Food : Sauerkraut

Real Food V: Sauerkraut

Sauerkraut is part of a tradition of fermented foods that reaches far into human prehistory. Fermentation is a means of preserving food while also increasing its nutritional value. It increases digestibility and provides us with beneficial bacteria, especially those that produce lactic acid. Raw sauerkraut is a potent digestive aid, probably the reason it's traditionally eaten with heavy food.

Sauerkraut is produced by a process called ‘anaerobic’ fermentation, meaning ‘without oxygen’. It’s very simple to achieve in practice. You simply submerge the cabbage in a brine of its own juices and allow the naturally present bacteria to break down the sugars it contains. The process of ‘lacto-fermentation’ converts the sugars to lactic acid, making it tart. The combination of salt, anaerobic conditions, and acidity makes it very difficult for anything to survive besides the beneficial bacteria, so contamination is rare. If it does become contaminated, your nose will tell you as soon as you taste it.

Store-bought sauerkraut is far inferior to homemade. It's soggy and sterile. Ask a German: unpasteurized kraut is light, crunchy and tart!

My method is inexpensive and requires no special equipment. I've tested it many times and have never been disappointed.

Materials

• Wide-mouth quart canning jars (cheap at your local grocery store)
• Beer bottles with the labels removed, or small jars that fit inside the canning jars
• Three tablespoons of sea salt (NOT iodized table salt-- it's fatal to our bacteria)
• Five pounds of green cabbage

Recipe

1. Chop cabbage thinly. Ideally the slices should be 2 mm or so wide, but it doesn’t matter very much. You can use a food processor, mandolin or knife.
2. Put all the cabbage together in a large bowl and add the salt. If the salt is not very dense (sometimes finely ground sea salt can be fluffy), you can add up to 5 tablespoons total. Mix it around with your hands. Taste some. It should be good and salty.
3. Let the salted cabbage sit in the bowl for 30 minutes or so. It should be starting to get juicy.
4. Pack the cabbage tightly into the canning jars. Leave 2-3 inches at the top of the jar. When you push on the cabbage in the jar, you should be able to get the brine to rise above the cabbage. Try to get rid of air bubbles.
5. Put water into the beer bottles and place them into the canning jars. The weight of the bottles will keep the cabbage under the brine. It’s okay that some of the brine is exposed to the air; the cabbage itself is protected.
6. Let it sit for 2 weeks at room temperature! As the fermentation proceeds, bubbles will form and this will raise the level of the brine. This is normal. You might get some scum on top of the liquid; just check for this and scrape it off every few days. It won’t affect the final product. If the brine drops to the level of the cabbage, add salt water (1 tsp/cup, non-chlorinated water) to bring it back up.
7. Taste it! It should be tart and slightly crunchy, with a fresh lactic acid flavor. If fully fermented, it will keep in the fridge for a long time.

Here are some photos from making sauerruben, which is like sauerkraut but made with turnips:

Food : Idlis

Real Food IX: Idlis

Traditional cultures throughout the world went to great lengths to maximize the nutritional value of the ingredients they had. Fermentation is a technique that was widely used for preparing grains and legumes. Humans are not well adapted to grains or legumes, in large part due to their assortment of anti-nutrients (substances that prevent the absorption of nutrients) and other toxins. Fermentation is a very effective way to eliminate anti-nutrients, making grains and legumes more nutritious and easily digested.

Idlis are steamed, naturally leavened cakes made from a fermented mixture of ground rice and beans. They're mild, savory and fluffy, and pair well with nearly any dish. I think they fill in well for bread. Due to the combination of rice and beans, they contain a fair amount of high-quality complete protein. They are also very economical. Idlis have their roots in Southern Indian cuisine more than 1,000 years ago. They may have originated as a fermented bean dish, with rice added to the recipe later in history.

The recipe takes 2-3 days to complete, but actually doesn't require much work. First, the beans and rice are soaked separately, then they are ground and mixed, then they are allowed to ferment for 24-48 hours and steamed. This type of days-long soaking and fermentation process is common in many grain-based cultures worldwide.

The recipe traditionally calls for short-grain white rice and urad dal (split black gram). I've been using short-grain brown rice with good results. You will only be able to find urad dal in an Indian grocer, specialty store or online. If you can't find urad dal, try experimenting with other types of mild dry beans.

Ingredients and materials

• One cup urad dal or other dried bean
• Two cups short-grain brown or white rice
• One teaspoon fenugreek (optional)
• Two teaspoons non-iodized salt
• Filtered or otherwise dechlorinated water
• Muffin tray
• Large pot for steaming (optional)

Recipe

1. Soak urad dal and rice separately for 6 hours (longer if you're using a different type of bean). Add fenugreek to the rice before soaking (optional). It's used traditionally to speed fermentation.
2. Pour water off the urad dal and rice/fenugreek mixture. Don't rinse.
3. Grind the urad dal in a food process or or blender with a minimum amount of water until it's a smooth paste. The water must not be chlorinated or it will kill our bacteria! Brita-type water filters remove chlorine, as does boiling or leaving water uncovered overnight.
4. Grind the rice/fenugreek mixture coarsely with a minimum amount of dechlorinated water.
5. Mix the ground urad dal, ground rice and salt. The salt must be non-iodized, or the batter will not ferment! Pickling salt, kosher salt and unrefined sea salt work well. Add dechlorinated water until it's a thick paste, stirrable but not liquid.
6. Ferment for 24-48 hours. You know it's ready when the dough has risen significantly, and the odor has gone from harsh and beany to mild and savory. Fermentation time will depend on the ambient temperature.
7. Fill muffin trays about half-way with batter and steam until a knife inserted into them comes out clean, 15-20 minutes. You can also bake them at 350 F. It's not traditional, but I like them baked almost as much. If you really want to be traditional, you can buy an idli steamer.

Here are photos of my last batch. Soaking the urad dal and rice:


Batter, pre-fermentation:


Batter, post-fermentation (48 hours). It more than doubled in volume. The color didn't actually change, that's just my camera.


Ready to steam or bake.


After baking. One escaped! Into my belly.


Thanks to Soumya dey and Wikipedia for the top photo

A few thoughts on Minerals, Milling, Grains and Tubers

A few thoughts on Minerals, Milling, Grains and Tubers

One of the things I've been noticing in my readings on grain processing and mineral bioavailability is that it's difficult to make whole grains into a good source of minerals. Whole grains naturally contain more minerals that milled grains where the bran and germ are removed, but most of the minerals are bound up in ways that prevent their absorption. 

The phytic acid content of whole grains is the main reason for their low mineral bioavailability. Brown rice, simply cooked, provides very little iron and essentially no zinc due to its high concentration of phytic acid. Milling brown rice, which turns it into white rice, removes most of the minerals but also most of the phytic acid, leaving mineral bioavailability similar to or perhaps even better than brown rice (the ratio of phytic acid to iron and zinc actually decreases after milling rice). If you're going to throw rice into the rice cooker without preparing it first, white rice may actually deliver an overall higher level of certain minerals than brown rice, though brown rice may have other advantages such as a higher feeling of fullness per calorie. Either way, the mineral availability of rice is low. Here's how Dr. Robert Hamer's group put it when they evaluated the mineral content of 56 varieties of Chinese rice:

This study shows that the mineral bio-availability of Chinese rice varieties will be [less than] 4%. Despite the variation in mineral contents, in all cases the [phytic acid] present is expected to render most mineral present unavailable. We conclude that there is scope for optimisation of mineral contents of rice by matching suitable varieties and growing regions, and that rice products require processing that retains minerals but results in thorough dephytinisation.

It's important to note that milling removes most of the vitamin content of the brown rice, and most of the fiber, both of which could be disadvantageous depending on what your overall diet looks like. 

Potatoes and other tubers contain much less phytic acid than whole grains, which may be one reason why they're a common feature of extremely healthy cultures such as the Kitavans. I went on NutritionData to see if potatoes have a better mineral-to-phytic acid ratio than grains. They do have a better ratio than whole grains, although whole grains contain more total minerals. 

Soaking grains reduces their phytic acid content, but the extent depends on the grain. Gluten grain flours digest their own phytic acid very quickly when soaked, due to the presence of the enzymephytase. Because of this, bread is fairly low in phytic acid, although whole grain yeast breads contain more than sourdough breads. Buckwheat flour also has a high phytase activity. The more intact the grain, the slower it breaks down its own phytic acid upon soaking. Some grains, like rice, don't have much phytase activity so they degrade phytic acid slowly. Other grains, like oats and kasha, are toasted before you buy them, which kills the phytase. 

Whole grains generally contain so much phytic acid that modest reductions don't free up much of the mineral content for absorption. Many of the studies I've read, including this one, show that soaking brown rice doesn't really free up its zinc or iron content. But I like brown rice, so I want to find a way to prepare it well. It's actually quite rich in vitamins and minerals if you can absorb them. 

One of the things many of these studies overlook is the effect of pH on phytic acid degradation. Grain phytase is maximally active around pH 4.5-5.5. That's slightly acidic. Most of the studies I've read soaked rice in water with a neutral pH, including the one above. Adding a tablespoon of whey, yogurt, vinegar or lemon juice per cup of grains to your soaking medium will lower the pH and increase phytase activity. Temperature is also an important factor, with approximately 50 C (122 F) being the optimum. I like to put my soaking grains and beans on the heating vent in my kitchen. 

I don't know exactly how much adding acid and soaking at a warm temperature will increase the mineral availability of brown rice (if at all), because I haven't found it in the literature. The bacteria present if you soak it in whey, unfiltered vinegar or yogurt could potentially aid the digestion of phytic acid. Another strategy is to add the flour of a high-phytase grain like buckwheat to the soaking medium. This works for soaking flours, perhaps it would help with whole grains as well?

So now we come to the next problem. Phytic acid is a medium-sized molecule. If you break it down and it lets go of the minerals it's chelating, the minerals are more likely to diffuse out of the grain into your soaking medium, which you then discard because it also contains the tannins, saponins and other anti-nutrients that you want to get rid of. That seems to be exactly what happens, at least in the case of brown rice. 

So what's the best solution for maximal mineral and vitamin content? Do what traditional cultures have been doing for millenia: soak, grind and ferment whole grains. This eliminates nearly all the phytic acid, dramatically increasing mineral bioavailiability. Fermenting batter doesn't lose minerals because there's nowhere for them to go. In the West, we use this process to make bread. In Africa, they do it to make ogi, injera, and a number of other fermented grain dishes. In India, they grind rice and beans to make idli and dosas. In the Phillipines, they ferment ground rice to make puto. Fermenting ground whole grains is the most reliable way to improve their mineral bioavailability and nutritional value in general. 

But isn't having a rice cooker full of steaming brown rice so nice? I'm still working on finding a reliable way to increase its nutritional value.

Dietary Fiber and Mineral Availability

Dietary Fiber and Mineral Availability

Health authorities tell us to eat more fiber for health, particularly whole grains, fruit and vegetables. Yet the Diet and Reinfarction Trial, which determined the effect of eating a high-fiber diet on overall risk of death, came up with this graph:



Oops!  At two years, the group that doubled its fiber intake had a 27% greater chance of dying and a 23% greater chance of having a heart attack. The extra fiber was coming from whole grains. The difference wasn't statistically significant, so we can't make too much out of this. But at the very least, it doesn't support the idea that increasing grain fiber will extend your life. 

Why might fiber be problematic? I read a paper recently that gave a pretty convincing answer to that question: "Dietary Fibre and Mineral Bioavailability", by Dr. Barbara F. Hartland. By definition, fiber is indigestible. We can divide it into two categories: soluble and insoluble. Insoluble fiber is mostly cellulose and it's relatively inert, besides getting fermented a bit by the gut flora. Soluble fiber is anything that can be dissolved in water but not digested by the human digestive tract. It includes a variety of molecules, some of which are quite effective at keeping you from absorbing minerals. Chief among these is phytic acid, with smaller contributions from tannins (polyphenols) and oxalates. The paper makes a strong case that phytic acid is the main reason fiber prevents mineral absorption, rather than the insoluble fiber fraction. This notion was confirmed here. 

Whole grains would be a good source of minerals, if it weren't for their very high phytic acid content. Even though whole grains are full of minerals, replacing refined grains with whole grains in the diet (and especially adding extra bran) actually reduces the overall absorption of a number of minerals (free text, check out table 4). This has been confirmed repeatedly for iron, zinc, calcium, magnesiumand phosphorus. 

Refining grains gets rid of the vitamins and minerals, but at least refined grains don't prevent you from absorbing the minerals in the rest of your food. Here's a comparison of a few of the nutrients in one cup of cooked brown vs. unenriched white rice (218 vs. 242 calories):

Brown rice would be quite nutritious if we could absorb all those minerals. There are a few ways to increase mineral absorption from whole grains. One way is to soak them in slightly acidic, warm water, which allows their own phytase enzyme to break down phytic acid. This doesn't seem to do much for brown rice, which doesn't contain much phytase. 

A more effective method is to grind grains and soak them before cooking, which helps the phytase function more effectively, especially in gluten grains and buckwheat. The most effective method by far, and the method of choice among healthy traditional cultures around the world, is to soak, grind and ferment whole grains. This breaks down nearly all the phytic acid, making whole grains a good source of both minerals and vitamins. 

The paper "Dietary Fibre and Mineral Bioavailability" listed another method of increasing mineral absorption from whole grains. Certain foods can increase the absorption of minerals from whole grains high in phytic acid. These include: foods rich in vitamin C such as fruit or potatoes; meat including fish; and dairy. 

Another point the paper made was that the phytic acid content of vegetarian diets is often very high, potentially leading to mineral deficiencies. The typical modern vegetarian diet containing brown rice and unfermented soy products is very high in phytic acid, and therefore it may make sense to ensure plentiful sources of easily absorbed minerals in the diet, such as dairy. The more your diet depends on plant sources for minerals, the more careful you have to be about how you prepare your food.

Cigarette Smoking

Cigarette Smoking-- Another Factor in the Obesity Epidemic

Obesity rates in the US have more than doubled in the last 30 years, and rates of childhood obesity and extreme adult obesity have tripled.  One third of US adults are considered obese, and another third overweight.  This is the "obesity epidemic".

The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved.  However, there's another probable contributor that's often overlooked: declining smoking rates.  

Here's a graph of cigarette consumption over the last century in the US (1):

You can see that cigarette smoking has declined quite a bit since its peak in 1963-- a decrease of 63 percent to be exact.  It didn't start declining in earnest until 1976 however-- just before the obesity epidemic began.

How Does is Work? 

The main active ingredient in cigarettes is nicotine.  Nicotine acts by binding to a specific type of receptor on neurons (nerve cells) called the nicotinic acetylcholine receptor.  Acetylcholine is one of the main signaling molecules (neurotransmitters) that neurons use to communicate with one another.  Nicotine suppresses food intake, increases energy expenditure, and lowers body fatness.  Smokers tend to be leaner than non-smokers, even though they usually have a cluster of unhealthy lifestyle habits (2, 3), and they rapidly gain weight when they quit (4, 5).  Administering nicotine to rodents under controlled conditions also reduces food intake and body weight substantially (6).

Since the brain (and particularly the hypothalamus) is the organ in charge of regulating food intake and body fatness, one might guess that nicotine acts there either directly or indirectly.  As predicted, nicotine infused directly into the hypothalamus reduces food intake (7), and a recent high-impact paper demonstrated in mice that nicotine exerts its effects on food intake primarily via POMC cells, a type of neuron in the hypothalamus that is important for the regulation of food intake and body fatness (8). 

Have Declining Smoking Rates Contributed to the Obesity Epidemic?

Public health authorities have been waging a war on cigarette smoking since it was firmly established as a risk factor for a number of serious conditions (e.g., cancer and heart attacks)*.  There's no doubt that regularly smoking cigarettes is bad for your health-- in fact it's probably one of the most unhealthy habits there is.  However, smoking kept us leaner than we should have been in the 1950s, 1960s, and 1970s, likely preventing the gradual changes in the US diet and lifestyle from exerting their full effect on our waistline.  As the appetite suppressive effects of cigarettes went away, and our diet became increasingly commercialized, per capita daily calorie intake increased by about 20 percent, and the adult obesity rate doubled.

Here's a graph that I find striking (based on CDC and NHANES data):

Notice that the plateaus (1960 to late 70s) and the steepest slopes (late 70s to 2006) line up almost perfectly.


* My grandmother quit smoking cold turkey in the late 1970s.  When I asked her why, she said "because I found out it was bad for me".

Iodine

Iodine

Iodine is an essential trace mineral. It's required for the formation of activated thyroid hormones T3 and T4. The amount of thyroid hormones in circulation, and the body's sensitivity to them, strongly influences metabolic rate. Iodine deficiency can lead to weight gain and low energy. In more severe cases, it can produce goiter, an enlargement of the thyroid gland.

Iodine deficiency is also the most common cause of preventable mental retardation worldwide. Iodine is required for the development of the nervous system, and also concentrates in a number of other tissues including the eyes, the salivary glands and the mammary glands. 

There's a trend in the alternative health community to use unrefined sea salt rather than refined iodized salt. Personally, I use unrefined sea salt on principle, although I'm not convinced refined iodized salt is a problem. But the switch removes the main source of iodine in most peoples' diets, creating the potential for deficiency in some areas. Most notably, the soil in the midwestern United States is poor in iodine and deficiency was common before the introduction of iodized salt.

The natural solution? Sea vegetables. They're rich in iodine, other trace minerals, and flavor. I like to add a 2-inch strip of kombu to my beans. Kombu is a type of kelp. It adds minerals, and is commonly thought to speed the cooking and improve the digestion of beans and grains. 

Dulse is a type of sea vegetable that's traditionally North American. It has a salty, savory flavor and a delicate texture. It's great in soups or by itself as a snack.

And then there's wakame, which is delicious in miso soup. Iodine is volatile so freshness matters. Store sea vegetables in a sealed container. It may be possible to overdo iodine, so it's best to eat sea vegetables regularly but in moderation like the Japanese.

Seafood such as fish and shellfish are rich in iodine, especially if fish heads are used to make soup stock. Dairy is a decent source in areas that have sufficient iodine in the soil.

Cod liver oil is another good source of iodine, or at least it was before the advent of modern refining techniques. I don't know if refined cod liver oil contains iodine. I suspect that fermented cod liver oil is still a good source of iodine because it isn't refined.

The Tokelau Island Migrant Study: Background and Overview

The Tokelau Island Migrant Study: Background and Overview

Tokelau's troubles began in 1765 with its 'discovery' by British commodore John Byron. Traditionally, residents of the three small coral atolls collectively called Tokelau (Nukunonu, Fakaofo and Atafu) lived an isolated subsistence lifestyle, relying almost exclusively on coconut, seafood, wild fowl and fruit for food. The first reliable account of the Tokelauan population, by an American expedition in 1841, found the people there healthy and happy. Here's an excerpt from Migration and Health in a Small Society: the Case of Tokelau (1992):

The expedition considered the people living there to be healthy and handsome... They all appeared to be thriving on their 'meager diet' of fish and coconut, for no evidence of cultivation was seen... People of both sexes were tattooed with geometric designs and figures of turtles and fish. The numerous reports and journals of the Expedition leave the impression of a generally admirable people - amiable (though cautious), peaceful, orderly, and resourceful.

Between 1841 and 1863, the population of Tokelau was reduced to a fraction of its original size by epidemics and kidnapping by slave ships. The old social and religious order was broken, and the inhabitants were converted to Christianity by overzealous and competing Protestant and Catholic missionaries. During this time, Tokelauans also gained new food sources from other Polynesian islands, including breadfruit trees, pulaka (a starchy tuber), pigs and chickens. Breadfruit is a starchy fruit used like plantain.

Tokelau became a territory of New Zealand in 1925, and Tokelauans were granted New Zealand citizenship in 1948. In 1963, a government-assisted migration program was established to (voluntarily) bring Tokelauans to the New Zealand mainland, as the population of Tokelau had reached a cozy 1,870 people. When a cyclone devastated coconut and breadfruit crops in 1966, Tokelauans began taking advantage of the assisted migration program in earnest. By 1971, roughly half of Tokelauans lived on the New Zealand mainland.

There are two reasons why the Tokelau Island Migrant study is unique. First, it's one of the best-documented transitions from a traditional to a modern lifestyle, studied over decades on Tokelau and in New Zealand. Regular visits by physicians recorded the health of the population as it shifted from a relatively traditional diet to a more Western one. The second thing that makes this population unique is they traditionally have an extraordinarily high saturated fat intake from coconut. They derive between 54 and 62 percent of their calories from coconut, which is 87% saturated. This gives them perhaps the highest documented saturated fat intake in the world. This will be a test of the "diet-heart hypothesis", the idea that dietary fat, cholesterol and especially saturated fat contribute to cardiovascular disease!

Through the late 1960s, cargo ships visited Tokelau every three months, making only small contributions to the islanders' diets. In 1968, just two percent of Tokelauans' calories came from sugar. By 1978, the number had risen to 8 percent, and by 1982, 14 percent. The increase came chiefly from refined sugar and sweetened imported foods. In 1961, ships brought 12 lb of flour per person per year to Tokelau, increasing to 60 lb per year by 1980. During this time, importation of low-quality canned meats such as "mutton flaps" and chicken backs, and sweets also increased. Rice imports declined in the 1970s. The diet of migrants to New Zealand rapidly became highly Westernized, containing a higher proportion of refined carbohydrates such as flour and sugar, more red meat and poultry, and less coconut and seafood.

Here's a nice quote from Migration and Health in a Small Society: the Case of Tokelau, to set the tone for the rest of the posts in this series:

In the mid- and late twentieth century, 'Western diseases'- that is, diseases of affluence (Trowell and Burkitt 1981)- have become the major health risk for Polynesians, because of exposure to cosmopolitan diet patterns and life-style.
The varying cultures and resource bases of islands in the Pacific have influenced the degree to which their populations have been modernized and thus exposed to Western diseases. At one end of the spectrum are relatively traditional subsistence societies such as those on Tokelau and on the low islands- for example Pukapuka, Manihiki, and Rakahanga in the Northern Cook Islands. These atolls are characterized by the almost complete absence of soil, by the inhabitants' dependence on coconut in varied forms, and by a bountiful supply of fish as a major part of the traditional diet. Their populations are notable for their low levels of blood pressure, high rates of infectious disease, and low rates of coronary heart disease, obesity and diabetes. At the other end of the spectrum are those Polynesian societies, such as the Hawaiians and the Maori of New Zealand, who were submerged by 'Western' settlers and the dominating cultures they brought with them. These populations have inevitably acquired the diseases of the 'West', sometimes to an exaggerated degree.

That quote could have been straight out of Nutrition and Physical Degeneration, despite being published 60 years later. Good science is timeless. Join me in future posts as I explore the health of Tokelauan society as it transitions from a traditional diet and lifestyle to a modern one.

Dental Health

The Tokelau Island Migrant Study: Dental Health

I'm always on the lookout for studies that can confirm or deny the information in Nutrition and Physical Degeneration. Traveling around the world in the 1920s and 1930s, Dr. Weston Price found a number of non-industrial cultures that had excellent dental and overall health, including a high resistance to tooth decay, perfectly straight teeth, and wisdom teeth that erupted without impacting. These same cultures developed extreme dental problems, including severe dental decay and crooked teeth in the younger generation, upon adopting modern European foods. These foods always included white flour and refined sugar, with variable contributions from canned goods and vegetable oils.

I have detailed information on the Tokelauan diet beginning in 1968 and ending in 1982. The traditional diet until the 1960s consisted of coconut, fish, breadfruit, pulaka, fruit, pigs, chickens and wild fowl. These are typical Polynesian foods. From the 1960s through the 1980s, Tokelauans gradually adopted flour and sugar as major carbohydrate sources, partially displacing starchy breadfruit and pulaka intake as well as coconut. They also began eating low-quality canned meats that partially replaced fish in their diet. Total calorie intake fluctuated between 1,500 and 2,000 kilocalories but did not trend in any particular direction over time. Here's a graph of macronutrient changes:


I found a study on the dental health of Tokelauans that I thought would be a fitting way to kick off this series. It's titled "Changed oral conditions, between 1963 and 1999, in the population of the Tokelau atolls of the South Pacific". I was only able to get my hands on the abstract, but that was enough. In 1963, Tokelauans were consuming roughly 15 lb of white flour and 10 lb of sugar per person per year. By 1980, the numbers were 60 lb and 69 lb for flour and sugar, and the trend was showing no sign of slowing down (see the graph in the previous post). I don't have numbers for 1999, but they're likely to be higher than in 1980, given the trend. For comparison, in 2006, the average American ate 117 lb of flour per year.

Let's look at a graph. This represents the DMF score (decayed, missing or filled teeth) of Tokelauans 15-19 and 35-44 years old, in 1963 and 1999. I've connected the two data points with lines to give an idea of the trend.

Dental decay increased eight-fold in adolescents and more than four-fold in adults. I don't know what their dental health was like before 1963, but I can only guess it was better than when this study was conducted, due to the fact that the Tokelauan diet was already partially modernized in 1963. The authors conclude "a serious decline in oral health has occurred over the past 35 years."

Does this sound familiar? It should be, because it's been known at least since the 1930s. Here's a quote from Nutrition and Physical Degeneration, describing the Tongan islanders, another Polynesian group: 

The limited importation of foods to the Tongan Islands due to the infrequent call of merchant or trading ships has required the people to remain largely on their native foods. Following the war, however, the price of copra went up from $40.00 per ton to $400.00, which brought trading ships with white flour and sugar to exchange for the copra. The effect of this is shown very clearly in the condition of the teeth. The incidence of dental caries [cavities] among the isolated groups living on native foods was 0.6 per cent, while for those around the port living in part on trade foods, it is 33.4 per cent. The effect of the imported food was clearly to be seen on the teeth of the people who were in the growth stage at that time [i.e., they developed crooked teeth]. Now the trader ships no longer call and this forced isolation is very clearly a blessing in disguise. Dental caries has largely ceased to be active since imported foods became scarce, for the price of copra fell to $4.00 a ton. The temporary rise in tooth decay was apparently directly associated with the calling of trader ships.

0.6 percent is one tooth in every 167. In other words, less than one in five people had even a single cavity. That's without the benefit of tooth brushing, fluoride or any of the tools of modern dentistry. 33.4 percent tooth decay in Tongans living on modern foods means they had 11 cavities per person, a bit less than Tokelauans had in 1999. 

Weston Price's anecdote above is remarkably similar to something that happened on Tokelau in 1979. The atolls didn't receive their normal shipments of European foods for a five-month period, during which they resorted to traditional foods. Here's an excerpt from the New Zealand Herald from June 11, 1979:

What will happen the day the country runs out of fuel and the ships stop bringing those "essential" foods like sugar and flour? Tokelauans recently found out what the answer to that question was- they got healthier. One of the victims of cyclone Meli earlier this year was the passenger cargo ship Cenpac Rounder, chartered five times per year by the Tokelau Affairs office in Apia. Left high and dry on a reef South of Fiji it was badly damaged and could not be moved. So ever since January the three Tokelau atolls have not received fresh supplies. Late last month the first ship called in, chartered by the Tokelau Affairs office. The Secretary of the office said that when the ship arrived the atolls had run out of fuel. So the fishermen had returned to the traditional sail, a sight on the lagoon that had almost been forgotten, thanks to the outboard motor. There was no sugar, flour, tobacco and starch foods either- and the atoll hospitals reported a shortage of business during the enforced isolation. It was reported that the Tokelauans had been very healthy during that time and had returned to the pre-European diet of coconuts and fish. Many people lost weight and felt very much better including some of the diabetics.

Cholesterol and Cardiovascular Health

The Tokelau Island Migrant Study: Cholesterol and Cardiovascular Health

Let's get right to the meat of this study. It's relevant to the hypothesis that saturated fat is a cause of cardiovascular disease.  Tokelauans traditionally obtained 40-50% of their calories from saturated fat, in the form of coconut meat. That's more than any other group I'm aware of.

So are the Tokelauans dropping like flies of cardiovascular disease?  I don't have access to the best data of all: actual heart attack incidence data. But we do have some telltale markers. In 1971-1982, researchers collected data from Tokelau and Tokelauan migrants to New Zealand on cholesterol levels, blood pressure and electrocardiogram (ECG) readings. 

The Tokelauan diet, as I've described in detail in previous posts, is traditionally based on coconut, fish, starchy tubers and fruit. By 1982, their diet also contained a significant amount of imported flour and sugar. Migrants to New Zealand had a much more varied diet that was also more typically Western: more carbohydrate, coming chiefly from wheat, sugar and potatoes; more processed sweet foods and drinks; more red meat; more vegetables; more dairy and eggs. Sugar intake was 13 percent of calories, compared to 8 percent on Tokelau. Saturated fat intake in NZ was half of what it was on Tokelau, while total fat intake was similar. Polyunsaturated fat intake was higher in NZ, 4% as opposed to 2% in Tokelau. I don't have data to back this up, but I think it's likely that the n-6:n-3 ratio increased upon migration.

Blood pressure did not change significantly over time in Tokelau from 1971 to 1982, if anything it actually declined slightly. It was consistently higher in NZ than in Tokelau at all timepoints. Men were roughly three times more likely to be hypertensive in NZ than on Tokelau at all timepoints (4.0% vs. 12.0% in the early 1970s). Women were about twice as likely to be hypertensive (8.1% vs. 15.0%).

On to cholesterol. Total cholesterol in male Tokelauans was a bit lower on average than in New Zealand, but neither was particularly elevated (182 vs. 199 mg/dL). LDL was also a bit higher in NZ males (119 vs. 132 mg/dL). Triglycerides were lower in Tokelauan men than in NZ (80 vs. 114 mg/dL). There were no differences in total cholesterol, LDL cholesterol or triglycerides between Tokelauan and NZ women.  It's interesting that serum lipids don't correspond at all to saturated fat intake.

But does it cause heart attacks? The best data I have from this study are ECG readings. These use electrodes to monitor the electrical activity of the heart. There are certain ECG patterns that suggest that a person has had a heart attack (Minnesota codes 1-1 and 1-2). The data I am going to present here are all age-standardized, meaning they are comparing between groups of the same age. On Tokelau in 1982, 0.0% of men 40-69 years old showed ECG readings that indicated a probable past heart attack. In NZ in 1980-81, 1.0% of men 40-69 years old showed the same ECG readings. In Tecumseh U.S.A. in 1965, 3.5% of men 40-69 years old showed the same ECG pattern. I don't have data for women.

These data don't prove that no one ever has a heart attack on Tokelau. Tokelauans do have heart attacks sometimes, and they also have strokes (at least in modern times). But they do allow us to compare in quantitative terms between genetically similar people living in two different environments. 

This is consistent with what has been observed on Kitava and other traditional Pacific island cultures: a vanishingly small incidence of cardiovascular disease while they retain their traditional diet and lifestyle (and sometimes even when some processed Western food has been introduced). When diets and lifestyles become modern, there is invariably a rise in the incidence of chronic disease.

These data raise serious questions about the role of saturated fat in cardiovascular disease. Tokelau underlines the fact that a non-industrial diet and lifestyle may be a more significant protective factor than the quality of ingested fat.

Unless otherwise noted, the data in this post are from the book Migration and Health in a Small Society: the Case of Tokelau.

Gout

The Tokelau Island Migrant Study: Gout

Gout is a disorder in which uric acid crystals form in the joints, causing intense pain. The body forms uric acid as a by-product of purine metabolism. Purines are a building block of DNA, among other things. Uric acid is normally excreted into the urine, hence the name.

On Tokelau between 1971 and 1982, gout prevalence fell slightly. In migrants to New Zealand, gout prevalence began at the same level as on Tokelau but increased rapidly over the same time period. Here are the prevalence data for men, from Migration and Health in a Small Society: the Case of Tokelau (I don't have data for women):

This paper found that the age-standardized risk of developing gout was 9 times higher in New Zealand than on Tokelau for men, and 2.7 times higher for women.

The Tokelau Island Migrant Study: Background and Overview
The Tokelau Island Migrant Study: Dental Health
The Tokelau Island Migrant Study: Cholesterol and Cardiovascular Health
The Tokelau Island Migrant Study: Weight Gain
The Tokelau Island Migrant Study: Diabetes
The Tokelau Island Migrant Study: Asthma

Stuck at the Starting Gate?

The Diet-Heart Hypothesis: Stuck at the Starting Gate?

The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack. 

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because the evidence that typical dietary amounts cause heart disease in humans is weak.  Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the main source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 eggs per week (click for larger image):The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not have a large impact on serum cholesterol in the long term, perhaps because humans are adapted to eating cholesterol. Most people are able to adjust their own cholesterol metabolism to compensate when the amount in the diet increases. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology. 

The first half of the diet-heart hypothesis states that eating saturated fat raises blood cholesterol. This has been accepted without much challenge by diet-health authorities for nearly half a century. In 1957, Dr. Ancel Keys proposed a formula (Lancet 2:1959. 1957) to predict changes in total cholesterol based on the amount of saturated and polyunsaturated fat in the diet. This formula, based primarily on short-term trials from the 1950s, stated that saturated fat is the primary dietary influence on blood cholesterol.

According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were significant flaws in the data from the very beginning, which were pointed out in this critical 1973 literature review in the American Journal of Clinical Nutrition (free full text).

The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect sometimes had more to do with LA lowering blood cholesterol than saturated fat raising it. This is not at all what I was expecting to find when I began looking through these trials.

Reading through the short-term controlled trials, I was surprised by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and non-optimal study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and consistently demonstrable.  

The long-term data are not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA certainly does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).  The small changes that did occur could have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions. 

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Diseaseby Dr. Harumi Okuyama et al.):What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). 

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not the case. The Masai traditionally get a high proportion of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating practically nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man?Junk food. 

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s).  Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Does dietary saturated fat influence total cholesterol and LDL over the long term?  I don't have the answers, but I do think it's interesting that the evidence is much less consistent than it's made out to be.  It may be that if dietary saturated fat influences total cholesterol or LDL concentration in the long term, the effect is is secondary to other factors.  That being said, it's clear that linoleic acid, in large amount, reduces circulating total cholesterol and LDL.

High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease.

New Review Paper by Yours Truly: High-Fat Dairy, Obesity, Metabolic Health and Cardiovascular Disease

My colleagues Drs. Mario Kratz, Ton Baars, and I just published a paper in the European Journal of Nutrition titled "The Relationship Between High-Fat Dairy Consumption and Obesity, Cardiovascular, and Metabolic Disease".  Mario is a nutrition researcher at the Fred Hutchinson Cancer Research Center here in Seattle, and friend of mine.  He's doing some very interesting research on nutrition and health (with an interest in ancestral diets), and I'm confident that we'll be getting some major insights from his research group in the near future.  Mario specializes in tightly controlled human feeding trials.  Ton is an agricultural scientist at the University of Kassel in Germany, who specializes in the effect of animal husbandry practices (e.g., grass vs. grain feeding) on the nutritional composition of dairy.  None of us have any connection to the dairy industry or any other conflicts of interest.

The paper is organized into three sections:

1. A comprehensive review of the observational studies that have examined the relationship between high-fat dairy and/or dairy fat consumption and obesity, metabolic health, diabetes, and cardiovascular disease.
2. A discussion of the possible mechanisms that could underlie the observational findings.
3. Differences between pasture-fed and conventional dairy, and the potential health implications of these differences.

 We wrote this paper because after reviewing the evidence, we found it to be surprising and fairly contradictory to conventional ideas on nutrition and health.  I wrote the sections on obesity, metabolic health and diabetes, Mario wrote the sections on cardiovascular disease and fatty acids, and Ton wrote the section on husbandry practices and dairy fat composition.  Mario was the lead author and did most of the editing/formatting, submitted the manuscript, etc.  Our paper went through a rigorous peer review process.

Here are our basic findings:

• High-fat dairy consumption is not associated with obesity, in fact, 11 out of 16 studies found that higher dairy fat intake is associated with lower body fat and/or less fat gain over time.  None identified an association between high-fat dairy consumption and fat gain, although some did find an association between low-fat dairy consumption and fat gain.
• High-fat dairy consumption is not associated with poorer metabolic health.  Six of 11 studies found that higher high-fat dairy consumption is associated with better metabolic health, while only one found that it was associated with one marker of poorer metabolic health (and this study used an odd design). 
• The association between high-fat dairy intake and diabetes risk is inconsistent.  Zero of eight studies found that high-fat dairy consumption is associated with diabetes risk, and three found that it was protective.  However, three studies also found that low-fat dairy intake was inversely associated with diabetes risk, compared to no association with high-fat dairy, suggesting by inference that the fat content of the dairy could be harmful.  These studies all adjusted for body fatness.  Since body fatness is a key risk factor for diabetes, and dairy fat intake is inversely associated with body fatness, this is obviously a major confound.  We discussed this and other potential confounds in the paper.
• The evidence on cardiovascular disease is inconsistent, with a number of studies suggesting a protective association, a few suggesting a harmful one, and several suggesting no association.
• Dairy fat is a complex substance.  There are major differences in the fatty acid composition of dairy from pasture-raised vs. conventionally raised cows, and many of these fatty acids are bioactive and could influence human health.
• We also discuss the limitations of observational studies in some detail, and many other issues that I won't touch on here.

What This Paper Means 

This is the first comprehensive review of studies on the association between high-fat dairy intake and obesity, metabolic, and cardiovascular health.  Typical dietary advice includes the recommendation to eat low-fat or skim dairy products.  This is based on the hypothesis that avoiding the (mostly saturated) fat in dairy will reduce the risk of obesity, metabolic problems, and cardiovascular disease.  This idea is logical, but not every idea that is logical is correct when tested scientifically, particularly when it pertains to a complex natural food.  We asked the question "what does the evidence say about this hypothesis?"

The research to date suggests that high-fat dairy overall does not have a negative impact on obesity risk, metabolic problems, diabetes risk, or cardiovascular disease.  In fact, these studies offer fairly strong support to the hypothesis that high-fat dairy may protect against obesity.  However, there was variability between studies and this may be explained by factors such as a) differences in the quality of dairy products between countries/regions, b) the form in which dairy is consumed (e.g., traditional cheeses vs. ice cream and pizza), and c) other confounding factors discussed in the paper. 

Please keep in mind that these studies are observational and therefore can not establish cause and effect. They're best viewed as a springboard for future research.

What This Paper Doesn't Mean

I want to be very clear about this.  This paper does not mean that adding butter to all your food will make you lose fat or become healthier.  In fact, if you do that you will most likely gain fat and become less healthy.  Say what??  The studies we reviewed examined the role of high-fat dairy in the context of normal varied diet patterns.  They did not compare people eating normally to people who put extra butter on everything, which is an excellent way to increase your calorie intake.  Essentially they compared people eating high-fat dairy to people eating other types of fats as part of a mixed diet.  The difference is subtle but critical to understand: addition vs. replacement. 

So does this mean that replacing other types of fats with dairy fat (pasture-raised in particular), in the context of a normal varied diet, could lead to less fat gain and perhaps even better health over time?  Perhaps.  That is what the studies suggest overall.  But again, these are observational studies with major limitations, so we'll have to wait for more evidence before we can hang our hats on the idea.  In the meantime, it's clear that typical dietary recommendations to favor low-fat dairy over high-fat dairy are on thin ice.

Yogurt

Real Food III: Yogurt

Fermented milk is regarded by many cultures as a delicious health food. It has cropped up all over the world in different forms: kefir from Caucasia, laban from the Middle East, dahi from India, creme fraiche from Western Europe, piima from Finland, mursik from Kenya, and yogurt from your grandmother's house. But these same people would scarcely recognize the colored, sweetened gel that passes for yogurt in grocery stores today.

Most if not all dairy-eating cultures ferment their milk. Why is this? There are three main reasons. First of all, unpasteurized milk spontaneously ferments at room temperature, usually becoming delicious "clabbered milk"- whereas pasteurized milk becomes putrid under the same conditions. So fermented milk is difficult to avoid. The second, related reason, is that fermentation prolongs the life of milk in the absence of refrigeration. Fully fermented milk is stable for weeks at room temperature.

The third reason is that these cultures know cultured milk is delicious and nutritious. Fermentation with specially selected cultures of lactic acid-producing bacteria and sometimes yeast work to break milk down into a form that is more easily assimilated. They partly (or fully) digest the lactose, which can be a problem for some people, turning it into tangy lactic acid. They also partially digest casein, a protein in milk that is difficult for some to digest. And finally, the lower pH of fermented milk makes its minerals more bioavailable.

Traditionally, milk was fermented in its unpasteurized state, but raw milk is hard to find in many industrialized countries. Raw milk has its complement of enzymes intact, such as lactase and lipase, which aid in its digestion. It also contains lactose-digesting bacteria that make milk easier for some to digest, and contribute to intestinal health. These are all eliminated by pasteurization. Fortunately, fermentation restores some of the benefits of raw milk. It reintroduces lactic-acid bacteria, along with their digestive enzymes. With that in mind, here's a simple yogurt recipe:


Ingredients/equipment:

1/2 gallon whole, raw or pasteurized, cow or goat milk (add extra cream if you wish)
Starter culture (commercial starter or 2 tbsp of your favorite live-culture yogurt)
Thermometer
Glass jars with lids
Cooler or yogurt maker

Recipe:

1. Heat the milk to 110-115 F (43 C). If the temperature exceeds 115 F, let it cool.

2. Add the starter culture. If the starter is yogurt, whisk it into the milk.

3. Pour the milk into glass jars and keep it at about 110 F for 4-10 hours. 4 hours will yield a mild yogurt, 10 will be tangy. If you don't have a yogurt maker, this is the tricky part. You can use a cooler filled with 100 F water to maintain the temperature and spike it with hot water after a few hours, or you can ferment it in your oven with the pilot light on if the temperature is in the right range.


If you want a thicker yogurt, bring the milk to 180 F (82 C) and let it cool to 110 F before adding the starter. Add fruit, honey or other flavors before fermenting. Enjoy!

As a final note, I'll mention that milk simply does not agree with some people. If you've tried raw milk and homemade yogurt, and they cause intestinal discomfort or allergies, let them go.