Growing Concerns about Fructose, the Fruit Sugar

Fructose, or fruit sugar, is a simple sugar, found in many fruits and in some vegetables also. It occurs naturally, either on its own or bound to glucose to give the disaccharide known as sucrose or table sugar. ( It is also the principal component of the polysaccharide inulin. ) Sucrose is the sugar that is isolated in large quantities from sugar beet or sugar cane. Fructose is the sweetest of all the sugars and more than twice as sweet as glucose. This fact, together with its cheapness to produce, is why fructose is widely used as a sweetener. The downside to all of this is that the body does not handle fructose well and in animal experiments it has been shown to cause liver toxicity. While many tissues can metabolize glucose, the liver is the principal site for fructose metabolism. The use of fructose as a sweetener has been perpetuated by the development of high fructose corn syrup, a product of the laboratory and in no way natural. It is intensely sweet, high in calories and is considered a major cause of the obesity epidemic. The fact is that fructose, whether in free form, or in sucrose or high fructose corn syrup, can be detrimental to our health, certainly if consumed in excess. Here’s how.

1. Fructose is rapidly converted to fat. It is highly lipogenic, stimulating the synthesis of triglycerides in the liver and resulting in increased fat deposition (1). The effect of fructose on fat synthesis is much greater than that produced by an equivalent amount of glucose.

2. Fructose inhibits the satiety mechanism. In animal studies, rats that were fed fructose developed leptin resistance that was not seen in starch-fed rats. Leptin is a protein hormone that acts on receptors in the brain to reduce appetite. Obviously, if fructose inhibits the actions of leptin, the result will be overeating and weight gain (2). When leptin-resistant rats were fed a classic high-fat, high-sugar Western diet, they gained weight much more rapidly than their starch-fed littermates (2). Starch is a polysaccharide that can be broken down to glucose and, unlike fructose, it stimulates leptin production which suppresses appetite.

3. Fructose stimulates the production of uric acid (3). For the body to metabolize fructose, energy and phosphate are required, both of which are provided by the conversion of adenosine triphosphate (ATP) to the diphosphate (ADP) and then the monophosphate (AMP) resulting in a buildup of AMP which is converted to uric acid. Serum uric acid levels have been shown to increase dramatically after ingesting fructose (3,4,5).

4. Uric acid raises blood pressure. It is becoming increasingly clear that uric acid can cause blood pressure to rise, a condition known as hypertension ( reviewed in 6 ), and high serum uric acid levels are often found in people newly diagnosed with the condition (7). When uric acid levels were lowered in adolescents diagnosed with hypertension, blood pressure returned to normal levels in two-thirds of the patients (8).

5. Fructose induces insulin resistance. There is growing evidence that fructose can induce the condition known as insulin resistance (9). This is where the tissues do not respond adequately to insulin and so do not absorb circulating glucose in the normal manner with the result that blood glucose levels rise above the normal range and produce adverse effects. The induction of insulin resistance by fructose occurs independently of weight gain and differences in caloric intake (10,11) and the effect may be mediated by increased uric acid levels. Insulin resistance precedes the development of type 2 diabetes and is characteristic of it.

6. Fructose and metabolic syndrome. It is now clear that high fructose consumption represents a serious threat to our health. Either directly or indirectly, it promotes fat synthesis, high blood pressure, and insulin resistance, all of which are characteristic of a condition known as metabolic syndrome, a collection of traits probably best described by Gerald Reaven (12) that greatly increase our risk of heart disease, stroke and type 2 diabetes. Metabolic syndrome now affects over 55 million people in the United States (13) and is indicative of chronic disease. It used to be found only in adults but now occurs in adolescents also.

How can we reduce our fructose intake? First we need to recognize the sources of fructose. The lowest levels of fructose in fruits are to be found, not surprisingly, in tart fruits, including lemons, limes and cranberries. The levels in most berries and citrus fruits are less than 10 grams per serving. Going over 10 grams per serving we find persimmon (10.6 g), watermelon (11.3g), pear (11.8g), raisins (12.3g), seedless grapes (12.4g), mango (16.2g), dried apricots (16.4g) and dried figs (23g). Table sugar (sucrose) is 50% fructose and high fructose corn syrup and honey contain about 55% fructose. Agave syrup cannot be considered a health food and contains as much as 59-67% of fructose. The sugar in sodas contains 50% fructose and there are also high levels in apple sauce, canned fruits and all sugar-rich products. It is certainly better to eat fresh fruits rather than dried ones and servings should be restricted to 2-3 per day of low-fructose-containing fruits (Ref.). Use table sugar sparingly and replace it with glucose (dextrose) or the artificial sweetener Stevia.

References

1. Stanhope, K. L. & Havel, P. J. (2008) Fructose Consumption: Potential Mechanisms for Its Effects to Increase Visceral Adiposity and Induce Dyslipidemia and Insulin Resistance. Curr. Opin. Lipidol. 19:16–24.
2. Shapiro, A. , Mu, W., Roncal, C.A., Cheng, K.Y., Johnson, R.J. & Scarpace, P.J. (2008) Fructose-Induced Leptin Resistance Exacerbates Weight Gain in Response to Subsequent High Fat Feeding. Am. J. Physiol. Regul. Integr. Comp. Physiol. 295: R1370–R1375.
3. Perheentupa, J. & Raivio, K. (1967) Fructose-Induced Hyperuricaemia. Lancet 2:528–531.
4. Fiaschi, E., Baggio, B., Favaro, S., Antonello, A., Camerin, E., Todesco, S. & Borsatti, A. (1977) Fructose-Induced Hyperuricemia in Essential Hypertension. Metabolism 26:1219–1223.
5. Stirpe, F., Della Corte, E., Bonetti, E., Abbondanza, A. , Abbati, A. & De Stefano, F. (1970) Fructose-Induced Hyperuricaemia. Lancet 2:1310–1311.
6. Feig, D. I., Kang, D. H. & Johnson, R. J. (2008) Uric acid and Cardiovascular Risk. N. Engl. J. Med. 359:1811–1821.
7. Feig, D. I. & Johnson, R.J. (2003) Hyperuricemia in Childhood Primary Hypertension. Hypertension 42:247–252.
8. Feig, D. I., Soletsky, B. 7 Johnson, R. J. (2008) Effect of Allopurinol on the Blood Pressure of Adolescents with Newly Diagnosed Essential Hypertension. JAMA 300:922–930.
9. Johnson, R. J., Perez-Pozo, S. E., Sautin, Y. Y., Manitius, J., Sanchez-Lozada, L. G., Feig, D. I., Shafiu, M., Segal, M., Glassock, R. J.,Shimada, M., Roncal, C. & Nakagawa, T. (2009) Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes? Endocrine Reviews 30 (1): 96-116.
10. Havel P. J. (2005) Dietary Fructose: Implications for Dysregulation of Energy Homeostasis and Lipid/Carbohydrate Metabolism. Nutr Rev 63:133–157.
11. Nakagawa, T., Hu, H., Zharikov, S., Tuttle, K. R., Short, R. A., Glushakova, O., Ouyang, X., Feig, D. I., Block, E. R., Herrera-Acosta, J., Patel, J. M. & Johnson, R. J. (2006) A Causal Role for Uric Acid in Fructose-Induced Metabolic Syndrome. Am J Physiol 290:F625–F631.
12. Reaven, G. M. (1997) Banting Lecture 1988. Role of Insulin Resistance in Human Disease. Nutrition 13:65.
13. Ford, E. S., Giles, W. H. & Mokdad, A. H. (2004) Increasing Prevalence of the Metabolic Syndrome Among U.S. Adults. Diabetes Care 27:2444–2449.

© Christopher J. Jones