Health Problems From Excess Fruit Sugar Intake


The art of bee-keeping and the extraction of honey is mentioned in ancient texts in China, India and Egypt. The use of sugarcane extracts in the West probably started in Persia around 510 BC. Sugar was traded in London in 1319 AD at around RM 300/kg (today’s price). Supplies from the Caribbean countries during the 1800s and the discovery of alternative sources of sugar caused prices to plummet. Prices dropped even more with industrial-scale conversion of glucose to high-fructose corn syrups (HFCS). In the 1700s 5 g/day of sugars were consumed, now it’s 180 g/day (Johnson et al. 2009). That sugar, particularly fructose, consumption increasing almost 40-fold within a short timespan seems to have taken a toll on health worldwide. The WHO has declared Malaysia as the most obese country in the Far East. Sugary food items have certainly contributed to this statistic. Most dietary fructose is added sugar found mainly in cereals and beverages. Today’s children may be the highest consumers of fructose (Marriott et al. 2009).



Fructose is a naturally occurring sugar and the main monosaccharide (single sugar) found in honey, fruit, and some vegetables. A Western diet contributes around 50 g of fructose daily or more than 15% of our daily energy intake. Sweetened beverages can provide up to 45% of dietary intake of fructose, while fruits and vegetables provide around 25%, with remainder coming from sucrose (white sugar) or HFCS added to baked food items and ready-to-eat cereals. Vegetables such as carrots, onions, and sweet potatoes contain equal or lesser amounts of fructose than glucose. Fruit juices contain more fructose than glucose.

Fructose is more than twice as sweet as glucose and 1.5 times sweeter than sucrose. HFCS was first introduced in 1967 and its consumption levels increased by more than 1000% between 1970 and 1990. HFCS contributes to more than 40% of caloric sweeteners added to Western food and beverages (Bray et al. 2004). Fructose, glucose, and galactose (milk sugar) are the 3 major dietary monosaccharides and all of which are known to promote lipogenesis (body fat generation). This means if you avoid dietary fats but consume excess carbohydrates/starches/sugars you would still put on weight.



In 2011 the United Nation declared that metabolic syndrome and other non-communicable diseases (cancer, stroke, dementia) are a greater threat to both the developed and developing countries than is acute infectious diseases including HIV. Even 40% of normal-weight adults manifest specific components of metabolic syndrome (Voulgari et al. 2011), which is a cluster of health disorders such as abdominal obesity linked to excess visceral fat, fatty liver, insulin resistance, diabetes type II, dyslipidemia, heart disease, and hypertension.

Fructose absorption in our gastro-intestinal tract is enhanced when glucose (rice, bread, biscuit, bun) is added to our diet. Since the transport system for fructose is absent in most cells, our liver and kidney are the main sites for fructose metabolism. Consequently, excess fructose intake inflicts stress to these vital internal organs.

Surprisingly, fructose consumption does not elevate blood sugar or insulin levels leading to a lower glycemic index (GI) compared to glucose consumption (Teff et al. 2004). In the past decade, commercial slimming diets seem to have used this abnormal feature of fructose to promote their formulae. Fructose has a low 19 (glucose index = 100) on the GI, which is a measure of a food’s generation of our insulin response and is widely used for quantifying a food’s potential for weight (fat) gain. But using GI to measure fructose would conceal its potential health hazards.

Epidemiological studies offer growing evidence that consumption of sweetened beverages is associated with a higher energy intake, increased body weight, and higher risk of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses directly causes adverse metabolic effects. Consumption of sweetened beverages is clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through a significant increase in body fat (Tappy and Le, 2010). In humans, fructose consumed in moderate to high quantities in the diet increases blood triglycerides and alters liver glucose homeostasis, but does not appear to cause muscle insulin resistance or high blood pressure in the short-term (Le and Tappy, 2006).





This refers to one’s inability to completely absorb fructose evidenced by unpleasant gastro-intestinal symptoms including IBS. Up to 50% of the population is unable to absorb 25 g of fructose (Gibson et al. 2007) and up to 80% of healthy people are unable absorb 50 g fructose load (Braden 2009). An estimated 1 in 20,000 new borns may be lacking in aldolase, which is the enzyme needed to metabolise fructose. Feeding high fructose food to these infants can lead to their abdominal pain, hypoglycemia (low blood sugar), vomiting, growth retardation, liver or kidney damage/failure and is potentially life-threatening (Collins 1993). Strict dietary exclusion of fructose helps them regain normal growth.



Research shows a substantial increase in blood triglyceride (stored fat) levels after fructose-containing diets (Hallfrisch 1990). Indeed, following fructose intake, triglycerides may rise by some 200% higher than after glucose intake, lactate production is up to 5,000% higher while insulin (sugar-controlling hormone) and leptin (appetite suppressing hormone) levels both rise less in response to fructose than to glucose (Teff et al. 2009). The risks of cardiovascular disease, obesity and the metabolic syndrome have all been linked to consumption of sugar-sweetened beverages in many research studies (Bray 2012). Chronic elevation in blood triglyceride levels has been associated with higher risk of heart disease especially in women (Heyden et al. 1980). Fructose – but not glucose – stimulates lipid (fat) production in the liver and so increases circulating levels of triglycerides, particularly when fructose-beverage is consumed at night (Stanhope et al. 2009).

A basic feature of Western “fast food” is ample supply of saturated fats, trans fats, and sugary beverages. High fructose intake is associated with higher levels of low density (‘bad’) cholesterol even in children (Aeberli et al. 2007).



Except for citrus fruits, increasing daily calorie intake from sweet fruits, flour or cereal products, corn products, sea food, and added sugars has been linked to higher incidence of kidney stones (De et al. 2014). Fructose intake is linked to higher risk of developing gout in men, especially if their fructose comes from multiple sources (Choi and Curhan, 2008). There seems to be an 85% higher risk of gout development if men consume more than two sweet beverages (including 3+1 coffee/tea, syrup, bottled/canned drinks) per day compared to infrequent consumers. Fructose-induced uric acid generation causes mitochondrial oxidative stress that further stimulates fat accumulation (Johnson et al. 2013). While a lower blood level of uric acid acts as an antioxidant in the extracellular environment, it produces pro-oxidative effects inside our cells.



Just 60 g of fructose can acutely raise blood pressure (Brown et al 2008) and 24 ounces of sweetened beverages can do likewise (Le t al. 2012). Indeed, fructose can increase blood pressure and thermogenesis more than glucose. However, population studies offer strong evidence that a higher daily intake of freshly harvested organic vegetables and citric fruits lowers blood pressure in hypertensive adults.



Besides alcoholic beverages, fructose plays a role in the development of fatty liver (Basaranoghu et al. 2013). Liver has a very high fructose extraction rate and fruit sugar does not get converted to glycogen (stored sugar) directly and so contributing directly to increased caloric consumption which is not accurately measured by GI.



A high fructose intake of some 50% of total dietary energy can lead to insulin resistance (pre-diabetes) and lipogenesis, as well as decreased insulin receptor activation (Rizkalla et al. 1992). Insulin resistance (high blood insulin) in children of obese mothers would have started during their fetal stage and this condition carries lifelong adverse implications for their metabolic health.



Fructose is more lipogenic (fat generating) than glucose or refined starches. This sugar increases weight (fat) gain since it is able to stimulate hunger while blocking our satiety responses (Shapiro et al. 2008). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight individuals (Stanhope et al 2009).



A maternal 60% fructose diet can significantly increase serum triglycerides, FFAs, and insulin in offspring (Ching et al, 2011). Obesity is a low-grade chronic inflammatory condition linked to many metabolic health disorders such as heart disease, hypertension, diabetes, and even some cancers. It is not the cause of metabolic syndrome, but a marker for metabolic dysfunction.



Epidemiological studies have provided evidence that higher intakes of freshly harvested organic citric fruits and vegetables reduce risk of cancer (Vainio and Weiderpass, 2006). However, excess fructose intake is associated with increased risk of pancreatic and intestinal cancers, as well as promoting more aggressive cancer behaviors and metastasis (Port et al. 2012). Cancer cells generate lactic acid as part of anaerobic glycolysis, which is their main survival mechanism. More lactate seems to be formed from fructose than from glucose consumption. Consequently, most nutritional therapists disagree with use of honey as part of adjunct cancer therapy due to its rather high fructose content.



Fish oil can significantly decrease triglyceride levels after high-fructose diets compared with high-fructose diets without fish oil (Harris 1997). EPA/DHA in fish oil reverses dyslipidemia but not insulin resistance, nor does it lower fasting glucose or cholesterol levels in diabetes type II people (Borkman et al. 1989). Omega-3 fats from fatty fish, sardines, grass-fed meat, or flax seed sources, whether in dietary or supplemental sources, seem equally protective against cardiovascular diseases (Hopper et al. 2004). Farmed fish such as salmon tend to be high in pro-inflammatory omega-6 fats. Trans-resveratrol helps neutralize some of damages inflicted by endothelial (artery wall) dysfunction and insulin resistance (Akar et al. 2012). For further advice on evidence-based nutritional treatment for metabolic disorders, refer to for more information.



Aeberli I, et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr. 2007;86(4):1174-8.

Akar F, et al. High-fructose corn syrup causes vascular dysfunction associated with metabolic disturbance in rats: protective effect of resveratrol. Food & Chem Toxicol. 2012;50:2135–41.

Basaranoglu et al. Fructose as a key player in the development of fatty liver disease. W J Gastroenterol. 2013;19(8):1166-72.

Borkman M et al. Effects of fish oil supplementation on glucose and lipid metabolism in NIDDM. Diabetes. 1989;38(10):1314-9.

Braden B. Methods and functions: Breath tests. Best Prac Res Clin Gastroenterol. 2009;23:337–352.

Bray GA, et al. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutri. 2004:79(4): 537–43.

Bray GA. Fructose and risk of cardiometabolic disease. Curr Atherosclero Rep. 2012;14(6):570-8.

Brown CM, et al. Fructose ingestion acutely elevates blood pressure in healthy young humans. Am J Physiol Regul Integr Comp Physiol. 2008;294:R730–R737.

Ching RHH, et al. Supplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspring. J Nutri. 2011; 141(9): 1664–72.

Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336(7639):309-12.

Collins J. Metabolic disease. Time for fructose solutions to go. Lancet. 1993;341:600.

De SK, et al. Changing trends in the American diet and the rising prevalence of kidney stones. Urology. 2014;84(5):1030-3. Gibson PR, et al. Review article: Fructose malabsorption and the bigger picture. Aliment Pharmacol Ther. 2007;25:349–63.

Hallfrish, J. Metabolic effects of dietary fructose. FASEB 1990;4:2652-60.

Harris WS: n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr.1997;65:1645S–54S.

Heyden S, et al. (1980) Fasting triglycerides as predictors of total and CHD mortality in Evans County, Georgia. J Chron. Dis. 1980;33:275-82.

Hooper L et al. Omega 3 fatty acids for prevention and treatment of cardiovascular disease. Omega 3 fatty acids for prevention and treatment of cardiovascular disease. Cochrane Database Syst Rev. 2004;(4):CD003177.

Johnson RJ, et al. Sugar, Uric Acid, and the Etiology of Diabetes and Obesity. Diabetes 2013; 62(10): 3307-15.

Johnson RJ, et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. 2009;30:96-116.

Le KA, Tappy L. Metabolic effects of fructose. Curr Opin Clin Nutr Metab Care. 2006;9(4):469-75.

Le MT, et al. Effects of high-fructose corn syrup and sucrose on the pharma-cokinetics of fructose and acute metabolic and hemodynamic responses in healthy subjects. Metabolism 2012;61:641–651.

Marriott BP, et al. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr. 2009;139:1228S–35S.

Port AM, et al. Fructose consumption and cancer: is there a connection? Curr Opin Endocrinol Diabetes Obes. 2012;19(5):367-74.

Rizkalla SW, et al. Comparative effects of 6 week fructose, dextrose and starch feeding on fat-cell lipolysis in normal rats: effects of isoproterenol, theophylline and insulin. Mol Cell Biochem 1992;109:127–32.

Shapiro A, et al. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol 2008;295:R1370–5.

Stanhope KL, 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;119(5):1322-34.

Tappy L, Le KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010;90(1):23-46.

Teff KL, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrin Metab. 2004; 89(6):2963–72.

Teff KL, et al. Endocrine and metabolic effects of consuming fructose-and glucose-sweetened beverages with meals in obese men and women: influence of insulin resistance on plasma triglyceride responses. J Clin Endocrinol Metab. 2009;94(5):1562-9.

Vainio H, Weiderpass E. Fruit and vegetables in cancer prevention. Nutr Cancer. 2006;54(1):111-42.

Voulgari C, et al. Increased heart failure risk in normal-weight people with metabolic syndrome compared with metabolically healthy obese individuals. J Am Coll Cardiol. 2011;58:1343–50.

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About Author

Dato’ Steve Yap

Masters’ in Metabolic & Nutritional Medicine (USF Med Sch);

Advanced Fellow, Anti-Aging Regenerative Functional Medicine (USA);

Fellow, Integrative Cancer Therapies (USA);

Nutritional Therapy Council Certified Practitioner (UK);

President, Federation of Complementary & Natural Medical Associations M’sia;

Complementary Medicine Director, DSY Wellness Longevity Center (

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