The problem of obesity, especially, experienced by the children, has taken the epidemic scales recently in the UAE. In fact, epidemiological researches established that there is a genetic predisposition to obesity. The genetic factors can influence any processes that regulate the energetic balance and body weight, including food behavior and power expenses. However, it is necessary to differentiate the effects of the genetic factors of obesity from the influence of the environmental factors; it is also necessary to define their interaction in the development and preservation of childhood obesity. The uncontrolled consumption of junk food, the sedentary way of life, the lack of any physical activity and eating habits contribute greatly to the development of childhood obesity in the UAE. Actually, the assessment of the contribution of the genetic and environmental factors to the phenotypical dispersion of child obesity in the UAE testifies to the polygenic model of the determination of obesity.
Keywords: obesity, genetic predisposition, polygenic inheritance, corpulence, metabolic syndrome
In the majority of the economically developed world countries, there is an increasing tendency in the number of patients, who report food behavior disorders, which can cause severe endocrine diseases and permanent psychosocial adaptation. The change in food behavior represents the type of pathological adaptation that composes the cornerstone of the food dependence that leads to addictive behavior. In fact, the addictive people acquire new problems in the form of the alimentary and constitutional obesity from overeating that can represent a conditioning agent of the escape from reality and normalization of an emotional state (Cheung & Mao, 2012, p. 2). The current situation with child obesity in the world causes more health problems than hunger and infectious diseases. Actually, obesity was most common for adults of 30-40 years old a few years ago; however, there is an increasing trend of child and teenager obesity at present time. Moreover, the indicators of obesity double every thirty years (AlBooshi, 2016, p. 198). In fact, the genetic factors combined with the low level of physical activity and the addiction to junk food, which contains a high content of carbohydrates, salt, fat, and processed sugar, cause the growing concern about the health of the world population.
What is important, the UAE is among the countries with high rates of obesity. According to the AlBlooshi et al. (2016), only 25.6% of men and 39.9% of women in the UAE have excess weight; thus, the country occupies the seventh place among the countries with the fattest women (p. 198). The general level of child obesity in the UAE reached an alarming level of 40 % of children, who suffer from the excess weight (Al Junaibi, Abdule, Sabri, Hag-Ali, & Nagelkerke, 2013, p. 68).
Obesity was previously investigated in the UAE by using different methods for BMI interpretation; Centers for Disease Control (CDC), IOTF or World Health Organization (WHO). By using the CDC method in children 6-16 y, the prevalence of overweight and obesity was 17% and 8%, respectively. By using the IOTF method in children 5-17 y, the prevalence of overweight and obesity was 22% and 14%, respectively. By using the WHO method in children 6-18 y, the prevalence of overweight and obesity was 17% and 16%, respectively (AlBooshi, 2016, p. 197).
Actually, there are many factors that contribute to a high level of child obesity in the UAE. Low levels of physical activity and overeating of unhealthy food lead to aggravated obesity. In fact, the predisposition to obesity appears in early childhood. Unfortunately, the government does not control or monitor the consumption of junk foods and soft drinks. However, genetics is among the main factors that lead to obese children. Thus, the given research paper will discuss, whether genetics leads to high child obesity rates in the UAE or there is another combination of factors, which contribute to the development of childhood obesity.
Genetic Causes of Child Obesity in the UAE
In fact, the genetic factors influence the formation of certain parameters of the child body constitution. According to Zhao and Grant (2011), more than 40% of the body features are genetically caused (p.1). What is important, obesity is a multiple-factor disease: more than 250 genes and chromosomal sites are responsible for the development of child obesity (Zhao & Grant, 2011, p. 2). At present, the world researchers have been studying the role of some separate genes in the development of childhood obesity in the UAE. Actually, they focus on the changes in the leptin gene, the predecessor of the convertase hormone, proopiomelanocortin, melanocortin-4 and SIM 1 (Cheung & Mao, 2012, p. 3). What is important, the researches help to understand the molecular mechanisms that regulate the power balance in the human body. However, such an evolution of childhood obesity in the UAE for the last 20 years cannot be explained only by the impact of the genetic factors, as the lifestyle is also an influential factor in such a situation. Most likely, both the increase in the consumption of energetic meals and the insufficient physical activity of children play a crucial role in the increasing trend of child obesity. Moreover, the consumption of energy increases at the expense of food intake outdoors, which is a common way of life in the UAE. Due to the abundance of developed fast-food networks, there is a convenient opportunity to eat fast or to have a snack (Al Junaibi et al., 2013, p. 68). In fact, the technical progress caused a decrease in the daily physical activity of children all over the world and, especially, in the UAE. Thus, the constant use of cars and different automatized equipment limits the physical activity of children and leads to the sedentary life and insufficient social activity (Kumar, Raju, & Gowda, 2010, p. 255). However, genetic factors are responsible for the emergence and development of childhood obesity in the UAE.
Actually, the existence of the genetic predisposition to obesity is undoubtful. The probability of the development of excess body weight in the presence of obese parents equals around 70-80%, while these indicators amount to no more than 30 % of the population in general (Cheung & Mao, 2012, p. 3). However, some scientists state that food addictions are not transferred from parents to their children in the UAE. Some scientists suppose that the genetic component defines the actual health of a child for no more than 5%, and the remaining 95% depends on the influence of the environment (AlBlooshi et al., 2016, p. 197). If the 20th century was mainly characterized by the studies of genetics, the 21st century allowed for the studies in the field of epigenetics that provided the possibilities to “switch” the active genes. The genes responsible for the emergence of a specific disease can be present in the human body, but they can activate only under certain conditions. Therefore, the main task is to create such conditions under which such genes will not become active. However, despite the new researches, there is still a lot of scientific proof that obesity of a close parent can cause child obesity.
Actually, the research of the twins and adopted children showed that genetic factors are the most important determinants of obesity. The contribution of these factors to a bodyweight index, which ranges from the insufficient to the excess weight, is determined by the polygenic inheritance (Zhao & Grant, 2011, p. 2). Besides, very few corpulent people have certain obesity genes. At present, it is unknown, which genetic factors are inherited, but they either regulate the total energy consumption, in general. or the level of the main exchange, in particular. In fact, the decrease or increase in body weight is connected to the change of power efficiency, which is usually defined by the genetic determinants. Taking into account the role of the heredity in child obesity, it becomes clear, why some children are obese and why it is difficult for them to lose weight. However, despite the influence of genetic factors, a great number of obese children were successful in reducing weight. Moreover, it is possible because a bodyweight is significantly influenced by environmental factors, including medical actions. At least, the partial genetic predisposition to obesity is caused by the hyper sensibility to the influence of the external factors that promote the gain of fat (Cheung & Mao, 2012, p. 4). However, polygenic inheritance is among the main contributors to the development of childhood obesity.
In fact, genetic factors play an important role in the etiology of obesity of children. There are two groups of obesity syndromes – the syndromes combined with the development of obesity and monogenic forms of obesity (Puiu, Emandi, & Arghirescu, 2013, p. 276; Loos, Barroso, O’rahilly, & Wareham, 2007, p. 187). According to Zhao and Grant (2011), syndrome obesity includes the Albright osteodystrophy, Prader-Willi syndrome, Down syndrome, Cohen syndrome, etc. (p. 2). Actually, these forms of obesity have wide clinical polymorphism. The features of the syndrome forms of obesity include different age of the obesity debut – from the first months of life up to the period of the late childhood – different degrees of expressiveness – from moderated to morbid – and the existence of the peculiar phenotypical features (Puiu, Emandi, & Arghirescu, 2013, p. 282). As a rule, all the patients have neurologic disorders, the expressed delay of psychomotor development and reduced intelligence. However, the genetic effect on child obesity is observed rather seldom. For example, the Prader-Willi syndrome is characterized by hyperphagia, obesity, diabetes, hypotonia and intellectual backwardness (Puiu, Emandi, & Arghirescu, 2013, p. 277; Zhao & Grant, 2011, p. 3). The Laurence-Moon-Bardet-Biedl syndrome is inherited in a form of a recessive genetic sign that is characterized by hyperphagia, obesity, intellectual backwardness, hypogonadism, pigmentary retinitis and polydactyly (Puiu, Emandi, & Arghirescu, 2013, p. 280). Neither anatomic nor biochemical basis for these types of obesity is found out, although, there is an interest in the hypothalamus or the highest nervous centers. Thus, the observations of the people convincingly demonstrate that the genetic factors can act as the primary determinants, but not the main indicators of obesity. However, genetic factors can influence any processes that regulate the power balance and body weight, including food behavior and power expenses.
In the process of child development, fatty deposits are accumulated unevenly. In fact, fat is intensively accumulated within the first 9 months of life that is followed by the peculiar stabilization of the process; however, the slight increase of fat is usually experienced during 5-7 years and the active accumulation of fat in tissues is enabled during puberty (Puiu, Emandi, & Arghirescu, 2013, p. 275). In this regard, there are three critical periods, when the chance of the development of obesity considerably increases. Actually, they include early age (0 – 3 years), preschool age (5 – 7 years) and teenage age, or the puberty period (from 12-14 to 16-17 years) (Kumar, Raju, & Gowda, 2010, p. 257). However, the majority of the UAE families, who plan to have a child, change the way of life and eating habits and also reconsider the nutritional plan. Thus, they control their food intake and avoid the accumulation of fat, which can negatively affect the newborn child. Despite the precautions and efforts to keep a healthy way of life that influences the genetics of a fetus, there are some risks to transfer the genetic predisposition to obesity to children.
Both early age obesity and obese parents increase the risk of its development in maturity. The randomized research conducted by AlBooshi, et al. (2016) reports the results of the sample analysis among young people (21-29 years) living in the UAE: the risk of the development of obesity fluctuated from 8% (among the people, who experienced obesity at the age of 1-2 years and the parents were not obese) up to 79% (among the people, who became obese at the age of 10-14 and at least one parent was obese) (p. 198). Thus, the probability to become obese in maturity increases depending on the age of emergence and severity of childhood obesity. However, other researches state that there is no correlation among the following factors: the probability of obesity, the age of its emergence and the severity of the disease (Memedi, Tasic, Nikolic, Jancevska, & Gucev, 2013, p. 85). One of the recent researches conducted by Cheung and Mao (2012) found out that the disease could appear at any age irrespective of the presence of obese parents. The eating habits of parents cause the development of obesity in children in the UAE. At the same time, the children of 1-2 years, who suffered from obesity but had non-obese parents, had practically no risk of the development of obesity in maturity, while those, who developed obesity after the age of six, increased the risk of the development of obesity in maturity up to 50% (p. 4). Besides, the presence of obesity of either one or both parents also increased the risk of obesity in maturity. In a situation, when at least one parent is obese, the risk for thin children to develop obesity at a mature age is three times higher.
In fact, there are the family forms of obesity, when the inheritance coefficient reaches 25%, which testifies to the rather high contribution of the genetic factors to the development of the syndrome. According to Al Junaibi et al. (2013), the risk of the development of childhood obesity in the UAE reaches 80% if both parents are obese. However, the risk amounts to 50% if only a mother suffers from obesity and it decreases to 40% if a father is obese (p. 69). In case of the absence of obesity of parents, the risk of the development of obesity in children amounts to about 7-9% (Al Junaibi et al., 2013, p. 68; Loos et al., 2007, p. 187). However, the extent of the development of childhood obesity caused by the inheritance of metabolic disorders has not been found out yet. Besides, there is no resistant deviation in metabolism, which would transfer from parents to the children and would not depend on the family eating habits (Puiu, Emandi, & Arghirescu, 2013, p. 275). However, the children can inherit the complexes of diseases, which compose obesity, from their parents.
If a child has the predisposition to corpulence inherited from the parents, it will represent the risk of obesity. However, much evidence states that childhood obesity is not always caused by genetics, but by the predisposition to corpulence. Thus, it is important to understand this difference. Under the conditions of the identical (average) nutrition and the way of life of children in the UAE, the children inclined to the gain of weight will most likely be obese, but those, who do not have the predisposition to corpulence, may even lose weight. Moreover, the predisposition to obesity or to the loss of weight can be noted even in the adopted children. Thus, the eating habits of parents, the passive way of life and the lack of the physical activity caused by the increase of the income of the population play the key role in the growth of the child obesity rates in the UAE (Al Junaibi et al., 2013, p. 70). However, the possibility to be obese can be inherited from the corpulent parents.
The variability of the genes, which leads either to the malfunction or to the amount of the protein coded by this gene, has a huge value in the genetic predisposition. In particular, it concerns the variability of the genes that cause obesity. According to Chesi and Grant (2015), there are several gene mutations, which can cause obesity. In fact, these mutations often promote the development of type II diabetes and other endocrine diseases. At the same time, obesity as an outcome of all the mutations stated above is connected to the hyper nutrition. People do not receive a signal when the body receives a sufficient amount of fat needed for the adequate accumulation of energy. If the mutation in the hormone of leptin is corrected by the means of injections of the absent protein in the presence of mutations in all other genes, the correction of food consumption through all known ways, including the use of the operational methods, is required (Memedi et al., 2013, p. 86). However, gene mutations provoke the development of diabetes in children (Chesi & Grant, 2015, p. 718). Thus, the genetic factor plays a big role in the increase of childhood obesity rates in the UAE.
At present, the researches in the sphere of the obesity genes are conducted all over the world, including the UAE; probably, there are several obesity genes, localized on the different chromosomes. In fact, the data supports the fact of the existence of a prepotent gene of obesity with the weak expressiveness. Moreover, the scientists suppose that this gene is closely linked to the meta 7 oncogene to a chromosome. However, after the repeated researches, the contribution to obesity was shifted to the IRX3 gene and the other seven genes, changes in which can lead to the gain of weight (Chesi & Grant, 2015, p. 721). However, the development of these genes is possible only in 5% of the whole population of the planet (Cheung & Mao, 2012, p. 5). Despite the statement that genes do not influence the development of obesity, many scientific types of research state that genes increase the risk to become obese.
While discussing the genetic aspects of childhood obesity, it is necessary to mention the existence of two main types of obesity – hypertrophic and hyperplastic (multicellular). In fact, the genetically determined and acquired number of adipocytes is the cornerstone of this division. The birth and growth of the number of these cells occur in “the critical period” of the child’s life – from the 30th week of pregnancy until the end of the first year of the post-natal life (Kumar, Raju, & Gowda, 2010, p. 256). According to Chesi and Grant (2015), the leading factors, which define the number of fatty cells in an organism, compose the level (quality) of food and genetically caused secretion of the growth hormone – somatotropin hormone (STH). Actually, the increase in the synthesis of STH of pregnant women with diabetes and the presence of the number of adipocytes in a fetus and the newborn baby testify to it (Chesi & Grant, 2015, p. 722). In fact, the growth hormone increases the cellular proliferation of various bodies. The overeating by a pregnant woman and a child stimulate the reproduction of adipocytes in the first months of life and, therefore, promote the development of hyperplastic obesity. Thus, this form of obesity often develops at an early age and has a more severe course. Moreover, it is almost not curable. In fact, the resistance to the therapy is connected to the irreversibility of the quantity rather than the sizes of adipocytes. However, the accumulation of adipocytes can lead to obesity only in some cases. Instead, in the majority of cases, hyperdynamic and the nutritional excesses lead to the development of the obesity genes, which result in the spread of the disease to the future generations in the geometrical progression (Al Junaibi et al., 2013, p. 71). However, owing to the somatotropin hormone, the adipocytes greatly contribute to the development of childhood obesity.
What is important, one of the main methodological approaches to the studying of the genetic nature of child obesity in the UAE represents the search for the possible interrelations between the genetically caused signs – the so-called “genetic markers” – and pathology. Among the genetic markers, the leukocyte anti-genes of people are of considerable interest. Actually, the human leukocyte anti-genes (HLA) terms of approach to the disease have a direct connection to the character of a clinical course and the forecast (Cheung & Mao, 2012, p. 6).
In fact, obesity can be manifested in some pathological states connected by the uniform origin. The hypothesis of the so-called “metabolic syndrome” (MS) emphasizes that all the signs are caused by the primary genetically determined tissues of the insulin resistance (Memedi et al., 2013, p. 87). While discussing metabolic syndrome, Puiu, Emandi, and Arghirescu (2013) state that metabolic syndrome can lead to obesity:
The origins of obesity and metabolic dysfunction can be traced back to the intrauterine period of life, at which time the developing fetus is influenced by suboptimal conditions during critical periods of cellular proliferation, differentiation, and maturation by producing structural and functional changes in cells, tissues, and organ systems. These changes, in turn, may have long-term consequences to increase the individual’s risk of developing obesity and metabolic dysfunction (p. 272).
Actually, the full picture of MS includes the existence of resistance to insulin, the excess body weight, the primary adjournment of fats, essential hypertension, the characteristic changes in a lipid blood range and the violation of tolerance to glucose accruing to diabetes. Moreover, due to the combination of all the signs, the children with MS have a high risk of the development of atherosclerosis, arterial hypertension, coronary heart disease, strokes, diabetes, etc. In fact, abdominal child obesity is the earliest manifestation of the syndrome of insulin resistance. Although, some of the researches state that child obesity has no connection to the development of hypertension, heart diseases, diabetes, etc., as they can face even the children with the normal weight indicators without metabolic syndrome (Loos et al., 2007, p. 187). However, insulin resistance is caused by the metabolic syndrome that leads to obesity.
Unfortunately, not all the factors of the genetic predisposition, which influence the development of obesity, have been revealed until the present time. Moreover, the mechanisms of the effective correction of genetic mutations have not been found yet. However, the available knowledge helps to predict the consequences of genetic child obesity. The analysis of the presence of the gene mutation in one of the discussed genes will allow identifying the group of people, who require immediate and radical treatment. However, such high obesity rates, especially, among children in the UAE, can be explained not only by the impact of the genetic factors but also on the way of life.
In conclusion, the given study provides arguments that support the impact of the genetic factors on child obesity in the UAE. In fact, the inherited genetic predisposition to obesity is the most common reason for the emergence of children with excess weight both at the newborn period and at the age of 10-15. The obesity of children can be considered to represent a family disease in the UAE. The children, who have relatives with the factors of the metabolic syndrome or whose mothers had the obese course of pregnancy and arterial hypertension in the anamnesis, require special attention. Actually, it is obvious that the obese children show a considerable genetic predisposition to the main components of the metabolic syndrome and are often affected by hyperdynamic, the excess hyper high-calorie food that provokes the development and progression of obesity that leads to metabolic syndrome. Besides, an additional factor contributes to the formation of arterial hypertension that represents one of the components of metabolic syndrome. However, the way of life, the lack of physical activity and the overconsumption of fatty junk foods also cause child obesity. Obesity in the UAE is caused by the prevalence of the sedentary way of life, the violation of the eating regime and nutritional balance, etc. However, the genetic factors compose the main reasons for child obesity, as there is a big possibility that a child will also have problems with a weight if both parents are obese.
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