Q&A on fructose, soy and meal frequency

I was in the middle of writing an overview on polyunsaturated fats when I received a comment from a reader Doug with some interesting questions. I started my answer in Comments but it quickly blew out of proportions so I have decided to post it. One of the main reasons being is that I get these questions very often and I would like to answer them fully once and for all.

Question 1: Why is fructose a “neolithic” agent of disease? Ancient man had fruit and I have seen intelligent speculation that it was just as sugary as modern fruit (especially in tropical regions). Wouldn’t it be more precise to say “refined sugar” instead of “fructose”? And isn’t the real culprit here high-fructose-corn-syrup?

Fructose is a hepatotoxin, its major damage site being the liver. Like other toxins its action can be plotted on a dose-response curve: the more you have the greater the damage. Alcohol is another example of hepatotoxin: may be even beneficial in moderation (possibly via polyphenols and action on blood vessels) but deadly in large quantities.

The other issue with any toxins is their idiosyncratic nature: some people can take a lot, some people will develop problems with small amount. If your liver is already damaged via alcohol, hepatitis viruses, autoimmune process, fatty liver disease, then the safe level of fructose is probably zero.

Ancient man definitely ate fruit, however the quantities of fructose were probably incomparable to modern standards. Unlike today, when fruit is available in the supermarket all year around, fruit was mostly seasonal and fruit trees were not cultivated in orchards. Subtropical climates probably favoured higher fruit consumption, Northern Europeans – hardly any.

HFCS is not used in all Western countries: Australia we only use sugar but we are still on track to overtake the US in the obesity race.

So the bottom line is the dose maketh the poison. If you wouldn’t eat 6 oranges in one sitting why drink it? The quantity of fructose in 1 apple is about 4g, the standard soda is around 30g.

I also addressed some of these issues in my previous fructose post.

Question 2: Do the Japanese eat fermented soy? I know that soy comprises a large part of their diet and yet they are very healthy as a group; the healthiest in the industrial world? What type of soy are they eating and how does it differ from the soy eaten in the West?

It has been shown (Dietary Intake and Sources of Isoflavones Among Japanese, Kenji Wakai, Isuzu Egami, Kumiko Kato, Takashi Kawamura, Akiko Tamakoshi, Yingsong Lin, Toshiko Nakayama, Masaya Wada, Yoshiyuki Ohno, Nutrition and Cancer,Vol. 33, Iss. 2, 2009) that 90% of soy intake in Japan comes from fermented/precipitated sources: tofu, miso, natto and fried tofu. It is mostly used as a condiment, not a staple food. Some estimate  that the average daily soy intake is around 10g, the equivalent of 2 teaspoons. And while the overall cardiovascular mortality of the Japanese is much better than in the US, the differences in the diet are too great to draw any conclusions from 1 ingredient. 30.3% of Japanese are daily smokers vs 17.5% Americans, it doesn’t mean that we should start smoking to match their health status.

Question 3: I have read good arguments for frequent meals and infrequent meals. It seems that there is science to support either lifestyle. What is your argument against frequent meals and how do you answer the objections that there are many studies that show that people who ate more frequent meals had BETTER insulin sensitivity?

Most of the studies favouring high meal frequency were performed with SID (standard industrial diet). Eating cornflakes for breakfast makes most people mighty hungry by mid-morning and more likely to binge out on sugary and unhealthy food. In this context higher meal frequency would indeed lead to better glucose control. However, the story changes when you introduce protein and/or fat into the meal. In this study obese men fed higher protein meal reported better satiety on larger LESS frequent meals.

Also do not forget that most studies comparing meal frequency do not  take HUNGER into account. The meals are spread out in a pre-determined fashion, making the study subjects eat “by the clock”. Resetting your metabolism on better nutrition will actually allow you to follow your hunger/satiety signals, not the traditional morning tea time.

Anybody who follows primal nutrition will tell you, snacks become obsolete after a while. Meal frequency decreases spontaneously when your body is fully replete with nutrients. Low meal frequency is not something to force your body into, it just happens under the right conditions.

For more info I recommend Martin Berkhan, the intermittent fasting king. His website contains links to many research studies supporting this hypothesis.

I hope this answers some of Doug’s and possibly others’ questions. Now back to my fats!


15 thoughts on “Q&A on fructose, soy and meal frequency

  1. From what I understand, if you want to ensure you can eat more fructose while being far less likely to damage your liver–or at least, less likely to cause non-alcoholic fatty liver disease–make sure you’re getting enough choline in your diet.

    Beef liver’s one of the best sources, along with egg yolks. Both these foods have been vilified in the standard industrial diet. I do not think this is a coincidence.

    • Hi Dana, you are right, choline deficiency is probably widespread in the community. We need choline for the formation of acetylcholine (neurotransmitter) and processing alcohol/fructose/fat into triglycerides to transport out of the liver. I think there has been a couple of studies showing a possible decrease or reversal of fatty liver disease with choline. But I think reducing the toxins in the first place might be a better alternative to trying to mop them up afterwards, considering we are not sure of the mechanism yet. So hooray for liver and egg yolks and take it easy on liver toxins.

  2. Love this one A! This is key – If you wouldn’t eat 6 oranges in one sitting why drink it? The quantity of fructose in 1 apple is about 4g, the standard soda is around 30g.
    People think that fruit juices (of course freshly squeezed is healthy) they freak out when I say “hope you enjoyed your can of coke”… same fructose, fructose is fructose in the body.
    Off to enjoy my almond spread with some fructose.

  3. I hope this answers some of Doug’s and possibly others’ questions.

    Oh yes. Thank you. Your answers were extremely helpful.


  4. I enjoy your perspectives and appreciate that you are fitting this in between clinical rotations, absorbing enormous quantities of curriculum and live your life, to boot!
    If the interest is there, would you consider what you would advise for a person who eats a paleo + fermented dairy diet, gets adequate sun and activity who is a newly diagnosed DILI from an investigational drug? AST/ALT 1.1 (534/476), adequate albumin, low globulin, bili direct .5, total 1.4, and alk phos 151. Mag, Ca++, Na+, and K+ all low-mid normal (I supplement with mag citrate). I didn’t have any inkling this was going on as study parameters were all normal. Had what I thought was a gallbladder attack (RUQ intolerable pain, nausea) and the results were a shock (stopped taking the drug two weeks prior to sx). I have done the google and pubmed and nosed around the liver websites and have come up pretty empty. I started NAC and milk thistle, but there really isn’t any strong evidence – it’s just something to do.
    No jaundice/icterus or edema, but I’m very fatigued, sleep a lot which is a total flip from severe chronic insomnia, nausea ever present and constant dull but tolerable RUQ pain. Am hoping that a pain/nausea flare doesn’t return as the hospital experience was traumatic – will not return.


    • Geez, aek, this reminds me of all the med students enrolling in drug studies to get themselves through med school. Obviously I can’t give any medical advice (not even qualified for another 5 months), I am sure you understand. Aren’t the study investigators looking after you? They bloody well should be. I assume that your liver enzymes are trending down from your hospital trip. If that’s the case then you just have to give your liver time to regenerate. Milk thistle gets brought up a lot. Don’t know if there are any definite studies on it but it has a good reputation and doesn’t seem to be harmful. NAC may be useful theoretically if the drug in question depletes glutathione in the same pathway as acetominaphe. Get the medics to monitor you for further liver damage, eliminate any liver toxins: alcohol (not even a liquor chocolate), fructose and other NADs (sounds like you are doing this already), good supportive non-inflammatory diet with some choline, give it time. Usual disclaimer: if symptoms persists, blah blah blah. Nasty for you, I’m sure. Please let me know how you pull up after this.

  5. Thanks so much for your response. In the US, the contracted research organizations are for profits and thus are literal bounty hunters as they get paid their fees on a per subject enrolled basis. The CRO doing this study is not only not doing anything, but is refusing to give me the contact information for Novartis, which is the manufacturer of the drug. Since this would give a result that Novartis doesn’t want, I’m sure that it’s deliberately being covered up and buried. The IRB is also a for profit contractor, and they don’t even have the Novartis info themselves, nor would they help me obtain it. I can’t afford care, and as there is no treatment – and certainly no care – for this anyway, I’m not seeing anyone for followup. As I’m too fatigued now to do anything, I’m down to leaving my bed solely for essential grocery shopping and household chores. My biggest fear and dread is that I’ll get another attack of unbearable pain without any ability to get relief. I’d be better off dead for everyone’s concern.

    • Aek, what you say is very sad and disturbing. I truly hope things will work out for you. Sending you some strength and good wishes across the Pacific.

  6. I enjoy your posts. I never was fan of sweet fruits or anything sweet; I get a lot of push from my wife. Once I moved to Paleo diet it seems I have developed some taste for sweet and now I eat quite a bit of fried sweet potato, carrot. My paleo style is high carb, high fat and low protein. Mostly I have read that people don’t crave for sweets when they move to Paleo, somehow my experience is opposite. I assume this is because earlier I used to eat sweet items which were rich in fructose but now I am eating sweet food items which are rich in glucose.

  7. Anastasia, thanks so much! Your previous response gave me some much needed reassurance that my diet may indeed have been protective all along, and that I’m pretty much on the right track for maintaining it with a couple of tweaks. I’ve been “doing the Google” and am amazed at how very little there is regarding self management/lifestyle techniques out there. Wish I still had access to primary texts in my field, but am not so sure that they would be of much use, either. I did find a few studies that demonstrated conflicting results with varying types of fats in rats with induced liver toxicity: one was that sat fats were protective and omega 3’s were contributory to mortality (!), and the other was almost the reverse. The unknown is what was in the remainder of the diets – and my guess is that therein lies the key (grin).

    Since Man’s Greatest Hospital won’t return my calls or give me even the names/titles of the people who mistreated me, I wrote a Yelp review. It’s been rated as funny! I guess it is. http://www.yelp.com/biz/massachusetts-general-hospital-boston-4#hrid:NrSkTJGKtyrbMUA9YNLhAA

    I didn’t address your comment about your fellow med students enrolling in clin trials, but as they are covered by differing IRB rules and study protections from those in the US, they may well want to have a relook at exactly what those are and the protections/lack of in the consents. There is a blog, 1 boring old man, written by a semi-retired academic psychiatrist, which is taking a hard, long look at some of these issues – his conclusions are more eye opening than a triple shot espresso. Thanks again – you made such a tremendous difference!

  8. One more thanks, Anastasia – I finally dragged myself out of bed and to the physician’s office for repeat labs, and except for the ALT which is just a wee bit above nl, everything else is back to rights. CRP is .1

    I wish the fatigue would go away, but I think I’m going to push myself a little bit each day to rebuild activity endurance and to get some sun. It’s alarming how fast I lost muscle tone and strength during this bout.

    I really appreciated having your perspective on diet. I hope that eventually therapeutic diets will incorporate these principles and practices. Sure made a difference in my case.



    • That’s great news! You are clearly doing all the right things and allowing your body to heal. Muscle memory is still there so it shouldn’t be a problem to get that strength and tone back. A bit of gentle exercise (I’m a yoga fan) will go a long way. All the best.

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