Real Food IV: Lard

Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.

The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.

If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.


Ingredients and Equipment:

• Lard
• Cheesecloth
• Baking dish
• Jars
  

1. Preheat the oven to 225 F.

2. Cut off any pieces of meat clinging to the fat.

3. Cut fat into small (~1-inch) cubes.

4. Place them into a non-reactive baking dish and then into the oven.

5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.

6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.

7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.

8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.

Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.

Okinawa and Lard

The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, sweet potatoes, exercise, and the fact that some of them may have been mildly calorie restricted for part of their lives.

The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat. Of course, they also eat the pork the lard came from.

I'm not saying lard will make you live to 100, but a moderate amount certainly won't stop you...

Olive Oil Buyer's Guide

Olive oil is one of the few good vegetable oils. It is about 10% omega-6 (n-6) fatty acids, compared to 50% for soybean oil, 52% for cottonseed oil and 54% for corn oil. Omega-6 fatty acids made up a smaller proportion of calories before modern times, due to their scarcity in animal fats. Beef suet is 2% n-6, butter is 3% and lard is 10%. Many people believe that excess n-6 fat is a contributing factor to chronic disease, due to its effect on inflammatory prostaglandins. I'm reserving my opinion on n-6 fats until I see more data, but I do think it's worth noting the association of increased vegetable oil consumption with declining health in the US.

Olive oil is also one of the few oils that require no harsh processing to extract. As a matter of fact, all you have to do is squeeze the olives and collect the oil. Other oils that can be extracted with minimal processing are red palm oil (9% n-6), hazelnut oil (10% n-6) and coconut oil (2% n-6). These are also the oils I consider to be healthy. Due to the mild processing these oils undergo, they retain their natural vitamin and antioxidant content.

You've eaten corn, so you know it's not an oily seed. Same with soybeans. So how to they get the oil out of them? They use a combination of heat and petroleum solvents. Then, they chemically bleach and deodorize the oil, and sometimes partially hydrogenate it to make it more shelf-stable. Hungry yet? This is true of all the common colorless oils, and anything labeled "vegetable oil".

Olive oil is great, but don't run out and buy it just yet! There are different grades, and it's important to know the difference between them. The highest grade is extra-virgin olive oil, and it's the only one I recommend. It's the only grade that's not heated or chemically refined in any way. Virgin olive oil, "light" olive oil (refers to the flavor, not calories), "pure" olive oil, or simply olive oil all involve different degrees of chemical extraction and/or processing. This applies primarily to Europe. Unfortunately, the US is not part of the International Olive Oil Council (IOOC), which regulates oil quality and labeling.

The olive oil market is plagued by corruption. Much of the oil exported from Italy is cut with cheaper oils such as colza. Most "Italian olive oil" is actually produced in North Africa and bottled in Italy, and may be of inferior quality. The USDA has refused to regulate the market so they get away with it. If you find a deal on olive oil that looks too good to be true, it probably is.

Only buy from reputable sources. Look for the IOOC seal, which guarantees purity, provenance and freshness. IOOC olive oil must contain less than 0.8% acidity. Acidity refers to the percentage of free fatty acids (as opposed to those bound in triglycerides), a measure of damage to the oil. Fortunately, the US has a private equivalent to the IOOC, the California Olive Oil Council (COOC). The COOC seal ensures provenance, purity and freshness just like the IOOC seal. It has outdone the IOOC in requiring less than 0.5% acidity. COOC-certified oils are more expensive, but you know exactly what you're getting.

Thanks to funadium for the CC photo

Masai and Atherosclerosis

I've been digging deeper into the health of the Masai lately. A commenter on Chris's blog pointed me to a 1972 paper showing that the Masai have atherosclerosis, or hardening of the arteries. This interested me so I got my hands on the full text, along with a few others from the same time period. What I found is nothing short of fascinating.

First, some background. Traditional Masai in Kenya and Tanzania are pastoralists, subsisting on fermented cow's milk, meat and blood, as well as traded food in modern times. They rarely eat fresh vegetables. Contrary to popular belief, they are a genetically diverse population, due to the custom of abducting women from neighboring tribes. Many of these tribes are agriculturalists. From Mann et al: "The genetic argument is worthless". This will be important to keep in mind as we interpret the data.

At approximately 14 years old, Masai men are inducted into the warrior class, and are called Muran. For the next 15-20 years, tradition dictates that they eat a diet composed exclusively of cow's milk, meat and blood. Milk is the primary food. Masai cows are not like wimpy American cows, however. Their milk contains almost twice the fat of American cows, more protein, more cholesterol and less lactose. Thus, Muran eat an estimated 3,000 calories per day, 2/3 of which comes from fat. Here is the reference for all this. Milk fat is about 50% saturated. That means the Muran gets 33% of his calories from saturated fat. This population eats more saturated fat than any other I'm aware of.

How's their cholesterol? Remarkably low. Their total serum cholesterol is about half the average American's. I haven't found any studies that broke it down further than total cholesterol. Their blood pressure is also low, and hypertension is rare. Overweight is practically nonexistent. Their electrocardiogram readings show no signs of heart disease. They have exceptionally good endurance, but their grip strength is significantly weaker than Americans of African descent. Two groups undertook autopsies of male Masai to look for artery disease.

The first study, published in 1970, examined 10 males, 7 of which were over 40 years old. They found very little evidence of atherosclerosis, even in individuals over 60. The second study, which is often used as evidence against a high-fat diet, was much more thorough and far more interesting. Mann et al. autopsied 50 Masai men, aged 10 to 65. The single most represented age group was 50-59 years old, at 13 individuals. They found no evidence of myocardial infarction (heart attack) in any of the 50 hearts. What they did find, however, was coronary artery disease. Here's a figure showing the prevalence of "aortic fibrosis", a type of atherosclerotic lesion:


It looks almost binary, doesn't it? What could be causing the dramatic jump in atherosclerosis at age 40? Here's another figure, of total cholesterol (top) and "sudanophilia" (fatty streaks in the arteries, bottom). Note that the Muran period is superimposed (top).


There appears to be a pattern here. Either the Masai men are eating nothing but milk, meat and blood and they're nearly free from atherosclerosis, or they're eating however they please and they have as much atherosclerosis as the average American. There doesn't seem to be much in between.

Here's a quote from the paper that I found interesting:

We believe... that the Muran escapes some noxious dietary agent for a time. Obviously, this is neither animal fat nor cholesterol. The old and the young Masai do have access to such processed staples as flour, sugar, confections and shortenings through the Indian dukas scattered about Masailand. These foods could carry the hypothetical agent."

This may suggest that you can eat a wide variety of foods and be healthy, except industrial grain products (particularly white flour), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.

Activator X

Activator X, the almost-mythical vitamin discovered and characterized by Weston Price, has been identified! For those of you who are familiar with Weston Price's book 'Nutrition and Physical Degeneration', you know what I'm talking about. For the rest of you, allow me to explain.

Weston Price was a dentist and scientist in the early part of the 20th century. Practicing dentistry in Cleveland, he was amazed at the poor state of his patients' teeth and the suffering it inflicted. At the time, dental health was even worse than it is today, with some children in their teens already being fitted for dentures. Being a religious man, he could not bring himself to believe that 'physical degeneration' was what God intended for mankind. He traveled throughout the world looking for cultures that did not have crooked teeth or dental decay, and that also exhibited general health and well-being. And he found them. A lot of them.

These cultures were all considered 'primitive' at the time, and were not subject to the lifestyles or food choices of the Western world. He documented, numerically and with photographs, the near-absence of dental cavities and crooked teeth in a number of different cultures throughout the world. He showed that like all animals, humans are healthy and robust when occupying the right ecological niche. Price had a deep respect for the nutritional knowledge these cultures curated.

He also documented the result when these same cultures were exposed to Western diets of white flour, sugar and other industrially processed foods: they developed rampant cavities, their children grew with crooked teeth due to narrow dental arches, as well as a number of other strikingly familiar health problems. I think it's worth mentioning that Price's findings were universally corroborated by doctors in contact with the same cultures at the time. They are also corroborated by the archaeological record. Many of his findings were published in respected peer-reviewed journals. 'Nutrition and Physical Degeneration' is required reading for anyone interested in the relationship between nutrition and health.

Naturally, Price wanted to understand what healthy diets had in common besides the absence of white flour and sugar. Having studied cultures as diverse as the carnivorous Inuit, the dairy-eating Masai and agricultural groups in the Andes, he realized that humans are capable of thriving on very diverse foods. However, he did find one thing in common: they all ate some amount of fat-soluble, animal-derived vitamins. Even the near-vegetarian groups ate insects or small animals that were rich in these vitamins. He looked for, but did not find, a single group that was entirely vegetarian and had the teeth and health of the groups he described in 'Nutrition and Physical Degeneration'.

There were three vitamins he found abundantly in the diets of healthy non-industrialized people: A, D, and an unknown substance he called 'activator X'. He considered them all to be synergistic and critical for proper mineral metabolism (tooth and bone formation and maintenance) and general health. He had a chemical test for activator X, but he didn't know its chemical structure and so it remained unidentified. He found activator X most abundantly in grass-fed butter (but not grain fed!), organ meats, shellfish, insects, and fish eggs. Many of these foods were fed preferentially to pregnant or reproductive-age women in the groups he studied.

Price used extracts from grass-fed butter (activator X), in combination with high-vitamin cod liver oil (A and D), to prevent and reverse dental cavities in many of his patients. 'Nutrition and Physical Degeneration' contains X-rays of case studies showing re-calcification of severe cavities using this combination.

After reading his book, I wasn't sure what to make of activator X. If it's so important, why hasn't it been identified in the 60+ years since he described it? I'm happy to say, it finally has. In the summer of 2007, Chris Masterjohn wrote an article for the Weston Price foundation website, in which he identified Weston Price's mystery vitamin: it's vitamin K2, specifically the MK-4 isoform (menatetrenone).

It occurs exactly where Weston Price described it, and research is beginning to find that it's also critical for mineral metabolism, bone and tooth formation and maintenance. Its function is synergistic with vitamins A and D. To illustrate the point, where do A, D and K2 MK-4 all occur together in nature? Eggs and milk, the very foods that are designed to feed a growing animal. This is true from sea urchins to humans, confirming the ubiquitous and critical role of these nutrients. K2 has not yet been recognized as such by the mainstream, but it is every bit as important to health as A and D. The scientific cutting edge is beginning to catch on, however, due to some very tantalizing studies.

In the next post, I'll go into more detail about K2, what the science is telling us and where to get it.

Vitamin K2, menatetrenone (MK-4)

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.

He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.

Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.

Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.

Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.

Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status. 

The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.

I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.

Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.

Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.

Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).

Real Food VIII: Ghee

All this talk about butter is making me hungry. Richard mentioned in the comments that he bought some ghee recently and has been enjoying it, so I thought I'd post a recipe. Ghee is the Hindi word for clarified butter. It's butter that has had everything removed but the fat. Rich in fat-soluble vitamins and lacking the sometimes problematic lactose and casein, ghee has rightfully been considered a health food in India since ancient times.

Another advantage of ghee is its high smoke point, which is higher than butter because it doesn't contain any protein or sugars. Consequently, food sauteed in ghee has a clean, rich taste.

The recipe is simple but touchy. I recommend using the best butter you can get your hands on. 100% grass-fed, unsalted cultured butter is the best.

Ingredient and materials

• Butter (1 lb minimum)
• Wide-mouth glass jars
• Cheesecloth
• Rubber bands
  

Recipe

1. Place the butter in a saucepan and turn the heat to medium until it's melted.
   
2. Once it begins to boil, turn the heat down to low. It's very important to calibrate the heat correctly. Typically, you will want the burner on its lowest setting. The idea is to evaporate the water without burning the oil. It should boil, but slowly.
3. The melted butter starts out cloudy but gradually clears up as the water evaporates. At the same time, a crust will form on the surface of the ghee and the bottom of the pan. Keep the heat very low.
   
4. Push a portion of the top crust to the side with a spoon to see inside of the saucepan. When the butter looks clear and bubbles only rise from the bottom every few seconds, it's done. You have to be very careful because once the water has evaporated, the fat heats up quickly and burns the crust. This gives the ghee an acrid flavor and color. Make sure to handle the pot cautiously, because hot oil can give severe burns.
   
5. Allow the ghee to cool until it's warm but not hot. Place a piece of cheesecloth over the lid of your jar. Secure it with a rubber band. Pour the ghee through the cheesecloth, into the jar.
   
6. Store ghee in the refrigerator or at room temperature. It keeps much longer than butter.

The picture above is of my last batch of ghee.

Celiac and Fat-Soluble Vitamins

One of the things I've been thinking about lately is the possibility that intestinal damage due to gluten grains (primarily wheat) contributes to the diseases of civilization by inhibiting the absorption of fat-soluble vitamins. If it were a contributing factor, we would expect to see a higher incidence of the common chronic diseases in newly-diagnosed celiac patients, who are often deficient in fat-soluble vitamins. We might also see a resolution of chronic disease in celiac patients who have been adhering faithfully to a long-term, gluten-free diet.

One thing that definitely associates with celiac disease is bone and tooth problems. Celiac patients often present with osteoporosis, osteopenia (thin bones), cavities or tooth enamel abnormalities (thanks Peter).

An Italian study showed that among 642 heart transplant candidates, 1.9% had anti-endomyosal antibodies (a feature of celiac), compared with 0.35% of controls. That's more than a 5-fold enrichment! The majority of those patients were presumably unaware of their celiac disease, so they were not eating a gluten-free diet.

Interestingly, celiac doesn't seem to cause obesity; to the contrary. That's one facet of modern health problems that it definitely does not cause.

The relationship between cancer and celiac disease is very interesting. The largest study I came across was conducted in Sweden using retrospective data from 12,000 celiac patients. They found that adult celiac patients have a higher overall risk of cancer, but that the extra risk disappears with age. The drop in cancer incidence may reflect dropping gluten following a celiac diagnosis. Here's another study showing that the elevated cancer risk occurs mostly in the first year after diagnosis, suggesting that eliminating gluten solves the problem. Interestingly, celiac patients have a greatly elevated risk of lymphoma, but a lower risk of breast cancer.

There's a very strong link between celiac and type I diabetes. In a large study, 1 in 8 type I diabetic children had celiac disease. This doesn't necessarily tell us much since celiac and type I diabetes are both autoimmune disorders.

One last study to add a nail to the coffin. Up to this point, all the studies I've mentioned have been purely observational, not able to establish a causal relationship. I came across a small study recently which examined the effect of a high-fiber diet on vitamin D metabolism in healthy (presumably non-celiac) adults. They broke the cohort up into two groups, and fed one group 20g of bran in addition to their normal diet. The other group got nothing extra. The bran-fed group had a vitamin D elimination half-life of 19.5 days, compared to 27.5 for the control group. In other words, for whatever reason, the group eating extra bran was burning through their vitamin D reserves 30% faster than the control group.

Unfortunately, the paper doesn't say what kind of bran it was, but it was probably wheat or oat (**Update- it's wheat bran**). This is important because it would determine if gluten was involved. Either way, it shows that something in grains can interfere with fat-soluble vitamin status, which is consistent with the staggering negative effect of refined wheat products on healthy non-industrialized cultures.

Add to this the possibility that many people may have some degree of gluten sensitivity, and you start to see a big problem. All together, the data are consistent with gluten grains interfering with fat-soluble vitamin status in a subset of people. As I discussed earlier, this could contribute to the diseases of civilization. These data don't prove anything conclusively, but I do find them thought-provoking.

Thanks to Dudua for the CC photo

The Inuit: Lessons from the Arctic

The Inuit (also called Eskimo) are a group of hunter-gatherer cultures who inhabit the arctic regions of Alaska, Canada and Greenland. They are a true testament to the toughness, adaptability and ingenuity of the human species. Their unique lifestyle has a lot of information to offer us about the boundaries of the human ecological niche. Weston Price was fascinated by their excellent teeth, good nature and overall robust health. Here's an excerpt from Nutrition and Physical Degeneration:

"In his primitive state he has provided an example of physical excellence and dental perfection such as has seldom been excelled by any race in the past or present...we are also deeply concerned to know the formula of his nutrition in order that we may learn from it the secrets that will not only aid in the unfortunate modern or so-called civilized races, but will also, if possible, provide means for assisting in their preservation."

The Inuit are cold-hardy hunters whose traditional diet consists of a variety of sea mammals, fish, land mammals and birds. They invented some very sophisticated tools, including the kayak, whose basic design has remained essentially unchanged to this day. Most groups ate virtually no plant food. Their calories came primarily from fat, up to 75%, with almost no calories coming from carbohydrate. Children were breast-fed for about three years, and had solid food in their diet almost from birth. As with most hunter-gatherer groups, they were free from chronic disease while living a traditional lifestyle, even in old age. Here's a quote from Observations on the Western Eskimo and the Country they Inhabit; from Notes taken During two Years [1852-54] at Point Barrow, by Dr. John Simpson:

These people [the Inuit] are robust, muscular and active, inclining rather to spareness [leanness] than corpulence [overweight], presenting a markedly healthy appearance. The expression of the countenance is one of habitual good humor. The physical constitution of both sexes is strong. Extreme longevity is probably not unknown among them; but as they take no heed to number the years as they pass they can form no guess of their own ages.

One of the common counterpoints I hear to the idea that high-fat hunter-gatherer diets are healthy, is that exercise protects them from the ravages of fat. The Inuit can help us get to the bottom of this debate. Here's a quote from Cancer, Disease of Civilization (1960, Vilhjalmur Stefansson):

"They are large eaters, some of them, especially the women, eating all the time..." ...during the winter the Barrow women stirred around very little, did little heavy work, and yet "inclined more to be sparse than corpulent" [quotes are the anthropologist Dr. John Murdoch, reproduced by Stefansson].

Another argument I sometimes hear is that the Inuit are genetically adapted to their high-fat diet, and the same food would kill a European. This appears not to be the case. The anthropologist and arctic explorer Vilhjalmur Stefansson spent several years living with the Inuit in the early 20th century. He and his fellow Europeans and Americans thrived on the Inuit diet. American doctors were so incredulous that they defied him and a fellow explorer to live on a diet of fatty meat only for one year, under the supervision of the American Medical Association. To the doctors' dismay, they remained healthy, showing no signs of scurvy or any other deficiency (JAMA 1929;93:20–2).

Yet another amazing thing about the Inuit was their social structure. Here's Dr. John Murdoch again (quoted from Cancer, Disease of Civilization):

The women appear to stand on a footing of perfect equality with the men, both in the family and the community. The wife is the constant and trusted companion of the man in everything except the hunt, and her opinion is sought in every bargain or other important undertaking... The affection of parents for their children is extreme, and the children seem to be thoroughly worthy of it. They show hardly a trace of fretfulness or petulance so common among civilized children, and though indulged to an extreme extent are remarkably obedient. Corporal punishment appears to be absolutely unknown, and children are rarely chided or punished in any way.

Unfortunately, those days are long gone. Since adopting a modern processed-food diet, the health and social structure of the Inuit has deteriorated dramatically. This had already happened to most groups by Weston Price's time, and is virtually complete today. Here's Price:

In the various groups in the lower Kuskokwim seventy-two individuals who were living exclusively on native foods had in their 2,138 teeth only two teeth or 0.09 per cent that had ever been attacked by tooth decay. In this district eighty-one individuals were studied who had been living in part or in considerable part on modern foods, and of their 2, 254 teeth 394 or 13 per cent had been attacked by dental caries. This represents an increase in dental caries of 144 fold.... When these adult Eskimos exchange their foods for our modern foods..., they often have very extensive tooth decay and suffer severely.... Their plight often becomes tragic since there are no dentists in these districts.

Modern Inuit also suffer from very high rates of diabetes and overweight. This has been linked to changes in diet, particularly the use of white flour, sugar and processed oils.

Overall, the unique lifestyle and diet of the Inuit have a lot to teach us. First, that some humans are capable of being healthy eating mostly animal foods. Second, that some humans are able to thrive on a high-fat diet. Third, that humans are capable of living well in extremely harsh and diverse environments. Fourth, that the shift from natural foods to processed foods, rather than changes in macronutrient composition, is the true cause of the diseases of civilization.

Composition of the Hunter-Gatherer Diet

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.

The researchers broke food down into three categories: hunted animal foods, fished animal foods and gathered foods. "Gathered foods" are primarily plants, but include some animal foods as well:

Although in the present analysis we assumed that gathering would only include plant foods, Murdock indicated that gathering activities could also include the collection of small land fauna (insects, invertebrates, small mammals, amphibians, and reptiles); therefore, the compiled data may overestimate the relative contribution of gathered plant foods in the average hunter-gatherer diet.

There are a number of striking things about the data once you sum them up. First of all, diet composition varied widely. Many groups were almost totally carnivorous, with 46 getting over 85% of their calories from hunted foods. However, not a single group out of 229 was vegetarian or vegan. No group got less than 15% of their calories from hunted foods, and only 2 of 229 groups ate 76-85% of their calories from gathered foods (don't forget, "gathered foods" also includes small animals). On average, the hunter-gatherer groups analyzed got about 70% of their calories from hunted foods. This makes the case that meat-heavy omnivory is our preferred ecological niche. However, it also shows that we can thrive on a plant-rich diet containing modest amounts of quality animal foods.

The paper also discusses the nature of the plant foods hunter-gatherers ate. Although they ate a wide variety of plants occasionally, more typically they relied on a small number of staple foods with a high energy density. There's a table in the paper that lists the most commonly eaten plant foods. "Vegetables" are notably underrepresented. The most commonly eaten plant foods are fruit, underground storage organs (tubers, roots, corms, bulbs), nuts and other seeds. Leaves and other low-calorie plant parts were used much less frequently.

The paper also gets into the macronutrient composition of hunter-gatherer diets.  He writes that

...the most plausible... percentages of total energy from the macronutrients would be 19-35% for protein, 22-40% for carbohydrate, and 28-58% for fat.

He derives these numbers from projections based on the average composition of plant foods, and the whole-body composition of representative animal foods (includes organs, marrow, blood etc., which they typically ate). 

However, some groups may have eaten more fat than this.  Natives on the North American Pacific coast rendered fat from fish, seals, bears and whales, using it liberally in their food. Here's an excerpt from The Northwest Coast by James Swan, who spent three years living among the natives of the Washington coast in the 1850s:

About a month after my return from the treaty, a whale was washed ashore on the beach between Toke's Point and Gray's Harbor and all the Indians about the Bay went to get their share... The Indians were camped near by out of the reach of the tide, and were all very busy on my arrival securing the blubber either to carry home to their lodges or boiling it out on the spot, provided they happened to have bladders or barrels to put the oil in. Those who were trying out [rendering] the blubber cut it into strips about two inches wide, one and a half inches thick, and a foot long. These strips were then thrown into a kettle of boiling water, and as the grease tried out it was skimmed off with clam shells and thrown into a tub to cool and settle. It was then carefully skimmed off again and put into the barrels or bladders for use. After the strips of blubber have been boiled, they are hung up in the smoke to dry and are then eaten. I have tried this sort of food but must confess that, like crow meat, "I didn't hanker arter it".

I was very impressed by the paper overall. I think it presents a good, simple model for eating well: eat whole foods that are similar to those that hunter-gatherers would have eaten, including at least 20% of calories from high-quality animal sources. Organs are mandatory, vegetables may not be. Sorry, Grandma.

Media Misinterpretations

The New York Times just published an article called "The Overflowing American Dinner Plate", in which they describe changes in the American diet since 1970, the period during which the obesity rate doubled. Bill Marsh used USDA estimates of food consumption from 1970 to 2006. Predictably, he focuses on fat consumption, and writes that it has increased by 59% in the same time period.

The problem is, we aren't eating any more fat than we were in 1970. The US Centers for Disease Control NHANES surveys show that total fat consumption has remained the same since 1971, and has decreased as a percentage of calories. I've been playing around with the USDA data for months now, and I can tell you that Marsh misinterpreted it in a bad way. Here are the raw data, for anyone who's interested. They're in easy-to-use Excel spreadsheets. I highly recommend poking around them if you're interested.

The reason Marsh was confused by the USDA data is that he confused "added fats" with "total fat".  While total fat intake has remained stable over this time period, added fats have increased by 59%. The increase is almost exclusively due to industrially processed seed oils (butter and lard have decreased). Total fat has remained the same because we now eat low-fat cuts of meat and low-fat dairy products to make up for it!

Another problem with the article is it only shows percent changes in consumption of different foods, rather than absolute amounts. This obscures some really meaningful information. For example, grain consumption is up a whopping 42%. That is the largest single food group change if you exclude the misinterpreted fat data. Corn is up 188%, rice 170%, wheat 21%. But in absolute amounts, the increase in wheat consumption is larger than corn or rice! That's because baseline wheat consumption dwarfed corn and rice. We don't get that information from the data presented in the article, due to the format.

So now that I've deconstructed the data, let's see what the three biggest changes in the American diet from 1970 to 2006 actually are:

• We're eating more grains, especially white wheat flour
  


• We're eating more added sweeteners, especially high-fructose corn syrup


• Animal fats from milk and meat have been replaced by processed seed oils
  

Wheat + sugar + processed vegetable oil = fat and unhealthy. Sounds familiar, doesn't it?

Letter to the Editor

I wrote a letter to the New York Times about their recent article "The Overflowing American Dinnerplate", which I reviewed here. The letter didn't get accepted, so I will publish it here:

In the article "The Overflowing American Dinner Plate", Bill Marsh cites USDA data showing a 59% increase in fat consumption from 1970 to 2006, coinciding with the doubling of the obesity rate in America. However, according to Centers for Disease Control NHANES nutrition survey data, total fat intake in the US has remained relatively constant since 1971, and has actually decreased as a percentage of calories. The apparent discrepancy disappears when we understand that the USDA data Marsh cites are not comprehensive. They do not include the fat contained in milk and meat, which have been steadily decreasing since 1970.

The change Marsh reported refers primarily to the increasing use of industrially processed vegetable oils such as soybean oil. These have gradually replaced animal fats in our diet over the last 30 years. Since overall fat intake has changed little since the 1970s, it cannot be blamed for rising obesity.

Vegetable Oil and Homicide

One of the major dietary changes that has accompanied the downward slide of American health is the replacement of animal fats with industrially processed vegetable oils. Soybean oil, corn oil, cottonseed oil and other industrial creations have replaced milk and meat fat in our diet, while total fat consumption has remained relatively constant. The result is that we're eating a lot more polyunsaturated fat than we were just 30 years ago, most of it linoleic acid (omega-6). Corn oil may taste so bad it inspires you to violence, but its insidiousness goes beyond the flavor. Take a look:


This figure is from a paper that Dr. Joe Hibbeln sent me recently, of which he is the first author. This followed an interesting e-mail conversation with Robert Brown, author of Omega Six: the Devil's Fat. He put me in touch with Dr. Hibbeln and Dr. William Lands (NIH, NIAAA), both of whom warn of the dangers of excessive linoleic acid consumption from modern vegetable oils. Dr. Lands has been researching the relationship between dietary fat and inflammation since the 1970s, and has been a critic of modern vegetable oils for just as long. Both Dr. Hibbeln and Dr. Lands were very generous in sending me a number of their papers. The figure above shows the homicide rate vs. linoleic acid consumption of five countries over the course of 40 years. Each point represents one year in one country. The U.S. has the distinction of being in the upper right.

I asked Dr. Hibbeln how he selected the five countries, and he told me the selection criteria were 1) available homicide and linoleic acid consumption statistics, 2) "first world" countries, and 3) countries representing a diversity of linoleic acid intakes. I'm satisfied that there was probably not a significant selection bias.

What's interesting about the graph is that not only does the homicide rate track with linoleic acid consumption across countries, but it also tracks within countries over time. For example, here is the same graph of the US alone:


And here is the UK, which doesn't suffer as much from the confounding factor of firearm availability:


I don't think we can draw any solid conclusions from this, but it is worth noting that epidemiological associations don't get much better. In the next few posts, I'll explore the data from intervention trials that support the hypothesis that excessive omega-6 consumption, and insufficient omega-3 consumption, cause serious problems for psychiatric and physical health.

The Omega Ratio

The theory advanced by Dr. Lands and Hibbeln is that the ratio of omega-6 to omega-3 fatty acids in the diet is the crucial factor for mental and physical health, rather than the absolute amount of each. Omega-6 and -3 fats are essential long-chain polyunsaturated fatty acids. The number refers to the position of the double bond near the methyl end of the carbon chain.

The ratio of omega-6 to omega-3 (hereafter, n-6 and n-3) in the diet determines the ratio in tissues. Since these molecules have many cellular roles, it doesn't stretch the imagination that they could have an effect on health. Hunter-gatherer and healthy non-industrial cultures typically have a favorable ratio of n-6 to n-3, 2:1 or less. In the US, the ratio is currently about 17:1 due to modern vegetable oils.

DHA, a long-chain n-3 fatty acid, is concentrated in neuronal synapses (the connections between neurons) and is required for the normal functioning of neurons. n-6 fats compete with n-3 fats for space in cellular membranes (which have a fixed amount of total polyunsaturated fat), so a high intake of n-6 fats, particularly linoleic acid, displaces n-3 fatty acids. Lower tissue levels of DHA and total n-3 correlate with measures of hostility in cocaine addicts. Feeding mice a diet high in linoleic acid increases aggressive behavior, and increses the likelihood of rats to kill mice.

If the ratio of n-6 to n-3 in the diet predicts psychiatric problems, we'd expect to see an association with n-3 intake as well. Let's take a look:

This is homicide mortality vs. n-3 intake for 24 countries, published here. The association is significant (p> 0.001) even without correcting for n-6 intake. Of course, one could see this as a cloud of points with a few well-placed outliers. Here are some closer associations from the same paper:

It's clear that both a high n-6 intake and a low n-3 intake correlate with negative psychiatric outcomes. Together, the data are consistent with the hypothesis that the ratio of n-6 to n-3 impacts brain function. Dr. Hibbeln and Dr. Lands do not claim that this ratio is the sole determinant of psychiatric problems, only that it is a factor.

Now to address the big criticism that was brought up by very astute readers of the last post, namely, that the data were purely correlative. Believe me, I wouldn't even have posted on this topic if I didn't have intervention data to back it up. In addition to the animal data I mentioned above, here are more studies that support a causal role of fatty acid balance in psychiatric problems:

• EPA supplementation (a long-chain n-3 fatty acid) reduced aggression and depression in a group of women with borderline personality disorder.
• DHA supplementation improved aggression in young Thai students.
• n-3 supplementation improved symptoms of bipolar disorder.
• EPA supplementation improved symptoms of unipolar depression.
• n-3 supplementation improved perinatal depression.
• n-3 supplementation improved symptoms of major depression.
• DHA and EPA supplementation reduced suicidal behaviors and improved markers of well-being in patients with recurrent self-harm.
• n-3 supplementation decreased anger and anxiety in substance abusers.
  

Most of those were placebo-controlled trials. If we can see a significant effect of n-3 supplementation in short-term trials, imagine how well it would work as a long-term preventive measure.

Omega Fats and Cardiovascular Disease

I noticed something strange when I was poring over data about the Inuit last month. Modern Inuit who have adopted Western food habits get fat, they get diabetes... but they don't get heart attacks. This was a paradox to me at the time, because heart disease mortality typically comes along with the cluster of modern, non-communicable diseases I call the "diseases of civilization".

One of the interesting things about the modern Inuit diet is it's most often a combination of Western and traditional foods. For example, they typically use white flour and sugar, but continue to eat seal oil and fish. Both seal oil and fish are a concentrated source of long-chain omega-3 (n-3) fatty acids.The 'paradox' makes much more sense to me now that I've seen this:

It's from the same paper as the graphs in the last post. Note that it doesn't take much n-3 to get you to the asymptote. Here's another one that might interest you:

The finding in this graph is supported by the Lyon diet heart study, which I'll describe below. One more graph from a presentation by Dr. Lands, since I began by talking about the Inuit:


Cardiovascular disease mortality tracks well with the n-6 content of blood plasma, both across populations and within them. You can see modern Quebec Inuit have the same low rate of CVD mortality as the Japanese. The five red triangles are from MRFIT, a large American intervention trial. They represent the study participants divided into five groups based on their plasma n-6. Note that the average percentage of n-6 fatty acids is very high, even though the trial occurred in the 1970s! Since n-3 and n-6 fats compete for space in human tissue, it makes sense that the Inuit are protected from CVD by their high n-3 intake.  [Update: I don't read too much into this graph because there are so may confounding variables.  It's an interesting observation, but take it with a grain of salt.. SJG 2011].

Now for a little mechanism. Dr. Lands' hypothesis is that a high n-6 intake promotes a general state of inflammation in the body. The term 'inflammation' refers to the chronic activation of the innate immune system. The reason is that n-3 and n-6 fats are precursors to longer-chain signaling molecules called eicosanoids. In a nutshell, eicosanoids produced from n-6 fatty acids are more inflammatory and promote thrombosis (clotting) more than those produced from n-3 fatty acids. Dr. Lands is in a position to know this, since he was one of the main researchers involved in discovering these mechanisms. He points out that taking aspirin to 'thin' the blood and reduce inflammation (by inhibiting inflammatory eicosanoids) basically puts a band-aid over the problem caused by excess n-6 fats to begin with.  [Update- this mechanism turns out not to be so straightforward. SJG 2011]

The Lyon Diet Heart Study assessed the effect of n-3 fat supplementation on CVD risk. The four-year intervention involved a number of diet changes designed to mimic the American Heart Association's concept of a "Mediterranean diet". The participants were counseled to eat a special margarine that was high in n-3 from alpha-linolenic acid. Overall PUFA intake decreased, mostly due to n-6 reduction, and n-3 intake increased relative to controls. The intervention caused a 70% reduction in cardiac mortality and a large reduction in all-cause mortality, a smashing success by any measure.

In a large five-year intervention trial in Japan, JELIS, patients who took EPA (a long-chain n-3 fatty acid) plus statins had 19% fewer cardiac events than patients taking statins alone. I don't know why you would give EPA by itself when it occurs with DHA and alpha-linolenic acid in nature, but it did nevertheless have a significant effect. Keep in mind that this trial was in Japan, where they already have a much better n-6/n-3 ratio than in Western nations.

In my opinion, what all the data (including a lot that I haven't included) point to is that a good n-6 to n-3 ratio may be important for vibrant health and proper development. In the next post, I'll talk about practical considerations for achieving a good ratio.

A Practical Approach to Omega Fats

Hunter-gatherers and healthy non-industrial cultures didn't know what omega-6 and omega-3 fats were. They didn't balance nutrients precisely; they stayed healthy by eating foods that they knew were available and nourishing. Therefore, I don't think it's necessary to bean count omega fats, and I don't think there's likely to be a single ideal ratio of n-6 to n-3. However, I do think there's evidence for an optimal range. To find out what it is, let's look at what's been done by healthy cultures in the past:

• Hunter-gatherers living mostly on land animals: 2:1 to 4:1


• Pacific islanders getting most of their fat from coconut and fish: 1:2


• Inuit and other Pacific coast Americans: 1:4 or less


• Dairy-based cultures: 1:1 to 2:1


• Cultures eating fish and grains: 1:2 or less

It looks like a healthy ratio is between 4:1 and 1:4 n-6 to n-3. Some of these cultures ate a good amount of n-3 polyunsaturated fat, but none of them ate much n-6 [One rare exception is the !Kung. SJG 2011]. There are three basic patterns that I've seen: 1) low fat with low total n-6 and n-3, and a ratio of less than 2:1; 2) high fat with low total n-6 and n-3 and a ratio of 2:1 or less; 3) high fat with low n-6 and high n-3, and a low carbohydrate intake.

I think there's a simple way to interpret all this. Number one, don't eat vegetable oils high in n-6 fats. They are mostly industrial creations that have never supported human health. Number two, find a source of n-3 fats that can approximately balance your n-6 intake. In practical terms, this means minimizing sources of n-6 and eating modest amounts of n-3 to balance it. Some foods are naturally balanced, such as grass-fed dairy and pastured lamb. Others, like coconut oil, have so little n-6 it doesn't take much n-3 to create a proper balance.

Animal sources of n-3 are the best because they provide pre-formed long-chain fats like DHA, which some people have difficulty producing themselves. Flax oil may have some benefits as well. Fish oil and cod liver oil can be a convenient source of n-3; take them in doses of one teaspoon or less. As usual, whole foods are probably better than isolated oils. Weston Price noted that cultures throughout the world went to great lengths to obtain fresh and dried marine foods. Choose shellfish and wild fish that are low on the food chain so they aren't excessively polluted.

I don't think adding gobs of fish oil on top of the standard American diet to correct a poor n-6:n-3 ratio is optimal. It may be better than no fish oil, but it's probably not the best approach. I just read a study, hot off the presses, that examines this very issue in young pigs. Pigs are similar to humans in many ways, including aspects of their fat metabolism. They were fed three diets: a "deficient" diet containing some n-6 but very little n-3; a "contemporary" diet containing a lot of n-6 and some n-3; an "evolutionary" diet containing a modest, balanced amount of n-6 and n-3; and a "supplemented" diet, which is the contemporary diet plus DHA and arachidonic acid (AA).

Using the evolutionary diet as a benchmark, none of the other diets were able to achieve the same fatty acid profile in the young pigs' brains, blood, liver or heart. They also showed that neurons in culture require DHA for proper development, and excess n-6 interferes with the process.

With that said, here are a few graphs of the proportion of n-6 in common foods. These numbers all come from nutrition data. They reflect the percentage n-6 out of the total fat content. First, animal fats:


Except salmon oil, these are traditional fats suitable for cooking. Except schmaltz (chicken fat), they are relatively low in n-6. Next, vegetable oils:


These range from very low in n-6 to very high. Most of the modern, industrially processed oils are on the right, while most traditional oils are on the left. I don't recommend using anything to the right of olive oil on a regular basis. "HO" sunflower oil is high-oleic, which means it has been bred for a high monounsaturated fat content at the expense of n-6. Here are the meats and eggs:

n-3 eggs are from hens fed flax or seaweed, while the other bar refers to conventional eggs.

A few of these foods are good sources of n-3. At the top of the list is fish oil, followed by n-3 eggs, grass-fed butter, and the fat of grass-fed ruminants. It is possible to keep a good balance without seafood, it just requires keeping n-6 fats to an absolute minimum. It's also possible to overdo n-3 fats. The traditional Inuit, despite their good overall health, did not clot well. They commonly developed nosebleeds that would last for three days, for example. This is thought to be due to the effect of n-3 on blood clotting. But keep in mind that their n-3 intake was so high it would be difficult to achieve today without drinking wine glasses full of fish oil.

How to Fatten Your Liver

Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.

This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH₂-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.

Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).

Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.

Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.

Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!

Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.

There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.

What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.

In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.

In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.

DART: Many Lessons Learned

The Diet and Reinfarction Trial (DART), published in 1989, is one of the most interesting clinical trials I've had the pleasure to read about recently. It included 2,033 British men who had already suffered from an acute myocardial infarction (MI; heart attack), and tested three different strategies to prevent further MIs. Subjects were divided into six groups:

• One group was instructed to reduce total fat to 30% of calories (from about 35%) and replace saturated fat (SFA) with polyunsaturated fat (PUFA).


• The second group was told to double grain fiber intake.


• The third group was instructed to eat more fatty fish or take fish oil if they didn't like fish.


• The remaining three were control groups that were not advised to change diet; one for each of the first three.
  

Researchers followed the six groups for two years, recording deaths and MIs. The fat group reduced their total fat intake from 35.0 to 32.3% of calories, while doubling the ratio of PUFA to SFA (to 0.78). After two years, there was no change in all-cause or cardiac mortality. This is totally consistent with the numerous other controlled trials that have been done on the subject. Here's the mortality curve:

Here's what the authors have to say about it:

Five randomised trials have been published in which a diet low in fat or with a high P/S [polyunsaturated/saturated fat] ratio was given to subjects who had recovered from MI. All these trials contained less than 500 subjects and none showed any reduction in deaths; indeed, one showed an increase in total mortality in the subjects who took the diet.

So... why do we keep banging our heads against the wall if clinical trials have already shown repeatedly that total fat and saturated fat consumption are irrelevant to heart disease and overall risk of dying? Are we going to keep doing these trials until we get a statistical fluke that confirms our favorite theory? This DART paper was published in 1989, and we have not stopped banging our heads against the wall since. The fact is, there has never been a properly controlled clinical trial that has shown an all-cause mortality benefit for reducing total or saturated fat in the diet (without changing other variables at the same time). More than a dozen have been conducted to date.

On to fish. The fish group tripled their omega-3 intake, going from 0.6 grams per week of EPA to 2.4 g (EPA was their proxy for fish intake). This group saw a significant reduction in MI and all-cause deaths, 9.3% vs 12.8% total deaths over two years (a 27% relative risk reduction). Here's the survival chart:

Balancing omega-6 intake with omega-3 has consistently improved cardiac risk in clinical trials. I've discussed that here.

The thing that makes the DART trial really unique is it's the only controlled trial I'm aware of that examined the effect of grain fiber on mortality (without simultaneously changing other factors). The fiber group doubled their grain fiber intake, going from 9 to 17 grams by eating more whole grains. This group saw a non-significant trend toward increased mortality and MI compared to its control group. Deaths went up from 9.9% to 12.1%, a relative risk increase of 18%. I suspect this result was right on the cusp of statistical significance, judging by the numbers and the look of the survival curve:

You can see that the effect is consistent and increases over time. At this rate, it probably would have been statistically significant at 2.5 years.

I think the problem with whole grains is that the bran and germ contain a disproportionate amount of toxins, such as the mineral-binding phytic acid.  The bran and germ also contain a disproportionate amount of nutrients. To have your cake and eat it too, soak, sprout or ferment grains. This reduces the toxin load but preserves or enhances nutritional value. Wheat may be a problem whether it's treated this way or not.

Subjects in the studies above were eating grain fiber that was not treated properly, and so they were increasing their intake of some pretty nasty toxins while decreasing their nutrient absorption. Healthy non-industrial cultures would never have made this mistake. Grains must be treated with respect, and whole grains in particular.