Larger Than Life
12 July 2014
[A look at the epidemiology, resultant effects, and potential solutions for obesity and obesity related health risks. Examines inherent causation of the disease as well as environmental factors.]
Since the onset of the bubonic plague, the world has yet to see a disease so devastating that it threatens the health and prosperity of generations to come. Obesity, which is identified as a measurement of body mass index (BMI) over 29.5, has always existed. However, the disease itself has established itself in the form of an epidemic. Since the 1980s the worldwide obesity rate has seen a twofold increase up to its current level; nearly 10% of the world’s population, a staggering 670 million people is classified as obese (Obesity and Overweight). While the prevalence of the disease is cause for concern, the other health complications associated with obesity are truly problematic. Obesity can be attributed to many negative health complications such as diabetes, heart disease, myocardial hypertrophy, hypertension, and other health effects. However, obesity is a disease that is completely preventable. In looking at ways to positively affect the prevalence rate of obesity, attention must be paid to the causality of the disease. By further examining the mechanisms by which obesity develops and operates, health professionals and organizations will be readily equipped to slow and reverse the development of obesity throughout the world. The epidemiology of obesity is a resultant of a mixing of different effects. A toxic food environment and genetic predisposition both play a decisive role in the manifestation of obesity.
In a world where the effective management of one’s personal time is of the utmost importance, convenience is often given preference over quality. This is especially true of food culture. Gone are the days where most come home and sit down for family dinner every night. Over the course of the past two decades, the amount of time families spend together around the dinner table has seen a decrease of approximately 33% (Gurian). Conversely, fast food has become a staple throughout food markets. The convenience of a drive thru, not having to wait a long time for a meal, and comparatively low costs has made fast food an attractive option. In America alone, during 2007–2010, adults consumed, on average, 11.3% of their total daily calories from fast food (Fryar, Ervin). Assuming an average diet of 2000 calories a day, 7 days a week for one year, the average adult American consumed 247,470 calories from fast food over this three year period. One pound of fat is equivalent to around 3500 calories. By this calculation, 240,000 calories worth of fast food is approximately 70 lbs worth of pure fat. This statistic reveals the heart of the problem. While only representative of a minor part of the total food consumption of an average American, fast food’s presence at this scale is problematic.
A well versed food-science representative from Coca-Cola may argue that calories are just calories, but this is simply not the case; 150 calories from a coke soda does not have the same effect on the body as 150 calories of fruit or orange juice. Comparatively, fast food does not possess the same holistic nutritional profile as real, whole foods. Take a Big Mac from McDonalds and compare it to its caloric equivalent in baked chicken, rice and spinach (prepared in the absence of additives). The Big Mac consists of 550 calories, 47% of which are from fat, as well as 10g of sugar and nearly 1000mg of sodium (over 40% of the recommended Daily Value (DV)) (Big Mac :: McDonalds.com). On the other hand, a meal comprised of chicken, rice and spinach, possessing the same total caloric value, renders nearly zero calories from fat of any kind, and other key vitamins and minerals. Regardless of the nutritional benefits of consuming whole foods, consumers are eating more fast food than they used to. This is having a pronounced effect on the prevalence of obesity. A study published by the American Journal of Health Promotion discovered that nearly 70% of variance in obesity rates between states in America is a resultant of fast food restaurant prevalence (Maddock). Fast food, despite its convenience, cost effectiveness and ease of access, is costing consumers more than just a trip to the drive through. Fast food represents a toxic food environment. Healthy eating has been replaced with convenience eating, and with this change fast food companies have taken shortcuts and cut corners in developing their food products. Instead of healthy, nutritious and diverse, food values have turned into cheap, fast and fried.
Outside of bad food consumption choices, consumers also face the daunting challenge of dealing with the unseen mechanism of genetics. Genetic disposition to obesity cannot be influenced or controlled. However, just as with the case of heritable dispositional susceptibility to heart disease or cancer, genetics plays a profound role in the development of obesity. A study done by a group of nutritional scientists published in “Lipids in Health and Disease” shows the correlation between genetic susceptibility to varying regulation of leptin gene expression which, “which may lead to obesity in these obese mutant rat strains” (Kalashikam et al.). Leptin, a hormone in the human body, is the main factor in the control of adipose (fat) tissue metabolism. Genetic disposition for poor regulation of leptin levels has a correlating effect with the prevalence of obesity. If the body cannot produce enough leptin to appropriately take care of adipose tissue levels, then the body will have difficulty in metabolizing fat tissue for energy. This results in overweight and the eventual development of obesity. Another study looked at obesity prevalence of American adolescents in comparison to immigrants from outside of the country,
“In the United States, Asian American and Hispanic American adolescents are more than twice as likely to be obese as first-generation immigrants from their countries of origin. These observations support a model in which susceptibility to obesity is determined largely by genetic factors, but the environment prompts phenotypic expression” (Qi, Young).
It is clear then, regardless of gene-environment interactions, genetic factors are the underlying mechanism in which obesity expresses itself. Lastly, “Obesity Epidemiology” reveals data from published studies on twins and interpreted results of what those findings correlate to in obesity’s developmental mechanism, “Findings from family and twin studies suggest that obesity and obesity-related traits have a substantial heritable component” (Hu). Genetic disposition and susceptibility to obesity is not something that develops throughout one’s lifetime, but rather a heritable trait passed from generation to generation.
Finding new ways to stop and prevent obesity is essential in establishing continued prosperity for future generations. Obesity threatens to eradicate many of the comforts consumers have come to enjoy. Enjoying a leisurely walk in the park or a nice stroll down the beachfront becomes nearly impossible due to the debilitating physical effects of obesity; the afflicted experiences much difficulty in performing even light to moderate physical activity. Moreover, there is a severely heightened risk for the development life threatening diseases associated with obesity. “Compared with men and women in the normal weight range (BMI lower than 25), men with BMIs of 30 or higher had a sevenfold higher risk of developing type 2 diabetes, and women with BMIs of 30 or higher had a 12-fold higher risk” (Health Risks). Obesity’s influence extends further than just a bigger waist circumference or self-esteem issues. Not only does obesity cause an increased vulnerability to diabetes, it also leads to amplified risk for heart disease and stroke, “As BMI increases, so do blood pressure, low-density lipoprotein (LDL, or “bad”) cholesterol, triglycerides, blood sugar, and inflammation. These changes translate into increased risk for coronary heart disease, stroke, and cardiovascular death” (Health Risks). Considering that obesity is a heritable, the inability to effectively halt the rising prevalence of obesity could have far-reaching implications for generations to come. If the disease continues to jump from one generation to the next coupled with increased susceptibility—the result could be an exponential increase in obesity rates as well as subsequent death from associated risk factors.
The obesity epidemic extends beyond manageable circumstances. Heritability of obesity has resulted in the development of a calamity that is difficult to combat. If genetics cannot change, then what can? The answer lies in addressing the toxic food environment that surrounds the obesity epidemic. Better nutrition education on the part of organizations across the globe, programs to help support the dissemination of this information, and alternatives to lethal fast food would be an optimal starting point in the battle against obesity. However, these initial efforts will not have a lasting effect on the relative occurrence of obesity. It is the environment that controls available food options, how much people eat, and societal perception of obesity. Change in the socioeconomic and political environment of the consumer constitutes the only method of establishing permanence in reducing obesity rates worldwide.
"Big Mac :: McDonalds.com." Big Mac :: McDonalds.com. McDonalds. Web. 03 July 2014.
Fryar, Cheryl D., M.S.P.H., and Bethene R. Ervin, Ph.D., R.D. "Caloric Intake From Fast Food Among Adults: United States, 2007–2010." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 21 Feb. 2013. Web. 01 July 2014.
"Genes Are Not Destiny." Obesity Prevention Source. Web. 03 July 2014.
Gurian, Anita, PhD. "Family Meals Matter-staying Connected | AboutOurKids.org." Family Meals Matter-staying Connected | AboutOurKids.org. NYU Child Study Center. Web. 03 July 2014.
"Health Risks." Obesity Prevention Source. Harvard School of Public Health. Web. 02 July 2014.
Hu, Frank B. Obesity Epidemiology. Oxford: Oxford UP, 2008. Print.
Maddock, J. "The Relationship Between Obesity and the Prevalence of Fast Food Restaurants: State-Level Analysis." American Journal of Health Promotion. 2044 Dec. 19. Web. 03 July 2014.
"Obesity and Overweight." WHO. World Health Organization, May 2014. Web. 01 July 2014.
Qi, Lu, and Young Ae Cho. "Gene-environment Interaction and Obesity." PubMed.gov. National Center for Biotechnology Information, U.S. National Library of Medicine, Dec. 2008. Web. 25 June 2014.