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Wednesday, November 19, 2008 The Fructose Index is the New Glycemic Index 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.

They found some important trends. Granulocytes from people over 50 years old had a reduced ability to kill cancer cells, as did granulocytes from people with cancer. This raises the possibility that cancer is not simply the result of getting too old, but a very specific weakening of the immune system. The most important finding, however, was that the granulocytes' kung-fu grip declined dramatically during the winter months. Here's Dr. Cui: Nobody seems to have any cancer-killing ability during the winter months from November to April.

I'm always on the lookout for foods rich in vitamin K2 MK-4, because it's so important and so rare in the modern food system. I heard some internet rumors that marrow might be rich in fat-soluble vitamins. Google let me down, so I decided to look through the rat studies on K2 MK-4 in which they looked at its tissue distribution. I found one that looked at the K2 MK-4 content in different tissues of rats fed vitamin K1. Marrow was rich in K2, along with testes. It contains 10-20 times more MK-4 than liver by weight, and more than any of the other organs they tested (serum, liver, spleen, kidney, heart, testes, marrow, brain) except testes. They didn't include values for salivary gland and pancreas, the two richest sources.

Friday, January 16, 2009 The Tokelau Island Migrant Study: Weight Gain Between 1968 and 1982, Tokelauans in nearly all age groups gained weight, roughly 5 kilograms (11 pounds) on average. They also became slightly taller, but not enough to offset the gain in weight. By 1980-82, migrants to New Zealand had become especially heavy, with all age groups weighing more than non-migrants by about 5 kg (11 lb) on average, and 10 kg (22 lb) more than Tokelauans did in 1968.

Weston Price established the importance of the MK-4 isoform of vitamin K2 (hereafter, K2) with a series of interesting experiments. He showed in chickens that blood levels of calcium and phosphorus depended both on vitamin A and K2, and that the two had synergistic effects on mineral absorption. He also showed that chickens preferred eating butter that was rich in K2 over butter low in K2, even when the investigators couldn't distinguish between them. Young turkeys fed K2-containing butter oil along with cod liver oil (A and D) also grew at a much faster rate than turkeys fed cod liver oil alone.

"As far as I can tell, MK-4 is capable of performing all the functions of vitamin K. MK-4 can even activate blood clotting factors, which is a role traditionally ascribed to vitamin K1. Babies are often born clotting deficient, which is why we give newborns vitamin K1 injections in the U.S. to prevent hemorrhaging. In Japan, they give children MK-4 to prevent hemorrhage, an intervention that is very effective. Could that have to do with the fact that Japan has half the infant mortality rate of the U.S.? Today, I found another difference between MK-4 and MK-7. I was reading a paper about SXR-independent effects of vitamin K2 on gene expression. The investigators found that MK-4 strongly activates transcription of two specific genes in osteoblast cells. Osteoblasts are cells that create bone tissue. The genes are GDF15 and STC2 and they're involved in bone and cartilage formation. They tested K1 and MK-7, and in contrast to MK-4, they did not activate transcription of the genes in the slightest. This shows that MK-4 has effects on gene expression in bone tissue that MK-7 doesn't have. That being said, MK-7 may still have a place in a healthy diet. Just because it can't do everything MK-4 can, doesn't mean it has no role. It may be able to fill in for MK-4 in some functions, or reduce the dietary need for MK-4. But no one really knows at this point. Hunter-gatherers would have had a source of longer menaquinones, including MK-7, from livers. So it's possible that we're adapted to a modest MK-7 intake on top of MK-4. "

"Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell."

"The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. To judge by the grave pronouncements of our most visible experts, you would think these studies had found an association between the two. It turns out, they haven't. The fact is, the vast majority of high-quality observational studies have found no connection whatsoever between saturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years."

"Not everyone has access to pastured eggs. "Omega-3 eggs" come from hens fed an omega-3 enriched diet*. Not only do they have a much higher omega-3 content than conventional eggs, they also contain less AA. One study found that omega-3 eggs contain 39% less AA than conventional and organic eggs. Omega-3 eggs were also rich in short- and long-chain omega-3 fats. Omega-3 eggs are certainly not nutritionally equivalent to pastured eggs, but they're a step in the right direction. "

"Wednesday, May 27, 2009 Eicosanoids and Ischemic Heart Disease, Part II Here's where it gets more complicated and more interesting. The ratio of omega-6 to omega-3 matters, but so does the total amount of each. This is a graph from a 1992 paper by Dr. Lands: In sum, this suggests that the single best way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.

"came across a gem of a study the other day, courtesy of Dr. John Briffa's blog. It's titled "Margarine Intake and Subsequent Coronary Heart Disease in Men", by Dr. William P. Castelli's group. It followed participants of the Framingham Heart study for 20 years, and recorded heart attack incidence*. Keep in mind that 20 years is an unusually long follow-up period. "

Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells. After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.

I bumped into a fascinating paper today by Dr. Loren Cordain titled "Plant-Animal Subsistence Ratios and Macronutrient Estimations in Worldwide Hunter-Gatherer Diets." Published in 2000 in the American Journal of Clinical Nutrition, the paper estimates the food sources and macronutrient intakes of historical hunter-gatherers based on data from 229 different groups. Based on the available data, these groups did not suffer from the diseases of civilization. This is typical of hunter-gatherers. Initial data came from the massive Ethnographic Atlas by Dr. George P. Murdock, and was analyzed further by Cordain and his collaborators. Cordain is a professor at Colorado State University, and a longtime proponent of paleolithic diets for health. He has written extensively about the detrimental effects of grains and other modern foods. Here's his website.

"We've been having an interesting discussion in the comments about a recently published paper by Dr. Stephen C. Benoit and colleagues (free full text). They showed that a butter-rich diet causes weight gain and insulin resistance in rats, compared to a low-fat diet or a diet based on olive oil. They published a thorough description of the diets' compositions, which is very much appreciated! They went on to show that infusing palmitic acid (a 16-carbon saturated fat) directly into the brain of rats also caused insulin resistance relative to oleic acid (an 18-carbon monounsaturated fat, like in olive oil). Here's a representation of palmitic acid. The COOH end is the acid end, and the squiggly line is the fatty end. Thus it's called a "fatty acid", various forms of which are the fat currency of the body."

The Diet-Heart Hypothesis: Subdividing Lipoproteins Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids. Lipoproteins Can be Subdivided into Several Subcategories In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source): The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease. Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder. Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily

"Tuesday, July 8, 2008 Wheat is Invading China Dr. Michael Eades linked to an interesting study yesterday on his Health and Nutrition blog. It's entitled "Vegetable-Rich Food Pattern is Related to Obesity in China." It's one of these epidemiological studies where they try to divide subjects into different categories of eating patterns and see how health problems associate with each one. They identified four patterns: the 'macho' diet high in meat and alcohol; the 'traditional' diet high in rice and vegetables; the 'sweet tooth' pattern high in cake, dairy and various drinks; and the 'vegetable rich' diet high in wheat, vegetables, fruit and tofu. The only pattern that associated with obesity was the vegetable-rich diet. The 25% of people eating closest to the vegetable-rich pattern were more than twice as likely to be obese as the 25% adhering the least. The authors of the paper try to blame the increased obesity on a higher intake of vegetable oil from stir-frying the vegetables, but that explanation is juvenile and misleading. A cursory glance at table 3 reveals that the vegetable-eaters weren't eating any more fat than their thinner neighbors. Dr. Eades suggests that their higher carbohydrate intake (+10%) and higher calorie intake (+120 kcal/day) are responsible for the weight gain, but I wasn't satisfied with that explanation so I took a closer look.