The Relationship Between Increased Fructose
Consumption and Weight Gain
This research reviewed the recent studies which explored the causal relationship between high fructose consumption and obesity in contemporary American population. The study was prompted by the researcher’s knowledge on the so called “epidemic” of obesity that has alarmed health experts not only in the United States but all over the world. This study, which aimed to determine whether there was strong evidence to support the idea that increases fructose consumption, found out that there is strong research-based evidence to prove the aforementioned causal relationship.
The growing concern over the nation’s ever-widening waistlines has prompted health practitioners into a reexamination of the current American culture and lifestyle in an attempt to discover the factors that influence obesity risks in the United States. Among the most prominent today, though not entirely new, is the idea that an individual’s weight largely depends upon both hereditary predisposal and the environment.
However, while one’s genes determines the amount of calories that the body can metabolize, environmental influences on dietary habits play a crucial role in an individual’s physical health and structure (Hill and Peters, 1998). For instance, the rise of sweetened beverages such as soft drinks which have become almost a staple in American living, also led to increased fructose consumption for majority of the people beginning with the time in the 1980s when fructose started to replace glucose as the main sweetening ingredient of commercial beverages.
This study therefore posits that increased fructose consumption leads indirectly to obesity.
Background/Review of Existing Data
For the past ten years, American health experts have been increasingly disturbed by the significant rise in the number of Americans with weight problems. A study by Cutler, et. al. (2003) points to the growth in mass-prepared and mass-produced food that increased the caloric intake of every American, making obesity cases in the United States rise faster than its contemporaries in other advanced countries. According to the researchers, “technological innovations—including vacuum-packing, improved preservatives, deep freezing, artificial flavors, and microwaves—have enabled food manufacturers to cook food centrally and ship it to consumers for rapid consumption (Cutler, et. al., 2003).” As a consequence of the greater availability and cheapness of food afforded by mass production, people also had the chance to consume food in greater volumes, which also meant rising caloric intake that later led to weight management problems.
However, the notion—that the added calories from the excessive intake of soft drinks and other sweetened beverages are chiefly responsible for weight gain—is now being challenged by developments in scientific research. Although there is great ambivalence as to the exact relationship between high fructose diets and obesity in humans since most of the experiments have hitherto been limited to animals, experts are convinced that fructose may play a significant factor in weight gain.
As early as 1990, experiments have been utilized to prove the contention that fructose consumption had weight gain-inducing on the body. Tordoff and Alleva (1990), for instance, compared the effects of aspartame (APM) and high-fructose corn syrup on the weight of human individuals. The result of their study—that “drinking large volumes of APM-sweetened soda, in contrast to drinking HFCS-sweetened soda, reduces sugar intake and thus may facilitate the control of calorie intake and body weight (Tordoff and Alleva, 1990),” spawned research into the characteristics of HFCS and fructose in general which contributed to weight gain among both male and female humans.
A recently concluded study at the University of Cincinnati led by Matthias Tschöp, MD, associate professor in UC’s psychiatry department and a member of the Obesity Research Center at UC’s Genome Research Institute, argues that “the total amount of calories consumed when fructose is added to diets may not be the only explanation for weight gain (Kimmon, 2005).” The study, which aimed to determine whether fructose indeed contributed to obesity and the particular way that it did or did not contribute to weight gain, found out that fructose consumption in mice contributed to obesity by affecting the hormonal processes that prevents mice’ ability to effectively metabolize fat (Tschop, et. al., 2005).
Prior to this, Bray, et. al. (2004), in an attempt to discover the causes of obesity among humans, investigated the relationship between obesity and the highfructose corn syrup (HFCS) consumption by analyzing the Americans’ food consumption patterns in a span of thirty-three (33) years using the United States’ food consumption tables. They found out that a sharp increase of one hundred percent (100%) HFCS intake from 1970 onwards which, they argued, reflected the pattern of a rapid increase in obesity among Americans. They illustrated the difference in the human body’s reaction to fructose from that of glucose, suggesting that “fructose does not stimulate insulin secretion or enhance leptin production,” a hormone that “acts as key afferent signal in the regulation of food intake and body weight.(Bray, et al., 2004)”
In a similar study, Bantle, et. al. (2000) found out that “dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men,” adding that diets high in added fructose are potentially unhealthy especially for men and recommending the use of glucose as a better alternative.
A study conducted by Havel, et. al. (2002) support these findings. The study, which aimed to explore the causal relationship between fructose, obesity, and insulin resistance syndrome, contend that fructose—which by its nature is not involved in the stimulation of insulin secretion—reduced leptin concentrations and production necessary in the regulation of appetite and in proper energy homeostasis. This increased the chances that an individual on a high fructose diet would gain weight (Havel, et al., 2002).
Aside from this was the fact that unlike glucose consumption, which “kicks off a cascade of biochemical reactions,” and “ increases production of insulin by the pancreas, which enables sugar in the blood to be transported into cells, where it can be used for energy (Squires, 2003),” fructose “appears to behave more like fat with respect to the hormones involved in body weight regulation…that suggests that consuming a lot of fructose, like consuming too much fat, could contribute to weight gain (Squires, 2003).”
Based from the aforementioned researches, it is clear that there is a rapidly emerging consensus among health and dietician experts that high levels of fructose consumption increase the probability of weight gain by inhibiting the response from leptin and insulin. The evidences gathered from studies conducted as far back as 1990 supports the argument that an increase in fructose intake through sweetened beverages would lead to obesity.
Although majority of these studies were conducted using laboratory animals in controlled settings which severely undermined the role of other causal factors such as physical activity and hereditary predisposal to weight gain, the results suggest that there might be reason to believe that the rising number of obesity problems in the United States and elsewhere in the world is due to the increased consumption of fructose—which has replaced glucose as major sweetener in most processed food and beverage—in the human diets.
The findings of this study point towards the adoption of the idea that, indeed, increased fructose consumption leads to obesity. This occurs from the 1) suppression of leptin and insulin, hormones responsible for appetite regulation, and 2) non-matabolism of fructose into energy similar to glucose but into fat instead (in animals, at least).
However, the inconclusive nature of the existing studies and data on the role of fructose in humans leads the researcher to recommend exhaustive research into the same area, preferably one that takes into consideration the sociological processes aside from the biological processes that influence dietary habits which in turn influence the likelihood of obesity and weight gain into taking place.
Tschop, Matthias, et al. Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice. Obesity Research. V. 13 No. 7 (July 2005) pp.1146-1156.
Bray, George, et. al. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. American Journal for Clinical Nutrition V. 79 (USA, 2004) pp. 537-543.
Cutler, David, et. al. Why have Americans Become More Obese? The Journal of Economic Perspectives. V. 17, No. 3. (Summer, 2003) pp. 93-118
Havel, Peter, et. al. Fructose, weight gain, and the insulin resistance syndrome.The American Journal for Clinical Nutrition. V. 76. (USA, 2002) pp. 911–922.
Bantle, John, et. al. Effects of dietary fructose on plasma lipids in healthy subjects. American Journal for Clinical Nutrition. V. 72. (USA, 2000) pp. 1128-1134.
Hill, James and Peters, John. Environmental Contributions to the Obesity Epidemic. Science. V. 280 (1998),
Tordoff, Michael, and Alleva, Annette. Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight. American Journal for Clinical Nutrition V. 51 (USA, 1990) pp. 963-969.
News and Website Articles
Squires, Sally. Sweet but Not So Innocent? High-Fructose Corn Syrup May Act More Like Fat Than Sugar in the Body. Washington Post. (March 11, 2003) p. HE01.
Kimmon, Dama. New link between soft drinks and weight gain. Medical News Today. (July 31, 2005) www.medicalnews.org