Fructose Confusion

October 10, 2011 Written by JP       [Font too small?]

Albert Einstein once famously quipped, “Everything should be made as simple as possible, but not simpler.” The topic of sugar aptly illustrates his point. Some would have you believe that all calorically equivalent, naturally sourced sweeteners are basically the same. Just eat them in moderation and there’s really little danger. However, a careful examination of the medical literature suggests otherwise. In particular, fructose stands out as a sweetener that ought to be limited in one’s diet. In recent months, fructose has been implicated as: a) reducing the calorie and fat “burning” (net fat oxidation and resting energy expenditure) potential of overweight men and women; b) contributing to abdominal pain, digestive symptoms and sleep disturbance in children; c) elevating various risk markers for cardiovascular disease including LDL (“bad”) cholesterol and triglycerides; d) a primary contributor to the development of abdominal obesity, hypertension and metabolic syndrome in a population study consisting of over 2,500 adults.

Many of the pitfalls associated with fructose can be avoided by simply steering clear of products containing agave nectar or syrup, crystalline fructose and high fructose corn syrup. Excessive fruit and fruit juice consumption can likewise present issues for some individuals. Another strategy to consider is the regular inclusion of sulfur rich foods in your diet such as garlic, onions and shallots. Several experiments in animal models have determined that these aromatic bulbs can mitigate some of the blood sugar, cardiovascular and inflammatory activity initiated by fructose intake.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

To learn more about the studies referenced in today’s column, please click on the following links:

Study 1 - Consumption of Fructose-Sweetened Beverages for 10 Weeks Reduces (link)

Study 2 - Fructose Malabsorption in Children with Recurrent Abdominal Pain:(link)

Study 3 - Consumption of Fructose and High Fructose Corn Syrup Increase (link)

Study 4 - Dietary Fructose and Risk of Metabolic Syndrome in Adults: (link)

Study 5 - Garlic & Onion Attenuates Vascular Inflammation and Oxidative Stress (link)

Study 6 - Garlic Improves Insulin Sensitivity & Associated Metabolic Syndromes (link)

Study 7 - Hypoglycemic Effect of Aqueous Shallot and Garlic Extracts (link)

High Fructose Intake Can Contribute to Hypertension & Kidney Disease

Source: Int J Nephrol. 2011; 2011: 315879. (link)

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Posted in Diet and Weight Loss, Food and Drink, Nutrition

11 Comments & Updates to “Fructose Confusion”

  1. anne h Says:

    Isn’t it great when research confirms what we already know – or at least suspect?
    Love the garlic/onion story, for example.

  2. JP Says:

    Thank you, Anne. Indeed. As a garlic, onion and shallot lover this is most welcome news to me. Luckily, my wife feels the same way! ;)

    Be well!

    JP

  3. Tammy Says:

    Thanks for your article! Had a question: are agave and high fructose corn syrup the same? I had read that agave is low-glycemic so theoretically better than table sugar. What’s your take on agave? Let me know if you already have a post on that topic!

  4. JP Says:

    Hi, Tammy.

    Agave and HFCS aren’t the same. However, they both contain a high percentage of fructose. Here’s some information I’ve posted previously about agave:

    http://www.healthyfellow.com/185/agave-danger/

    http://www.healthyfellow.com/810/natural-products-expo-west-part-two/

    Be well!

    JP

  5. WP Ho Says:

    Thanks for the informative post. I’ve heard that the percentage of fructose and sucrose for instance will affect its health impact. Fruits for instance have a more balance proportion (and of course vitamins, minerals and fibers) that make them less of a problem. What’s your take on this? Thanks!

  6. JP Says:

    Fruits are certainly preferable to processed sources of fructose, IMO. Concentrated fruits are a step downward – example: fruit juice or fruit concentrates. The primary reasons why whole fruits are superior to agave or crystalline fructose, for instance, is that many fruits contain a significant amount of fiber and various phytochemicals which can blunt blood sugar / insulin response to some degree. Berries are an excellent example of fruits which may actually improve faulty blood sugar control as seen in the metabolic syndrome.

    Be well!

    JP

  7. Tony Phylactou Says:

    I had my first gout attack about 10 years ago.
    At the beginning I was having attacks every 6 months. Then gradually I was getting them
    every 3 months, then every month and eventually every week.
    It started at my big toe and then it was moving sometimes in my knees,and generally all
    around my joints, in my feet.And the pain was agonising.
    I have tried all the cures you can imagine.I tried ACV, lemons, drinking a lot of water, but
    to no avail.I tried water fasting, juice fasting,baking soda, again without success.
    I almost gave up meat, limiting it to only once a week ,gave up alcohol completely,again
    no success.
    I was living on vegetables, lots and lots of fresh fruit, milk ,cheese beans and so on .My
    eating habits could not be healthier ,or so I thought.But my gout was worsening.
    Then I decided to increase the amount of fruit I was consuming, thinking that if some fruit
    is healthy, more fruit will be more healthy.Some days I was eating fruit only ,others over 10
    portions a day.
    And alas my gout instead of improving it became chronic ,it was there all the time.
    I was desperate I did not know what to do.
    And then one day accidentally I read an article about fructose,which is contained in fruit in
    large quantities.It said that it increases uric acid, in a matter of minutes.
    Fructose is also present in table sugar, and in HFCS, which is used in soft drinks.
    I put two and two together and realised what I was doing wrong.
    I stopped eating fruit and all other sugars, for a period of 3 weeks,and by magic I saw a
    dramatic improvement.Pain was gone, swelling was gone, I was fine.
    I re introduced fruit again in my diet but reducing them to 1 or 2 a day, and my gout completely
    disappeared.
    I do eat more meat now, and occasionally have an alcoholic drink, and thank God everything
    seems to be fine.
    Fructose was my enemy.

  8. JP Says:

    That’s a powerful testimonial, Tony. Thank you for sharing your success with us!

    Be well!

    JP

  9. JP Says:

    Updated 02/17/17:

    http://www.clinicalnutritionjournal.com/article/S0261-5614(17)30047-X/abstract

    Clin Nutr. 2017 Feb 3.

    Acute metabolic and endocrine responses induced by glucose and fructose in healthy young subjects: A double-blinded, randomized, crossover trial.

    BACKGROUND AND OBJECTIVE: A rise in fructose consumption has been implicated in the etiology of obesity, diabetes and cardiovascular disease. Serum uric acid (UA) elevates after fructose ingestion, increasing the risk of cardiovascular disease. However, the impact of fructose ingestion on nitric oxide (NO) has not yet been confirmed. The aim of this study was to investigate the postprandial metabolic and endocrine responses following an acute ingestion of fructose and glucose in healthy subjects.

    METHOD: This was a double-blinded, randomized, crossover postprandial trial. Eighteen healthy young subjects (9 males and 9 females) with a mean age of 23.6 ± 2.3 years and mean BMI of 20.2 ± 1.5 kg/m2 completed the experiment that was conducted in Hangzhou, China. Volunteers were randomized to two groups (A and B): after an 8-h overnight fast, volunteers either ingested 300 mL of 25% glucose (group A) or fructose (group B) solution at 0830 within 5 min. After a one-week washout period, volunteers were crossed over to receive the alternate test solution. Blood pressure was measured at 0 h, 1 h, 2 h and 3 h and venous blood was drawn at 0 h, 0.5 h, 1 h, 2 h and 3 h after ingestion of the test solution.

    RESULTS: Eighteen subjects completed the study. Serum NO level tended to be lower at 1 h (59.40 ± 3.10 μmol/L and 68.1 ± 3.40 μmol/L, respectively, p ≤ 0.05) and 2 h (62.70 ± 3.10 μmol/L and 70.10 ± 3.50 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC (area under curve) of NO was significantly lower after fructose ingestion than after glucose (p ≤ 0.05). UA level was higher at 1 h (512.17 ± 17.74 μmol/L and 372.11 ± 17.41 μmol/L, respectively, p ≤ 0.01) and 2 h (440.22 ± 16.07 μmol/L and 357.39 ± 14.80 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of UA was significantly higher after fructose ingestion than after glucose (p ≤ 0.01). Correlation analyses revealed that NO was negatively associated with UA at T0.5h (r = -0.62, p ≤ 0.01), T1.0h (r = -0.69, p ≤ 0.001), T2.0h (r = -0.86, p ≤ 0.001) and T3.0h (r = -0.85, p ≤ 0.001) after fructose ingestion. SBP (systolic blood pressure) tended to be higher at 1 h (125.33 ± 1.95 mmHg and 112.06 ± 1.77 mmHg, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of SBP was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). The 3 h-AUC of TG, TC, HDL-C and LDL-C showed no differences between fructose and glucose. LDH (lactate dehydrogenase) level was higher at 1 h (195.00 ± 5.6 U/L and 177.67 ± 6.8 U/L, respectively, p ≤ 0.05) and 2 h (197.01 ± 6.32 U/L and 185.50 ± 7.37 U/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of LDH was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). AR was significantly higher at 1 h (19.86 ± 0.52 ng/mg Hb and 16.98 ± 0.29 ng/mg Hb, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of AR (p ≤ 0.05) was significantly higher after fructose ingestion than after glucose (p ≤ 0.05).

    CONCLUSION: Ingestion of a 75 g fructose load led to acute but unfavorable changes in certain metabolic and endocrine responses including increased serum concentrations and 3 h-AUC of UA, AR and LDH, increased SBP, and decreased endothelial NO production when compared with the same amount of ingested glucose.

    Be well!

    JP

  10. JP Says:

    Updated 02/19/19:

    http://www.journal-of-hepatology.eu/article/S0168-8278(17)30002-8/abstract

    J Hepatol. 2017 Feb 6.

    Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents.

    BACKGROUND & AIMS: Recent research has suggested that dietary fructose intake may increase serum uric acid (UA) concentrations. Both UA concentration and fructose consumption maybe also increase in NAFLD. It is not known whether dietary fructose consumption and UA concentration are independently associated with non-alcoholic steatohepatitis (NASH). Our aim was to investigate the factors associated with NASH in children and adolescents with proven NAFLD, and to test whether UA concentrations and fructose consumption are independently associated with NASH.

    METHODS: Obese children with NAFLD were studied (n=271). NASH was diagnosed by a NAFLD activity score ⩾5 and the fatty liver inhibition of progression (FLIP) algorithm. Fructose consumption (g/day) was assessed by food frequency questionnaire, and UA (mg/dl) was measured in serum. Binary logistic regression with adjustment for covariates and potential confounders was undertaken to test factors independently associated with NASH.

    RESULTS: NASH occurred in 37.6% of patients. Hyperuricaemia (UA ⩾5.9mg/dl) was present in 47% of patients with NASH compared with 29.7% of non-NASH patients (p=0.003). Both UA concentration (OR=2.488, 95% CI: 1.87-2.83, p=0.004) and fructose consumption (OR=1.612, 95% CI 1.25-1.86, p=0.001) were independently associated with NASH, after adjustment for multiple (and all) measured confounders. Fructose consumption was independently associated with hyperuricaemia (OR=2.021, 95% CI: 1.66-2.78, p=0.01). These data were confirmed using the FLIP algorithm.

    CONCLUSIONS: Both dietary fructose consumption and serum UA concentrations are independently associated with NASH. Fructose consumption was the only factor independently associated with serum UA concentration.

    LAY SUMMARY: Currently, it is not known whether dietary fructose consumption and uric acid (UA) concentration are linked with non-alcoholic steatohepatitis (NASH) in children and adolescents. Our aim was to test whether UA concentrations and fructose consumption are independently associated with NASH in children and adolescents with proven non-alcoholic fatty liver disease (NAFLD). We show that both dietary fructose consumption and serum UA concentrations are independently associated with NASH and fructose consumption was independently linked with high serum UA concentrations.

    Be well!

    JP

  11. JP Says:

    Updated 12/07/18:

    https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-018-1105-0

    BMC Nephrol. 2018 Nov 8;19(1):315.

    Fructose increases risk for kidney stones: potential role in metabolic syndrome and heat stress.

    BACKGROUND: Fructose intake, mainly as table sugar or high fructose corn syrup, has increased in recent decades and is associated with increased risk for kidney stones. We hypothesized that fructose intake alters serum and urinary components involved in stone formation.

    METHODS: We analyzed a previously published randomized controlled study that included 33 healthy male adults (40-65 years of age) who ingested 200 g of fructose (supplied in a 2-L volume of 10% fructose in water) daily for 2 weeks. Participants were evaluated at the Unit of Nephrology of the Mateo Orfila Hospital in Menorca. Changes in serum levels of magnesium, calcium, uric acid, phosphorus, vitamin D, and intact PTH levels were evaluated. Urine magnesium, calcium, uric acid, phosphorus, citrate, oxalate, sodium, potassium, as well as urinary pH, were measured.

    RESULTS: Ingestion of fructose was associated with an increased serum level of uric acid (p < 0.001), a decrease in serum ionized calcium (p = 0.003) with a mild increase in PTH (p < 0.05) and a drop in urinary pH (p = 0.02), an increase in urine oxalate (p = 0.016) and decrease in urinary magnesium (p = 0.003).

    CONCLUSIONS: Fructose appears to increase urinary stone formation in part via effects on urate metabolism and urinary pH, and also via effects on oxalate. Fructose may be a contributing factor for the development of kidney stones in subjects with metabolic syndrome and those suffering from heat stress.

    Be well!

    JP

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