High Fructose Corn Syrup and Obesity in America

Introduction

A primary concern for many Americans is undesirable weight gain, which relates to food choices made daily. But what if people are aware of their food choices, but not what is in the actual food itself? With obesity on a constant rise, as well as other major health issues, many individuals are searching for reasons and answers. As most humans are omnivores, we consume various amounts of carbohydrates, sugars, and other fatty substances. In particular, high fructose corn syrup which is found in many of the daily food choices we consume. Yet ask yourself do you know what high fructose corn syrup is, or where it is found? In a society where maintaining a healthy lifestyle is important people need to investigate what he or she is putting in their bodies, such as high fructose corn syrup.

What is high fructose corn syrup?

High-fructose corn syrup (HFCS) is a fructose-glucose liquid inducement substitute to sucrose (also known as table sugar) which was first presented to food and beverage manufacturing in the 1970s. It is not expressively diverse in structure or metabolism from other fructose-glucose sweeteners like honey, sucrose, and fruit juice concentrates. High fructose corn syrup was extensively incorporated by food formulators, and its consumption increased around the mid-1970s and mid-1990s, mainly as a spare for sucrose. This was primarily because of its sweetness similar to that of sucrose, better-quality constancy and functionality, and ease of use. High-fructose corn syrup (HFCS), also called isoglucose, is mainly a blend of two sugars, fructose and glucose. Soda and ice cream often merger 55 percent fructose and 45 percent glucose, while the HFCS used in canned fruits and condiments is generally a 42/48 percent mix (with other ingredients). White sugar is a 50/50 split. In the United States, heavy corn supports and sugar-import barricades have made HFCS some 20 percent cheaper than sugar. The United States accounted for nearly 80 percent of global construction in 2004 and U.S. patrons accepted 58 pounds of the syrup per person last year in numerous harvests, conferring to the U.S. Department of Agriculture (USDA). Other producers include Japan, Argentina, the European Union, and China.

Some claim that HFCS's global growth and the parallel rise in obesity are related. The troubled dietitians debate that, unlike glucose, which activates appetite-suppressing indications in the body, fructose does not tell its consumers to stop. The theory rests unconfirmed, but a growing body of literature has recommended the syrup may certainly respond the satiation-hormone leptin.

Conflicting research, reinforced by the American Beverage Institute, claims HFCS is no dissimilar than other sweeteners and is "safe in control." The food manufacturing began to substitute cane and beet sugar with HFCS after sugar prices quadrupled in the 1970s, and a few years later soft-drink businesses followed suit. The syrup's affordability in the United States has aided soda businesses retail greater bottles and greatly expand ingesting of the calorie-rich drinks. You won't find it on the U.S.D.A. pyramid, but there's a food category that includes breakfast cereals, ice cream, granola bars, hot dog buns, baby food, soft drinks, yogurt, soup, ketchup and barbecue sauce.

Those and countless other products found on the shelves of any grocery store are united by a common ingredient: high-fructose corn syrup.

The increasing use of the sweetener over the past three decades roughly corresponds with a dramatic rise in obesity and related health problems among Americans, and some experts on nutrition say that's no coincidence. The question of whether high-fructose corn syrup presents a distinct health threat or is unfairly blamed for the effects of general overconsumption is a divisive one, spawning disagreement even among scientists with no financial stake in the answer. For decades, processed foods were usually sweetened with liquified sugar, also called sucrose. But food researchers in the 1970s found a way to modify cornstarch into a syrup with a higher level of fructose, or fruit sugar, in relation to glucose, another form of sugar. Because the corn product is cheaper, easier to use and more durable than sugar derived from cane or beets, food manufacturers quickly adopted the new ingredient. (Diet sodas and other products contain newer sugar substitutes, such as aspartame and sucralose that carry few or no calories.)

The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.

The digestive and absorptive processes for glucose and fructose are different. When disaccharides such as sucrose or maltose enter the intestine, they are cleaved by disaccharides. A sodium-glucose cotransporter absorbs the glucose that is formed from cleavage of sucrose. Fructose, in contrast, is absorbed further down in the duodenum and jejunum by a non-sodium-dependent process. After absorption, glucose and fructose enter the portal circulation and either are transported to the liver, where the fructose can be taken up and converted to glucose, or pass into the general circulation. The addition of small, catalytic amounts of fructose to orally ingested glucose increases hepatic glycogen synthesis in human subjects and reduces glycemic responses in subjects with type 2 diabetes mellitus (12), which suggests the importance of fructose in modulating metabolism in the liver. However, when large amounts of fructose are ingested, they provide a relatively unregulated source of carbon precursors for hepatic lipogenesis.

The metabolism of fructose differs from that of glucose in several other ways as well (3). Glucose enters cells by a transport mechanism (Glut-4) that is insulin dependent in most tissues. Insulin activates the insulin receptor, which in turn increases the density of glucose transporters on the cell surface and thus facilitates the entry of glucose. Once inside the cell, glucose is phosphorylated by glucokinase to become glucose-6-phosphate, from which the intracellular metabolism of glucose begins. Intracellular enzymes can tightly control conversion of glucose-6-phosphate to the glycerol backbone of triacylglycerol’s through modulation by phosphofructokinase. In contrast with glucose, fructose enters cells via a Glut-5 transporter that does not depend on insulin. This transporter is absent from pancreatic β cells and the brain, which indicates limited entry of fructose into these tissues. Glucose provides “satiety” signals to the brain that fructose cannot provide because it is not transported into the brain. Once inside the cell, fructose is phosphorylated to form fructose-1-phosphate (26). In this configuration, fructose is readily cleaved by aldolase to form trioses that are the backbone for phospholipid and triacyglycerol synthesis. Fructose also provides carbon atoms for synthesis of long-chain fatty acids, although in humans, the quantity of these carbon atoms is small. Thus, fructose facilitates the biochemical formation of triacylglycerols more efficiently than does glucose (3). For example, when a diet containing 17% fructose was provided to healthy men and women, the men, but not the women, showed a highly significant increase of 32% in plasma triacylglycerol concentrations (27).

In the United States, HFCS is found in almost all foods containing caloric sweeteners. These include most soft drinks and fruit drinks, candied fruits and canned fruits, dairy desserts and flavored yogurts, most baked goods, many cereals, and jellies. Over 60% of the calories in apple juice, which is used as the base for many of the fruit drinks, come from fructose, and thus apple juice is another source of fructose in the diet. Lists of HFCS-containing foods can be obtained from organizations concerned with HFCS-related allergies (33). It is clear that almost all caloric sweeteners used by manufacturers of soft drinks and fruit drinks are HFCS (4, 34). In fact, about two-thirds of all HFCS consumed in the United States are in beverages. Aside from beverages, there is no definitive literature on the proportion of caloric sweeteners that is HFCS in other processed foods. HFCS is found in most processed foods; however, the exact compositions are not available from either the manufacturer or any publicly available food-composition table.

What’s in the name of HFCS?

Corn is high in starch, which is simply chains of glucose molecules held together. When chains are broken apart, individual glucose molecules are released and form glucose syrup. In the 1970s, scientist learned how to convert some of that glucose into fructose, and the resulting product was named high- fructose corn syrup. At the time, all other corn syrups were made of glucose. Although accurate relative to the term glucose syrup, the name high-fructose corn syrup has, over the years, been a source of confusion for consumers and scientists, alike. Commercially, various forms of HFCS are available with different percentages of fructose and glucose. The most commonly used are HFCS-42 and HFCS-55 which contain 42% and 55% fructose respectively. Thus, despite the name, HFCS is not particularly high in fructose compared to sucrose. In 1983, the FDA approved HFCS as Generally Recognized as safe (GRAS), and that decision was reaffirmed in 1996. To be included in the FDA’s GRAS list, evidence must exist that the ingredient is safe under the conditions of its intended use, and the approval process involves an extensive review of the science, including estimated dietary intake. The FDA decision to approve and subsequently reaffirm HFCS as GRAS was based in part on the substantial similarity between HFCS and table sugar.

Diabetes and HFCS

Research is clear that sugar do not cause diabetes. The American Association of Clinical Endocrinologists identifies the following as risk factors for diabetes: family history of diabetes, cardiovascular disease, over-weight or obese state, sedentary lifestyle, ethnicity previously identified impaired glucose tolerance or impaired fasting glucose, hypertension, increased levels of triglycerides and/or low levels of high-density lipoprotein cholesterol, history of gestational diabetes, history of delivery an infant weighing over nine pounds, polycystic ovary syndrome and psychiatric illness. Suffice it to say that diabetes is multifactorial. People who are old enough might remember that,

Benefits of HFCS

Compared with other sweeteners, HFCS has historically been relatively inexpensive. And while that HFCS is economical, HFCS is often the sweetener of choice because of its many positive attributes, which extend well beyond cost. HFCS sweetness and flavor profile is similar to table sugar. It also controls microbial growth more than sucrose and controls crystallization. High fructose helps retain texture in canned and baked goods. Another benefit of HFCS is that it reduces crystallization in canned, frozen and baked goods. It promotes ideal and controlled browning in baked goods and breakfast cereals. In the same way HFCS stables temperatures fluctuations and wide ranges of acidity. It blends easily with other ingredients. In the same way HFCS lowers freezing points which contribute to pourability of frozen beverage concentrates.

High Fructose Conspiracy

The use of high fructose corn syrup (HFCS) has increased over the past several decades in the United States while overweight and obesity rates have risen dramatically. Some scientists hypothesize that HFCS consumption has uniquely contributed to the increasing mean body mass index (BMI) of the U.S. population. The Center for Food, Nutrition, and Agriculture Policy convened an expert panel to discuss the published scientific literature examining the relationship between consumption of HFCS or "soft drinks" (proxy for HFCS) and weight gain. The authors conducted original analysis to address certain gaps in the literature. Evidence from ecological studies linking HFCS consumption with rising BMI rates is unreliable. Evidence from epidemiologic studies and randomized controlled trials is inconclusive. Studies analyzing the differences between HFCS and sucrose consumption and their contributions to weight gain do not exist. HFCS and sucrose have similar monosaccharide compositions and sweetness values. The fructose: glucose (F:G) ratio in the U.S. food supply has not appreciably changed since the introduction of HFCS in the 1960s. It is unclear why HFCS would affect satiety or absorption and metabolism of fructose any differently than would sucrose. Based on the currently available evidence, the expert panel concluded that HFCS does not appear to contribute to overweight and obesity any differently than do other energy sources. Research recommendations were made to improve our understanding of the association of HFCS and weight gain.

Overweight and obesity have become increasingly problematic in the United States from an individual and a population perspective. According to the body mass index (BMI) categories defined by the Centers for Disease Control and Prevention (CDC), about 65% of the U.S. adult population aged 20-74 years is currently overweight. In addition, 31% of all overweight adults are classified as obese. In 1976-80, only 47% and 15% of adults in the United States were considered overweight and obese, respectively (CDC, 2004). About 16% of American children and adolescents aged 6-19 years are also currently overweight. Two decades ago, about 6% of individuals in this age group were classified as overweight (CDC, 2004). Prior to 1976-80, such dramatic overweight and obesity rates were not observed in the United States.

Overweight and obese individuals are subject to societal stigmatization and are at increased risk for deleterious health conditions, including type 2 diabetes, cardiovascular diseases, hypertension, osteoarthritis, and some cancers (CDC, 2004). Overweight and obesity increase health care costs (USDA, 2004) and mortality rates (Mokdad et al., 2004, 2005; Flegal et al., 2005). Overweight and obesity are influenced by many genetic and environmental contributors, including race/ethnicity, age, physical activity, sedentary behaviors, food consumption patterns, smoking, technological advancements, and psychological factors (CDC, 2004; Columbia Univ., 2000; Rashad and Grossman 2004). Researchers, government officials, politicians, and activist organizations are contributing significant resources in an attempt to understand and reduce the overweight and obesity "epidemic" in the United States.

All sources of energy consumed in excess of energy needs can contribute to increased BMI and risk of overweight and obesity. However, several arguments suggest that, in addition to providing energy, high fructose corn syrup (HFCS) may contribute to the development of overweight and obesity via other mechanisms. In the United States, HFCS has increasingly replaced refined sugar (sucrose) in many foods and most sweetened beverages. Outside the United States, HFCS is not used extensively, and sucrose continues to be the primary caloric sweetener.

Some evidence suggests that high consumption of fructose plays a role in the epidemics of obesity, hypertension, diabetes, and kidney disease. In the U.S., these epidemics have been paralleled by a rise in sugar consumption. High intake of free fructose (found in high-fructose corn syrup, but not in sucrose) is associated with hypertension and hyperlipidemia in animals and with dyslipidemia and insulin resistance in adults. Further, small particle size of low-density lipoprotein (LDL) is associated with obesity, the metabolic syndrome, and central adiposity in older children and adults. Investigators in Switzerland examined the relation between dietary fructose consumption and obesity, distribution of body fat, plasma lipids, and LDL particle size in a convenience sample of 74 children (age range, 6-14 years) recruited from schools and pediatric clinics; 43 children were overweight (mean BMI, 23.4), and 31 were normal weight (mean BMI, 15.9).

Dietary intake was measured by two 24-hour dietary recalls and a 1-day weighed food record. LDL particle size, triglycerides, and serum cholesterol were measured after a 12-hour fast. Overweight children had significantly higher plasma triglyceride levels, lower high-density lipoprotein (HDL) levels, and smaller LDL particle size than normal-weight children. LDL particle size was associated with overall adiposity and central adiposity. The only dietary factors that correlated significantly with LDL particle size were total fructose intake and grams of fructose per 1000 kcal consumed; higher fructose consumption was inversely associated with LDL particle size, independent of adiposity. Fructose intake did not correlate with any other lipid variable. Some claim that HFCS's global expansion and the parallel increase in obesity are linked. The concerned dietitians argue that, unlike glucose, which triggers appetite-suppressing signals in the body, fructose does not tell its eaters to stop. The theory remains unproven, but a growing body of literature has suggested the syrup may indeed counteract the satiation-hormone leptin. Conflicting research, supported by the American Beverage Institute, insists HFCS is no different than other sweeteners and is "safe in moderation."

The latest health concern stems from a recent Environment Health study that found mercury in samples from two HFCS manufacturers. Chemicals mixed during production to stabilize pH may have contributed the toxic metal, the study said. The industry accuses the research of using "scant data of questionable quality."

The environmental impact of HFCS depends on how the corn is grown. Conventional farming practices use significant water resources, pesticides, and fertilizers, leading to widespread water pollution and nutrient-depleted soil. Corn production has also become a major contributor to climate change. In The Omnivore's Dilemma, author Michael Pollan estimates that between one-quarter and one-third gallons (about 1.0 to 1.25 liters) of oil are needed per bushel of corn to create the pesticides, fertilizers, and tractor gasoline, and to harvest, dry, and transport the corn. The U.S. high-fructose corn syrup industry used about 490 million bushels of corn last year, according to USDA.

Fructose is a sweet tasting sugar that is found naturally in fruits and some vegetables and has been part of the human diet--in modest amounts--for eons. The increasing consumption of sugar has dramatically increased our exposure to fructose (1). Sugar consumption has risen more than 40-fold since the Declaration of Independence was signed 250 years ago, and more than 40% of the added sugars in our diet are in sugar-sweetened beverages and fruit drinks (2,3). Thus, the principal sources of fructose in our diet are now sugar and high-fructose corn syrup, each of which has about 50% fructose. The intake of soft drinks has risen fivefold since 1950 (4,5) (Fig. 1) and with it the intake of fructose. The rise in the consumption of high-fructose corn syrup in beverages has paralleled the rise in the prevalence of obesity and the metabolic syndrome and is associated with the appearance of nonalcoholic fatty liver disease (6-8). Although association does not prove causation, it has stimulated research to understand whether current levels of fructose intake in beverages pose a health risk.

Over the past decade fructose from either sucrose or high-fructose corn syrup has received growing attention as it has been associated with a widening group of health-related problems. Several meta-analyses have shown a relationship between the consumption of sugar-sweetened soft drinks and obesity (9-11). The relation of these beverages to obesity can be attributed to the increased caloric intake and to the fact that beverages do not suppress the intake of other foods to an appropriate degree--thus beverage calories serve as "add-on" calories enhancing the risk of obesity (12) (Fig. 1). Meta-analyses have also suggested that the consumption of sugar-sweetened beverages is related to the risk of diabetes, the metabolic syndrome, and cardiovascular disease