Assassination Of Jfk Essays (406 words) - Lee Harvey Oswald

Assassination Of Jfk JAKE Lee Harvey Oswald On November 22, 1963 JFK was assassinated. Though to this day it is unknown weather the accused killer Oswald, acted alone or was a patsy as he claimed. Lee Harvey Oswald was the perfect fall guy for such a conspiracy. He was a former US marine that defected to USSR. He was a Marxist with communist believes. He did support Kennedy's view on Cuba and was said to have handed out pro Castro propaganda. Oswald may have not supported the President, he may have even wanted him dead. Though he was not capable of the assassination alone. Oswald worked in the Book Depository building where the shots were allegedly fired from. I believe it would have been impossible for Oswald to have killed the president, for a number of reasons. Oswald was right handed the Italian Rifle he was said to have used was set up for someone that was left handed. From the window he was supposedly perched at their was a huge tree blocking his vision. Oswald was also said to be a very poor shot when he was in the Marines. Whoever the gunmen were, they fired their five to six shots very accurately. The fatal head wound shown the presidents head to have moved back and to left indicating that the shot came from the front. Oswald was behind the president and could not have inflicted that wound. Moments prior to the shooting Oswald was on the second floor of the building drinking a Coke. When he was confronted in the building after the shooting he was said to have been calm and collective. You would think after someone had committed the murder of the century they would be a little more tense. Oswald did not appear to be tense at all. He exited the building from the front door of the building. If he had committed the murder he would probably have escaped from the building through a different door. Oswald was a mere pawn in the conspiracy and the assassination of JFK. He was not the trigger man just a mere patsy as he said. Their are thousands of files that have been reviewed by two committees since the assassination. One of them the Warren commission believed that Oswald was the lone assassin. The other The house Select Committee believes if Oswald did do it than he did not act alone. They believed a conspiracy was probable. History Reports

FAMILIAL INFLUENCE ON CHILDHOOD OBESITY Essays

FAMILIAL INFLUENCE ON CHILDHOOD OBESITY Essays FAMILIAL INFLUENCE ON CHILDHOOD OBESITY Essay FAMILIAL INFLUENCE ON CHILDHOOD OBESITY Essay FAMILIAL INFLUENCE ON CHILDHOOD OBESITY Scope Nature of the Problem The children population currently struggling with obesity has massively expanded, representing a huge health care burden both at present and in the future. The extent of the epidemic is worsened because it is a critical risk factor for other diseases, including cardiovascular diseases, musculoskeletal disorders, cancer and diabetes. Upwards of 17% of adolescents and children in the United States, suffer from obesity, representing more than 12.5 million patients (World Health Organization, 2012). These represents a near 300% increase in the levels since 1980, with considerable ethnic and racial disparities in the prevalence rates, with male Hispanics and non-Hispanic black girls being the worst affected population groups. Similar trends are evident elsewhere in the world, with the World Health Organization (WHO) estimating that upwards 40 million children across the world are either overweight or obese. : Research Hypothesis Family behaviors and attitudes are important in whether or not children become overweight or obese Justification There is a growing body of theoretical, scientific evidence indicating that children assimilate their family and parents health philosophies. They engage in activities and eat foods that their families allow, encourage or provide them with, and refrain from those that are forbidden. This influence of families and parents on childrens eating and exercise habits is critical in the development of disease, while at once building lasting habits that prevent or predispose them to obesity or high body weight (Austin, 2011). With the establishment of empirical evidence to back up the theoretical models, this research findings will help to create and impetus for the development better parental attitudes and skills, which will ultimately lead to the reduction of theoverall disease burden and the overall health care costs facing populations and governments. Potential family-based interventions/treatments can be developed with the establishment of firm evidence of family environments on the poss ibility of obesity development. In addition, if the research hypothesis can lead to the prevention of incidental diseases associated with childhood obesity, while at once boosting the productivity of the future generations. Methodology The research design will use both secondary and primary data. The secondary data would comprise of peer-reviewed journal and book sources on childhood obesity causes, preventive methods and the possible predisposition of children due to familial factors (Austin, 2011). The primary data would be obtained from a cross-sectional sample of 400 children aged between 6 and 13. The sample would comprise (i) 100 Hispanics (ii) 100 Blacks (iii) 100 Whites and (iv) Minority groups. Half of the respondents must be (i) obese (ii) overweight. The research staff would go to schools and hospitals, and request parents and the children to participate in the study. As many as 700 possible participants would be selected, from whom a random sample of 450 would be selected to participate in the study. Respondents would complete research questionnaires sent by post, email or by telephone interviews based on the questionnaire, with information includingtheir diet, eating habits, parental attitudes towards eating and exercise, knowledge of obesity and the number of times that food is cooked in the home (Kothari, 2009). Others would include the children body mass index, maternal depression, family functioning and self-esteem etc. Once questionnaires are completed, they will be checked for completeness and correctness, before the final random sample of 400 is selected for coding, and analysis. Data would be analyzed by a specialized statistical computer software, SPSS and varied reports would be provided. Initial Findings The causes of obesity, a non-communicable and perfectly preventable disease, are well known and include excessive intake of high energy and sugar foods, low vegetables intake and lack adequate physical activity. Genetic predisposition, family demographics, parenting practices, increasing sedentary lifestyles due to computer use and television viewing etc, increasing consumerism and hectic family schedules have equally been identified as (Delahanty, et al., 2012). Other causal factors include the emergence of the fast foods industry, which is almost solely responsible for the rise in high-fat foods across the world.It is however evident that proper parenting and control can limit these risk factors, effectively making the heightened rates of obesity a direct consequence of the failure in parenting (Austin, 2011). According to the ecosystems model, the relationships among families, individuals, society, institutions and psychosocial groups interactions have a considerable effect on the functioning and behavior. On the other hand, another theoretical model, the ecological model asserts that family dynamics are critical in whether or not children develop weight problems or obesity. This possibility is determined by food choices, which are influenced by the family demographic characteristics (HU, 2011). Families in which both parents worked and single parent families were more likely to eat fast foods, compared to other families, which in turn influence the eating habits of children. In addition, low income families vegetable consumption by as much as 22%, as do dual worker families (Delahanty, et al., 2012). Other factors including the parents beliefs and attitudes about the nutritional and exercise needs of the children impact the body weight of the children. References Austin, B. (2011). [Commentary on] The Blind Spot in the Drive for Childhood Obesity Prevention: Bringing Eating Disorders Prevention Into Focus as a Public Health Priority. American Journal of Public Health, Jun2011, Vol. 101 Issue 6 . Delahanty, L. M., Pan, Q., Jablonski, ,. K., Watson, C., McCaffery, J., Kahn, S., et al. (2012). Genetic Predictors of Weight Loss and Weight Regain After Intensive Lifestyle Modification, Metformin Treatment, or Standard Care in the Diabetes Prevention Program. Diabetes Care , vol. 35 no. 2 363-366. HU, F. (2011). Globalization of diabetes: the role of diet, lifestyle, and genes. diabetes lifestyle, Harvard School of Public Health, in PubMed . Kothari, D. C. (2009). Research methodology: methods and techniques. New York: New Age International. Mazzeo, D., Arens, S., Germeroth, C., Hein, H. (2012). Stopping childhood obesity before it begins. Phi Delta Kappan, Vol. 93 Issue 7 , , p10-15. World Health Organization. (2012, May 17). Obesity and overweight. Retrieved June 3, 2012, from www.who.org: who.int/mediacentre/factsheets/fs311/en/