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!

Forbidden fructose

Not a day goes by without a well-meaning somebody reminding us that we don’t eat enough fruit and vegetables. The nagging of the nutritionists rivals that of my grandmother who used to force her famous “borscht” down my throat. The limp and tasteless bits of cabbage would stick to the roof of my mouth making me gag and my shaking hand would invariably spill the red liquid on her white tablecloth, resulting in an extra serving of beetroot goodness. I am obviously still deeply scarred.

The bright images of squeaky clean green apples and shiny red capsicums are often displayed in contrast to the pictures of insipid and suspicious-looking burgers with visible grease glistening on the meat patty, with horror movie music theme in the background. You have to be a moron not to realise which one is better for you, right?

Is it any wonder that a word “fructose”, which we immediately associate with “fruit”, sounds so wholesome? Fructose is indeed the predominant sugar in fruit. But it is a little more than that.

For something that sounds so healthy, fructose has been implicated in several nutritional crimes of late. Several studies have found that excess fructose consumption can cause insulin resistance in the liver, NAFLD (non-alcoholic fatty liver disease), gout, hypertension and abdominal obesity, colloquially known as a “spare tyre”. Does it make sense from physiological point of view?

Simple science

Actually, it does. While fructose is a simple sugar (=monosaccharide) just like glucose, it is actually processed in the body quite differently. After being absorbed from your intestine, it goes directly to the liver. The liver is like your body’s own Border Control. It receives raw materials, a.k.a. nutrients, from the gut, examines them for suitability (is it poison? is it a building block?) and then packages the good stuff up, loads them onto specialised freight trucks (transport molecules) and sends them via blood to customers, the cells in your tissues.

As you already know, the liver helps the pancreas keep the blood glucose on a tight leash, either by releasing more of it or by diverting extra glucose to fat stores. However, unlike glucose, fructose is too toxic to be floating around your body. Like a conscientious customs officer, your liver recognises the danger and neutralises it  by converting ALL fructose into triglycerides (fat). Triglycerides can be sent to the safe heaven of your fat tissues in their own trucks called LDLs (did you just have a little “Eureka” moment?), or they can be stored in the liver itself. Not good either way. Nobody likes love handles or their liver resembling fois gras.

Incidentally, do you know what else is processed in a similar way by the liver? Alcohol. So what would happen from a love match between alcohol and fructose? Bacardi Breezer, anyone?

Back to reality

Hang on, you ask, are you saying that fruit will make me fat and diabetic? No. The concentration of fructose in fruit is unlikely to harm you. In a manner of a true toxin, fructose has a dose-response relationship: the more you have, the worse it is.

The real question is: what other foods contain fructose? You are probably familiar with HFCS, high fructose corn syrup, a ubiquitous sweetener in the land of stars and stripes. HFCS is a product of industrial engineering genius: it is cheap, subsidised by the government (yay for corn subsidies) and is sweeter than sucrose, table sugar. It has been justly vilified and we often think we are lucky that it never took off in Oz.

However, your humble sucrose is not much better. HFCS normally used in soft drinks has 55%/45% fructose/glucose content. The white stuff that you put in your coffee is 50/50. Let’s say you don’t use sugar in your coffee and you don’t drink Coke, does it let you off the fructose hook? Sorry, no. Fructose is used in pretty much every processed and packaged product, whether on its own or as part of sugar. Fortunately for manufacturers, they don’t have to put fructose on nutrition labels. But you can estimate fructose content of foods yourself by dividing the amount of sugar on the label in half. (Be careful, it doesn’t work with dairy products, as their main sugar is lactose, not sucrose).

Here is a little table I prepared earlier.

  Sugar content (g) Estimated fructose content (g)
Apple green,
small

9.6

4.8

Apple juice,
250mL

26

13

Banana bread,
57g piece

14.7

7.4

Lipton Iced Tea, 375mL bottle

22.1

11.1

Nutrigrain
cereal, 40g

12.8

6.4

Coca Cola,
600mL bottle

63.6

31.8

As you can see, you have to have a hell of a lot of apples to come close to the level of fructose an average Australian/American consumes daily in the course of their processed food addiction.

What about fruit juice? Not too long ago fruit had to be squeezed by hand. Homemade juice sans the electrical juicer can be used as a babysitting tool: it will keep your kids busy for hours as they diligently work up a sweat trying to earn one glass of precious sugary orange liquid. If you want to be really mean, tell them to make apple juice by hand. Nobody in their right mind will eat 6 to 8 oranges in one sitting, but apparently a glass of juice, made from the same amount of fruit, is a healthy addition to our diet with breakfast, lunch and dinner.

Due to its current love affair with GI, Diabetes Australia tells diabetics that “a healthy eating plan for diabetes can include some sugar“. Glucose has a GI of 100, but table sugar, with only 50% of glucose, is 65. But the other 50%, fructose, is the real killer. Unfortunately, the very thing which makes the GI of sugar lower is the reason NOT to give it to diabetics. Its effects on the liver make it a ticking time bomb: you can’t see the blood glucose rise but your liver is developing insulin resistance with every bite of that low-fat banana bread.

So what do you do?
1. Whenever you drink soft drinks, juices, sports drinks, it is not just
the calorie load and fat-storing effects of insulin you have to worry about. It
is the direct toxicity to the liver. So don’t.
2. Avoid sweets and cakes with high load of sugar.
3. Avoid processed pre-packaged foods, bars, biscuits, as they have a lot
of hidden sugar.
4. If your goal is to lose fat, limit your fruit consumption to 2 a day.
5. If you have a diagnosed fatty liver, temporarily avoid fruit. It has
nothing that you can’t find in vegetables.

More information:
1. A must to see: “Sugar: the Bitter Truth”
Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin. Series: UCSF Mini Medical School for the Public [7/2009] [Health and Medicine] [Show ID: 16717]
2. Dr Eades on sugar vs HFCS
3. Double danger of HFCS
4. Fructose content in popular beverages differs from data labels
5. Review: Fructose, weight gain and the insulin resistance syndrome