本文是美国健康论文范例，题目是“Socio-economic Impact of Obesity Management on the US Economy（肥胖管理对美国经济的社会经济影响）”，肥胖在美国迅速成为一种严重的流行病，部分原因是美国人的饮食习惯和缺乏运动。根据疾病控制中心的数据，美国73%的成年人和43%的儿童超重或肥胖。在20岁以上的非裔美国人中，超过三分之二的人超重或肥胖(Gaines, 2010)。一般来说，非裔美国妇女和西班牙裔美国妇女的超重和肥胖率高于白人妇女，在南部和中西部较高，并随年龄增长而增加(Ogden等，2014;Gregg等人，2009年;Sherry等人，2010)。根据世界卫生组织的数据，肥胖者的身体质量指数(BMI)大于等于30。2型糖尿病和高血压是两种最终影响非裔美国人的疾病，这主要是由体重增加引起的，因为这些额外的体重使人容易患上这些疾病(Gaines, 2010)。肥胖是心脏病，糖尿病和一些癌症的主要风险因素之一，这些是今天美国人的主要死因。肥胖及其相关并发症对健康的影响越来越比吸烟更有害，因此已成为全世界可预防的主要死亡原因之一。
OBESITY肥胖
Obesity is fast becoming a serious epidemic in the United States due partly to eating habits and physical inactivity amongst Americans. According to the Centre for Disease Control, Seventy-three percent of adults and 43 percent of all children in the United States are overweight or obese. Among African-Americans 20 years and over, more than two-thirds are overweight or obese (Gaines, 2010). Generally, the rate of overweight and obesity are higher for African-American and Hispanic women than Caucasian women, higher in the south and Midwest and increases with age (Ogden et al., 2014; Gregg et al., 2009; Sherry et al., 2010). According to the World Health Organization, body mass index (BMI) of an obese person has a value greater than or equal to thirty. Type 2 diabetes and high blood pressure are two diseases that ultimately affect African Americans and this is predominantly caused by an increase in weight as those extra pounds predisposes a person to these diseases (Gaines, 2010). Obesity is one of the primary risk factor for heart diseases, diabetes and a number of cancers and these are major causes of death in American today. The health implication of obesity and the complications associated with it is increasingly becoming more detrimental than cigarette smoking and has therefore become one of the major preventable causes of death worldwide.
This investigation paper focuses on the brief history of obesity; this will take obesity from its discovery over 2000 years to this present day. An understanding of the BMI classification, aetiological determinants, pathophysiology and health effects is important if obesity prevalence will be curtailed. Furthermore, the socio economic impact of obesity management on the United States economy will be looked into. Finally, its treatment options, prevention and trends of the disease will be discussed.
HISTORY OF OBESITY
The Ancient Greeks were the first to acknowledge obesity as a health disorder and this was further recognized by the Ancient Egyptians in a similar way. According to Hippocrates, corpulence is not only a disease itself, but the harbinger of other diseases (Haslam & James, 2005). Hippocrates which was the Ancient Greek Father of Western medicine acknowledged obesity in his work and details of various diseases including diabetes was first given by him. Another Indian surgeon Sushruta, also discovered the association between obesity, diabetes and heart diseases and he was the first person to find out the significant signs, symptoms, causes and health implications. In the Ancient days, man always strived for food due to scarcity or famine and this resulted in obesity being regarded as a sign of wealth and good fortune in the middle age. However, all this changed when the scientific society of the 20th century revealed the medical implications of obesity (Caballero B., 2007)
With the inception of the industrial revolution, body size and strength of soldiers and workers became pertinent as this was attributed to the military and economic power of Nations (Caballero, 2007). The increase in the average body mass index from underweight to the normal on the BMI charts played an important role in the development of industrialized societies (Caballero, 2007). Therefore in the 19th century, there was an increase in weight and height generally. However, during the 20th century, the genetic potentials for height was reached and this resulted to weight increasing more than height in this century and thus resulted in the average increase in BMI (Caballero, 2007). In human evolution, for the first time, the number of adults with excess weight exceeded the number of those who were underweight which further led to obesity (Caballero, 2007).
The perceptions of the public as regards healthy body weight varied from those regarded as normal in the western society, but this perception was changed in the beginning of the 20th century. There was a reduction in the weight seen as normal since 1920s and this was evident by the 2% increase in average height of the Miss America pageant winners and a 12% decrease in weight between year 1922 and 1999 (Rubinstein & Caballero, 2000). Also, the perception of most people as regards healthy weight has changed, for example in Britain the weight at which people regarded themselves to be overweight was considerably higher in 2007 than in 1999 (Johnson & Wardle, 2008). Obesity is still regarded as an indication of wealth and well-being in many parts of Africa and this has become more widespread since the HIV epidemic began (Haslam & James, 2005).
BODY MASS INDEX (BMI) CLASSIFICATION体重指数(bmi)分级
According to the World Health Organization, Body Mass Index (BMI) is a simple index of weight-for-height that is commonly used to classify underweight, normal weight, overweight and obesity in adults. It is defined as the weight in kilograms divided by the square of the height in metres (kg/m2) (W.H.O. 2004). For example, an adult who weighs 60kg and whose height is 1.65m will have a BMI of 22.0.
根据世界卫生组织的说法，身体质量指数(BMI)是一个简单的体重与身高的指数，通常被用来区分成年人的体重不足、正常体重、超重和肥胖。它的定义是体重(以公斤为单位)除以身高(以米为单位)的平方(kg/m2)(世卫组织，2004年)。例如，一个体重60公斤、身高1.65米的成年人，其BMI为22.0。
BMI = 60 kg / (1.65 m2) = 60 / 2.72 = 22.04
LEAN BODY MASS
Lean Body Mass is a component of body composition, it is calculated by subtracting body fat weight from total body weight. Total body weight is lean plus fat.
In equations: LBM = BW − BF
Lean Body Mass equals Body Weight minus Body Fat
LBM + BF = BW
Lean Body Mass plus Body Fat equals Body Weight
Lean Body Weight (men) = (1.10 x Weight(kg)) – 128 ( Weight2/(100 x Height(m))2)
Lean Body Weight (women) = (1.07 x Weight(kg)) – 148 ( Weight2/(100 x Height(m))2)
Ideal Body Weight (men) = 50 + 2.3 ( Height(in) – 60 )
Ideal Body Weight (women) = 45.5 + 2.3 ( Height(in) – 60 )
Body Mass Index = Weight(kg) / Height(m)2
The table below further explains the classification of BMI in relation to the weight and height of an individual.
BMI values are age dependent and are the same for both males and females (WHO, 2000). The health risks associated with increasing BMI are many and the interpretation of BMI values in relation to risk may vary for different populations in different geographical locations (WHO, 2004).
AETIOLOGY DETERMINANTS OF OBESITY
Obesity is a heterogeneous group of conditions with numerous causes, it is not merely a single disorder and it is predominantly expressed phenotypically (Susan A.J, 1997). Obesity is hereditary, but the genetic component does not follow simple Mendelian principles and the effect of the genotype on the aetiology of obesity may be decreased or increased by factors that are non-genetic (Susan A.J, 1997). Several factors determine the body weight, and these are interactions of genetic, environmental and psychosocial factors which are in relation to the amount of energy consumed and the amount of energy expended and the resulting acting through the physiological mediators of energy intake and energy expenditure and the resulting equilibrium between both (Susan A.J, 1997).
ENDOCRINE AND HYPOTHALAMIC DISORDERS内分泌和下丘脑紊乱
Certain endocrinological disorders may lead to obesity, but this applies to a very small percentage of the total number of cases (Susan A.J, 1997). The endocrinological determinants of obesity have been reviewed recently (Bouchard C., Perusse L., Leblanc C., Tremblay A, & Theriault, 1988). The single disorder that causes obesity in this group is hypothyroidism in which increased weight occurs largely as a result of reduced energy expenditure (Susan A.J, 1997). Other endocrinological factors contributing to obesity include Cushing’s syndrome and disorders of corticosteroid metabolism, where weight gain is typically accompanied by a distinctive prototype of fat deposition in the trunk, sex hormone disorders including hypogonadism in men and ovariectomy in women, insulinoma and growth hormone deficiency (Susan A.J, 1997). The key causes of weight gain in these cases are the amount of energy intake. Certain hypothalamic tumors or damage to the hypothalamic part of the brain as a result of excessive exposure to radiation, infectious agents or head trauma can also lead to obesity with defect in appetite control and hyperphagia (Susan A.J, 1997). A hypothalamic disorder is also believed to be the foundation of a number of congenital abnormalities which could also result in obesity, e.g. Prader-Willi syndrome, which is an abnormality that could be a primary cause of obesity (Susan A.J, 1997).
某些内分泌失调可能导致肥胖，但这只适用于极少数病例(Susan A.J, 1997)。最近对肥胖的内分泌决定因素进行了综述(Bouchard C.， Perusse L.， Leblanc C.， Tremblay A， & Theriault, 1988)。在这一人群中，导致肥胖的唯一疾病是甲状腺功能减退症，其中体重增加主要是由于能量消耗减少(Susan a.j.， 1997)。其他导致肥胖的内分泌因素包括库欣综合征和皮质类固醇代谢紊乱，体重增加通常伴随着躯干脂肪沉积的独特原型，性激素紊乱包括男性性腺机能减退和女性卵巢切除术，胰岛素瘤和生长激素缺乏(Susan A.J, 1997)。在这些情况下，体重增加的主要原因是摄入的能量。某些下丘脑肿瘤或由于过度暴露于辐射、感染剂或头部外伤而对大脑下丘脑部分造成的损伤也可导致食欲控制缺陷和暴食症的肥胖(Susan A.J, 1997)。下丘脑紊乱也被认为是许多先天性异常的基础，这些先天性异常也可能导致肥胖，例如Prader-Willi综合征，这种异常可能是肥胖的主要原因(Susan A.J, 1997)。
GENETIC INFLUENCE
At a population level, the genetic influence of obesity is expressed in terms of heritability (Susan A.J, 1997). This refers to the percentage of the total difference in a character which is attributable to genetic factors (Susan A.J, 1997). The heritability of obesity may be considered either in terms of the total fatness of an individual or the distribution of body fat in an individual (Susan A.J, 1997). Several discoveries have been made over the years regarding the influence of genetics on chronic diseases like cardiovascular disease and obesity (R. C. Whitaker, J.A. Wright, M.S. Pepe, K.D. Seidel, &W.H. Dietz., 1997). Recent reports indicate that at least 32 genes contribute to common forms of obesity. Many of these genes are thought to be related to the development of obesity through the deregulation metabolic hormones in the body (Susan A J, 1997).
The obesity related variant in the fat mass and obesity-associated protein also known as alpha-ketoglutarate-dependent dioxygenase FTO, has aroused interest in pediatrics due to its relationship with increased weight and ponderal index at 2 weeks of age (A. Lopez-Bermejo, C.J. Petry, M. Diaz, et al., 2008). FTO is located on the long arm of the chromosome 16 and is expressed in the brain, specifically the hypothalamic nuclei (Khung E. Rhee et al. 2012). Those who are homogenous for the at-risk allele have been found to be 3kg heavier than those who do not have the allele (T.M. Frayling, N. J. Timpson, M. N. Weedon et al. 2007). This weight gain is likely due to the gene’s involvement in the regulation of energy intake (Khung E. Rhee et al. 2012). According to recent studies, individuals carrying the at-risk allele prefer dense energy foods (J.E Cecil, R. Tavendale, P. Watt, M. M. Hetherington, & C.N.A Palmer, 2008), have reduced feeling of satiety (J. Wardle, S. Carnell, C.M.A. Haworth, I.S. Farooqi, S. O’Rahilly, & R. Plomin, 2008), display loss of control over eating (M. Tanofsky-Kraff, J.C. Han, K. Anandalingam et al. 2009), consume more fat and calories (even after adjusting for BMI) (N. J. Timpson, P.M. Emmett, T.M. Frayling, et al. 2008) and display a greater tendency towards consuming palatable foods after eating a meal (J. Wardle, C.Llewellyn, S. Sanderson, & R. Plomin, 2009). Therefore, FTO isn’t associated with energy expenditure, but it increases the susceptibility of individuals to higher calorie consumption and decreased satisfaction. A meta- analysis of 45 studies found that adults who were physically active attenuate the odds of obesity associated with FTO by almost 30% (T.O. Kilpelainen, L. Qi, S. Brage, et al. 2011). Thus carrying a gene for obesity does not necessarily predestine one to be obese (D. Meyre, K. Proulx, H. Kawagoe-Takaki et al. 2010), but rather increases the risk in the face of an obesogenic environment (Khung E. Rhee et al. 2012).
Numerous studies in different ethnic groups suggest that the familial correlation in the total body fatness, expressed as body mass index, (BMI; kg/m2) from parent to offspring is about 0.2 and for sibling-sibling relationships about 0.25 (Bouchard C, Perusse L, Leblanc C, Tremblay A, Theriault G. 1988). As would be expected, studies of twins show a much higher concentration, particularly in monozygotic pairs (Susan A.J, 1997). However, these findings do not segregate the independent effects of genetic transmission and a shared environment (Susan A.J, 1997). Further studies of twins reared apart attribute 50-70% of the difference in BMI in later life to genetic factors (Stunkard A, Harris J, Pedersen N, McClearn G. 1990). Adoption studies, where an individual is compared both to their biological parent and their adopted parents, have also demonstrated the importance of genetic influences (Susan A.J, 1997). There is a strong relationship between the BMI of the adoptee and their biological parents across the entire range of fatness, but no relationship between the adoptee and their adoptive parents (Stunkard A, Sorensen T, Hanis C. et al. 1986).
Studies of fat distribution have considered both the ratio of subcutaneous to total fat mass and the distribution of subcutaneous fat in the trunk relative to the limbs (Susan A.J, 1997). Data from the Quebec Family Study, suggest that the size of the internal fat stores are more strongly influenced by genetic factors than subcutaneous depots (Bouchard C., Perusse L., Leblanc C., Tremblay A, Theriault, 1988). Familial clustering suggests that genetic factors may account for 37% of the variance in the trunk to extremity skin fold thickness ratio (Rice T, Bouchard C, Perusse L, Rao D. 1995). These combined evidence from these genetic analysis suggests that obesity is a polygenic disorder and that a considerable proportion of the variance is non-additive (Susan A.J, 1997). This would explain the higher correlations between siblings than those between parent and offspring, and the 2-fold greater correlation between monozygotic than dizygotic twins (Susan A.J, 1997). These genetic influences seem to operate through susceptible genes; the occurrence of the gene increases the risk of developing a characteristic but not essential for its expression nor is it, in itself, sufficient to explain the development of the disease (Susan A.J, 1997). Unlike animal models, where a number of single genes can lead to obesity, no human obesity gene has yet been characterized, but the heterogeneous nature of human obesity does not preclude the identification of small number of individuals with a single defect which leads to obesity (Susan A.J, 1997). In man, a number of genetically determined conditions result in excess body weight or fatness (e.g Prader-Willi syndrome or Bardet-Biedl syndrome), but these account for only a very small proportion of the obese population (Susan A.J, 1997).
PHYSIOLOGICAL MEDIATORS
Energy expenditure
Studies in animals have postulated that at the time of overfeeding, a remarkable increase in metabolic rate may deplete the excess energy thus reducing the rate of weight gain below theoretical values (Rothwell N., Stock M., 1983). Genetically obese animals tend to gain more weight than their lean controls even when they are pair-fed, thus implying a greater metabolic rate (Thurby P., Trayhurn P., 1979). One possible explanation for this effect is the decrease in diet-induced thermogenesis which is lessened in animal models of obesity due to a decrease in the sympathetic activation of brown adipose tissue (Rothwell N., Stock M., 1983). These unequivocal effects on energy expenditure in obese animals contrast with the paucity of evidence in humans (Susan A Jebb, 1997). Susan A.J (1997) stated that in obese humans, there have been constant reports of abnormally low energy intake which indirectly imply that there must be a defect in energy expenditure. There are three basic elements to energy expenditure which have each been the focus of extensive research.
Basal Metabolic Rate
In 1997, Susan A Jebb defined basal or resting metabolic rate as the energy expended by an individual at rest, following an overnight fast and at a comfortable environmental temperature in the thermo neutral range. Several studies of basal metabolic rate have concluded that obese subjects have a higher BMR compared to their lean counterparts. Researchers like Swinburn B. & Ravussin E, reported that approximately 80% of the inter- individual variance in BMR can be accounted for by age, fat-free mass, fat mass and gender. Nevertheless, this still gives room for some likelihood that inter-individual difference in BMR which may influence individuals with a relatively low BMR to become obese (Susan A. Jebb, 1997).
Diet induced thermogenesis
A number of studies have suggested that the post-prandial increase in energy expenditure is attenuated in obese subjects, perhaps due to decreased Sympathetic Nervous System activity (Astrup A. 1996). Similar effects have also been demonstrated in the post-obese. However this is not a consistent finding, even among studies from the same laboratory. A recent review by Ravussin E. & Swinburn B. (1993) identified 28 studies in favour of a defect in thermogenesis in humans and 17 against. However, since thermogenesis accounts for only a fraction of total energy expenditure (approximately 10%), the potential for a significant effect on total energy expenditure is insufficient (Susan A. Jebb 1997).
Physical activity
The most significant component of energy expenditure is physical activity which may represent 20-50% of total energy expenditure. Studies of fidgeting movements in Pima Indians within a whole-body calorimeter have shown significant inter-individual variations in the daily energy cost of these actions from 400-3000 kJ/day, with low levels predictive of subsequent weight gain at least in males but not females (Zurlo F., Ferraro R., Fontvielle A. et. al. 1988). However, in free-living conditions, the freedom to undertake conscious physical activity or exercise increases the inter-individual variability even further (Susan A Jebb). Research in this area has been hampered by imprecision in the methods to measure physical activities which have included various actometers, heart rate monitoring, activity diaries and direct observation (Susan A. Jebb, 1997).
The energy requirements of an individual encompass the summation of basal expenditure, thermogenesis and physical activity. A whole-body calorimeter can be used to measure the total energy expenditure of an individual. The analysis of total energy expenditure in 319 obese subjects clearly demonstrates a significant increase in energy expenditure with increasing body weight such that individuals with a BMI in excess of 35 kg/m2 have energy expenditure approximately 30% higher than those with BMI less than 25 kg/m2 (Susan A Jebb, 1997). The outstanding difficulty with these studies , as stated by Susan A. Jebb in 1997 is that the increase in energy expenditure seen in obese subjects as a result of their increased body size may mask pre-existing metabolic defects in the pre-obese state which exposes the individual to excessive weight gain. However, in experimental overfeeding researches, there is no remarkable difference in the degree of weight gain between lean and obese subjects when matched for their excess energy intake (Diaz E. Prentice A. M et. al. 1992). Studies of total energy expenditure in post-obese subjects have not arrived at a definite conclusion; some studies show no difference in energy expenditure in the post-obese relative to never-obese controls (Goldberg G.R., et. al. 1991), whilst others show a modest suppression of energy expenditure (Geissler C. Miller D., Shah M. 1987). In general, there is little evidence to support the hypothesis that human obesity may be due to a specific defect in energy expenditure in predisposed individuals (Susan A Jebb, 1997). Susan A Jebb further stated that advocates of a metabolic basis to obesity, argue that only very small differences in energy expenditure are neccessary to produce significant weight gain over many years, and this difference may be lower than the limits of precision of even the most advanced methodology.
Energy Intake能量摄入
The failure to identify a defect in the metabolic control of energy expenditure and the contrary observation of high levels of energy expenditure, and the contrary observation of high levels of energy expenditure in obese subjects has led to a focus on food intake to explain the aetiology of obesity (Susan A Jebb, 1997). The increase in energy expenditure associated with the development of obesity should automatically help to prevent continued weight gain; hence the failure of this auto-regulatory system suggests that there must be a considerable error in the regulation of food intake (Susan A Jebb, 1997). Furthermore, habitually lean individuals are able to regulate intake to match energy requirements over a wide range of energy requirements yet those who become obese seem unable to achieve this balance (Susan A Jebb, 1997).
未能识别缺陷的代谢控制能量消耗和相反的观察高水平的能量消耗,以及高水平的能量消耗的相反的观察在肥胖受试者已经导致了人们开始关注对食物摄入肥胖原因的解释(苏珊·杰布,1997)。与肥胖发展相关的能量消耗增加应该自动有助于防止体重持续增加;因此，这种自动调节系统的失败表明，在食物摄入的调节中一定存在相当大的错误(Susan a Jebb, 1997)。此外，习惯苗条的人能够调节摄入量，以满足各种各样的能量需求，但那些肥胖的人似乎无法达到这种平衡(Susan a Jebb, 1997)。
Breakthrough in discerning the role of energy intake in the aetiology of obesity has been critically disconcerted by under-reporting which is now largely recognized as a feature of obesity (Susan A Jebb, 1997). Comparisons of energy intake and energy expenditure indicate consistent shortfalls in self-reported intake, averaging approximately 30% of energy requirements in obese subjects (Prentice A.M., Black A.E., Coward W.A., 1986; Lichtman S., Pisarska K., Berman E., et al., 1993). This phenomenon also extends to post-obese subjects and to others who may be very weight conscious (Susan A Jebb, 1997).
Under-reporting may be cause by several factors and it is natural for individuals to change their eating pattern when they are to record their food intake. This is usually associated with a reduction in intake as subjects consciously or sub-consciously adopt a self-imposed ‘diet’. (Susan A Jebb, 1997). Therefore they might give accurate results about their intake for that duration, but it may not be a true representation of their habitual pattern. Forgetfulness, underestimation of meal size and lack of basic knowledge of food consumption can also lead to under-reporting. Although, it is possible to have falsification and fabrication of dietary records, there are also instances of self-deception or deliberate manipulation of dietary records.
少报可能是由几个因素造成的，对于个人来说，在记录他们的食物摄入量时，改变他们的饮食模式是很自然的。这通常与摄入量的减少有关，因为受试者有意识或潜意识地采用了自我强加的“饮食”。(Susan A Jebb, 1997)。因此，他们可能会给出准确的结果，关于他们在那个时间段的摄入量，但这可能不是他们习惯模式的真实代表。健忘、低估饭量和缺乏食物消费的基本知识也会导致少报。虽然，有可能有伪造和伪造饮食记录，也有自我欺骗或故意操纵饮食记录的例子。
Recent research into the appetite control system by Blundell J.; Bouchard C., Bray G. (1996), has identified a network of synchronous interactions which govern eating behavior. These effects are mediated through the central nervous system particularly the hypothalamus, where a number of neuropeptides appear to regulate feeding behavior via effects on hunger and satiety (Susan A Jebb, 1997). Laboratory studies of feeding behavior by Spiegel T., et al., in 1989, proposed that, following a convert energy preload, obese subject may be less able to accurately compensate for the energy content of the preload at a subsequent meal than lean subjects. However, these studies are usually of short duration in laboratory settings and may not accurately reflect eating behavior in a naturalistic setting, where knowledge of foods consumed and conditioned learning may invoke other regulatory processes (Susan A Jebb, 1997).
There is also significant evidence that the individual macronutrients (protein, fat, carbohydrate and alcohol) have different influences on eating behavior, majorly due to their effects on satiety (Stubbs R., 1995). Experimental studies of manipulated foods and retrospective analyses of dietary records suggest that protein is the most satiating (DeCastro J., 1987; Hill A., Blundell J., 1990). Carbohydrate is also an efficient inhibitor of later food consumption, at least in the short terms, meal-to-meal context (Rolls B., et al. 1994). Fat seems to have a satiating capacity (Lawton C., Burley V., 1993). Fat hyperphagia occurs during a single meal due to subjects overeating high fat foods and is also known as passive over consumption. In 1994, Poppitt S., stated that fat has two times the energy per gram of carbohydrate or protein which may be due to the level of energy density and not necessarily a characteristic of dietary fat. Appetite is said to be stimulated by alcohol and according to DeCastro J & Orozco (1990), in free living circumstances, alcohol consumption with meals is associated with higher energy intakes, but this may also reflect that alcohol is more likely to be consumed on special occasions which in themselves are associated with increased food intake.
Basically, taste preference can have an effect on the amount of food consumed and the kind of food. The individual preference for certain meals would make them more likely to consume more of that meal. Therefore, sensory preferences plays a role on energy balance since is it associated with energy intake. According to Witherley S, Pangborn R & Stern J (1980), several reports of sensory preferences for particular food groups in association with obesity, but inter-subject variability is so great as to obscure any underlying obese-lean differences. The relationship between sensory preference for fat versus sugar and BMI was pinpointed by Drewnowski in 1992. Obese women had preference for foods with high fat to sugar ratio while women with low BMI had preference for high sugar to fat ratio, therefore increase in weight is closely related to increase for fatty foods.
Eating frequency has effect on weight gain, because people who eat several small meals at intervals have less weight than those that eat fewer meals in larger quantity and therefore large quantity of food consumed at a time may be a risk factor for obesity, however, studies as regards this, showed no remarkable relationship (Bellisle F, McDevitt R, Prentice A.M. 1997). Research in this area is contradicted by under-reporting of food consumption in obese subjects and by post-hoc variations in eating patterns as a result of obesity and efforts to control weight (Susan A Jebb, 1997). Eating frequency in obese subjects is however an unreliable blueprint to the eating patterns involved in the aetiology of obesity (Susan A Jebb, 1997).
ENVIRONMENTAL INFLUENCE
Obesogenic environment which was first coined in the 1990s, in a bid to explain the present obesity epidermic. According to King D (2007), obesogenic environment is the sum of the influences that the surroundings, opportunities or conditions of life have on promoting obesity in individuals and populations. This encompasses the cultural, social and infrastructural conditions that affect the ability of a person to embrace a healthy lifestyle. Individuals in a population respond to unhealthy environment and the more urbanized the environment, the more individuals are pressurized to adopt unhealthy habits. The pressure from the surrounding makes it difficult for individuals to change their lifestyle and practice healthy habits when the environment itself is unhealthy. Environmental factors may have a critical effect in the development of obesity by unmasking genetic or metabolic susceptibilities (Susan A.J, 1997). Environmental influences on diet involve a wide range of factors including accessibility to food and high calorie drinks. Eating habits are commonly influenced by the availability and accessibility of unhealthy food, which is an important consideration in the effect on obesity. Studies in the United States recommend that the availability of high quality, affordable ‘healthy’ food is limited for people who reside in low-income communities and such scarcity is associated with unhealthy diet and obesity (White 2007) .However despite several epidemiological studies that shows environmental influences play an important role in the aetiology of obesity, it is a fact that some people within the same ‘unhealthy environment’ still managed to maintain a healthy weight (Susan A.J, 1997).
PSYCHO-SOCIAL INFLUENCES心理社会影响
Food is sometimes used as a coping mechanism by individuals with weight issues, especially when they are unhappy, nervous, stressed, bored and depressed. In many obese individuals there seems to be a perpetual cycle of mood disturbance, overeating, and weight gain (Jennifer C. Collins & Jon E. Bentz 2009). When they feel frustrated, they rely on food for comfort, even though this coping mechanism may pacify their mood, the resultant weight gain that results may cause a dysphoric mood due to their inability to control their stress (Jennifer C. Collins & Jon E. Bentz, 2009). Eventually a guilty feeling may restart the cycle and might steer a habitual pattern of eating food to get comfort. This habitual pattern is specifically significant if there is a genetic risk factor for obesity or an ‘obesogenic’ environment where foods high in calorie & density are readily accessible and sedentary lifestyle is present. Regrettably, these situations are popular in America.
食物有时被有体重问题的人用作一种应对机制，尤其是当他们不开心、紧张、有压力、无聊和抑郁的时候。在许多肥胖的个体中，情绪紊乱、暴饮暴食和体重增加似乎是一个永恒的循环(Jennifer C. Collins & Jon E. Bentz, 2009)。当他们感到沮丧时，他们依靠食物来获得安慰，尽管这种应对机制可能会安抚他们的情绪，结果体重的增加可能会导致由于他们无法控制他们的压力而引起的烦躁情绪(Jennifer C. Collins & Jon E. Bentz, 2009)。最终，一种负疚感可能会重新启动这个循环，并可能会改变吃东西来获得安慰的习惯模式。如果存在肥胖的遗传风险因素，或者存在容易获得高热量和密度食物的“致肥”环境，并且存在久坐不动的生活方式，那么这种习惯模式就尤为重要。遗憾的是，这种情况在美国很普遍。
In addition to depression and anxiety, other risk factors include problematic eating behaviors such as “mindless eating,” frequent snacking on high calories foods, overeating, and night eating (Glinski J., Wetzler S., Goodman E.2001). American Psychiatric Association has currently included Binge eating disorder (BED) in an appendix of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) and is characterized by: recurrent episodes of eating during a discrete period of time (at least 2 days a week over a 6 month period); eating large quantity of food than majority of the people would eat at the same time; a feeling of loss of control during the episodes; and guilt or distress following the episodes (Jennifer C. Collins & Jon E. Bentz, 2009). According to Wadden T.A., Sarwer D. B., Fabricatore A. N., Jones L., Stack R., & Williams N.S (2007), BED is estimated to occur in approximately 2% of the general population and between 10% and 25% of the bariatric population. An important differentiation pointed out by the American Psychiatric Association, between BED and bulimia/anorexia is that BED is not associated with any regular compensatory behaviors, such as purging, fasting, or excessive exercise. It can therefore be implied that the majority of individuals with BED are overweight.
Night eating, which was first identified in 1955 as another disorder that can lead to remarkable weight gain, though night eating syndrome (NES) is not currently recognized by the American Psychiatric Association as a distinct diagnosis in the DSM-IV-TR. Night eating syndrome is characterized by excessive late night consumption (> 35% of daily calories after the evening meal), unhealthy eating patterns, “morning anorexia,” insomnia, and distress (Stunkard A. J., Grace W. J. & Wolff H. G. 1955). NES occurs in approximately 1% of the general population and an estimated 5-20% of the bariatric population (Wadden T.A., Sarwer D. B., Fabricatore A. N., Jones L., Stack R., & Williams N.S. 2007). More recently, NES has been seen as a disorder of circadian rhythm that includes a delay of appetite in the mornings and the continuation of appetite and over consumption of food during the night (Jennifer C. Collins & Jon E. Bentz, 2009).
PATHOPHYSIOLOGY OF OBESITY肥胖的病理生理学
There are several possible pathophysiological mechanisms involved in the advancement and prolongation of obesity. This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedman’s laboratory (Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., Friedman, J.M., 1994). These researchers proposed that leptin was a satiety element. However, soon after J. F. Caro’s laboratory could not ascertain any mutations in the leptin gene in humans with obesity. In 1995, Considine, RV; Considine, EL; Williams, CJ; Nyce, MR; Magosin, SA; Bauer, TL; Rosato, EL; Colberg, J., & Caro, J.F. proposed a contrary view that Leptin expression was increased, postulating the possibility of Leptin-resistance in human obesity. Since the discovery of leptin, insulin, ghrelin, orexin, cholecystokinin, adipokines, peptide tyrosine tyrosine, as well as many other mediators have been researched. The adipokines are intermediators produced by adipose tissue; their action is thought to revise many obesity-related diseases. Leptin and ghrelin are considered to be interrelated in their effect on appetite, with ghrelin produced by the stomach regulating short-term appetitive control (i.e. hunger pangs when the stomach is empty and satiety when the stomach is stretched). Leptin is created by adipose tissue to signal fat storage reservoirs in the body, and mediates long-term appetitive controls (i.e. to eat more when fat storages are low and less when fat storages are high). Although administration of leptin may be effective in a small subset of obese humans who have deficiency in leptin, most obese humans are considered to be leptin resistant and have been found to have high levels of leptin (Hamann A., & Matthaei S. 1996). This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese people (Flier J.S. 2004).
肥胖的发生和延长可能与多种病理生理机制有关。在1994年J.M. Friedman的实验室发现瘦素基因之前，这一领域的研究几乎无人涉足(Zhang, Y.， Proenca, R.， Maffei, M.， Barone, M.， Leopold, L.， Friedman, j.m.， 1994)。这些研究人员提出，瘦素是一种饱腹感因素。然而，不久之后，j·f·卡罗的实验室无法确定肥胖人群中的瘦素基因有任何突变。1995年，Considine, RV;很远,EL;威廉姆斯,CJ;Nyce先生;Magosin SA);鲍尔,TL;Rosato EL;Colberg, J.， & Caro, J. f .提出了相反的观点，认为瘦素表达增加了，并假设在人类肥胖中存在瘦素抵抗的可能性。自发现瘦素以来，胰岛素、胃饥饿素、增食欲素、胆囊收缩素、脂肪因子、肽酪氨酸等许多介质都得到了研究。脂肪因子是脂肪组织产生的中间体;他们的行动被认为可以改善许多与肥胖有关的疾病。瘦素和胃饥饿素被认为对食欲的影响是相互关联的，胃饥饿素由胃调节短期的食欲控制产生(即，当胃空的时候会感到饥饿，当胃被拉伸的时候会感到饱足)。瘦素是由脂肪组织产生的，用来向体内的脂肪储存库发出信号，并调节长期的食欲控制(即脂肪储存低时吃得多，脂肪储存高时吃得少)。虽然对一小部分缺乏瘦素的肥胖人群施用瘦素可能有效，但大多数肥胖人群被认为是瘦素抵抗，并被发现有高水平的瘦素(Hamann a .， & matthai S. 1996)。这种抵抗力被认为可以部分解释为什么在大多数肥胖人群中使用瘦素并不能有效地抑制食欲(Flier J.S. 2004)。
Leptin and ghrelin act on the hypothalamus and are produced peripherally. They control appetite through their actions on the central nervous system. They act on the hypothalamus, a region of the brain central to the coordination of food consumption and energy expenditure. There are several circuits within the hypothalamus that contribute to its performance in integrating appetite, the melanocortin pathway being the most well understood (Flier J.S. 2004). The circuit starts with an region of the hypothalamus, the arcuate nucleus, that has outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brain’s feeding and satiety centers, respectively (Boulpaep, Emile L., Boron, & Walter F. 2003).
According to Flier J.S. (2004), the arcuate nucleus contains two distinct groups of neurons; the first group co expresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH and the second group coexpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH (Flier J.S. 2004). Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding (Flier J.S. 2004). Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group (Flier J.S. 2004). Researches done by Flier J.S., 2004, thus concluded that a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.
EFFECT ON HEALTH影响健康
Obesity is a severe medical condition and a chronic health issue worldwide. The association between body weight and mortality is a subject of concern, especially in regards to the optimal weight for longevity (JoAnn E. Manson, M.D., Walter C. Willett, M.D., et al, 1995). The significance of understanding the true relationship between weight and mortality is underlined by the increasing prevalence of obesity in the United States (Kuczmarski RJ, et al, 1994) especially women (Harlen WR, et al, 1988). Obesity is a major risk factor for cardiovascular diseases (e.g., heart disease, stroke and high blood pressure), diabetes (e.g. type 2 diabetes), musculoskeletal disorders (e.g., osteoarthritis), some cancers (e.g., endometrial, breast, and colon cancer), high total cholesterol or high levels of triglycerides, liver and gallbladder diseases, sleep apnea and respiratory problems, reproductive health complications such as infertility and mental health conditions (WHO, 2012).
肥胖是世界范围内的一种严重的疾病和慢性健康问题。体重和死亡率之间的关系是一个值得关注的主题，特别是关于长寿的最佳体重(JoAnn E. Manson, m.d.， Walter C. Willett, m.d.， et al .， 1995)。了解体重和死亡率之间真实关系的重要性被美国日益普遍的肥胖所强调(Kuczmarski RJ, et al, 1994)，特别是女性(Harlen WR, et al, 1988)。肥胖是心血管疾病的主要危险因素(例如,心脏病,中风和高血压)、糖尿病(如2型糖尿病),肌肉骨骼疾患(如关节炎)、某些癌症(如子宫内膜癌、乳腺癌和结肠癌),高总胆固醇或甘油三酯水平高,肝脏和胆囊疾病,睡眠呼吸暂停和呼吸问题、生殖健康并发症，如不孕症和精神健康状况(世卫组织，2012年)。
Obesity and Cancer
Obese people are more vulnerable to cancer and their prognosis is extremely worse when diagnosed. Men that are obese are 33% more likely to die from cancer and obese women also have a 50% higher likelihood of dying from breast cancer (Weight Management Centre, 2010). Additional to obesity, cancer has recently been linked to diet and physical activity status (Bray 2004, Barnard 2004, Wiseman 2008). The cancers most significantly associated with obesity in women are cervical, uterine, kidney, breast and endometrial cancer and in men are colon, pancreatic and liver cancer (Calle, Rodriguez, Walker-Thurmond & Thun 2003). One study, using National Cancer Institute Surveillance, Epidemiology, and End Results data, estimated that in 2007 in the United States, about 34,000 new cases of cancer in men (4 percent) and 50,500 in women (7 percent) were due to obesity. The percentage of cases attributed to obesity varied widely for different cancer types but was as high as 40 percent for some cancers, particularly endometrial cancer and esophageal adenocarcinoma (National Cancer Institute, 2012).
Obesity and cardiovascular disorders
Cardiovascular disease (CVD) is one of the major cause of death in U.S. Obese people are more liable to die from CVD largely due to accelerated atherosclerosis, hyperlipidaemia, loss of glyceamic control and hypertension. Until recently the relationship between obesity and coronary heart disease was viewed as indirect, i.e., through covariates related to both obesity and coronary heart disease risk (Lew E.A., Garfinkel L., 1979) including hypertension; dyslipidemia, particularly reductions in HDL cholesterol; and impaired glucose tolerance or non–insulin-dependent diabetes mellitus. Insulin resistance and accompanying hyperinsulinemia are typically associated with these comorbidities (Reaven G.M., 1988). Although most of the comorbidities linking obesity to coronary artery disease increase as BMI increases, they also relate to the total distribution of body fat. Long-term longitudinal studies, however, indicate that obesity as such not only relates to but independently predicts coronary atherosclerosis (Manson J.E., et al., 1995; Garrison R. J., et al. 1985; Rabkin S.W., 1977). Messerli F. H. (1982) stated that left ventricular hypertrophy is mostly seen in patients with obesity and is related to systemic hypertension and may be related to the severity of obesity. Hypertension is approximately three times more commonly found in obese individuals than normal-weight persons (Van Itallie T.B., 1985). This relationship may be directly related such that when weight increases, there is an increase in blood pressure (Kannel W.B., Brand N., et al., 1967) and when weight decreases, blood pressure also decreases (Reisin E., Frohlich E.D., et al., 1983).
Obesity and mental health
Individuals diagnosed with obesity tend to be less favorable on all levels of the psychological assessment and may exhibit several symptoms ranging from mere sadness to chronic depression. Evident are more episodes of mood swings, anxiety, personality and eating disorders, basically related to or associated with obesity experienced by individuals with obesity (Pickering, Grant, Chou, Compton 2007). Obesity may be an inception of psychiatric manifestations and vice versa and is related to psychosocial deterioration and bias based on weight. This comprises of loss of self-worth, and reduced self-esteem associated with stigmatization. Stigmatization can further lead to desolation and withdrawal and thus many obese individuals seek solace in binge eating, thereby gaining more weight. Based on reports from Roberts, Deleger, Strawbridge & Kaplan 2003; Herva, Laitinen, Miettunen, Veijola, Karvonen & Lasky 2006; Kasen, Cohen, Chen &Must 2008, concern, shame and guilt associated with low self-worth, which is finally related to excessive food consumption completes the obesity-mental disorder circle.
There is bias and discrimination associated with obesity. They generally report reduced quality of life and functional wellbeing, collectively called Health-related quality of life (HRQOL) (Puhl & Brownell 2001; Wadden & Phelan 2002). This relationships is majorly expressed by women (Fontaine 2001) and for people with severe obesity (Hudson, Hiripi, Pope & Kessler 2007; Scott, Bruffaerts, Siomn, Alonso, Angermeyer, de Girolamo et al. 2008).
Obesity and diabetes
Diabetes is usually a terminal illness. i.e. it is a lifelong chronic disease characterized by high levels of sugar in the blood. One of the major risk factors for diabetes is obesity. Obesity is directly associated with Diabetes 2. The association between obesity and type 2 diabetes are firmly established and without the intervention of a healthy diet and proper exercise, obesity can lead to type 2 diabetes over a very short period of time. In fact, obesity is believed to account for 80-85% of the risk of developing type 2 diabetes, while recent research suggests that obese people are up to 80 times more likely to develop type 2 diabetes than those with a BMI of less than 22 (National Health Service, 2014). It is a known fact that obesity carries a greater risk of developing type 2 diabetes, especially if you have excess weight around your abdomen. Studies postulates that abdominal fat causes fat cells to releases ‘pro-inflammatory’ chemicals, which can reduce the body’s sensitivity to the insulin, this can also disrupt the function of insulin responsive cells and their ability to react to insulin. This is known as insulin resistance which is a primary activator for type 2 diabetes. Excess abdominal fat is a major high-risk form of obesity.
SOCIO-ECOMOMIC/ FINANCIAL COST OF OBESITY肥胖的社会经济/财政成本
In 1999-2000, nearly 65 percent of U.S. adults were either obese or overweight. Obesity accounts for $117 billion a year in direct and indirect economic costs. Obesity is associated with 300,000 deaths per year, and is fast becoming the leading cause of preventable deaths” (Mancino, Lin, and Ballenger, 2004). Certainly, obesity has become a large problem in America. Recent increase in meal portions and reduction in availability of natural food production may propose why people find it challenging to maintain a healthy diet. Although, certain People have been successful at maintaining a healthy nutritional status and avoiding this unhealthy situation. Gary Becker’s human capital theory is a groundwork that helps to clarify the effect of weight status on the economy in terms of the labor market outcomes for the individual. Human capital is the educational qualification, job experience/training, and the health condition that workers devote their time in to boost their capacity and skills to be “rented out” to employers (Ehrenberg and Smith, 2005). Healthy weight status in relation to labour is a type of human capital investment. According to Robert Pindyck and Daniel Rubinfeld (2004), “When an investment decision is made, the investor commits to a current outlay of expenses in return for a stream of expected future benefits.” These stated costs for a healthy weight may include buying of food with high nutritional values and creating time for physical activities. As an investment, the individual sacrifices money, time and other resources to attain a healthy weight to become more productive in the future and, hence, earn higher income. Obese workers miss more days of work and inflict more cost on employers especially in medical and disability claims and also workers compensation claims. As a result, firms end up with extra costs associated with obesity, this is one of the economic effects of obesity.
1999年至2000年，近65%的美国成年人肥胖或超重。肥胖每年造成1170亿美元的直接和间接经济损失。每年有30万人死于肥胖，并正迅速成为可预防死亡的主要原因”(Mancino, Lin, and Ballenger, 2004)。当然，肥胖在美国已经成为一个大问题。最近饭量的增加和天然食物生产的减少可能解释了为什么人们觉得保持健康饮食具有挑战性。虽然，有些人成功地保持了健康的营养状况，并避免了这种不健康的状况。加里·贝克尔的人力资本理论是一个基础，有助于澄清体重状况对经济的影响，就个人的劳动力市场结果而言。人力资本是指劳动者为提高自己的能力和技能而投入的教育资格、工作经验/培训和健康状况，以便“出租”给雇主(Ehrenberg和Smith, 2005年)。与劳动相关的健康体重状况是一种人力资本投资。根据Robert Pindyck和Daniel Rubinfeld(2004)的观点，“当作出投资决定时，投资者承诺将当前的支出用于回报预期的未来收益。”这些健康体重的声明成本可能包括购买高营养价值的食物和为体育活动创造时间。作为一种投资，个人牺牲金钱、时间和其他资源来获得健康的体重，从而在未来变得更有生产力，从而获得更高的收入。肥胖员工会耽误更多的工作时间，给雇主带来更多的成本，尤其是在医疗和残疾索赔以及员工赔偿索赔方面。因此，公司最终会与肥胖相关的额外成本，这是肥胖的经济影响之一。
Obesity places significant burden on the society through health care expenditures and disability payments combined through group health insurance and public programs. The estimated annual medical cost of obesity in the U.S. was $147 billion in 2008 U.S. dollars; the medical costs for people who are obese were $1,429 higher than those of normal weight (CDC, 2011). Obesity there has direct and indirect effect on the Nation’s resources, as more money is spent on the obese due to the high risk of comorbidity with other life threatening diseases like type 2 diabetes, osteoarthritis and cardiovascular diseases.
TREATMENT
There are several weight-loss schemes available but many are ineffectual and short-term, especially for those who are morbidly obese. The strategies for weight loss with non-surgical programs usually involve a combination of diet modification, behavior modification therapy and appropriate exercise.
Dietary Modification
Dietary modifications for obesity are designed to create a negative energy intake-energy expenditure balance (i.e., calories consumed < calories expended) by reducing daily energy intake below the required level. The required energy varies by weight, sex and level of physical exercise such individuals with higher weights, more activity have greater energy needs, including men (Melanson K. & Dwyer J. 2002). Uniformly, higher energy deficits results in higher weight losses. Low calorie diet is recommended for obese individuals and they are advised to check calorie content of meals before consumption. Very low calorie diet is recommended for morbidly obese individuals with little or no success in low diet consumption.
Behaviour Therapy
The oldest report of the use of behavioral therapy in the management of obesity occurred in 1967. Since then, it has been widely used in the management of obesity (Gupta R. & Misra A. 2007). Behavior therapy involves setting out goals and principles to patients to aid their adherence to the diet modification and activity goals for weight loss. Conventional tactics include self-monitoring of food intake and exercise, reduced portion of meals and number of times of food intake, intellective restructuring, problem solving, and prevention of regression. The primary aim of behavior modification therapy is to change eating pattern and exercise practices to promote weight loss (CDC, 2011).
Components of behavioral therapy
Self-monitoring: This is one of the main elements of behavior therapy in obesity. Self-monitoring includes maintaining food dairies and activity logs (Guare J.C., et. Al., 1989).
Stimulus Control: This is the second key element in behavior therapy. In this element, focus is placed on altering the environment that initiates eating and modifying it to help prevent overeating. Stimulus control includes proper purchase of food items, excluding energy-dense processed food and introducing more fruits and vegetables (Wing R.R., 2004)
Slower eating: Reducing the speed of eating so as to allow signals for fullness come into play.
Goal setting: Setting realistic goals for one’s self or setting goals for patients as appropriate (Bandura A. & Simon K.M., 1977).
Behavioral contracting: Reinforcing of successful outcomes or rewarding good behaviors plays a key role (Volpp K. G., et. al., 2008).
Education: Nutritional education is a necessary component of a successful behavior therapy for obesity. A structured meal plan in conjunction with consultation with a dietician will be helpful (Pedersen S. D., et. al., 2007).
Social support: Behavioral modification is more sustainable in the long term when there is social support. Enhancing social support is essential for behavioral therapy (Avenell A. et. al., 2004).
Physical activity
Physical activity is the third component of non-surgical weight loss interventions and lifestyle modification. The advantages of physical activities include promoting negative energy balance by maximizing calorie expenditure, preserving fat-free part during weight loss, and improving cardiovascular fitness. Physical activity, however, is ineffective in weight loss in the absence of diet modification. The greatest benefit of physical activity is in facilitating the maintenance of weight loss (Pronk N.P & Wing R.R. 1992). Case studies have shown that people who exercise regularly are more successful in maintaining weight losses than are those who do not exercise. Kayman S., Bruvold W., Stern J.S. 1990; Klem M.L., Wing R.R., McGuire M.T., Seagle H.M., Hill J.O.1997). Additional evidence comes from randomized trials. Participants who receive diet plus exercise maintain greater weight losses 1 year after treatment than do those who receive diet alone, although the differences are not always statistically significant (Wing, R.R. 1999).
PREVENTION预防
Obesity is a long-lasting medical condition, which is linked with several debilitating and life-threatening conditions. The increasing rate of obesity globally is a public health concern (Srinivas N., et. al., 2004). Hence an effective way to control obesity requires strategies that would tackle the major issues relating to prevention (Srinivas N., et. al., 2004). The treatment and prevention of obesity are interrelated. The prevention of obesity involves several levels i) Primary ii) Secondary iii) Tertiary (Timothy P.G., 1997).
肥胖是一种长期的疾病，它与几种衰弱和威胁生命的疾病有关。全球肥胖率的上升是一个公共卫生问题(Srinivas N.等人，2004年)。因此，控制肥胖的有效方法需要能够解决与预防相关的主要问题的策略(Srinivas N.等人，2004年)。肥胖的治疗和预防是相互关联的。肥胖的预防包括以下几个层次:i)一级ii)二级iii)三级(Timothy P.G.， 1997)。
Primary prevention: The goal of primary prevention is to reduce the number of new cases. Diet modification/ healthy diet habits is a primary way of preventing obesity. Sedentary life style which is one of the causes of obesity can be prevented by appropriate exercises and activities that help burn out excess calories in the body and also prevent accumulation of fat. Simple habits ranging from 30 minutes walk in a day to weekly work out at the gymnasium can go a long way in maintaining a healthy weight. Health education is also very important in this aspect because some individuals in the community are unaware of the health implications of their habits. Appropriate health education programs should be organized to increase awareness. Accessibility to healthy food is also an important factor in the prevention of obesity. Formulations of policies that would facilitate healthy eating habit should be adopted by the Government; this would go a long way in reducing the economic effects of obesity and the burden on the Nation’s resources. Policy and environmental approaches that make healthy choices available, affordable and easy can be used to extend the propagation of strategies designed to raise awareness and support people who would like to make healthy lifestyle changes (CDC, 2011).
Secondary prevention: Secondary prevention is to lower the rate of established cases in the community (Srinivas N., et. al., 2004). Secondary prevention includes strategies to diagnose and treat an existing medical condition in its early stage to avoid complications. (Jeffery G.K., 2014).
Tertiary prevention: Tertiary prevention is to stabilize or reduce the amount of disability related to obesity ((Srinivas N., et. al., 2004). For those who are already obese and showing signs and symptoms of complications, there are clinical preventive maintenance and treatment regimes (Srinivas N., et. al., 2004). These treatment includes medications and increase in fruit and vegetable consumption. Some extreme cases may include surgery and this is used usually when BMI exceeds 30kg/m2 or 40 kg/m2 and when other treatment options have failed. Examples of surgical procedures to treat obesity and its complications includes gastric partitioning and gastric by-pass (Srinivas N., et. al., 2004).
三级预防:三级预防是为了稳定或减少与肥胖相关的残疾数量((Srinivas N.等，2004年)。对于那些已经肥胖并出现并发症迹象和症状的人，有临床预防性维持和治疗方案(Srinivas N.等人，2004年)。这些治疗包括药物治疗和增加水果和蔬菜的摄入。一些极端的病例可能包括手术，通常在BMI超过30kg/m2或40kg /m2以及其他治疗方案失败时使用手术。外科手术治疗肥胖及其并发症的例子包括胃分区和胃旁路(Srinivas N.等，2004年)。
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