I stumbled upon an interesting editorial recently in the American Journal of Clinical Nutrition from Dr. Richard Johnson's group, entitled "How Safe is Fructose for Persons With or Without Diabetes?" It was a response to a meta-analysis in the same journal pronouncing fructose safe up to 90 grams per day. That's the amount in eight apples or four cans of soda. Not quite what our hunter-gatherer ancestors were eating! The editorial outlined the case against excessive fructose, which I feel is quite strong. That led me to another, more comprehensive paper from Dr. Johnson's group, which argues that the amount of fructose found in a food, which they call the "fructose index", is more relevant to health than the food's glycemic index. The glycemic index is a measure of the blood sugar response to a fixed amount of carbohydrate from a particular food. For example, white bread has a high glycemic index because it raises blood sugar more than another food containing the same amount of carbohydrate, say, lentils. Since chronically elevated blood sugar and its natural partner, insulin resistance, are part of the metabolic syndrome, it made sense that the glycemic index would be a good predictor of the metabolic effect of a food. I believed this myself for a long time. My faith in the concept began to erode when I learned more about the diets of healthy traditional cultures. For example, the Kitavans get 69% of their calories from high-glycemic index carbohydrates (mostly starchy root vegetables), with little added fat-- that's a lot of fast-digesting carbohydrate! Overweight, elevated insulin and other symptoms of the metabolic syndrome are essentially nonexistent. Throughout Africa, healthy cultures make dishes from grains or starchy tubers that are soaked, pounded, fermented and then cooked. The result is a pile of mush that is very easily absorbed by the digestive tract, which is exactly the point of going through all the trouble. The more I thought about the glycemic index and its relationship to insulin resistance and the metabolic syndrome, the more I realized there is a disconnect in the logic: elevated post-meal glucose and insulin do not necessarily lead to chronically elevated glucose and insulin. Here's what Dr. Mark Segal from Dr. Johnson's group had to say:We suggest that the [glycemic index] is better aimed at identifying foods that stimulate insulin secretion rather than foods that stimulate insulin resistance. The underlying concept is based on the principle that it is the ingestion of foods that induce insulin resistance that carries the increased risk for obesity and cardiovascular disease and not eating foods that stimulate insulin secretion.
Well said! I decided to take a look through the literature to see if there had been any trials on the relationship between a diet's glycemic index and its ability to cause satiety (fullness) and affect weight. I found a meta-analysis from 2007. Two things are clear from the paper: 1) in the short term, given an equal amount of carbohydrate, a diet with a low glycemic index is more satiating (filling) than one with a high glycemic index, leading to a lower intake of calories. 2) this effect disappears in the long-term, and the three trials (1, 2, 3) lasting 10 weeks or longer found no consistent effect on caloric intake or weight*. As a matter of fact, the only statistically significant (p less than 0.001) weight difference was a greater weight loss in one of the high-glycemic index groups!
As I've said many times, the body has mechanisms for maintaining weight and caloric intake where they should be in the long term. As long as those mechanisms are working properly, weight and caloric intake will be appropriate. The big question is, how does the modern lifestyle derail those mechanisms?
Dr. Johnson believes fructose is a major contributor. Table sugar, fruit, high-fructose corn syrup and honey are all roughly 50% fructose by calories. Total fructose consumption has increased about 19% in the U.S. since 1970, currently accounting for almost one eighth of our total calorie intake (total sugars account for one quarter!). That's the average, so many people actually consume more.
Fructose, but not starch or its component sugar glucose, causes insulin resistance, elevated serum uric acid (think gout and kidney stones), poorer blood glucose control, increased triglycerides and LDL cholesterol in animal studies and controlled human trials. All of these effects relate to the liver, which clearly does not like excessive fructose (or omega-6 oils). Some of these trials were conducted using doses that are near the average U.S. intake. The effect seems to compound over time both in humans and animals. The overweight, the elderly and the physically unfit are particularly vulnerable. I find this pretty damning.
Drs. Johnson and Segal recommend limiting fructose to 15-40 grams per day, which is the equivalent of about two apples or one soda (choose the apples!). They also recommend temporarily eliminating fructose for two weeks, to allow the body to recover from the negative long-term metabolic adaptation that can persist even when intake is low. I think this makes good sense.
The glycemic index may still be a useful tool for people with poor glucose control, like type II diabetics, but I'm not sure how much it adds to simply restricting carbohydrate. Reducing fructose may be a more effective way to address insulin resistance than eating a low glycemic index diet.
*Here was the author's way of putting it in the abstract: "Because of the increasing number of confounding variables in the available long-term studies, it is not possible to conclude that low-glycaemic diets mediate a health benefit based on body weight regulation. The difficulty of demonstrating the long-term health benefit of a satietogenic food or diet may constitute an obstacle to the recognition of associated claims." In other words, the data not supporting our favorite hypothesis is an obstacle to its recognition. You don't say?
Several commenters have asked for my opinion on recent statements by prominent health researchers that many Americans are suffering from unrecognized vitamin A toxicity. Dr. John Cannell of the Vitamin D Council is perhaps the most familiar of them. Dr. Cannell's mission is to convey the benefits of vitamin D to the public. The Vitamin D Council's website is a great resource.Vitamin A is a very important nutrient. Like vitamin D, it has its own nuclear receptors which alter the transcription of a number of genes in a wide variety of tissues. Thus, it is a very fundamental nutrient to health. It's necessary for proper development, vision, mineral metabolism, bone health, immune function, the integrity of skin and mucous membranes, and many other things. Vitamin A is a fat-soluble vitamin, and as such, it is possible to overdose. So far, everyone is in agreement.The question of optimal intake is where opinions begin to diverge. Hunter-gatherers and healthy non-industrial cultures, who almost invariably had excellent dental and skeletal development and health, often had a very high intake of vitamin A (according to Dr. Weston Price and others). This is not surprising, considering their fondness for organ meats. A meager 2 ounces of beef liver contains about 9,500 IU, or almost 200% of your U.S. and Canadian recommended daily allowance (RDA). Kidney and eye are rich in vitamin A, as are many of the marine oils consumed by the Inuit and other arctic groups. If we can extrapolate from historical hunter-gatherers, our ancestors didn't waste organs. In fact, in times of plenty, some groups discarded the muscle tissue and ate the organs and fat. Carnivorous animals often eat the organs first, because they know exactly where the nutrients are. Zookeepers know that if you feed a lion nothing but muscle, it does not thrive. This is the background against which we must consider the question of vitamin A toxicity. Claims of toxicity must be reconciled with the fact that healthy cultures often consumed large amounts of vitamin A without any ill effects. Well, you might be surprised to hear me say that I do believe some Americans and Europeans suffer from what you might call vitamin A toxicity. There is a fairly consistent association between vitamin A intake and bone mineral density, osteoporosis and fracture risk. It holds true across cultures and sources of vitamin A. Chris Masterjohn reviewed the epidemiology here. I recommend reading his very thorough article if you want more detail. The optimum intake in some studies is 2-3,000 IU, corresponding to about 50% of the RDA. People who eat more or less than this amount tend to suffer from poorer bone health. This is where Dr. Cannell and others are coming from when they say vitamin A toxicity is common.The only problem is, this position ignores the interactions between fat-soluble vitamins. Vitamin D strongly protects agains vitamin A toxicity and vice versa. As a matter of fact, "vitamin A toxicity" is almost certainly a relative deficiency of vitamin D. Vitamin D deficiency is also tightly correlated with low bone mineral density, osteoporosis and fracture risk. A high vitamin A intake requires vitamin D to balance it. The epidemiological studies showing an association between high-normal vitamin A intake and reduced bone health all sported populations that were moderately to severely vitamin D deficient on average. At optimal vitamin D levels, 40-70 ng/mL 25(OH)D, it would take a whopping dose of vitamin A to induce toxicity. You might get there if you eat nothing but beef liver for a week or two.The experiment hasn't been done under controlled conditions in humans, but if you believe the animal studies, the optimal intake for bone mineral density is a high intake of both vitamins A and D. And guess what? A high intake of vitamins A and D also increases the need for vitamin K2. That's because they work together. For example, vitamin D3 increases the secretion of matrix Gla protein and vitamin K2 activates it. Is it any surprise that the optimal proportions of A, D and K occur effortlessly in a lifestyle that includes outdoor activity and whole, natural animal foods? This is the blind spot of the researchers who have warned of vitamin A toxicity: uncontrolled reductionism. Vitamins do not act in a vacuum; they interact with one another. If your theory doesn't agree with empirical observations from healthy cultures, it's back to the drawing board.High-vitamin cod liver oil is an excellent source of vitamins A and D because it contains a balanced amount of both. Unfortunately, many brands use processing methods that reduce the amount of one or more vitamins. See the Weston Price foundation's recommendations for the highest quality cod liver oils. They also happen to be the cheapest per dose. I order Green Pasture high-vitamin cod liver oil through Live Superfoods (it's cheaper than ordering directly). This suggests that vitamin A toxicity may be less of a concern when vitamin D status is good.