Obesity: History, BMI Classification, Determinants and Effects

fleshiness History, BMI Classification, De depotinants and EffectsOBESITY corpulency is fast graceful a serious plaguey in the United States payable partly to con affectionatenesse habits and personal in application amongst Ameri lots. According to the Centre for Disease Control, lxxiii part of bragging(a)s and 43 percent of all children in the United States ar grievous or heavy. Among Afri advise-Ameri plentys 20 years and over, to a greater extent than than than deuce-thirds ar over loading down or telling (Gaines, 2010). Generally, the survey of over pitch and fleshiness ar soaringer(prenominal)(prenominal) for African-American and Hispanic wo hands than Caucasian women, spirited in the s bulge outh and midwestern United States and pluss with age (Ogden et al., 2014 Gregg et al., 2009 Sherry et al., 2010). According to the World wellness Organization, dead embody mass indication (BMI) of an grave person has a value greater than or come about to to thirty. Type 2 diabetes and steep blood air pressure be two sicknesss that ultimately affect African Americans and this is predominantly get alongd by an increase in encumbrance as those extra pounds predisposes a person to these diseases (Gaines, 2010). corpulency is wholeness of the primary bump factor for effect diseases, diabetes and a number of crab louses and these argon major causes of death in American today. The wellness implication of corpulency and the complications associated with it is increasely becoming more detrimental than cigargontte smoking and has thusly compel ace of the major preventable causes of death worldwide.Thisinvestigation wallpaper focuses on the brief history of corpulency this provide take fleshiness from its find over 2000 years to this present day. An understandingof the BMI classification, aetiological determinants, pathophysiology andhealth do is important if fleshiness prevalence will be curtailed.Furthermore, the socio fr ugal impact of corpulency counsel on the UnitedStates miserliness will be looked into. Finally, its discourse options, taproomand trends of the disease will be discussed. annals OF OBESITYThe old-fashioned Greeks were the initiatory to acknowledge fleshiness as a health disorder andthis was hike up recognized by the Ancient Egyptians in a similar authority.According to Hippocrates, corpulence is non only a disease itself, only if theharbinger of other diseases (Haslam & James, 2005). Hippocrates which wasthe Ancient Greek spawn of Western medicine acknowledged fleshiness in his workand expatiate of various diseases including diabetes was first contri aloneen by him.Another Indian surgeon Sushruta, a corresponding discovered the linkup among fleshiness, diabetes and heart diseases and he was the first person to find outthe significant signs, symptoms, causes and health implications. In the Ancientdays, man always strived for forage repayable to scarcity or pauc ity and this extendedin fleshiness being regarded as a sign of riches and good fortune in the middleage. However, all this salmagundid when the scientific indian lodge of the twentieth centuryrevealed the medical implications of corpulency (Caballero B., 2007)Withthe inception of the industrial revolution, body surface and strength of soldiersand workers became pertinent as this was attri stilled to the military andeconomic advocator of Nations (Caballero, 2007). The increase in the add up bodymass office from skinny to the linguistic rule on the BMI charts played an important image in the ontogenesis of industrialized societies (Caballero, 2007). in that locationfore in the 19th century, in that respect was anincrease in lading and round top generally. However, during the 20th century, thegenetic potentials for height was reached and this mattered to cargoincrease more than height in this century and thus resulted in the modal(a)increase in BMI (Caballero, 2007). In human evolution, for the first sentence, thenumber of adults with extra weight exceeded the number of those who wereunderweight which further led to fleshiness (Caballero, 2007). Theperceptions of the humanity as regards levelheaded body weight varied from thoseregarded as median(prenominal) in the western federation, plainly this perception was changed inthe beginning of the 20th century. in that respect was a reduction in the weight seen asnormal since 1920s and this was evident by the 2% increase in average height ofthe Miss America pageant winners and a 12% belittle in weight mingled with year 1922and 1999 (Rubinstein & Caballero, 2000). Also, the perception of close to heap as regards healthy weight has changed, for example in Britain the weightat which people regarded themselves to be stoutness was considerably higher in2007 than in 1999 (Johnson & Wardle, 2008). Obesity is still regarded as anindication of wealth and well-being in galore(postnominal) parts of Africa and this has becomemore widespread since the HIV epidemic began (Haslam & James, 2005).BODY MASS INDEX(BMI) CLASSIFICATIONAccordingto the World Health Organization, frame muss Index (BMI) is a simple index ofweight-for-height that is normally used to classify underweight, normal weight,overweight and obesity in adults. It is delimit as the weight in kilogramsdivided by the squ ar of the height in metres (kg/m2) (W.H.O. 2004). Forexample, an adult who weighs 60kg and whose height is 1.65m will feed a BMI of22.0. BMI= 60 kg / (1.65 m2) = 60 / 2.72 = 22.04 LEAN BODY MASS cant over dust ken is a component of body composition, it is calculated by subtractingbody lucubrate weight from extreme body weight. Total body weight is lean plus plonk. In equations LBM= BW BFLean Body Massequals Body incubus minus Body FatLBM + BF = BWLean Body Massplus Body Fat equals Body WeightLean Body Weight(men) = (1.10 x Weight(kg)) 128 ( Weight2/(100 x Height(m))2)Lean Body Weight(wo men) = (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)2The table be ruggedfurther pardons the classification of BMI in relation to the weight and heightof an soul. table 1 The International Classification of adult underweight, overweight and obesity harmonize to BMI Source Adapted from WHO,1995, WHO, 2000 and WHO 2004.BMI values argon agedependent and are the same for twain males and females (WHO, 2000). The health risk of infections associated with increasing BMI are many and the interpretation of BMIvalues in relation to risk whitethorn vary for opposite states in different geographicallocations (WHO, 2004). aetiologyDETERMINANTS OF OBESITYObesity is a heterogeneous crowd of conditions with numerous causes, it is not merely a single disorder and it is predominantly expressed phenotypically (Susan A.J, 1997). Obesity is h ereditary, moreover the genetic component does not follow simple Mendelian principles and the violence of the geno token on the aetiology of obesity whitethorn be diminish or increased by factors that are non-genetic (Susan A.J, 1997). many(prenominal) factors condition the body weight, and these are interactions of genetic, environmental and psycho complaisant factors which are in relation to the fare of cleverness consumed and the amount of postcode expended and the resulting acting through the physiological mediators Table 1 The International Classification of adult underweight, overweight and obesity match to BMI of goose egg usance and sinew pulmonary tuberculosis and the resulting equilibrium between both (Susan A.J, 1997).ENDOCRINE ANDHYPOTHALAMIC DISORDERSCertainendocrinological disorders whitethorn lead to obesity, but this applies to a verysmall percentage of the full number of cases (Susan A.J, 1997). Theendocrinological determinants of obesity defy be en review articleed recently (BouchardC., Perusse L., Leblanc C., Tremblay A, & Theriault, 1988). The singledisorder that causes obesity in this group is hypothyroidism in which increasedweight occurs largely as a result of decrease vitality using up (Susan A.J, 1997).Other endocrinological factors contributing to obesity include Cushingssyndrome and disorders of corti courteroid metabolism, where weight pretend istypically accompanied by a distinctive prototype of fill out deposition in thetrunk, sex interior secretion disorders including hypogonadism in men and ovariectomy inwomen, insulinoma and growth hormone insufficiency (Susan A.J, 1997). The reportcauses of weight get through in these cases are the amount of free verve use. Certainhypothalamic tumors or damage to the hypothalamic part of the understanding as a resultof overabundanceive exposure to radiation, infectious agents or head trauma can alikelead to obesity with forsake in propensity find and hyp erphagia (Susan A.J,1997). A hypothalamic disorder is to a fault believed to be the foundation of anumber of congenital abnormalities which could in addition result in obesity, e.g.Prader-Willi syndrome, which is an abnormality that could be a primary cause ofobesity (Susan A.J, 1997).GENETIC lureAta universe of discourse take aim, the genetic modulate of obesity is expressed in terms ofheritability (Susan A.J, 1997). This refers to the percentage of the total passing in a character which is attributable to genetic factors (Susan A.J,1997). The heritability of obesity may be considered any in terms of thetotal fatness of an private or the distribution of body fat in an individualistic(Susan A.J, 1997). Several discoveries place upright been made over the years regardingthe twist of genetics on degenerative diseases like cardiovascular disease andobesity (R. C. Whitaker, J.A. Wright, M.S. Pepe, K.D. Seidel, &W.H. nutrimentz.,1997). Recent reports demonstrate that at lea st 32 genes contribute to commonforms of obesity. Many of these genes are thought to be related to to to the victimisation of obesity through the deregulation metabolic hormones in the body(Susan A J, 1997).The obesity related mixed in the fat massand obesity-associated protein also know as alpha-ketoglutarate-dependentdioxygenase foreign terrorist organization, has reddened interest in pediatrics due(p) to its relationshipwith increased weight and ponderal index at 2 workweeks of age (A. Lopez-Bermejo,C.J. Petry, M. Diaz, et al., 2008). FTO is located on the long arm of thechromo or so 16 and is expressed in the brain, particular propositionally the hypothalamicnuclei (Khung E. Rhee et al. 2012). Those who are homogenous for the at-riskallele devour been found to be 3kg heavier than those who do not nominate the allele(T.M. Frayling, N. J. Timpson, M. N. Weedon et al. 2007). This weight gain is possible due to the genes involvement in the regulation of push use of goods and services (KhungE. Rhee et al. 2012). According to recent studies, individuals carrying theat-risk allele prefer dense might fodders (J.E Cecil, R. Tavendale, P. Watt, M.M. Hetherington, & C.N.A Palmer, 2008), have inhibitd olfactory sensation of satiety (J.Wardle, S. Carnell, C.M.A. Haworth, I.S. Farooqi, S. ORahilly, & R.Plomin, 2008), queer sledding of keep back over ingest (M. Tanofsky-Kraff, J.C.Han, K. Anandalingam et al. 2009), consume more fat and small calories (even afteradjusting for BMI) (N. J. Timpson, P.M. Emmett, T.M. Frayling, et al. 2008) anddisplay a greater tendency towards consuming palatable fares after eating arepast (J. Wardle, C.Llewellyn, S. Sanderson, & R. Plomin, 2009). Therefore,FTO isnt associated with brawniness expenditure, but it increases the facultyof individuals to higher calorie custom and decreased satisfaction. Ameta- analysis of 45 studies found that adults who were physically activeattenuate the odds of obesity associated wit h FTO by al or so 30% (T.O.Kilpelainen, L. Qi, S. Brage, et al. 2011). Thus carrying a gene for obesitydoes 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 anobesogenic environment (Khung E. Rhee et al. 2012).Numerousstudies in different ethnic groups advert that the familial correlation in thetotal body fatness, expressed as body mass index, (BMI kg/m2) from parent tooffspring 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 beexpected, studies of twins come on a much higher concent proportionn, in particular inmonozygotic pairs (Susan A.J, 1997). However, these findings do not segregatethe independent encumbrances of genetic transmission and a shared environment (SusanA.J, 1997). Further studies of twins reared apart attribute 50-70% of the divergence in BMI in later life to genetic factors (Stunk ard A, Harris J,Pedersen N, McClearn G. 1990). Adoption studies, where an individual is comparedboth to their biological parent and their comeed parents, have also demo the importance of genetic influences (Susan A.J, 1997). There is astrong relationship between the BMI of the adoptee and their biological parentsacross the entire send of fatness, but no relationship between the adoptee andtheir adoptive parents (Stunkard A, Sorensen T, Hanis C. et al. 1986).Studiesof fat distribution have considered both the ratio of subcutaneous to total fatmass and the distribution of subcutaneous fat in the trunk relative to thelimbs (Susan A.J, 1997). Data from the Quebec Family Study, suggest that thesize of the internal fat stores are more strongly influenced by genetic factorsthan subcutaneous depots (Bouchard C., Perusse L., Leblanc C., Tremblay A,Theriault, 1988). Familial clustering suggests that genetic factors may business relationshipfor 37% of the dissonance in the trunk to extremi ty skin fold thickness ratio(Rice T, Bouchard C, Perusse L, Rao D. 1995). These combined curtilage fromthese genetic analysis suggests that obesity is a heritable disorder and that aconsiderable proportion of the variance is non-additive (Susan A.J, 1997). Thiswould explain the higher correlations between siblings than those betweenparent and offspring, and the 2-fold greater correlation between monozygoticthan dizygotic twins (Susan A.J, 1997). These genetic influences seem tooperate through supersensitised genes the occurrence of the gene increases therisk of developing a characteristic but not essential for its expression nor isit, in itself, sufficient to explain the breeding of the disease (Susan A.J,1997). Unlike carnal models, where a number of single genes can lead toobesity, no human obesity gene has yet been characterized, but theheterogeneous nature of human obesity does not preclude the realization ofsmall number of individuals with a single defect which leads to o besity (SusanA.J, 1997). In man, a number of genetically determined conditions result inexcess body weight or fatness (e.g Prader-Willi syndrome or Bardet-Biedlsyndrome), but these account for only a very small proportion of the obesepopulation (Susan A.J, 1997).PHYSIOLOGICALMEDIATORSEnergy expenditureStudiesin animals have postulated that at the cadence of give, a precious increasein metabolic rate may deplete the excess energy thus reducing the rate ofweight gain below theoretical values (Rothwell N., Stock M., 1983). Geneticallyobese animals tend to gain more weight than their lean controls even when theyare pair-fed, thus implying a greater metabolic rate (Thurby P., Trayhurn P.,1979). virtuoso affirmable explanation for this effect is the decrease in diet-inducedthermogenesis which is slightened in animal models of obesity due to a decreasein the sympathetic activating of brown adipose tissue (Rothwell N., Stock M.,1983). These unequivocal effects on energy expenditure in obese animalscontrast with the paucity of secern in human beings (Susan A Jebb, 1997). Susan A.J(1997) stated that in obese humans, in that location have been constant reports ofabnormally low energy intake which in maneuverly imply that at that place essential be a defectin energy expenditure. There are three basic elements to energy expenditurewhich have each been the focus of extensive research.Basal Metabolic targetIn1997, Susan A Jebb defined primary(a) or resting metabolic rate as the energyexpended by an individual at rest, following an nightlong fast and at acomfortable environmental temperature in the thermo nonsubjective range. Severalstudies of basal metabolic rate have cerebrate that obese subjects have ahigher BMR compared to their lean counterparts. Researchers like Swinburn B.& Ravussin E, account that al around 80% of the inter- individualvariance in BMR can be accounted for by age, fat-free mass, fat mass andgender. Nevertheless, this still gives manner for some likelihood thatinter-individual dissimilitude in BMR which may influence individuals with arelatively low BMR to become obese (Susan A. Jebb, 1997). Diet inducedthermogenesis Anumber of studies have suggested that the post-prandial increase in energyexpenditure is attenuated in obese subjects, perhaps due to decreasedSympathetic Nervous System activity (Astrup A. 1996). Similar effects have alsobeen demonstrated in the post-obese. However this is not a unvarying finding,even among studies from the same research lab. A recent review by Ravussin E.& Swinburn B. (1993) place 28 studies in favour of a defect inthermogenesis in humans and 17 against. However, since thermogenesis accountsfor only a fraction of total energy expenditure (approximately 10%), thepotential for a significant effect on total energy expenditure is insufficient(Susan A. Jebb 1997). somatogenic activity Themost significant component of energy expenditure is physical activity which mayrepresent 20-50% of total energy expenditure. Studies of fidgeting movements inPima Indians within a whole-body calorimeter have shown significantinter-individual variations in the daily energy cost of these actions from400-3000 kJ/day, with low levels prophetical of subsequent weight gain at leastin males but not females (Zurlo F., Ferraro R., Fontvielle A. et. al. 1988).However, in free-living conditions, the freedom to undertake conscious physicalactivity or role increases the inter-individual variability even further(Susan A Jebb). Research in this area has been hampered by imprecision in themethods to measure physical activities which have include various actometers,heart rate monitoring, activity diaries and direct observation (Susan A. Jebb,1997).Theenergy requirements of an individual encompass the summation of basalexpenditure, thermogenesis and physical activity. A whole-body calorimeter canbe used to measure the total energy expenditure of an individual. The analysisof total energy expe nditure in 319 obese subjects clearly demonstrates asignificant increase in energy expenditure with increasing body weight much(prenominal)that individuals with a BMI in excess of 35 kg/m2 have energy expenditureapproximately 30% higher than those with BMI less than 25 kg/m2 (Susan A Jebb,1997). The expectant difficulty with these studies , as stated by Susan A.Jebb in 1997 is that the increase in energy expenditure seen in obese subjectsas a result of their increased body size may mask pre-existing metabolicdefects in the pre-obese state which exposes the individual to excessive weightgain. However, in experimental overfeeding researches, there is no remarkabledifference in the dot of weight gain between lean and obese subjects whenmatched for their excess energy intake (Diaz E. Prentice A. M et. al.1992). Studies of total energyexpenditure in post-obese subjects have not arrived at a definite conclusionsome studies show no difference in energy expenditure in the post-obese rel ativeto never-obese controls (Goldberg G.R., et. al. 1991), whilst others show amodest suppression of energy expenditure (Geissler C. Miller D., Shah M. 1987).In general, there is little evidence to co-occurrence the dead reckoning that humanobesity may be due to a specific defect in energy expenditure in predisposedindividuals (Susan A Jebb, 1997). Susan A Jebb further stated that advocates ofa metabolic basis to obesity, solicit that only very small differences in energyexpenditure are neccessary to produce significant weight gain over many years,and this difference may be dismay than the limits of precision of even the mostsophisticated methodology.Energy IntakeThe 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 forage intake to explain the aetiology of obesity (Susan A Jebb, 1 997). The increase in energy expenditure associated with the development of obesity should automatically help to prevent continue 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, normally lean individuals are able to charm intake to match energy requirements over a wide range of energy requirements yet those who become obese seem unable to reach this symmetricalness (Susan A Jebb, 1997).Breakthrough in discerning the role of energyintake in the aetiology of obesity has been critically disconcerted byunder-reporting which is now largely recognized as a feature of obesity (SusanA Jebb, 1997). Comparisons of energy intake and energy expenditure betoken lucid shortfalls in self-reported intake, averaging approximately 30% ofenergy requirements in obese subjects (Prentice A.M., contraband A.E., Coward W.A.,1986 Lichtman S., Pisarska K., Berman E., et al., 1993). This phenomenon alsoextends to post-obese subjects and to others who may be very weight conscious(Susan A Jebb, 1997).Under-reportingmay be cause by several factors and it is natural for individuals to changetheir eating warning when they are to record their food intake. This is usually associated with a reductionin intake as subjects consciously or sub-consciously adopt a self-imposeddiet. (Susan A Jebb, 1997). Therefore they might give accurate results abouttheir intake for that duration, but it may not be a true representation oftheir habitual pattern. Forgetfulness, underestimation of meal size and lack ofbasic knowledge of food consumption can also lead to under-reporting. Although,it is possible to have falsification and fabrication of dietetic records, thereare also instances of self-deception or deliberate manipulation of dietaryrecords.Recentresearch into the zest control system by Blundell J. Bouchard C., labour G.(1996), has identified a network of synchronous interactions which governeating conduct. These effects are mediated through the central nervous systemparticularly the hypothalamus, where a number of neuropeptides appear toregulate feeding way 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 lessable to accurately compensate for the energy content of the preload at asubsequent meal than lean subjects. However, these studies are usually of shortduration in laboratory settings and may not accurately reflect eating behaviorin a naturalistic setting, where knowledge of foods consumed and conditionedlearning may submit other regulatory processes (Susan A Jebb, 1997). Thereis also significant evidence that the individual macronutrients (protein, fat,carbohydrate and alcohol) have different influences on eating behavior, majorlydue to their effects on satiety (Stubbs R., 1995). Experimenta l studies ofmanipulated foods and retrospective analyses of dietary records suggest thatprotein is the most satiating (DeCastro J., 1987 Hill A., Blundell J., 1990).Carbohydrate is also an efficient inhibitor of later food consumption, at leastin the short terms, meal-to-meal context (Rolls B., et al. 1994). Fat seems tohave a satiating capacity (Lawton C., Burley V., 1993). Fat hyperphagia occursduring a single meal due to subjects overeating high fat foods and is alsoknown as resistless over consumption. In 1994, Poppitt S., stated that fat has two generation the energy per gram of carbohydrate or protein which may be due to thelevel of energy density and not necessarily a characteristic of dietary fat.Appetite is said to be plagued by alcohol and according to DeCastro J &Orozco (1990), in free living circumstances, alcohol consumption with meals isassociated with higher energy intakes, but this may also reflect that alcoholis more likely to be consumed on special occasions whic h in themselves areassociated with increased food intake.Basically,taste preference can have an effect on the amount of food consumed and the kindof food. The individual preference for true meals would mention them more likely to consume more of that meal.Therefore, sensory preferences plays a role on energy balance since is itassociated with energy intake. According to Witherley S, Pangborn R & SternJ (1980), several reports of sensory preferences for particular food groups inassociation with obesity, but inter-subject variability is so great as to flurry any underlying obese-lean differences. The relationship between sensorypreference for fat versus net profit and BMI was pinpointed by Drewnowski in 1992. grave women had preference for foods with high fat to sugar ratio period womenwith low BMI had preference for high sugar to fat ratio, whence increase inweight is closely related to increase for fatty foods. take infrequency has effect on weight gain, because people who eat s everal small mealsat intervals have less weight than those that eat fewer meals in larger cadence and therefore large quantity of food consumed at a time may be a riskfactor for obesity, however, studies as regards this, showed no remarkablerelationship (Bellisle F, McDevitt R, Prentice A.M. 1997). Research in thisarea is contradicted by under-reporting of food consumption in obese subjectsand by post-hoc variations in eating patterns as a result of obesity andefforts to control weight (Susan A Jebb, 1997). Eating frequency in obesesubjects is however an unre conceivable blueprint to the eating patterns involved inthe aetiology of obesity (Susan A Jebb, 1997).ENVIRONMENTALINFLUENCEObesogenicenvironment which was first coined in the 1990s, in a bid to explain thepresent obesity epidermic. According to King D (2007), obesogenic environmentis the sum of the influences that the touchs, opportunities or conditionsof life have on promoting obesity in individuals and populations. Thisenco mpasses the cultural, social and infrastructural conditions that affect theability of a person to embrace a healthy lifestyle. Individuals in a populationrespond to unhealthy environment and the more urbanized the environment, themore individuals are pressurized to adopt unhealthy habits. The pressure fromthe surrounding makes it difficult for individuals to change their lifestyle andpractice healthy habits when the environment itself is unhealthy. environmentalfactors may have a critical effect in the development of obesity by unmaskinggenetic or metabolic susceptibilities (Susan A.J, 1997). environmentalinfluences on diet involve a wide range of factors including handiness tofood and high calorie drinks. Eating habits are commonly influenced by theavailability and accessibility of unhealthy food, which is an importantconsideration in the effect on obesity. Studies in the United States recommendthat the availability of high quality, affordable healthy food is limited forpeople wh o reside in low-income communities and much(prenominal) scarcity is associatedwith unhealthy diet and obesity (White 2007) .However despite several epidemiologicalstudies that shows environmental influences play an important role in theaetiology of obesity, it is a fact that some people within the same unhealthyenvironment still managed to chief(prenominal)tain a healthy weight (Susan A.J, 1997).PSYCHO-SOCIAL INFLUENCESFoodis sometimes used as a coping mechanism by individuals with weight issues, in particular when they are unhappy, nervous, stressed, bored and depressed. Inmany obese individuals there seems to be a perpetual cycle of mood disturbance,overeating, and weight gain (Jennifer C. Collins & Jon E. Bentz 2009). Whenthey feel frustrated, they rely on food for comfort, even though this copingmechanism may pacify their mood, the resultant weight gain that results maycause a dysphoric mood due to their unfitness to control their stress (JenniferC. Collins & Jon E. Bentz, 20 09). Eventually a guilty feeling may restartthe cycle and might steer a habitual pattern of eating food to get comfort.This habitual pattern is specifically significant if there is a genetic riskfactor 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. Inaddition to depression and anxiety, other risk factors include ruffianlyeating behaviors such as mindless eating, frequent snacking on high caloriesfoods, overeating, and night eating (Glinski J., Wetzler S., Goodman E.2001).American Psychiatric tie has currently included Binge eating disorder(BED) in an appendix of the Diagnostic and statistical Manual of MentalDisorders (DSM-IV-TR) and is characterized by recurrent episodes of eatingduring a distinguishable period of time (at least 2 days a week over a 6 monthperiod) eating large quantity of food than majority of the people would eat atthe s ame time a feeling of loss of control during the episodes and guilt or excruciation 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 thegeneral population and between 10% and 25% of the bariatric population. Animportant differentiation pointed out by the American Psychiatric Association,between BED and bulimia/anorexia is that BED is not associated with any regularcompensatory behaviors, such as purging, fasting, or excessive pattern. It cantherefore be implied that the majority of individuals with BED are overweight.Nighteating, which was first identified in 1955 as another disorder that can lead toremarkable weight gain, though night eating syndrome (NES) is not currentlyrecognized by the American Psychiatric Association as a distinct diagnosis inthe DSM-IV-TR. Night eating syndrome is characterized by excessive lat e nightconsumption ( 35% of daily calories after the evening meal), unhealthyeating patterns, dayspring anorexia, insomnia, and distress (Stunkard A. J.,Grace W. J. & Wolff H. G. 1955). NES occurs in approximately 1% of thegeneral population and an estimated 5-20% of the bariatric population (WaddenT.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 thatincludes a delay of appetite in the mornings and the continuation of appetiteand over consumption of food during the night (Jennifer C. Collins & Jon E.Bentz, 2009).PATHOPHYSIOLOGY OFOBESITYThereare several possible pathophysiological mechanisms involved in the advancementand continuation of obesity. This field of research had been almostunapproached until the leptin gene was discovered in 1994 by J. M. Friedmanslaboratory (Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L.,Friedman, J.M., 1994). These researchers proposed that l eptin was a satietyelement. However, soon after J. F. Caros laboratory could not as certain(a) anymutations in the leptin gene in humans with obesity. In 1995, Considine, RVConsidine, EL Williams, CJ Nyce, MR Magosin, SA Bauer, TL Rosato, ELColberg, J., & Caro, J.F. proposed a contrary view that Leptin expressionwas increased, postulating the possibility of Leptin-resistance in humanobesity. Since the discovery of leptin, insulin, ghrelin, orexin, cholecystokinin,adipokines, peptide tyrosine tyrosine, as well as many other mediators havebeen researched. The adipokines are intermediators produced by adipose tissuetheir action is thought to revise many obesity-related diseases. Leptin andghrelin are considered to be interrelated in their effect on appetite, withghrelin produced by the stomach regulating short-term appetitive control (i.e.hunger pangs when the stomach is empty and satiety when the stomach isstretched). Leptin is created by adipose tissue to request fat storagereservoi rs in the body, and mediates long-term appetitive controls (i.e. to eatmore when fat storages are low and less when fat storages are high). Although judgeship of leptin may be effective in a small subset of obese humans whohave deficiency in leptin, most obese humans are considered to be leptinresistant and have been found to have high levels of leptin (Hamann A., &Matthaei S. 1996). This resistance is thought to explain in part why ecesis of leptin has not been shown to be effective in suppressingappetite in most obese people ( measure J.S. 2004).Leptinand ghrelin act on the hypothalamus and are produced peripherally. They controlappetite through their actions on the central nervous system. They act on thehypothalamus, a realm of the brain central to the coordination of foodconsumption and energy expenditure. There are several circuits within thehypothalamus that contribute to its performance in integrating appetite, themelanocortin pathway being the most well understood (Flier J .S. 2004). Thecircuit starts with an region of the hypothalamus, the arcuate nucleus, thathas outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus(VMH), the brains feeding and satiety centers, respectively (Boulpaep, EmileL., Boron, & Walter F. 2003).Accordingto Flier J.S. (2004), the arcuate nucleus contains two distinct groups ofneurons the first group co expresses neuropeptide Y (NPY) and agouti-relatedpeptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs tothe VMH and the second group coexpresses pro-opiomelanocortin (POMC) andcocaine- and amphetamine-regulated transcript (CART) and has stimulatory inputsto the VMH and inhibitory inputs to the LH (Flier J.S. 2004). Consequently,NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neuronsstimulate satiety and inhibit feeding (Flier J.S. 2004). Both groups of arcuatenucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRPgroup while bear upon the POMC/ CART group (Flier J.S. 2004). Researches done by Flier J.S., 2004, thusconcluded that a deficiency in leptin signaling, either via leptin deficiencyor leptin resistance, leads to overfeeding and may account for some genetic andacquired forms of obesity. EFFECT ON healthObesityis a severe medical condition and a chronic health issue worldwide. Theassociation between body weight and mortality rate is a subject of concern, particularly in regards to the optimal weight for higher stead (JoAnn E. Manson,M.D., Walter C. Willett, M.D., et al, 1995). The significance of understandingthe true relationship between weight and mortality is underlined by theincreasing prevalence of obesity in the United States (Kuczmarski RJ, et al,1994) especially women (Harlen WR, et al, 1988). Obesity is a major risk factorfor cardiovascular diseases (e.g., heart disease, stroke and high bloodpressure), diabetes (e.g. type 2 diabetes), musculoskeletal disorders (e.g., degenerative joint disease), some ca ncers (e.g., endometrial, breast, and colon cancer),high total cholesterol or high levels of triglycerides, colored and gallbladderdiseases, sleep apnea and respiratory tasks, reproductive healthcomplications such as infertility and mental health conditions (WHO, 2012).Obesity and crabby personObesepeople 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 obesewomen also have a 50% higher likelihood of dying from breast cancer (WeightManagement Centre, 2010). special to obesity, cancer has recently been joined to diet and physical activity side (Bray 2004, Barnard 2004, Wiseman2008). The cancers most significantly associated with obesity in women arecervical, uterine, kidney, breast and endometrial cancer and in men are colon,pancreatic and liver cancer (Calle, Rodriguez, Walker-Thurmond & Thun2003). One study, using matter Cancer Institute Surveillance, Epidemiology,and End Result s data, estimated that in 2007 in the United States, about 34,000new cases of cancer in men (4 percent) and 50,500 in women (7 percent) were dueto obesity. The percentage of cases attributed to obesity varied widely fordifferent cancer types but was as high as 40 percent for some cancers,particularly endometrial cancer and esophageal adenocarcinoma (National CancerInstitute, 2012).Obesity andcardiovascular disordersCardiovasculardisease (CVD) is one of the major cause of death in U.S. Obese people are moreliable to die from CVD largely due to accelerated atherosclerosis,hyperlipidaemia, loss of glyceamic control and hypertension. Until recently therelationship between obesity and coronary heart disease was viewed as indirect,i.e., through covariates related to both obesity and coronary heart diseaserisk (Lew E.A., Garfinkel L., 1979) including hypertension dyslipidemia,particularly reductions in HDL cholesterol and impair glucose tolerance ornoninsulin-dependent diabetes mellitus. Insulin resistance and accompanyinghyperinsulinemia are typically associated with these comorbidities (Reaven G.M.,1988). Although most of the comorbidities linking obesity to coronary arterydisease increase as BMI increases, they also relate to the total distributionof body fat. Long-term longitudinal studies, however, indicate that obesity assuch 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 grow is mostly seenin patients with obesity and is related to systemic hypertension and may be relatedto the severity of obesity. Hypertension is approximately three times morecommonly found in obese individuals than normal-weight persons (Van ItallieT.B., 1985). This relationship may be directly related such that when weightincreases, there is an increase in blood pressure (Kannel W.B., Brand N., etal., 1967) and when weight decreases, blood p ressure also decreases (Reisin E.,Frohlich E.D., et al., 1983). Obesity and mentalhealthIndividualsdiagnosed with obesity tend to be less favorable on all levels of thepsychological assessment and may exhibit several symptoms ranging from meresadness to chronic depression. Evident are more episodes of mood swings,anxiety, personality and eating disorders, basically related to or associatedwith obesity experienced by individuals with obesity (Pickering, Grant, Chou,Compton 2007). Obesity may be an inception of psychiatric manifestations andvice versa and is related to psychosocial deterioration and bias ground onweight. This comprises of loss of self-worth, and reduced self-esteemassociated with stigmatization. Stigmatization can further lead to desolationand withdrawal and thus many obese individuals anticipate solace in binge eating,thereby gaining more weight. Based on reports from Roberts, Deleger,Strawbridge & Kaplan 2003 Herva, Laitinen, Miettunen, Veijola, Karvonen& Lasky 20 06 Kasen, Cohen, Chen &Must 2008, concern, shame and guiltassociated with low self-worth, which is finally related to excessive foodconsumption completes the obesity-mental disorder circle.Thereis bias and discrimination associated with obesity. They generally reportreduced quality of life and functional wellbeing, collectively calledHealth-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 2007Scott, Bruffaerts, Siomn, Alonso, Angermeyer, de Girolamo et al. 2008).Obesity anddiabetesDiabetesis usually a terminal illness. i.e. it is a long chronic diseasecharacterized by high levels of sugar in the blood. One of the major riskfactors for diabetes is obesity. Obesity is directly associated with Diabetes2. The association between obesity and type 2 diabetes are firmly establishedand without the intervention of a healthy diet and p roper exercise, obesity canlead to type 2 diabetes over a very short period of time. In fact, obesity is believed to account for80-85% of the risk of developing type 2 diabetes, while recent researchsuggests that obese people are up to 80 times more likely to develop type 2diabetes 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 2diabetes, especially if you have excess weight around your abdomen. Studiespostulates that abdominal fat causes fat cells to releases pro-inflammatorychemicals, which can reduce the bodys sensitivity to the insulin, this canalso disrupt the function of insulin responsive cells and their ability toreact to insulin. This is known as insulin resistance which is a primary activator for type 2diabetes. intemperance abdominal fat is a major high-risk form of obesity. SOCIO-ECOMOMIC/ financial COST OF OBESITYIn1999-2000, nearly 65 percent of U.S. adults were either obe se or overweight.Obesity accounts for $117 billion a year in direct and indirect economic cost.Obesity is associated with 300,000 deaths per year, and is fast becoming the leading(a) cause of preventable deaths (Mancino, Lin, and Ballenger, 2004).Certainly, obesity has become a large problem in America. Recent increase inmeal portions and reduction in availability of natural food production maypropose why people find it challenging to assign a healthy diet. Although,certain People have been flourishing at maintaining a healthy nutritional statusand avoiding this unhealthy situation. Gary Beckers human heavy(p) theory is agroundwork that helps to clarify the effect of weight status on the economy interms of the labor market outcomes for the individual. Human capital is the schoolingal qualification, job experience/training, and the health conditionthat workers devote their time in to boost their capacity and skills to berented out to employers (Ehrenberg and Smith, 2005). Healthy weight status inrelation to labour is a type of human capital investment. According to RobertPindyck and Daniel Rubinfeld (2004), When an investment decision is made, theinvestor commits to a current outlay of expenses in return for a stream of expected future benefits. Thesestated be for a healthy weight may include buying of food with highnutritional values and creating time for physical activities. As an investment,the individual sacrifices money, time and other resources to attain a healthyweight to become more productive in the future and, hence, earn higher income.Obese workers miss more days of work and inflict more cost on employersespecially in medical and disability claims and also workers requitalclaims. As a result, firms end up with extra costs associated with obesity,this is one of the economic effects of obesity. Obesityplaces significant burden on the society through health care expenditures anddisability payments combined through group health insurance and publicp rograms. The estimated annual medical cost of obesity in the U.S. was $147billion 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 directand indirect effect on the Nations resources, as more money is spent on theobese due to the high risk of comorbidity with other life threatening diseaseslike type 2 diabetes, osteoarthritis and cardiovascular diseases.TREATMENTThereare several weight-loss schemes available but many are ineffectual andshort-term, especially for those who are morbidly obese. The strategies forweight loss with non-surgical programs usually involve a combination of diet alteration, behavior modification therapy and appropriate exercise. DietaryModificationDietarymodifications for obesity are designed to create a negative energyintake-energy expenditure balance (i.e., calories consumed caloriesexpended) by reducing daily energy intake below the call for level. Therequired energ y varies by weight, sex and level of physical exercise suchindividuals with higher weights, more activity have greater energy needs,including men (Melanson K. & Dwyer J. 2002). Uniformly, higher energydeficits results in higher weight losses. start calorie diet is recommended forobese individuals and they are advised to check calorie content of meals beforeconsumption. Very low calorie diet is recommended for morbidly obeseindividuals with little or no success in low diet consumption.Behaviour TherapyTheoldest report of the use of behavioral therapy in the management of obesityoccurred in 1967. Since then, it has been widely used in the management ofobesity (Gupta R. & Misra A. 2007). Behavior therapy involves setting outgoals and principles to patients to aid their adherence to the dietmodification and activity goals for weight loss. Conventional tactics includeself-monitoring of food intake and exercise, reduced portion of meals andnumber of times of food intake, intellective re structuring, problem solving,and cake of regression. The primary aim of behavior modification therapyis to change eating pattern and exercise practices to promote weight loss (CDC,2011).Components ofbehavioral therapySelf-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) sluggish eating Reducing the speed of eating so as to consent to signals for fullness come into play.Goal setting Setting realistic goals for ones self or setting goals for patients as appropriate (Bandura A. & Simon K.M., 1977). Behavioral detec tion Reinforcing of successful outcomes or rewarding good behaviors plays a key role (Volpp K. G., et. al., 2008).Education Nutritional development is a necessary component of a successful behavior therapy for obesity. A structured meal plan in continuative 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 activityPhysicalactivity is the third component of non-surgical weight loss interventions andlifestyle modification. The advantages of physical activities include promotingnegative energy balance by maximizing calorie expenditure, preserving fat-freepart during weight loss, and improving cardiovascular fitness. Physicalactivity, however, is ineffective in weight loss in the absence seizure of dietmodification. The greatest benefit of physical acti vity is in facilitating the living of weight loss (Pronk N.P & Wing R.R. 1992). Case studies haveshown that people who exercise regularly are more successful in maintainingweight losses than are those who do not exercise. Kayman S., Bruvold W., SternJ.S. 1990 Klem M.L., Wing R.R., McGuire M.T., Seagle H.M., Hill J.O.1997). supernumerary evidence comes from randomized trials. Participants who receive dietplus exercise maintain greater weight losses 1 year after hatchment than dothose who receive diet alone, although the differences are not alwaysstatistically significant (Wing, R.R. 1999).PREVENTIONObesityis a long-lasting medical condition, which is linked with several debilitatingand life-threatening conditions. The increasing rate of obesity globally is a publichealth concern (Srinivas N., et. al., 2004). Hence an effective way to controlobesity requires strategies that would tackle the major issues relating toprevention (Srinivas N., et. al., 2004). The treatment and prevention ofobesity are interrelated. The prevention of obesity involves several levels i)Primary ii) supplementary iii) Tertiary (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. frank habits ranging from 30 minutes walk in a day to periodic 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 polici es 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 Nations 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 stagecoach 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). 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