>HFCS is a sweet substance made (mostly in the USA) from corn and used in a wide range of products as a substitute for sugar. HFCS was developed in response to a growing number of issues in sourcing cane sugar, such as high costs, climate changes, stability issues in acidic foods, and restrictions on trading. It was easier and cheaper for the United States to source corn domestically and to process it into a sugar source than to import cane sugar.
It took a number of years to develop HFCS into the product that is so widely used in the commercial food industry today. HFCS was developed from a harder breed of corn called “dent” which needs to go through a range of processes before it can be consumed (e.g. cleaning, soaking, washing, drying, milling before turning the resulting corn starch into liquid corn syrup via hydrolysis). At this point, the corn syrup is still high in glucose, but an additional enzymatic process is used to convert some of this glucose to fructose making HFCS. HCFS-42 and FCFS-55 are the most widely used types of HCFS. HCFS-42 is 42% fructose, HCFS-55 is 55% fructose but there are also types that are available at up to 90% fructose content.
HFCS is in a vast range of everyday products including cereals, yoghurts, cordials, fizzy drinks, fruit juices, cakes, biscuits ice cream, cereals, salad dressings, breads, sweets and chocolate bars. Generally, HCFS-42 is used in cereals and baked or processed foods.
HCFS is used for flavouring foods (e.g. to sweeten the acidity of tomato sauces), to alter textures (to make consistencies smoother, crisper or grainier), to brown/caramelise items, to preserve or to help with fermentation.
Due to HFCS’s rapid and largely unscrutinised introduction to so many of the foods that we eat, we are now consuming higher levels of fructose than ever before. Glucose, in comparison to fructose, is more readily available for energy use since it can be converted to ATP and burned off. Fructose is instead quickly metabolised in the liver leading to production of triglycerides, free fatty acids and VLDL cholesterol (increasing cardiovascular risks through the development of atherosclerosis) and fat storage in the liver that increases the risk of non-alcoholic fatty liver disease (Gaby, 2005, Ouyang et al, 2008). Fatty liver disease is, in turn, a common cause of insulin resistance and type 2 diabetes (Basciano et al, 2005).
Fructose also has the disadvantage that it fails to appropriately reduce our appetite with consumption; basically, we do not get the same messages of fullness as we would from glucose for example. In contrast, glucose suppresses the hormone ghrelin and stimulates leptin which helps us know that we are full. Obviously, with no indicator of fullness and this can have an impact in terms of overeating, weight-gain and associated health risks.
High fructose consumption has also been connected with risk of kidney stone formation (Taylor and Curhan, 2008), gout attacks (Choi et al, 2008), hypertension risk (Khitan and Kim, 2013) and metabolic syndrome (Nakagawa, 2005). This is due to the increased levels of uric acid that are produced, alongside other harmful by-products, when fructose is metabolised.
Controlled metabolic studies in humans have shown that consuming large amounts of fructose can lead to insulin resistance and chronically elevated insulin levels, as well as problems with cholesterol, triglycerides and blood sugars.
The problem with HCFS is that it is highly addictive (Levy et al, 2012); it gives you pleasure when you eat it and anxiety as withdrawal symptoms when you remove it. HCFS is in a very wide range of products, some of which you may not have been aware of such as: salad dressing, pizzas, tinned tuna, crackers, cereal, canned fruits and vegetables, ketchup, soup, yoghurts, mayonnaise, soft drinks and so on. The best way to avoid HCFS is to stay clear of fast foods and always read food labels before you buy (100% organic is always HCFS-free). There are a number of helpful websites that list regular food products that contain HCFS.
Basciano, H., Federico, L., & Adeli, K. (2005). Fructose, insulin resistance, and metabolic dyslipidaemia. Nutrition & Metabolism, 2, 5.
Choi, J.W, Ford, E.S., Gao, X., Choi, H.K. (2008). Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 59(1): 109-16.
Gaby, A.R. Adverse effects of dietary fructose. (2005) Altern Med Rev. 10(4): 294-306.
Khitan, Z. and Kim, D. (2013). Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension. Journal of Nutrition and Metabolism, 1-12. doi:10.1155/2013/682673
Nakagawa, T. (2005). A causal role for uric acid in fructose-induced metabolic syndrome. AJP: Renal Physiology, 290(3), 625-631.
Ouyang, X., Cirillo, P., Sautin, Y., et al. (2008). Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 48(6): 993-9.
Taylor, E.N, Curhan, G.C. (2008). Fructose consumption and the risk of kidney stones. Kidney Int. 73(2): 207-12.
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