Consumption of high-fructose corn syrup has distinct negative health effects compared to sucrose
the verdict
CONTESTED
contested - evenly split
refutedsupported
the weight of evidence
2 sources for · 8 against
The health effects and metabolic differences of high-fructose corn syrup compared to sucrose remain a subject of ongoing scientific controversy and mixed findings.
The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that supports the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, leading to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and high fructose corn syrup (HFCS), which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, CVD and T2DM, often independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0%, 10%, 17.5% or 25% of daily energy requirement (Ereq) as HFCS increased lipid/lipoprotein risk factors for CVD and uric acid in a dose-response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that enables determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, recent reports conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging (fMRI) of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. Some epidemiological studies show that sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high-sugar diets promoted increased body weight gain compared with consumption of ad libitum low- sugar diets. However, there are no studies in which energy intake and weight gain were compared in subjects consuming high or low sugar, blinded, ad libitum diets formulated to ensure both groups consumed a comparable macronutrient distribution and the same amounts of fiber. There is also little data to determine whether the form in which added sugar is consumed, as beverage or as solid food, affects its potential to promote weight gain. It will be very challenging to obtain the funding to conduct the clinical diet studies needed to address these evidence gaps, especially at the levels of added sugar that are commonly consumed. Yet, filling these evidence gaps may be necessary for supporting the policy changes that will help to turn the food environment into one that does not promote the development of obesity and metabolic disease.
This paper reviews evidence in the context of current research linking dietary fructose to health risk markers.Fructose intake has recently received considerable media attention, most of which has been negative. The assertion has been that dietary fructose is less satiating and more lipogenic than other sugars. However, no fully relevant data have been presented to account for a direct link between dietary fructose intake and health risk markers such as obesity, triglyceride accumulation and insulin resistance in humans. First: a re-evaluation of published epidemiological studies concerning the consumption of dietary fructose or mainly high fructose corn syrup shows that most of such studies have been cross-sectional or based on passive inaccurate surveillance, especially in children and adolescents, and thus have not established direct causal links. Second: research evidence of the short or acute term satiating power or increasing food intake after fructose consumption as compared to that resulting from normal patterns of sugar consumption, such as sucrose, remains inconclusive. Third: the results of longer-term intervention studies depend mainly on the type of sugar used for comparison. Typically aspartame, glucose, or sucrose is used and no negative effects are found when sucrose is used as a control group.Negative conclusions have been drawn from studies in rodents or in humans attempting to elucidate the mechanisms and biological pathways underlying fructose consumption by using unrealistically high fructose amounts.The issue of dietary fructose and health is linked to the quantity consumed, which is the same issue for any macro- or micro nutrients. It has been considered that moderate fructose consumption of ≤50g/day or ~10% of energy has no deleterious effect on lipid and glucose control and of ≤100g/day does not influence body weight. No fully relevant data account for a direct link between moderate dietary fructose intake and health risk markers.
Mineral balances in humans as affected by fructose, high fructose corn syrup and sucrose.
The utilization of selected minerals when sugars were supplemented to basal diets was investigated in two separate, laboratory-controlled human feeding studies. Fructose-fed subjects had higher fecal excretions of iron and magnesium than did subjects fed sucrose. Apparent iron, magnesium, calcium, and zinc balances tended to be less positive during the fructose feeding period as compared to balances during the sucrose feeding period. Conversely, high fructose corn syrup (HFCS) did not affect the mineral balances when compared to sucrose feeding. Subjects fed fructose experienced diarrhea which possibly decreased absorption of minerals and thus increased fecal mineral losses. No such adverse effects were noticed when HFCS was fed.
Published in Plant foods for human nutrition (Dordrecht, Netherlands) (1992)
Both controversy and confusion exist concerning fructose, sucrose, and high-fructose corn syrup (HFCS) with respect to their metabolism and health effects. These concerns have often been fueled by speculation based on limited data or animal studies. In retrospect, recent controversies arose when a scientific commentary was published suggesting a possible unique link between HFCS consumption and obesity. Since then, a broad scientific consensus has emerged that there are no metabolic or endocrine response differences between HFCS and sucrose related to obesity or any other adverse health outcome. This equivalence is not surprising given that both of these sugars contain approximately equal amounts of fructose and glucose, contain the same number of calories, possess the same level of sweetness, and are absorbed identically through the gastrointestinal tract. Research comparing pure fructose with pure glucose, although interesting from a scientific point of view, has limited application to human nutrition given that neither is consumed to an appreciable degree in isolation in the human diet. Whether there is a link between fructose, HFCS, or sucrose and increased risk of heart disease, metabolic syndrome, or fatty infiltration of the liver or muscle remains in dispute with different studies using different methodologies arriving at different conclusions. Further randomized clinical trials are needed to resolve many of these issues. The purpose of this review is to summarize current knowledge about the metabolism, endocrine responses, and potential health effects of sucrose, HFCS, and fructose.
Sugar is widely consumed over the world. Although the mainstream view is that high added or free sugar consumption leads to obesity and related metabolic diseases, controversies exist. This narrative review aims to highlight important findings and identify major limitations and gaps in the current body of evidence in relation to the effect of high sugar intakes on health. Previous animal studies have shown that high sucrose or fructose consumption causes insulin resistance in the liver and skeletal muscle and consequent hyperglycemia, mainly because of fructose-induced de novo hepatic lipogenesis. However, evidence from human observational studies and clinical trials has been inconsistent, where most if not all studies linking high sugar intake to obesity focused on sugar-sweetened beverages (SSBs), and studies focusing on sugars from solid foods yielded null findings. In our opinion, the substantial limitations in the current body of evidence, such as short study durations, use of supraphysiological doses of sugar or fructose alone in animal studies, and a lack of direct comparisons of the effects of solid compared with liquid sugars on health outcomes, as well as the lack of appropriate controls, seriously curtail the translatability of the findings to real-world situations. It is quite possible that "high" sugar consumption at normal dietary doses (e.g., 25% daily energy intake) per se-that is, the unique effect of sugar, especially in the solid form-may indeed not pose a health risk for individuals apart from the potential to reduce the overall dietary nutrient density, although newer evidence suggests "low" sugar intake (<5% daily energy intake) is just as likely to be associated with nutrient dilution. We argue the current public health recommendations to encourage the reduction of both solid and liquid forms of free sugar intake (e.g., sugar reformulation programs) should be revised due to the overextrapolation of results from SSBs studies.
High fructose corn syrup (HFCS) has replaced sucrose in many food products, which has prompted research comparing these two sweeteners in rodents. The present study examined the relative palatability of HFCS and sucrose for rats, offering 11% carbohydrate solutions to match the content of common beverages for human consumption. The animals initially preferred HFCS to sucrose but after separate experience with each solution they switched to sucrose preference. Approximating the composition of HFCS with a mixture of fructose and glucose (55:45) yielded a solution that was less attractive than sucrose or HFCS. However, HFCS contains a small amount of glucose polymers, which are very attractive to rats. A 55:42:3 mixture of fructose, glucose and glucose polymers (Polycose) was equally preferred to HFCS and was treated similarly to HFCS in comparisons vs. sucrose. Post-oral effects of sucrose, which is 50% fructose and 50% glucose, may be responsible for the shift in preference with experience. This shift, and the relatively small magnitude of differences in preference for HFCS and sucrose, suggest that palatability factors probably do not contribute to any possible difference in weight gain responses to these sweeteners.
Added sugars, particularly those containing fructose—high fructose corn syrup (HFCS), sucrose, honey, fruit juice concentrates, agave nectar, and crystalline fructose—have been blamed for a variety of adverse health consequences. Fructose containing sugars are among the most misunderstood nutrients in all of nutrition. While the consumption of added sugars has increased in the last 40 years in the American diet, the increase in sugars has not been disproportionate compared to flour and grain products. In fact, of the increase of over 450 cal in the overall diet in the USA between 1970 and 2010 only 34 cal came from all added sugars combined. Over this same time period, fructose consumption has changed very little. In this chapter we begin with an historical perspective on the manufacture of sugar and high fructose corn syrup including their production, consumption, and functionality. We then examine the modern scientific literature related to added sugars and their potential interaction with a variety of health related issues such as obesity, cardiovascular disease, diabetes, the metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). We then summarize emerging evidence on the interaction between sugars and the brain. Based on contemporary scientific research we conclude there is not a unique relationship between sugar consumption and changes in energy regulating hormones, obesity, diabetes, NAFLD or risk factors for cardiovascular disease, and that HFCS and sucrose
Fructose and high-fructose corn syrup (HFCS) have become central to the debate on metabolic health and the rising prevalence of type 2 diabetes. Chemically, fructose is a monosaccharide found naturally in fruits and honey, whereas HFCS is an industrially produced sweetener composed of varying proportions of free fructose and glucose. While fructose has unique metabolic effects, its impact is comparable to other sugars when consumed in excess. HFCS is widely used in processed foods and sugar-sweetened beverages (SSBs) due to its high sweetness and low production cost. However, its metabolic effects remain a topic of scientific and public health concern. Animal and human studies suggest that excessive fructose consumption contributes to metabolic disturbances, including insulin resistance, impaired glucose tolerance, and increased fat accumulation in the liver through <i>de novo</i> lipogenesis (DNL). Unlike glucose, fructose bypasses key regulatory steps in glycolysis, leading to unregulated hepatic uptake and lipid synthesis. Epidemiological studies have reported a higher prevalence of type 2 diabetes in countries with greater HFCS availability, independent of obesity rates. Despite this, there remains controversy regarding whether HFCS is a direct contributor to diabetes or if overall energy intake plays a more significant role. This study aims to analyze the chemical composition of fructose and HFCS and their potential role in the development of type 2 diabetes. Additionally, it briefly discusses the global policy measures, such as sugar taxation and public health interventions, aimed at reducing sugar consumption and mitigating diabetes risk.
It was first marketed in the United States in the early 1970s.[2] Its use in the United States has grown, relative to sucrose, partly because of government subsidies for the production of corn. Controversy
High fructose corn syrup has been linked to obesity, diabetes and other health problems.[3]
However, an expert[3] in food policy who is also a professor at New York University, cautioned that the study doesn't show that diabetes is caused by consumption of high-fructose corn syrup, … “I think it’s a stretch to say the study shows high-fructose corn syrup has anything special to do with diabetes," and that "diabetes is a function of development. The more cars, more TVs, more cellphones, more sugar, more meat, more fat, more calories, more obesity, the more diabetes you have."
An article in The American Journal of Clinical Nutrition titled “Straight talk about high-fructose corn syrup: what it is and what it ain't”[2] states:
- “High-fructose corn syrup (HFCS) ...
The effects of sucrose, fructose, and high-fructose corn syrup meals on plasma glucose and insulin in non-insulin-dependent diabetic subjects. We have previously shown that fructose and sorbitol given with a standard meal cause less increment in plasma glucose than sucrose and high fructose corn syrup (HFCS) in patients with NIDDM. However, there was no direct comparison of sucrose with HFCS. Sixteen men and one woman aged 54-67) with NIDDM were given either 35 g sucrose, 35 g fructose, or 43.75 g HFCS containing 35 g carbohydrate as part of a 400-calorie test meal. Blood samples were obtained at frequent intervals up to 3 h and were analyzed for glucose and insulin. As compared with a fructose meal, the mean increment in plasma glucose (delta PG) after a sucrose meal was significantly higher at 45 min and after an HFCS meal it was significantly higher at 30 and 45 min, but sucrose and HFCS meals did not differ.
Everything we examined (10)
This check searched the claim as stated. It did not run a separate search for evidence against it.