Wednesday, March 31, 2010

Paleo Basics: How Much Sugar in Wild Fruits?

I frequently see the claim that wild fruits have less sugar than cultivated varieties.  It must sound reasonable to those who state it, but what does the evidence show?

In "Australian Aboriginal plant foods: a consideration of their nutritional composition and health implications" Brand-Miller and Holt discuss the carbohydrate contents of wild fruits consumed by Australian Aborigines and report:
"The average nutrient analysis of all the dried AA [Australian Aborigine] fruits in Table 1 (n = 7) shows that they are high in carbohydrate (59 %, v. 65 % in cultivated sultanas and raisins), and contain moderate amounts of protein (8 %) and fat (4 %) depending on the state of desiccation."

They also report:
"The average nutrient composition of all the fruit samples analysed (n = 334) is shown in Table 1 (macronutrients) and Table 2 (micronutrients). On first inspection they appear to be a little higher in protein (2 v. 1 %) and fat (1 v. 0 %) compared with the average of 17 types of cultivated western fruits. These small differences could be explained in large part by the lower water content of the wild foods (72 v. 85 % in cultivated foods). 
"Native fruits also appear to be twice as high in both carbohydrate (21 v. 9 %) and fibre (8 v. 3 %). However, because the methods used are not ideal (see above), the carbohydrate is probably an overestimate and the fibre an underestimate."

So analyses show that wild fruits have, in the first comparison, about the same sugar content as cultivated varieties, and in the second comparison, at least as much sugar, probably more, and up to twice as much, as cultivated.  Neither analysis showed them to have significantly less carbohydrate.

Paleo Basics: Fructose Fact Vs. Fiction



In response to my post on the Kitavan diet, which includes plenty of fruit and likely 36g of fructose daily, "gn" asked me if I think it plausible to suppose that human ethnic groups differ in ability to deal with fructose loads, so that daily fruit won't harm dark-skinned Kitavans living in tropical climate (constant summer) for hundreds of generations, but will harm people of European descent whose ancestors had fructose supply only in late summer and fall seasons.

From this question, which I will address below,  I get the impression that the Lustig lecture embedded above has led many to believe that daily ingestion of fructose in any quantity has toxic effects, such as non-alcoholic-fatty-liver-syndrome (NAFLS), particularly to people of European descent.

Unfortunately, Lustig's lecture contains misleading hyperbole or exaggeration (e.g. within the first five minutes he says "The Japanese diet is all carbs and no fat, and the Atkins diet is all fat and no carbs" and later he claims that Japanese eat no sugar, a falsehood) and doesn't give important details about research on fructose metabolism. The main problem lies in a failure to define the dose of fructose required to produce the adverse effects. Let's take a look at some of the research to see what people have missed.

Fructose Research

Le et al investigated the effect of fructose overconsumption on blood lipids and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes.   In this study they found that fructose overconsumption  "increased ectopic lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity" and the effect appeared greater in offspring of parents who had type 2 diabetes.

To get this effect, they used a hypercaloric high-fructose diet supplying 3.5g fructose per kg of fat free mass, amounting to more than 35% of energy intake.  For a lean individual like myself, that would require putting down more than 222g/888kcal of fructose daily while also consuming more calories than I expend.   This is an unrealistic intake of fructose for a person eating a whole foods diet.  It would require consuming more than 444g of table sugar, 12 non-diet sodas, or about 18 medium size apples or bananas.

For another example, Ackerman et al studied fructose-induced fatty liver disease in rats.  To induce FLD in the rats, they used a diet consisting of 60% fructose by weight, which supplied all the carbohydrate in the diet.  Humans do not typically consume diets in which fructose is the sole carbohydrate and the major macronutrient by weight.

Brown et al looked at the effect of fructose on blood pressure in young healthy people.  They had 15 volunteers drink a 500ml  beverage containing a single dose of 60g fructose or glucose.  Both sugars produced an increase in heart rate, and the fructose dose produced an elevation in blood pressure that persisted for at least 2 hours.  To get a single dose of 60g fructose from sucrose (table sugar) would required ingesting about 120g sugar in one sitting--or, 157g of high-fructose corn syrup, or more than 4 apples or 4 bananas.  This says nothing about the effects of consuming the more typical 15g fructose per serving found in a serving of soda, let alone eating whole fruits, which contain other components (e.g. potassium) that tend to reduce blood pressure.  For my n=1 experiment, I have routinely eaten 3-4 pieces or servings (cups) of fruit in a day for more than 10 years in a row and my blood pressure remains at 110/60.

Swarbrick et al claimed to show that consumption of fructose-sweetened beverages increases postprandial triglycerides and fasting apoB concentrations, and suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.  To produce their results, they fed study subjects diets providing 25% of total energy as fructose.  For a 2000 kcalorie diet, that is 500 kcalories or 125g of fructose.  Again, this would require consuming a total of 250g of sugar from sucrose or high-fructose corn syrup, i.e. more than 6 non-diet sodas, or at least 10 pieces or cups of fruit in a day. 

As John White noted in the American Journal of Clinical Nutrition, in the typical U.S. diet, fructose contributes about 200–250 kcal/d, which amounts to about 7–8% of the current 2700-kcal/d per capita total calorie intake, a much smaller intake than used in these experiments, so they provide no evidence that typical intakes of fructose induce fatty liver disease.  He added:

"Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption."
I could go on but instead I will refer you to an excellent critical review of Lustig's lecture by Alan Aragon:  The bitter truth about fructose alarmism.  After reviewing 19 papers on the effects of dietary fructose disputing some of the anti-fructose claims made by Lustig, and finding Lustig's presentation lacking, Alan comments:

"So, what’s the upper safe limit of fructose per day (all sources considered)? Again, this depends on a number of variables, not the least of which are an individual’s physical activity level and lean body mass.Currently in the literature is a liberal camp reporting that fructose intakes up to 90 grams per day have a beneficial effect on HbA(1c), and  no significant effects are seen for fasting triacylglycerol or body weight with intakes up to 100 grams per day in adults [15]. The conservative camp suggests that the safe range is much less than this; roughly 25-40 grams per day [19].  Figuring that both sides are biased, the middle figure between the two camps is roughly 50 grams for active adults."  
Back To The Original Question

As I noted above, "gn" asked me if I find it plausible that Europeans have less tolerance for fructose than Kitavans.  Short answer: No.  Long answer:  All of the above studies were done on people of European descent, illustrating that Europeans have a quite high tolerance for fructose.  Further, fructose tolerance developed millions of years ago in the African primate lineage from which we all hale, due to primate consumption of fruit as a dietary staple.  When humans moved out of Africa about 50 thousand years ago, they would have lost fructose tolerance only if maintaining it proved a disadvantage in northern climates.  In other words, they would have lost fructose tolerance only if maintaining it resulted in death before reproduction.

I can't imagine a scenario in which the environment would select against fructose tolerance, i.e. in which maintenance of fructose tolerance despite a fructose-poor environment, would cause a person to lose fertility or die before having a chance to reproduce.  I also can't imagine a scenario in which the environment (seasonal variations in supply of fructose) would select for fructose-intolerance, i.e. favor the reproduction of fructose-intolerant individuals.  On the contrary, seasonal supply of fructose would continue to select for those who could eat naturally large amounts of fructose (i.e. fruits) when seasonally available, because those people maintaining the deeply ingrained primate ability to metabolize fructose would even in the north have a greater total available food supply than fructose-intolerant individuals.

I routinely eat three to five servings of fruits daily, i.e. 30 to 50g of fructose, and have done so most days for the past 10 years that I have eaten a practically paleo diet.  My ethnic background consists of Hungarian, French, and German.   My last blood profile showed my total lipoproteins at 231 mg/dL, my HDL at 85, and my triglycerides at 47.  Using the Friedewald equation they calculated the LDL at 138, but since I have very low triglycerides, using the Iranian formula calculator I calculate my LDL equals 104.  Since I have nearly twice as much HDL as triglycerides, and low fasting glucose, I have extremely low heart disease risk.  My liver enzyme levels and bilirubin all fell in low normal values, indicating no liver dysfunction.





"

Tuesday, March 30, 2010

Paleo Diet Analysis: Kitavan Analogue Diet

This weekend I spent some time reading Stephan Guyenet's excellent series of posts on the Kitavans, along with parts of Staffan Lindeberg's website and book Food and Western Disease: An Evolutionary Perspective, which also contain information on the Kitavans.

The Kitavans display exceptional health and live well into their 90s without heart disease, cancer, diabetes, obesity, high blood pressure, or other diseases of civilization. They eat eat a diet composed primarily of tubers (sweet potatoes, cassava, yam, taro), coconut, fruit (bananas, guava, watermelon, pineapple), vegetables, and fish. Far from a low carbohydrate or high animal protein diet, this supplies 69% carb, 21% fat, 10% protein. They maintain immunity to modern diseases and have low insulin levels (almost half those of Swedes).

I decided to create a Kitavan diet analogue for analysis. They have an average caloric intake of 2200 kcal per day, so I aimed for that figure and incorporated the foods Lindeberg lists as their staples (above). The food list looks like this (click on images to enlarge for ease of reading):



The diet supplies 376g carbohydrate, 63g fat, and 64g protein.  The macronutrient analysis looks like this:

By energy, 66% carbohydrate, 24% fat, 10% protein, close enough to Lindeberg's reported 69:21:10 to serve as a valid measure.  It contains 52g saturated fat and supplies 20% of calories as saturated fat, again not significantly different from Lindeberg's reported 17% of calories from saturated fat.  Polyunsaturates and monounsaturates each contribute only 1% of calories.


Kitavans, photo source:  Staffan Lindeberg

The four fruits (one serving of each) supply about 72g of the total carbohydrate, which would mean an intake of about 36g of fructose.  Since the Kitavans have low insulin levels and don't have heart disease, cancer, diabetes, dementia, or any other disorder, they seem to provide evidence against the claim that more than 15g/d of fructose causes insulin resistance, etc.

The micronutrient analysis looks like this in tabular then graphic display:



The menu shows shortages in vitamin D and calcium.  Kitavans get plenty of sunshine so don't need dietary vitamin D.  My analysis assumed that they don't consume soft fish bones or make broth from fish bones, probably an incorrect assumption, and also does not account calcium they may get from drinking water (mineral waters can supply up to 500mg per liter), so their calcium intake probably exceeds the level in this menu.

 Kitavan fisherman, photo source:  Staffan Lindeberg 

One note about zinc:  Two thirds of the zinc supplied by this menu comes from one single oyster. Oysters supply 150mg of zinc per 100g serving, so a Kitavan needs only one oyster daily to bring the zinc level to well above recommended levels. 

In short, the Kitavan diet easily supplies all the essential nutrients at recommended levels, and affords a high immunity to modern diseases along with excellent longevity, without a high protein or low carbohydrate intake.

Paleo Diet pH: Does It Matter, part VII

Some people appear to believe that Stefansson's 12 month trial of an all meat diet published in JAMA proved that an all meat diet provides adequate skeletal nutrition for prevention of osteoporosis.

According to the JAMA report on the all meat experiment, Stefansson consumed ends of bones supplying about 100mg calcium daily (less than by Inuit). The report on the experiment states:

"The increased amount of tartar on Stefansson's teeth and the lack of evidence of lowered blood calcium offers an interesting field for speculation. There was no decreased density in roentgenograms of the hands at the end of the experiment when compared with the hand of a man on a general diet."

Testing only the hands with X-ray does not tell us whether he lost vertebral or trochanter bone; and X-rays don't have the ability to detect the small amount of bone density lost in one year.

In fact, the National Institute of Arthritis, Musculoskeletal, and Skin Diseases (NIAMS) has this to say about X-ray tests for bone density:

"X-Ray Tests

If you have back pain, your doctor may order an x ray of your spine to determine whether you have had a fracture. An x ray also may be appropriate if you have experienced a loss of height or a change in posture. However, because an x ray can detect bone loss only after 30 percent of the skeleton has been depleted, the presence of osteoporosis may be missed."

So the test used to evaluate effects of an all meat diet on Stefansson's bone density would only have detected loss of bone if he had lost 30 percent of his bone mass. Simply put, at the time of the experiment, they did not have a technology capable of detecting smaller yet significant changes in his bone mass.

Further, they don't report before and after X-rays of Stefansson, they report comparing Stefansson's hands to those of a man "on a general diet." Which can't tell us whether the diet had any impact on Stefansson's bones.

The failure of Stefansson's blood calcium to decline is not surprising, since body can prevent drops in blood calcium by extracting calcium from the bones and tissues. Low calcium in blood causes PTH release, which extracts calcium from bone to raise blood calcium to normal levels. Thus, on a calcium deficient diet, blood calcium will not go below normal until bone stores of calcium have been exhausted.

Stefansson reportedly had increased dental tartar, which indicates increased salivary calcium and phosphorus. What makes this happen?

This study showed that administration of PTH increases calcium and phosphorus in saliva: http://www.ncbi.nlm.nih.gov/pubmed/404157

Thus, we can surmise that Stefansson probably had increased PTH, which was probably resorbing bone to maintain normal blood calcium, simultaneously raising the calcium content of his saliva, producing increase in tartar. The calcium and phosphorus should stay in bones, not be deposited on the outside of teeth.

I also want to note that Stefansson consumed organ meats that supply vitamin C (brains, liver, etc). To that extent Stefansson did replicate an Inuit diet. He in fact made it very clear that to live on an all-meat diet requires replicating the Inuit diet in several important respects, including eating far more fat than protein, eating organs, etc.

As an experiment, I ate an all meat diet for more than one month. I ate ends of bones, but not every day, and liver once weekly. Within a few weeks, I developed severe muscle cramps indicative of mineral (primarily potassium) deficiencies. When I added vegetables and fruits back to my diet, the cramps diminished. This tells me that an all meat diet does not adequately provide me with potassium, for which I have to eat plants.

Thursday, March 18, 2010

Arctic Paleo Diet: Modern Foods Can't Replicate An Inuit Diet

As we have discussed possible Inuit diet profiles for their nutrient contents relevant to bone health in the series pertaining to Eskimo Diet and Health, I have come to realize that the idea that you can replicate Inuit diet and health by eating a diet composed of any selection of modern meat and fat does not hold water.  For example, thanks to help from Greg, we found that to ensure adequate intake of manganese, Inuit had to eat shellfish; that a diet of meat and finfish alone fell short.

This fact came very clear to me when I read through the paper on vitamin C in the Inuit diet discovered by my able commenter Greg (Thanks Greg!): "Vitamin C in the Inuit diet: past and present," a master's thesis  written by Karen Fediuk of the School of Dietetics and Human Nutrition at McGill University, Montreal, Canada, July 2000.

This paper demonstrates that the Inuit ate a variety of wild plant and animal tissues that supplied vitamin C.   Further, even if you assume that Inuit only ate animal products most of the time, many of the marine animal tissues they consumed had very significant contents of vitamin C not found in modern livestock products, even from grass-fed animals.

For example, among common traditional Inuit foods, cisco eggs contain ascorbic acid at levels of 49mg/100g, whale skin 36mg/100g, and ringed seal brain up to 28mg/100g.  Compare these to spinach supplying ascorbic acid at 51mg/100g, oranges at 50mg/100g, cabbage at 47mg/100g, and tangerines at 31mg/100g.

Frozen and raw muscle meats consumed by Inuit contain ascorbic acid at 1mg/100g on average. In contrast, modern muscle meats generally supply no vitamin C at all in a 100g portion, and liver only about 20-30mg/100g.

Fediuk found that in a traditional Inuit diet, absent modern foods, vitamin C intake would range from 90mg/d up to 262mg/d, depending on season (table 13.5 from her thesis below):

This is plenty not only to prevent scurvy, but also to provide some of the benefits that accrue from higher tissue saturation with vitamin C.  In winter and spring, the sources of vitamin C for Inuit distribute as shown in this figure from Fediuk's paper:


In winter, kelp, boiled ringed seal meat, raw whale skin, and raw ringed seal meat provided 92% of Inuit winter intake of vitamin C, which according to the table above amounted to 90mg/d.  So these 4 items provided them with >80mg of vitamin C.  In late spring, raw whale skin provided 71% of their vitamin C intake, with mussels providing the next largest share at only 10% of the total 185mg/d intake (from table above).  That means the whale skin alone provided 131mg of vitamin C per day.  I know of no product of modern, even grass-fed, livestock that will come anywhere close to this (if anyone else does, please let me know).

In contrast, someone eating a strictly carnivorous meat-and-fat diet composed of modern livestock meats, even if strictly grass-fed, would not consume anywhere near this amount of vitamin C on a daily basis.  Therefore, a modern "zero carb" diet composed of terrestrial livestock is not a replica of an Inuit diet, and we can't expect it to produce the same health outcomes of a traditional Eskimo diet.

As I noted in Masai Use of Herbs, to replicate the diet and health of the Masai you have to eat the same quality of food (grass-fed cattle products) and use the herbs they use.  Similarly, to replicate the diet and health of the precontact Inuit (if that was desirable) would require eating exactly the same variety and types of foods as the Inuit ate–shellfish, fish with bones, seal eyeballs, walrus liver, seal brains, whale skin, kelp, berries, partially digested contents of caribou stomachs, and so on–in proportions similar to what Inuit ate.

If you do something different from the Eskimo diet, you can't rationally expect that you will have the same results.  Eskimos' experience certainly did not prove that a diet of modern meat and fat will keep you healthy without plant food intake.

One last interesting aspect of this paper.  According to Stefansson, Eskimos ate a diet providing 70-80% of energy as fat and only 20% as protein, claimed to be required to prevent protein poisoning.  Others have claimed that humans can tolerate no more than 35% of calories as protein for extended periods of time due to limits on the liver's ability to synthesize urea from waste nitrogen, and I have taken this as a demonstrated fact.

Therefore, I was surprised to find the following table in Fediuk's thesis:



The sources she cites estimated the coastal Inuit diet providing a minimum of 43% of calories  and a maximum of 56% as protein, and fat ranged from only 43% to 53%.  These figures all have carbohydrate intake of less than 7%, so I don't think we can dismiss them as results of incorporation of modern carbohydrates (i.e. post-contact diets).  They describe the Inuit diet as having roughly equal caloric portions of protein and fat, not the modern high-fat low-carb diet.

A 3000 kcalorie diet (necessary for a young active hunter) providing 43% of calories as protein contains 322g of protein; with 56% protein it would provide 420g of protein.  This exceeds levels Stefansson claimed and apparently demonstrated (in Effects on humans of 12 months exclusive meat diet) to be acutely toxic, at least in his own case. 

I will have to do some more research to determine whether protein intakes of this level (twice what I proposed in my models of Inuit diet), from meat (not purified proteins) could have any influence on bone mass.  It has been my impression so far that  studies supposedly proving that dietary meat protein has no detrimental effect on bone health have utilized much lower protein intakes in the range of 2-3 times the RDA, whereas if this data is correct, the Eskimos were consuming 6-10 times the RDA.

Tuesday, March 16, 2010

Paleo Diet pH: Does It Matter, part VI

Arctic Paleo Diet:  Eskimo Use of Plant foods

Although Vihljalmur Stefannson portrayed the traditional Eskimo diet as strictly carnivorous, Weston Price reported that Eskimos “were able to provide their bodies with all the mineral and vitamin requirements from sea foods, stored greens and berries and plants from the sea" (page 72 of Nutrition and Physical Degeneration).

Why the conflict?  Stefannson studied Eskimos of the far Northern parts of Canada, who did eat almost exclusively carnivorous diets, whereas Price apparently spent time with Alaskan Eskimos who use more plant foods.

I have gotten ahold of two old papers that discuss the use plant foods by native Eskimos: One written by  A.E. Porsild,  former Chief Botanist of the National Museum of Canada, entitled “Edible Plants of the Arctic,” for the Encyclopedia Arctica  , a project guided by Vilhjalmur Stefansson; and the other by J.P.Anderson, entitled “Plants used by the Eskimos of the Northern Bering Sea and Arctic Regions of Alaska,”  which appeared in the American Journal of Botany, Vol. 36, November 1939.

Porsild reports that Eskimo use of plant foods varied from place to place, with it supplying not more than 5 percent of the diet in the Bering Sea region, less in North Central Canada, and variable amounts among Greenland Eskimos, with more consumed in western than eastern Greenland.  In Porsild’s words:


“Among the Eskimo--the most widely distributed race of arctic aborigines the dependence on vegetable food varies from group to group according to tradition and according to what plants are available in the area occupied by them; thus, to the most northerly tribes the use of vegetable food is purely incidental and largely limited to the partly fermented and pre-digested content of the rumen of caribou and muskoxen, whereas in the diet of the Eskimo of southwestern Greenland, Labrador, and western and southwestern Alaska, vegetable food constitutes a regular, if not very large, item.”


As for quantity of plant food in Eskimo diets, Porsild states:


"Thus Weyer (1932) estimated that in the diet of the Eskimo of the Bering. Sea region vegetable food constituted no more than 5 per cent; among the Central Canadian Eskimo Stefansson (1914) and Jenness (1928) noted that it was scarcely used at all; in Greenland the part played by vegetable food has always been unimportant, except from a dietary point of view."


Based on his own expeditions, he states:


“Twenty-five years ago, I found that only a small number of plants was used by the Eskimo of northwestern Alaska. Among the more important were the leaves of Saxifraga punctata, the leaves and flowering axes of marshfleabane (Senecio congestus) and coltsfoot (Petasites frigiqys), all of which were made into a form of “sauerkraut” mixed with blubber; the root tubers of Eskimo potato (Claytonia tuberosa) and those of the vetch (Hedysaruvzalpinum) were gathered in considerable quantities and used during the winter cooked as a vegetable with meat. Of the several kinds of berries used, cloudberry or baked-apple (Rubus Chamamorus) and crowberry (Empetrum) were the most favoured. Both were eaten fresh or preserved frozen in sealskin bags.”


Thus, the Northwestern Eskimos ate some leaves, flowers, tubers and berries.  Regarding seaweeds, Porsild states:


“A number of edible species of seaweed or marine algae occur along rocky shores of the arctic seas and several are used regularly, if mostly in times of scarcity, by the Eskimo. In Greenland, several species, including Rhodymenia palmata and Laminaria spp. [kelps] are eaten raw, dipped in boiling water or with seal oil. Rodahl (1950) estimated that 50 per cent of the vitamin C intake of the east Greenland Eskimo is derived from marine algae.”


This indicates that Eskimos used kelp "regularly, if mostly in times of scarcity."  So was scarcity regular for Eskimos? In regards to vitamin C, Porsild states:


“The recent investigations by Rodahl (1944) and others, of the vitamin content of arctic plants, have demonstrated too, that it is just those arctic plants that are eaten by preference by nearly all arctic tribes, that have the highest content of ascorbic acid as well as of thiamine [emphasis added], and that the methods of preparation and of storing of vegetable foods used by these people are perhaps the best possible in the circumstances for the preservation of vitamins.”


Anderson visited Eskimo villages of the Northern Bering Sea and Arctic Alaska during the summer of 1938.  He states:


“The diet of the Eskimos is almost exclusively of animal origin.  The total portion that is directly vegetable is very small. The food plants growing in the vicinity of the villages indicated that but little had been gathered.”


Anderson also found the Eskimos using leaves (greens), taproots, tubers, seeds, and berries (including blueberries).   He also reports that they preserved plant foods for consumption out-of-season by either fermentation or storage in oil or fat.  I may devote another post to some of Anderson’s interesting observations on  Eskimo use of plant foods. 

According to the online Encyclopedia of Food and Culture entry on Inuit food and culture (http://www.enotes.com/food-encyclopedia/inuit),  the wild greens and berries “are much sought” by Inuit.  Anderson reports:


“Among monocotyledons, products of three species are consumed.  The enlarged farinaceous [starchy] bases of a sedge, Carex sp., are called mouse food from the custom of robbing the nest of field mice (Microtis), which gather them for winter food.  In some places fish is placed in the mouse nests so that the mice may live through the winter and be able to store a new supply of the sedge the following year.” 


Thus he seems to indicate that Eskimos would “sacrifice” fish to feed mice so that they (the Eskimos) could get some starchy tubers!   If so I would agree that Eskimos "eagerly sought" what plant foods they could get.  (In another post I may report on similar practices among the Chukchi, another Arctic population popularly but incorrectly viewed as strictly carnivorous.)

So it seems possible that Eskimos would have preferred a greater portion of plant foods in their diets, but found that their environment could hardly meet their desires without some encouragement (e.g. feeding fish to the tuber-collecting mice) or fetching partially digested grasses from the guts of caribou.

Therefore, for purposes of estimating nutrient intakes, a proper analogue of an Eskimo diet would have not more than five percent of calories from plants consisting primarily of some greens and berries, and little kelp.  I have created one with five percent of calories from dandelion greens, blueberries, and kelp (all species consumed by Eskimos), along with 50g (less than 2 ounces) of walrus liver, sardines with edible bones, and venison substituted for caribou, which possibly presents the best case scenario for an Eskimo:  


This diet supplies 74% of energy as fat, 22% as protein (9% less than some estimates of usual protein intake for a precontact Eskimo) and 4% carbohydrate;
 An analysis of micronutrients reveals a major excess of vitamin A and significant deficiencies of  vitamin C, magnesium, manganese, potassium, and thiamin:


This presents the micronutrient contents graphically:


Although the FitDay software does not analyze for boron content, I can say almost certainly this diet lacks adequate boron because of its very low content of vegetables and fruits.  Thus, with regard to bone mineral loss, this diet has several potential contributing factors:

1.  High vitamin A content relative to vitamin D status.  With less than 50g of walrus liver, this diet supplies 51, 537 IU (4183 mcg) of vitamin A, more than 4 times recommended intakes.  Current research suggests that chronic high vitamin A intakes coupled with low vitamin D status may increase the risk for bone loss.   In Vitamin A antagonizes calcium response to vitamin D in man,  Johansson and Melhus  report results of experiments in which they found that "an intake of vitamin A corresponding to about one serving of liver antagonizes the rapid intestinal calcium response to physiological levels of vitamin D in man."  Given that this diet supplies only 771 IU of vitamin D and Eskimos had limited or no sun exposure at least half of the year and poor solar ray angle in the summer, I think it highly likely that they had a very unfavorable ratio of vitamin A to vitamin D.

2.  Deficiency of vitamin C necessary for bone matrix formation.

3. Deficiencies of boron, magnesium and manganese, discussed in the Part V of this series.

4.  Deficiency of potassium.  Plant foods generally have a much higher potassium content than animal foods.  This Eskimo analogue diet supplies less than half of the recommended intake of potassium.  In "The effects of high potassium consumption on bone mineral density in a prospective cohort study of elderly postmenopausal women" Zhu et al report finding that "Potassium intake shows positive association with bone density in elderly women, suggesting that increasing consumption of food rich in potassium may play a role in osteoporosis prevention."  

Hence, it seems that even in the best case scenario, an Eskimo diet may have had chronic nutritional issues besides acid load that may have promoted their early onset and rapid progression of bone loss.



If you take away all the plant foods and the liver, you get this:

Which when analyzed has the following macronutrient profile:


This shows how it measures up in micronutrients:


Now it has all the same deficiencies as the best case scenario, plus only supplies 10% of the vitamin A requirement and only 61% of the vitamin E requirement.  It seems Eskimos would have more likely had the regular intake of liver promoting excessive vitamin A levels.  The other deficiencies would have a negative effect on bone health.


Relating to pH, it now seems likely that it will be impossible to separate the effect of pH of food from the nutritional content.  Plant foods provide the best sources of the nutrients deficient in these Eskimo analogues, and also have alkaline residues. Therefore, I feel inclined to say that the accelerated bone loss of Eskimos occured due to an imbalance of vitamins A and D along with a lack of nutrients better supplied by plant foods than animal foods.   Whether we can have any confidence that lack of base-forming organic acids also plays a role or not I will explore in a future post.


Looking at the best case scenario Eskimo diet above, I estimate its pH residue as follows (fat is neutral so we can ignore it):


280g sardines @ 13.5 mEq per 100g = +38
196g venison @ ~8 mEq per 100g = +16 (used beef, venison not in database)
50g liver @ ~14 mEq per 100g = +7 (used veal liver, walrus liver not in database)
148g blueberries @  ~ –6.5 mEq =  –10 (used black currants, blueberries not in database)
105g dandelion greens @  ~ –2.0 = –2 (used chicory, dandelion not in database)


Net +49 mEq, acidic.


At this point, still wonder if nutrient deficiencies can alone account for the uniquely high occurence of type II bone remodeling in the Eskimos.  More on that in an upcoming post.

Thursday, March 11, 2010

Paleo Diet pH: Does It Matter? Part V

Researchers who have discovered the unusual early onset and accelerated progression of bone loss in Eskimos have explored various possible explanations for it.  Basically, we can simply look at all the factors we know may affect bone mass accrual or release and evaluate the Eskimo diet and lifestyle to see if any one or several of those factors stands out as an influence strong enough to produce the observed bone loss.

Activity

Bones lose mineral content when not subjected to loads.  Primitive Eskimos led vigorous lives of hunting, kayaking, walking through snow, carrying loads of food, fuel, or children, so it seems unlikely that inactivity caused bone losses found in precontact Eskimos.  

Eskimos compared to Pueblos had more evidence of bone demineralization activity.  It seems unlikely that the Pueblo life in the high desert had higher bone loads than Eskimos.  Walking through the desert is less strenuous than walking in snow with snow shoes and heavy clothing, carrying loads of meat probably is more strenuous than picking corn cobs.

In the 1970s, modern Eskimos getting about 50% of subsistence from hunted wild foods had more demineralization than modern Wisconsin whites who got most if not all of their foods by driving automobiles to supermarkets.  Very unlikely that the whites had higher intensity activity overall.

Vitamins

Vitamin A – Modern population data indicates that excessive vitamin A intake relative to vitamin D and K levels may promote osteoporosis.  Eskimos who ate animal livers frequently, particularly liver from species high on the food chain (e.g. polar bears), may have ingested levels of vitamin A that would promote osteoporosis.

Vitamin D – Eskimos had extensive summer sun exposure with sufficient skin exposure to generate some vitamin D.  Those that ate marine animals would also have gotten large doses of vitamin D from fish and sea mammals.   Weston Price reported Eskimos getting at least 10 times the vitamin D found in modern diets.  Lack of vitamin D would have caused rickets and poor craniofacial development, neither of which appear to have occurred in either precontact Eskimos or those Weston Price found still eating native diets.  The Wainwright Eskimos studied by Mazess got about 50% of their energy from wild foods including fish supplying vitamin D, whereas the whites having higher bone mineral content ate none of those foods.  Vitamin D deficiency seems an unlikely cause of Eskimo age-related bone loss.

Vitamin K – Inadequate vitamin K, particularly K2, results in loss of bone matrix.  Eskimos who ate ruminant animal fats and livers from caribou would very likely have gotten adequate vitamin K2.  This would seem confirmed by the excellent craniofacial development of Eskimos studied by Weston Price, since lack of vitamin K2 would have resulted in poor craniofacial development.

Vitamin B-12 – Deficiency of vitamin B-12 in pregnancy and childhood appears to impair bone mineralization in youth.  Eskimos ate plenty of meat and fish rich in vitamin B-12.

Vitamin C – Deficiency of vitamin C would impair formation and repair of the cartilage bone matrix.  Eskimos apparently did not suffer from vitamin C deficiency severe enough to impair bone growth during development since most reports including Weston Price have found Eskimos have normal bone growth and development in youth.  However, their vitamin C intake fell far short of the 400-500 mg estimated daily intake of an equatorial hunter-gatherer,  which is only a fraction of the the intake a comparably sized non-human primate would consume from a wild diet.  I consider it possible that their vitamin C intake was suboptimal for maintaining bone matrix during aging.  

Mineral Intake

Boron – Modern studies have found higher resistance associated with lower risk of osteoporotic bone fractures among people consuming higher amounts of boron.  Fruits, vegetables, and nuts provide most of the boron in modern diets. I have not yet found information of the boron content of fish and meat, the main mineral sources in the Eskimo diet.

Calcium – Eskimos consumed calcium in meat and bones, primarily fish bones.  They had an estimated variable intake ranging from 500 mg to 2000 mg daily.   Since in most studies including the reports of Weston Price it appears that they developed and maintained normal bones and bone density comparable to non-Eskimos up to the third decade of life, it does not seem likely that calcium deficiency caused their early onset osteoporosis.

Copper – Copper supports collagen formation for bone structure and deficiency results in decreased bone formation and bone deformities, and increases loss of calcium from bone.   In the Eskimo diet, meat, particularly organ meats, would have supplied copper.  Since Price found isolated Eskimos had no bone deformities, precontact Eskimos probably had adequate copper intake for development. 

Magnesium – The bones contain 60 percent of the magnesium in the body.  Rude et al found that dietary magnesium deficiency induces bone loss, decrease in osteoblasts, and an increase in osteoclasts in rats maintained at levels of 10%, 25%, and 50% of recommended intakes.  They also found that magnesium restriction in humans induces changes that would promote osteoporosis.  Of foods eaten by Eskimos, meat does not supply much magnesium but seafoods and kelp do.  Nuts and green leafy vegetables supply high amounts.  

Manganese – Manganese plays a role in collagen formation and is required for normal bone formation and development.  

Phosphorus – Calcium phosphate forms the primary component of bones and teeth. Phosphate deficiency would result in failure to form normal bones.   Humans rarely experience phosphorus deficiency, and since meat and fish supply plenty of phosphorus, Eskimos would not have experienced phosphate deficiency unless during starvation. 

On the other hand,  studies on humans consuming diets with a low calcium:phosphorus ratio produce elevations of parathyroid hormone and urinary calcium (see for example Kemi et al  or Calvo).
 
An Eskimo Analogue Diet

To get some idea of the nutrient profile of a precontact Eskimo diet, I created an Eskimo analogue diet and subjected it to nutrition analysis.  I composed it of sardines with edible bones, venison (as an alternative to caribou, not in the database), kelp (8 ounces) and animal fat.  About 50% of the protein comes from the sardines, and the rest from venison.  The diet supplies 3000 kcal, with 21% of calories from protein and 77% from fat, approximately the ratio recommended by Stefansson.  

 
This slide displays the macronutrient values and ratio of this food selection:



This slide gives the micronutrient analysis in tabular form:



And this slide gives the micronutrient analysis in graphic form:

 Using this selection of foods, this diet has adequate calcium but shows significant deficiencies of vitamin A, vitamin C, manganese, potassium, and thiamin.  I know that the Eskimos met their vitamin A needs by eating liver regularly.  They obtained vitamin C from adrenal glands, and the need for vitamin C is probably reduced by low carbohydrate intake.  The manganese content only 36% of recommended levels.  As noted above, this deficiencies could have an adverse effect on bones.  

Absent the kelp, this diet provides only 16% of the recommended intake of manganese.  This means that increased kelp consumption would provide the most efficient way to increase manganese intake without increasing protein intake.  Since one-half pound of kelp provides 20% of the daily requirement for manganese, to reach 80% of the recommended level would require adding more than one pound of kelp to the diet, for a total of more than 1.5 pounds of kelp daily.  That seems possible and would also increase intake of other minerals including calcium.  It would fit with the mineral intake of Eskimos reported by Weston Price.

Including the half-pound of kelp, the diet also provides early 1500 mg of calcium and about 2100 mg of phosphorus.  Assuming precontact Eskimos ate like this, the diet does not have a low calcium to phosphorus ratio, so this would probably exclude a low calcium:phosphorus ratio in the precontact Eskimo diet as a factor to their bone condition.  

Summary


Thus it seems unlikely to me that isolated coastal Eskimos who ate kelp suffered from any activity or mineral deficiency that could account for their unusual bone metabolism and mineral loss with age.  Inland Eskimos who ate less fish and kelp may have had a more difficult time getting adequate calcium and magnesium,  since without the kelp this diet would have only 42% of the recommended level of magnesium and about 400 mg less calcium, and without the sardines the calcium intake would fall very low.

It does seem possible that excessive vitamin A could have played a role, at least in some cases where people consumed liver from certain species.  Subacute deficiency of vitamin C may also have played a role.   On page 72 of NPD, Dr. Price summarized the omnivorous Eskimo diet:  "Eskimos were able to provide their bodies with all the mineral and vitamin requirements from sea foods, stored greens and berries and plants from the sea."  I don't know what other greens or berries the Eskimos ate, but they would have increased the vitamin C content as well.  Thus, I do not feel certain that either of these can completely account for the degree of bone mineral loss observed in Eskimos.

I do want to emphasize the importance of kelp in this menu.  If you take it out of the outlined diet, this makes the diet deficient in vitamin E, magnesium, manganese, potassium, and thiamin.  It appears that by Weston Price's report, high nutrient density plant foods (seaweeds, greens, and berries) played an important nutritive role in the Eskimo diet.

Addendum 3/13/2010:

Shortly after I posted this I noticed that I did not feel confident in my supposition that Eskimos ate the amount of kelp I proposed in my analogue diet, but I did not have time to edit it.  This reminded me that when I posted on the Masai Use of Herbs, in response to a comment I stated that I would post on plant foods used by Eskimos.  Then I received comments from Stephan and Tom (below) that expressed the same doubt.  I got ahold of two old reports on plants used as food by Eskimos, and from these two papers it appears that coastal Eskimos did not use kelp in anywhere near the quantity I thought possible.  It appears that they actually used more of land plants than seaweeds.

So in my next post on this subject I will present a revised Eskimo analogue diet.  Suffice it to say the without kelp, the Eskimo diet has multiple mineral deficiencies that could promote osteoporosis.

Sunday, March 7, 2010

Paleo Diet pH IV: Weston Price on pH

It appears to me that some people into paleo diet and Weston A Price Foundation seem to think that Weston Price has the final say in all debates, that nutrition research ended with Price and anyone who contradicts or appears to contradict Weston Price has to “correct” his/her view to reflect what they believe Weston Price taught. 

Well, I have read Nutrition and Physical Degeneration cover-to-cover several  times. I have also read several of the articles Price published in medical, nutrition, and dental journals, including the one he entitled “Acid-Base Balance of Diets Which Produce Immunity to Dental Caries Among the South Sea Islanders and Other Primitive Races” (available online here). I use his works in several classes that I teach. I think I have a pretty good grasp of Price’s findings.

I did not come away from reading Price with the impression that he had he had discovered every significant nutrition fact. Price did not have omniscience.

Secondly,  Price's research suffers from some weaknesses.  Price did not spend much time with any of the groups he studied, nor did he perform extensive medical testing to determine the incidence of any diseases other than dental decay and malocclusion among them. Interviewing frontier doctors does not count as basic research; those guys could have made mistakes as well. Price assumed that people with good development and resistance to dental decay would also have resistance to all other disorders afflicting humans. This is not a justifiable assumption. A diet could support exceptional development and resistance to dental decay yet have adverse effects on aging.  Finally, he made almost no attempt to accurately report the quantities of foods consumed by the various groups.  He used vague terms like "largely composed of milk products" or such.  Such reports preclude making firm conclusions about amounts of various foods consumed by each group.

Third, I want to emphasize that he only intensively studied dental disorders and developmental skeletal disorders, not disorders of aging, like osteoporosis. He looked at skeletons of some groups, but nowhere in his book does he report determining the age of death of the skeletons. He doesn't even list dental decay rates in age-adjusted figures.

In the aforementioned article, Price wrote:
“My investigations are showing that primitive groups have practically complete freedom from deformity of the dental arches and irregularities of the teeth in the arches and that various phases of these disturbances develop at the point of contact with foods of modern civilization.

“It is not my belief that this is related to potential acidity or potential alkalinity of the food but to the mineral and activator content of the nutrition during the developmental periods, namely, prenatal, postnatal and childhood growth. It is important that the very foods that are potentially acid have as an important part of the source of that acidity the phosphoric acid content, and an effort to eliminate acidity often means seriously reducing the available phosphorus, an indispensable soft and hard tissue component.

It is my belief that much harm has been done through the misconception that acidity and alkalinity were something apart from minerals and other elements. Many food faddists have undertaken to list foods on the basis of their acidity and alkalinity without the apparent understanding of the disturbances that are produced by, for example, condemning a food because it contains phosphoric acid, not appreciating that phosphorus can only be acid until it is neutralized by combining with a base.”

Notice that he did not claim that his investigations showed that all primitive groups have complete freedom from all diseases of civilization. He only claimed resistance to “deformity of the dental arches and irregularities of the teeth in the arches.”

Next, he says he does not hold a “belief” in the acid-base theory with regards to dental decay and deformity. He specifically states that he thinks that he thinks that resistance to these disorders comes via “mineral and activator content of the nutrition during the developmental periods, namely, prenatal, postnatal and childhood growth.” [emphasis added] He says nothing about his whether he “believes” that the potential acidity or alkalinity of food might affect the occurrence of other skeletal or metabolic diseases associated with aging. He does not mention age-related osteoporosis and did not study it.

Then he goes on to use a broad brush to discount people who do believe that acidity or alkalinity of foods might impact health. He calls them “food faddists.” This term would not apply to the serious scientists who I have already and will in upcoming articles refer to in regards to research on Eskimo bone health or the effects or metabolic acidity on bone metabolism.

Next, he suggests that these “faddists” don’t understand the importance of foods rich in phosphorus and “condemn” them. This certainly does not apply to me, Loren Cordain, S.Boyd Eaton, Staffan Lindeberg, Thomas Remer, Friedrich Manz, Anthony Sebastian, Lynn Frasseto, or  Jurgen Vormanne.

I don’t “condemn” meat, fish, poultry, eggs, or nuts, all rich in phosphorus and protein, and acidogenic. If you look at my diet and dietary recommendations, you can see that I eat plenty of meat and that it plays an important role in my dietary recommendations.

However, I don’t blindly worship meat, etc. either. I remain aware of the basic principal of toxicology, that anything – even things essential for health -- can produce toxic effects in large enough dose.

Experiment has established that for humans dietary protein becomes acutely toxic at levels of 240-280 g per day due to limits on the liver’s ability to synthesize urea from the ammonia generated when cells convert excess protein to glucose. [See Maximal Rates of Excretion and Synthesis of Urea in Normal and Cirrhotic Subjects, full text.]

Thus, we know that excess protein can act as an acute toxin for humans. We can reasonably suspect that anything that acts as an acute toxin in large amounts can act as a chronic toxin in reduced amounts. As with other nutrients, we can reasonably expect that people will suffer from deficiency diseases if they get too little protein and toxicity diseases if they get too much, and that between these extremes we will find an optimum intake that maximizes the benefits while avoiding detriments.

Price himself seemed to acknowledge that some primitive diets might have protected against decay and malocclusions but not produced the optimum development for humans. In chapter 9 of NPD, he wrote:

Neurs, Malakal, Sudan. The Neurs at Malakal on the Nile River are a unique tribe because of their remarkable stature. Many of the women are six feet tall and the men range from six feet to seven and a half feet in height. Their food consists very largely of animal life of the Nile, dairy products, milk and blood from the herds.

A study of 1,268 teeth of thirty-nine individuals revealed only six teeth with dental caries, or 0.5 per cent. Only three individuals had caries, or 7.7 per cent.

Dinkas, Jebelein, Sudan. This tribe lives on the Nile. Its members are not as tall as the Neurs. They are physically better proportioned and have greater strength. They use fish from the Nile and cereals for their diet. They decorate their bodies profusely with scars.

An examination of 592 teeth of twenty-two individuals revealed only one tooth with caries, or 0.2 per cent.”

You will notice that this passage, typical of NPD, contains no attempt to even identify whether either of these groups suffered from any diseases other than tooth decay. Further, Price’s description of the Dinka diet is, like most of his other dietary descriptions, sketchy.  He makes no effort to accurately quantify their dietary composition. According to Everyculture.com:

“Dinka have traditionally produced all the material resources needed to sustain their livelihood via a combination of horticulture (gardening) with pastoralism (nomadic herding), fishing and occasional hunting. Millet is the mainstay of the Dinka diet [Emphasis added]. Depending on the season, it is supplemented with cow milk, fish, meat, beans, tomatoes, or rice.”

[Read more: Dinka .]

This almost certainly fails to itemize and quantify all the foods in the Dinka diet (judging by my experience with Ethiopian food, most likely the Dinka also eat a wide variety of vegetables and herbs), but at least it identifies millet as their main food. Thus, it appears that Price believed that the almost exclusively animal-sourced Neur diet produced more tooth decay and weaker, disproportionately developed people when compared to the grain-dominated Dinka diet.

How such statements by Price get converted to the idea that healthy people got all their vitamins and minerals from animal sources, and that plant foods are not important to health,  is beyond my comprehension.

Price also prescribed diets containing whole wheat, apparently unaware of the hazards associated with gluten exposure.  

Yet what appears to me as a Weston Price Personality Cult seems bent on suggesting that Price demonstrated and believed that the only groups eating predominantly animal-sourced diets--particularly milk products-- had in every case the best development and health. 

Friday, March 5, 2010

Why I Eat Walnuts

 
Image Source:  Mariani Nut

Some contemporary hunter-gatherer tribes displaying a high immunity to diseases of civilization consume fairly large amounts of nuts.  Although some nuts richly supply omega-6 fats and an excess intake of corn, soy, or safflower oils rich in these fats may have ill effects, I hesitate to generalize these effects to all whole foods rich in such oils.  Since whole foods contain a myriad of compounds,  I believe that we have to evaluate each food as a whole, not reduce any food to a predominant nutrient.

The !Kung got up to 50% of their calories from the mongongo nut. The mongongo supplies 57 g fat/100g, and 43% of that fat occurs as PUFA, nearly all linoleic acid (omega-6). Assuming 2000 kcal/d and 1/3 of calories as mongongo, they would get ~16g linoleic/d just from the nuts, then some from game fats.

However, a 100g portion of mongongos also provides approximately 193 mg of calcium, 527 mg magnesium, 3.7 mg iron, 2.8 mg copper, 4 mg zinc, 0.3 mg thiamine, 0.2 mg riboflavin, 0.3 mg niacin, and a stunning 565mg of vitamin E.  This very high vitamin E content makes the oil very stable and resistant to oxidation and 'rancidity' for a very long time, in spite of the African heat.

Inland Australian Aborigines consumed considerable amounts of wild walnuts, almonds, candlenut, pine nuts, and even acorns.

I consume fairly large amounts of nuts, particularly walnuts and almonds, more of the former and less of the latter. Walnuts appear to have a number of positive effects on health. I have collected some articles and abstracts of research on the health effects of walnuts. I have not read all of these in full text yet, but a perusal of PubMed shows a clear pattern of independent research on walnuts suggesting significant health benefits.


Cancer Prevention

According to the American Association for Cancer Research, a team led by Elaine Hardman, Ph.D., associate professor of medicine at Marshall University School of Medicine, studied mice that consumed a diet containing the human equivalent of two ounces of walnuts per day. A separate group of mice ate a control diet.

"Standard testing showed that walnut consumption significantly decreased breast tumor incidence, the number of glands with a tumor and tumor size.

'These laboratory mice typically have 100 percent tumor incidence at five months; walnut consumption delayed those tumors by at least three weeks,' said Hardman."

Carvalho et al tested extracts of walnuts for human cancer cell antiproliferative and antioxidant activities. They found that the extract of walnut seed inhibited growth of human renal and colon cancer cells.

Aithal et al found that juglone, a naphthoquinone from walnut, kills cultured melanoma tumor cells.

Spaccarotella et al studied the effects of walnut consumption on prostate and vascular health in men at risk for prostate cancer. The 21 subjects consumed 75g of walnuts daily, replacing other calories in the diet. They found that walnuts may improve biomarkers of prostate and vascular status.

 
Image source:  Pretty Garlic

Cardiovascular Health

Casas-Agustench et al conducted a human trial in which subjects consumed a mix of 15g walnuts with 7.5g almonds and 7.5g hazelnuts daily. Comapred to a control group, those eating the nut mix had a reduction of fasting insulin and insulin resistance.

Ma et al conducted a human trial in which type 2 diabetic subjects consumed with 56 g (366 kcal) walnuts/day for eight weeks. They found that the walnut-consumers displayed a significant improvement in endothelium-dependent vasodilatation, suggesting a potential reduction in overall cardiac risk.


Ros et al had 21 people with high cholesterol consume either a Mediterranean diet or a similar diet in which walnuts replace about 32% of the monounsaturated fat (which amounted to 40-65g walnuts daily, varied as a proportion of caloric intake). They reported that, compared to the Mediterranean diet, the walnut diet improved endothelium-dependent vasodilation, reduced levels of vascular cell adhesion molecule-1, and significantly reduced total cholesterol and LDL cholesterol. The reductions of cholesterol correlated with increases of both dietary {alpha}-linolenic acid and LDL {gamma}-tocopherol content, and changes of endothelium-dependent vasodilation correlated with those of cholesterol-to-HDL ratios.

Cognitive Health

Willis et al fed aged rats a control, or a 2, 6 or 9% walnut diet for 8 weeks before motor and cognitive testing. They found that the 2% walnut diet improved performance on rod walking, while the 6% walnut diet improved performance on the medium plank walk; the higher dose of the 9% walnut diet did not improve psychomotor performance and on the large plank actually impaired performance. All of the walnut diets improved working memory in the Morris water maze, although the 9% diet showed impaired reference memory. Thus the effect appeared dose-dependent, with no benefit and possible detriment for consuming walnuts as more than 6% of diet. So it appears that moderate intake of walnuts can improve cognitive and motor performance in aged rats.  If you have an aged rat, make sure to give him/her some walnuts!

Thursday, March 4, 2010

Paleo Diet pH: Does It Matter? – Part III

Here are a few more studies that lead me to believe that even precontact Eskimos had an early onset and accelerated rate of bone mineral loss with age that we can most easily explain as an effect of their diet composition.

Type I and Type II Resorption Cavities

In 1979, Richman, Ortner, and Schulter-Ellis studied differences in intracortical bone remodeling in three aboriginal American populations, Eskimos, Arikara, and Pueblo.[1] Specifically, they studied the occurrence of two different types of resorption/remodeling cavities in the bones.

 
Image source:  Wikipedia

In normal Type I remodeling the resorption cavity (resulting from the breakdown of mineralized bone) courses lengthwise through the mineralized sections (lamellae), surrounded by osteons (an osteon consists of a haversian canal surrounded by lamellae).

In Type II remodeling the cavity appears as a small dilation of the haversian canal of an osteon. The haversian canal contains the blood vessels servicing the osteocytes. It appears that Type II remodeling results from resorption of minerals for maintenance of physiological homeostasis.

The Smithsonian Institution preserved and housed all the skeletal material studied.

The 51 Eskimo skeletons came from Northern Alaska. Regarding their ages, Richman et al state:

“According to records in the dividision of Physical Anthropology, Smithsonian Institutino, material is both pre- and post- contact, from the late 1700s to early 1900s. However, settlers had little effect on Eskimo diet and life style [7], allowing consideration of the skeletal material as belonging to a homogeneous group.”

To establish that contact in this period had little influence on Eskimo diet, they cite: Rainey FG. The Whale Hunters of Tigara. Anthropological Papers of the American Museum of Natural History, 41. New York, 1947. I don’t have access to this paper. However, given that when Weston Price reached the Eskimos in the 1930s many still remained exclusively on their native diets, I am inclined to accept that contact had very little significant influence on Northern (i.e. more isolated) Eskimos in the early 1900s.
Eskimo Family. Image source:  Wikipedia

The 65 Pueblo skeletons came from pre- and post- contact periods also: 919 AD to the 1600s. Richman et al cite another researcher, Corrucini, who detected no differences in osteometric or odontometric traits in the pre- and post- contact specimens. About 90% of the Pueblo diet consisted of maize, beans, squash, and sunflower, with protein-poor maize accounting for 80-85% of the total. Thus they ate a 90%+ vegetarian, cereal-based, low protein diet.

 
Taos Pueblo, c. 1920.  Wikipedia


The 57 Arikara (Plains dwellers) skeletons also came from both pre- and post-contact times (1550-1845). Arikara ate maize, but unlike the Pueblo they combined it with meat and vegetables. The Arikara diet included red meat, fowl, fish, internal organs, fat, blood, eggs, berries, and tubers.

 
Arikara Warrior.  Wikipedia.


Richman et al found that “The populations did not differ significantly in numbers of type I resorption cavities or type I forming osteons. However, highly significant result were obtained with respect to type II resorption cavities and type II forming osteons.” The Eskimos had about 4 times more type II osteons than the Peublos, and almost twice as many type II osteons as the Arikara, indicating that the Eskimo bones had experience considerably more type II remodeling than the other two groups.

Eskimos had the highest occurrence of Type II resorption cavities, while Pueblos had a significantly lower number of these cavities and Arikaras had an intermediate number (which was not significantly different from either Eskimos or Pueblos). They found no evidence that age affected the incidence of type II remodeling (i.e. the incidence of type II remodeling did not differ with age in any of the populations). This indicates that the type II remodeling arose from a metabolic condition, not aging.

Richman et all suggested that the acidogenic character of the Eskimo diet would lead to greater urinary losses of calcium, which would cause a greater need to resorb bone calcium to correct blood calcium levels. This would explain why the Eskimo bones had the most evidence the type II resorption that occurs in the haversian canals adjacent to the blood vessels serving the osteocytes.

What About Precontact Eskimo Bones?

In 1979, Laughlin, Harper, and Thompson reported [2]:

“Our data from St. Lawrence Island (Yupik) Eskimos demonstrate a low degree of bone mineralization in both males and females, thus suggesting that a low bone mineral profile and rapid bone loss with advancing age is a condition common to all Eskimos regardless of their particular micro-environment (table 3). It is also apparent that this pattern has been the case in Eskimos for a considerable time prior to European contact.” [Italics added.]

These researchers also found that Eskimo bones had thinner cortices than those of Caucasians; their bones thus had both thinner and less dense cortices.

In 1981, Thompson and Gunness-Hey published “Bone Mineral-Osteon Analysis of Yupik-Inupiaq Skeletons”[3]. They analyzed nine different variables in skeletons from both post-contact and pre-contact Eskimo skeletons in comparison to skeletons of U.S. caucasians. They found “Eskimo femora to be thinner than those of U.S. whites.” Eskimo bones also had a greater porosity. They also reported:

“Similarities in cortical thickness, bone mineral index, and cortical bone density values between Kodiak Island (precontact) and St. Lawrence Island (postcontact) skeletons suggest no differences in bone remodeling between periods of contact among Eskimos from the same linguistic division (Yupik).”

Thus, these investigators appear convinced that precontact Eskimos had the same pattern of early-onset and accelerated bone mineral loss as partially modernized Eskimos.

Finally, in a paper entitled "The paleopathology of the cardiovascular system" (full text), Zimmerman reports the results of autopsies he performed on several naturally frozen bodies of ancient Eskimos.   The oldest one, dated to about 400 AD, was a 53 year old female from St. Lawrence Island.  It appears she died in an avalanche.  She had coronary and aortic atherosclerosis.

Two others came from Barrow, the northernmost community in Alaska, and dated to 1520 AD +/- 70 years, well before European contact.  The remains indicated that an entire family had died in their sleep trapped and killed by ice in a storm on the Arctic Ocean.  One female was 25 to 30 years of age and one 42 to 45 years of age.  The elder exhibited atherosclerosis.  According to Zimmerman, both "showed severe osteoporosis, the bone spicules being remarkably thinned and decalcified."  Read that again.  He found severe osteoporosis in a pre-contact Eskimo woman who was at time of death not more than 30 years of age. 

In upcoming posts I will discuss some of the other evidence of the effect of meat on metabolic acidity that leads me to select and recommend a diet with a net alkaline residues.

Thanks to Loren Cordain for assistance with this series, and especially for finding the Zimmerman paper.

1. Richman EA, Ortner DJ, and Schulter-Ellis FP. Differences in intracortical bone remodeling in three aboriginal American populations: Possible Dietary Factors. Calcif Tissue Int (1979) 28:209-214.
2. Laughlin WS, Harper AB, Thompson DD. New Approaches to the Pre- and Post-contact History of Arctic Peoples. Am J Phys Anthrop (1979) 51:579-588.
3. Thompson DD and Gunness-Hey M. Bone Mineral-Osteon Analysis of Yupik-Inupiaq Skeletons. American Journal of Physical Anthropology (1981) 55:1-7.

Monday, March 1, 2010

Paleo Diet pH: Does It Matter? – Part II

As I reported in Eskimo Osteoporosis?, I felt astonished when I found that a report by Mazess, commonly cited as documenting osteoporosis among precontact Inuit, actually reported that middle-aged Inuit had an apparently normal bone mineral density. As I said in that post, that report did not give good evidence one way or another for bone density of elderly Inuit. I decided to read some of the other papers published on this topic.

In 1972, Mazess and Jones published data documenting age-related bone loss in skeletons of extinct Sadlermiut Eskimos.[1] In this study 17% of the skeletal remains studied came from a stratum at least several hundreds of years old, 44% came from remains deposited before 1899, and 39% from remains deposited between 1899 and 1903. Contact had very little influence on Eskimo diet and lifestyle through these periods. In these skeletons Mazess and Jones found that skeletons from individuals probably aged 36 years or older showed a more rapid rate of bone mineral loss than comparably aged non-Eskimos.

In 1974, Mazess and Mather published another report, Bone Mineral Content of North Alaskan Eskimos.[2] This report looked at Inuit people living in Wainwright, Pt. Hope, and Pt. Barrow, ranging from age 5 years to 82 years, both male and female. This investigation found that Inuit have bone density comparable to age-matched Caucasians in the U.S. up until the age of 40, after which they show a more rapid loss of bone mass resulting in bone mineral densities averaging 10-15% lower than U.S. Caucasians. The process of bone loss starts in the third decade of life in Eskimos of both sexes, whereas in Caucasians in the U.S. it does not start until the forties in females and fifties in males. In the 70-82 year age group, Inuit men had bone density almost 16% lower than Caucasian men, and Inuit women had bone density almost 30% (29.8%) lower than Caucasian women.

Mazess and Mather state:

“Apparently some continuous process accompanies aging in Eskimos that accelerates and exacerbates the aging bone loss evident in so many other populations. In white females, the rate of bone loss between ages 45 and 74 is approximately 9.5% per decade, and there is a change to almost 4.5% per decade thereafter. In white males, the onset of loss is later, and the rate of loss after age 55 is nearly 4.5% per decade. The present results indicate that Eskimo males lost almost 6 to 7% per decade, and Eskimo females close to 10 to 12% per decade after the late thirties and early forties. The rate of loss in Eskimos appeared to approximate 2 to 3% per decade greater than that of corresponding whites. As the onset of loss was earlier than in whites by age 50, the Eskimos had substantially lower bone mineral than whites.”

Some advocates of Inuit-style diets have criticized this and similar studies, correctly pointing out that it looked only at partially modernized Eskimos. They suggest that Weston Price’s work documented excellent skeletal health among the primitive Inuit and these studies fail to contradict Price’s findings. I do not find this argument persuasive; in fact, I find it very flawed.

According to the diet surveys carried out by the International Biological Programme in 1971 and 1972 which is cited by Draper [3], Wainwright adults at that time (when Mazess collected skeletal data) obtained nearly half of their calories, three-quarters of their protein, and half of their fats from native foods. Carbohydrate provided 32 per cent of their calories, compared to an estimated 2 per cent in premodern Arctic Eskimos. Protein provided 25 per cent of calories, not much less than the estimated 32 per cent in the premodern Eskimos. For comparison, 12 per cent would be typical for US or Northern European populations.

Therefore, the Eskimos ate the most native and least modern foods when compared to Caucasians. Since Mazess and Mather found that the Caucasians (eating the most modernized diet) had the later onset and less severe progression of osteoporosis, their study actually showed that either modernization or Caucasian race protected against the accelerated loss of bone mass found in the partially modernized Eskimos.

I find it hard to imagine any adaptive value of early bone loss in humans, so I don't find it plausible to explain this difference via genetics.

Hence, if the Eskimo diet protected against osteoporosis, we should see the lowest rate of bone loss in the group with the most Eskimo-style diet and activity patterns and the highest rate of bone mass loss in people having the most modernized diet and activity patterns. In other words, Mazess and Mather should have found the greatest rate of bone loss in the Caucasians, not the Eskimos. However, they found the opposite. This means that the fully modernized diet consumed by the Caucasians protected against bone loss.

It follows that some feature of the primitive Eskimo diet accelerates aging-related bone loss, or that some feature of the modernized diet retards aging-related bone loss. According to Draper, at the time of data collection, the Eskimos got 32% of energy from carbohydrate, 43% from fat, and 25% from protein; whereas the modern U.S. diet supplied 46% of energy from carbohydrate, 42% from fat, and 12% from protein. Thus, compared to whites, Eskimos consumed a similar amount of fat, 30% less carbohydrate, and twice as much protein.

Hence this data would generate the reasonable and testable hypothesis that either reducing carbohydrate-rich foods or increasing protein intake promotes early onset and rapid progression of bone loss in Eskimos. It does not support the hypothesis that wild game protects against osteoporosis, because the group with the diet highest in wild game (the Eskimos) had the earliest onset and most rapid progression of osteoporosis. It also does not support the hypothesis that modern carbohydrates promote osteoporosis, because the group with the lowest intake of modern carbohydrates (the Eskimos) had the earliest onset and most rapid progression of osteoporosis.

In short, even if we didn’t already have the earlier Mazess study on precontact Eskimo skeletons showing the same accelerated loss of bone mass compared to modern U.S. citizens, the fact that these Eskimos were partially modernized in diet and lifestyle only more firmly points to their native diet -- specifically, its high protein content -- as the most probable dietary cause for their osteoporosis.

By comparing the Eskimos to fully modernized whites, Mazess demonstrated that the fully modernized diet reduces aging-related losses of bone mass compared to a partially modernized Eskimo diet, which effectively shows that the acceleration of bone loss did not result from the modernized portion of the Eskimo diet or lifestyle.

This does not conflict with Weston Price’s findings. Price focused his investigation on disorders of skeletal development), not disorders of skeletal aging. He did not investigate the effects of the Eskimo diet on the aging skeleton at all. Mazess and Mather also found that the Eskimos have normal bone development, but they found something Price missed, namely, accelerated bone aging, compared to non-Eskimos.

The evidence for the role of dietary protein (as a source of metabolic acid) in osteoporosis goes beyond Eskimos and includes clinical trials.

Stay tuned for the next installment.

Notes:

1. Mazess RB and Jones R. Weight and density of Sadlermiut Long Bones. Human Biology (September 1972) 44;3:537-548.
2. Mazess RB and Mather W. Bone Mineral Content of North Alaskan Eskimos. AJCN (1974) 27:916-925.
3. Draper HH. The Aboriginal Eskimo Diet in Modern Perspective. American Anthropologist, New Series, Vol. 79, No. 2 (Jun., 1977), pp. 309-316.