In 2010, Dr. Robert Lustic, MD of the University of California at San Francisco, posited that the increasing consumption of fructose drives the worsening obesity and metabolic syndrome epidemic1. Unlike glucose, fructose is a simple sugar that is metabolized by the liver, similarly to alcohol and other toxins. In this article, we will explain why fructose is the more harmful form of carbohydrate, and why you should avoid it.
What is Fructose?
Fructose is a simple sugar naturally found in honey and fruits. It is also half of the table sugar (sucrose). Fructose is about twice as sweet as glucose and typically sweeter than table sugar2.
When we consume table sugar, our gut breaks down each molecule of sucrose into a molecule of fructose and a molecule of glucose.
In processed foods, high-fructose corn syrup may be used in place of sucrose as sweeteners, because they are sweeter and less expensive. High-fructose corn syrup may contain up to 60% fructose3,4.
Therefore, all sweetened foods and beverages contain fructose.
Why is Sugar Toxic?
All of your cells are made to use glucose as fuel – they can readily take up glucose and burn it for energy. Whereas, only the liver can take up and use fructose by converting it into other forms of energy that the body can use.
The liver handles fructose very similarly to how it handles alcohol or other toxins, but the dose makes the poison1. In small doses, fructose gets stored as glycogen in the liver. However, an average modern American adult may consume up to 126 grams of sugar/day5. That’s over eight tablespoons (half a cup) of sugar every day!
Depleting the liver of energy
Too much fructose can deplete the energy (ATP) in liver cells, reducing the liver’s detoxification capacity. In order to produce more energy, the liver further breakdown ATP, which can increase uric acid, leading to high blood pressure and gout6,7.
Inflammation, triglycerides, and insulin resistance
Like alcohol, fructose also gets converted into fat, which can increase triglycerides and free fatty acids in the blood8,9. The conversion process leads to increased inflammation and insulin resistance in the liver, which can cause fatty liver10. In addition, the increase in free fatty acids can lead to insulin resistance in muscle cells11.
How to Avoid the Toxic Effects of Fructose
It is normal to like sugar because, in the old days, consuming sweets increased your chance of survival. However, nowadays, it is important to be mindful of your fructose consumption by:
- Learning to read food labels and identify all forms of added sugar in your foods
- Focusing on whole, natural, and unprocessed foods
- Doing a sugar detox to reset your brain and palate, and eliminate sugar cravings
- Lustig, R. H. Fructose: metabolic, hedonic, and societal parallels with ethanol. J. Am. Diet. Assoc. 110, 1307–21 (2010).
- Wiebe, N. et al. A systematic review of the effect of sweeteners on glycemic response and clinically relevant outcomes. BMC Med. 9, (2011).
- White, J. S. Straight talk about high-fructose corn syrup: What it is and what it ain’t. American Journal of Clinical Nutrition 88, (2008).
- Walker, R. W., Dumke, K. A. & Goran, M. I. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition 30, 928–35
- Where people around the world eat the most sugar and fat – The Washington Post. Available at: https://www.washingtonpost.com/news/wonk/wp/2015/02/05/where-people-around-the-world-eat-the-most-sugar-and-fat/?noredirect=on. (Accessed: 12th September 2019)
- Nakagawa, T., Tuttle, K. R., Short, R. A. & Johnson, R. J. Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome. Nature clinical practice. Nephrology 1, 80–86 (2005).
- Fiaschi, E. et al. Fructose-induced hyperuricemia in essential hypertension. Metabolism. 26, 1219–23 (1977).
- Fried, S. K. & Rao, S. P. Sugars, hypertriglyceridemia, and cardiovascular disease. Am. J. Clin. Nutr. 78, 873S-880S (2003).
- Teff, K. L. et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. in Journal of Clinical Endocrinology and Metabolism 89, 2963–2972 (2004).
- Diraison, F., Moulin, P. H. & Beylot, M. Contribution of hepatic de novo lipogenesis and reesterification of plasma non-esterified fatty acids to plasma triglyceride synthesis during non-alcoholic fatty liver disease. Diabetes Metab. 29, 478–485 (2003).
- Montell, E. et al. DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells. Am. J. Physiol. Metab. 280, E229–E237 (2001).