Yet another reason to avoid fructose

Have you seen the Corn Refiners Association commercial campaigns to educate the American public on the safety of fructose? If you haven't, you can view these interesting specimens on You Tube:

"Get the facts--You're in for a sweet surprise: Fructose is safe in moderation!"

Two Moms

Two lovers


Beyond the fact that fructose stimulates liver production of glycerol, which thereby increases liver VLDL production and raises blood levels of triglycerides; likely stimulates appetite; increases cholesterol levels; fructose has also been clearly implicated in increasing blood levels of uric acid.

Uric acid is the substance that, in some people, precipitates in joints and causes gout, the painful inflammatory arthritis that has been increasing in prevalence over the last four decades since the introduction of fructose in 1967. While blood levels of uric acid in the early part of the 20th century averaged 3.5 mg/dl, more recent population assessments have averaged 6.0 mg/dl or higher. (Non-human mammals who don't eat processed foods, drink fruit drinks or beer, and don't eat candy have uric acid levels of <2.0 mg/dl.)

Uric acid is looking like it may prove to be an important risk factor for coronary disease and atherosclerotic plaque. It is no news that people with higher blood levels of uric acid are more likely to experience adverse cardiovascular events like heart attack. People with features of the metabolic syndrome also have higher uric acid blood levels; the more characteristics they have, the higher the uric acid level. However, the prevailing view has been that uric acid is simply an accompaniment of these processes, but not causal.

However, more recent observations suggest that increased levels of uric acid may instead be a cause of metabolic syndrome and high blood pressure.

Increased blood levels of uric acid have been shown to:

--Increase blood pressure
--Induce kidney damage (even in the absence of uric acid kidney stones)
--Antagonize insulin responses

A diagnosis of gout is not required to experience all of the adverse phenomena associated with uric acid. (For not entirely clear reasons, some people, perhaps based on pH or other factors, are more prone to trigger crystallization of uric acid in joints, similar to the phenomena of sugar crystallization when making rock candy.)

Which brings us back to fructose, a sweetener that clearly substantially increases uric acid levels. I suppose that the mothers and lovers in the Corn Refiners' commercials are right to a degree: Our kids will survive, as will you and I, despite increases in triglycerides, enhanced diabetic tendencies, amplified appetites, and increased uric acid due to fructose in our diet. We will also likely survive despite being 100 lbs overweight, partly due to the effects of fructose.

But if long-term health is your desire for you and your family, fructose has no role whatsoever to play.

Interestingly, the obviously expensive and slick ad campaigns from the Corn Refiners' videos have triggered some helpful video counterarguments:

High-fructose corn syrup
Conspiracy for Fat America
High-fructose corn syrup truth


A full discussion of uric acid, the scientific data behind uric acid as a coronary risk factor, and the nutritional means to reduce uric acid will be the topic of a thorough discussion in an upcoming Special Report on the Track Your Plaque website.

Comments (5) -

  • Kevin

    12/12/2008 8:02:00 PM |

    There was an article this week in USA Today about new research pertaining to high fructose corn syrup (independent of your uric acid argument). Check it out here: http://www.usatoday.com/news/health/2008-12-08-fructose-corn-syrup_N.htm

    -Kevin on behalf of the Corn Refiners Association

  • BenignaMarko

    12/18/2008 5:28:00 PM |

    This all sounds doable.  It does seem that fructose is causing such health problems that the FDA should make sure it is removed from products.  We all know that we consume too much everything, so, can't they make the stuff without the fructose?  There is so much to worry about in recent years, we might as well not eat.
    Benigna Marko

  • Anonymous

    1/4/2009 10:36:00 PM |

    I don't deny the research posted in this post.  However, things are not as simple as they seem.

    I have done quite a lot of research on Multiple Sclerosis, and high levels of uric acid are actually implicated in LOWER levels of MS.  Uric acid actually can work as an antioxidant in the body; gout and MS are almost mutually exclusive.  You will almost never see someone who has gout having MS, and vice versa.

    In fact, increasing uric acid in MS patients has been shown to DECREASE RELAPSE RATES (see abstract below.)

    So, things are not as simple as they appear.  

    Just thought I'd post this information.

    -gb

    FROM MEDLINE


    5: Vojnosanit Pregl. 2006 Oct;63(10):879-82.Links
        Therapeutic value of serum uric acid levels increasing in the treatment of multiple sclerosis.
        Toncev G.

        Clinical Center Kragujevac, Center of Neurology, Kragujevac, Srbija.

        BACKGROUND/AIM: Uric acid was successfully used in both, prevention and treatment of the animal model of multiple sclerosis (MS). Recently it has been shown that inosine, a ribosylated precursor of uric acid, might be used to elevate serum uric acid levels in MS patients. The aim of this study was to evaluate the safety and efficacy of oral inosine as a single drug treatment in patients with MS. METHOD: We administered inosine orally to 32 MS patients from 2001-2004 year at doses from 1-2 g daily (given twice) depending on the pretreatment serum uric acid levels. The mean follow-up interval was 37.69+/-6.55 months. The other 32 MS patients, without any treatment except for a relapse period (matched by age, sex, duration of disease and functional disability), were used as controls. The follow-up interval of these patients was 36.39 +/- 2.68 months. The neurological disability was evaluated by the Expanded Disability Status Scale score (EDSS). RESULTS: During the observed period the treated MS patients were found to have the lower relapses rate than the non-treated MS patients (Chi-square test, p = 0.001). None of the patients have showed any adverse effect of inosine treatment. The non-treated MS patients were found to have a higher increasing in the mean EDSS score than the treated ones (two-way ANOVA-repeated measures/factor times, p = 0.025). CONCLUSION: Our results suggested that the treatment approaches based on the elevation of serum uric acid levels might prove beneficial for some MS patients


    1: Eur J Neurol. 2008 Apr;15(4):394-7. Epub 2008 Feb 26.Click here to read Links
        Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment.
        Guerrero AL, Martín-Polo J, Laherrán E, Gutiérrez F, Iglesias F, Tejero MA, Rodríguez-Gallego M, Alcázar C.

        Neurology Unit, Hospital Río Carrión, Palencia, Spain. aguerrero@hcuv.sacyl.es

        Uric acid (UA), a product of purine metabolism, may be an antioxidant, perhaps acting as a scavenger of peroxynitrite. Patients with gout have a reduced incidence of multiple sclerosis (MS). A number of studies found that patients with MS have low serum levels of UA, although it has not been established whether this represents a primary deficit or a secondary effect. UA has also been proposed as a marker of disease activity and response to immunosuppressive or immunomodulatory treatment. We retrospectively reviewed 83 relapsing-remitting or secondary progressive MS patients (64 females and 19 males) followed in our Neurology Unit. We collected data concerning demographic variables as age and sex, and clinical variables as age of onset, clinical type, disease duration, EDSS score and total number of relapses. We considered UA levels in three different situations: during a relapse, during remission period and during remission period under immunomodulatory treatment [Interferon Beta 1a i.m. (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a s.c. (Rebif; Serono Europe Limited, London, UK), Interferon Beta 1b (Betaferon; Bayer Schering Pharma AG, Berlin, Germany) or Glatiramer Acetate (Copaxone; TEVA Neuroscience LLC, Kansas City, MO, USA)]. A Wilcoxon matched pairs test was carried out to determine differences between groups. A P-value less than 0.05 was considered statistically significant. In 33 patients, we were able to compare at least one UA value obtained during a relapse with at least one when remission without treatment. Mean serum UA levels were significantly lower when measured during a relapse (r: 0.39, P: 0.024). In 27 cases, we compared at least one remission value without treatment with at least one obtained during remission and immunomodulatory treatment. Mean serum UA levels significantly increased when determined during Interferon Beta or Glatiramer Acetate therapy (r: 0.84, P < 0.001). Although we do not know exactly whether and how UA is involved in MS pathogenesis, our data suggest that UA might reflect disease activity or treatment response in MS.

  • karl

    2/28/2009 3:56:00 AM |

    I read that Fructose is 10 times more reactive than glucose in forming AGE - Advanced Glycogen End-products - the process thought to start CAD.

    I avoid all sugar - but wonder if the extra 5-10% might make a difference.

  • Free Teleconferencing

    2/22/2011 11:49:58 AM |

    Very... Nicee... Blog.. I really appreciate it... Thanks..Smile

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"It's genetic"

"It's genetic"

At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.


There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

Comments (17) -

  • steve

    11/18/2008 2:58:00 PM |

    all excellent points,but the question is: how do you find someone who will tell you why?  Most will look at advanced cholesterol testing and based on that prescribe a statin and a low fat diet.  Speaking of diet, it is unclear how much sat fat you think acceptable on a daily basis.  It is nice to say it is ok to have and we have gone overboard in its elimination, but unfair not to then say how much in your view is ok

  • Anonymous

    11/18/2008 4:25:00 PM |

    Thank you, thank you, thank you... I'm still trying to convince my dad that his lifestyle is still important after his idiot cardiologist told him it was all genetic and all he could do it take meds and hope for the best... I hate when docs downplay diet and exercise.  Ugh!

    On another note, I've been told that because I have ApoE 4 I should not consume alcohol or take fish oil.  What do you know about that?

  • vin

    11/18/2008 4:25:00 PM |

    My grandmother, who died 20 years ago at the age of 85, used to say "it is god's will" whenever someone died young (or old). It is what the modern day cardiologist now puts it down to genetics.

    That is progress over the last 100 years.

  • Jessica

    11/18/2008 7:14:00 PM |

    I think the potential that Vitamin D has relating to heart health is significant.

    Although I'm not the best at verbalizing why this is the case, when I learn a condition is "genetic" and it tends to strike later in life, I think, "but you've had that gene your entire life. Why is it that NOW it's expressing itself?"

    Genetic predispositions to conditions may explain why someone has a condition, but it doesn't explain why the condition occurs when it does.

    Could it be that identifying and correcting D deficiencies early in life will provide our cells (DNA) with the power to continue suppressing genes that should never be expressed?

  • Anonymous

    11/18/2008 7:59:00 PM |

    I think you missed one of the biggest "genetic" factors: crappy living habits: junk food, no exercise. These pass down from generation to generation too. But, like some of the others you mentioned, these conditions are treatable.

  • Anonymous

    11/19/2008 12:03:00 AM |

    www.amocare.com is a free service that has hospitals located in the U.S. that perform heart surgery for around 70% the cost of the price of the average cost. American Medical Outsourcing will help you with the entire process of the treatment. Heart bypass surgery usaly cost $45k-$55k. with AMO, the cost is around $10k-$13k. Go to www.amocare.com for more info.

  • Anonymous

    11/19/2008 4:01:00 PM |

    I'm curious as to why you approved the comment of the amocare spammer?

  • Katherine

    11/20/2011 6:08:47 PM |

    About six months ago I started eating a paleo lifestyle.  Since then I've had two cholestrol panels.  After two months, my LDL was 180.  Four months later, my LDL was 290.  HDL is 68 and Trigs are 41.  I've also lost about 10-14 pounds.  My dad has high cholesterol (LDL) and my grandmother on my mom's side had a heart attack at 66 and died.  I've recently had a FH test and I'm awaiting the results.  Now after reading this, having having a test run on the ApoE4 seems like a good idea as well.  Would the ApoE4 be appropriate?  Was the FH test a waste of time?

  • Dr. William Davis

    11/21/2011 1:38:03 PM |

    Both can be helpful, if only to confirm whether there is a genetic basis or not.

  • Katherine

    11/24/2011 2:16:31 PM |

    Dr. Davis,
    You've said "ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution),"  What do you think is the best solution?

  • Dr. William Davis

    11/25/2011 2:10:35 PM |

    Because the majority of apo E4 people have extravagant numbers of small LDL particles triggered by carbohydrate consumption, I still advise first eliminating wheat and slashing carbs.

  • Gene K

    11/25/2011 4:21:21 PM |

    I am apo E4/3, and I was able to bring down my small LDL particles to under 90. My daily carb consumption includes a small cup of dark berries, hummus, non-starchy vegetables (broccoli, eggplant, cauliflower, zucchini), and natto. I saw a big drop in small LDL particles after I greatly reduced consumption of oils (olive oil specifically), but I don't know whether this change alone had a role in causing the reduction of my smLDL.

  • Gene K

    11/25/2011 4:27:53 PM |

    (cont'd) As far as fats, I don't eat red meat, but plenty of fatty fish and lean poultry plus an egg every day. Tons of yellow mustard (turmeric), too.

  • Dr. William Davis

    11/27/2011 2:15:58 PM |

    HI, Gene--

    I believe the best way to view this is that oils/fats amplify LDL particles in all its forms. If in the presence of carbohydrates, oils/fats will increase small LDL because it is the dominant form.

  • Katherine

    11/28/2011 8:50:14 PM |

    I have eliminated wheat and eat about 30 total carbs a day while my LDL is 289.  I am actively losing weight which is sounds like may have influenced my numbers.  Is the Apo E4 associated only with increased LDL's or is it with elevated Trigs as well?  My Trigs are 37.

  • Ronnie

    12/13/2011 3:16:58 AM |

    My doctor tested me for ApoE without telling me and mailed me my results....I'm a 3/4.  My LDL-P was 1206, Triglycerides 115, HDL-C 72, sdLDL 37 mg/dl.  I'm 60, female, thin (5'2" 109 lbs), have exercised my entire life, non smoker, occasionally drink one glass of white wine.  Parents never had heart disease although I have a sister with CAD which I always chalked up to poor lifestyle habits (terrible diet, sedentary).  I never expected this and I'm not handling this news well at all.  While some people may want to know their ApoE genotype, I wasn't one of them.  I greatly resent my doctor doing this test without consulting me first and the way I received the results through the mail.   I have no idea what to do this information.  Do I consult with a geneticist, a cardiologist or a lipid specialist?

  • Robin Michael

    5/1/2013 5:50:50 PM |

    Dr. Davis,

    I joined TYP specifically because my Heart Diagnostics Lab results (taken before I started Wheat Belly plan) showed my to be APOE E4 3/4 genotype.  My other numbers: total cholesterol=154, LDL-C=85, HDL-C=56, Triglycerides=58. On Lipitor generic 10mg, Lisinopril 20mg and Amlodipine 5mg. I find the WB plan to be easy, but am moderately high fat diet including labne for breakfast, eggs for lunch with avocado, sour cream, and fish/chicken and salad/green vegetable for dinner. Carbs are limited to less than 50g per day. I generally cook with olive oil, and sometimes toasted sesame oil. I eat very little fruit, limited my intake to a few berries in the morning, a plum or half an apple at lunch.

    Do you recommend lowering my fat intake? Anything else?

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