Wheat Again

The USDA has published this chart of U.S. consumption of wheat flour between 1830 and 2008.

Before 1850, U.S. consumption of wheat was lower than between 1850 and 1910.  The USDA explains:

"Wheat production was difficult in New England and in much of the South in the colonial era (1600s and 1700s), making wheat flour too expensive for regular use. High transportation costs also made long-distance transport of wheat and flour from regions better suited for wheat growing unprofitable. Therefore, colonists in these regions turned to other crops, especially corn. The wealthy were the principal consumers of wheat bread."

In the U.S., wheat flour (and thus wheat bread) consumption peaked in the late 19th century at about 220 pound per capita per annum.  That means that in the late 19th century, U.S. citizens were consuming an average of about 10 ounces of wheat flour daily.

That would provide about 950 kcalories, 37 g protein, and 200 g carbohydrate from whole wheat flour alone.   It is equivalent to consuming 12 slices of whole wheat bread daily.

About 1910 the per capita wheat flour consumption dropped below 200 pounds, and now it is about 150 pounds per annum, so we have seen a 32 percent drop in wheat flour consumption since the late 19th century.

So, during the 20th century, what replaced grain consumption?  The USDA says :

"Historically, economic development has been accompanied by the substitution of meat for grain in the diet, and this was true in the United States starting in the 1870s."

The substitution of meat for grains as a consequence of economic development represents part of what nutritionists have called the  nutrition transition ,  which Popkin characterizes here :

"Major dietary change includes a large increase in the consumption of fat and added sugar in the diet, often a marked increase in animal food products contrasted with a fall in total cereal intake and fiber."

Put another way, up until the late 19th century, the U.S. was an agrarian nation.  Agrarian nations typically derive most of their sustenance from cereal grains and this was true of the U.S. for its first 100 years, during which corn and wheat provided the majority of calories consumed by the majority of people.

So far as I can tell, rates of obesity, diabetes, and cardiovascular disease in the U.S. went up during a time when consumption of wheat and corn was well below that of the late 19th century.

According to an article by B.C. Curtis posted on the Food and Agriculture Organization website, the French consume almost twice as much wheat per capita as people of the United States.

According to World Health Organization data, the U.S. has about 2.5 times as many heart disease deaths as France.

France also has an obesity rate one-third of that of the U.S.A..

It doesn't look like consumption of bread increases the risk of heart disease or obesity in France.

We do have evidence indicating that whole grains including whole wheat protect against heart disease.

Groen (pdf) studied the effect of dietary wheat bread on serum cholesterol.  He found first that Trappist monks, Yemenite Jews, and Arab Bedouins consumed an average of 600, 500, and 750 g of bread daily, compared to an average of 150 g bread daily in a Western diet, but the bread eaters had low serum cholesterol levels and very low risk of ischemic heart disease.

The Bedouins consumed the most bread (750 g daily) and the least animal protein (5 g daily) and total fat (38 g) and had the lowest serum cholesterol.

One slice of bread weighs about 30 g, so the Trappists ate about 20 slices daily, the Yemenites about 17 slices, and the Bedoins about 25 slices daily, compared to about 5 slices in the typical Western diet.  These levels of bread intake are common among people who eat bread as a staple food.

Groen compared the effects on serum cholesterol of low-fat, low-sugar diets  in which most of the protein came from animal sources, or most of the protein came from wheat gluten.  The study suggested that a gluten-rich diet may produce a lower cholesterol level than one based on animal protein.

Groen also found that replacing bread with equal caloric amounts of sugar raised serum cholesterol.

Study Indicates Prostate Cancer Is Reversible By Diet

According to the National Cancer Institute, each year in the U.S., 240,890 men get diagnosed with prostate cancer, and 33,720 men die from it.

According to the American Cancer Society,

"About 1 man in 6 will be diagnosed with prostate cancer during his lifetime. More than 2 million men in the United States who have been diagnosed with prostate cancer at some point are still alive today.

"Prostate cancer is the second leading cause of cancer death in American men, behind only lung cancer. About 1 man in 36 will die of prostate cancer."

I have a family history of prostate cancer, so I have a personal interest in prevention and remedy for this disease of civilization.

According to some people, whole grains and legumes cause or promote the diseases of civilization, including cancer.

If this disease is caused by eating grains and legumes, then any diet based on grains and legumes should promote cancer.  If you give men living with prostate cancer a diet rich in whole grains and legumes, you should see a promotion of the cancer.

My friend, Gordon Saxe, M.P.H., Ph.D., M.D., professor of medicine at U.C.S.D.,  has actually tested this hypothesis, albeit unintentionally.

Gordon has lead pilot research in which men with diagnosed with prostate cancer were taught to eat a diet consisting of whole grains, legumes, vegetables, fruits, nuts, and seeds, while eliminating animal  products, based on evidence [discussed here] that this dietary pattern may reduce the risk or progression of prostate cancer.

If whole grains and legumes promote prostate cancer then these men should have had an accelerated progression of their cancers.  However, in the first study, over six months, this intervention produced just the opposite effect:  a 100-fold reduction in the rate of rise of their disease, as measured by the rate of change in levels of prostate-specific antigen (PSA).  As stated by Saxe et al:

"The rate of PSA increase decreased in 8 of 10 men, while 3 had a decrease in absolute PSA. Results of the signed rank test indicated a significant decrease in the rate of increase in the intervention period (p = 0.01). Estimated median doubling time increased from 6.5 months (95% confidence interval 3.7 to 10.1) before to 17.7 months (95% confidence interval 7.8 to infinity) after the intervention. Nine of 10 participants in the study had reduction in the rate of rise of their PSA, a marker for progression of disease."

When 9 of 10 people respond in the very same way to an intervention, in this case with a reduction in rate of rise of PSA, this tends to suggest that the effect is no accident and most likely indicates a definite therapeutic effect of the intervention.

In the second study, involving 14 men, Saxe et al produced a similar result.  In this second study they explored the biological mechanisms involved:

"During the first 3 months of the intervention, as both median WHR and body weight declined significantly, the median rate of PSA rise not only declined but became negative, reflecting a slight reduction in absolute PSA and possibly disease regression in patients with absolute reductions. Conversely, during the second 3 months of the intervention, when median body weight increased (though not significantly), median PSA began to rise again, albeit more slowly than during the period prior to Baseline."

This second study suggested that weight-related metabolic changes may have mediated the reduction in rate of PSA increase.  In other words, the intervention resulted in a loss of body fat and concommitant metabolic changes related to reduction of body fatness, including an increase in sex hormone binding globulin, that influence prostate cancer.

"Assuming that the attenuation of PC progression was mediated by weight-related metabolic changes, a question arises as to what aspect of intervention brought about the observed reduction in adiposity. Earlier ⁵³, we described large increases during months 0–3 in intake of whole grains and vegetables, food groups which are fiber and water-rich, very low in fat, and therefore of low energy density. However, intake of these foods declined slightly during months 3–6. Weight loss during the first three months may possibly have resulted from replacing energy-rich foods with energy-poor foods, and the slight increase in body weight during the second three months may have resulted from a small degree of dietary recidivism." 

So this intervention, based on increasing intake of whole grains, legumes, etc., resulted in body fat reduction during the period when the subjects ate the most of these foods, and body weight increased during the period when these subjects ate less of these foods.  This clearly undermines the idea that diets rich in grains and legumes cause two of the major diseases of civilization, i.e. obesity and cancer.

Saxe et al consider the possibility that any diet that induces weight loss may reduce cancer progression.

"A second question that naturally arises regarding the reduction in adiposity is whether it matters, in terms of effects on prostate cancer progression, how it is achieved. One aspect of this question has to do with the preferred dietary strategy for reducing energy intake. Another facet regards whether it is more desirable to increase energy expenditure or decrease intake to achieve this end. Although our study and its findings did not address these issues, they remain important ones that warrant consideration in the planning and design of future behavioral approaches to the management of progressive PC. What can be said is that while both a plant-based diet and a high-protein, low-carbohydrate diet high in foods of animal origin (such as the popular Atkins diet) may both result in weight loss, the former is far more consistent with the dietary cancer prevention guidelines of various agencies (69).⁵⁴ "

Some people reject those cancer prevention guidelines of various agencies, which emphasize increased consumption of whole plant foods and decreased consumption of animal products, claiming that whole grains and legumes are the true causes of diseases of civilization.   These two studies, among others, weaken that claim. 

So far, the only studies I can find testing the effect of a low-carbohydrate diet on prostate cancer were done with mice, not men.  In this one, researchers from Duke Prostate Center fed mice with prostate cancer either a "Western" diet,  "low-fat high-carbohydrate" diet, or a zero-carbohydrate diet.  The results:

"Fifty-one days after injection [with xenograft tumors], NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice."

I don't have access to the full text, but if done in a typical fashion, all diets would have been pellets made from isolated nutrients (e.g. casein, starch, sugar, etc.) so this can't tell us much about what would happen in humans if we compared a whole foods vegan diet (whole grains, legumes, vegetables, fruits, nuts, seeds) to a zero-carbohydrate diet (meat and fat only).  The effects of a casein-based zero-carbohydrate diet on mice might be very different from the effects of a meat-based zero-carbohydrate diet on humans.

In a second study, Masko et al fed mice diets containing 0, 10, or 20 percent carbohydrate and again injected them with prostate cancer cells.  As a 'control' they fed a group of mice a 12% fat diet, but they did not inject cancer cells into these mice--which to me means they weren't much of a control group, because they differed from the others not only in dietary composition but also in absence of tumor injection.

The full text of this study tells us the components of all diets:  corn oil, lard, milk fat, casein, dl-methionine, dextrine, maltodextrine, corn starch, sucrose, and isolated vitamins and minerals. 

In the low-fat arm, 72% of calories came from carbohydrate, and 50% of total calories came from sucrose, which means that about 25% of total calories came from refined fructose.  Meanwhile, in the 10% and 20% carbohydrate arms, all of the carbohydrate was provided in the form of corn starch. 

This makes me wonder again about diet composition in the other Duke University study cited above.  Were those mice on the low fat diet also eating a 50% sucrose/25% fructose diet?  If so, did this rig the study, intentionally or not, so that the low fat group would have more body fat and shorter lifespan than the zero-carbohydrate group? 

Moving on, all the mice got all of their protein from casein-plus-methionine, none ate any meat.  Most people eating low carbohydrate diets eat cooked meats, not isolated casein, as their main protein source.  Meat is nutritionally complex, and affected by cooking process, in ways that may result in it having a different effect on prostate cancer than casein-plus-methionine.  For example, unlike the casein-methionine mix fed to these mice, meat contains heme iron and if cooked at high heat, heterocyclic amines, all of which have been linked to prostate cancer causation or promotion [e.g. Sinha et al full text].  So it is not clear how a study of mice eating a low carbohydrate diet wherein casein is the main protein will apply to people eating low carbohydrate diets wherein cooked meat, poultry, and fish are the main protein sources.

Masko et al found that the survival rates of the mice in the 0, 10, and 20 percent carbohydrate groups were similar.  They liked this finding because, as they say, people find it extremely difficult to follow zero-carbohdyrate diets, so now they are ready to test the 20 percent carbohydrate diet on human prostate cancer patients. 

Masko et al also found that the mice in the 20% carbohydrate group had the lowest insulin level, about which they comment:

"It was unexpected that the lowest levels of insulin were observed in mice fed with 20% carbohydrate, but there are possible explanations for this phenomenon. First, there is always the possibility for a type I error in the analysis. Second, it is known that low-carbohydrate diets promote insulin sensitivity in animals (38) and humans (39, 40). Thus, it is possible that a diet containing a small amount of carbohydrates may actually improve insulin sensitivity compared with a diet completely lacking of carbohydrates."

Perhaps unknown to Masko et al, it is also 'possible' that a diet containing an even large amount of carbohydrate may actually improve insulin sensitivity compared to a diet with only 20% carbohydrate. In 1971, Brunzell et al [abstract only] evaluated the effect of increased dietary carbohydrate at the expense of fat in humans, both non-diabetic and mildly diabetic.  In the New England Journal of Medicine they reported that after feeding these subjects a diet providing 85 percent of energy as carbohydrate for 10 days,

"Fasting plasma glucose levels fell in all subjects and oral glucose tolerance (0 to 120-minute area) significantly improved ..... Fasting insulin levels also were lower on the high carbohydrate diet; however, insulin responses to oral glucose did not significantly change. These data suggest that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin."

 An diet supplying 85 percent of energy as carbohydrate is by necessity very low in fat, so perhaps Brunzell et al could have emphasized that this very low fat diet increased insulin sensitivity.  The mice of Masko et al that got the 20 percent carbohydrate diet had a lower fat intake than the mice on the zero-carbohydrate diet; rather than increasing carbohydrate being responsible for promoting insulin sensitivity, perhaps it is reducing fat (replacing it with starch) that does the trick. 

Anyway, the Masko et al study has a few features that make me skeptical that they will have similar results in humans.  I feel curious to see if their approach will have results as good as those found by Saxe et al.

Phytate Facts

Concerned about phytates in seed foods (nuts, seeds, grains, legumes) blocking mineral absorption and causing ill health?

You can relax.  Context matters. 

Consuming foods rich in ascorbate (vitamin C) with foods rich in phytate can cancel the negative effects of phytate on mineral absorption.[1, pdf]  Just eat some fruits and vegetables with foods that supply phytate.

Some studies have shown substantial degradation of phytate in the human gut (70-86%), indicating that humans adapt to diets high in phytate by increasing small intestinal production of phytase. [2 full text link, 3]

I have never seen any evidence that dietary phytate causes mineral deficiencies except in the context of overall poor quality diet, such as people attempting to live on diets composed entirely of unleavened grains and legume flours without adequate intake of vegetables, fruits, and other mineral sources.

If you live in a modern industrialized nation, when was the last time you had someone tell you that a physician diagnosed her with multiple mineral deficiencies caused by excessive dietary phytate?

I have never seen it.

Anticancer Effects of Phytates

Everything has a front and a back.

According to researchers from Linus Pauling Institute of Science and Medicine, phytates appear to have anticancer effects by binding excess minerals in tissues, depriving tumors of essential minerals.[4 pdf]

Vucenik and Shamsuddin discuss the anticancer properties of phytate in detail; all information and quotes remaining in this post come from their report in the Journal of Nutrition.[5 full text]

Almost all mammalian cells contain phytate in the inositol hexaphosphate (IP6) form and others with smaller numbers of phosphate groups (IP1-5).  When we ingest dietary phytate, intracellular levels of IP6 increase, and from this cells increase the levels of the other forms, which appear involved in "cellular signal transduction, regulation of cell function, growth, and differentiation."

Dietary phytate enters the blood stream and reaches tissues, including tumors, far from the gut.

Tumor cells take up phytate, probably by pinocytosis or receptor-mediated endocytosis.

Phytate inhibits malignant growth in human leukemic, colon cancer, breast cancer, cervical cancer, prostate cancer, and liver cancer cells.

"IP₆ inhibited the growth of all tested cell lines in a dose- and time-dependent manner. The growth of cells of hematopoietic lineage was inhibited: human leukemic hematopoietic cell lines, such as K-562 (26,27) and human normal and leukemic hematopoietic cells (27). The antiproliferative activity of IP₆ was further reported in human colon cancer HT-29 cells (28), estrogen receptor–positive and estrogen receptor–negative human breast cancer cells (32), cervical cancer (25), prostate cancer (15,33,34), and HepG2 hepatoma cell lines (31). IP₆ also inhibited the growth of mesenchymal tumors, murine fibrosarcoma (39), and human rhabdomyosarcoma (38)."

Phytate also causes malignant cells to mature and differentiate into normal cells:

"The potential of IP₆ to induce differentiation and maturation of malignant cells, often resulting in reversion to the normal phenotype, was first demonstrated in K-562 hematopoietic cells (26). IP₆ was further shown to increase differentiation of human colon carcinoma HT-29 cells (28,29), prostate cancer cells (33), breast cancer cells (32), and rhabdomyosarcoma cells (38)."

Phytates provide an intracellular antioxidant function by binding with iron, which suppresses formation of the most hazardous hydroxyl radicals:

"The antioxidant role of IP₆ is known and widely accepted; this function of IP₆ occurs by chelation of Fe³⁺ and suppression of ·OH formation (11). Therefore, IP₆ can reduce carcinogenesis mediated by active oxygen species and cell injury via its antioxidative function."

Phytate also stimulates the immune response and protects against carcinogen-induced depression of natural killer cell activity.

"Besides affecting tumor cells, IP₆ can act on a host by restoring its immune system. IP₆ augments natural killer cell activity in vitro and normalizes the carcinogen-induced depression of natural killer cell activity in vivo (59). "

Phytate only adversely affects malignant cells, not normal cells:

" The most important expectation of a good anticancer agent is for it to only affect malignant cells and not affect normal cells and tissues. That property was recently shown for IP₆. When the fresh CD34⁺ cells from bone marrow was treated with different doses of IP₆, a toxic effect (inhibition of the clonogenic growth or as cytotoxicity on liquid cultures) was observed that was specific to leukemic progenitors from chronic myelogenous leukemia patients but no cytotoxic or cytostatic effect was observed on normal bone marrow progenitor cells under the same conditions."

 This indicates that normal cells are adapted to phytate.  Of course, since phytate is abundant in the plant world and also present in almost every mammalian cell.

Phytate inhibits all of the several pathways supporting malignancy:

" From the behavior and characteristics of malignant cells, several principal pathways of malignancy have been established, such as proliferation, cell cycle progression, metastases and invasion, angiogenesis, and apoptosis; interestingly, IP₆ targets and acts on all of them."

 In one pilot clinical trial, six patients with advanced colorectal cancer (Dukes C and D) with multiple liver and lung metastasis received oral phytate plus chemotherapy.  One of the patients refused additional chemotherapy after one session and she was treated only with IP₆ plus inositol.  What happened?

"...her control ultrasound and abdominal computed tomography scan 14 mo after surgery showed a significantly reduced growth rate. A reduced tumor growth rate was noticed overall and in some cases a regression of lesions was noted."

Say again?  A simple, natural dietary ingredient reversed the progress of cancer!

Which reminds me:

"Pioneering experiments showing this novel anticancer feature of IP₆ were performed by Shamsuddin et al. (18–20), who were intrigued by the epidemiologic data indicating that only diets containing a high IP₆ content (cereals and legumes) showed a negative correlation with colon cancer." 

Most hunter-gatherer groups would have consumed significant phytate from nuts and seeds of various sorts, including legumes.

Dietary Phytate Safety
   
Vucenik and Shamsuddin agree that chronic phytate ingestion does not cause mineral deficiencies whether gotten from food or isolated form unless the overall diet lacks essential minerals:

"Some concerns have been expressed regarding the mineral deficiency that results from an intake of foods high in IP₆ that might reduce the bioavailability of dietary minerals. However, recent studies demonstrate that this antinutrient effect of IP₆ can be manifested only when large quantities of IP₆ are consumed in combination with a diet poor in oligoelements (60–63). A long-term intake of IP₆ in food (60,61) or in a pure form (64) did not cause such a deficiency in humans. Studies in experimental animals showed no significant toxic effects on body weight, serum, or bone minerals (Table 5) or any pathological changes in either male F344 or female Sprague-Dawley rats for 40 wk (40,51,52). Grases et al. (65) confirmed our findings and also reported that abnormal calcification was prevented in rats given IP₆."

 Phytate has many benefits:  

"In humans, IP₆ not only has almost no toxic effects, but it has many other beneficial health effects such as inhibition of kidney stone formation and reduction in risk of developing cardiovascular disease. IP₆ was administered orally either as the pure sodium salt or in a diet to reduce hypercalciuria and to prevent formation of kidney stones, and no evidence of toxicity was reported (64,65,79,80). A potential hypocholesterolemic effect of IP₆ may be very significant in the clinical management of hyperlipidemia and diabetes (75,76,81). IP₆ inhibits agonist-induced platelet aggregation (82) and efficiently protects myocardium from ischemic damage and reperfusion injury (83), both of which are important for the management of cardiovascular diseases. "

Perhaps avoiding and removing phytates from food doesn't serve your best interests?

Perhaps we evolved to consume significant amounts of phytates, and cancer is a disease facilitated by a dietary deficiency of phytates?

The Real Gladiator Diet

Source: U of Texas Course Intro To Greece

What did the gladiators eat?

According to Andrew Curry, author of "The Gladiator Diet," an article in the journal Archaeology, Karl Grossschmidt, a paleo-pathologist at the Medical University of Vienna, did an analysis of bones of gladiators found in an 1800 year old graveyard near Ephesus, in what is now western Turkey.

"Contemporary accounts of gladiator life sometimes refer to the warriors as hordearii--literally, "barley men." Grossschmidt and collaborator Fabian Kanz subjected bits of the bone to isotopic analysis, a technique that measures trace chemical elements such as calcium, strontium, and zinc, to see if they could find out why. They turned up some surprising results. Compared to the average inhabitant of Ephesus, gladiators ate more plants and very little animal protein."

Interesting.  The top athletes, with their lives on the line, ate 'very little' animal protein compared to non-athletes.  According to Grossschmidt, gladiators ate this way to get fat:

"The vegetarian diet had nothing to do with poverty or animal rights. Gladiators, it seems, were fat. Consuming a lot of simple carbohydrates, such as barley, and legumes, like beans, was designed for survival in the arena. Packing in the carbs also packed on the pounds. "Gladiators needed subcutaneous fat," Grossschmidt explains. "A fat cushion protects you from cut wounds and shields nerves and blood vessels in a fight." Not only would a lean gladiator have been dead meat, he would have made for a bad show. Surface wounds "look more spectacular," says Grossschmidt. "If I get wounded but just in the fatty layer, I can fight on," he adds. "It doesn't hurt much, and it looks great for the spectators."

What an interesting hypothesis.  Grossschmidt apparently believes that barley and beans are "simple carbohydrates" that "pack on the pounds" making people fat, and that a gladiator would prefer to be fat than lean and muscular.

I challenge Grossschmidt to consume a diet of barley and beans, with less than 10% of his diet as animal products, for a year, to find out if he grows fat eating that way.  Since cooked barley supplies only about 200 calories per cup, he can look forward to eating 6 cups daily just to get to 1200 kcal.  Add one cup of lentils (230 kcal), 4 cups of cooked kale (280 kcal), 4 ounces of sardines (240 kcal), and an ounce of almonds (180 kcal) and you have a nutritionally dense meal plan supplying about 2130 kcal and more than 11 cups of food.  See if you can eat it all, then enough additional to 'pack on the pounds.'

I also suggest that he produce some evidence that gladitors were fat.  He could spend a little time looking at reliefs and other art depicting gladiators of the time.  I found a good selection online from a University of Texas course, Introduction to Greece, here.  I put one of them at the head of this article.  Those men obviously have little subcutaneous or intra-abdominal fat, with ribs, rectus abdominus, deltoids, and upper back muscles clearly defined; they won't qualify as 'fat' by any standard.

Here are a few more from the same source:

Funny, I don't see any fat gladiators.  I didn't cherry-pick, you can look for yourself here.  These depictions don't look that much different from a modern vegetarian combat athlete, Chris Campbell, who won a bronze wrestling in the 1992 Olympics at age 37:

Source:  Information Processing

You can see how fat and weak Campbell got eating all those "simple sugars." 

I can't imagine any reason artists would falsely depict gladiators as lean and muscular, if they really were fat.  I wonder where Grossschmidt got his idea?

Grossschmidt apparently believes that "a lean gladiator would have been dead meat" compared to a fat one. I have to doubt that Grossschmidt has any experience in the fighting arts.  Fat slows you down, making you an easy target.  The goal of a gladiator was to survive, not to put on a good show; only a fool would choose to get fat for battles against armed opponents where you only walk away if you can move faster and hit harder than the other guy.

Grossschmidt also believes that those gladiators had to supplement calcium to their barley and vegetable diet:

"But a diet of barley and vegetables would have left the fighters with a serious calcium deficit. To keep their bones strong, historical accounts say, they downed vile brews of charred wood or bone ash, both of which are rich in calcium. Whatever the exact formula, the stuff worked. Grossschmidt says that the calcium levels in the gladiator bones were "exorbitant" compared to the general population. "Many athletes today have to take calcium supplements," he says. "They knew that then, too."

What? Despite having low animal protein intake, and eating a diet based on 'toxic' neolithic barley supplying much-feared gluten, phytates, and other "anti-nutrients" supposed to interfere with calcium absorption, these gladiators had 'exhorbitant' calcium levels in their bones?  Strong bones in agriculturalists?  How could that happen?

Well, let's see if they needed calcium supplements.  Ephesus lies on the west coast of Turkey, near the mouth of the Menderes River, so I will assume the gladiators ate some fish.  I'll build the diet of barley, lentils, kale, olives, acorns, and sardines, all possible foods for those people.  Here's a nutritional analysis of a hypothetical barley diet with less than 10% of calories from sardines:

Click to Enlarge

As you can see, to get to 3400 kcal required by a large, physically active martial artist using swords, tridents, and similar arms, the barley men would have to eat 10 cups of cooked barley in a day.  Now imagine having to eat several more daily to 'pack on the pounds.'  Good luck with that!

With only 4 ounces of sardines (supplying only 236 calories, less than 10% of total) and two cups of lentils, it supplies 116 g of protein, enough for a 220 pound athlete.  The diet supplies energy in the following  proportions: 70/18/12, carbohydrate/fat/protein. It supplies all required nutrients in adequate amounts (most nutrients at 2-4 times the RDA) except vitamin E, which is 77% of RDA, probably adequate for most people eating a diet this low in fat (71 g/d), but we could boost this by exchanging one cup of  barley for one cup of olives (that brings the vitamin E to 97% of RDA and fat to 22% of calories). 

I also tested 3000 calories of this diet by removing 2 cups of barley.  It became 67/20/13 (carb/fat/pro) and still supplied 110 g protein, enough for a 220 pound athlete.  It still supplied at least 100% of the RDA for all listed nutrients except vitamin E, still at 77%.

Now, back to the 'exorbitant' levels of calcium in these athlete's bones. First, ancient athletes were familiar with resistance training, using all types of heavy objects to increase strength.   Physical training with heavy weapons and other sources of resistance stresses the bones, increasing mineral deposition, so we should expect athletes like gladiators to have high bone mineral density.

Second, humans appear to absorb more calcium from some plants, especially cabbage-family green leafy vegetables, than from milk.  In one study humans absorbed a greater proportion of calcium from kale (and probably similar brassica vegetables) (41%) than from milk (32%) [1]. As an aside, Heaney et al found that humans absorbed calcium from leavened whole wheat bread at at higher rate than from milk [2].

Third, we have evidence from other paleo diet research suggesting that a diet with a high ratio of plant to animal protein may promote greater bone mineral density.  Richman et al compared bones of three aboriginal American populations:  Pueblos, Arikaras, and Inuit [3 ].   These groups had similar genetic backgrounds, all descended from the few humans who first populated the Americas. 

Richman et al looked for type II osteons, characteristic of increased bone mineral resorption involved in maintaining physiological homeostasis, such as buffering to maintain the pH of urine in the range safe for kidney tubules.  They found that the Pueblos had the least evidence of this type of remodeling, and Eskimos had four times as many type II osteons as the Pueblos.  The diet of the Pueblos consisted largely (80%) of maize and 90% of plant foods, while the Eskimo diet consisted 90% of meat.  The Arikaras consumed more meat than Pueblo and less than Eskimos, and had twice as many type II osteons the Pueblos.

When I first reviewed this study, I missed the fact that it contradicted the theory that people are less adapted to grains than to meat.  If the antinutrients in grains impair calcium and vitamin D metabolism, the Pueblos should have had the worst bone health because they had the highest cereal grain intake, supposedly blocking vitamin D action and calcium absorption; but in fact they had the lowest markers of resorption. 

We have plenty of evidence that isolated Inuit had severe and early onset osteoporosis [4, 5].  Similar to the Pueblos, largely vegetarian Bantu women eating grain-based diets have extremely low rates of osteoporosis despite very low (200-450 mg/d) intakes of calcium and a high number of pregnancies (~10 per woman) with prolonged breastfeeding [6 ]. 

We have some evidence that a diet with a high ratio of animal protein to vegetable protein increases urinary calcium losses and that this may result in demineralization of the bones [7 , 8 , 9 , 10, among others].  While some consider this research inconclusive so far [11], it seems to me that the bulk of research points in the direction of diets with high ratios of animal protein increasing the risk of bone mineral loss, although the mechanism may be unclear and other factors may modify this risk (resistance training, vitamin D, vitamin K, dietary acid-base ratio, sodium intake, to name a few).  Anyway, it appears possible that the gladiators' high ratio of vegetable to animal protein contributed to their maintaining a high bone mineral density. 

I conclude that a diet of barley, lentils, olives, acorns, green vegetables, and small amount of small fish can provide plenty of calcium, which when combined with hard physical training will produce very dense, strong bones.  Maybe those gladiators did add wood ash or bone meal, but they may have been overdosing on unnecessary calcium, the same way the many modern athletes take unnecessary supplements hoping for greater performance.

Meat and Fat Diet Delivers Satisfying Results

I really enjoy hearing from people who have taken classes from me and gotten the awesome results you can get by putting paleo principles into practice.

Leslee Ridgeway took nutrition classes from me when I taught at Southwest Institute of Healing Arts,  and has applied the paleo principles in her own life and spread the word.  Here's part of her report: 

For example, I have a four year old and it's very hard to do the low carb thing all the way through with t ball practice and all the societal things we go to that are so backwards with nutrition. I am trying to teach and raise him the best I can without making him feel like he an outcast. Not that it is determined by diet, but it is proving difficult to adjust. His mood and behavior are like night and day difference since getting the fat and protein he needs and low sugar. I have been trying to make some stuff for him that might not be as bad, even though I have decided to pass on it for myself because of my attempts to be closer to a ketogenic diet. 

PS. My family has had a lot of health problems through the years. I suggested everyone test for gluten sensitivity after reading the book you recommended, "Dangerous Grains". So far my sister has been diagnosed with a severe gluten intolerance, and possibly has Celiac, she was referred to a doctor for more testing. She is very young and has a chance at becoming far more healthy because of that (she has thyroid disease). Several others are being tested based on the genetic trends. There are at least 50 people I know that are learning to change their diet because of the things you shared with me, that I in turn share with them.

Kids absolutely will thrive if you feed them meat and fat and limit their sugar intake.   Feed people dangerous grains and they will have a lot of health problems.  This all follows from our ancestral hunter heritage.

Grilled salmon with steamed kale

Practically Paleo Perspective: Rice

A commenter asked me for my opinion on rice, so here you have it.

[Updated 4/20/12:  The original version of this post illustrates some of the poor reasoning I fell into as a result of reading books and blogs by people advocating paleo diet, while ignoring the bulk of research on diet and health.  My critiques and corrections of the original appear in brackets.]

Botany and Antinutrients

Rice is the seed of a monocotyledonous plant known to botanists as Oryza sativa. 

Like other seeds, whole (brown) rice contains chemical defenses against predation, primarily present in the hull and bran of the seed.  They include phytin (phytate), trypsin inhibitor, oryzacystatin and haemagglutinin-lectin.

Phytate binds minerals including calcium, zinc and iron; it also binds with protein.  Heat (cooking) does not denature phytate.  Studies have found that subjects fed brown rice diets have poorer mineral balance when compared to subjects fed milled rice diets.  On the other hand, phytate protects against dental caries, so white rice promotes dental decay more than brown rice.

[4/20/12:   Phytate fears are not founded on good science.  Science does not support claims that dietary phytate causes harm to humans.  Humans adapt to phytate ingestion, dietary vitamin C cancels the negative effect of phytate on mineral absorption, phytate adversely affects mineral balance only if the diet is deficient in minerals, and research has shown that dietary phytate has a strong health benefits for prevention and treatment of cardiovascular disease and cancer; it even inhibits the growth of malignant tumors.]

Trypsin inhibitor occurs in rice bran.  Steaming rice bran at 100 degrees C (212 F) inactivates trypsin inhibitor.  [4/20/12:  This means that boiled brown rice has no active trypsin inhibitor.] Polishing rice eliminates trypsin inhibitor.

Haemagglutinins  or lectins consist of globulins that agglutinate mammalian red blood cells and precipitate glycoconjugates or polysaccharides. Lectins bind to specific carbohydrate receptor sites on the intestinal mucosal cells and thus interfere with the absorption of nutrients across the intestinal wall.  Rice lectin agglutinates human A, B and O group erythrocytes.  According to the FAO, rice lectin sharply loses activity when heated to 100 degrees C. [4/20/12: Hence, since we boil rice at 100 degrees C before eating it, we don't have to worry about this lectin.]

Oryzacystatin is an inhibitor of protein-digesting enzymes.  Oryzacystatin remains 100% active after at least 30 minutes of boiling.

Rice also contains an allergenic protein that occurs primarily in the milled rice, not the bran, and remains stable (60%) even after boiling for 60 minutes at 100 C (212 F).

[4/20/12: Rice allergies occur in only 10% of atopic patients in Japan and less in Europeans and Americans.  Compare this to beef allergy:

"The prevalence of beef allergy is between 3% and 6.5% among children with atopic dermatitis and can be up to 20% in cow's milk allergic children. Several studies reported an incidence of 1-2% of food-induced anaphylactic reactions caused by ingestion of beef. In another study an even higher figure of 9% of anaphylactic events from foods were induced by beef."

These data appear to indicate a much greater incidence of anaphylactic events triggered by beef than by rice.]
 
Nutritional value

Rice has a very high carbohydrate content and low levels of micronutrients compared to vegetables or fruits.  The following table compares the levels of selected vitamins and minerals in 50-kcal portions of brown rice and a selection of vegetables and fruits.  Red numbers indicate items with the highest levels among the foods compared. Click on image to see larger version.

Notice that brown rice does not have the highest level of any of the nutrients listed.  White potatoes have twice as much riboflavin (B2), 2.5 times as much folate, vitamin C not present in rice, 10 times more potassium, more than 3 times as much iron, and 25% more calcium than brown rice.    Sweet potatoes supply carotenes (provitamin A) and vitamin C not present in brown rice, three times as much B2, 5.5 times as much folate, 9 times as much potassium, slightly more iron, and more than 3 times as much calcium.  Winter squash also makes brown rice pale in comparison.

Strawberries have 10 times as much B2, 12.5 times as much potassium, nearly 3 times as much iron, and more than 5 times as much calcium.

No matter which vegetable or fruit you compare to brown rice, you find the vegetable or fruit makes brown rice pale in comparison.

Then if you compare brown to white rice:

Brown Rice vs. White Rice
Nutrient	Brown Rice (1 cup)	White Rice (1 cup)
Energy (kcal)	218	241
Protein (g)	4.5	4.4
Carbohydrate (g)	46	53
Fat (g)	1.6	0.4
Fiber (g)	3.5	NA
Thiamin (mg)	0.2	0.3 (synthetic)
Riboflavin (mg)	0.02	0.03 (synthetic)
Niacin (mg)	2.6	2.8 (synthetic)
Pyridoxine (mg)	0.29	0.11
Folacin (mcg)	7.8	109.8 (synthetic)
Calcium (mg)	19.5	1.9
Iron	1.0	2.7 (fortified)
Magnesium	86	15
Phosphorus	150	61
Potassium	154	48
Zinc	1.2	0.74

Laying aside the synthetic fortification, brown rice supplies nearly 3 times as much pyridoxine, 10 times as much calcium, almost 6 times as much magnesium, more than 3 times as much phosphorus, more than 3 times as much potassium, and almost twice as much zinc.  Therefore, white rice doesn't hold a candle to brown rice, and brown rice doesn't hold a candle to white potatoes.

[4/20/12:  Turn this around, and judge by energy, protein, and carbohydrate delivery per unit volume, and you find that brown rice surpasses non-starchy vegetables and fruits.  We need some foods for energy and macronutrients, and some foods for micronutrients.  Brown rice is a nutrient-dense starch and energy source compared to white rice.]

White or brown, rice is basically filler with little nutritional value compared to vegetables and fruits.  If you eat rice, you crowd out more nutrient-dense sources of carbohydrate. 

[4/20/12:  Wow, what a ridiculous argument!  Both brown and white rice are much more nutrient-dense than fats like butter, lard, and olive oil, so I would have been more correct to state that fats are fillers compared to brown rice.  When I compared the micronutrient content of two equicaloric diets, one high in meat and supplying most of its energy from fat, and the other low in meat and supplying most of its energy from starches like brown rice, the starch-based diet won hands down.]

Ecology

Environmentalist vegetarians like to blame livestock for global warming, but according to Wikipedia:

In many countries where rice is the main cereal crop, rice cultivation is responsible for most of the methane emissions....Methane is twenty times more effective as a greenhouse gas than carbon dioxide.

[4/20/12:  This is an example of the half-truths used to support paleo perspectives.  How about taking a look at relative contributions of rice compared to animal products?  A study published in the American Journal of Clinical Nutrition calculated the amounts of greenhouse gases (carbon dioxide, nitrous oxide, and methane) emitted in the production of 22 different commonly consumed foods, in kg of CO2 equivalents per kg of final product:   Rice, 1.3;  eggs, 2.5; rapeseed oil, 3.0; chicken, 4.3; cod, 8.5; pork, 9.3; cheese, 11; beef, 30.  So the favored foods of low carb and paleo diets produce 2 to 23 times as much greenhouse gas emissions as rice.]

Further, rice fields are the principal breeding grounds for mosquitos that carry malaria.

So there you have my perspective on rice.   I do not recommend regular consumption of either brown or white rice. [Line through added on 4/20/12.]

[4/20/12:  I now highly recommend eating rice and other grains as staple foods, and I no longer recommend eating eggs, poultry, fish, pork, or beef or beef products.  Grains are far superior to meats and fats as human energy sources and for health support, and have much less deleterious effect on the environment.  Science has shown us that meat- and fat-based paleo dieting is not beneficial to human health, animal welfare, or for ecosystem preservation.]