Excess Omega-6 Fat Damages Infants' Livers

A nurse friend of mine sent me an e-mail a few weeks ago with a very interesting observation:

On the unit I work on we get lots of babies who have "short gut syndrome" due to a variety of causes who have to be on parenteral nutrition to supplement their nutrition while their GI system grows and hopefully heals fast enough. The big problem (among many) with TPN (total parenteral nutrition) is that it destroys the liver and kids get horribly jaundiced (which also causes brain damage) and often they die of liver failure or need a liver transplant before their GI system grows enough to take them off TPN.

Boston Children's has done some amazing work showing that this is largely due to the fact that the lipids part of the TPN was a soybean based oil so they started using Omegaven instead which is a fish oil based IV lipid solution. So far the results have been amazing and reversed the damage in lots of kids livers and prevented it in those started on Omegaven at birth.

Babies born with short gut syndrome can't absorb nutrients properly due to their unusually short small intestine. They're temporarily fed intravenously (total parenteral nutrition; TPN), until their intestines can develop enough to digest food normally.

The typical TPN formula contains soybean and safflower oils as the fat, both of which are over 50% omega-6 linoleic acid. Soybean oil also contains 7% omega-3 alpha-linolenic acid. You can't get the kids started too early on a "heart-healthy" diet!

The solution was to replace the vegetable oil with fish oil, which prevents or rapidly reverses the severe liver damage caused by TPN rich in omega-6 vegetable oils. I don't think this is a great solution, but it certainly beats vegetable oil. The ideal solution would be to replace the vegetable oil with a fat that approximates the composition of breast milk: mostly monounsaturated and saturated fat, with a little bit of linoleic acid, alpha-linolenic acid and long-chain fats such as AA and DHA. You could do this pretty easily with a mix of lard and fish oil; or palm oil and fish oil; or coconut oil, olive oil and fish oil. Breast milk composition varies with diet, and the amount of linoleic acid in the breast milk of Western populations is unusually high.

Excess linoleic acid, particularly when combined with excess fructose and insufficient omega-3 fat, is toxic to the liver. Modern Western nations are experiencing an epidemic of non-alcoholic fatty liver disease (NAFLD), which animal studies indicate is probably the result of replacing animal fats with polyunsaturated vegetable oils and increasing sugar intake (see links below for more detail). Fatty liver was seen primarily in alcoholics three decades ago. An estimated 1/4 of Americans now have NAFLD. It's the number one cause of liver damage in the U.S.

Where the liver goes, the rest of the body follows.

How to Fatten Your Liver
Nonalcoholic Fatty Liver Disease
The Liver: Your Metabolic Gatekeeper
More Liver Functions

Nutrition and Infectious Disease

Dr. Edward Mellanby's book Nutrition and Disease contains a chapter titled "Nutrition and Infection". It begins:

There is general agreement among medical men that the susceptibility of mankind to many types of infection is closely related to the state of nutrition. The difficulty arises, when closer examination is given to this general proposition, as to what constitutes good and bad nutrition, and the problem is not rendered easier by recent advances in nutritional science.

Dr. Mellanby was primarily concerned with the effect of fat-soluble vitamins on infectious disease, particularly vitamins A and D. One of his earliest observations was that butter protected against pneumonia in his laboratory dogs. He eventually identified vitamin A as the primary protective factor. He found that by placing rats on a diet deficient in vitamin A, they developed numerous infectious lesions, most often in the urogenital tract, the eyes, the intestine, the middle ear and the lungs. This was prevented by adding vitamin A or cabbage (a source of beta-carotene, which the rats converted to vitamin A) to the diet. Mellanby and his colleagues subsequently dubbed vitamin A the "anti-infective vitamin".

Dr. Mellanby was unsure whether the animal results would apply to humans, due to "the difficulty in believing that diets even of poor people were as deficient in vitamin A and carotene as the experimental diets." However, their colleagues had previously noted marked differences in the infection rate of largely vegetarian African tribes versus their carnivorous counterparts. The following quote from Nutrition and Disease refers to two tribes which, by coincidence, Dr. Weston Price also described in Nutrition and Physical Degeneration:

The high incidence of bronchitis, pneumonia, tropical ulcers and phthisis among the Kikuyu tribe who live on a diet mainly of cereals as compared with the low incidence of these diseases among their neighbours the Masai who live on meat, milk and raw blood (Orr and Gilks), probably has a similar or related nutritional explanation. The differences in distribution of infective disease found by these workers in the two tribes are most impressive. Thus in the cereal-eating tribe, bronchitis and pneumonia accounted for 31 per cent of all cases of sickness, tropical ulcers for 33 per cent, and phthisis for 6 per cent. The corresponding figures for the meat, milk and raw blood tribe were 4 per cent, 3 per cent and 1 per cent.

So they set out to test the theory under controlled conditions. Their first target: puerperal sepsis. This is an infection of the uterus that occurs after childbirth. They divided 550 women into two groups: one received vitamins A and D during the last month of pregnancy, and the other received nothing. Neither group was given instructions to change diet, and neither group was given vitamins during their hospital stay. The result, quoted from Nutrition and Disease:

The morbidity rate in the puerperium using the [British Medical Association] standard was 1.1 per cent in the vitamin group and 4.7 in the control group, a difference of 3.6 per cent which is twice the standard error (1.4), and therefore statistically significant.

This experiment didn't differentiate between the effects of vitamin A and D, but it did establish that fat-soluble vitamins are important for resistance to bacterial infection. The next experiment Dr. Mellanby undertook was a more difficult one. This time, he targeted puerperal septicemia. This is a more advanced stage of puerperal sepsis, in which the infection spreads into the bloodstream. In this experiment, he treated women who had already contracted the infection. This trial was not as tightly controlled as the previous one. Here's a description of the intervention, from Nutrition and Disease:

...all patients received when possible a diet rich not only in vitamin A but also of high biological quality. This diet included much milk, eggs, green vegetables, etc., as well as the vitamin A supplement. For controls we had to use the cases treated in previous years by the same obstetricians and gynecologists as the test cases.

In the two years prior to this investigation, the mortality rate for puerperal septicemia in 18 patients was 92%. In 1929, Dr. Mellanby fed 18 patients in the same hospital his special diet, and the mortality rate was 22%. This is a remarkable treatment for an infection that was almost invariably fatal at the time.

Dr. Mellanby was a man with a lot of perspective. He was not a reductionist; he knew that a good diet is more than the sum of its parts. Here's another quote from Nutrition and Disease:

It is probable that, as in the case of vitamin D and rickets, the question is not simple and that it will ultimately be found that vitamin A works in harmony with some dietetic factors, such as milk proteins and other proteins of high biological value, to promote resistance of mucous membranes and epithelial cells to invasion by micro-organisms, while other factors such as cereals, antagonise its influence. The effect of increasing the green vegetable and reducing the cereal intake on the resistance of herbivorous animals to infection is undoubted (Glenny and Allen, Boock and Trevan) and may well indicate a reaction in which the increased carotene of the vegetable plays only a part, but an important part.

And finally, let's not forget the effect of vitamin D on infection resistance. Low vitamin D is consistently associated with a higher frequency of respiratory infections, and a controlled trial showed that vitamin D supplements significantly reduce the occurrence of flu symptoms in wintertime. Vitamins A and D are best taken together. Did someone say high-vitamin cod liver oil??

P.S.- I have to apologize, I forgot to copy down the primary literature references for this post before returning the book to the library. So for the skeptics out there, you'll either have to take my word for it, or find a copy of the book yourself.

Fructose vs. Glucose Showdown

As you've probably noticed, I believe sugar is one of the primary players in the diseases of civilization. It's one of the "big three" that I focus on: sugar, industrial vegetable oil and white flour. It's becoming increasingly clear that fructose, which constitutes half of table sugar and typically 55% of high-fructose corn syrup, is the problem. A reader pointed me to a brand new study (free full text!), published in the Journal of Clinical Investigation, comparing the effect of ingesting glucose vs. fructose.

The investigators divided 32 overweight men and women into two groups, and instructed each group to drink a sweetened beverage three times per day. They were told not to eat any other sugar. The drinks were designed to provide 25% of the participants' caloric intake. That might sound like a lot, but the average American actually gets about 25% of her calories from sugar! That's the average, so there are people who get a third or more of their calories from sugar. In one group, the drinks were sweetened with glucose, while in the other group they were sweetened with fructose.

After ten weeks, both groups had gained about three pounds. But they didn't gain it in the same place. The fructose group gained a disproportionate amount of visceral fat, which increased by 14%! Visceral fat is the most dangerous type; it's associated with and contributes to chronic disease, particularly metabolic syndrome, the quintessential modern metabolic disorder (see the end of the post for more information and references). You can bet their livers were fattening up too.

The good news doesn't end there. The fructose group saw a worsening of blood glucose control and insulin sensitivity. They also saw an increase in small, dense LDL particles and oxidized LDL, both factors that associate strongly with the risk of heart attack and may in fact contribute to it. Liver synthesis of fat after meals increased by 75%. If you look at table 4, it's clear that the fructose group experienced a major metabolic shift, and the glucose group didn't. Practically every parameter they measured in the fructose group changed significantly over the course of the 9 weeks. It's incredible.

25% of calories from fructose is a lot. The average American gets about 13%. But plenty of people exceed that, perhaps going up to 20% or more. Furthermore, the intervention was only 10 weeks. What would a lower intake of fructose, say 10% of calories, do to a person over a lifetime? Nothing good, in my opinion. Avoiding refined sugar is one of the best things you can do for your health.

U.S. Fructose Consumption Trends
Peripheral vs. Ectopic Fat
Visceral Fat
Visceral Fat and Dementia
How to Give a Rat Metabolic Syndrome
How to Fatten Your Liver

Cordain on Saturated Fat

I recently signed up for Dr. Loren Cordain's Paleo Diet newsletter, and I just received my first update. For those of you who aren't familiar with him, Dr. Cordain is a researcher at Colorado State University who studies the effects of hunter-gatherer and modern diets on health. He's made a number of important contributions to our understanding of nutrition and health. He's in my "Nutrition Hall of Fame" on the right sidebar.

His update was about saturated fat. In the past, I've disagreed with Dr. Cordain on this issue, because I thought he felt that saturated fat contributes to the risk of heart attack (although he never described it as a dominant factor). He has recommended trimming the fat off meats and using canola oil rather than just eating the fat. I don't know if I had misunderstood his stance, or if he's had a change of heart, but his current position seems quite reasonable to me. Here are a few brief quotes:

By examining the amounts of saturated fats in pre-agricultural hominin diets, an evolutionary baseline can be established for the normal range and limits of saturated fats that would have conditioned the human genome. While these diets varied due to geography, climate, etc., there is evidence that all hominin species were omnivorous. Thus, dietary saturated fats would have always been present in hominin diets.

There is also evidence that the hominin species that eventually led to Homo began to include more animal food in their diet approximately 2.6 million years ago. Clear evidence shows tool usage to butcher and disarticulate carcasses...

This data suggests that the normal dietary intake of saturated fatty acids that conditioned our species genome likely fell between 10 to 15% of total energy, and that values lower than 10% or higher than 15% would have been the exception.

And the conclusion:

Consequently, population-wide recommendations to lower dietary saturated fats below 10% to reduce the risk of CAD have little or no evolutionary foundation in pre-agricultural Homo sapiens... So we do not need to restrict ourselves to only tuna and turkey breast, avoiding every last gram of saturated fat.

AMEN, brother. I'd like to point out that the average American eats about 11% of his calories as saturated fat (down from 13% in the 1970s), on the low side of what Cordain considers normal for Homo sapiens. This is from the NHANES nutrition surveys.

The effect of a food on an animal's health has everything to do with what that animal is adapted to eating. Feeding a rabbit cholesterol gives it high blood cholesterol and atherosclerosis, but you can't give a dog high cholesterol or atherosclerosis by feeding it cholesterol, unless you kill its thyroid first. Feeding studies in Masai men showed that replacing their fatty, cholesterol-rich milk and blood diet with a cholesterol-free refined diet low in saturated fat caused their total cholesterol and body weight to increase rapidly. Adding purified cholesterol to the cholesterol-free diet did not affect their blood cholesterol concentration. Feeding cholesterol-rich eggs also has a negligible effect on blood cholesterol in most people.

I do still have a slight difference of opinion with Cordain on the saturated fat issue. While I think his numbers for pre-agricultural saturated fat intake are reasonable, his range is probably too narrow. Non-agricultural diets are so variable, I would expect the range to be more like 5 to 30% saturated fat. 5% would represent diets low in fat such as certain Australian Aboriginal diets, and 30% would represent the intake of Northern hunter-gatherers relying heavily on ruminants in fall and winter. During this time, ruminants store most of their fat subcutaneously, and their subcutaneous fat is roughly half saturated. Given that such a wide range of saturated fat intakes are part of our species' ecological niche, it follows that saturated fat is unlikely to be an important determinant of health in the context of an otherwise healthy lifestyle.

A Testament to the Flexibility of the Human Mind

I'm sure you've heard that humans have five senses: sight, hearing, touch, taste and smell. But we actually have far more senses than that. The canonical list doesn't include equilibrioception-- our sense of balance-- the result of fluid sloshing around in the inner ear. It also doesn't include proprioception, the ability to detect the position of our limbs using nerve endings in our tendons and muscles.

Furthermore, the sense of touch is actually several different senses, each detected and transmitted by its own special type of neuron. The sense of touch includes vibration sense, pressure sense, heat sense, cold sense and pain sense. The sense of smell can be divided into roughly 400 senses in humans, each one tuned in to a different class of airborne molecules. Vision can be divided into cells maximally responsive to four different wavelengths of light. I could go on but the rest are less exciting.

This brings me to what I really want to write about, the development (or perhaps refinement) of a new human sense: echolocation. Echolocation is the ability to gather sensory information about your surroundings by bouncing sounds off of objects and listening to the echo that returns. It's what bats use to hunt in the dark, and dolphins use to navigate muddy water and find food under the sand. There are a number of blind people who have developed the ability to use clicking sounds to "see" their surroundings, and it's remarkably effective. This represents a new use of the human mind, or at least a refinement of a rudimentary sense. Here are a few links if you'd like to watch/read more about it:

Human echolocation- Wikipedia
Daniel Kish- You Tube
The boy who sees without eyes- You Tube

Images of Tooth Decay Healing due to an Improved Diet

This one's for the skeptics out there. As I mentioned in my previous post, Drs. Edward and May Mellanby and Dr. Weston Price reported that under the right circumstances, tooth decay can be reversed by proper nutrition. Here are images taken from the book Nutrition and Disease, by Dr. Mellanby, showing the re-calcification of decayed human teeth due to the growth of tertiary dentin (formerly known as secondary dentin). These are sections (slices) of teeth that have been treated with a chemical that darkens decayed areas. They represent four different teeth at different stages of decay reversal. Click on the image for a larger view:


Here's the text that accompanies the figure:

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. Illustrations of this healing process can be seen in Figs. 21 (b), (c) and (d). 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.

The following reference contains a summary of Dr. May Mellanby's experiments on healing tooth decay in children using diet: Mellanby, M. et al. British Medical Journal. Issue 1, page 507. 1932. The diet they used was typically a combination of some source of vitamin D (cod liver oil or irradiated ergosterol), plus liberal full-fat dairy, meats, eggs, vegetables, potatoes and grains low in phytic acid such as white bread. The most effective version of his diet, however, did not include grains.

In the book Nutrition and Physical Degeneration, Dr. Price provides X-rays showing the re-calcification of a mouth full of cavities using a similar diet.

Modern Diet-Health Epidemiology: a Self-Fulfilling Prophecy? Part II

Certain ideas about diet and health, for better or for worse, have worked their way deeply into the American psyche in the last few decades. We're constantly advised by health authorities, the news media, food advertisements, our doctors and our friends to eat less saturated fat, red meat and sugar, and more fruit, vegetables and whole grains. There is some dissent of course, but this has been the mainstream message for roughly four decades. And people are listening. We've replaced animal fats with unsaturated vegetable oils, red meat with poultry, whole milk with low-fat milk, and we're eating more fruit and vegetables than ever before. Here are two graphs of U.S. Department of Agriculture data to illustrate the point:Whole grains are a very instructive case. Dr. Dennis Burkitt popularized the idea that fiber is good for health. He spent a number of years in eastern Africa, where he observed that natives on their traditional high-grain-fiber diets were free of many modern degenerative conditions, particularly those involving the digestive system. He found that as these cultures began to rely on Western foods such as white flour and sugar, their health declined dramatically. This is the same observation Dr. Weston Price made, however the two men interpreted their findings differently. Price attributed the effect to a loss of micronutrients, while Burkitt attributed it to the loss of fiber.

There are a number of observational studies that have examined the relationship between whole grain intake and health. The massive Iowa Women's Health Study, for example, showed that women with a high intake of grain fiber had a 17% lower risk of death from all causes combined. In the same group, women in the top quintile (top 20%) of whole grain consumption had a 30% lower risk of heart attack than women in the lowest quintile. These two papers were published in 2000 and 1998. Here's where it starts to get interesting. From the second paper:

Higher whole-grain intake was associated with having more education, a lower body mass index and waist-to-hip ratio [and] being a non-smoker, doing more regular physical activity, and using vitamin supplements and hormone replacement therapy.

Do whole grains prevent smoking too? An alternative explanation is that the women who were eating whole grains were all-around more conscientious and concerned about their health than those eating refined grains. And why not? They "knew" from mainstream diet advice that whole grains are healthier than refined grains. When is the last time you saw someone smoking a cigarette while eating whole grain muesli with skim milk and half a grapefruit for breakfast? Is it easier to imagine someone smoking while eating a donut and sweetened coffee? Women who eat whole grains, on average, are those that care about their health and adopt patterns that they perceive as healthy throughout their lives. This includes behaviors large and small, both measurable and unmeasurable. The investigators factored smoking into their model, but you can't factor in things you didn't measure or don't understand.

Maybe it will come as no surprise, then, that the only controlled trial that has ever evaluated the effect of increasing grain fiber on all-cause mortality showed a trend toward increased mortality in the group that doubled its grain fiber intake. Here's the graph of survival in the two groups. This was the Diet and Reinfarction Trial. It's important to mention that the fiber group probably increased its grain fiber haphazardly, using bran and unfermented grains, rather than the traditional processing techniques of healthy grain-based cultures Burkitt described.

Here's the theory. When the public decides that a particular behavior is healthy, at that point it becomes difficult to accurately measure its impact on health using observational studies. This is due to the fact that healthy, conscientious people tend to gravitate toward the recommendation. If a theory manages to become implanted early on, it will become a self-fulfilling prophecy as healthy, conscientious people adopt the behavior and are detected by subsequent observational studies. People who don't care about their health or aren't motivated enough to make a change will keep living how they used to, and that will also be detected.
You can adjust for some of these factors if you measure them. Researchers commonly adjust for age, gender, smoking, exercise and sometimes other factors when they're trying to nail down the effect of a particular factor on health. But you can't measure all the little things that accompany a health-conscious lifestyle. Do the participants take the stairs or the elevator? Do they take supplements, and if so, which ones? How much sunlight do they get? Do they have positive relationships with their friends and family? How often do they shave (kidding)? What is the quality of the foods they buy? How often do they visit the doctor, and how often do they follow her advice? I believe there are too many confounds to measure and correct for. In my opinion, this means that observational data gathered from populations that already have opinions about the factor you're trying to study may tend to reinforce prevailing notions regardless of their accuracy.

This brings us to the recent study on meat intake and mortality. It was a massive observational study that followed the diet and health of 617,119 elderly Americans for 10 years. Researchers found that the highest quintile of red meat intake was at an elevated risk of cancer and cardiovascular disease, and had an overall risk of dying about 1/3 greater than those in the lowest quintile. That's a pretty somber finding for those of us who love a juicy steak. But let's look at a few of the things that came along with red meat intake. I'm going to post a few graphs of factors that associated with red meat. They're organized by ascending quintiles of red meat intake; in other words, the people eating the least (left) through the most (right) red meat.
As compared to men eating the least red meat, men eating the most were three times more likely to smoke, half as likely to exercise regularly, and 22% less likely to take vitamin supplements! These are clearly people who are less concerned about their health in general. The investigators adjusted their model for a number of confounds: education, marital status, family history of cancer, race, body mass index, smoking history, exercise, alcohol intake, vitamin supplementation, fruit and vegetable intake, and hormone replacement therapy. This adjustment weakened but did not eliminate the association between red meat intake and mortality.
But again, you can't adjust for variables you don't measure. How about vitamin D status? Sugar intake? Quality and frequency of doctor's visits? Mental health? Dental health? Quality of food? There's no way to measure all the little things a health-conscious person will do to take care of himself. These unmeasured (and sometimes unmeasurable) factors can add up to have a major impact on health. So in the end, what are these studies really measuring? The association between diet and health, or the association between a health-conscious lifestyle and health? There's no way to know without a controlled trial. I rest my case, ladies and gents.
Here are a few other critiques of the study that are worth reading. Chris Masterjohn points out that the investigators' method of measuring meat intake was stunningly inaccurate, and they may have been measuring wishful thinking more than meat itself. Dr. Michael Eades points out that two other studies appeared at the same time, without fanfare, that contradicted the study's findings. And Jenny Ruhl discusses the implications of the bizarre finding that red meat intake also associates with the risk of accidental death.

Modern Diet-Health Epidemiology: a Self-Fulfilling Prophecy? Part I

Epidemiology is the study of population statistics to learn about health. It can provide simple information such as the prevalence of hepatitis C in a particular region, or it can provide more complex information such as the association between dietary patterns and gout. It has brought us many great things, from its roots in understanding the transmission of communicable diseases, to the identification of smoking as the probable cause of lung cancer.

Observational studies are a mainstay of epidemiology. In observational studies, investigators gather data passively rather than manipulating variables. For example, if you want to know if people who wear tight shoes develop bunions, you would find a group of people who wear tight shoes and one that doesn't. You would try your best to make sure the groups are the same in every way besides shoe tightness: age, gender, weight, etc. Then you would follow them for 10 years to see how many people in each group develop bunions. You would then know whether or not wearing tight shoes is associated with bunions.

Observational data can never tell us that one thing caused another, only that the two are associated. The tight shoes may not have caused the bunions; they may simply have been associated with a third factor that was the true cause. For example, maybe people who wear tight shoes also tend to eat corn flakes, and corn flakes are the real cause of bunions. Or perhaps bunions actually cause people to wear tight shoes, rather than the reverse. Observational data can't resolve these questions definitively.

To establish causality, you have to do a controlled trial. In the case of our example, we would select 2,000 people and assign them randomly to two groups of 1,000. One group would wear tight shoes while the other would wear roomy shoes. After 10 years, we would see how many people developed bunions in each group. If the tight shoe group had more bunions, we could rightly say that tight shoes cause bunions. The reason this works is the randomization process (ideally) eliminates all differences between the groups except for the one you're trying to study. You should have the same number of corn flake eaters in each group if the randomization process worked correctly.

A less convincing but still worthwhile alternative would be to put tight and loose shoes on mice to see if they develop bunions. That's what researchers did in the case of the tobacco-lung cancer link. Controlled studies in animals reinforced the strong suggestion from epidemiological studies that smoking increases the risk of lung cancer.

Finally, another factor in determining the likelihood of associations representing causation is plausibility. In other words, can you imagine a way in which one factor might cause another or is the idea ridiculous? For example, did you know that shaving infrequently is associated with a 30% increase in cardiovascular mortality and a 68% increase in stroke incidence in British men? That's a better association than you get with some blood lipid markers and most dietary factors! It turns out:

The one fifth (n = 521, 21.4%) of men who shaved less frequently than daily were shorter, were less likely to be married, had a lower frequency of orgasm, and were more likely to smoke, to have angina, and to work in manual occupations than other men.

So what actually caused the increase in disease incidence? That's where plausibility comes in. I think we can rule out a direct effect of shaving on heart attacks and stroke. The authors agree:

The association between infrequent shaving and all-cause and cardiovascular disease mortality is probably due to confounding by smoking and social factors, but a small hormonal effect may exist. The relation with stroke events remains unexplained by smoking or social factors.

In other words, they don't believe shaving influences heart attack and stroke directly, but none of the factors they measured explain the association. This implies that there are other factors they didn't measure that are the real cause of the increase. This is a critical point! You can't determine the impact of factors you didn't measure! And you can't measure everything. You just measure the factors you think are most likely to be important and hope the data make sense.

This leads us to another important point. Investigators can use math to estimate the relative contribution of different factors to an association. For example, imagine the real cause of the increased stroke incidence in the example above was donut intake, and it just so happens that donut lovers also tend to shave less often. Now imagine the investigators measured donut intake. They can then mathematically adjust the association between shaving and stroke to subtract out the contribution of donuts. If no association remains, then this suggests (but does not prove) that the association between shaving and stroke was entirely due to shaving's association with donuts. But the more math you apply, the further you get from the original data. Complex mathematical manipulation of observational data requires certain assumptions, and while it is useful for extracting more information from the dataset, it should be viewed with caution in my opinion.

Of course, you can't adjust for things you didn't measure, as the study I cited above demonstrates. If factors you didn't measure are influencing your association, you may be left thinking you're looking at a causal relationship when in fact your association is just a proxy for something else. This is a major pitfall when you're doing studies in the diet-health field, because so many lifestyle factors travel together. For example, shaving less travels with being unmarried and smoking more. Judging by the pattern, it also probably associates with lower income, a poorer diet, less frequent doctor visits, and many other potentially negative things.

If the investigators had been dense, they may have decided that shaving frequently actually prevents stroke, simply because none of the other factors they measured could account for the association. Then they would be puzzled when controlled trials show that shaving doesn't actually influence the risk of stroke, and shaving mice doesn't either. They would have to admit at that point that they had been tricked by a spurious association. Or stubbornly cling to their theory and defend it with tortuous logic and by selectively citing the evidence. This happens sometimes.

These are the pitfalls we have to keep in mind when interpreting epidemiology, especially as it pertains to something as complex as the relationship between diet and health. In the next post, I'll get to the meat of my argument: that modern diet-health epidemiology is a self-fulfilling prophecy and a rather unreliable way to detect causal relationships.

Dental Anecdotes

Here are a few anecdotes gleaned from past comments that describe improvements in oral health due to a change in diet. Please feel free to add your own (positive or negative) experience to the comments. I may add it to the post.

Stan: My teeth stopped decaying and some breakage (broken tooth due to mechanical damage, 5 years ago) begun sealing itself with new enamel on my high animal fat, low carb diet of the last 10 years. I still have all my teeth including wisdom teeth. My teeth no longer develop plaque/scale and thus no need to descale, and I no longer develop cold sores on my gums. I haven't been to a dentist since 1999 (I am 53). [From another comment] I can fully confirm the astounding effect of a diet very high in animal produce and low in plants, on my teeth. My tooth decay has totally stopped! I wrote about that before but it is worth repeating: - my teeth would not decay even if mechanically damaged, broken in half etc. The broken exposed parts of a tooth, even if the core is open, just seals itself over time.

Dave: Our family has had similar experiences. In particular, my daughter had a poorly formed molar (she was a spring baby, before we started Vitamin D, hmmmm). The tooth had quite a large crater in it. I put her on D3 and cod liver oil/butter oil. We finally got a dentist she'd cooperate with enough for X-rays. The result was exactly as described above: a thick layer of dentin had formed. The dentist was thoroughly puzzled, which I enjoyed immensely :-)

Arnoud: For years my dentist has been insisting on more frequent and more aggressive cleaning techniques.... to no avail. Last year I started Vitamin D supplementation, and a more Paleo style of diet, and the 'chronic' inflammation of my gums resolved themselves within days, literally. My dentist claims it is a coincidence. I think not!

Martin: Once I changed my diet to one close to what is listed in this entry, and added a vitamin D3 supplement, my dental health greatly improved. No more cavities, and beyond that, no more rapid build-up of dental plaque. To prevent gum problems, I used to have to get my teeth cleaned four times a year, now, once a year is enough, and it seems to me, even that might not be necessary.

Thresshold: I am a cavity-every-six-months person, who arrested decay for 3 years by going on a Protein Power-like diet. No limit on non-starchy veggies, lots of meat-- turkey, beef --lots of nuts, olive oil, egg a day. No grains. Very little fruit, no sugar. Plenty of supplemented vitamin A and D, E, C, Bs, some dolomite.

Jeff: I just had a dentist visit, first in almost 3 years. No cavities for the first time in a while. Your advice and a Paleo diet are the reason, in my mind.

Dr. Dan: Before paleo I had bleeding gums and sore teeth. Now that I have been on it I have not had them and my flatmate just commented how white my teeth are looking.

Cheeseslave: I have also eliminated cavities since I changed the way I eat. I avoid all phytic acid (I try to only eat sprouted bread or naturally fermented sourdough) and I soak or sprout all my grains, legumes, nuts and seeds. I also take cod liver oil, and eat a nutrient-dense diet consisting of mostly meat and dairy.

Dr. B. G.: Myself, I had periodontal disease (esp immed after pregnancy and lactation -- wonder W-H-Y ??!) however at the last check up -- I have no more pockets of '5' and am released to come in only 2x annually instead of all the extra (painful) de-planing and cleanings. This was improved by: vitamin A, vitamin D 5000 IU every am, high dose fish oil, flaxseed and egg yolks and saturated fats and some K2 supplements. [From another comment] I have to admit -- my dental problems reversed prior to total Paleo eating (eg, wheat-free). On vitamin D and fish oil alone my cavities sealed. In fact I had gone back to see the DDS but he couldn't find one tiny 'sticky' spot. When he decided to fill it irregardless (and I was an idiot to not walk out b/c who knew that cavities could heal/seal...on their own??), then I had to leave him. At that point, the dental hygienist had already let me return to a 'normal' insured 2 cleanings/yr schedule, instead of the $$ 4/year (where 2 were out-of-pocket). With going 100% wheat-free, vits ADEK and adding a little (fresh highquality) flaxseed oil, my gums are super healthy and no throbbing at all for the last 9mos!

Brock: When I went to my dentist for the first time in a while last September I was told I had six cavities. My dentist told me to schedule to get them filled in, but I never did. I just had the intuitive feeling that the human body ought to be able to heal itself, and that for some reason my dentist just didn't know how. So, I started Googling. My search lead me here and to the Weston Price Foundation. I bought Dr. Price's book and changed by diet months ago. I eat mostly paleo but mainly just focus on avoiding wheat, corn, sugar and n6 fats. I supplement with Vitamins A, C, D, E and K2. Long story short, my six cavities have closed up and my teeth have noticeably improved in color and "feel". Swelling in my gums is down. I can often go for weeks now without brushing my teeth without any noticeable side effects. It's great.

Andrew S.:I had a lot of cavities growing up, and as a young adult. I started up a new company, didn't have health insurance, and didn't go to the dentist in a while -- and started eating whole, natural foods, with a bit of supplementation (mostly cod liver oil). I was surprised when I visited the dentist for the first time in years to not have any decay.

Robert Andrew Brown: I too have gone from regular cavities, indifferent gum health, sensitive teeth, and a host of dental work to prove it, to none since balancing the Omega 3s and 6s, and regular 'industrial' cod liver oil. Small carries that were sensitive and on the list for restorative work have re mineralised and skinned over but not refilled. I have only recently started seriously increasing vitamin D and reintroducing grass fed butter.

Wow

Last Thursday, the post "Reversing Tooth Decay" made it to the front page of Reddit, a news aggregator site. I ended up getting 46,429 hits that day, and another 8,646 the next day. I normally hover between 1,500 and 3,000.

It was a wild ride. I'd like to send out a big thanks to whoever posted the article to Reddit, and everyone who voted for it. I appreciate you helping to spread the message.

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 calci�fying 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!