Is fructose bad for you

Is fructose bad for you?

Pawel Malczewski
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Short Summary

Foods high in fructose, such as refined sugar products, sugar based soft drinks and fruit juices, when consumed frequently, have harmful effects in most people.

High fructose consumption is the key factor leading to metabolic syndrome and increases the risk of obesity, type 2 diabetes, cardiovascular diseases, gout, non-alcoholic metabolic liver disease, and some forms of cancer.

However, when consumed in the form of whole fruit and vegetables, it does not present a health risk for most people. In this case, it is beneficial for health. For a quick answer click here.

Explanation

NOTE: Hereditary fructose intolerance. This article refers to people with no fructose related diseases such as hereditary fructose intolerance. (1)National Library of Medicine. Hereditary fructose intolerance. Available here.

High fructose diet affects some people more than others

For an athletic, insulin sensitive person on a balanced diet, the effects of fructose metabolism may be negligible. However, for an obese person, who is insulin resistant and with a sedentary lifestyle, the high fructose diet may have severe health consequences.

It should be noted that genetics also plays an important role in how people react to fructose.

While some studies may have shown a negligible impact on some healthy, slim and insulin sensitive individuals, we should be more concerned about the effects of fructose on the overall population, most of which (over 60% in U.S., UK, Canada or Australia) is overweight and to whom the negative effects especially apply.

In summary, the health effects of fructose depend on:

  • level of overweight;
  • genetics;
  • level of insulin sensitivity;
  • fasting / glycogen depleted state (e.g. after a marathon, the glycogen energy reserves would be exhausted);
  • other medical conditions;
  • level of physical activity.

Fructose is harmful when consumed from some sources but not from others

    • Fructose from healthy sources. Dietary fructose in the form of whole vegetables and fruit, as a part of a balanced diet, doesn’t cause any harm due to the relatively low contents of fructose and high amounts of other nutrients that accompany it, such as fiber. Whole fruit and vegetables have a beneficial effect on our health. (2)Slavin JL, Lloyd B. Health Benefits of Fruits and Vegetables. Adv Nutr July 2012 Adv Nutr vol. 3: 506-516, 2012. Available here.
    • Fructose from refined carbs and high fructose sweeteners. Concentrated fructose in refined carbohydrates (see examples below), on the other hand, put enormous stress on our liver and have a negative effect on our health. The reason is that the metabolic process of an excessive amount of fructose in the liver produces various harmful substances such as uric acid and triglycerides and has a damaging effect directly on the liver and the entire body. This applies especially, but not exclusively, to overweight and obese people.

High fructose food sources:

  • refined sugar products (e.g. table sugar, candy or sweet pastry);
  • fructose-based sweeteners (e.g. maple or agave syrup);
  • soft drinks containing sugar (e.g. Coke or Fanta);
  • fruit juices (all juices extracted from fruit, with fiber removed resulting in the presence of a high amount of fructose and a medium to high GL.). Note: fruit juice is considered as a refined food because of the removed fiber.

Is fructose toxic?

Here is a definition of chronic toxicity taken from Harrison’s Principles of Internal Medicine. NOTE: it should not to be confused with Acute Toxicity. (3)Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Harrison’s Principles of Internal Medicine. 19th Edition. Mc GrawHill Education. Available here.
“TOXICITY: The degree to which a substance can harm humans or animals.

Chronic toxicity is the ability of a substance or mixture of substances to cause harmful effects over an extended period, usually upon repeated or continuous exposure, sometimes lasting for the entire life of the exposed organism. “

It is important to bear in mind that toxicity may be caused by various substances, even water (read more..).

Any substance can become toxic if it is consumed in excessive amounts. It is not very common for us to over-consume certain nutrients but when it happens we get sick as in the case of selenium in Brazil nuts. (read more..)

Fructose is not a toxin per se, although we can live without it. However, it is an unusual nutrient, since it is particularly easy to over-consume due to a number of reasons:

  • It tricks our mind into thinking that we are still hungry by acting on our hunger and satiety hormones; (4)Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, Heiman M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. The Journal of Clinical Endocrinology & Metabolism Vol 89, No 6. Available here.
  • Fructose consumption is linked to an addictive-like behavior, although science is still not clear whether fructose consumption can be considered as addictive in a strict dependency sense or only habitual; (5)Ziauddeen H, Farooqu S, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nature Reviews Neuroscience 13, 279-286 (April 2012). Available here.
  • It is involved in the vicious cycle of obesity where the excess of fructose in the diet leads to weight gain and weight gain leads to craving for more fructose (more on this below).
  • It is available in a concentrated form such as in sweeteners, soft drinks or fruit juices, which allows us to have a lot of it in one sitting;
  • Clever/misleading marketing – we are led to believe that since fructose is the “healthier sugar” and that fruit juices are healthy, the servings are excessively large.

These points explain why it is common that after drinking a bottle of Coke, the appetite is not suppressed but actually increases.

While an occasional small dose of fructose generally causes no harm, there is an overwhelming number of harmful side-effects of excess dietary fructose, making it toxic and, as it was made clear, over-consumption is easy.

Why is fructose bad for us?

In summary, the most significant impact on human health of a high fructose diet is the development of metabolic syndrome and increased risk of diseases such as obesity, cardiovascular diseases and type 2 diabetes. (6)Stanhope KL, Schwarz JM, Havel PJ. Adverse metabolic effects of dietary fructose: Results from recent epidemiological, clinical, and mechanistic studies. Curr Opin Lipidol. 2013 Jun; 24(3): 198–206. Available here.

The following is the list of known effects of high fructose consumption:

  • Energy production
    Part of the fructose consumed is turned into energy by the liver cells. (7)Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.
  • Glucose production
    Part of the fructose is turned into glucose. The proportion of that conversion depends on fitness, health level and on gender. Part of this glucose is stored as glycogen. (8)Décombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71. Available here.
  • Visceral fat accumulation
    Fructose metabolism (similar to alcohol but in contrast to glucose) promotes the accumulation of fatty acids in the abdominal area, resulting in visceral obesity.

    Visceral fatty tissue is located around the organs and its visible signs are commonly referred to as “beer gut”, since it is usually associated with alcohol. (9)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.

    Visceral fat is associated with metabolic syndrome, cardiovascular diseases and type 2 diabetes. (10)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.

  • Uric acid production
    Fructose intake rapidly increases the production of uric acid (by the liver), which reduces the production and availability of nitric oxide.

    Nitric oxide (NO) protects the organs (e.g. liver) from vascular damage, increases the blood flow by widening blood vessels (vasodilation) and reduces blood pressure in people with hypertension. In order to be able to perform its function of distributing glucose to the muscle cells, insulin needs nitric oxide to increase the blood flow to these areas.

    If the nitric oxide is reduced, insulin action is affected. The result is that there is a circulating insulin that cannot do its job which is referred to as “insulin resistance”.

    Uric acid also causes gout, leads to kidney damage, inflammation and hypertension and increases the risk of metabolic syndrome and obesity. (11)Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, et al. A causal role for uric acid in fructose-induced metabolic syndrome. American Journal of Physiology – Renal Physiology Published 1 March 2006 Vol. 290 no. 3, F625-F631. Available here. (12)Stirpe F, Della Corte E, Bonetti E, Abbondanza A, Abbati A, De Stefano F. Fructose-induced hyperuricaemia. Lancet. 1970 Dec 19;2(7686):1310-1. Available here. (13)Steinberg HO, Brechtel G, Johnson A, Fineberg N, Baron AD. Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. J Clin Invest. 1994 Sep; 94(3): 1172–1179. Available here. (14)Singh JA, Reddy SG, Kundukulam J. Risk Factors for Gout and Prevention: A Systematic Review of the Literature. Curr Opin Rheumatol. 2011 Mar; 23(2): 192–202. Available here. (15)Cox CL, Stanhope KL, Schwarz JM ,,Graham JL, Hatcher B, Griffen SC, et al. Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans. Nutrition & Metabolism2012. Available here. (16)Kanbay M, Segal M, Afsar B, Kang DH, Rodriguez-Iturbe B, Johnson RJ. The role of uric acid in the pathogenesis of human cardiovascular disease. Heart doi:10.1136/heartjnl-2012-302535. Available here.

  • Triglyceride production
    Part of the fructose that is metabolized in the liver is converted into triglycerides, leading to increased levels of triglycerides in the blood, a condition called dyslipidemia/hyperlipidemia. This affects those who are overweight and obese more than athletic and slim individuals. (17)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.Dyslipidemia is associated with hypertension, cardiovascular disease and metabolic syndrome. (18)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here. (19)Bray GA. How bad is fructose? Am J Clin Nutr October 2007. Vol. 86 no. 4 895-896. Available here. (20)Olofsson SO, Boren J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. J Intern Med. 2005 Nov;258(5):395-410. Available here. (21)Hyson D, Rutledge JC, Berglund L. Postprandial lipemia and cardiovascular disease. Curr Atheroscler Rep. 2003 Nov;5(6):437-44. Available here. (22)Kanbay M, Segal M, Afsar B, Kang DH, Rodriguez-Iturbe B, Johnson RJ. The role of uric acid in the pathogenesis of human cardiovascular disease. Heart doi:10.1136/heartjnl-2012-302535. Available here. (23)Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. Available here.
  • “Bad cholesterol” increase and “good cholesterol” reduction
    Excessive fructose consumption increases the amount of atherosclerosis’ forming particles: cholesterol, apoB, LDL, small dense LDL and oxidized LDL, and reduces HDL lipoproteins, which leads to heart disease. (24)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here. (25)Aeberli I, Zimmermann MB, Molinari L, Lehmann R, l’Allemand D, Spinas GA, et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr October 2007. vol. 86 no. 4 1174-1178. Available here.
  • Increase of VLDL particles
    Excessive fructose leads to elevated triglycerides production which, together with cholesterol, are packaged inside VLDLs particles and released to the bloodstream.High levels of VLDLs are associated with metabolic syndrome and cardiovascular diseases. (26)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here. (27)Bray GA. How bad is fructose? Am J Clin Nutr October 2007. Vol. 86 no. 4 895-896. Available here. (28)Olofsson SO, Boren J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. J Intern Med. 2005 Nov;258(5):395-410. Available here. (29)Hyson D, Rutledge JC, Berglund L. Postprandial lipemia and cardiovascular disease. Curr Atheroscler Rep. 2003 Nov;5(6):437-44. Available here.
  • Increase of insulin and insulin-like growth factors
    High levels of fructose lead to insulin resistance. (30)Tappy L, Le KA, Tran C, Paquot N. Fructose and metabolic diseases: New findings, new questions. Volume 26, Issues 11–12, 2010, Pages 1044–1049 Available here. (31)Kelishadi R, Mansourian M, Heidari-Beni M. Association of fructose consumption and components of metabolic syndrome in human studies: a systematic review and meta-analysis. Nutrition. 2014 May;30(5):503-10. Available here. As a result, there is an increase in circulating insulin and insulin-like growth factors.

    Insulin resistance is associated with an increased risk of colon cancer and metabolic syndrome. Metabolic syndrome is linked with cancers such as: liver, colorectal and bladder cancers in men and endometrial, pancreatic, breast postmenopausal, rectal and colorectal in women.
    (32)Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here. (33)Giovannucci E. Insulin, insulin-like growth factors and colon cancer: a review of the evidence. J Nutr. 2001 Nov;131(11 Suppl):3109S-20S. Available here. (34)Esposito K., Chiodini P, Colao A, Lenzi A, Giugliano D. Metabolic Syndrome and Risk of Cancer – A systematic review and meta-analysis. Diabetes Care November 2012 vol. 35 no. 11 2402-2411. Available here.

  • Increase amount of blood glucose
    Fructose increases fasting blood glucose (measure of blood glucose after a period of fasting) which leads to insulin resistance. (35)Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
  • Increase in lipid droplets in the liver
    Part of the lipids produced from fructose remains in the liver and are called lipid droplets. These particles cause a non-alcoholic fatty liver disease.

    This condition is similar to the one caused by ethanol metabolism in alcoholics. An advanced stage of this condition results in cirrhosis – scaring of the liver tissue. (36)Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here. (37)Ackerman Z, Oron-Herman M, Grozovski M, Rosenthal T, Pappo O, Link G, Sela BA. Fructose-Induced Fatty Liver Disease. Hypertension. 2005; 45: 1012-1018. Available here. (38)Wijarnpreecha K, Thongprayoon C, Edmonds PJ, Cheungpasitporn W. Associations of sugar- and artificially sweetened soda with nonalcoholic fatty liver disease: a systematic review and meta-analysis. Oxford University Press. Sep 2015. Hcv172. Available here. (39)Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. AASLD. Hepatology. Volume 57, Issue 6 June 2013 Pages 2525–2531. Available here.

  • Increase part of fructose not absorbed
    The amount of absorbed fructose by the body is limited. The unabsorbed fructose passes to the colon where it is fermented by gut bacteria.

    This process may lead to gas, bloating and diarrhea. (40)Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. AASLD. Hepatology. Volume 57, Issue 6 June 2013 Pages 2525–2531. Available here. (41)Rao SS, Attaluri A, Anderson L, Stumbo P. The Ability of the Normal Human Small Intestine to Absorb Fructose: Evaluation by Breath Testing. Clin Gastroenterol Hepatol. 2007 Aug; 5(8): 959–963. Available here. (42)Suri SZ, Empie MW. Fructose metabolism in humans – what isotopic tracer studies tell us. Nutr Metab (Lond). 2012; 9: 89. Available here.

  • Increase leptin production
    Leptin is a hormone generated by fat cells and signals our brain to stop eating. The more fat that our body has, the more leptin is produced. Too much leptin in circulation leads to leptin resistance. Since excess fructose leads to obesity, the resulting increased leptin production leads to leptin resistance. Leptin resistance is also caused by another effect of fructose: insulin resistance.

    This results in a leptin resistance vicious cycle: more appetite, overeating, more fat accumulated in fatty cells, and increased resistance to leptin. (43)Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34. Available here. (44)Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest. 2000;106(4):473–481. doi:10.1172/JCI10842. Available here. (45)Pallayova M. The Vicious Cycle of Leptin-Insulin Resistance Predicts Impaired Glucose Metabolism in Obese Adults with Obstructive Sleep Apnea. J Clin Sleep Med. 2012 Apr 15; 8(2): 227–228. Available here.

  • Production of inflammatory substances
    “JNK1” is a substance produced in the liver from fructose breakdown that causes inflammation.Chronic inflammation in the liver is associated with insulin resistance in the liver but also as secondary insulin resistance in muscles, and fatty cells. (46)Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here. (47)De Luca C, Olefsky JM. Inflammation and insulin resistance Volume 582, Issue 1, 9 January 2008, Pages 97–105. Available here.

Positive effects of fructose

Fructose is not required for any processes in the body. However, in small amounts it can be useful (but not essential) for two functions:

  • After strenuous exercise – since fructose speeds up the replenishing of the glycogen stores; (48)Décombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71. Available here.
  • For the male reproduction system – since fructose is useful as a preferred energy source for the semen. Please note, however, that dietary fructose sources are not essential, since our bodies are capable of converting glucose to fructose for this purpose. (49)Frenette G, Thabet M, Sullivan R. Polyol Pathway in Human Epididymis and Semen. Journal of Andrology. Volume 27, Issue 2, pages 233–239, March-April 2006. Available here.

Summary of medical conditions that may arise from the excess fructose consumption.

  • Insulin resistance, and related increased insulin production and presence in blood (hyperinsulinemia);
  • Leptin resistance, and related increased leptin production and high levels of leptin in blood (hyperleptinemia);
  • Hypertension;
  • Obesity, especially central and visceral obesity;
  • Inflammation;
  • Type 2 Diabetes;
  • Fructose intolerance;
  • Metabolic syndrome;
  • Cancers;
  • Non-alcoholic fatty liver disease;
  • Heart disease

Conclusion

Back to top
Since the majority of fructose we consume comes from sweeteners or refined sugar products, the question of whether “fructose is good for us”, mainly refers to those food sources. It also refers to the majority of the population that are affected by this high fructose diet.

In that context the answer is: fructose has a damaging effect on our body and can be considered as chronically toxic when consumed frequently and in high amounts. A high fructose diet leads to many serious medical conditions and should be considered unhealthy. This applies specially to overweight and obese people.

It is important to note, however, that dietary fructose which comes in the form of whole fruit and vegetables, consumed as part of a balanced diet, not only doesn’t present any harm to our health, but has shown many benefits.

References   [ + ]

1. National Library of Medicine. Hereditary fructose intolerance. Available here.
2. Slavin JL, Lloyd B. Health Benefits of Fruits and Vegetables. Adv Nutr July 2012 Adv Nutr vol. 3: 506-516, 2012. Available here.
3. Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. Harrison’s Principles of Internal Medicine. 19th Edition. Mc GrawHill Education. Available here.
4. Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, Heiman M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. The Journal of Clinical Endocrinology & Metabolism Vol 89, No 6. Available here.
5. Ziauddeen H, Farooqu S, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nature Reviews Neuroscience 13, 279-286 (April 2012). Available here.
6. Stanhope KL, Schwarz JM, Havel PJ. Adverse metabolic effects of dietary fructose: Results from recent epidemiological, clinical, and mechanistic studies. Curr Opin Lipidol. 2013 Jun; 24(3): 198–206. Available here.
7. Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.
8. Décombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71. Available here.
9. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
10. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
11. Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, et al. A causal role for uric acid in fructose-induced metabolic syndrome. American Journal of Physiology – Renal Physiology Published 1 March 2006 Vol. 290 no. 3, F625-F631. Available here.
12. Stirpe F, Della Corte E, Bonetti E, Abbondanza A, Abbati A, De Stefano F. Fructose-induced hyperuricaemia. Lancet. 1970 Dec 19;2(7686):1310-1. Available here.
13. Steinberg HO, Brechtel G, Johnson A, Fineberg N, Baron AD. Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent. J Clin Invest. 1994 Sep; 94(3): 1172–1179. Available here.
14. Singh JA, Reddy SG, Kundukulam J. Risk Factors for Gout and Prevention: A Systematic Review of the Literature. Curr Opin Rheumatol. 2011 Mar; 23(2): 192–202. Available here.
15. Cox CL, Stanhope KL, Schwarz JM ,,Graham JL, Hatcher B, Griffen SC, et al. Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans. Nutrition & Metabolism2012. Available here.
16. Kanbay M, Segal M, Afsar B, Kang DH, Rodriguez-Iturbe B, Johnson RJ. The role of uric acid in the pathogenesis of human cardiovascular disease. Heart doi:10.1136/heartjnl-2012-302535. Available here.
17. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
18. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
19. Bray GA. How bad is fructose? Am J Clin Nutr October 2007. Vol. 86 no. 4 895-896. Available here.
20. Olofsson SO, Boren J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. J Intern Med. 2005 Nov;258(5):395-410. Available here.
21. Hyson D, Rutledge JC, Berglund L. Postprandial lipemia and cardiovascular disease. Curr Atheroscler Rep. 2003 Nov;5(6):437-44. Available here.
22. Kanbay M, Segal M, Afsar B, Kang DH, Rodriguez-Iturbe B, Johnson RJ. The role of uric acid in the pathogenesis of human cardiovascular disease. Heart doi:10.1136/heartjnl-2012-302535. Available here.
23. Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. Available here.
24. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
25. Aeberli I, Zimmermann MB, Molinari L, Lehmann R, l’Allemand D, Spinas GA, et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr October 2007. vol. 86 no. 4 1174-1178. Available here.
26. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
27. Bray GA. How bad is fructose? Am J Clin Nutr October 2007. Vol. 86 no. 4 895-896. Available here.
28. Olofsson SO, Boren J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. J Intern Med. 2005 Nov;258(5):395-410. Available here.
29. Hyson D, Rutledge JC, Berglund L. Postprandial lipemia and cardiovascular disease. Curr Atheroscler Rep. 2003 Nov;5(6):437-44. Available here.
30. Tappy L, Le KA, Tran C, Paquot N. Fructose and metabolic diseases: New findings, new questions. Volume 26, Issues 11–12, 2010, Pages 1044–1049 Available here.
31. Kelishadi R, Mansourian M, Heidari-Beni M. Association of fructose consumption and components of metabolic syndrome in human studies: a systematic review and meta-analysis. Nutrition. 2014 May;30(5):503-10. Available here.
32. Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.
33. Giovannucci E. Insulin, insulin-like growth factors and colon cancer: a review of the evidence. J Nutr. 2001 Nov;131(11 Suppl):3109S-20S. Available here.
34. Esposito K., Chiodini P, Colao A, Lenzi A, Giugliano D. Metabolic Syndrome and Risk of Cancer – A systematic review and meta-analysis. Diabetes Care November 2012 vol. 35 no. 11 2402-2411. Available here.
35. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May 1; 119(5): 1322–1334. Available here.
36. Lustig RH. Fructose: It’s “Alcohol Without the Buzz. Adv Nutr March 2013 Adv Nutr vol. 4: 226-235, 2013. Available here.
37. Ackerman Z, Oron-Herman M, Grozovski M, Rosenthal T, Pappo O, Link G, Sela BA. Fructose-Induced Fatty Liver Disease. Hypertension. 2005; 45: 1012-1018. Available here.
38. Wijarnpreecha K, Thongprayoon C, Edmonds PJ, Cheungpasitporn W. Associations of sugar- and artificially sweetened soda with nonalcoholic fatty liver disease: a systematic review and meta-analysis. Oxford University Press. Sep 2015. Hcv172. Available here.
39. Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. AASLD. Hepatology. Volume 57, Issue 6 June 2013 Pages 2525–2531. Available here.
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