A New Way to Soak Brown Rice

I've been looking for a way to prepare whole brown rice that increases its mineral availability without changing its texture. I've been re-reading some of the papers I've accumulated on grain processing and mineral availability, and I've found a simple way to do it.

In the 2008 paper "Effects of soaking, germination and fermentation on phytic acid, total and in vitro soluble zinc in brown rice", Dr. Robert J. Hamer's group found that soaking alone didn't have much of an effect on phytic acid in brown rice. However, fermentation was highly effective at degrading it. What I didn't realize the first time I read the paper is that they fermented intact brown rice rather than grinding it. This wasn't clear from the description in the methods section but I confirmed it by e-mail with the lead author Dr. Jianfen Liang. He added that the procedure comes from a traditional Chinese recipe for rice noodles. The method they used is very simple:

1. Soak brown rice in dechlorinated water for 24 hours at room temperature without changing the water. Reserve 10% of the soaking liquid (should keep for a long time in the fridge). Discard the rest of the soaking liquid; cook the rice in fresh water.
2. The next time you make brown rice, use the same procedure as above, but add the soaking liquid you reserved from the last batch to the rest of the soaking water.
3. Repeat the cycle. The process will gradually improve until 96% or more of the phytic acid is degraded at 24 hours.

This process probably depends on two factors: fermentation acidifies the soaking medium, which activates the phytase (phytic acid-degrading enzyme) already present in the rice; and it also cultivates microorganisms that produce their own phytase. I would guess the latter factor is the more important one, because brown rice doesn't contain much phytase.

You can probably use the same liquid to soak other grains.

Reversing Tooth Decay

In the last post, I discussed the research of Drs. Edward and May Mellanby on the nutritional factors affecting tooth formation. Dr. Mellanby is the man who discovered vitamin D and identified the cause of rickets. Nutrition has a profound effect on tooth structure, and well-formed teeth are inherently resistant to decay. But is there anything you can do if your teeth are already formed?

Teeth are able to heal themselves. That's how traditional cultures such as the Inuit can wear their teeth down to the pulp due to chewing leather and sand-covered dried fish, yet still have an exceptionally low rate of tooth decay. It's also how the African Wakamba tribe can file their front teeth into sharp points without causing decay. Both cultures lost their resistance to tooth decay after adopting nutrient-poor Western foods such as white flour and sugar.

Teeth are made of four layers. Enamel is the hardest, most mineralized outer shell. Dentin is another protective mineralized layer that's below the enamel. Below the dentin is the pulp, which contains blood vessels and nerves. The roots are coated with cementum, another mineralized tissue.

When enamel is poorly formed and the diet isn't adequate, enamel dissolves and decay sets in. Tooth decay is an opportunistic infection that takes advantage of poorly built or maintained teeth. If the diet remains inadequate, the tooth has to be filled or removed, or the person risks more serious complications.

Fortunately, a decaying or broken tooth has the ability to heal itself. Pulp contains cells called odontoblasts, which form new dentin if the diet is good. Here's what Dr. Edward Mellanby had to say about his wife's research on the subject. This is taken from Nutrition and Disease:

Since the days of John Hunter it has been known that when the enamel and dentine are injured by attrition or caries, teeth do not remain passive but respond to the injury by producing a reaction of the odontoblasts in the dental pulp in an area generally corresponding to the damaged tissue and resulting in a laying down of what is known as secondary dentine. In 1922 M. Mellanby proceeded to investigate this phenomenon under varying nutritional conditions and found that she could control the secondary dentine laid down in the teeth of animals as a reaction to attrition both in quality and quantity, independently of the original structure of the tooth. Thus, when a diet of high calci­fying qualities, ie., one rich in vitamin D, calcium and phosphorus was given to the dogs during the period of attrition, the new secondary dentine laid down was abundant and well formed whether the original structure of the teeth was good or bad. On the other hand, a diet rich in cereals and poor in vitamin D resulted in the production of secondary dentine either small in amount or poorly calcified, and this happened even if the primary dentine was well formed.

Thus, in dogs, the factors that affect tooth healing are the same factors that affect tooth development:

1. The mineral content of the diet, particularly calcium and phosphorus
   
2. The fat-soluble vitamin content of the diet, chiefly vitamin D
   
3. The availability of minerals for absorption, determined largely by the diet's phytic acid content (prevents mineral absorption)
   

What about humans? Drs. Mellanby set out to see if they could use their dietary principles to cure tooth decay that was already established. They divided 62 children with cavities into three different diet groups for 6 months. Group 1 ate their normal diet plus oatmeal (rich in phytic acid). Group 2 ate their normal diet plus vitamin D. Group 3 ate a grain-free diet and took vitamin D.

In group 1, oatmeal prevented healing and encouraged new cavities, presumably due to its ability to prevent mineral absorption. In group 2, simply adding vitamin D to the diet caused most cavities to heal and fewer to form. The most striking effect was in group 3, the group eating a grain-free diet plus vitamin D, in which nearly all cavities healed and very few new cavities developed. Grains are the main source of phytic acid in the modern diet, although we can't rule out the possibility that grains were promoting tooth decay through another mechanism as well.

Dr. Mellanby was quick to point out that diet 3 contained some carbohydrate (~45% reduction) and was not low in sugar: "Although [diet 3] contained no bread, porridge or other cereals, it included a moderate amount of carbohydrates, for plenty of milk, jam, sugar, potatoes and vegetables were eaten by this group of children." This study was published in the British Medical Journal (1) and the British Dental journal. Here's Dr. Edward Mellanby again:

The hardening of carious areas that takes place in the teeth of children fed on diets of high calcifying value indicates the arrest of the active process and may result in “healing” of the infected area. As might be surmised, this phenomenon is accompanied by a laying down of a thick barrier of well-formed secondary denture... Summing up these results it will be clear that the clinical deductions made on the basis of the animal experiments have been justified, and that it is now known how to diminish the spread of caries and even to stop the active carious process in many affected teeth.

Dr. Mellanby first began publishing studies showing the reversal of cavities in humans in 1924. Why has such a major medical finding, published in high-impact peer-reviewed journals, faded into obscurity?

Dr. Weston Price also had success curing tooth decay using a similar diet. He fed underprivileged children one very nutritious meal a day and monitored their dental health. From Nutrition and Physical Degeneration (p. 290):

About four ounces of tomato juice or orange juice and a teaspoonful of a mixture of equal parts of a very high vitamin natural cod liver oil and an especially high vitamin butter was given at the beginning of the meal. They then received a bowl containing approximately a pint of a very rich vegetable and meat stew, made largely from bone marrow and fine cuts of tender meat: the meat was usually broiled separately to retain its juice and then chopped very fine and added to the bone marrow meat soup which always contained finely chopped vegetables and plenty of very yellow carrots; for the next course they had cooked fruit, with very little sweetening, and rolls made from freshly ground whole wheat, which were spread with the high-vitamin butter. The wheat for the rolls was ground fresh every day in a motor driven coffee mill. Each child was also given two glasses of fresh whole milk. The menu was varied from day to day by substituting for the meat stew, fish chowder or organs of animals.

Dr. Price provides before and after X-rays showing re-calcification of cavity-ridden teeth on this program. His intervention was not exactly the same as Drs. Mellanby, but it was similar in many ways. Both diets were high in minerals, rich in fat-soluble vitamins (including D), and low in phytic acid.

Price's diet was not grain-free, but used rolls made from freshly ground whole wheat. Freshly ground whole wheat has a high phytase (the enzyme that degrades phytic acid) activity, thus in conjunction with the long yeast rises common in Price's time, it would have broken down nearly all of its own phytic acid. This would have made it a source of minerals rather than a sink for them. He also used high-vitamin pastured butter in conjunction with cod liver oil. We now know that the vitamin K2 in pastured butter is important for bone and tooth development and maintenance. This was something that Dr. Mellanby did not understand at the time, but modern science has corroborated Price's finding that K2 is synergistic with vitamin D in promoting skeletal and dental health.

If I were to design the ultimate dietary program to heal cavities that incorporates the successes of both doctors, it would look something like this:

• Rich in animal foods, particularly full-fat pastured dairy products (if tolerated). Also meat, organs, fish, bone broths and eggs.
  
• Fermented grains only; no unfermented grains such as oatmeal, breakfast cereal, crackers, etc. No breads except true sourdough (ingredients should not list lactic acid). Or even better, no grains at all.
  
• Limited nuts; beans in moderation, only if they're soaked overnight or longer in warm water (due to the phytic acid).
  
• Starchy vegetables such as potatoes and sweet potatoes.
  
• A limited quantity of fruit (one piece per day or less), but no refined sweets.
  
• Cooked and raw vegetables.
  
• Sunlight, high-vitamin cod liver oil or vitamin D3 supplements.
  
• A generous amount of pastured butter.
• No industrially processed food.
  

This diet would maximize mineral absorption while providing abundant fat-soluble vitamins. It probably isn't necessary to follow it strictly. For example, if you eat more mineral-rich foods such as dairy and bone broths, you can probably get away with more phytic acid. Or you might be able to heal cavities eating like this for only one or two meals a day, as Dr. Price demonstrated.

The Benefits of Growing Algae in Your Water Filter

One of the factors that's often overlooked in our efforts to replicate the health of non-industrial cultures is water quality. Traditional cultures don't drink sterilized, chlorinated, fluoridated tap water. They drink from natural flowing streams and lakes, complete with their natural minerals, and... algae.

With every gulp, they ingest millions or even billions of tiny green organisms entirely missing from the modern water supply (1).

Fortunately, we can drink algae water too. As a matter of fact, millions of lazy people are doing it right now! All you have to do is buy a clear water filter, use it regularly and leave it in the sun. Over time, you'll develop your very own film of algae that will constantly shed into the water you drink. Here are some of the benefits of algae water:

• Adds oxygen to the water, increasing your energy on a cellular level!
• Probiotics in every cup
• Algae are full of vitamin K. Who needs spinach!
• Make your own biofuel

4 out of 5 scientists agree that a cup of algae water equals 3.7 servings of vegetables (2).

April fools!

Preventing Tooth Decay

Meet Sir Edward Mellanby, the discoverer of vitamin D. Along with his wife, Dr. May Mellanby, he identified dietary factors that control the formation and repair of teeth and bones. He also identified the cause of rickets (vitamin D deficiency) and the effect of phytic acid on mineral absorption. Truly a great man! This research began in the 1910s and continued through the 1940s.

What he discovered about tooth and bone formation is profound, disarmingly simple and largely forgotten. I remember going to the dentist as a child. He told me I had good teeth. I informed him that I tried to eat well and stay away from sweets. He explained to me that I had good teeth because of genetics, not my diet. I was skeptical at the time, but now I realize just how ignorant that man was.

Tooth structure is determined during growth. Well-formed teeth are highly resistant to decay while poorly-formed teeth are cavity-prone. Drs. Mellanby demonstrated this by showing a strong correlation between tooth enamel defects and cavities in British children. The following graph is drawn from several studies he compiled in the book Nutrition and Disease (1934). "Hypoplastic" refers to enamel that's poorly formed on a microscopic level.
The graph is confusing, so don't worry if you're having a hard time interpreting it. If you look at the blue bar representing children with well-formed teeth, you can see that 77% of them have no cavities, and only 7.5% have severe cavities (a "3" on the X axis). Looking at the green bar, only 6% of children with the worst enamel structure are without cavities, while 74% have severe cavities. Enamel structure is VERY strongly related to cavity prevalence.

What determines enamel structure during growth? Drs. Mellanby identified three dominant factors:

1. The mineral content of the diet
2. The fat-soluble vitamin content of the diet, chiefly vitamin D
   
3. The availability of minerals for absorption, determined largely by the diet's phytic acid content
   

Teeth and bones are a mineralized protein scaffold. Vitamin D influences the quality of the protein scaffold that's laid down. For the scaffold to mineralize, the diet has to contain enough minerals, primarily calcium and phosphorus. Vitamin D allows the digestive system to absorb the minerals, but it can only absorb them if they aren't bound by phytic acid. Phytic acid is an anti-nutrient found primarily in unfermented seeds such as grains. So the process depends on getting minerals (sufficient minerals in the diet and low phytic acid) and putting them in the right place (fat-soluble vitamins).

Optimal tooth and bone formation occurs only on a diet that is sufficient in minerals, fat-soluble vitamins, and low in phytic acid. Drs. Mellanby used dogs in their experiments, which it turns out are a good model for tooth formation in humans for a reason I'll explain later. From Nutrition and Disease:

Thus, if growing puppies are given a limited amount of separated [skim] milk together with cereals, lean meat, orange juice, and yeast (i.e., a diet containing sufficient energy value and also sufficient proteins, carbohydrates, vitamins B and C, and salts), defectively formed teeth will result. If some rich source of vitamin D be added, such as cod-liver oil or egg-yolk, the structure of the teeth will be greatly improved, while the addition of oils such as olive... leaves the teeth as badly formed as when the basal diet only is given... If, when the vitamin D intake is deficient, the cereal part of the diet is increased, or if wheat germ [high in phytic acid] replaces white flour, or, again, if oatmeal [high in phytic acid] is substituted for white flour, then the teeth tend to be worse in structure, but if, under these conditions, the calcium intake is increased, then calcification [the deposition of calcium in the teeth] is improved.

Other researchers initially disputed the Mellanbys' results because they weren't able to replicate the findings in rats. It turns out, rats produce the phytic acid-degrading enzyme phytase in their small intestine, so they can extract minerals from unfermented grains better than dogs. Humans also produce phytase, but at levels so low they don't significantly degrade phytic acid. The small intestine of rats has about 30 times the phytase activity of the human small intestine, again demonstrating that humans are not well adapted to eating grains. Our ability to extract minerals from seeds is comparable to that of dogs, which shows that the Mellanbys' results are applicable to humans.

Drs. Mellanby found that the same three factors determine bone quality in dogs as well, which I may discuss in another post.

Is there anything someone with fully formed enamel can do to prevent tooth decay? Drs. Mellanby showed (in humans this time) that not only can tooth decay be prevented by a good diet, it can be almost completely reversed even if it's already present. Dr. Weston Price used a similar method to reverse tooth decay as well. I'll discuss that in my next post.

Skin Texture, Cancer and Dietary Fat

Richard and I exchanged a series of e-mails last week in which he remarked that Thai people generally have nice skin, which is something I've also noticed in Thai immigrants to the U.S. I believe you can often tell what kind of fat a person eats by looking at their face, especially as people age or bear children.

People who eat predominantly traditional fats like butter and coconut oil usually have nice skin. It's smoother, rosier and it ages more gracefully than the skin of a person who eats industrial fats like soy and corn oil. Coconut is the predominant fat in the traditional Thai diet. Coconut fat is about 87% saturated, far more than any animal fat*. Coconut oil and butter are very low in omega-6 linoleic acid, while industrial vegetable oils and margarine contain a lot of it.

I saw a great movie last week called "The Betrayal", about a family of Lao refugees that immigrated to the U.S. in the late 1970s. The director followed the family for 23 years as they tried to carve out a life for themselves in Brooklyn. The main fats in the traditional Lao diet are lard and coconut milk. The mother of the family was a nice looking woman when she left Laos. She was thin and had great skin and teeth, despite having delivered half a dozen children at that point. After 23 years in the U.S., she was overweight and her skin was colorless and pasty. At the end of the movie, they return to Laos to visit their family there. The woman's mother was still alive. She was nearly 100 years old and looked younger than her daughter.

Well that's a pretty story, but let's hit the science. There's a mouse model of skin cancer called the Skh:HR-1 hairless mouse. When exposed to UV rays and/or topical carcinogens, these mice develop skin cancer just like humans (especially fair-skinned humans). Researchers have been studying the factors that determine their susceptibility to skin cancer, and fat is a dominant one. Specifically, their susceptibility to skin cancer is determined by the amount of linoleic acid in the diet.

In 1994, Drs. Cope and Reeve published a study using hairless mice in which they put groups of mice on two different diets (Cope, R. B. & Reeve, V. E. (1994) Photochem. Photobiol. 59: 24 S). The first diet contained 20% margarine; the second was identical but contained 20% butter. Mice eating margarine developed significantly more skin tumors when they were exposed to UV light or a combination of UV and a topical carcinogen. Researchers have known this for a long time. Here's a quote from a review published in 1987:

Nearly 50 years ago the first reports appeared that cast suspicion on lipids, or peroxidative products thereof, as being involved in the expression of actinically induced cancer. Whereas numerous studies have implicated lipids as potentiators of specific chemical-induced carcinogenesis, only recently has the involvement of these dietary constituents in photocarcinogenesis been substantiated. It has now been demonstrated that both level of dietary lipid intake and degree of lipid saturation have pronounced effects on photoinduced skin cancer, with increasing levels of unsaturated fat intake enhancing cancer expression. The level of intake of these lipids is also manifested in the level of epidermal lipid peroxidation.

Here's a quote from a study conducted in 1996:

A series of semi-purified diets containing 20% fat by weight, of increasing proportions (0, 5%, 10%, 15% or 20%) of polyunsaturated sunflower oil mixed with hydrogenated saturated cottonseed oil, was fed to groups of Skh:HR-1 hairless mice during induction and promotion of photocarcinogenesis. The photocarcinogenic response was of increasing severity as the polyunsaturated content of the mixed dietary fat was increased, whether measured as tumour incidence, tumour multiplicity, progression of benign tumours to squamous cell carcinoma, or reduced survival... These results suggest that the enhancement of photocarcinogenesis by the dietary polyunsaturated fat component is mediated by an induced predisposition to persistent immunosuppression caused by the chronic UV irradiation, and supports the evidence for an immunological role in dietary fat modulation of photocarcinogenesis in mice.

In other words, UV-induced cancer increased in proportion to the linoleic acid content of the diet, because linoleic acid suppresses the immune system's cancer-fighting ability!

It doesn't end at skin cancer. In animal models, a number of cancers are highly sensitive to the amount of linoleic acid in the diet, including breast cancer. Once again, butter beats margarine and vegetable oils. Spontaneous breast tumors develop only half as frequently in rats fed butter than in rats fed margarine or safflower oil (Yanagi, S. et al. (1989) Comparative effects of butter, margarine, safflower oil and dextrin on mammary tumorigenesis in mice and rats. In: The Pharmacological Effects of Lipids.). The development of breast tumors in rats fed carcinogens is highly dependent on the linoleic acid content of the diet. The effect plateaus around 4.4% of calories, after which additional linoleic acid has no further effect.

Conversely, omega-3 fish oil protects against skin cancer in the hairless mouse, even in large amounts. In another study, not only did fish oil protect against skin cancer, it doubled the amount of time researchers had to expose the mice to UV light to cause sunburn!

Thus, the amount of linoleic acid in the diet as well as the balance between omega-6 and omega-3 determine the susceptibility of the skin to damage from UV rays. This is a very straightforward explanation for the beautiful skin of people eating traditional fats like butter and coconut oil. It's also a straightforward explanation for the poor skin and sharply rising melanoma incidence of Western nations (source). Melanoma is the most deadly form of skin cancer. If you're dark-skinned, you're off the hook:

I believe the other factor contributing to rising melanoma incidence is sunscreen. Most sunscreens block sunburn-causing UVB rays but not melanoma-causing UVA rays. The fact that they allow you to remain in the sun for longer without burning means they increase your exposure to UVA. I've written about this before. Sunscreen also blocks vitamin D formation in the skin, a process that some researchers believe also promotes cancer. I'll end with a couple more graphs that are self-explanatory (source). "PUFA" stands for polyunsaturated faty acids, and primarily represents linoleic acid:





*Not only do Thais have clear skin, they also have clear arteries. Autopsies performed in the 1960s showed that residents of Bangkok had a low prevalence of atherosclerosis and a rate of heart attack (myocardial infarction) about 1/10 that of Americans living in Los Angeles.

More Thoughts on the Glycemic Index

In the last post, I reviewed the controlled trials on the effect of the glycemic index (GI) of carbohydrate foods on health. I concluded that there is no convincing evidence that a low GI diet is better for health than a high GI diet, and in fact the long-term trials suggest that a high GI diet may even be better for insulin sensitivity.

Despite the graphs I presented in the last post, for the "average" individual the GI of carbohydrate foods can affect the glucose and insulin response to carbohydrate foods somewhat, even in the context of an actual meal. If you compare two meals of very different GI, the low GI meal will cause less insulin secretion and cause less total blood glucose in the plasma over the course of the day (although the differences in blood glucose may not apply to all individuals).

But is that biologically significant? In other words, do those differences matter when it comes to health? I would argue probably not, and here's why: there's a difference between post-meal glucose and insulin surges and chronically elevated glucose and insulin. Chronically elevated insulin is a marker of metabolic dysfunction, while post-meal insulin surges are not (although glucose surges in excess of 140 mg/dL indicate glucose intolerance). Despite what you may hear from some sectors of the low-carbohydrate community, insulin surges do not necessarily lead to insulin resistance. Just ask a Kitavan. They get 69% of their 2,200 calories per day from high-glycemic starchy tubers and fruit (380 g carbohydrate), with not much fat to slow down digestion. Yet they have low fasting insulin, very little body fat and an undetectable incidence of diabetes, heart attack and stroke. That's despite a significant elderly population on the island.

Furthermore, in the 4-month GI intervention trial I mentioned last time, they measured something called glycated hemoglobin (HbA1c). HbA1c is a measure of the amount of blood glucose that has "stuck to" hemoglobin molecules in red blood cells. It's used to determine a person's average blood glucose concentration over the course of the past few weeks. The higher your HbA1c, the poorer your blood glucose control, the higher your likelihood of having diabetes, and the higher your cardiovascular risk. The low GI group had a statistically significant drop in their HbA1c value compared to the high GI group. But the difference was only 0.06%, a change that is biologically meaningless.

OK, let's take a step back. The goal of thinking about all this is to understand what's healthy, right? Let's take a look at how healthy cultures eat their carbohydrate foods. Cultures that rely heavily on carbohydrate generally fall into three categories: they eat cooked starchy tubers, they grind and cook their grains, or they rely on grains that become very soft when cooked. In the first category, we have Africans, South Americans, Polynesians and Melanesians (including the Kitavans). In the second, we have various Africans, Europeans (including the villagers of the Loetschental valley), Middle Easterners and South Americans. In the third category, we have Asians, Europeans (the oat-eating residents of the outer Hebrides) and South Americans (quinoa-eating Peruvians).

The pattern here is one of maximizing GI, not minimizing it. That's not because high GI foods are inherently superior, but because traditional processing techniques that maximize the digestibility of carbohydrate foods also tend to increase their GI. I believe healthy cultures around the world didn't care about the glycemic index of foods, they cared about digestibility and nutritional value.

The reason we grind grains is simple. Ground grains are digested more easily and completely (hence the higher GI).  Furthermore, ground grains are more effective than intact grains at breaking down their own phytic acid when soaked, particularly if they're allowed to ferment. This further increases their nutritional value.

The human digestive system is delicate. Cows can eat whole grass seeds and digest them using their giant four-compartment stomach that acts as a fermentation tank. Humans that eat intact grains end up donating them to the waste treatment plant. We just don't have the hardware to efficiently extract the nutrients from cooked whole rye berries, unless you're willing to chew each bite 47 times. Oats, quinoa, rice, beans and certain other starchy seeds are exceptions because they're softened sufficiently by cooking.

Grain consumption and grinding implements appear simultaneously in the archaeological record. Grinding has always been used to increase the digestibility of tough grains, even before the invention of agriculture when hunter-gatherers were gathering wild grains in the fertile crescent. Some archaeologists consider grinding implements one of the diagnostic features of a grain-based culture. Carbohydrate-based cultures have always prioritized digestibility and nutritional value over GI.

Finally, I'd like to emphasize that some people don't have a good relationship with carbohydrate. Diabetics and others with glucose intolerance should be very cautious with carbohydrate foods. The best way to know how you deal with carbohydrate is to get a blood glucose meter and use it after meals. For $70 or less, you can get a cheap meter and 50 test strips that will give you a very good idea of your glucose response to typical meals (as opposed to a glucose bomb at the doctor's office). Jenny Ruhl has a tutorial that explains the process. It's also useful to pay attention to how you feel and look with different amounts of carbohydrate in your diet.

Integrated Nutrition, Lifestyle and Health Database

Ricardo from the website Canibais e Reis has just released a fantastic resource for anyone who's interested in the relationship between nutrition, lifestyle and health. It's an excel spreadsheet that integrates information from several international sources, including:

• UN Food and Agriculture Organization Statistical Yearbook
• FAOSTAT food consumption database
• British Heart Foundation Health Statistics database
• World Health Organization Global Health Atlas

This database provides a wealth of information on 86 different countries, and even includes a macro feature that automatically plots variables. This is an empowering resource for those of us who like to do our own research and come to our own conclusions, and I thank Ricardo for his hard work.

You can read more about the database and download it here.