Obesity: History, BMI Classification, Determinants and Effects

fleshiness History, BMI Classification, Determinants and EffectsOBESITY fleshiness is fast becoming a serious epidemic in the United States cod partly to take in habits and physiologic in application amongst Ameri keisters. According to the Centre for Disease operate, Seventy-three percent of adults and 43 percent of all children in the United States atomic number 18 ponderous or orotund. Among African-Americans 20 years and over, more than than two- ternarys are over pack or grave (Gaines, 2010). Generally, the rate of lowering and fleshiness are heightser for African-American and Hispanic women than whiteness women, senior higher(prenominal)er in the south and Midwest and augments with age (Ogden et al., 2014 Gregg et al., 2009 Sherry et al., 2010). According to the World Health Organization, body mass force (BMI) of an obese person has a appreciate great than or equal to thirty. Type 2 diabetes and high blood pressure are two unhealthinesss that ultimately aff ect African Americans and this is predominantly caused by an emergence in weight as those extra pounds predisposes a person to these diseases (Gaines, 2010). corpulency is one of the primary risk factor for heart diseases, diabetes and a subprogram of malignant neoplastic diseases and these are major causes of death in American today. The wellness implication of fleshiness and the complications associated with it is increasingly becoming more detri intellectual than cigarette smoking and has thence blend in one of the major preventable causes of death worldwide.Thisinvestigation paper focuses on the brief history of fleshiness this will takeobesity from its find over 2000 years to this present day. An understandingof the BMI classification, aetiological determinants, pathophysiology andhealth effect is important if obesity prevalence will be curtai lead.Furthermore, the socio economic impact of obesity management on the UnitedStates preservation will be looked into. Finall y, its preaching options, stripeand trends of the disease will be discussed. HISTORY OF OBESITYTheAncient Greeks were the scratch to acknowledge obesity as a health disorder andthis was further recognized by the Ancient Egyptians in a similar way.According to Hippocrates, adiposis is not only a disease itself, but theharbinger of other diseases (Haslam & James, 2005). Hippocrates which wasthe Ancient Greek Father of Western medicine acknowledged obesity in his workand details of various diseases including diabetes was first given by him.Another Indian surgeon Sushruta, to a fault discovered the joining betweenobesity, diabetes and heart diseases and he was the first person to find outthe evidentiary signs, symptoms, causes and health implications. In the Ancientdays, man always strived for food due to scarcity or deficit and this resultedin obesity being regarded as a sign of wealth and good fortune in the middleage. However, all this changed when the scientific society of th e twentieth degree Celsiusrevealed the medical implications of obesity (Caballero B., 2007)Withthe inception of the industrial revolution, body size of it and strength of soldiersand workers became pertinent as this was attributed to the military andeconomic power of Nations (Caballero, 2007). The step-up in the total bodymass index from underweight to the normal on the BMI charts played an importantrole in the development of industrialized societies (Caballero, 2007). thitherfore in the 19th century, at that place was anincrease in weight and height elementrally. However, during the 20th century, the inheritable potentials for height was reached and this resulted to weightincreasing more than height in this century and thus resulted in the averageincrease in BMI (Caballero, 2007). In human evolution, for the first time, thenumber of adults with supernumerary weight exceeded the number of those who wereunderweight which further led to obesity (Caballero, 2007). Theperceptions of the public as regards rose-cheeked body weight varied from thoseregarded as normal in the western society, but this perception was changed inthe start of the 20th century. There 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% strike in weight between year 1922and 1999 (Rubinstein & Caballero, 2000). Also, the perception of closepeople as regards well weight has changed, for example in Britain the weightat which people regarded themselves to be overweight was considerably higher in2007 than in 1999 (Johnson & Wardle, 2008). corpulency is palliate regarded as anindication of wealth and well-being in many parts of Africa and this has becomemore widespread since the HIV epidemic began (Haslam & James, 2005).BODY MASS power(BMI) CLASSIFICATIONAccordingto the World Health Organization, Body cumulus Index (BMI) is a simple index ofweight-for-height that is normally us ed to classify underweight, normal weight,overweight and obesity in adults. It is defined as the weight in kilogramsdivided by the square of the height in metres (kg/m2) (W.H.O. 2004). Forexample, an adult who weighs 60kg and whose height is 1.65m will make believe a BMI of22.0. BMI= 60 kg / (1.65 m2) = 60 / 2.72 = 22.04 LEAN BODY MASS toppleBody Mass is a lot of body composition, it is calculated by subtractingbody flump weight from total body weight. Total body weight is lean plus fat. In equations LBM= BW BFLean Body Massequals Body Weight 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(women) = (1.07 x Weight(kg)) 148 ( Weight2/(100 x Height(m))2) nonesuch(prenominal) 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 on a lower floorfurther explains the cl assification of BMI in relation to the weight and heightof an individual. delay 1 The International Classification of adult underweight, overweight and obesity according to BMI Source Adapted from WHO,1995, WHO, 2000 and WHO 2004.BMI values are agedependent and are the uniform for both(prenominal) males and females (WHO, 2000). The healthrisks associated with increasing BMI are many and the interpretation of BMIvalues in relation to risk may vary for assorted communitys in different geographicallocations (WHO, 2004).AETIOLOGYDETERMINANTS OF OBESITYObesity is a heterogeneous conclave of conditions with numerous causes, it is not merely a single disorder and it is predominantly express phenotypically (Susan A.J, 1997). Obesity is hereditary, but the genetic component does not follow simple Mendelian principles and the effect of the geno typecast on the aetiology of obesity may be decreased or increased by factors that are non-genetic (Susan A.J, 1997). Several factors determ ine the body weight, and these are interactions of genetic, purlieual and psychosocial factors which are in relation to the amount of push consumed and the amount of vital force expended and the resulting acting through the physiological mediators Table 1 The International Classification of adult underweight, overweight and obesity according to BMI of faculty stirring and energy outgo and the resulting equilibrium between both (Susan A.J, 1997).ENDOCRINE ANDHYPOTHALAMIC DISORDERSCertainendocrinological disorders may lead to obesity, but this applies to a very low-down part of the total number of cases (Susan A.J, 1997). Theendocrinological determinants of obesity exact been revaluationed recently (BouchardC., Perusse L., Leblanc C., Tremblay A, & Theriault, 1988). The singledisorder that causes obesity in this group is hypothyroidism in which increasedweight occurs chiefly as a result of reduced energy usance (Susan A.J, 1997).Other endocrinological factors contributing to obesity include Cushingssyndrome and disorders of corticosteroid metabolism, where weight gain istypically tended to(p) by a distinctive prototype of fat deposition in thetrunk, sex endocrine disorders including hypogonadism in men and ovariectomy inwomen, insulinoma and growth hormone deficiency (Susan A.J, 1997). The keycauses of weight gain in these cases are the amount of energy pulmonary tuberculosis. Certainhypothalamic tumors or damage to the hypothalamic part of the mind as a resultof excessive exposure to radiation, infectious agents or head trauma can in any caselead to obesity with defect in appetence control and hyperphagia (Susan A.J,1997). A hypothalamic disorder is alike believed to be the foundation of anumber of congenital abnormalities which could also result in obesity, e.g.Prader-Willi syndrome, which is an unregularity that could be a primary cause ofobesity (Susan A.J, 1997).GENETIC INFLUENCEAta population level, the genetic square up of obesity is e xpressed in terms ofheritability (Susan A.J, 1997). This refers to the percentage of the totaldifference in a character which is attributable to genetic factors (Susan A.J,1997). The heritability of obesity may be considered either in terms of thetotal fatness of an individual or the distribution of body fat in an individual(Susan A.J, 1997). Several discoveries break been made over the years regardingthe influence of genetics on chronic diseases like cardiovascular disease andobesity (R. C. Whitaker, J.A. Wright, M.S. Pepe, K.D. Seidel, &W.H. Dietz.,1997). late reports indicate that at least 32 genes contribute to commonforms of obesity. many of these genes are thought to be related to thedevelopment of obesity through the deregulation metabolic hormones in the body(Susan A J, 1997).The obesity related straining in the fat massand obesity-associated protein also known as alpha-ketoglutarate-dependentdioxygenase FTO, has aroused interest in pediatrics due to its relationshipwith 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 thechromosome 16 and is expressed in the brain, specifically the hypothalamicnuclei (Khung E. Rhee et al. 2012). Those who are homogenised for the at-riskallele 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 islikely due to the genes elaboration in the regulation of energy intake (KhungE. Rhee et al. 2012). According to recent studies, individuals carrying theat-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 repletion (J.Wardle, S. Carnell, C.M.A. Haworth, I.S. Farooqi, S. ORahilly, & 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 aft(prenominal)adjus ting for BMI) (N. J. Timpson, P.M. Emmett, T.M. Frayling, et al. 2008) anddisplay a greater tendency towards consuming pleasant-tasting foods after eating ameal (J. Wardle, C.Llewellyn, S. Sanderson, & R. Plomin, 2009). Therefore,FTO isnt associated with energy outgo, but it increases the susceptibilityof individuals to higher calorie consumption and decreased satisfaction. Ameta- analysis of 45 studies found that adults who were physically activeattenuate 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 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 suggest that the familial correlation in thetotal body fatness, expressed as body mass index, (BMI kg/m2) from parent tooffspring is close to 0.2 and for s ibling-sibling relationships about 0.25(Bouchard C, Perusse L, Leblanc C, Tremblay A, Theriault G. 1988). As would beexpected, studies of twins show a much higher concentration, in particular inmonozygotic pairs (Susan A.J, 1997). However, these findings do not segregatethe self-sufficing effects of genetic transmission and a shared environment (SusanA.J, 1997). Further studies of twins reared apart attribute 50-70% of thedifference in BMI in later purport to genetic factors (Stunkard A, Harris J,Pedersen N, McClearn G. 1990). Adoption studies, where an individual is comparedboth to their biological parent and their espouse parents, have alsodemonstrated the importance of genetic influences (Susan A.J, 1997). There is a sloshed relationship between the BMI of the adoptee and their biological parentsacross the entire range of fatness, but no relationship between the adoptee andtheir adoptive parents (Stunkard A, Sorensen T, Hanis C. et al. 1986).Studiesof fat distribution have co nsidered 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 inborn 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 considerfor 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 fromthese genetic analysis suggests that obesity is a polygenic 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 susceptible 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 development of the disease (Susan A.J,1997). Unlike animal 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 identification ofsmall number of individuals with a single defect which leads to obesity (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 time of overfeeding, 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). One possible explanation for this effect is the decrease in diet-inducedthermogenesis which is littleened in animal models of obesity due to a decreasein the sympathetic activation of brown adipose tissue (Rothwell N., Stock M.,1983). These unequivocal effects on energy expenditure in obese animals seam 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 ofabnormally low energy intake which in instanter imply that there must be a defectin energy expenditure. There are three basic elements to energy expenditurewhich have each been the focus of extensive research.Basal MetabolicRateIn1997, Susan A Jebb defined chief(a) or resting metabolic rate as the energyexpended by an individual at rest, following an overnight fa st and at acomfortable environmental temperature in the thermo neutral range. Severalstudies of basal metabolic rate have concluded that obese subjects have ahigher BMR compared to their lean counterparts. Researchers like Swin discharge B.& Ravussin E, reported that approximately 80% of the inter- individualvariance in BMR can be accounted for by age, fat-free mass, fat mass andgender. Nevertheless, this still gives room for some likelihood thatinter-individual difference 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 consistent finding,even among studies from the same laboratory. A recent review by Ravussin E.& Swinburn B. (1993) determine 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).Physical 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 insouciant energy cost of these actions from400-3000 kJ/day, with low levels predictive 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 license to undertake conscious physicalactivity or exercise 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 included various actometers,heart rate monitoring, activity diaries and direct observation (Susan A. Jebb,1997).Theenergy requirements of an individual encompass the increase 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 expenditure in 319 obese subjects clearly demonstrates asignificant increase in energy expenditure with increasing body weight suchthat 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 outstanding 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 ex cessive weightgain. However, in experimental overfeeding researches, there is no remarkabledifference in the degree 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 relativeto 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 reinforcer the guesswork 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, argue that only very small differences in energyexpenditure are neccessary to produce significant weight gain over many years,and this difference may be lower than the limits of precision of even the mostadvanced methodology.Energy IntakeThe affliction 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 stick intake to match energy requirements over a wide range of energy requirements yet those who become obese seem unable to achieve this equilibrate (Susan A Jebb, 1997).Breakthrough in discerning the role of energyintake in the aetiology of obe sity 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 indicateconsistent shortfalls in self-reported intake, averaging approximately 30% ofenergy 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 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 pattern 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 period, 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 dietary records, thereare also instances of self-deception or deliberate manipulation of dietaryrecords.Recentresearch into the appetite control system by Blundell J. Bouchard C., Bray G.(1996), has identified a network of synchronous interactions which governeating behavior. These effects are talk terms through the central nervous systemparticularly the hypothalamus, where a number of neuropeptides appear toregulate 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 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 acc urately resile eating behaviorin a naturalistic setting, where knowledge of foods consumed and conditionedlearning may invoke 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). Experimental 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 passive over consumption. In 1994, Poppitt S., stated that fat has twotimes 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 stirred 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 which 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 forcertain meals would make 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 toobscure any underlying obese-lean differences. The re lationship between sensorypreference for fat versus sugar and BMI was pinpointed by Drewnowski in 1992. orotund women had preference for foods with high fat to sugar ratio while womenwith low BMI had preference for high sugar to fat ratio, therefore increase inweight is closely related to increase for fatty foods. take infrequency has effect on weight gain, because people who eat several small mealsat intervals have less weight than those that eat fewer meals in largerquantity 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 unreliable 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 surroundings, opportunities or conditionsof invigoration have on promoting obesity in individuals and populations. Thisencompasses 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 andradiation diagram 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, 199 7). Environmentalinfluences on diet involve a wide range of factors including accessibility 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, low-priced healthy food is limited forpeople who reside in low-income communities and such 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 contain a healthy weight (Susan A.J, 1997).PSYCHO-SOCIAL INFLUENCESFoodis sometimes used as a coping mechanism by individuals with weight issues, particularly when they are unhappy, nervous, stressed, bore and depressed. Inmany obese individuals there seems to be a perpetual cycle of supposition 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 inability to control their stress (JenniferC. Collins & Jon E. Bentz, 2009). Eventually a viciousnessy 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 problematiceating behaviors such as mindless eating, frequent snacking on high caloriesfoods, overeating, and night eating (Glinski J., Wetzler S., Go odman E.2001).American Psychiatric tie-in 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 discrete 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 same time a feeling of loss of control during the episodes and guilt ordistress 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 exercise. It canth erefore be implied that the majority of individuals with BED are overweight.Nighteating, which was first identified in 1955 as some other 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 late nightconsumption ( 35% of daily calories after the evening meal), unhealthyeating patterns, morning 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, 20 09).PATHOPHYSIOLOGY OFOBESITYThereare several possible pathophysiological mechanisms involved in the advancementand prolongation 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 leptin was a satietyelement. However, soon after J. F. Caros laboratory could not ascertain 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 tiss uetheir 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 potbelly 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 signal fat storagereservoirs 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). Althoughadministration 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 whereforeadministration of leptin has not been shown to be effective in suppressingappetite in most obese people ( aviator 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 region 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 pass 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 ampheta mine-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). some(prenominal) groups of arcuatenucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRPgroup while stimulating 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 deathrate 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 understandingthe true re lationship 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.,osteoarthritis), some genus Cancers (e.g., endometrial, breast, and colon cancer),high total cholesterol or high levels of triglycerides, liver and gallbladderdiseases, sleep apnea and respiratory problems, reproductive healthcomplications such as infertility and mental health conditions (WHO, 2012).Obesity and CancerObesepeople are more vulnerable to cancer and their prognosis is extremely worse whendiagnosed. 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). Additional to obesity, cancer has recently beenlin ked to diet and physical activity status (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 National Cancer Institute Surveillance, Epidemiology,and End Results 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 alpha-lipoprotein cholesterol and impaired 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 separately 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 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 pressure 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 mere sorrow 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 deter ioration and bias based 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 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 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, d e Girolamo et al. 2008).Obesity anddiabetesDiabetesis usually a terminal illness. i.e. it is a lifelong 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 proper 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. Excess 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 obese or overweight.Obesity accounts for $117 billion a year in direct and indirect economic be.Obesity is associated with 300,000 deaths per year, and is fast becoming theleading 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 maintain a healthy diet. Although,certain People have been boffo at maintaining a healthy nutritional statusand avoiding this unhealthy situation. Gary Beckers human capita l 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 theeducational qualification, job experience/training, and the health conditionthat workers devote their time in to hike 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 coronation. 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 costs 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 an d cut back more cost on employersespecially in medical and disability claims and also workers compensationclaims. 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 publicprograms. 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 played out 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 forw eight loss with non-surgical programs usually involve a combination of diet variety, 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 required level. Therequired energy 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 losings. downhearted 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. S ince 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. customary tactics includeself-monitoring of food intake and exercise, reduced portion of meals andnumber of times of food intake, intellective restructuring, problem solving,and prevention 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). remark 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 co ntrol 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 bring home the bacon 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 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 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 of dietmodification. The greatest benefit of physical activity is in facilitating themaintenance 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).Additional evidence comes from randomized trials. Participants who receive dietplus exercise maintain greater weight losses 1 year after treatment than dothose who receive diet alone, although the differences are not alwaysstatistically significant (Wing, R.R. 1999). ginmillObesi tyis 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) Secondary 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. Simple habits ranging from 30 minutes walk in a day to hebdomadary work out at the gymnasium can go a lon g 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 organise 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 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 strategi es 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. 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