Free «How Childhood Obesity Affects Adulthood Personality and Illness» UK Essay Paper
Obesity (from Latin ‘adipositas’ - literally means ‘obesity’ and ‘obesitas’ - literally means completeness, obesity, well-fed) - is a deposition of fat, increasing of body weight caused by fat. Adipose tissue can be deposited as sediments in the physiological areas, as well as in the breast, thighs and abdomen. Currently obesity is considered as a chronic disease of the exchange that occurs at any age, manifested by excessive weight gain, mainly due to excessive accumulation of adipose tissue, accompanied by increased incidence of overall morbidity and mortality. Incidence of the obesity in a civilized society is rising dramatically, despite the absence of changes in the genetic pool that is independent of hereditary factors (Esposito & Guigliano, 2006).
Obesity is the result of an imbalance between the absorption and energy spending in the body processes. Regulation of body weight is done by a complex interactions of a set of interconnected systems that oversee the energy system of the body: the absorbed energy measured in calories is equal to expended energy. Obesity contributes to a positive energy balance and deposit caused by lack of physical exercises and readily available source of carbohydrates. Excess of carbohydrates is accumulated and stored in the body form of triglycerides in the adipose tissue. Negative energy balance between absorbed and consumed energy, even for a short period of time, is a threat to the life of the organism and human. Therefore, to maintain energy balance the body must adjust level of hormones, reduce energy costs, improve nutrient absorption, correct feeding behavior or decrease appetite, and adjust the level of missing energy to mobilize energy from fat stores. Each of these units and factors are subjects to certain genes.
1. At present days obesity is one of the biggest actual problems for the world, which associated with its anomalous progressive spread. WHO experts predict double increase in the number of obese in 2025 compared to 2000. Nowadays more the a billion people of the planet have an excess body weight. In United States of America more then 50% of adults have overweight problems and about 30% obese more or less. Obesity is categorized as one of the major risk factors for many diseases such as: diabetes, hypertension, coronary heart disease, liver and gall bladder and many others ((Esposito & Guigliano, 2006).
Buy How Childhood Obesity Affects Adulthood Personality and Illness essay paper onlineBecome our VIP client
* Final order price might be slightly different depending on
the current exchange rate of chosen payment system.
2. One of the greatest challenges facing public health in the 21st century is obesity among children. Before childhood obesity was rare, and for many years, real evidence of a link between the presence of childhood obesity and body weight of an adult was missing. However, research and the findings conducted that up to 10% of children can be clinically obese and that far from a considerable number of young people who have excess weight, maintain it into adulthood. It is estimated that in 2010 the number of children with excess body weight in the world exceeds 42 million and about 35 million of them live in developing countries.
The huge medical and social significance of the obesity and the diseases associated with obesity in childhood determines the urgency of further research in this direction.
Overweight and obesity are defined as "abnormal or excessive fat accumulation that represents a risk to health.". In 2006 WHO has developed and approved typical data for child development that are recommended for assessment of physical development, in particular weights.
The role of hereditary factors in the development of obesity is now beyond doubts. The existence of family forms of obesity in which the inheritance factor reaches 25% is well known fact, which indicates a high level of influence of genetic factors in the development of this disease. For today it is confirmed that several monogenic forms of obesity are caused by mutations in a gene leptin, gene of its receptor, convertase-1 pro-hormone, melanocortin receptor 4R-and-proopiomela nokortina (Masuzaki et al., 1997). Clinica manifestations of monogenic variants are characterized by the early disease, morbid obesity, hyperphagia, secondary hypogonadism. About 50 known mutations in the insulin receptor. Basically those disease are rare (leprehuanizma syndrome, insulin resistance syndrome of type A, Mendenhall Ranson syndrome).
It is believed that critical to the development of obesity are the following periods:
1. During early age. At 1st year of age of the child overfeeding leads to more fat cells, but not their size. With time control and correct adjustment of diet during this period is likely a favorable outcome.
2. Prepubertal (5-7 years), when obesity can have recurrent characteristics. Is often persistent and involves constant obesity in adulthood, because in this period the excess number of adipocytes is not reduced, a provision for the fat depots.
3. Adolescence. The vast majority adolescents, overweight, save it as an adult. This obesity is largely due to restructuring of the neuro-endocrine system associated with puberty and often forms the so-called hypothalamic syndrome puberty.
Candidate-genes increase the risk of overweight of children only during the action of environmental factors, including exogenous. Overeating, drinking excessive amounts of fat, carbohydrates, supply disruptions, the so-called syndrome of "night" food is a common cause of obesity. Physical inactivity is the accompanying risk factor in the development of obesity.
Social factors play a very important role in the development of obesity, even for young children. These include the low educational level of parents and the social status of the family, single-parent family with one child, stress in the family, extraordinary situation in the school and the surrounding environment - all these factors cause mental injury to a child and can trigger his obesity (Masuzaki et al., 1997).
Limited Time offer!
Get 19% OFF
In the pathogenesis of obesity are considered more main links regulation of appetite and the energy balance:
1. central (ventromedial hypothalamus)
2. afferent system (leptin and other factors saturation)
3. efferent system
4. gastrointestinal (GI) tract and liver metabolic processes.
Hunger center (appetite) and saturation center located respectively in ventrolateral and ventromedial hypothalamic nuclei. Emotional and behavioral aspects of eating regulated centers located in the cortical part of the orthorhombic lymph system (cingulate cortex, hippocampus), as well as in the amygdala (Speiser 2005).
One of the most common metabolic disorders in obesity in children is a phenomenon of IR. The frequency and intensity of R & D increases with the mass of adipose tissue, especially in the visceral region. Among the factors released by adipocytes, we study the effect of free fatty acids (FFA), the level of which increases with accumulation of visceral fat (Lavin, 1994). FFA prevent the binding of insulin hepatocytes, causing development of R & D at the hepatic level, reducing the absorption of insulin by liver (Lackey & Kolassa, 2004).
Considered important in the pathogenesis and the role of leptin, the neurohormonal mediator of adipocyte-produced results. Leptin regulates food intake, energy consumption, body weight. To a large extent it has an inhibitory effect on taken food, not on the periodic bursts of increasing appetite. The action of leptin appears at the level of the hypothalamus, where it binds to the ob-receptors, causing activation signals that inhibit food intake and increase energy expenditure. Circulating level of leptin is proportional to the amount of children’s fat. The mechanism of leptin secretion is not fully understood, it is known that it is secreted in the pulse mode with an interval of 444 minutes. Peak secretion accounts for night (24.00-4.00), and the lowest - in the morning and at noon. Leptin levels increase glucocorticoids, acute infections, inflammation, decreases with colds, smoking, thyroid stimulating hormone, melatonin (Wynne, 2005). In the past two decades, much researches have been conducted to neuropeptide Y, to its role in the control of body weight and appetite control. Neuropeptide Y increases food intake, because of the hunger feeling, through the centers of hunger and satiety.
Active consideration in the development of obesity ES. ES regulates energy balance in the body for the main functional levels, involving limbic system, hypothalamus, gastrointestinal tract, adipose tissue. Exogenous and endogenous cannabinoids contribute to weight gain. During obesity there is noticed increased activity of ES (Clement & Ferre, 2003).
It should be noted the role of the gastrointestinal hormone like grelin - a peptide secreted in the stomach, duodenum, and intestine. It directly stimulates the appetite by regulating food intake and energy balance in the body. Grelin level is higher during the hunger, and quickly decreases after having a meal, allows to suggest its role in feeding behavior. Changes in grelin gene can cause obesity in early childhood, or serve as a protective mechanism for the accumulation of fat, but the ultimate role of the polymorphism of grelin in the control of body weight is not specified (Clement & Ferre, 2003). Much attention is paid to the study of mutations selected in fat RRAR-Y receptor associated with the exchange of glucose and fat. The most common obesity manifests are during the first years, in 5-6 years, during puberty.
The most common form of obesity, which accounts to 83.7% of all of its forms, is a constitutional-exogenous obesity, which is manifested in infants by type paratrofi. Distribution of subcutaneous fat of children depends on the sex, age, severity, and duration of disease. In general fat is deposited relatively uniformly. However, the period of puberty of girls fat layer is more pronounced in the pelvic area, and boys - on the trunk (waist types of obesity).
Genetic screening is required for children to avoid monogenic forms of obesity.
Let’s earn with us!
Get 10% from your friends orders!
Treatment of obesity include diet therapy, physical activity, drug therapy may be needed.
Poor diet, lack of systematic or excessive use of low-quality food, fast food, low content of fruits and vegetables in the diet, increased emphasis on sweet, flour, fried and fatty foods are the main factors for the development of children obesity. Some other factors are low levels of physical activity and mobility, hormonal disorders, disruption of the thyroid or adrenal glands, elevated levels of anxiety, depression, high level of stress (Wynne, 2005).
It is important to understand that if the weight is defined as having excess body weight for specific age and height through adipose tissue, muscle, bones, body fluids or more of these factors at the same time then obesity is just the number of fat tissue in the body which is not harmless and the risks of adverse effects on children with developed obesity in early age are much higher than for adults acquired this condition in adulthood(Bado et al., 2004).
The main risks associated with childhood obesity are: reduced learning activity and attention, depression and impaired social adaptive skills, delayed sexual development, cardio problems, probable development of diabetes, Alzheimer’s disease in adults, predisposition to cancer, probability of apnea (Branca et al., 2009). These facts show how high the risk of childhood obesity for every child now. It is important to understand that child will develop unhealthy eating habits and lifestyle which will be almost impossible to rebuild by the early teen years.
Children do not eat healthy food on daily basis, more than 40% of children eat fast food every day for the entire year.
Want to know what your projected final grades might look like?
Check out our easy to use grade calculator! It can help you solve this question.Calculate now