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A recent article proposed that excessive consumption of fructose, particularly in the form of high-fructose corn syrup (HFCS), may contribute more significantly to metabolic disorders compared to sucrose in the human diet. The surge in HFCS use, notably in soft drinks in the United States, has mirrored the escalating obesity rates.
This new theory on fructose underscores a genetic “survival of the fittest” explanation for how heightened fat accumulation due to fructose exacerbates the impact of increased caloric intake from Western diets, especially affecting adolescents and young adults, leading to metabolic disorders. The concept suggests that fructose intake induces low adenosine triphosphate levels, triggering increased energy consumption and disrupting energy regulation. The ongoing interest revolves around the correlation between heightened HFCS usage and the obesity prevalence in the United States. The cost-effectiveness of using HFCS in sugary beverages, owing to technological advancements in its production from corn and its substitution for sugar, has led to reduced prices of these drinks. While a direct link between sugary drinks and obesity remains unproven, there has been an observed rise in the risk of type 2 diabetes, cardiovascular diseases (CVD), nonalcoholic fatty liver disease (NAFLD), and even cancer. Research investigating HFCS, weight gain, and metabolic diseases persists despite inconclusive evidence establishing causation.
The connection between sugary drink consumption and obesity is attributed to an overall increase in total caloric intake, as these liquid calories fail to suppress the intake of solid foods, resulting in an imbalance in calorie consumption. This understanding stems from studies conducted by R. Mattes and B. Rolls in the 1990s and early 2000s.
This ongoing research on HFCS and metabolic diseases holds significance, especially considering the high consumption of sugary beverages among adolescents and young adults in the United States and globally, putting them at risk of early-onset metabolic disorders like type 2 diabetes, NAFLD, and CVD.
Concerns regarding fructose arise from its association with the rise in HFCS usage in sugary beverages, coinciding with the increased prevalence of obesity in the United States around the 1970s and 1980s. Researchers noted this correlation and began focusing on potential mechanisms to attribute the effects to HFCS or fructose specifically, aiming to caution the public about the risks associated with consuming sugary beverages containing HFCS and fructose, potentially leading to metabolic diseases. There’s a suggestion to explore methods to eliminate harmful HFCS from the food supply, akin to the elimination of industrially produced trans fatty acids. In 2018, the World Health Organization advocated for a total ban on trans fats, attributing them to causing around 500 million premature deaths annually worldwide. Similarly, most trans fats are formed through an industrial process altering vegetable oils, leading to a shelf-stable, inexpensive partially hydrogenated oil, which has been linked to increased LDL cholesterol and decreased HDL, elevating the risk of heart attacks and strokes.
The turning point for banning trans fats involved challenges in convincing the scientific community and industries about their harmful effects, partly due to prevalent beliefs that margarine and Crisco oils were healthier alternatives compared to lard and butter. Substantial evidence from epidemiological studies showing elevated LDL and reduced HDL in individuals consuming more trans fats reinforced the notion that saturated fats were not the sole culprits in heart disease. Perhaps a pivotal moment in this campaign was when a researcher, experienced in testing trans fat deposition, sued the US Food and Drug Administration (FDA) for delayed action despite accumulating evidence.
Do we possess similar evidence to advocate for an FDA ban on HFCS? What we do have is the temporal association between HFCS introduction into the food supply in 1970 and the escalating obesity rates from 1960 to 2000.
The surplus energy in sugary drinks might act as a pleasurable stimulus, overriding the body’s natural energy balance mechanisms, particularly since the excess energy comes in liquid form and might bypass the hypothalamic satiety signal.
Nevertheless, proving that fructose in HFCS solely drives the increase in obesity rates is more challenging than attributing the rise in LDL cholesterol and drop in HDL cholesterol to trans fats. Obesity rates have surged globally, even in regions where sugary drinks do not contain HFCS.
However, the intriguing notion that HFCS could disrupt the satiety pathway, leading to excess calorie intake, gains traction, especially if we can pinpoint the rise in obesity rates among children and adolescents to increased HFCS consumption in sugary beverages. From a nutritional perspective, there seems to be no justification to add sugar or HFCS to liquids. Furthermore, if HFCS indeed poses a metabolic disadvantage, it strengthens the case for its prohibition, mirroring the status of trans fats as a toxin in the food supply.
