Obesity and Sedentary Lifestyles

Obesityand Sedentary Lifestyles

Obesityand Sedentary Lifestyles

Obesitymay be one of the most prevalent ailments in the contemporary humansociety. More often than not, it is not considered to be a seriouscondition especially considering that the patients would not befeeling pain or limited in the accomplishment of varied functions.However, many are the times when the seriousness of the ailment isunderlined by the chronic ailments for which it is a predisposingfactor including asthma, diabetes, heart diseases and respiratoryailments, as well as high blood pressure. This has necessitated thatscholars and healthcare researchers examine the epidemic in a morecritical way in an effort to determine the causes and risks, as wellas the ways in which it can be prevented and even treated. Recenttimes have underlined the fact that the modern western lifestyles areto blame for the current rates of obesity as well as the associatedchronic ailment pandemics. This assertion seems to be plausible giventhat such problems only started about 4 decades ago at a populationlevel. In addition, they do not result from any microbial agent andhave taken place too fast for any genome modifications to beconsidered as a factor. Nevertheless, lifestyle underlines thevolitional behaviors or tendencies on the part of the affectedperson. This comes with a pejorative implication for socialscientists as it is often considered to ignore the deeperenvironmental, economic and social determinants pertaining to bothdisease and lifestyle while concentrating on individualresponsibility. Essentially, it is often considered to be an elementof victim blaming. Scholars, therefore, determine that a considerablymore holistic view would revolve around the examination of the “causeof the cause” rather that the cause of the disease. This becomesparticularly in the examination of the chronic and non-communicableailments (NCDs) that are usually associated with obesity in contrastto communicable or infectious ailments that have historicallyprevailed.

Asmuch as there is no universal way for defining obesity or overweight,it may be defined as excess body fat. Of course, there exists nocut-off point regarding the acceptable levels of fatness or obesityespecially among children. Nevertheless, the obesity levels may beexpressed as a percentage with varied ways of doing this beingdefined subject to the environment in question. In research,techniques such as magnetic resonance imaging (MRI), multi-frequencybioelectrical impedance analysis (BIA) and underweight weighing(densitometry) are used. In the clinical environment, however, variedtechniques may be used including skin fold thickness, waistcircumference and especially Body Mass Index (BMI). Individuals areconsidered to be obese in instances where the BMI is between 25 and29.9. However, BMI is used only in the case of adults and not forchildren since the latter have changing body shape as they progressin normal growth. However, in seeking to come up with properpreventative and treatment measures for the condition, it has becomeimperative that scholars examine the causes. This paper examines theliterature undertaken on the same with a view to determining theimpact of lifestyle in the development of the ailment.

In“Genes, Lifestyles and Obesity”, Marti et al (2004 29) sought toexamine or review the role that lifestyle factors and genes play inthe risk for obesity, as well as the potential interactions betweenthe two. The researchers concentrated on physical activity patternsand the dietary habits of the individuals when examining thelifestyle factors. To examine this, the researchers revieweddescriptive reports pertaining to varied genes that are potentiallyimplicated or definitely ascribed in the excessive accumulation offat resulting in obesity as evaluated by varying research approaches.In addition, they reviewed the involvement or the roles thatmacronutrient composition and intact, and the role thatactivity-associated expenditure plays in the onset of obesity. Thisresults from the acknowledgement that a positive balance of energybetween the consumed energy and expended energy in the daily life ofan individual would underlie weight gain. The excessive accumulationof fat in the adipose tissue causing obesity is the result ofpersistent overconsumption of drinks and foods well beyond the energyexpenditure requirements where the lifestyle, dietary, neuroednocrinealterations, sociological factors and hereditary components areinvolved. The results of the study demonstrated that the genotype,coupled with the macronutrient composition and low energy cost ofphysical activities or sedentary lifestyles are determinants in theprevalence of obesity. This underlines the fact that the daily lifeenvironmental factors and genes play a role in the obesity pandemic.The environmental factors, in this case, would involve reduced livingand domestic work activities, as well as social and cultural mediatedfood intake. Essentially, the interaction between genetic compositionand environmental factors would increase the difficulty ofinterpreting the roles that lifestyles and genetics play in the riskof obesity.

Whilethis article offers an insight into the different aspects of obesityand its causes, it is imperative that the researchers examine whetherthere exists variations in the roles that these factors play in theobesity pandemic. As earlier stated, there has been an increase inthe rates of obesity in the contemporary human society. Of course,this could not be a signal of the changes in the genetic compositionbut rather a change of lifestyle from the relatively physicalactivities-oriented lives to sedentary ones where everything isavailed by technology. On the other hand, initial observations havedemonstrated that the vulnerability of an individual to obesity ishigher in some families compared to others. Further, the survival ofhumans and animals in instances where there is food deprivation can,in evolution terms, be a predisposing factor for the widespreaddistribution of genotypes that favor weight gain. It would beimperative that one acknowledges that the most likely factor thatshould be credited with the high rates of or the current obesityepidemic is the lifestyle, perhaps coupled with the environment.Indeed, there is a continuing decline in the daily expenditure ofenergy, which his yet to be matched by sufficient or equivalentreductions in the intake of energy. This comes as a risk factor, notonly for obesity but other chronic ailments as well.


In“ChildhoodObesity: is parental nurturing to blame”La rocca, (2009 1) seeks to examine the contribution of parentalnurturing to childhood obesity. According to La rocca , the majorcontributing factors are lack of exercise and nutrition . There is agrowing epidemic of obesity in children in the entire United Stateswith the current trends spreading among the minorities including theAfrican American and the Hispanics. Are parental nurturing influencesresponsible for growing epidemic in children? Parents influencechildhood behaviour by promoting particular values and attitudes, byrewarding or reprimanding certain behaviour and acting as rolemodels. If such values are implemented correctly, they can lead tohealthy lifestyles. However, certain behaviours that parents rewardare major contributors of obesity, such as forcing the child to clearthe plate of food which may result to over feeding as the childcannot tell whether she/he is full or not. Similarly, overlydiscouraging snacks such as junk food will develop a certain likingof junks in the child. A restrictive diet may cause the child to feeldeprived of certain food, and therefore, the child will look at everychance to consume the restricted foods.

Whileparents eating habits may have influenced the children eating habitsthe issue is much broader than just blaming them. Parents eatinghabits are not the only cause of obesity. Some parents constantlymake the effort of encouraging their children to eat healthy dietsand physical activities but the children still suffer from weightgain. This is due to factors beyond parents control such as thenationwide advertising on fast foods that targets children.Similarly, children are also influenced by their peers and otherenvironmental factors such as accessibility to junk foods. Childrenhappen to listen more to their peers more than their parents.Parental effort measures only are not by themselves sufficient toeradicate the problem of obesity. The dietary and physicalbehaviours of children is influenced by many sectors of economyranging from schools, community, childcare setting, medical careproviders, entertainment industries, food and beverages industriesand government agencies. Similarly, some factors such as geneticmakeup are beyond parental control. People with particular genes aremore prone to gaining weight even if they eat healthy foods or areexposed to physical activities. Their bodies are incapacitated tonormal utilization of energy making them gain weight cumulativelyresulting in high BMI and obesity. Another consideration is obesitycaused by medical prescriptions. Parents therefore, are torn betweenallowing their children to consume the drugs and deal with weightgain later or not to administer the drugs at all. Many of the drugsused to treat diabetes, bipolar disorder, weight loss prescriptionsmay have an opposite effect, depression and high blood pressureprescriptions can cause weight gain. Patients and doctors need to beaware of such weight gain related prescriptions which are overlyunrecognized as drivers of obesity problem.

Thereality is that the environment we live in encourages lifestylebehaviours that leads to obesity where some families see it normal toeat large portions of energy- dense fast foods. It is therefore verydifficult to change things for just one person. A comprehensiveapproach will be achieved if the families take a stand, and thecommunity around them supports their stands. Also the governmentshould control the prevalence of fast food adverts in the televisionand also increase awareness among the families about healthy diets.Increasing awareness will ensure that parents are aware of what ahealthy weight comprise of and start intervention measures earlybefore it becomes too much. Also, parents will be able to educatetheir children on the proper eating habits, knowing when they arehungry, importance of consuming the necessary amount of foods and thedisadvantages of always sitting in the house watching television andplaying computer games. The Government can also ensure supply ofphysical activity resources ensuring that the cycling paths along theroads are well maintained, public open spaces and parks, safe andless expensive recreational centres, and improved quality of physicaleducation benefits in schools to encourage physical activities.


In“Dietarybehaviors, physical activity and sedentary lifestyle associated withoverweight and obesity, and their socio-demographic correlates, amongPakistani primary school children”Mushtaq et al (20112) conducted a study aimed at analyzing theimpact of dietary behaviours, physical activities and sedentarylifestyles on the health of primary school going children andwhether there is a correlation between socio demographics andprevalence of obesity. They observed that, physical activities,sedentary lifestyles and dietary behaviours are independentpredictors of higher BMI among the children. Higher BMI is mostlyassociated with obesity. Children who frequently skip meals such asbreakfast were more likely to suffer from diabetes and the risk islower among children who take breakfast regularly. The act ofskipping breakfast was more common among female children than males. Similarly, skipping breakfast was also represented bysocio-demographic characteristics, with children from higher socialclass and those from urban areas with high income neighbourhoods,higher parental education and fewer siblings being more prone toskipping breakfast behaviour. A school- based breakfast programespecially in urban areas should be introduced so as to improve thenutrition standard. Also, higher consumption of snacks and junk foodswas more common in boys than in girls. This can be associated to thefact that girls possess higher nutrition knowledge than boys due totheir self perception of body image. Parents also, are less likelyto encourage boys to lose weight due to preference towards big andmuscular bodied men. Eating fast foods and snacks have a positivecorrelation with higher BMI and being overweight after adjusting forage, gender and genetics. Recommendable solution would be restrictionof fast food related adverts focusing on children, while at the sametime applying taxes on energy dense foods and their packaging. Thiswill push their prices up, making them less affordable and lessattractive to children. Studies also show that physical activity isinversely proportional to the BMI. Physical activities also help inlosing weight as it increases a child’s energy utilization loweringthe risk of becoming overweight. Children who spend more timewatching televisions and playing computer games are at a high risk ofbecoming obese due to lack of physical exercise. Dietary behaviours,physical activities and sedentary lifestyles are independentpredictors of overweight and higher BMI among children. Independentof the region that one comes from, childhood obesity was moreprevalent in environment that facilitated intake of energy densefoods while at the same time inhibiting physical activities thatfacility high energy utilization.

Accordingto Mushtaq, the main causes of obesity are poor diets, lack ofphysical activities and sedentary lifestyles. Whereas the factorsmay be true contributors of weight gain, his study does not inform uson the extent to which each factors contributes to weight gain. Hehas used positive correlation to justify the factors as the maincause of obesity this exposes him to limitations of correlation wherea change in one variable is not the causal effect of the change inanother variable. Since the data shows a positive relationship, itdoes not necessarily mean that there is necessarily an underlyingcausal relationship. Other external factors may be present. Forexample, Mushtaq failed to recognize that some people are more proneto weight gain due to their genetic makeup while in for other people,no matter what amount of fast foods they consume, they cannot gainweight due to their genetic makeup In essence, impact of energyintake and nutrient composition on the development of obesity isaffected by the occurrence of mutations which make some individualsmore prone to weight gain than others. Future studies should alsofocus on the influence of gene X nutrient interactions to determinewhether obesity can be inherited. Studies also seem to becontradictory, whereas Mushtaq believes that consumption of fastfoods is a major cause of obesity, other studies argue that too muchrestriction on junk foods may raise uncontrollable need in thechildren to indulge in fast foods whenever their parents are notwatching them. Studies present s a strong evidence that children dietbeyond fast food consumption is strongly linked to poor nutrition and obesity.()While reducing fast food is important, the rest of thechild’s diet should not be overlooked. Children who rely heavily onfast food also do not get healthy diets at home as their parents lackfinances or time to make healthy diets. This is also a concern thatshould not be ignored.

Inconclusion, the issue of obesity can be really sensitive especiallywhere people make unsupported conclusions on its main cause.Theabove articles have discussed their concerns pertaining to the maincauses of obesity ranging from parental influence, genetic makeup,lifestyles and poor diet concerns. Whereas controlling the abovefactors will contribute positively to eradicate obesity, care shouldbe taken not to make worse the effects of obesity. Where parents areblamed on their children obesity, they may shy off from seeking helpas they are considered incapable of providing their children withhealthy diets. Similarly, families who have a child suffering fromobesity should talk openly without ridicule so as not to inducestigma on the child thus lowering their self esteem. Above all,experts agree that the most comprehensive approach to obesity iscreating awareness to parents, children and the entire society on allthe possible causes of weight gain, possible control and interventionmeasures in order to eradicate obesity. It is also important forparents to model a healthy lifestyle to their children.


  1. Ackard, D. M., Neumark-Sztainer, D., Story, M., &amp Perry, C. (2003). Overeating among adolescents: Prevalence and associations with weight-related characteristics and psychological health.&nbspPediatrics, 111, 67-74.

  2. Ali, M., Blades, M., Oates, C., &amp Blumberg, F. (2009). Young children`s ability to recognize advertisements in web page designs.&nbspBritish Journal of Developmental Psychology, 27(1), 71-83.

  3. Benjamin SE, Cradock A, Walker EM, Slining M, Gillman MW (2008): Obesity prevention in child care: A review of U.S. state regulations. BMC Public Health 2008, 8:188.

  4. Bray GA. Treatment for obesity: a nutrient balance/nutrient partition approach.&nbspNutr Rev&nbsp1991&nbsp49: 33–45.

  5. Crespo, C. J., Smit, E., Troiano, R. P., Bartlett, S. J., Macera, C. A., &amp Andersen, R. E. (2001). Television watching, energy intake, and obesity in U.S. children.&nbspArchives of Pediatric and Adolescent Medicine, 155, 360-365.

  6. Kokkoris P, Pi-Sunyer FX. Obesity and endocrine disease.&nbspEndocrinol Metab Clin N Am&nbsp2003&nbsp32: 895–914.

  7. Jafar TH, Qadri Z, Islam M, Hatcher J, Bhutta ZA, Chaturvedi N (2008). Rise in childhood obesity with persistently high rates of undernutrition among urban school-aged Indo-Asian children. Arch Dis Child, 93(5):373-378. 9. East High Scales, China Scale Manufacturer, Nanjing, China: ZT Mechanical Physician Scale

  8. Jequier E, Tappy L. Regulation of body weight in humans.&nbspPhysiol Rev1999&nbsp79: 451–480

  9. Martínez JA. Body-weight regulation: causes of obesity.&nbspProc Nutr Soc2000&nbsp59: 337–345.

  10. Martínez J, Fruhbeck G. Regulation of energy balance and adiposity: a model with new approaches.&nbspJ Physiol Biochem&nbsp1996&nbsp52: 255–258.

  11. Schwartz MW, Baskin DG, Kaiyala KJ, Woods SC. Model for the regulation of energy balance and adiposity by the central nervous system.&nbspAm J Clin Nutr&nbsp1999&nbsp69: 584–596

  12. Rosenbaum M, Leibel LR, Hirst J. Obesity.&nbspN Engl J Med&nbsp1997&nbsp337: 396–407

  13. Weber J. Energy balance in obesity.&nbspProc Nutr Soc&nbsp2003&nbsp62: 539–543.

  14. Flier JS. Obesity wars: molecular progress confronts an expanding epidemic.&nbspCell&nbsp2004&nbsp116: 337–350

  15. Lytle LA, Nichaman MZ, Obarzanek E (1993). Validation of 24-hour recalls assisted by food records in third-grade children. J Am Diet Assoc 1993, 93:1431-1436.

  16. Durkin MS, Islam S, Hasan ZM, Zaman SS (1994): Measures of socioeconomic status for child health research: comparative results from Bangladesh and Pakistan. Soc Sci Med 1994, 38:1289-1297.

  17. Martínez JA. Obesity in young Europeans: genetic and environmental influences.&nbspEur J Clin Nutr&nbsp2000&nbsp54: S56–S60.

  18. Martínez JA, Moreno MJ, Marques-Lopes I, Marti A. Causes of obesity.&nbspAnal Sis San Nav&nbsp2002&nbsp25: 17–27.

  19. Hill JO, Wyatt HR, Melanson EL. Genetic and environmental contributions to obesity.&nbspMed Clin N Am&nbsp2000&nbsp84: 333–346.

  20. Hill JO, Wyatt HR, Reed GW, Peters JC. Obesity and the environment: where do we go from here?&nbspScience&nbsp2003&nbsp299: 853–855

  21. Comuzzie AG, Allison DB. The search for human obesity genes.&nbspScience1998&nbsp280: 1374–1377.&nbsp

  22. Hill JO, Peters JC. Environmental contributions to the obesity epidemic.Science&nbsp1998&nbsp280: 1371–1374.&nbsp

  23. Damcott CM, Sack P, Shuldiner AR. The genetics of obesity.&nbspEndocrinol Metab Clin N Am&nbsp2003&nbsp32: 761–786.

  24. Poskitt EM (2005): Tackling childhood obesity: diet, physical activity or lifestyle change? Acta Paediatr 2005, 94:396-398. 8.

  25. Noland M, Danner F, DeWalt K, McFadden M, Kotchen JM (1990): The measurement of physical activity in young children. Res Q Exerc Sport 1990, 61:146-153.

  26. McPherson RS, Hoelscher DM, Alexander M, Scanlon KS, Serdula MK (2000): Dietary assessment methods among school-aged children: validity and reliability. Prev Med, 31:S11-S33.

  27. Kohl HW, Fulton JE, Caspersen CJ (2000): Assessment of physical activity among children and adolescents: a review and synthesis. Prev Med 31: S54-S76.

  28. Koplan, J. P., Liverman, C. T., &amp Kraak, V. A., (Eds.) (2005).&nbspPreventing childhood obesity: Health in the balance. Washington, DC: Committee on Prevention of Obesity in Children and Youth, Food and Nutrition Board, Institute of Medicine of the National Academies.

  29. Sweeting H (2007): Measurement and definitions of obesity in childhood and adolescence: a field guide for the uninitiated. Nutr J 2007, 6:32.

  30. Martínez-González MA, Martínez JA, Hu FB, Gibney MJ, Kearney J. Physical inactivity, sedentarism lifestyle and obesity in the European Union.&nbspInt J Obes Relat Metab Disord&nbsp1999&nbsp23: 1–10

  31. Miller , S. A., Taveras , E. M. Rifas-Shiman, S. L., &amp Gillman, M. W. (2008). Association between television viewing and poor diet quality in young children.&nbspInternational Journal of Pediatric Obesity,&nbsp3(3), 168-176.

  32. Neumark-Sztainer, D., Croll, J., Story, M., Hannan, P. J., French, S. A., &amp Perry, C. (2002). Ethnic/racial differences in weight-related concerns and behaviors among adolescent girls and boys: Findings from Project EAT.&nbspJournal of Psychosomatic Research, 53, 963-974.

  33. Davison, K. K., &amp Birch, L. L. (2002). Processes linking weight status and self concept among girls form ages 5 to 7 years.Developmental Psychology®, 38, 735-748.

  34. Geller F, Reichwald K, Dempfle A, Illig T, Vollmert C, Herpertz S, Siffert W, Platzer M, Hess C, Gudermann T, Biebermann H, Wichmann HE, Schafer H, Hinney A, Hebebrand J (2004). Melanocortin-4 receptor gene variant I103 is negatively associated with obesity.&nbspAm J Hum Genet&nbsp2004&nbsp74: 572–581

  35. Hebebrand J, Friedel S, Schauble N, Geller F, Hinney A (2003). Perspectives: molecular genetic research in human obesity.&nbspObes Rev&nbsp2003&nbsp4: 139–146.

  36. Kyle UG, Morabia A, Schutz Y, Pichard C. Sedentarism affects body fat mass index and fat-free mass index in adults aged 18 to 98 years.Nutrition&nbsp2004&nbsp20: 255–260.

  37. Kaiser Family Foundation (2007).&nbspFood for thought: Television food advertising to children in the United States.Washington, D.C.: Author.

  38. Puhl, R. M., &amp Latner, J. D. (2007). Stigma, obesity, and the health of the nation`s children.&nbspPsychological Bulletin®, 133, 557-580.

  39. Ogden, C. L., Carroll, M. D., &amp Flegal, K. M. (2008) High body mass index for age among U.S. children and adolescents, 2003–2006.&nbspJournal of the American Medical Association, 299, 2401–2405.

  40. Pratt, C. A., Stevens, J., &amp Daniels, S. (2008). Childhood obesity prevention and treatment recommendations for future research.&nbspAmerican Journal of Preventive Medicine, 35, 249-252.

  41. Lanningham-Foster L, Nysse LJ, Levine JA. Labor saved calories lost: the energy impact of domestic labor-saving devices.&nbspObes Res&nbsp2003&nbsp11: 1178–1181

  42. Perusse L, Bouchard C (2000). Gene–diet interactions in obesity.&nbspAm J Clin Nutr2000&nbsp72: 1285S–1290S

Mushtaqet al, (2011) International Journal of Behavioral Nutrition andPhysical Activity,

InternationalJournal of Obesity&nbsp(2004)&nbsp28,&nbspS29–S36.doi:10.1038/sj.ijo.080280