Overconsumption of Sucrose and Fructose may contribute to certain types of Cancer
Though it is hard to establish, the link between cancer and glucose does exist. This is especially disturbing given the fact that the link between diabetes and glucose has been of particular interest to the science community for the past three decades. The bottom line is that most of the problematic cum chronic illnesses in the world today are to a large extent lifestyle diseases. In fact, research has advanced to the extent that the link between strains of diabetes and those of cancer can now be easily ascertained. This therefore implies that sugar it all its forms has devastating impacts on the health of human being. This assertion should be taken seriously given the fact that sugar is the largest source of calorie for most people in the globe. Americans specifically prefer high fructose corn syrup. To this effect, statistics indicate that well over 50% of American consume a half a pound of sugar per day which easily translates to a mind boggling 180pounds of sugar on an annual basis per person.
Based on this premise, the scope of this thesis shall be limited to establishing the link between sucrose and fructose and specific strains of cancer. Basically, the thesis shall beyond reasonable doubt determine that overconsumption of fructose and sucrose can and has in the past been found to cause certain typologies of cancer. This is based on the assertion as earlier mentioned that diabetes can also be a carcinogen; specifically, the dietary patterns influence insulin levels in the body which in turn do results to a condition referred to as hyperinsulinemia which research has determined that is responsible for certain strains of cancer. Therefore, among other strains of cancer, fructose and sucrose increase the risk factor of diabetes mellitus type patients to contracting colon and colorectal cancer. This field of study is however shrouded by a lot of contradictions given that some researchers support this line of thought while others do vehemently negate it. Generally, the carcinogenic effects of fructose and sucrose especially amongst diabetes patients have been a topic of extreme intellectual interest in the past three decades and the scope of this thesis shall enjoin this debate with the objective of establishing the fact that two aforementioned sugar typologies can indeed cause cancer.
2. What Researchers have Clearly Determined
There are good fats and bad fats, good amino acids and bad one too exist. Based on this premise, researchers have similarly established that they are good calories and also that bad calories too do exist. Therefore, sugar too does pose great and grave danger to the public and advocates of this notion have been lobbying different governments for the past decade to impose regulatory measure on sugar as they do on alcohol and tobacco products.in fact, sugar can be likened more to tobacco rather than alcohol. This is the case because whether used in regulated amounts or unregulated ones, studies have established that sugar consumption indeed does cause fatal risk to public health. Indeed, this notion is disturbing given the fact that sugar and it supplements are core components of the dietary regime of almost every individual in the world either in manufactured or natural form.
Before the thesis embarks on the fact finding mission to establish whether fructose and sucrose are carcinogens, we shall briefly look at some of the health risks that are non-contentious and that are caused by the two strains of sugar. Obesity, which has been declared a global epidemic due to the fact that 68% of people in America alone suffer from this lifestyle disease, has been fodder for public debate and intellectual discourse on the global arena. Some of the already determined causes of obesity in the world include but are not limited to dietary regimes. Specifically, obesity can be caused by unchecked fat consumption, increased carbohydrate intake, overconsumption of high-fructose content food to mention but a few. However, it is significant to point out the fact that the link between obesity and fructose is purely epidemiological implying that it is not clear to establish a cause and effect relationship. This is the case because the risk factor of fructose and sucrose cannot be delineated clearly from that posed by other high calories dietary sources.
In addition to causing obesity, it is now a well-established fact that sugar consumption can cause oral disorders specifically dental caries. In fact, statistical estimates indicate that 52% of people with dental caries in the world consume a lot of sugar. To this effect, during the Second World War when the globe was hit by an unprecedented sugar shortage, cases of dental caries decreased significantly. Basically, isolated and primitive communities that are low on sugar intake have a low prevalence rate to dental caries a situation that changes significantly if such societies are exposed to westernized diets that are high in fructose and glucose content. The dental caries causing type of sugar is limited to disaccharides and monosaccharide that food manufacturers in the world use as additives to their products globally.
This therefore does not include natural occurring sugars commonly referred as free sugar. However it must be mentioned that research conducted in Sweden has established that ingestion of fructose and sucrose within a meal at most four times a day does not have a significant impact on the prevalence of dental caries amongst people. It has in fact been established that it is the fructose and sucrose ingestion between meals that predisposes most people to contracting dental caries. In addition to this, it has been wrongfully presumed that withdrawal from high ingestion of fructose and sucrose automatically translates to reduced risk exposure to dental caries. In fact, withdrawal results to intensification of the oral disorder amongst fructose and sucrose junkies who are trying to reform.
Finally, it is a well-known fact that sucrose and fructose significantly contribute to the contraction and consequent progression of diabetes mellitus. Interestingly, these two types of sugars are the most preferred sweeteners for diabetic patients more so in the developed nations and to a large extent worldwide. In fact, before the introduction of insulin therapy, fructose was a significant component in the treatment of diabetes and it was till the discovery of insulin therapy that fructose treatment was abandoned. Basically, just like the case was in dental caries, sugar additives have a higher risk factor compared to free sugar as far as diabetes is concerned. However, the link between fructose and diabetes is hard to establish given that fructose dietary content rarely constitutes national surveys and therefore it is hard to determine the quantity of the monosaccharide that progresses diabetes mellitus.
3. Fructose and Sucrose as Carcinogens of Pancreatic Cancer
Diabetic mellitus and glyemic rich diet have been found as some of the risk factors that do predispose people to pancreatic cancer. This is especially daunting given the fact that pancreatic cancer is the fourth most deadly form of cancer in America which in more often than not result to high mortality rates if left unchecked. As earlier mentioned, sugar sweetened drinks are the major source of absorbable sugars such as fructose and sucrose which are strongly linked to diabetes and obesity. Many studies conducted not only in America but also in the rest of the world have established that patients with diabetes mellitus are at a higher risk of contracting pancreatic cancer. Specifically, research has established the existence if causal-effect relationship existing between absorbable sugars such sucrose and fructose and pancreatic cancer that is evident in the following manner.
Studies have found a strong correlation exists between post load plasma glucose and pancreatic cancer and henceforth the supporting the premise that impaired glucose intolerance, insulin resistance, and hyperinsulinemia play a role in pancreatic cancer aetiology. This therefore implies that high glyemic dietary intake predisposes the unsuspecting public to not only diabetes mellitus but also pancreatic cancer. It is therefore necessary for one to understand what highly glyemic diet comprises; this term is used loosely to describe diet content rich in fructose and sucrose which are two highly absorbable types of sugar. As aforementioned, the most common sources of fructose and sucrose in the world are sugar-sweetened soft drinks that are popular globally. Overconsumption of these soft drinks therefore consequently results to an increase in the blood glucose levels contributing to a high glycaemic index of dietary regime henceforth promoting obesity and diabetes. A recent study dubbed the Nurses’ Health Study (NHS) has concluded that high fructose and sucrose intake as a result of overconsumption of soft drinks might increase the prevalent of pancreatic cancer in the society. In addition, due to the cola content of most of these soft drinks, their overconsumption also subsequently results to insulin resistance and thereby effectively increasing the chances of one contracting cancer.
Despite that fructose and sucrose intake are pancreatic cancer carcinogens, there is little evidence to support the fact that the risk factors varies significantly between high and moderate to low consumers of these two types of absorbable sugar. This implies that the risk factor is statistically similar as far as pancreatic cancer is concerned whether one is a modest consumer of fructose and sucrose or not. In fact studies whose main objectives were to establish the known carcinogens of pancreatic cancer have yielded varied results depending on the factor combination resorted to by the researchers.
For instance while some studies conducted amongst male smokers have established a strong link between pancreatic cancer and high carbohydrates dietary intake, others have established that specifically a high glycaemic load especially among obese women as a result of overconsumption of fructose and sucrose can too cause pancreatic cancer. This implies that the link between pancreatic cancer and fructose consumption can only be established provided that there is a right and specific combination of predisposing the most common of which being obesity and diabetes mellitus. To conclude, it is thus clear that abnormal glucose metabolism and hyperinsulinemia do enhance pancreatic carcinogenesis. Though, this does not delimit the cancer causing aspect to fructose and sucrose because it can be as result of the other dietary constituents other than the two absorbable sugars.
4. Fructose and Sucrose as Carcinogens for Colorectal Cancer
Just like in the case of pancreatic cancer, empirical evidence has now established a relationship between hyperinsulinemia and colorectal cancer. Some of the already established causes of colorectal cancer such as obesity and physical inactivity have a direct impact on insulin metabolism in the human body. As a result, studies have indicated consistently that obese people or people with a history of obesity are more likely to contract colon cancer compared to their non-obese counterparts. In addition to this, research has also established the fact that absorbable sugars such as fructose and sucrose that are responsible for insulin fluctuations within the human body are also responsible for colon cancer. In fact, overconsumption of fructose and sucrose is a predisposing factor to colorectal cancer.
As it is been established above, glycaemic can indeed cause colorectal. The contentious part however and that has been a subject of heated intellectual debate is the long term effects of glycaemic diet especially as far as colon cancer is concerned. However, we must constantly remind ourselves that the objective of this intellectual discourse is limited to whether or not fructose and sucrose are carcinogens for colorectal cancer and any other contentious issue is of course irrelevant as far the scope of this section of the thesis is concerned. A growing body of information alludes to the fact that fructose and sucrose rich dietary ingestion can cause colorectal cancer. This is the case because hyperinsulinemia and glucose resistant which are the two most evident direct consequences of overconsumption of fructose and sucrose do indeed result to the creation of a conducive environment that amongst other things encourages tumour growth within the colon.
This is the case because fructose and sucrose ingestion adversely affect insulin metabolism to some extent. Specifically, “insulin stimulates pathways that increase levels of insulin-like growth factor, and both insulin and insulin-like growth factor promote mitosis and cell proliferation but inhibit apoptosis in normal and cancer cells of the colonic epithelium.” Concentrated fructose and sucrose levels in the body are harmful to the extent that they inhibit glycogenesis in the liver. The consequent result of reduced glucose metabolism is the fact that insulin levels within rise exponentially henceforth glucose absorption occurs in alternative sites rather than the kidney such as muscle tissues. This high glucose absorption in alternative sites results to insulin resistance a situation that impairs glycaemic control if overconsumption of fructose and sucrose is maintained over a prolonged period.
Dietary ingestion of easily absorbable foods and more so specifically those rich in fructose and glucose can trigger such insulin reaction within the colon as a result of sudden blood glucose increase. However, research has revealed that colorectal cancer is caused by several carcinogen including absorbable sugars such as fructose and sucrose. The challenge that most studies have encountered in the studies trying to establish the relationship between colon cancer and over consumption of fructose and sucrose is the factor most other carcinogenic variables are not only hard to identify but also not easily measurable. The only other factors that can be easily ascertained in addition to whether or not absorbable sugars such fructose and sucrose were over consumed is the risk profile of the subjects in question to colorectal cancer.
Risk profile basically refers to other underlying factors that play a major role in predisposing a person to contracting colon cancer and they include but are not limited to body mass index (BMI), physical activity/inactivity, alcohol consumption, and smoking. Depending on an individual’s risk profile, the impacts of overconsumption of sucrose and fructose will have varying effects as far as colorectal cancer is concerned. This thus implies that the nature of a person’s risk profile to a large extent determines the degree to which overconsumption of absorbable sugars is likely to result to colon cancer. Based on this premise, it can thus be safely concluded that most studies seeking to establish the link between colorectal cancer and fructose/sucrose intake have an error margin implying that in reality they are either exaggerated or underestimated depending the other factors in play. It is however clear that overconsumption of fructose and sucrose rich diets triggers insulin-like growth factors that create an ideal breeding ground for colorectal carcinogenesis. It is however unclear whether this relationship is statistically significant or not. Further studies are henceforth necessary to determine whether the relationship between fructose and sucrose consumption is statistically significant specifically in relation colorectal cancer.
Despite the factor that fructose and sucrose are known carcinogens as demonstrated in the thesis, little research has been dedicated to this specific field of cancerous studies. Theoretically, sucrose and fructose are two different absorbable sugars that are sources of calorie in addition to glucose. The situation is however different practically especially amongst manufacturers whereby fructose is the preferred cheapest substitute for sucrose. This implies that for practical purpose, the two absorbable sugars are used interchangeably. The refining process used to produce most foods containing fructose is to a large extent to blame for the lethal nature of the absorbable sugar especially in relation to cancer. This is the case because the refining process not only concentrates the fructose and sucrose levels in foods but also eliminates substances such as polyphenols present in the naturally occurring forms of these sugars that slow down their digestion and absorption in the human body.
Academy of Nutrition and Dietetics. “Position of the Academy of Nutrition and Dietetics: Use of Nutritive and Nonnutritive Sweeteners.” Journal of the Academy of Nutrition and Dietetics 2012;112 (2012): 739-758.
Adams, Mike. The top five cancer-causing foods. 24 April 2007. 17 August 2012
Appleton, Nancy and G. N. Jacobs. Suicide By Sugar: A Startling Look at Our #1 National Addiction. New York: Square One Publishers, 2009.
Higginbotham, Susan, et al. “Briefcommunication: Dietary Glycemic Load and Risk of Colorectal Cancer in the Women’s Health Study.” Journal of the National Cancer Institute, Vol. 96, No. 3, February 4, 2004 (2004): 229-233.
Liu, S. P., et al. “Glycine N-methyltransferase-/- mice develop chronic hepatitis and glycogen storage disease in the liver.” Hepatology. 2008 Feb;47(2):769 (2008): 13-25.
Michaud, Dominique S., et al. “Dietary Glycemic Load, Carbohydrate, Sugar, and Colorectal Cancer Risk in Men and Women.” Cancer Epidemiology, Biomarkers & Prevention (2005): 138-144.
Moynihan, Paula J. “The role of diet and nutrition in etiology and prevention of oral diseases.” Bulletin of the Workd Health Organization, September 2005, 8(5) (2005): 694-670.
Rippe, James M. “The Health Implications of Sucrose, High-Fructose Corn Syrup, and Fructose: What Do We Really Know?” Journal of Diabetes Science and Technology Volume 4, Issue 4, July 2010 (2010): 1008-1011.
Schernhammer, Eva S., et al. “Sugar-Sweetened Soft Drink Consumption and Risk of Pancreatic Cancer in Two Prospective Cohorts.” Cancer Epidemiology, Biomarkers & Prevention 2005;14(9). September 2005 (2005): 2098-2105.
Weeks, Dr. Shannon. The Devil in the Fructose. 4 January 2011. 17 August 2012