Essential Fatty Acids Omega 3 FA: Converted into Eicosapentaenoic Acid/EPA & Docosahexaenoic Acid/DHA (omega 3 → EPA → DHA) EPA: Converted into Leucotrienes (series 5) & Prostoglandins & Thromboxanes (series 3) Dilate blood vessels, reduce clotting, lower LDL & increase HDL, decrease inflammation DHA Utilized for nervous system development and overall development Omega 6 FA Arachidonic acid: Converts into Leucotrienes (series 4) & Prostoglandins & Thromboxanes (series 2) constrict blood vessels, promote clotting, increase LDL & decrease HDL, increase inflammation

High Fructose Corn Syrup Until 1957 there was no such thing as high fructose corn syrup because, until that time, people had operated with the understanding – a correct understanding, in fact – that there is no fructose in corn syrup. Corn syrup contains another sugar molecule, considerably less sweet than fructose, called glucose. In 1957, a pair of researchers named Marshall and Kooi developed in their laboratory an enzyme called glucose isomerase that remarkably – actually, astonishingly – could work on corn syrup to rearrange the molecular composition of glucose and convert it to fructose. Glucose isomerase brings about the isomerization, or rearrangement, of glucose, hence the name. The more that the natural glucose in corn syrup is converted by the enzyme to fructose, the sweeter the syrup becomes. High fructose corn syrup means that a high percentage of the glucose is converted to fructose. Corn syrup, typically a mildly sweet sweetener, suddenly had the potential to become strikingly sweet.

High Fructose Corn Syrup When the glucose in corn syrup is converted to fructose, corn syrup can be sweeter than sugar, depending on how much of the glucose is actually converted to fructose. The two standard high fructose corn syrups sold today are 42% high fructose corn syrup and 55% high fructose corn syrup. 42%, which refers to the percentage of glucose converted to fructose, is about as sweet as sucrose, or liquid sugar; 55% high fructose corn syrup is sweeter than liquid sugar. And in the U.S., where corn is plentiful, corn syrup is not expensive to produce. High fructose corn syrup was as sweet, if not sweeter than sugar, and cheap to make.

High Fructose Corn Syrup When, therefore, high fructose corn syrup began to be produced on an industrial scale in the 1970’s, high fructose corn syrup rapidly swallowed up much of the sweeteners market. A Time Magazine article in 1974 described the stupefaction of sugar producers when, in part due to the emergence of high fructose corn syrup, they began to notice that the annual consumption of sugar was falling. “It was like telling them,” the author noted, “that people were breathing less air.” According to a 1997 USDA report, in 1970 sucrose accounted for about 83% of sweeteners Americans ate, but by 1997 sucrose was only about 43%. High fructose corn syrup made up virtually the rest, or about 56% of the sweeteners that Americans consumed in 1997

High Fructose Corn Syrup Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. High-Fructose Corn Syrup - Original Ad High Fructose Corn Syrup - Revised Ad

High Fructose Corn Syrup Hepatic fructose metabolism: A highly lipogenic pathway. Fructose is readily absorbed from the diet and rapidly metabolized principally in the liver. Fructose can provide carbon atoms for both the glycerol and the acyl portions of triglyceride. Fructose is thus a highly efficient inducer of de novo lipogenesis. High concentrations of fructose can serve as a relatively unregulated source of acetyl CoA. In contrast to glucose, dietary fructose does NOT stimulate insulin or leptin (which are both important regulators of energy intake and body adiposity). Stimulated triglyceride synthesis is likely to lead to hepatic accumulation of triglyceride, which has been shown to reduce hepatic insulin sensitivity, as well as increased formation of VLDL particles due to higher substrate availability, increased apoB stability, and higher MTP, the critical factor in VLDL assembly. Basciano et al. Nutrition & Metabolism 2005 2:5   doi:10.1186/1743-7075-2-5

FIGURE 1. Estimated intakes of total fructose ( FIGURE 1. Estimated intakes of total fructose (*), free fructose ({blacktriangleup}), and high-fructose corn syrup (HFCS, {diamondsuit}) in relation to trends in the prevalence of overweight ({blacksquare}) and obesity (x) in the United States Bray, G. A et al. Am J Clin Nutr 2004;79:537-543 Copyright ©2004 The American Society for Nutrition

HFCS Availability Availability of HFCS in the food supply In 1970 HFCS represented < 1% of all caloric sweeteners available for consumption in the United States, but the HFCS portion of the caloric sweetener market jumped rapidly in the 1980s and by 2000 represented 42.0% of all caloric sweeteners (Table 1) (8). HFCS-42 was initially the only HFCS component, but by the early 1980s, HFCS-55 had become the major source and constituted 61.2% of all HFCS in 2000. These data are based on per capita food disappearance data. In the absence of direct measures of HFCS intake, these data provide the best indirect measure of the HFCS available for consumption in the United States. The data are useful for studying trends but probably overestimate intake patterns. Although it is useful to understand that HFCS intake represents more than two-fifths of the total intake of caloric sweeteners in the United States, it is also important to recognize that the proportion of HFCS in some foods is much higher than that in other foods. American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004

HFCS in Foods Foods containing HFCS 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. American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004

Obesity Trends and HFCS Trends in obesity and HFCS availability There are important similarities between the trend in HFCS availability and the trends in the prevalence of obesity in the United States (Figure 1). Using age-standardized, nationally representative measures of obesity at 5 time points from 1960 to 1999 (35) and data on the availability of HFCS collected annually over this same period, we graphed both patterns. The data on obesity are from the National Center for Health Statistics for the following periods: 1960–1962 (National Health Examination Survey I), 1971–1975 [National Health and Nutrition Examination Survey (NHANES)], 1976–1980 (NHANES II), 1988–1994 (NHANES III), and 1999 (NHANES 1999–2000) (35). The HFCS data are those from Table 1. The prevalence of overweight (BMI of 25–29.9) and the prevalence of obesity (BMI > 30) were fit with fourth-order polynomial curves so that the limited number of data points could be fitted into a curve to capture the US trends. We also included estimates of free-fructose intake and total fructose intake. Total fructose is the sum of free fructose and fructose that is part of the disaccharide sucrose. Free fructose is the monosaccharide in HFCS and is also obtained in small amounts from other sources. Free-fructose intake closely follows the intake of HFCS. Total fructose intake increased nearly 30% between 1970 and 2000. American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004

HFCS Consumption Estimated HFCS consumption The intake of caloric sweeteners in the United States has increased rapidly, and nationally representative data from 1994 to 1998 from the USDA allow us to estimate an intake of 318 kcal/d for the average US resident aged 2 y. This value is one-sixth of the intake of all calories and close to one-third of the intake of all carbohydrates and represents a significant increase over the past 2 decades (Table 2). As the intake of caloric sweeteners increased, so did the fructose load, which increased from 158.5 to 228 kcal · person-1 · d-1 between 1977–1978 (36) and 1994–1998 (38, 39). American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004