Pre and post-natal risk and determination of factors for child obesity

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Term Occurence Count Dictionary
childhood obesity 10 endocrinologydiseases
cortisol 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
metabolic syndrome 5 endocrinologydiseases
obesity 66 endocrinologydiseases

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cortisol 16097 including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol , increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. Laboratory
Select Disease Character Offset Disease Term Instance
childhood obesity 728 pre-conception weight and weight gain during pregnancy are two of the most important prenatal determinants of childhood obesity . Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity,
childhood obesity 834 childhood obesity. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity , and this effect extends into adulthood. Obesity and the metabolic syndrome in children originate in
childhood obesity 6935 pre-conception weight and weight gain during pregnancy are two of the most important prenatal determinants of childhood obesity . Several factors may influence the association of maternal weight and weight gain during pregnancy with
childhood obesity 7363 practices [[11]]. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity , and this effect extends into adulthood. In turn, childhood obesity increases chances of later life
childhood obesity 7431 associated with foetal macrosomia and childhood obesity, and this effect extends into adulthood. In turn, childhood obesity increases chances of later life obesity, thus type 2 diabetes, and cardiovascular disease in the offspring
childhood obesity 8424 findings suggested that a very low birth weight and a very high birth weight are both associated with childhood obesity . Although the link between very high birth weight and childhood obesity is studied more, the link between
childhood obesity 8496 weight are both associated with childhood obesity. Although the link between very high birth weight and childhood obesity is studied more, the link between low birth weight and obesity may be the result of accelerated growth
childhood obesity 9351 endocrine disrupting chemicals (EDCs) or to other chemicals plays a role in the development of diabetes and childhood obesity . Some scientists have coined the term “obesogens” for chemicals that they believe may promote weight
childhood obesity 11140 them solid foods, since the early introduction of solids (prior to six months) increases the risk for childhood obesity [[20]]. Also, hypercaloric, hyperglucidic, hyperproteic nutrition, poor in fibres during the critical
childhood obesity 11589 early infancy and a high consumption of sweetened drinks in childhood is prospectively associated with childhood obesity risk. The consumption of sugar-sweetened beverages, particularly carbonated soft drinks, may be a key
diabetes mellitus 7729 increased risk of childhood and early adult obesity in the offspring. Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin. Irving L et al. showed that adiponectin supplementation
hyperlipidemia 21218 adult age and might contribute to the appearance of the metabolic syndrome (HTA, insulin resistance, hyperlipidemia , and abdominal obesity). The knowledge on the connection between obesity and intestinal microbiota allowed
metabolic syndrome 909 with foetal macrosomia and childhood obesity, and this effect extends into adulthood. Obesity and the metabolic syndrome in children originate in intrauterine life. The current obesity epidemic is probably the result of our
metabolic syndrome 17723 link between the microbes in the human gut and the development of obesity, cardiovascular disease, and metabolic syndrome s, such as type 2 diabetes, is becoming clearer. The microbiota participatesinthe development and maintenance
metabolic syndrome 18358 endotoxemia is suggested to contribute to low-grade inflammation, a characteristic trait of obesity, and the metabolic syndrome . Finally, the activation of the endocannabinoid system by lipopolysaccharidesand/or high-fat diets is
metabolic syndrome 20928 chronic inflammation, appetite, thermogenesis, or the turnover of macronutrients). Obesity and the metabolic syndrome in children originate in the intrauterine life. The role of maternal nutrition during pregnancy is important
metabolic syndrome 21173 expression in the feotus, which will last until adult age and might contribute to the appearance of the metabolic syndrome (HTA, insulin resistance, hyperlipidemia, and abdominal obesity). The knowledge on the connection between
obesity 99 Title: Journal of Medicine and LifePre and post-natal risk and determination of factors for child obesity LM TrandafirOR Temneanu*Mother and Child Department, “Grigore T. Popa” University of Medicine and
obesity 484 non-genetic factors. The way the available information should be efficiently and strategically used in the obesity and overweight prohylaxisprogrammes for children all over the world is still unclear for most of the
obesity 738 weight and weight gain during pregnancy are two of the most important prenatal determinants of childhood obesity . Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity,
obesity 756 during pregnancy are two of the most important prenatal determinants of childhood obesity. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity, and this effect
obesity 844 obesity. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity , and this effect extends into adulthood. Obesity and the metabolic syndrome in children originate in
obesity 984 adulthood. Obesity and the metabolic syndrome in children originate in intrauterine life. The current obesity epidemic is probably the result of our evolutive inheritance associated with the consumption of highly
obesity 1197 processed food with an increased calorific value. The determination of risk factors involved in child obesity are: genetic predisposition, diet, sedentary behaviors, socioeconomic position, ethnic origin, microbiota,
obesity 1665 patients should be considered for modifiable lifestyle risk factors and screened for the complications of obesity .IntroductionThe epidemic of obesity we are witnessing today is a consequence of the natural biological
obesity 1701 modifiable lifestyle risk factors and screened for the complications of obesity.IntroductionThe epidemic of obesity we are witnessing today is a consequence of the natural biological and technological evolution of humankind.
obesity 2150 an economical energetic metabolism, known as “the thrifty genotype hypothesis” [[1]].The current obesity epidemic is probably the result of our evolutive inheritance associated with the consumption of highly
obesity 2476 have kept their traditional life style with daily physical exercise, in their case, the prevalence of obesity being considerably lower [[2]].Even though the appearance of agriculture 14000 years ago ensured a more
obesity 2941 bio-availability of food and its energetic value. Lately, we have witnessed an increased prevalence of obesity among the developed countries as well as in the developing or less developed countries. However, in
obesity 3083 well as in the developing or less developed countries. However, in the less developed countries, the obesity epidemic is present mostly in urban areas, easily giving access to food, which is highly energetic and
obesity 3280 energetic and affordable [[3]].Obesity in children teeangers represents a significant forecaster of obesity in adulthood and a risk factor for the numerous complications it generates. Thus, 20% of the obese newly
obesity 3546 children will become obese teenagers and 80% of the obese teenagers will become obese adults.Nowadays, obesity is considered a condition presenting a complex, multi-factorial etiology that implies genetic and non-genetic
obesity 3759 non-genetic factors. The way the available information should be efficiently and strategically used in the obesity and overweight prohylaxisprogrammes for children all over the world is still unclear for most of the
obesity 4161 [[4]]. Individual behaviors, environmental factors and genetics all contribute to the complexity of the obesity epidemic (Fig. 1). Fig. 1Multi-factor etiology of obesityThe determination of risk factors involved
obesity 4219 genetics all contribute to the complexity of the obesity epidemic (Fig. 1). Fig. 1Multi-factor etiology of obesity The determination of risk factors involved in child obesity Genetic predispositionIn obesity cases, only
obesity 4278 (Fig. 1). Fig. 1Multi-factor etiology of obesityThe determination of risk factors involved in child obesity Genetic predispositionIn obesity cases, only 20-50% of the variation in the body weight is influenced
obesity 4311 etiology of obesityThe determination of risk factors involved in child obesity Genetic predispositionIn obesity cases, only 20-50% of the variation in the body weight is influenced by the environment factors, while
obesity 4495 environment factors, while 50-80% is explained by genetic changes [[5]]. The most frequent forms of obesity are the polygenic ones. Several genes contribute to weight gain by controlling appetite, energy expenditure,
obesity 4682 appetite, energy expenditure, and metabolism, but can only partially account for the development of obesity . There are currently more than 600 genes, markers and chromosomal regions known to be associated to
obesity 4798 are currently more than 600 genes, markers and chromosomal regions known to be associated to Ob, the obesity gene. The obesity gene was discovered in 1994. This gene codifies a protein that is synthesized by adipocytes
obesity 4816 than 600 genes, markers and chromosomal regions known to be associated to Ob, the obesity gene. The obesity gene was discovered in 1994. This gene codifies a protein that is synthesized by adipocytes and is called
obesity 5223 hypothalamus and it is involved in regulating the energy balance [[6]]. The monogenic determinism of obesity is rarely seen and it is characterised by the deficit of leptin, pro-opiomelanocrotin and leptin receptors
obesity 5455 in the gene encoding leptin (LEP) typically lead to an absence of circulating leptin and to extreme obesity . Otherepigenetic biomarkers of obesity are represented by FGF2, PTEN, CDKN1A and ESR1 implicated in
obesity 5494 typically lead to an absence of circulating leptin and to extreme obesity. Otherepigenetic biomarkers of obesity are represented by FGF2, PTEN, CDKN1A and ESR1 implicated in adipogenesis, SOCS1/SOCS3, in inflammation,
obesity 6335 and may contribute to the appearance of hypertension, insulin resistance, hyperlipemia, and abdominal obesity . The parental conditions and lifestyles, which may involve maternal size/obesity, the use of nutritional
obesity 6416 hyperlipemia, and abdominal obesity. The parental conditions and lifestyles, which may involve maternal size/ obesity , the use of nutritional supplements, alcohol or drug abuse, as well the administration of therapeutical
obesity 6945 weight and weight gain during pregnancy are two of the most important prenatal determinants of childhood obesity . Several factors may influence the association of maternal weight and weight gain during pregnancy with
obesity 7285 levels during pregnancy, fetal growth, birth weight, and infant feeding practices [[11]]. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity, and this effect
obesity 7373 [[11]]. Maternal obesity and gestational weight gain are associated with foetal macrosomia and childhood obesity , and this effect extends into adulthood. In turn, childhood obesity increases chances of later life
obesity 7441 foetal macrosomia and childhood obesity, and this effect extends into adulthood. In turn, childhood obesity increases chances of later life obesity, thus type 2 diabetes, and cardiovascular disease in the offspring
obesity 7481 and this effect extends into adulthood. In turn, childhood obesity increases chances of later life obesity , thus type 2 diabetes, and cardiovascular disease in the offspring [[12]]. The exposure to gestational
obesity 7667 exposure to gestational diabetes is associated with an increased risk of childhood and early adult obesity in the offspring. Mothers with obesity or gestational diabetes mellitus have low circulating levels
obesity 7706 associated with an increased risk of childhood and early adult obesity in the offspring. Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin. Irving L et al. showed
obesity 7905 al. showed that adiponectin supplementation in pregnancy prevents fetal overgrowth caused by maternal obesity . Moreover, the authors demonstrated that adiponectin functions as an endocrine link between maternal
obesity 8147 by regulating the placental function. Therefore, the improvement of adiponectin levels in women with obesity and/or gestational diabetes may serve as an effective intervention strategy in preventing the intrauterine
obesity 8278 diabetes may serve as an effective intervention strategy in preventing the intrauterine transmission of obesity and metabolic disease [[13]].Recent findings suggested that a very low birth weight and a very high
obesity 8434 suggested that a very low birth weight and a very high birth weight are both associated with childhood obesity . Although the link between very high birth weight and childhood obesity is studied more, the link between
obesity 8506 both associated with childhood obesity. Although the link between very high birth weight and childhood obesity is studied more, the link between low birth weight and obesity may be the result of accelerated growth
obesity 8569 very high birth weight and childhood obesity is studied more, the link between low birth weight and obesity may be the result of accelerated growth immediately after birth. Babies who were “deprived of nutrition”
obesity 9069 risk of children being overweight.An early age at BMI rebound is associated with a greater risk of obesity , but this may be a statistical artifact.DietIn addition to fetal “over-nutrition” or “under-nutrition”,
obesity 9361 disrupting chemicals (EDCs) or to other chemicals plays a role in the development of diabetes and childhood obesity . Some scientists have coined the term “obesogens” for chemicals that they believe may promote weight
obesity 9483 scientists have coined the term “obesogens” for chemicals that they believe may promote weight gain and obesity . Such chemicals may promote obesity by increasing the number of fat cells, changing the amount of calories
obesity 9519 “obesogens” for chemicals that they believe may promote weight gain and obesity. Such chemicals may promote obesity by increasing the number of fat cells, changing the amount of calories burned at rest, altering energy
obesity 11150 foods, since the early introduction of solids (prior to six months) increases the risk for childhood obesity [[20]]. Also, hypercaloric, hyperglucidic, hyperproteic nutrition, poor in fibres during the critical
obesity 11325 poor in fibres during the critical periods of childhood are involved in the increase of the risk of obesity . Weight gain usually involves the combination of consuming too many calories and not expending enough
obesity 11599 and a high consumption of sweetened drinks in childhood is prospectively associated with childhood obesity risk. The consumption of sugar-sweetened beverages, particularly carbonated soft drinks, may be a key
obesity 11755 beverages, particularly carbonated soft drinks, may be a key contributor to the epidemic of overweight and obesity , by virtue of these beverages- high-added sugar content, low satiety, and incomplete compensation for
obesity 12135 that the increase in the consumption of sugar-sweetened beverages is associated with overweight and obesity in children. Free sugars include monosaccharides and disaccharides added to foods and beverages by the
obesity 12588 the same amounts of milk and soda [[22]].Researchers have hypothesized that TV watching could promote obesity in several ways: displacing time for physical activity; promoting poor diets; giving more opportunities
obesity 13906 TV watching. However, there is evidence that these other forms of “sit time” can contribute to obesity . There is evidence that spending too much time sitting—at work or at home—increases the risk of
obesity 14266 such as leisure-time Internet and computer use, in order to reduce the prevalence of overweight and obesity . Longitudinal studies are required to further examine the potential causal relationships between the
obesity 15485 sedentary behaviours and other activities in the context of our modern lifestyle in order to prevent obesity at all ages [[30]]. It has also been suggested that physically active young people more readily adopt
obesity 16314 studies and multiple epidemiological studies have linked short-sleep duration and poor-sleep quality to obesity risk [[32]].Children who get less sleep in infancy and early childhood may be at greater risk of being
obesity 16610 countries, generations born prior to 1950’s–1960 did not show socioeconomic differentials in adiposity/ obesity in childhood (as they did as adults). Children from low and middle-income countries tend to be stunted
obesity 16826 underweight but, with sufficient nutrition, gain healthy weight and with overnutrition, are prone to obesity . Some evidence showed that contemporary populations of children present higher rates of obesity in those
obesity 16922 to obesity. Some evidence showed that contemporary populations of children present higher rates of obesity in those from the lowest socioeconomic groups in the high-income countries. Children living in low-income
obesity 17686 Asian-American children.MicrobiotaThe link between the microbes in the human gut and the development of obesity , cardiovascular disease, and metabolic syndromes, such as type 2 diabetes, is becoming clearer. The
obesity 18341 metabolic endotoxemia is suggested to contribute to low-grade inflammation, a characteristic trait of obesity , and the metabolic syndrome. Finally, the activation of the endocannabinoid system by lipopolysaccharidesand/or
obesity 20388 medications affecting the appetite should be considered in the evaluation of the paediatric patient with obesity . However, the vast majority of patients will not have any of these identifiable conditions. Regardless
obesity 20627 patients should be considered for modifiable lifestyle risk factors and screened for the complications of obesity .ConclusionsIt is important to know the epigenetic stimuli playing a part in the changing of the epi-obesogene
obesity 21248 to the appearance of the metabolic syndrome (HTA, insulin resistance, hyperlipidemia, and abdominal obesity ). The knowledge on the connection between obesity and intestinal microbiota allowed the identification
obesity 21298 insulin resistance, hyperlipidemia, and abdominal obesity). The knowledge on the connection between obesity and intestinal microbiota allowed the identification of the biomarkers of predisposition to weight gain
obesity 21581 towards an optimum life style remains the main prophylactic and therapeutic measure in the management of obesity associated with metabolic complications

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