the exceptional sweetness of sugar

Our first encounter with sugar's extraordinary flavor began with a dollop of buttercream and a spoonful of strawberry ice cream rather than the normal pureed carrots, a gustatory revelation that falls through the gap of early childhood. However, as Jabr (20130) says, the experience of initial sweetness is often well maintained before our bodies' resistance to glucose switches abruptly. Our cells depend on sugar for nutrition, indicating that we have an inherent fondness for sweetness. Most physicians believe that overindulging of sugar is the first stage of self-poisoning (Gornall, 2015). They argue that taking too much sugar has more significant risks than love handles and tooth cavities. Whatsoever, the majority of people agree that taking adequate amounts of sugar is not bad but excessive intake of sugar is the problem since it causes obesity, diabetes, and cardiovascular diseases.

Nevertheless, O'Connor (2016) argues that the dangers of sugar depend on the kind of sugar one takes and not the amount, a statement that he fails to base on scientific grounds. Most sugars constitute a combination of two molecules, fructose and glucose in distinct ratios. For instance, the sugar contained in an apple fruit is identical to table sugar, which may be added to homemade apple pie. Both of them are sucrose, and they undergo breakdown in the intestine to form fructose and glucose. This arouses questions as to which sugar is good and which one is bad given that all undergo metabolism that breaks them into glucose and fructose. According to Schaefer, Gleason, and Dansinger (2009), over a third of American adults and about 12.5 million adolescents and children have obesity. This triggers our thirst of knowledge on the type of sugar that causes obesity and their resultant effects on the body.

Agreeing to Zerbe’s (2017) proposition, there is the tendency of many people blaming dietary fat as the primary cause of cardiovascular diseases. This happens due to lack of adequate exposure to scientific evidence on the same. While particular artificial, inflammatory fats such as trans fats trigger heart attacks (Kodali, 2014), sugar is the main reason for such diseases. In 2016, researchers uncovered big sugar industry scandal, which indicated lobby sponsoring phoney Havard research in the 1960s so that researchers could withdraw their efforts towards the health effects due to sugar intake (Kearns, Schmidt, & Glantz, 2016). The researchers arrived at their conclusion that coronary heart diseases could only be avoided by circumventing or eating less of cholesterol and substitute saturated fats with polyunsaturated fats (Fernandez, 2016). My understanding does not, however, admit to these assertions as they are not true. Furthermore, past literature review strongly criticized findings that linked sucrose to heart diseases while ignoring the shortcomings of the studies that were investigating dietary fats. All these compounded resulted to misdirections about the major cause of heart diseases (Kearns, Schmidt, & Glantz, 2016). However, Schidmt states that “there is now a considerable body of evidence linking added sugars to hypertension and cardiovascular disease, which is the No. 1 cause of premature death in the developed world” (Fernandez, 2016). From my standpoint, the statement is true and has a strong scientific base.

The argument ascertaining sugar as very toxic can be described using technical details regarding the distinctive ways that human bodies gain energy from different sugars for physiological processes. This case is based on a study conducted by Schaefer, Gleason, and Dansinger (2009). While we argue on this, it is essential to understand that majority of Americans consume sugar in two main forms, high-fructose corn syrup, and the table sugar (Jabr, 2013). Each sugar molecule is made of glucose and fructose molecules that are bonded to each other (Schaefer, Gleason, & Dansinger, 2009). The two sugars constitute identical chemical formulas but slightly distinct atomic compositions/structures. Also, these two sugar constituents have sweetness embedded in them, which makes them be consumed more often.

Beth Haney (2015) asserts that, irrespective of what type of sugar we eat, our body cells are only interested with glucose, fructose, and not the compact glucose. She further states that intestinal enzymes break down sucrose into glucose and fructose in seconds. This is not true for their constituent molecules as they take entirely different direction of metabolism. According to my understanding, glucose is absorbed into our bloodstream where it travels to the tissues, which contains cells to convert the glucose into energy while fructose heads to the liver that contains specific cells to break down fructose (Jabr, 2013). According to Brandt (2016), glucose metabolism results in products such as energy, carbon dioxide and water. Also, glucose is stored in the form of glycogen in the liver or is converted to fatty acids that are deposited as TG in adipose tissues when there is excess energy. Under situations of chronic energy excess, according to Gunnars (2013), adipose cells and muscles develop resistance to the insulin effects leading to less intake of glucose. It is in this case that diabetes type two develops when the pancreas is unable to meet demands for the production of insulin. In contrast, the liver contains a few cells that convert fructose into energy, placing fructose only in one organ. The liver changes the fructose into glucose and lactase. As a result, the liver is taxed in that it uses a lot of energy to convert fructose into other molecules, which eventually exhausts its energy leading to the production of uric acid linked to kidney stones, gout, and high blood pressure. These conditions, however, could be caused by other factors that researchers do not expound when discussing sugar metabolism and its effects.

The human body is designed to regulate the quantity of glucose in the blood (Nursing, Allied Health and Other Health-related Educational Grant Program, 2017). When the glucose is absorbed into the body, the pancreas is stimulated to secrete insulin, the hormone that aids in the removal of excess blood glucose and boosts the production of leptin, a hormone that suppresses hunger. Conversely, insulin secretion is not triggered by fructose but instead triggers an increase in hormone grehlin that keeps us hungry. Thus, having too much fructose in the body encourages people to eat more than their body requires. Moreover, high levels of fructose in the body lead to increase in fat production in places such as the liver and increased levels of triglycerides circulation raising the risks for clogging of arteries and cardiovascular problems. Thus, the higher the amount of sugar a person takes, the higher the risk of cardiovascular problems.

Norman (2017) contends that fatty liver results to insulin resistance, which makes body cells to become less responsive than usual, which in turn exhausts the pancreas until it is unable to regulate the levels of blood glucose. Basing on a study by Ouaamari, Zhou, Liew, Shirakawa, & Dirice, etc. (2015), I agree with Norman since fructose metabolism product (uric acid) enhances insulin resistance associated with obesity and type two diabetes, which emphasises on the adverse effects of sugar. These disorders take place at the same time. Jabr argues that the metabolism of fructose causes chain reactions of potentially toxic chemical alterations in our bodies, which Lusting and Taubes terms as “the rotten apple of the sugar family.” When discussing sugar as a toxin, they specifically incline on fructose. However, the past five years have seen nutritionists and biochemists challenging the idea of fructose being a risk factor for our health (Deshmukh, Cox, Jensen, Meissner, & Mann, 2015). They argue that replacement of fructose with other sugars such as glucose will not provide any solution. Initially, John White (2017), a fructose expert claims that despite a decline in the consumption of fructose, there is no significant improvement in the level of obesity seems to rise in the US. However, I argue that the coincidence of trends does not determine anything. In several meta-analyses studies, such as the one carried out by John Sienvenpiper and his colleagues (2014), there is no serious implications of taking fructose on blood pressure, body weight, and the uric acid production. I consent this finding since other studies (Schaefer, Gleason, & Dansinger, 2009) do not provide the quantities of fructose that can be consumed to dim fructose toxic to the body.

Much as there mixed propositions whether sugar is good for humans, research has stood firm to support this. However, my point is that the risks associated with sugar ingestion depend on the type of sugar and not every sugar. For instance, an article on Healthline, stresses that added sugar is bad for the teeth, overloads the liver, can lead to fatty liver disease, can result in insulin resistance that progresses to cause type two diabetes and cancer. To add on this, sugar affects hormonal balance and the brain functioning, which is enhanced by the sugar’s different fat-promoting implications. In this case, sugar causes the release of large amounts of dopamine, making it addictive to take. In both Children and Adults, sugar intake leads to obesity, which h poses a person into risks of diabetes and other cardiovascular diseases. Sugar does cause this disorders by raising the levels of cholesterol. Nevertheless, we cannot do away with sugar as our bodies require energy for physiological processes. It, therefore, means we have a role to play to ensure our blood glucose remains between 70mg/dl and 110mg/dl. Below and above this can raise or lower blood pressure resulting in heart problems. Moreover, it is critical to understand that people’s tolerance to glucose is different and thus people should be able to monitor their blood sugar levels by better choices of what they chose to eat. Some researchers state that all sugars are bad for the body when taken more than what the body requires. However, this is not supported as sugars from fruits, and unprocessed natural products do not seem to pose higher risk compared to added sugar.



References

Brandt, M. (2016). Chapter 5: Endocrine Regulation of Glucose Metabolism. Chicago: University of Chicago Press,.

Deshmukh, A. S., Cox, J., Jensen, L. J., Meissner, F., & Mann, M. (2015). Secretome Analysis of Lipid-Induced Insulin Resistance in Skeletal Muscle Cells by a Combined Experimental and Bioinformatics Workflow. American Chemical Society, 14(11), 4885–4895.

Fernandez, E. (2016, September 12). Sugar Papers Reveal Industry Role in Shifting National Heart Disease Focus to Saturated Fat. University of Califonia San Franscico. Retrieved from https://www.ucsf.edu/news/2016/09/404081/sugar-papers-reveal-industry-role-shifting-national-heart-disease-focus

Gornall, J. (2015). Sugar’s web of influence 2: Biasing the science. BMJ, 350(215). Retrieved from http://dx.doi.org/10.1136/bmj.h215

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Haney, B. (2015). Effects of Sugar on Our Bodies: The Good, the Bad, and the Options. New York, U.S.: Luxe Aesthetic and Wellness Center.

Jabr, F. (2013, July 15). Is Sugar Really Toxic? Sifting through the Evidence. Scientific American. Retrieved from https://blogs.scientificamerican.com/brainwaves/is-sugar-really-toxic-sifting-through-the-evidence/

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Kearns, C. E., Schmidt, L. A., & Glantz, S. A. (2016). Sugar Industry and Coronary Heart Disease ResearchA Historical Analysis of Internal Industry Documents. Special Communication, 1(1). doi:10.1001/jamainternmed.2016.5394

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Nursing, Allied Health and Other Health-related Educational Grant Program. (2017, October 01). Glucose Regulation. Retrieved from Austin Community College: http://www.austincc.edu/apreview/EmphasisItems/Glucose_regulation.html

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