Sedentariness_&_Obesity

It comes as no surprise that obesity is more prevalent now than ever before in human history. The creation of larger cars, wider seats in public facilities and the massive food portions seen at restaurants indicate that everyone is starting to take notice of the fact that our average size has increased. Though the actual numbers vary significantly between different parts of the world, it is safe to assume that North American’s are steadily becoming more overweight and obese. Obesity is classified by a BMI of 30 or higher and affects approximately 300 million worldwide. (WHO, 2010). Obesity poses more significant health risks than simply being overweight and can lead to a wide spectrum of health conditions such as Type II diabetes, elevated blood pressure and cholesterol and heart disease. Obesity is associated with earlier death, and overall higher rates of myocardial infarctions (heart attacks) as well as many types of cancer (Dietz, 1998). Though obesity is linked to health complications in both adults and children, this paper will focus on the main contributors of childhood obesity. The children facing the obesity epidemic today will become the adults of tomorrow and therefore it is increasingly important to address the etiology and pathology of the widespread childhood obesity epidemic. Sedentariness, nutritional factors and medical/genetic malfunctions, and the means by which they affect obesity, will be discussed in this paper. Obesity is a health condition brought on by the synthesis of many factors and sedentariness plays a large role but is not the sole cause of the current childhood obesity epidemic. Sedentariness and Obesity: Obesity rates in children have almost tripled in the last 25 years (WHO, 2010). Though sedentariness is not the only reason for this, it is a very significant part of the obesity epidemic. There has been a recent global shift to a more sedentary lifestyle with the advent of “mechanized transport and labour-saving technology” (84 – Wikipedia: obesity) that matches the increasing incidence of obesity worldwide. Numerous studies have been conducted that further strengthen the link between increased sedentariness and obesity rates, specifically in children. The explosive introduction of hand-held games, cell-phones and PDA’s means that children are less likely to spend leisure time engaged in physical activity. Sedentariness affects obesity in a few different ways but its main force comes from its ability to displace time for physical activity (Lopez et al, 2008). The displacement of physical activity time causes children to have a decreased overall level of energy expenditure and though this is important in adults as well, in children it can create habits that become deeply rooted throughout their lives. The importance of physical activity is diverse in the mechanisms with which it affects the growth and development of a child. Physical activity during childhood contributes significantly to the development of skeletal mass and building bone mineral density (Janz, Burns & Levy, 2005). Without adequate physical activity during childhood, once fully-grown, these adults would have suboptimal levels of skeletal mass which substantially increases their risk for injury as well as affects posture, overall strength and agility (Janz, Burns & Levy, 2005). This weakened skeletal system could indirectly contribute to obesity as it puts less emphasis on sports and physical activity. In a study conducted by the Department of Community Health and Epidemiology at Queens University in Kingston, Ontario, results indicated that overweight and obesity prevalence was particularly high in countries located in North America, Great Britain, and south-western Europe. In these countries, physical activity levels are generally lower and sedentary activity times are significantly higher in overweight/obese individuals compared to normal weight youth (Janssen et al, 2004). Lack of physical activity has drastic effects on one’s energy balance. Though the topic of how to lose weight and maintain weight loss is heavily debated, it is generally agreed upon that one’s caloric intake should approximately match their energy expenditure to maintain a healthy weight. Fat storage occurs when caloric intake exceeds caloric expenditure. Excessive caloric intake and decreased energy expenditure due to physical inactivity both disrupt the energy balance and increases the prevalence of obesity in a population. Excess adiposity can affect many bodily functions and circulating fat in the body can contribute to atherosclerosis and heart disease (Lopez et al, 2008). Thus, we can see the importance of maintaining energy balance to avoid the accumulation of adipose tissue within the body and in turn, obesity. Nutritional factors and obesity: The other side of the energy balance problem has to do with improper nutritional intake. An unhealthy diet can magnify the effects that lack of physical activity has on obesity. Over the past few decades, the structure of dietary intakes has changed drastically and modern urban societies have transitioned towards a diet high in saturated fats and sugar but low in fibre (Popkin & Gordon-Larsen, 2004). Fibre promotes a feeling of satiety as well as interferes with fat absorption and is therefore essential in weight loss or healthy weight maintenance. Ample food availability could also potentially be responsible for increased intake as well as large food companies resorting to low cost sweeteners to mass produce making sugar-type substitutes more available potentially encouraging overconsumption. (Popkin & Gordon-Larsen, 2004). A diet characterized by low fibre intake and overconsumption along with a sedentary lifestyle is likely to lead to obesity. In a study conducted by Nicklas et al at the Children's Nutrition Research Center in Houston, Texas in 2003, specific eating patterns were shown to be associated with overweight status and obesity. Consumption of soft drinks, fruit flavour drinks, sweets, and overall consumption of low-quality foods were positively associated with overweight status. The study also indicated that total amount of food consumed, particularly from snacks, was positively associated with overweight status. (source). These eating patterns are consistent with children in developed countries across the world. This relates to the importance of maintaining energy balance, and with consistent over consumption of food and decreasing physical activity, increased fat storage is likely to occur leading to an overall rise in overweight and obese children. Other factors and obesity: Sedentariness and poor nutrition are the most obvious and significant factors in the childhood obesity epidemic. However, the extensive field of genetics play a key role in the occurrence an obese phenotype from the passing of genes linked to somatic traits and overall size as well as from genetic malfunctions. The FTO gene (fat mass and obesity associated gene) has been identified as being correlated with obesity. Two alleles of this FTO gene account for an almost twofold increase in risk for obesity. (Frayling et al, 2007) Many genetic diseases have also been discovered that have are directly related to obesity in subjects of all ages. MOMO syndrome is a rare genetic disorder that is characterized by high birth weight and obesity through childhood and adult life. The mechanism by which the autosomal dominant mutation that characterises MOMO syndrome causes obesity is unclear to date, but the resultant obesity has been seen in all cases. (Ferreira, 1993) Leptin-receptor malfunction can also cause obesity (course). A large number of genes are responsible for appetite, metabolism and many somatic traits thus any mutation of those genes could result in obesity. Many disorders can lead to obesity as well, the most common being hypothyroidism, a disease characterized by a thyroid gland malfunction. The thyroid gland is responsible for the release of Thyroxin, and this release is stimulated by the “thyroid stimulating hormone” from the anterior pituitary gland. The anterior pituitary gland itself is regulated by a releasing factor from the hypothalamus called “thyroid releasing hormone”. This hormonal system is regulated by a tightly monitored feedback system. Disturbances in any part of this chain of hormones and releasing factors, or in the intrinsic feedback mechanism, can lead to overproduction or underproduction of Thyroxin. In the case of hypothyroidism, Thyroxin levels are lower than optimal. Given that Thyroxin is responsible for metabolic function within the body this can result in significant weight gain (course) Hypothyroidism can be caused by a variety of disorders that affect the hypothalamic-pituitary-hepatic axis. Hashimoto's thyroiditis is an autoimmune disorder that presents in children and results in the degradation of the thyroid gland causing hypothyroidism and ultimately weight gain. Congenital hypothyroidism is another example of a HPH-axis disorder that results in a deficiency of thyroid hormone at birth increasing one’s obesity risk dramatically. Another example of a disorder leading to obesity is a hormone disorder known as Cushing’s syndrome which occurs in the body when exposed to elevated Cortisol levels for a prolonged period of time. Obesity is known to increase the risk for developing Cushing’s syndrome and the syndrome itself causes obesity, specifically in the upper body. The release of Cortisol in the body follows a similar pattern to the release of Thyroxin in that the hypothalamus releases a corticotrophin-releasing hormone stimulating the release of adrenocorticotropin from the anterior pituitary gland. This stimulates the release of Cortisol from the adrenal glands and a disruption to this pathway at any place could cause distorted levels of Cortisol. The control of the body’s fat storage, distribution and metabolism is a result of countless factors and consequently there are many ways that these systems could malfunction. Genetics, hormonal systems and congenital disorders are all viable contributors to obesity, and though may not account for the majority of obesity cases, it is clear that sedentariness is not the sole cause of childhood obesity. The childhood obesity epidemic is a large concern worldwide but specifically in developed countries and can cause detrimental effects on a child’s health and overall well being. Over the past few decades it has been recognized as a serious public health concern and more research is being conducted to create innovative treatments for this broad problem. The many different contributors to childhood obesity as discussed in this paper, sedentariness, poor nutrition, genetic/endocrine malfunctions and others, all lead to obesity in their own way. Physical activity and a healthy diet work in synchrony to maintain a healthy energy balance and avoid excess fat storage from caloric excess. Genetic/endocrine malfunctions are harder to treat, and since they have symptoms that extend beyond obesity alone, it is important to attempt to treat these in a holistic manner and not by simply decreasing body weight. Works Cited Dietz, William H. "Health Consequences of Obesity in Youth: Childhood Predictors of Adult Disease." Journal of the American Academy of Pediatrics 101.3 (1998): 518-25 Janssen, I., P. Katzmarzyk, W. Boyce, M. King, and W. Pickett. "Overweight and Obesity in Canadian Adolescents and Their Associations with Dietary Habits and Physical Activity Patterns." Journal of Adolescent Health 35.5 (2004): 360-67. Janz, K., T. Burns, and S. Levy. "Tracking of Activity and Sedentary Behaviors in ChildhoodThe Iowa Bone Development Study." American Journal of Preventive Medicine 29.3 (2005): 171-78. Popkin, B. M., and P. Gordon-Larsen. "The Nutrition Transition: Worldwide Obesity Dynamics and Their Determinants." International Journal of Obesity 28 (2004): S2-S9. Rey-López, Juan Pablo, Germán Vicente-Rodríguez, Mireia Biosca, and Luis A. Moreno. "Sedentary Behaviour and Obesity Development in Children and Adolescents." Nutrition, Metabolism and Cardiovascular Diseases 18.3 (2008): 242-51 WHO | World Health Organization." World Health Organization. 2010. Web. 18 Nov. 2010. .