Cause and effect of childhood obesity in America - Research Paper Example

CAUSES AND EFFECTS OF CHILDHOOD OBESITY Obesity has been identified as a disease that has gradually been acquiring epidemic proportions incontemporary times. The most recent development in the progress of this condition is that it has surfaced in a growing number of incidences among the young – children and adolescents. What has originated as a medical condition for the middle aged who have, by virtue of their age, experienced a slowdown of metabolism, has alarmingly become prevalent among the young who, supposedly, are at a stage typically characterized by high metabolism and energy expenditure. Many causes of childhood obesity have been cited, among which are genetics and contemporary living, the hallmarks of which are an increasingly sedentary lifestyle, preference for fast foods high in fat content, the influence of television and the internet, and lack of daily exercise. Childhood obesity also results in adverse effects for the young until they grow to adulthood, such as the early onset of a multitude of physiological problems, and the psychological effects of loss of self-esteem and public ridicule. There is also the very real discrimination when it comes to finding employment and attaining promotions, because of the negative perception attached to their condition. This study examines the causes and effects of childhood obesity, and tries to explain the process by which these elements are linked. Causes and Effects of Childhood Obesity Introduction The words “obese” and “overweight” are usually taken to mean the same thing, when, actually, they are not. Overweight means an increased body weight which does not necessarily mean an increase in body fat. It is measures relative to height, age and race, above an accepted standard. Obesity, however, is “defined simply as a condition of abnormal or excessive fat accumulation in adipose tissue, to the extent that health may be impaired.” (MASO, 2009) An athlete may be overweight although he is muscularly built and may exercise a lot, if his weight exceeds the standard. He is not, however, obese, because his extra weight is not due to fat. The individual is obese when his weight is at least 30% higher than the “normal” or standard weight. He is morbidly obesity when he weighs more than 50% above the standard, or more than 100 pounds heavier than normal. The Body Mass Index (BMI) is the commonly accepted measure of the proportion of weight-to-height. It is the person’s weight, expressed in kilograms, divided by the square of his height expressed in meters. Individuals who have a BMI of 25 to 29.9 are classified as overweight; those who have a BMI of 30 or more are classified as obese. (MASO, 2009) Obesity is usually conceived of as a disease among adults, when metabolism slows down. Of late, however, a growing proportion of children and adolescents are categorized as “obese”. This has led to the perception that childhood obesity has attained the status of an “epidemic,” and a programmed and concerted effort to arrest its spread is required. (Ludwig & Gortmaker, 2004) Better yet than finding a cure is finding a way to prevent obesity, and to do this necessitates an understanding of how the process by which the body accumulates fat. The mechanics of energy and nutrient balance Fat mass is the measure of a body’s adipose (or fatty) tissue that is designed to store energy. According to Maffeis (2000), normally, a baby’s fat mass (expressed as a percentage of body weight) accumulates dramatically from approximately 14% at birth to around 25% at the age of six months. It then gradually decreases until the age of six years, when it tends to increase again until maturity. A sophisticated regulatory system controls this process, to allow the person to attain the best body composition needed for adult life. Studies found that when feeding happens above or below one’s requirements, involuntary reactions are triggered which are designed to maintain the weight genetically programmed. Ordinarily, children’s weight control mechanisms are extremely efficient; in one study, children were allowed six days to freely indulge in their favourite food, but despite this there was no significant change in their total daily energy intake even if there was a large difference in energy intake of single meals. (Maffeis, 2000) Recently, it was discovered that more and more children in industrialized countries no longer follow the typical growth patterns. They show greater adiposity (fatty tissue), indicating that the body’s self-regulation of fat mass is either not present, has not worked efficiently, or has been eluded in some way, by the influence of either genetic, environmental, or metabolic factors. Each source of energy gain that is not expended creates a positive energy balance, which is the difference between energy intake and total daily energy expenditure. Prolonged accumulation of positive energy balance induces fat storage. For a six-year-old girl, storage of less than 2% of energy intake each day results in an increase of 30% of her fat mass within one year. Thus, it appears that even slight adjustments in the energy balance mechanism seems to be mainly responsible for fat gain and, subsequently, obesity. (Maffeis, 2000) The metabolic process Maffeis (2000), in examining the aetiology of childhood obesity, described the metabolic process. Nutrients that provide energy intake come in the form of carbohydrates, protein and fat. Although also an energy source, the contribution of fibre is nearly negligible. Thus, energy balance is the sum of the energy intake in all three nutrients, less energy released due to oxidation into the system during expenditure. It must be understood, though, that carbohydrate intake induces carbohydrate oxidation, and protein intake induces protein oxidation. Furthermore, carbohydrate does not convert to new adipose tissue unless all the carbohydrate stores are fully saturated. In contrast, fat intake does not induce fat oxidation. This points to the fact that carbohydrate and protein balance are essentially self-regulating, while fat balance is determined by the balances of the other two nutrients. It is only when the sum of carbohydrate and protein oxidation rates are insufficient to fuel total energy expenditure that fat oxidation occurs. This is significant in understanding the role of fat. The body follows an oxidative hierarchy, preferring to first oxidize carbohydrates and protein before fat. The role of fat in the body is to promote fat gain. Ingested fat is preferentially stored, and is the body’s way of preserving energy. This is a mechanism developed in the anatomy of our prehistoric ancestors, who understandably fed heavily only when the hunt yielded the occasional kill. The body reached such efficiency that it stored energy as fat, to be expended at such time when food was low or not available. (Maffeis, 2000) It was supposed that obese children had a low total energy expenditure than their non-obese counterparts. Recent studies have surprisingly contradicted this. Obese children on the average have a higher total energy expenditure than other children. However, they also have a commensurately much higher energy intake, and in the forms this intake comes in. Many studies conducted on European children show an overconsumption of fat and animal protein, coupled with an under-consumption of fibre. (Reilly, 2007; Lederman, Akabas and Moose, 2004) Both genetic and environmental factors promote a positive energy balance which causes obesity. Genetics predispose individuals to fat gain; environmental influences and lifestyle choices actualize either the relatively high energy intake or low energy expenditure. Genetic causes of obesity According to Maffeis (2000), among the factors involved in childhood obesity, inheritance appears to be the most important cause, and parents’ obesity the greatest risk factor. The author stated that body mass index (BMI) inheritance accounts for 25% to 40% of the variability in adiposity among individuals. In this study it was found that identical twins born to obese parents are likely to become obese than those born to non-obese parents. Although the twins are reared apart, about 70% of the variance of the BMI, which is not accounted for by age, sex, or other covariates, may be attributed to genetic variation. Furthermore, it was determined that adopted children who grew into adulthood had a closer similarity in BMI to their biological parent than their adopted parents. (Maffeis, 2000) In most cases, genes involved in weight gain do not directly cause obesity but they increase the susceptibility to fat gain in subjects exposed to a specific environment. There have been several chromosomes identified that appear to be associated with obesity. In the case of two grossly obese children, severe deficiency in leptin (the product of the ob gene) has been demonstrated, with the same mutation in the ob gene noted. (Maffeis, 2000; Rossner, 1998) 1. A nine-year-old girl was treated with recombinant-methionyl human leptin for six months, during which time significant weight loss was induced. (Maffeis, 2000) 2. Congenital leptin receptor deficiency, and CART (cocaine and amphetamine regulated transcript, a novel anorectic peptide), which is regulated by leptin, has been discovered. This is important because the CART peptide signals satiety (the feeling of being full) in the hypothalamus. In one study, recombinant CART peptide inhibited feeding when injected into rats. Further study in this area is being undertaken to determine the possible application of this discovery. (Maffeis, 2000) 3. Mutations of pro-hormone convertase 1 (PC1) gene, known to activate pro-insulin processing and promote early-onset obesity, have also been recently reported in humans. (Kinoshita, Hanaki, Nagaishi, Kawashima, Adachi, Nanba & Kanzaki, 2007) Environmental and lifestyle causes of obesity The role of the environment in the development of obesity is observable in the rapid increase in incidences of obesity accompanying the dynamic changes in lifestyle in the second half of this century. These environmental factors include the following: 1. Eating habits of the mother during gestation Maffeis (2000) determined that the effect of environmental causes begins in the uterus. The fetus interacts fully with the mother and her metabolism, and it is likely that it is profoundly affected by her metabolic regulatory mechanisms. During gestation, hypothalamic centres of hunger and satiety are differentiated and hyperplasia of adipose tissue occurs in the third trimester. It has been demonstrated that over- or under-feeding during pregnancy appears to influence obesity in later life. For instance, in the west Netherlands, the events of World War II induced a famine that was theorized to have seriously affected women then pregnant. A study was made of young adult males born during this period. It was determined that undernutrition during the first two trimesters of pregnancy was associated with a significantly higher prevalence of obesity among the subjects, while undernutrition occurring during the last trimester did not result in subsequent obesity. Another effect caused during pregnancy was that of children born to mothers who were diabetic. Such children were, independent from other factors, more frequently obese than children of non-diabetic mothers. It is likely that hyperglycaemia and hyperinsulinaemia exposure of the fetus is a risk factor for obesity in later life. (Maffeis, 2000) These findings are supported by Persons and Sevdy (2008), who also determined that large-for-gestational-age (LGA) infants tended to remain heavier through 83 months of life, an developed skinfold measurements considerably divergent at the age of 6 years. They thus concluded that intrauterine growth is positively associated with obesity in early childhood. 2. Early experiences with food, feeding practices and family food choices affect children’s nutritional habits. In particular, the parents are responsible for food availability and accessibility in the home and they affect food preferences of their children. What the parents prepare for family meals and where they decide to bring the family when they dine out greatly influence the food the children get accustomed to, and determine their future food preferences when they do get to choose their own meals. They are conditioned to the taste and kinds of food of their parents. (Consumer Alert, 2004; Ludwig & Gortmaker, 2004)) 3. Diet composition, in particular fat intake, influence the development of obesity. The high energy density and palatability of fatty foods as well as their less satiating properties promotes food consumption. From our prehistoric ancestors, human tastes are skewed to like fatty foods because the occasional hunt means a prehistoric community will only be able to occasionally eat meat. Liking fatty foods will enable human bodies to store energy more efficiently until the next successful hunt, whenever that may be. In today’s supermarket society, however, meat is always available, and our programmed taste for fat is working to make us obese. (McIntyre and Sullivan, 2004) 4. Technology has promoted an inactive lifestyle among children. A sedentary lifestyle has contributed greatly to the loss of exercise and, therefore, reduction in energy expenditure among children, creating greater positive energy balance. TV viewing, computer gaming and internet surfing, which are inactivity and food intake promoters, were identified as a relevant risk factor in children. Sedentarity, i.e. a low physical activity level, is accompanied by a low fat oxidation rate in muscle and a low fat oxidation rate is a risk factor of fat gain or fat re-gain after weight loss. Further, heavy advertising on TV increase the attractiveness of fastfoods and commercially prepared, preserved food that entice children to indulge in them. (Maffeis, 2000; Rossner, 1998) Causes explored in recent studies 1. Childhood sexual abuse, a potential risk factor A study conducted by Gustafson and Sarwer (2004) have found empirical correlation between childhood sexual abuse and obesity. The authors note that childhood sexual abuse is more common than is commonly believed, affecting some one-third of women and one-eighth of men. They state that numerous psychological episodes such as depression, anxiety, substance abuse, somatization, and eating disorders (particularly binge eating) have been linked with the low self-esteem experienced by sexual abuse survivors, but there are relatively few studies that deal on sexual abuse and obesity. It is theorized that a possible “adaptive function” exists for obesity in childhood in response to sexual abuse. The relationship between the two have not yet, however been confirmed. (Gustafson & Sarwer, 2004) 2. Family status In the UK, findings suggest that children hailing from families of lower socio-economic status tend to be relatively more obese than the general population. The same seems to be the case for children from ethnic minority groups, although this still has to be confirmed. (Lederman, et al., 2004) 3. Lack of information Research supports the fact that many parents, as well as health, educational, and counselling professionals are aware of the magnitude of the risks of childhood obesity. Childhood obesity has been characterized as “practically invisible” (Baur, 2005 as cited in Reilly, 2007). Failure to fully appreciate the problem and its consequences delays treatment and renders insufficient whatever attempts are taken to remedy the condition. Furthermore, few who are aware of the problem are inclined to prioritize it because of its seeming hopelessness; as Stunkard’s cynical comment states, “Most obese persons will not stay in treatment for obesity. Of those who stay in treatment, most will not lose weight; and of those who lose weight, most will regain it.” (Stunkard, 1972 as quoted in Rossner, 1998) Common effects of childhood obesity: Childhood obesity tends to lead to adverse consequences in adulthood. Following are the various diseases or disorders suffered by obese children which may begin in childhood and progress through adolescence to adulthood. 1. Neurological Pseudotumor cerebri, or “false brain tumor,” is likely to develop among obese persons due to high pressure within the skull caused by the buildup or poor absorption of cerebrospinal fluid (CSF). It symptoms are headache, nausea, vomiting, and pulsating sounds within the head – all symptoms which mimic large brain tumors. (MedicineNet.com). 2. Pulmonary Sleep apnoea is a common disorder wherein the afflicted has one or more pauses in breathing and shallow breaths as he sleeps. The disruptions are caused by the narrowing or blockage of the airways as one sleeps. This could disrupt sleep three or more nights a week, and often results in poor sleep quality that makes the afflicted tired during the day. (National Heart Lung and Blood Institute, (NHLBI)) Asthma is a chronic lung disease that inflames and narrows the airways, causing recurring periods of wheezing, chest tightness, shortness of breath and coughing. (NHLBI) Another pulmonary disorder is exercise intolerance is the inability to exercise excessively. It is characterized by a variety of symptoms such as shortness of breath, swelling, muscle weakness, fatigue, etc. (WebMD.com) 3. Gastrointestinal Gallstones are chrystallized solid masses of cholesterol and other substances found in the bile, sometimes smaller than a grain of stand and sometimes as large as a golf ball. They seldom cause trouble but require intervention when they block a duct. Nonalcoholic steatohepatitis (NASH) is a liver inflammation caused by a buildup of fat in the liver that can result in progressive liver damage over time. NASH commonly affect people who are middle-aged, obese, have high cholesterol and triglycerides, or diabetes. (MedicineNet.com) 4. Cardiovascular Obesity gives rise to many cardiovascular diseases, including dyslipidaemia (abnormal levels of lipids like cholesterol and triglycerides), hypertension (high blood pressure), coagulopathy (bleeding disorders), chronic inflammation (long-term unchecked inflammation) and endothelial dysfunction (abnormality in the interior lining of blood vessels). (WebMD.com) 5. Renal Glomerulosclerosis is the scarring of the kidney’s blood vessels that are responsible for filtering urine from the blood. The scarring disturbs the kidneys’ filtering process and allows protein to lead from the blood into the urine. Different kinds of this disease may be caused by diabetes, infection or drug use. Scarred glomeruli cannot be repaired, and when end-stage renal disease (ESRD) is reached, the kidneys fail completely and the patient must go on dialysis or get a kidney transplant. (WebMD.com) 6. Musculoskeletal Orthopaedic problems (particularly in the foot, knee and hip) result from the increased load the musculoskeletal system, particularly the joints, are made to carry. Slipped capital femoral ephiphysis is a condition that affects teenagers in particular, wherein the growth center of the hip slips backward on the top of the thighbone. (eOrthopod.com) Blount’s disease is a growth disorder of the shine bone among young children and adolescents. (Medline Plus Medical Encyclopedia). There could also occur forearm fracture and flat feet due to obesity. 7. Endocrine Adverse effects on the metabolism of glucose leading to type 1 and type 2 (non-insulin-dependent) diabetes, particularly for obese adolescents. Type 2 diabetes, which used to be unrecognised in adolescence, already accounts for half of all new diagnoses of diabetes in certain populations. (Ebbeling, Pawlak and Ludwig, 2002). Precocious puberty, polycystic ovary syndrome (girls) and hypogonadism (boys) are other endocrine disorders due to obesity. (WebMD.com) 9. Persistence of obesity At least 7 percent of obese adolescents will grow into obese adults (Reilly, 2007). Breaking out of the cycle will necessitate a complete change of lifestyle, which is almost difficult to attain even with the desire to do so. 10. Social, educational and economic displacement Obese individuals suffer from a host of social, economic and educational prejudice. Because of teasing and stigmatisation among their peers, obese children tend to suffer from psychosocial morbidity, particularly among adolescents and girls. The obese child develops poor self-esteem, depression and eating disorders. (Reilly, 2007) When they grow into adulthood, the obese individuals tend to experience discrimination at work. Difficulty in getting a job is a particularly prevalent and oppressive effect of the social prejudice against obesity because a person’s very lifelihood and economic well-being is affected. Chernov (2006) conducted a study that identified some of the reasons why obese people are discriminated against. Most commonly expressed by employers are: (1) negative portrayal of store image (customers perceive the store negatively if they have an obese employee); (2) higher insurance costs coupled with the uncertain future health conditions of the obese applicant; and (3) physical limitations of the obese applicant to comply with the dictates of the job. Of these three excuses, only the third, physical limitations, may constitute a legitimate reason for not hiring an obese person. And oftentimes, even if the person has been hired, he has trouble being promoted and is often passed over in career advancement opportunities. Conclusion The future of obese children is bleak, given conventional realities. In many segments of society, the seriousness of obesity is not even recognized yet. It is high time that the medical profession, as well as educational and healthcare professionals, and most of all the parents, are beginning to view the problem as an epidemic. It is hoped that in the future, the following statement would no longer prove true, that “The most common metabolic disease in the United States was treated with scorn, contempt and indifference.” (Rossner, 1998, p.1) Appendix REFERENCES Baur, L., “Childhood obesity: practically invisible”, International Journal of Obesity – First Steps, 2005, as cited in Reilly, John J., “Childhood Obesity: An Overview”, Children & Society, vol. 21, pp. 390-396, 2007. “Case Commentary” contributed by Yach, Derek & Marks, Amy Seidel, International Journal of Medical Marketing, vol. 4 no. 3, pp. 288-294, 2004 Consumer Alert, “No quick fix for childhood obesity”, Consumer Comments, vol. 28 issue 4, Fall 2004. 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