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!