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.