It really is. The ingredient that gives pop that sweet, mesmerizing taste. I could guzzle liters of it without blinking. If I could live off soda (and the occasional steak), I would in an instant. My pop consumption is off the charts due to its addicting, refreshing tastes. And I’m not the only one. According to a self-performed study, Americans drink the equivalent of roughly 24 cans of pop a week, translating to 288 ounces (over 8.5 liters!).(1)
What should we know about high fructose corn syrup and its effect on the body? HFCS is a popular industrially due to being cheaper and artificially sweeter than its natural sugar alternatives. I’m sure you are well acquainted with controversy surrounding this common ingredient in not only pops, but many other beverages and processed foods. You’ve probably seen the corn propoganda commercials where they claim “your body can’t tell the difference” and I’m sure you have a local dietitian (2) around the neighborhood that busts out a torch and pitchfork every time you pop a tab on your favorite soft drink. While both sides have some valid points (my heart/diet hopes desperately the former is unequivocally correct), research has shown a relationship between high fructose corn syrup intake and leptin and insulin levels in your body. Leptin and insulin play direct roles in obesity.
To understand the role of HFCS in this context, we must first understand the role of insulin and leptin in regulating our food intake. Our article this week essentially stated that low levels of leptin and insulin stimulate higher food intake, while normal or higher levels lead to decreased food intake. One crucial area in the brain responsible for this effect is the hypothalamic arcuate nucleus. In this case, we are interested in three types of neurons: POMC, NPY, and AgRP. POMC neurons decrease food intake and increase energy expenditure when activated, while NPY and AgRP increase food intake when activated. POMC neurons are stimulated by insulin and leptin, while NPY and AGRP neurons are more activated when leptin and insulin levels are low. In a normal functional body, these two systems work together to provide homeostasis in the body. If someone is losing too much weight, NPY and AgRP neurons will not stimulated by the lack of leptin/insulin and will “urge” the body to regain weight. If someone has an elevated level of insulin/leptin from increased food intake, POMC neurons will decrease food intake while NPY/AgRP’s effects will be essentially inhibited from their normal function. Insulin and leptin also can affect genetic expression of these neurons, inhibiting NPY while increasing the expression of POMC neurons. Consequently, insulin and leptin resistance can lead to increased food intake and obesity. Leptin and insulin are adiposity signals, meaning they rely on signals from fat stores for their function.
Ideally, we want to avoid low leptin/insulin levels or resistance. What role does HFCS play in the function/levels of leptin and insulin? A study in 2009 provided some not so exciting results for avid pop guzzlers.(3) Consumers of excess fructose (instead of typical glucose or sucrose) showed increased conversion of excess sugars into fats (in a process known as de novo lipogenesis (DNL)). HFCS also decreased insulin sensitivity. If the body can’t respond normally to insulin, it will act as if there is a deficiency which, as seen above, can lead to increased food intake and obesity. In another study, fructose consumption was linked to low ciruclation levels of insulin and leptin.(4) Fructose, unlike glucose, doesn’t stimulate insulin secretion. Insulin-regulated glucose metabolism is hypothesized to play a role in leptin secretion. Thus, both leptin and insulin are decreased, leading to increased caloric intake and further obesity. Besides influencing leptin and insulin levels, HFCS also alters metabolic hormones so we don’t feel full. These manufacturers know what they’re doing.
While it truly pains me to say this, high fructose corn syrup opponents may indeed have a point. It would be wise to reduce HFCS in order to prevent obesity and the diseases, such as type II diabetes, that often result. Sticking to natural sugars like sucrose and glucose in substitution for synthesized fructose can help reduce caloric intake (while it is probably unwise to overindulge in those sugars either). Even if we aware of these problems, can the possible consequences of high fructose diets deter us from indulging in soda and the plethora of other processed food containg HFCS? It’s up to the consumer.
(1) – Americans named Nathan Rodeberg.
(2) – Or dentist. The effect of pop on teeth will unfortunately not be addressed in this blog post.
(3) – Stanhope et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation 2009 119(5):1322-34.
(4) Teff et al. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. Journal of Endocrinology and Metabolism 2004 89 (6): 2963-2972.
(5) Google Images.
High Fructose Corn Syrup is Delicious
