Malocclusion: Disease of Civilization, Part VIII

Three Case Studies in Occlusion

In this post, I'll review three cultures with different degrees of malocclusion over time, and try to explain how the factors I've discussed may have played a role.

The Xavante of Simoes Lopes

In 1966, Dr. Jerry D. Niswander published a paper titled "The Oral Status of the Xavantes of Simoes Lopes", describing the dental health and occlusion of 166 Brazilian hunter-gatherers from the Xavante tribe (free full text). This tribe was living predominantly according to tradition, although they had begun trading with the post at Simoes Lopes for some foods. They made little effort to clean their teeth. They were mostly but not entirely free of dental cavities:

Approximately 33% of the Xavantes at Simoes Lopes were caries free. Neel et al. (1964) noted almost complete absence of dental caries in the Xavante village at Sao Domingos. The difference in the two villages may at least in part be accounted for by the fact that, for some five years, the Simoes Lopes Xavante have had access to sugar cane, whereas none was grown at Sao Domingos. It would appear that, although these Xavantes still enjoy relative freedom from dental caries, this advantage is disappearing after only six years of permanent contact with a post of the Indian Protective Service.

The most striking thing about these data is the occlusion of the Xavante. 95 percent had ideal occlusion. The remaining 5 percent had nothing more than a mild crowding of the incisors (front teeth). Niswander didn't observe a single case of underbite or overbite. This would have been truly exceptional in an industrial population. Niswander continues:

Characteristically, the Xavante adults exhibited broad dental arches, almost perfectly aligned teeth, end-to-end bite, and extensive dental attrition. At 18-20 years of age, the teeth were so worn as to almost totally obliterate the cusp patterns, leaving flat chewing surfaces.

The Xavante were clearly hard on their teeth, and their predominantly hunter-gatherer lifestyle demanded it. They practiced a bit of "rudimentary agriculture" of corn, beans and squash, which would sustain them for a short period of the year devoted to ceremonies. Dr. James V. Neel describes their diet (free full text):

Despite a rudimentary agriculture, the Xavante depend very heavily on the wild products which they gather. They eat numerous varieties of roots in large quantities, which provide a nourishing, if starchy, diet. These roots are available all year but are particularly important in the Xavante diet from April to June in the first half of the dry season when there are no more fruits. The maize harvest does not last long and is usually saved for a period of ceremonies. Until the second harvest of beans and pumpkins, the Xavante subsist largely on roots and palmito (Chamacrops sp.), their year-round staples.

From late August until mid-February, there are also plenty of nuts and fruits available. The earliest and most important in their diet is the carob or ceretona (Ceretona sp.), sometimes known as St. John's bread. Later come the fruits of the buriti palm (Mauritia sp.) and the piqui (Caryocar sp.). These are the basis of the food supply throughout the rainy season. Other fruits, such as mangoes, genipapo (Genipa americana), and a number of still unidentified varieties are also available.

The casual observer could easily be misled into thinking that the Xavante "live on meat." Certainly they talk a great deal about meat, which is the most highly esteemed food among them, in some respects the only commodity which they really consider "food" at all... They do not eat meat every day and may go without meat for several days at a stretch, but the gathered products of the region are always available for consumption in the community.

Recently, the Xavante have begun to eat large quantities of fish.

The Xavante are an example of humans living an ancestral lifestyle, and their occlusion shows it. They have the best occlusion of any living population I've encountered so far. Here's why I think that's the case:

• A nutrient-rich, whole foods diet, presumably including organs.
  
• On-demand breast feeding for two or more years.
• No bottle-feeding or modern pacifiers.
• Tough foods on a regular basis.
  

I don't have any information on how the Xavante have changed over time, but Niswander did present data on another nearby (and genetically similar) tribe called the Bakairi that had been using a substantial amount of modern foods for some time. The Bakairi, living right next to the Xavante but eating modern foods from the trading post, had 9 times more malocclusion and nearly 10 times more cavities than the Xavante. Here's what Niswander had to say:

Severe abrasion was not apparent among the Bakairi, and the dental arches did not appear as broad and massive as in the Xavantes. Dental caries and malocclusion were strikingly more prevalent; and, although not recorded systematically, the Bakairi also showed considerably more periodontal disease. If it can be assumed that the Bakairi once enjoyed a freedom from dental disease and malocclusion equal to that now exhibited by the Xavantes, the available data suggest that the changes in occlusal patterns as well as caries and periodontal disease have been too rapid to be accounted for by an hypothesis involving relaxed [genetic] selection.

The Masai of Kenya

The Masai are traditionally a pastoral people who live almost exclusively from their cattle. In 1945, and again in 1952, Dr. J. Schwartz examined the teeth of 408 and 273 Masai, respectively (#1 free full text; #2 ref). In the first study, he found that 8 percent of Masai showed some form of malocclusion, while in the second study, only 0.4 percent of Masai were maloccluded. Although we don't know what his precise criteria were for diagnosing malocclusion, these are still very low numbers.

In both studies, 4 percent of Masai had cavities. Between the two studies, Schwartz found 67 cavities in 21,792 teeth, or 0.3 percent of teeth affected. This is almost exactly what Dr. Weston Price found when he visited them in 1935. From Nutrition and Physical Degeneration, page 138:

In the Masai tribe, a study of 2,516 teeth in eighty-eight individuals distributed through several widely separated manyatas showed only four individuals with caries. These had a total of ten carious teeth, or only 0.4 per cent of the teeth attacked by tooth decay.

Dr. Schwartz describes their diet:

The principal food of the Masai is milk, meat and blood, the latter obtained by bleeding their cattle... The Masai have ample means with which to get maize meal and fresh vegetables but these foodstuffs are known only to those who work in town. It is impossible to induce a Masai to plant their own maize or vegetables near their huts.

This is essentially the same description Price gave during his visit. The Masai were not hunter-gatherers, but their traditional lifestyle was close enough to allow good occlusion. Here's why I think the Masai had good occlusion:

• A nutrient-dense diet rich in protein and fat-soluble vitamins from pastured dairy.
• On-demand breast feeding for two or more years.
• No bottle feeding or modern pacifiers.
  

The one factor they lack is tough food. Their diet, composed mainly of milk and blood, is predominantly liquid. Although I think food toughness is a factor, this shows that good occlusion is not entirely dependent on tough food.

Sadly, the lifestyle and occlusion of the Masai has changed in the intervening decades. A paper from 1992 described their modern diet:

The main articles of diet were white maize, [presumably heavily sweetened] tea, milk, [white] rice, and beans. Traditional items were rarely eaten... Milk... was not mentioned by 30% of mothers.

A paper from 1993 described the occlusion of 235 young Masai attending rural and peri-urban schools. Nearly all showed some degree of malocclusion, with open bite alone affecting 18 percent.

Rural Caucasians in Kentucky

It's always difficult to find examples of Caucasian populations living traditional lifestyles, because most Caucasian populations adopted the industrial lifestyle long ago. That's why I was grateful to find a study by Dr. Robert S. Corruccini, published in 1981, titled "Occlusal Variation in a Rural Kentucky Community" (ref).

This study examined a group of isolated Caucasians living in the Mammoth Cave region of Kentucky, USA. Corruccini arrived during a time of transition between traditional and modern foodways. He describes the traditional lifestyle as follows:

Much of the traditional way of life of these people (all white) has been maintained, but two major changes have been the movement of industry and mechanized farming into the area in the last 25 years. Traditionally, tobacco (the only cash crop), gardens, and orchards were grown by each family. Apples, pears, cherries, plums, peaches, potatoes, corn, green beans, peas, squash, peppers, cucumbers, and onions were grown for consumption, and fruits and nuts, grapes, and teas were gathered by individuals. In the diet of these people, dried pork and fried [presumably in lard], thick-crust cornbread (which were important winter staples) provided consistently stressful chewing. Hunting is still very common in the area.

Although it isn't mentioned in the paper, this group, like nearly all traditionally-living populations, probably did not waste the organs or bones of the animals it ate. Altogether, it appears to be an excellent and varied diet, based on whole foods, and containing all the elements necessary for good occlusion and overall health.

The older generation of this population has the best occlusion of any Caucasian population I've ever seen, rivaling some hunter-gatherer groups. This shows that Caucasians are not genetically doomed to malocclusion. The younger generation, living on more modern foods, shows very poor occlusion, among the worst I've seen. They also show narrowed arches, a characteristic feature of deteriorating occlusion. One generation is all it takes. Corruccini found that a higher malocclusion score was associated with softer, more industrial foods.

Here are the reasons I believe this group of Caucasians in Kentucky had good occlusion:

• A nutrient-rich, whole foods diet, presumably including organs.
  
• Prolonged breast feeding.
• No bottle-feeding or modern pacifiers.
• Tough foods on a regular basis.
  

Common Ground

I hope you can see that populations with excellent teeth do certain things in common, and that straying from those principles puts the next generation at a high risk of malocclusion. Malocclusion is a serious problem that has major implications for health, well-being and finances. In the next post, I'll give a simplified summary of everything I've covered in this series. Then it's back to our regularly scheduled programming.

The Diet-Heart Hypothesis: Stuck at the Starting Gate

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

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because there really isn't much evidence to debunk in humans. As far as I can tell, most diet-health researchers don't take this theory seriously anymore because the evidence has simply failed to materialize. Dr. Walter Willett doesn't believe it, and even Dr. Ancel Keys didn't believe it. Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the most concentrated source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 (click for larger image): The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not raise serum cholesterol in the long term, because humans are adapted to eating cholesterol. We simply adjust our own cholesterol metabolism to compensate when the amount in the diet increases, like dogs. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology.

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

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

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

I recently read a 2003 study that addresses this point directly. Muller et al. (free full text) compared the effects of three controlled diets on the blood cholesterol of 25 healthy women. The diets were:

1. High in saturated fat from coconut, low in LA
2. Same as #1, with half the saturated fat replaced by carbohydrate
3. Low in saturated fat, high in LA, with the same total fat as in #1
   

The diets were fed to the whole group for three week periods. Investigators found that diet #3 lowered cholesterol and LDL relative to diets #1 and #2. The total cholesterol of women on diets #1 and #2 were not statistically different (p= 0.09), and their LDL was virtually identical. Thus, a very large difference in saturated fat intake didn't affect total cholesterol or LDL when it was replaced by carbohydrate, but it did when it was replaced by LA. The most straightforward explanation is that LA lowers cholesterol and LDL, but saturated fat has little or no effect on either. From the discussion section:

The most important finding of this study was that lowering total saturated fat in the form of coconut oil, from 22.7 to 10.5 E% without change in the P/S ratio [polyunsaturated to saturated ratio], did not lower total or LDL cholesterol, but significantly reduced HDL cholesterol.

Among the heaps of poorly conducted studies, I was able to find one apparently well-controlled counterexample: Arterioscler. Thromb. Vasc. Biol. 18:441. 1988. In this 8-week study, increasing saturated fat (at the expense of carbohydrate and with LA constant) increased total cholesterol and LDL, while also increasing HDL, and decreasing Lp(a) and triglycerides. Decreasing saturated fat from 15% to 6% of calories (drastic), reduced total cholesterol by 9% and LDL by 11% (calculated by the Friedewald equation). The variation between trials may have to do with the specific saturated fatty acids used in each trial, their duration, or some other unknown confounder.

Reading through the short-term controlled trials, I was struck by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and poor study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and repeatably demonstrable. It clearly is not, so I'm left wondering why diet-health authorities are so certain of themselves on this point.

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

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Disease by Dr. Harumi Okuyama et al.): What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). If we can't even find a consistent association between dietary saturated fat and blood cholesterol in observational studies, how can we claim that saturated fat is a dominant influence on blood cholesterol?

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not at all the case. The Masai traditionally get almost 2/3 of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man? Junk food.

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. I think fructose (which makes up 50% of sucrose-- or table sugar-- and 55% of high-fructose corn syrup) is a more logical explanation for the high serum cholesterol and LDL of modern affluent societies, particularly considering the results of this study.

The inevitable conclusion is that if saturated fat influences total cholesterol or LDL concentration at all, the effect is modest and is dwarfed by other factors.

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.

Saturated Fat and Health: a Brief Literature Review, Part I

Even years ago, when I watched my saturated fat intake, I always had a certain level of cognitive dissonance about it. I knew that healthy non-industrial cultures often consumed large amounts of saturated fat. For example, the Masai of East Africa, who traditionally subsist on extremely fatty milk, blood and meat, do not appear to experience heart attacks. Their electrocardiogram readings are excellent and they have the lowest level of arterial plaque during the time of their lives when they are restricted (for cultural reasons) to their three traditional foods. They get an estimated 33% of their calories from saturated animal fat.

Then there are the Pacific islanders, who often eat large amounts of highly saturated coconut. Kitavans get 17% of their calories from saturated fat (Americans get about 10% on average), yet show no trace of heart disease, stroke or overweight. The inhabitants of the island of Tokelau, who I learned about recently, eat more saturated fat than any other culture I'm aware of. They get a whopping 55% of their calories from saturated fat! Are they keeling over from heart attacks or any of the other diseases that kill people in modern societies? Apparently not. So from the very beginning, the theory faces the problem that the cultures consuming the most saturated fat on Earth have an undetectable frequency of heart attacks and other modern non-communicable diseases.

Humans have eaten saturated animal fat since our species first evolved, and historical hunter-gatherers subsisted mostly on animal foods. Our closest recent relatives, neanderthals, were practically carnivores. Thus, the burden of proof is on proponents of the theory that saturated fat is unhealthy.

There have been countless studies on the relationship between saturated fat and health. The first studies were epidemiological. Epidemiological studies involve collecting data from one or more populations and seeing if any specific factors associate with the disease in question. For example, the Framingham Heart study collected data on diet, lifestyle and mortality from various diseases and attempted to connect diseases to lifestyle factors. This type of study is useful for creating hypotheses, but it can only determine associations. For example, it can establish that smokers tend to die more often from heart disease than non-smokers, but it can't determine that smoking is actually the cause of heart disease. This is because multiple factors often travel together. For example, maybe smokers also tend to take care of themselves less in other ways, sleeping less, eating more sugar, etc.

Epidemiological data are often incorrectly used to demonstrate causality. This is a big problem, and it irritates me to no end. There's only one way to show conclusively that a diet or lifestyle factor actually causes something else: a controlled trial. In a controlled trial, researchers break participants into two groups: an intervention group and a control group. If they want to know the effect of saturated fat on health, they will advise the participants in each group to eat different amounts of saturated fat, and keep everything else the same. At the end of the trial, they can determine the effect of saturated fat on health because it was the only factor that differed between groups. In practice, reducing saturated fat also involves either increasing unsaturated fat or decreasing total fat intake, so it's not perfect.

I'm not going to review the epidemiological data because they are contradictory and they are "lesser evidence" compared to the controlled trials that have been conducted. However, I will note that Dr. Ancel Keys' major epidemiological study linking saturated fat consumption to heart disease, the "Seven Countries" study, has been thoroughly discredited due to the omission of contradictory data (read: the other 15 countries where data were available). This was the study that sparked the anti-saturated fat movement. Older epidemiological studies and those conducted internationally tend to find nonexistent or weak links between saturated fat and health problems, while more recent American studies, such as the Nurses' Health study, have sometimes found strong associations. I'll address this phenomenon in another post.

In the next post, I'll get into the meaty data: the controlled trails evaluating the effect of saturated fat on health.

Thanks to Rockies for the CC photo.

More Masai

I left out one of the juicier tidbits from the last post because it was getting long. Investigators Kang-Jey Ho et al. wanted an explanation for why the Masai didn't have high serum cholesterol despite their high dietary cholesterol intake (up to 2,000 mg per day-- 6.7 times the US FDA recommended daily allowance).

They took 23 male Masai subjects aged 19 to 24 and divided them into two groups. The first group of 11 was the control group, which received a small amount of radioactive cholesterol in addition to a cholesterol-free diet that I will describe below. The second group of 12 was the experimental group, which they fed 2,000 mg cholesterol per day, a small amount of radioactive cholesterol as a tracer, and the exact same cholesterol-free diet as the control group. For the duration of the 24-week trial, the subjects ate the experimental diet exclusively. Here's what it was (in order of calories, descending):

• Nondairy coffee creamer (made of corn syrup solids and vegetable oil)
• Beans
• Sugar
• Corn
• Corn oil
• A vitamin pill

Not a healthy diet by most peoples' standards, but those items are nevertheless widely eaten in the US. Over the course of the 24-week study, the investigators found no difference in serum cholesterol between the control and experimental groups. This isn't really surprising. The body has mechanisms for regulating blood cholesterol, and if you aren't eating any it just synthesizes more to stay at its preferred level.

The really interesting thing is that serum cholesterol increased dramatically in both groups. It went from 125 mg/100 mL to over 170 mg/100 mL, despite a large decrease in the saturated fat they were eating. The change took about two weeks to occur, and remained fairly stable for the remainder of the trial.

Both groups also gained weight. In the first week, they gained an average of 3 pounds each. To be fair, the initial gain was probably most water, which is what happens when a person increases their carbohydrate and salt intake. The investigators freaked out and cut their calorie intake by 400 kcal, only allowing them 3,600 kcal per day. Initially, they were voluntarily consuming 4,000 kcal per day. I find that interesting as well. Something tells me they weren't chugging non-dairy creamer because it was so delicious, but because their confused hormones were telling them to EAT.

Even after putting the subjects on calorie restriction (not letting them eat as much as they wanted, by an average of 400 kcal/day), they continued gaining weight. By the end of the study, the 23 subjects had gained an average of 7.8 lbs per person.

To summarize, this is what the investigators saw when they put 23 unfortunate Masai men on a bottom-rung industrially processed diet: elevated cholesterol, hyperphagia (excessive eating), and weight gain. Sounds familiar, doesn't it?

Masai and Atherosclerosis

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

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

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

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

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


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


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

Here's a quote from the paper that sums it up well:

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

I know this blog is starting to sound like a broken record, but I'll say it again: you can eat a wide variety of foods and be healthy, except industrial grain products (particularly wheat), sugar, industrial vegetable oil and other processed food. The Masai are just one more example of a group that's healthy when eating a traditional diet.

What to do if Your Study Contradicts Conventional Wisdom

I just read a recent paper from the British Journal of Sports Medicine, "Daily Energy Expenditure and Cardiovascular Disease Risk in Masai, Ruran and Urban Bantu Tanzanians". The study caught my eye because I think we have a lot to learn from healthy traditionally-living populations worldwide.

The Masai have a very unique diet consisting almost exclusively of whole cow's milk, cow's blood and meat. As you might imagine, they eat a lot of fat, a lot of saturated fat and a modest amount of carbohydrate (from lactose). They also have low total cholesterol, low blood pressure, and virtually no overweight. They have been a thorn in the side of the lipid hypothesis for a long time.

The Bantu are an agricultural population that traditionally eat a diet low in fat and high in carbohydrate. Their staples are root vegetables, corn, beans, fish and wild game. The paper also describes a group of urban Bantu, which eats a diet intermediate in fat and carbohydrate. Incidentally, the investigators describe it as a "high-fat diet", despite the fact that the percentage fat is about the same as what Americans and Europeans eat, shamelessly exposing their bias.

The investigators recorded the three groups' diets, activity levels, physical characteristics and various markers of cardiovascular disease risk. Here's what they found: only 3% of Masai were obese, compared to 12% of rural Bantu and 34% of urban Bantu (they'd fit right in here!). The Masai, despite smoking like chimneys, had generally lower CVD risk factors than the other two populations, with the urban Bantu being significantly worse off than the rural Bantu.

Overall, the Masai came out looking really good, with the rural Bantu not too far behind. The urban Bantu look almost as bad as Americans. How do we make sense of these two conflicting facts? 1) The urban Bantu eat an amount of fat and saturated fat that's right in the middle of what the Masai and the rural Bantu eat, yet they seem the most likely to keel over spontaneously. 2) Saturated fat KILLS!! Answer: keep digging until you find something else to blame your results on.

They certainly did find something, and it's the reason the study was published in the British Journal of Sports Medicine rather than the American Journal of Clinical Nutrition. The Masai exercise more than either of the other two groups. I don't have too much trouble believing that. However, the authors used a dirty trick to augment their result: they normalized calorie expenditure to body weight. They present their data as kcal/kg/day. In other words, the fatter you are, the lower your apparent energy expenditure! It makes no sense to me. But it does inflate the apparent exercise of the Masai, simply because of the fact that they're thinner than the other two groups.

Due to this unscrupulous number massaging, here's what they got (data re-plotted by me):


I'm going to try to un-massage the data. Here's what it looks like when I factor bodyweight out of the equation. Calories expended (above resting metabolic rate) is on the Y-axis. The bars look a bit closer together...



Here's what it looks like when you add back resting metabolic rate. I assumed 1500 kcal/day. This graph is an approximation of their total energy expenditure per day:



Hmm, the differences keep getting smaller, don't they? I'm not challenging the fact that the Masai exercise more than the other two groups, but I do have a problem with this kind of manipulation of the data in misleading ways.

Their conclusion is that exercise is protecting the Masai from the deadly saturated fats in their diet. A more parsimonious explanation is that saturated fat per se doesn't cause heart disease. It's also more consistent with other healthy cultures that ate high-fat diets like the Inuit, certain Australian aboriginal groups, and some American Indian groups. It's also consistent with the avalanche of recent trials of low-carbohydrate diets, in which people consistently see improvements in weight, blood pressure, and CVD markers, among other things. Not that I have much faith in blood lipid markers of CVD.

My conclusion, from this study and others, is that macronutrients don't determine how healthy a diet is. The specific foods that compose the diet do. The rural Masai are healthy on a high-fat diet, the rural Bantu are fairly healthy on a low-fat, high carbohydrate diet. Only the urban Bantu show a pattern really consistent with the "disease of civilization", despite a daily energy expenditure very similar to the rural Bantu. They're unhealthy because they eat too much processed food: processed vegetable oil, processed grain products, refined sugar.

Thanks to kevinzim for the CC photo