The aim of this investigation was to evaluate the effect of energy-restriction, prescribed to overweight and obese participants, on anxiety and depression symptoms, as well as the potential predictive value of some baseline psychological features on weight loss. Overweight and obese participants (n = 305) were randomly assigned for 16 weeks to two hypocaloric diets with different macronutrient distribution: a moderately high-protein (MHP) diet and a low-fat (LF) diet. Anthropometrical, clinical, psychological, and lifestyle characteristics were assessed at baseline and at the end of the intervention. The nutritional intervention evidenced that weight loss has a beneficial effect on trait anxiety score in women (β = 0.24, p = 0.03), depression score in all population (β = 0.15, p = 0.02), particularly in women (β = 0.22, p = 0.03) and in subjects who followed the LF diet (β = 0.22, p = 0.04). Moreover, weight loss could be predicted by anxiety status at baseline, mainly in women and in those who were prescribed a LF diet. This trial suggests that weight loss triggers an improvement in psychological traits, and that anxiety symptoms could predict those volunteers that benefit most from a balanced calorie-restricted intervention, which will contribute to individualized precision nutrition

Nutrigenetic approaches for personalized management of obesity and metabolic syndrome traits

Altogether the results presented in this thesis clearly show that dietary and genetic factors could modulate susceptibility to obesity and its metabolic disorders. Notably, individuals with a high genetic predisposition to obesity, defined by a GRS based on 16 obesity and lipid metabolism related polymorphisms, showed higher adiposity measures and obesity risk than those individuals with a low genetic predisposition. Although scientific evidence suggests the heritability component of obesity, in the present study we observed that genetic factors explain a small percentage of BMI variation as has been found by other authors. However, when we include in the regression model phenotypic features such as age, physical activity and energy intake the percentage of BMI explanation increased. These results confirm that obesity should be treated as a multifactorial disease in which a large number of phenotypic and genotypic factors are involved. Furthermore, our research work also contributes to better understand not only the role of genetics on body weight loss but also how the diet could modify the association between a polymorphism and body weight regulation. Specifically, for the first time we reported the interaction between the ADCY3 rs10182181 genetic variant and dietary macronutrient distribution on changes in anthropometric and body composition measurements. In addition, the MTNR1B rs101830963 genetic variant interacted with dietary fat intake in response to a hypocaloric diet in terms of body composition and lipid metabolism traits. On the other hand, the fat/carbohydrate intake modified the association between the PPM1K rs1440581 variant and changes in insulin and insulin resistance traits after a dietary intervention to induced weight loss. Finally, the association between the NOS3 rs1799983 polymorphism and DBP and risk of hypertension was modified by MUFA and PUFA intake, and BMI, respectively. Nutrigenetics emerges as a good option to further investigate the interindividual susceptibility to metabolic disorders and the response to dietary interventions, and therefore provide personalized nutrition based on the genetic make-up for preventing and treating obesity and its related comorbidities

Nutrigenetic approaches for personalized management of obesity and metabolic syndrome traits

Altogether the results presented in this thesis clearly show that dietary and genetic factors could modulate susceptibility to obesity and its metabolic disorders. Notably, individuals with a high genetic predisposition to obesity, defined by a GRS based on 16 obesity and lipid metabolism related polymorphisms, showed higher adiposity measures and obesity risk than those individuals with a low genetic predisposition. Although scientific evidence suggests the heritability component of obesity, in the present study we observed that genetic factors explain a small percentage of BMI variation as has been found by other authors. However, when we include in the regression model phenotypic features such as age, physical activity and energy intake the percentage of BMI explanation increased. These results confirm that obesity should be treated as a multifactorial disease in which a large number of phenotypic and genotypic factors are involved. Furthermore, our research work also contributes to better understand not only the role of genetics on body weight loss but also how the diet could modify the association between a polymorphism and body weight regulation. Specifically, for the first time we reported the interaction between the ADCY3 rs10182181 genetic variant and dietary macronutrient distribution on changes in anthropometric and body composition measurements. In addition, the MTNR1B rs101830963 genetic variant interacted with dietary fat intake in response to a hypocaloric diet in terms of body composition and lipid metabolism traits. On the other hand, the fat/carbohydrate intake modified the association between the PPM1K rs1440581 variant and changes in insulin and insulin resistance traits after a dietary intervention to induced weight loss. Finally, the association between the NOS3 rs1799983 polymorphism and DBP and risk of hypertension was modified by MUFA and PUFA intake, and BMI, respectively. Nutrigenetics emerges as a good option to further investigate the interindividual susceptibility to metabolic disorders and the response to dietary interventions, and therefore provide personalized nutrition based on the genetic make-up for preventing and treating obesity and its related comorbidities

Low birth weight and small for gestational age are associated with complications of childhood and adolescence obesity: systematic review and meta-analysis

In recent decades, the incidence of type 2 diabetes (T2D) has increased dramatically in children and adolescents, posing a real public health problem. Beyond unhealthy diets and sedentary lifestyles, growing evidence suggests that some perinatal factors, such as low birth weight (LBW), are associated with higher risk of T2D in adulthood. In this regard, it remains unclear whether the increased risk is already present in childhood and adolescence. We conducted a systematic review and meta-analysis to clarify the association of LBW or being small for gestational age (SGA) with insulin resistance in childhood and adolescence. The systematic review resulted in 28 individual studies, and those with the same outcome were included within two random-effects meta-analyses. Compared with children or adolescents born with adequate size for gestational age, those SGA had 2.33-fold higher risk of T2D (95% confidence interval [CI]: 1.05–5.17). Furthermore, LBW and being SGA were associated with 0.20 higher mean homeostasis model assessment of insulin resistance (HOMA-IR) values (95% CI: 0.02–0.38). Given the high prevalence of preterm babies, from a population perspective, these results may be of great importance as they point to the existence of a potentially vulnerable subgroup of children and adolescents that could benefit from screening tests and early preventive strategies

Parity implications for anthropometrical variables, lifestyle behaviors and dietary habits in pregnant women

Altogether the results presented in this thesis clearly show that dietary and genetic factors could modulate susceptibility to obesity and its metabolic disorders. Notably, individuals with a high genetic predisposition to obesity, defined by a GRS based on 16 obesity and lipid metabolism related polymorphisms, showed higher adiposity measures and obesity risk than those individuals with a low genetic predisposition. Although scientific evidence suggests the heritability component of obesity, in the present study we observed that genetic factors explain a small percentage of BMI variation as has been found by other authors. However, when we include in the regression model phenotypic features such as age, physical activity and energy intake the percentage of BMI explanation increased. These results confirm that obesity should be treated as a multifactorial disease in which a large number of phenotypic and genotypic factors are involved. Furthermore, our research work also contributes to better understand not only the role of genetics on body weight loss but also how the diet could modify the association between a polymorphism and body weight regulation. Specifically, for the first time we reported the interaction between the ADCY3 rs10182181 genetic variant and dietary macronutrient distribution on changes in anthropometric and body composition measurements. In addition, the MTNR1B rs101830963 genetic variant interacted with dietary fat intake in response to a hypocaloric diet in terms of body composition and lipid metabolism traits. On the other hand, the fat/carbohydrate intake modified the association between the PPM1K rs1440581 variant and changes in insulin and insulin resistance traits after a dietary intervention to induced weight loss. Finally, the association between the NOS3 rs1799983 polymorphism and DBP and risk of hypertension was modified by MUFA and PUFA intake, and BMI, respectively. Nutrigenetics emerges as a good option to further investigate the interindividual susceptibility to metabolic disorders and the response to dietary interventions, and therefore provide personalized nutrition based on the genetic make-up for preventing and treating obesity and its related comorbidities

Correlation between serum advanced glycation end products and dietary intake of advanced glycation end products estimated from home cooking and food frequency questionnaires

Abstract Background & aims: To our knowledge the association between dietary advanced glycation end-products (dAGEs) and cardiometabolic disease is limited. Our aim was to examine the association between dAGEs and serum concentration of carboxymethyl-lysine (CML) or soluble receptor advanced glycation end-products (sRAGEs), and to assess the difference on dAGEs and circulating AGEs according to lifestyle and biochemical measures. Methods and results: 52 overweight or obese adults diagnosed with type 2 diabetes were included in this cross-sectional analysis. dAGEs were estimated from a Food Frequency Questionnaire (FFQ) or from a FFQ þ Home Cooking Frequency Questionnaire (HCFQ). Serum concentrations of CML and sRAGEs were measured by ELISA. Correlation tests were used to analyze the association between dAGEs derived from the FFQ or FFQ þ HCFQ and concentrations of CML or sRAGEs. Demographic characteristics, lifestyle factors and biochemical measures were analyzed according to sRAGEs and dAGEs using student t-test and ANCOVA. A significant inverse association was found between serum sRAGEs and dAGEs estimated using the FFQ þ HCFQ (r Z 0.36, p Z 0.010), whereas no association was found for dAGEs derived from the FFQ alone. No association was observed between CML and dAGEs. dAGEs intake estimated from the FFQ þ HCFQ was significantly higher among younger and male participants, and in those with higher BMI, higher Hb1Ac levels, longer time with type 2 diabetes, lower adherence to Mediterranean diet, and higher use of culinary techniques that generate more AGEs (all p values p < 0.05). Conclusions: These results show knowledge on culinary techniques is relevant to derive the association between dAGEs intake and cardiometabolic risk factors