Can breastfeeding prevent childhood obesity - Free Essay Example

Sample details Pages: 11 Words: 3274 Downloads: 3 Date added: 2017/06/26 Category Medicine Essay Type Analytical essay Tags: Childhood Essay Childhood Obesity Essay Obesity Essay Did you like this example? Can breastfeeding in the first six months prevent childhood obesity? Childhood obesity is becoming a worldwide concern given the potential health implications in the future. Obese children are more likely to suffer physical and mental health problems and are likely to develop into obese adults (Labayen, Ruiz et al. 2012), thereby increasing the long term risk of developing chronic conditions such as diabetes, cardiovascular diseases and stroke. Don’t waste time! Our writers will create an original "Can breastfeeding prevent childhood obesity?" essay for you Create order The cause of childhood obesity is multifactorial, including hereditary factors, comorbidities, dietary habits and physical activity. There is much debate as to the impact of breastfeeding during the early stages of life and how it correlates with childhood obesity compared with formula-fed newborns. Breast milk is nutritionally balanced to provide infants with all dietary requirements during the early stages of life. It also provides antibodies to reduce infection risks in newborns. Breast milk constitutes the appropriate amounts of protein, water, fat and sugar for a newborn and changes composition over time to adapt to a growing child’s needs. Formula tends to be higher in protein and fat than the baby actually requires and this excessive intake has been linked with adiposity (Hernell 2011). Marseglia et al have reviewed the potential impact of key breast milk constituents thought to play a role in reducing obesity risk (Marseglia, Manti et al. 2015). There hav e been a number of recent reviews discussing the association between breastfeeding and childhood obesity, all of which have concluded that breastfeeding confers a protective effect against childhood obesity and being overweight (Horta and Victora 2013, Aguilar Cordero, Sà ¡nchez Là ³pez et al. 2014, Lefebvre and John 2014, Yan, Liu et al. 2014). The largest reduction in obesity risk was 81%, reported in a study of females aged 11 years of who had been breastfed for more than three months compared with controls who had never been breastfed (Panagiotakos, Papadimitriou et al. 2008). The males in the same study had a reduced risk of 72% and both results were statistically significant. However, other literature reports either no association between breastfeeding and childhood obesity (Burdette, Whitaker et al. 2006, Huus, Ludvigsson et al. 2008, Jing, Xu et al. 2014), or an increased risk of obesity following breastfeeding of 9% (Kwok, Schooling et al. 2010), 10% (Novaes, Lamoun ier et al. 2012), 11% (Buyken, Karaolis-Danckert et al. 2008), 14% (Sabanayagam, Shankar et al. 2009), 18% He (2000), 29% (Al-Qaoud and Prakash 2009), 34% (Neutzling, Hallal et al. 2009), 40% (Toschke, Martin et al. 2007) and 83% (Araà ºjo, Victora et al. 2006), although none of which were statistically significant. Some studies suggest that there is a dose-response relationship, with increased duration of breastfeeding resulting in a decreased prevalence of being obese in childhood (von Kries, Koletzko et al. 2000, Fallahzadeh, Golestan et al. 2009, Griffiths, Smeeth et al. 2009, Yan, Liu et al. 2014). In contrast, other studies have reported no significant association between breastfeeding and its duration and obesity prevention (Burke, Beilin et al. 2005, Al-Qaoud and Prakash 2009, Sabanayagam, Shankar et al. 2009, Vehapoglu, Yaz?c? et al. 2014). One meta-analysis analysed the association between breastfeeding duration and obesity (Yan, Liu et al. 2014). As eligible s tudies reported different durations, the review categorised breastfeeding duration into less than three months, 3-4.9 months, 5-6.9 months and seven or more months. Those exclusively breastfed for at least seven months had a 21% decrease in the risk of childhood obesity, whilst those fed for less than three months only showed a 10% decrease. They concluded that the duration of breastfeeding was associated with a decreased likelihood of childhood obesity and reported a stepwise gradient of decreasing risk with increasing duration of breastfeeding. Single studies report a significant protective effect against childhood obesity when breastfeeding is done for at least one to three months (Goldfield, Paluch et al. 2006), three months (Twells and Newhook 2010), 13-25 weeks (McCrory and Layte 2012), four months (Scholtens, Gehring et al. 2007, Griffiths, Smeeth et al. 2009, Chivers, Hands et al. 2010), nine months (Nelson and Sethi 2005), 12 months (Burke, Beilin et al. 2005) and two or more years (Rathnayake, Satchithananthan et al. 2013). However, the differences in study design make it difficult to directly compare findings as the comparator groups can be formula-fed babies or babies’ breastfed for short durations. For studies investigating the impact of breastfeeding for at least six months on childhood obesity, the comparator group can be either newborns breastfed for less than six months (i.e. mixed feeding of variable durations) or newborns exclusively formula-fed. Additionally, the age of the children being assessed also differs in studies. When comparing those breastfed for at least six months with those breastfed less than six months, studies report a reduction in obesity risk of 60% when assessing two year olds (Weyermann, Rothenbacher et al. 2006), 54% and 43% in four year olds (Komatsu, Yorifuji et al. 2009, Simon, Souza et al. 2009), and 67% in six year olds (Thorsdottir, Gunnarsdottir et al. 2003). This suggests that the age of assessment affects the degree of risk reduction observed. However, when comparing against formula-fed newborns there are studies reporting reductions of 14%, 28% and 67% for three year olds (Poulton and Williams 2001, Armstrong, Reilly et al. 2002, Taveras, Rifas-Shiman et al. 2006), 6% for four year olds (Moschonis, Grammatikaki et al. 2008), 45% for seven year olds (Yamakawa, Yorifuji et al. 2013), 60% for nine year olds (Toschke, Martin et al. 2007), 64% for 11 year olds (Poulton and Williams 2001), 21% for 21 year olds (Poulton and Williams 2001) and 6% for 45 year olds (Michels, Willett et al. 2007). This data suggests that observing adults to determine the impact of breastfeeding on obesity is not advisable. Only one study reported an increased risk of obesity for newborns breastfed more than six months compared with formula-fed newborns, reporting a non-significant 40% increased risk of obesity in nine year olds (Toschke, Martin et al. 2007). Interestingly, very few detailed, for those breastfeeding for at least six months, whether the feeding duration was exclusively breastfeeding or mixed. Only two studies (Simon, Souza et al. 2009, Yamakawa, Yorifuji et al. 2013) reported on exclusive breastfeeding. There is evidence that exclusive breastfeeding also results in a decreased prevalence of being obese in childhood (Fallahzadeh, Golestan et al. 2009, Simon, Souza et al. 2009, Lefebvre and John 2014). Mayer-Davis et al (2006) compared exclusively breastfed newborns with exclusively formula-fed newborns and found that the breastfed children were significantly less likely to be overweight (34%) and that the results were not affected by maternal weight or diabetes status (Mayer-Davis, Rifas-Shiman et al. 2006). When exploring the differences between studies who defined breastfeeding as â€Å"Never – ever† and those reporting â€Å"exposure† to breastfeeding (implying mixed feeding practices of different types), a sy stematic review found a reduced likelihood of obesity in the exclusive feeding group of 20% and in the mixed group of 27% (Yan, Liu et al. 2014). This was supported by another review comparing â€Å"ever† breastfed with â€Å"exclusively breastfed for a specific number of months†, the latter showing a 27% decreased risk compared with the former at 21% (Horta and Victora 2013). That review postulated that if there is no critical window effect, but rather a cumulative effect of breastfeeding, studies that compared ever vs. never breastfed subjects will tend to underestimate any association. Any observed association between breastfeeding and later obesity does not prove causality (Butte 2001). There may be any number of potential confounders impacting on the relationship including geography, social deprivation status, parental weight status, smoking, marital status and education, ethnicity, gender, number of hospital admissions during the early stages of life, di et, sleep duration and physical activity. Whilst a number of studies discuss their impact, very few studies actually provide control for these factors in their analysis. The issue of geography is a potential confounder of any association between breastfeeding and obesity. In high-income countries, the babies usually receive formula, whereas many non-breastfed infants in low and middle income countries receive whole or diluted animal milk (Horta and Victora 2013). However, Hancox et al have reported that whilst breastfeeding reduced the risk of obesity slightly, there was no evidence that an association between breastfeeding and body mass index (BMI) was different in lower income countries compared with higher income countries (Hancox, Stewart et al. 2014). The socio-economic status of the mother may also contribute to the child’s weight status in childhood. The World Health Organisation (WHO) review analysed obesity risk in studies also controlling for social de privation and found a further 3% decrease in the risk of obesity to 37% compared with studies which did not (34%) (Horta and Victora 2013). Armstrong et al reported that the reduced prevalence in obesity for breastfed children also persisted after adjustment for socio-economic status, birth weight and gender (30% reduction) (Armstrong, Reilly et al. 2002). The impact of gender was prominent as Nelson et al reported that breastfeeding for at least nine months reduced the risk of being overweight more in girls than in boys (Nelson and Sethi 2005). A similar gender inequality was reported by Panagiotakos et al with girls breastfed for more than three months having a larger reduced risk of obesity than the boys (Panagiotakos, Papadimitriou et al. 2008). Sibling studies have been unable to rule out the impact of confounders on childhood obesity. One study which controlled for this as part of a sibling study reported the adolescent BMIs were 0.39 standard deviations lower in th e breastfed sibling than the non-breastfed sibling (Metzger and McDade 2010). However, another study of sibling pairs was unable to prove a protective effect for breastfeeding (Nelson and Sethi 2005). As well as the lack of control for confounders, other study limitations may affect the results reported. Definitions of obesity vary from a BMI of ?90th to ?97th, making any direct comparison of the outcome problematic. During their meta-analysis Yan et al investigated the association of breastfeeding and obesity, stratifying by the definitions of obesity and found a lower adjusted odds ratio for the BMI ? 97th group (25%) than the BMI ? 95th group (22%) (Yan, Liu et al. 2014). Most studies varied in the time when obesity was measured. As the definition of childhood can extend from one year olds to adolescents, there is an increasing influence of external and genetic factors on a child’s weight as potential confounders for any weight gain. When Scholtens et al looked at children breastfed for at least four months they reported a significantly lower BMI at age 1 compared to children not breastfed, but at age 7 this difference was no longer significant (Scholtens, Gehring et al. 2007). The WHO review reported a 38% decreased risk of obesity when assessing 10-19 year olds compared with 23% for 1-9 year olds and 11% for adults aged 20 and over, suggesting that endpoint for analysis is critical in determining the impact of breastfeed on obesity at various stages in childhood (Horta and Victora 2013). Finally, study design and follow up can affect the findings as high dropout rates affect long term follow ups, and the methodology used to analyse the results can produce unreliable results. Beyerlein et al investigated the impact of breastfeeding on children’s BMI in Germany but was unable to make any firm conclusions as the results differed according to whether they used linear or logistic regression (Beyerlein, Toschke et al. 2008). To summarise, there is a wealth of literature reporting the decreased risk of childhood obesity for newborns who are breastfed, although there was limited literature exploring those breastfed for at least six months. However, most studies cannot completely control for confounding maternal, child, cultural, genetic and environmental factors. The WHO recommend that infants should be exclusively breastfed for the first six months and that it should be supplemented with additional foods for the first two years (World Health Organisation 2015). Following close examination of the literature, we would conclude that breastfeeding for at least six months should reduce the risk of obesity in early childhood, although the protective effect may be lost in latter childhood depending upon the child’s upbringing. References Aguilar Cordero, M. J., A. M. Sà ¡nchez Là ³pez, N. Madrid Baà ±os, N. Mur Villar, M. Expà ³sito Ruiz and E. Hermoso Rodrà ­guez (2014). [Breastfeeding for the prevention of overweight and obesity in children and teenagers; systematic review]. Nutr Hosp 31(2): 606-620. Al-Qaoud, N. and P. Prakash (2009). Breastfeeding and obesity among Kuwaiti preschool children. Med Princ Pract 18(2): 111-117. Araà ºjo, C. L., C. G. Victora, P. C. Hallal and D. P. Gigante (2006). Breastfeeding and overweight in childhood: evidence from the Pelotas 1993 birth cohort study. Int J Obes (Lond) 30(3): 500-506. Armstrong, J., J. J. Reilly and C. H. I. Team (2002). Breastfeeding and lowering the risk of childhood obesity. Lancet 359(9322): 2003-2004. Beyerlein, A., A. M. Toschke and R. von Kries (2008). Breastfeeding and childhood obesity: shift of the entire BMI distribution or only the upper parts? Obesity (Silver Spring) 16(12): 2730-2733. Burdette, H. L., R. C. Whitaker, W. C. Hall and S. R. Daniels (2006). Breastfeeding, introduction of complementary foods, and adiposity at 5 y of age. Am J Clin Nutr 83(3): 550-558. Burke, V., L. J. Beilin, K. Simmer, W. H. Oddy, K. V. Blake, D. Doherty, G. E. Kendall, J. P. Newnham, L. I. Landau and F. J. Stanley (2005). Breastfeeding and overweight: longitudinal analysis in an Australian birth cohort. J Pediatr 147(1): 56-61. Butte, N. F. (2001). The role of breastfeeding in obesity. Pediatr Clin North Am 48(1): 189-198. Buyken, A. E., N. Karaolis-Danckert, A. Gà ¼nther and M. Kersting (2008). Effects of breastfeeding on health outcomes in childhood: beyond dose-response relations. Am J Clin Nutr 87(6): 1964-1965; author reply 1965-1966. Chivers, P., B. Hands, H. Parker, M. Bulsara, L. J. Beilin, G. E. Kendall and W. H. Oddy (2010). Body mass index, adiposity rebound and early feeding in a longitudinal cohort (Raine Study). Int J Obes (Lond) 34(7): 1169-1176. Fallahzadeh, H., M. Golestan, T. Rezvan ian and Z. Ghasemian (2009). Breast-feeding history and overweight in 11 to 13-year-old children in Iran. World J Pediatr 5(1): 36-41. Goldfield, G. S., R. Paluch, K. Keniray, S. Hadjiyannakis, A. B. Lumb and K. Adamo (2006). Effects of breastfeeding on weight changes in family-based pediatric obesity treatment. J Dev Behav Pediatr 27(2): 93-97. Griffiths, L. J., L. Smeeth, S. S. Hawkins, T. J. Cole and C. Dezateux (2009). Effects of infant feeding practice on weight gain from birth to 3 years. Arch Dis Child 94(8): 577-582. Hancox, R. J., A. W. Stewart, I. Braithwaite, R. Beasley, R. Murphy, E. A. Mitchell and I. P. T. S. Group (2014). Association between breastfeeding and body mass index at age 6-7 years in an international survey. Pediatr Obes. Hernell, O. (2011). Human milk vs. cows milk and the evolution of infant formulas. Nestle Nutr Workshop Ser Pediatr Program 67: 17-28. Horta, B. L. and C. G. Victora (2013). Long-term effects of breastfeeding: a systemat ic review, World Health Organisation: 74. Huus, K., J. F. Ludvigsson, K. Enskà ¤r and J. Ludvigsson (2008). Exclusive breastfeeding of Swedish children and its possible influence on the development of obesity: a prospective cohort study. BMC Pediatr 8: 42. Jing, H., H. Xu, J. Wan, Y. Yang, H. Ding, M. Chen, L. Li, P. Lv, J. Hu and J. Yang (2014). Effect of breastfeeding on childhood BMI and obesity: the China Family Panel Studies. Medicine (Baltimore) 93(10): e55. Komatsu, H., T. Yorifuji, T. Iwase, A. Sasaki, S. Takao and H. Doi (2009). Impact of breastfeeding on body weight of preschool children in a rural area of Japan: population-based cross-sectional study. Acta Med Okayama 63(1): 49-55. Kwok, M. K., C. M. Schooling, T. H. Lam and G. M. Leung (2010). Does breastfeeding protect against childhood overweight? Hong Kongs Children of 1997 birth cohort. Int J Epidemiol 39(1): 297-305. Labayen, I., J. R. Ruiz, F. B. Ortega, H. M. Loit, J. Harro, I. Villa, T. Veideb aum and M. Sjostrom (2012). Exclusive breastfeeding duration and cardiorespiratory fitness in children and adolescents. Am J Clin Nutr 95(2): 498-505. Lefebvre, C. M. and R. M. John (2014). The effect of breastfeeding on childhood overweight and obesity: a systematic review of the literature. J Am Assoc Nurse Pract 26(7): 386-401. Marseglia, L., S. Manti, G. DAngelo, C. Cuppari, V. Salpietro, M. Filippelli, A. Trovato, E. Gitto, C. Salpietro and T. Arrigo (2015). Obesity and breastfeeding: The strength of association. Women Birth. Mayer-Davis, E. J., S. L. Rifas-Shiman, L. Zhou, F. B. Hu, G. A. Colditz and M. W. Gillman (2006). Breast-feeding and risk for childhood obesity: does maternal diabetes or obesity status matter? Diabetes Care 29(10): 2231-2237. McCrory, C. and R. Layte (2012). Breastfeeding and risk of overweight and obesity at nine-years of age. Soc Sci Med 75(2): 323-330. Metzger, M. W. and T. W. McDade (2010). Breastfeeding as obesity prevention in th e United States: a sibling difference model. Am J Hum Biol 22(3): 291-296. Michels, K. B., W. C. Willett, B. I. Graubard, R. L. Vaidya, M. M. Cantwell, L. B. Sansbury and M. R. Forman (2007). A longitudinal study of infant feeding and obesity throughout life course. Int J Obes (Lond) 31(7): 1078-1085. Moschonis, G., E. Grammatikaki and Y. Manios (2008). Perinatal predictors of overweight at infancy and preschool childhood: the GENESIS study. Int J Obes (Lond) 32(1): 39-47. Nelson, A. and S. Sethi (2005). The breastfeeding experiences of Canadian teenage mothers. J Obstet Gynecol Neonatal Nurs 34(5): 615-624. Neutzling, M. B., P. R. Hallal, C. L. Araà ºjo, B. L. Horta, M. e. F. Vieira, A. M. Menezes and C. G. Victora (2009). Infant feeding and obesity at 11 years: prospective birth cohort study. Int J Pediatr Obes 4(3): 143-149. Novaes, J. F., J. A. Lamounier, E. A. Colosimo, S. C. Franceschini and S. E. Priore (2012). Breastfeeding and obesity in Brazilian childr en. Eur J Public Health 22(3): 383-389. World Health Organisation. (2015). Breastfeeding. Retrieved March 2015 from https://www.who.int/topics/breastfeeding/en/. Panagiotakos, D. B., A. Papadimitriou, M. B. Anthracopoulos, M. Konstantinidou, G. Antonogeorgos, A. Fretzayas and K. N. Priftis (2008). Birthweight, breast-feeding, parental weight and prevalence of obesity in schoolchildren aged 10-12 years, in Greece; the Physical Activity, Nutrition and Allergies in Children Examined in Athens (PANACEA) study. Pediatr Int 50(4): 563-568. Poulton, R. and S. Williams (2001). Breastfeeding and risk of overweight. JAMA 286(12): 1449-1450. Rathnayake, K. M., A. Satchithananthan, S. Mahamithawa and R. Jayawardena (2013). Early life predictors of preschool overweight and obesity: a case-control study in Sri Lanka. BMC Public Health 13: 994. Sabanayagam, C., A. Shankar, Y. S. Chong, T. Y. Wong and S. M. Saw (2009). Breast-feeding and overweight in Singapore school children. P ediatr Int 51(5): 650-656. Scholtens, S., U. Gehring, B. Brunekreef, H. A. Smit, J. C. de Jongste, M. Kerkhof, J. Gerritsen and A. H. Wijga (2007). Breastfeeding, weight gain in infancy, and overweight at seven years of age: the prevention and incidence of asthma and mite allergy birth cohort study. Am J Epidemiol 165(8): 919-926. Simon, V. G., J. M. Souza and S. B. Souza (2009). Breastfeeding, complementary feeding, overweight and obesity in pre-school children. Rev Saude Publica 43(1): 60-69. Taveras, E. M., S. L. Rifas-Shiman, K. S. Scanlon, L. M. Grummer-Strawn, B. Sherry and M. W. Gillman (2006). To what extent is the protective effect of breastfeeding on future overweight explained by decreased maternal feeding restriction? Pediatrics 118(6): 2341-2348. Thorsdottir, I., I. Gunnarsdottir and G. I. Palsson (2003). Birth weight, growth and feeding in infancy: relation to serum lipid concentration in 12-month-old infants. Eur J Clin Nutr 57(11): 1479-1485. Tosc hke, A. M., R. M. Martin, R. von Kries, J. Wells, G. D. Smith and A. R. Ness (2007). Infant feeding method and obesity: body mass index and dual-energy X-ray absorptiometry measurements at 9-10 y of age from the Avon Longitudinal Study of Parents and Children (ALSPAC). Am J Clin Nutr 85(6): 1578-1585. Twells, L. and L. A. Newhook (2010). Can exclusive breastfeeding reduce the likelihood of childhood obesity in some regions of Canada? Can J Public Health 101(1): 36-39. Vehapoglu, A., M. Yaz?c?, A. D. Demir, S. Turkmen, M. Nursoy and E. Ozkaya (2014). Early infant feeding practice and childhood obesity: the relation of breast-feeding and timing of solid food introduction with childhood obesity. J Pediatr Endocrinol Metab 27(11-12): 1181-1187. von Kries, R., B. Koletzko, T. Sauerwald and E. von Mutius (2000). Does breast-feeding protect against childhood obesity? Adv Exp Med Biol 478: 29-39. Weyermann, M., D. Rothenbacher and H. Brenner (2006). Duration of breastfeeding and risk of overweight in childhood: a prospective birth cohort study from Germany. Int J Obes (Lond) 30(8): 1281-1287. Yamakawa, M., T. Yorifuji, S. Inoue, T. Kato and H. Doi (2013). Breastfeeding and obesity among schoolchildren: a nationwide longitudinal survey in Japan. JAMA Pediatr 167(10): 919-925. Yan, J., L. Liu, Y. Zhu, G. Huang and P. P. Wang (2014). The association between breastfeeding and childhood obesity: a meta-analysis. BMC Public Health 14: 1267.

The King Of Ancient Greek Kingdom Of Macedon Alexander The...

From the king of Ancient Greek kingdom of Macedon Alexander the Great, Through every generation of the human race there has been a constant war, a war with fear. Those who have the courage to conquer it are made free and those who are conquered by it are made to suffer until they have the courage to defeat it, or death takes them. Alexander the Great was born in Pella on July 20, 356 B.C. His parents were king Philip II of Macedon and Queen Olympia, daughter of King Neoptolemus. He was raised in Pella s royal court and spent much of his childhood learning to be a leader. Most of the time his father was busy engaged in military campaigns and he hardly ever saw him. His mother served a powerful role for him and had encouraged him to believe that he was a descendant of heroes. He was tutored by legendary Greek philosopher Aristotle in 343 B.C. which was hired by his father the king Philip II in the Temple of the Nymphs at Meiza. 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Creatine Essay Example For Students

Creatine Essay If, about 5 years ago,you were to tell an athlete there was a supplement (which was not an anabolicsteroid or other bodybuilding drug) that would help bodybuilders and athletespack on as much as 10 rock-hard pounds of muscular bodyweight (which could leadto better performance for athletes) in less then 2 weeks; increase their benchpress by 25 lbs. (which also would help in enhancing performance) in a mere 10days; get a pump like you were loaded on Dianabol(Phillips 48) (apump that last for hours and hours which helps in muscle development); and, allthe while, help you run faster, jump higher, recover from exercise more quickly,they would probably tell you to get lost. Well all these facts and more have nowbeen proven to be effective on athletes. Creatine is the safest, mosteffective supplement out on the market today, says Ron Terjung, aphysiology professor at the University of Missouri. Millions of men are buyingthe dietary supplement, hoping it is the magic pill that can transform them fromscrawny to brawny. Creatine has made a strong impact on the athletic worldgiving many an edge on the competition and enhancing athletic performance. Thediscovery of Creatine leads back to 1832. A French scientist named Chevreul,identified a naturally occurring organic compound in meat and then was laterfound to be manufactured by the liver, kidneys and pancreas using three aminoacids. The scientist named the compound Creatine after the greek word forflesh(Phillips 8). Creatine is a compound that is naturally made in our bodiesto supply energy to our muscles. It is an energy rich metabolite that is foundmainly in muscle tissue. It is responsible for supplying the muscle with energyduring exercise. Chemically, it is called Methylguanido-acid. Creatine is formedfrom the three amino acids, argentine, methionine, and glycogen that undergo achemical process to form Creatine. Creatine is manufactured in the liver and maybe produced in the pancreas and kidneys. It is transported th rough the blood andtaken up by muscle cell, where it is converted into Creatine phosphate; alsocalled phosphocreatine. This reaction involves the enzyme Creatine kinase thathelps bond Creatine to a high-energy phosphate group. Once Creatine is bound toa phosphate group, it is permanently stored in a cell as phosphocreatine untilit is used to produce chemical energy called Adenosine Triphosphate (ATP). ATPthen loses a phosphate group and becomes Adenosine Diphosphate (ADP). Creatine,when present in the muscle in sufficient amounts donates a phosphate group toADP and it rapidly retransform to ATP, which is immediately available to themuscle to be used for a fuel for exercise. During brief explosive-typeexercises, the energy supplied to rephosphorylate adenosine diphosphate (ADP) toadenosine triphosphate (ATP) is determined largely by the amount ofphosphocreatine stored in the muscle. As phosphocreatine stores become depleted,performance is likely to rapidly deteriorate, due to the ina bility toresynthesize ATP at the rate required. Since the availability ofphosphocreatine stores in the muscle may significantly influence the amount ofenergy generated during brief periods of high intensity exercise, it has beenhypothesized that increasing muscle creatine through creatine supplementationmay increase the availability of phosphocreatine and allow for an acceleratedrate of resynthesis of ATP during and following high intensity, short durationexercises(Kreider 1). ATP is the primary source of fuel for muscularexercise. It is used before sugars (carbohydrates) and before fats. When musclesare used to lift weight, run or perform any type of work the ATP is broken downto ADP (adenosine diphosphate) and energy is released. The amount of ATP storedin the muscles will only fuel a maximum effort such as lifting a weight for 10to 15 seconds. After that, the muscle must rely on Creatine Phosphate to restockits supply of ATP. Increasing the muscles supply of Creatine phosphate he lpsincrease the rate in which the body can supply ATP. This increases the musclecapacity to do work and improves the energy level of the muscles. Typically, theaverage person metabolizes about two grams of Creatine per day, and the bodynormally synthesizes that same amount; thus, you generally maintain a Creatinebalance (Bamberger 59), but it is not uncommon for an athlete to have whatis called Creatine deficiency.(Phillips 15) which is not being able tocreate enough Creatine on your own. In these cases through a more balanced dietor by supplementing Creatine in their diet they regain the balance. This leadsto a point that proves in one way how Creatine has an advantage on enhancingathletes performance. Creatine is naturally found in foods. For example, theaverage helping of beef or fish contains about 1 gram of naturally occurringCreatine. Unfortunately, Creatine is very sensitive to heat and cookingvirtually destroys the effectiveness of Creatine. The amount of Creatine neededdepe nds on the athletes body weight and on the number of days Creatine has beensupplemented. Creatine should be loaded in relatively high amounts for the firstsix days of supplementation and then may be taken in daily dosage whilemaintaining positive performance. Creatine can bind water to the muscle givingan athlete a more muscular appearance. Competitive bodybuilders usually dropCreatine supplementation two weeks prior to a show to insure maximum definitionand vascularity. Creatine has not yet been definitely linked to any adversehealth effects, and thus has very few side effects. One side effect usuallycaused by over-dosage which some have complained about is stomach cramps. Reporting for forced girl in baidabo region EssayInnumerable ordinary weekend athletes use it. Its everywhere (Bamberger62). When I was a sophomore in high school, I was first introduced to thismiracle drug called creatine. Many of the guys on the football teamwere taking this, and soon did I. I did not really know what this white powderysubstance was, but all I know is that it seemed to jump my weight up 10 poundswithin about three weeks. My weightlifting maxs seemed to be increasing and Iwas full of energy. Some of us would load just before a footballgame to give us that extra boost of energy. To us, it seemed like legal steroidswith no side effects. Creatine seemed to improve performance for short-durationactivities like our 40 times, bursting off the snap of the ball, and ourweightlifting maxs. What I found was in order to make creatine effective, youmust work out at least three times a week consistently. Most people do notnotice any difference until about three weeks into the cycle. A recent studyfollowed 19 men who lifted weights regularly over 12 weeks. Those takingcreatine registered an average 6.3 percent gain in fat-free body mass, comparedwith a 3.1 percent gain in those not taking the supplement(Timberline 1). In1981, an article published in the New England Journal of Medicine by Dr. l. Silila. Reported that supplementation with Creatine in a group of patientssuffering from a condition called Gyrate Atrophy (a genetic ailment of the eyescaused by a metabolic inability to efficiently metabolize ornithine andsynthesize Creatine). Improved the test subjects strength, increased theirbodyweight by ten percent, and partially reversed the Type II muscle fiberatrophy associated with this disease(Silila 867). One athlete in this group oftest subjects improved his best time in the 100-meter sprint by two seconds. In1993, a study peer reviewed and published in Scandinavian Journal of Medicine,Science and sports (Balsom 143) demonstrated that Creatine supplementation couldsignificantly increase body mass (in only one week) and that it was responsiblefor improved performance in high-intensity intermittent exercise. Over the past4 years, at least 20 separate university studies have demonstrated that Creatinemonohydrate supplementation increases athletic performance; strength;recu peration; speed in the 100-, 200-, and 400-meter sprints. A lot of factual,scientifically proven data shows Creatine monohydrate works. It produces fastand significant results even in the most rigorous trials(Casey 31). The goal ofthe bodybuilder and most athletes is to use progressive resistance exercise toforce the muscles to adapt and grow in size and strength. This increasedworkload or progressive resistance can be achieved in several ways: byincreasing the force of contraction through increased resistance such as whenlifting a heavier weight, by increasing the duration of time that the muscle isunder tension or contracted, and by increasing the frequency of exercise. Creatine helps in all three ways: it helps build lean body mass which allowsstill greater force to be used; provides energy so the duration of exercise orwork can be lengthened; and speeds recovery, so exercise frequency can beincreased. I have also personally benefited from the use of Creatine. I havebenefited from all of the above, but have also gained more personal respect andconfidence for myself from the results I have accomplished with the use ofCreatine. BibliographyBalsom, P. Creatine Supplementation and Dynamic High-IntensityIntermittent Exercise. Scandinavian Journal of Medicine, Science andsports 3 (1993): 143-149. Bamberger, Michael. The Magic Potion.Sports Illustrated 4 (1998): 58-61. Casey, A. Creatine SupplementationFavorably Affects Performance and Muscle Metabolism During Maximal IntensityExercise in Human. American Journal of Physiology 271 (1996): 31-37. Creatine. Available online. Address. http://www.vitamin-planet.com/nutrition/creatine.htmCreatine Monohydrate Frequently Asked Questions. Available online. Address. http://www.rnlist.utl.pt/~rmlbgs/atpfaq.tex Phillips, Bill. Sports SupplementsReview. Golden, Colorado: Mile High Publishing, 1996 Kreider, B. Richard. CreatineSupplementation. (Internet) http://www.afpafitness.com/Creatine3.htmlSilila, I. Supplementary Creatine as a Treatment for Gyrate Atrophy of theChoroid and Retina. New England journal of Medicine 304 (1981):867-870.(Internet) Timberline, David. Muscles for Sale: Is Creatine Rightfor You? (Internet) http://www.accenthealth.com/mh/intheknow/1999/creatine.htmlWhat is the Deal with Creatine? Available online. Address. http://www.powersupplement.com/creatine.htmHealth Care