We used to think that fructose, fruit sugar, was a useful substitute for sucrose, “table sugar”; sadly we now know better.
Fructose intolerance happens when fructose is not absorbed well; fruits and fruit juices with higher levels of fructose can then cause gas, bloating, abdominal cramps and diarrhoea.
But in the long-term it is this is probably better than what happens if you do absorb it; the metabolic effects of fructose include as much weight gain as from sucrose, plus worse insulin resistance and damage to fat metabolism. Fructose leads to oxidative stress, and so increases LDL (‘bad’ cholesterol) and leads to high blood pressure and damage to arteries.
It has now been shown that fructose also increases uric acid (which can cause gout, arthritis and kidney stones) at the same time as depleting ATP, the cell’s main energy currency. Anybody with a high uric acid on blood testing is strongly advised to cut out fructose from their diet. With further laboratory tests we can now even detect a build-up of fructose products in the cell - and do so with worrying frequency.
Fructose is a naturally occurring simple sugar found in fruit, vegetables, and honey.
Sucrose (table sugar) consists of one molecule of glucose and one of fructose. This form of fructose is absorbed more slowly than pure fructose, but will still be as harmful to metabolism in the end.
High Fructose Corn Syrup (HFCS) is a sweetener in many processed foods and soft drinks. It is made up of almost half glucose and half fructose. An average 600 ml can of soft drink contains 32.6 grams (over 6 teaspoons) of fructose. HFCS is also used to sweeten baked goods, canned fruits, dairy products, ketchup and jams.
Sorbitol is a sugar alcohol used as an artificial sweetener and found naturally in fruits and fruit juices. It can also be found in many “diet foods” such as diet soft drinks, sugarless gum, sugar-free jelly/jam, and liquid medications. Sorbitol often creates similar symptoms to fructose – especially when fructose and sorbitol are ingested together.
The best way to take fruit is as the whole, fresh fruit; even freshly squeezed fruit juice will give you more fructose. But anything labelled as squash or fruit drink may well have even more fructose in the form of HFCS.
Dietary Sources of Fructose
(mg of Fructose per 100 grams):
- Bananas 4,850
- Grapes 8,130
- Apples 5,900
- Figs 22,900
- Cherries 6,000
- Pears 6,230
- Strawberry 2,500
- Blackberry 2,400
- Orange 2,250
- Blueberry 4,970
- Grapefruit 2,500
- Raisins 29,700
- Dates 32,000
- Prunes 12,500
- Persimmon 5,560
- Kiwi Fruit 4,350
- Watermelon 3,360
- Plums 3,070
- Raspberry 2,350
- Honeydew Melon 2,960
- Pineapple 2,050
- Cantaloupe 1,870
- Peach 1,530
- Nectarine 1,370
- Paprika 6,710
- Chilli powder 4,290
- Ginger 1,780
- Molasses: 12,800
- Tomato 1,370
- Cabbage 1,650
These Substances may Counteract the Toxic Effects of Fructose
N-Acetyl-Cysteine (NAC) may inhibit the ability of Fructose to increase Blood Pressure and cause Insulin Resistance.
Lipoic Acid may inhibit the ability of Fructose to cause Cross-Linking of Proteins.
Cinnamon may inhibit the ability of Fructose to cause Insulin Resistance.
Green Tea may inhibit the ability of Fructose to cause Insulin Resistance and to increase Triglyceride levels.
Tappy L, Leˆ K-A. Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiol Rev 90: 23– 46, 2010; doi:10.1152/physrev.00019.2009.
While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.
Choi, Y. K., et al. Fructose intolerance: an under-recognized problem. Am J Gastroenterol. 98(6):1348-1353, 2003.
Although the role of lactose intolerance in the pathogenesis of abdominal symptoms is well known, the role of fructose intolerance is unclear. The aims were 1) to examine the prevalence of fructose intolerance in patients with unexplained abdominal symptoms, and 2) to explore whether fructose concentration influences fructose breath test. Over 2 yr, patients with unexplained symptoms answered questionnaires and underwent fructose breath tests. Patients received 50 g fructose in 150 ml water (33% solution). Breath samples were collected for hydrogen and methane. In a second study, breath test was performed after giving either 10%, 20%, or 33% fructose solution. Data were analyzed retrospectively. A total of 183 patients (50 male, 133 female) had breath tests, of whom 134 (73%) were positive. Among these, 119 (89%) had elevated H(2), and 15 (11%) had elevated CH(4) or both gases. Questionnaires showed that flatus (83%), pain (80%), bloating (78%), belching (70%), and altered bowel habit (65%) were the most common symptoms. Breath test reproduced symptoms in 101 patients (75%). In the second study, 14/36 (39%) tested positive with a 10% solution, 23/33 (70%) with a 20% solution, and 16/20 (80%) with a 33% solution (10% versus 20% or 33%, p < 0.01). Fructose intolerance may cause unexplained GI symptoms. The higher yield of positive tests in our initial study may be due to referral bias or testing conditions; lower test dose produced a lower yield. Nonetheless, recognition and treatment of fructose intolerance may help many patients.
Ledochowski, M., et al. Fructose- and sorbitol-reduced diet improves mood and gastrointestinal disturbances in fructose malabsorbers. Scand J Gastroenterol. 35(10):1048-1052, 2000.
Fructose malabsorption is characterized by the inability to absorb fructose efficiently. As a consequence fructose reaches the colon where it is broken down by bacteria to short fatty acids, CO2 and H2. Bloating, cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are the consequences and can be seen in about 50% of fructose malabsorbers. The authors have previously shown that fructose malabsorption is associated with early signs of mental depression and low serum tryptophan concentrations. It was therefore of interest whether a fructose-
reduced diet could not only improve gastrointestinal complaints but also depressive signs seen in fructose malabsorbers. Fifty-three adults (12 males, 41 females), who were identified as fructose malabsorbers according to their breath-H2 concentrations, filled out a Beck’s depression inventory-questionnaire, and a questionnaire with arbitrary scales for measurement of meteorism, stool frequency and quality of life for a 4-week period before dietary intervention and 4 weeks after dietary change as for fructose- and sorbitol-reduced diet. Depression scores were reduced by 65.2% after 4 weeks of diet (P < 0.0001), and there was a significant reduction of meteorism (P < 0.0001) and stool frequency (P < 0.01). Improvement of signs of depression and of meteorism was more pronounced in females than in males. Fructose- and sorbitol-reduced diet in subjects with fructose malabsorption does not only reduce gastrointestinal symptoms but also improves mood and early signs of depression.