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 25, 2010

Practically Paleo Diet Supplementation: How Much Vitamin D?

About a year ago, one of my paleo-dieting, vitamin D-supplementing patients developed a salivary stone (sialolith), diagnosed by an oral surgeon.  A salivary stone consists of calcium phosphate blocking the salivary duct and saliva flow, resulting in swelling of the gland during meals when saliva production increases.

The patient refused the surgical treatment for this condition and consulted me for non-surgical treatment.   I began treating her with acupuncture and a Chinese herbal formula clinically proven effective for this condition.   Over the course of about 10 months of treatment consisting primarily of drinking an herbal tea every day, the stone dissolved, confirmed by the surgeon who diagnosed it.

In the meantime (several months into the treatment), she had her semi-annual vitamin D test which found a serum 25-hydroxyvitamin D level of 82ng/mL.   This came after six months of supplementing with 4000-5000 IU daily. When I saw this level I knew it fell in the range suggested as possibly optimum by Cannell at the Vitamin D Council (50-80ng/mL), but I advised her to reduce her vitamin D intake by half (from ~4000-5000 IU per day) and let it decline to 30- 50ng/mL.

Over the course of the next 7-8 months the patient had progressively less swelling during meals, and I could see the stone shrinking.   However, it shrank so much more slowly than I expected that I started to wonder if a high intake or elevated blood level of vitamin D counteracted the effect of the herbs, and contributed to the formation of this stone.  So I did a PubMed search to find out if anyone had ever investigated the relationship between vitamin D levels and formation of sialoliths.

I found one study  that looked for increased salivary stone formation in women taking vitamin D, calcium, and alendronate (PhosomaxÔ).  This study found no evidence of increased sialolithiasis in this group of women.  However, the abstract does not state the dose of vitamin D used, and I don’t want to pay to view the full text.  I feel pretty confident that this trial did not use a vitamin D dose greater than 2000 IU daily, whereas previous to her stone formation my patient was taking 4000-5000 IU.

Then I found the abstract of an experimental study by Westhofen et al: Calcium redistribution, calcification and stone formation in the parotid gland during experimental stimulation and hypercalcaemia.   In this study Westhofen et al induced hypercalcemia in rats by administration of dihydrotachysterol, a synthetic vitamin D analogue. They reported:


“During hypercalcaemia (induced by dihydrotachysterol), a calcium overloading of the cell membrane and intracellular buffer organelles without calcification was observed. Combined stimulation and hypercalcaemia induced an excessive calcium overloading of all intra-and extracellular calcium depots with excessive calcium release into the acinar lumina resulting in calcium phosphate aggregates and stone formation. Secretory stimulation and simultaneous hypercalcaemia exert potentiating effects on intracellular and intraluminal calcification proposing an importance for pathogenesis of human sialolithiasis.” [Emphasis added.]


Since vitamin D increases blood calcium by increasing both intestinal absorption and bone resorption, this suggested to me that excessive vitamin D could indeed increase the risk of forming salivary stones, particularly in people like my patient who form large deposits of calculus (thus have a tendency to high salivary calcium phosphate).

By the time I figured all this out, my patient’s stone had dissolved, confirmed by the same oral surgeon who diagnosed it.  By consuming vitamin D only intermittently, her vitamin D level fell to 39 ng/ML during the treatment period.

Then, in the process of working on my series on acid-base balance, I found that Eskimos probably had suboptimal intakes of magnesium.  I got a hold of a couple of studies looking at the effect of magnesium deficiency on bone health

Surveys since 1985 indicate that the typical U.S. individual does not ingest magnesium at amounts recommended by the RDA (1, 2) of 400mg for adult men and 310mg for adult women.  U.S. adults commonly consume 50% or less than recommended levels.  

Rude et al showed that restricting animals to magnesium intakes equivalent to just half of the adult human RDA resulted in “bone loss, decrease in osteoblasts, and an increase in osteoclasts by histomorphometry” (3).  Six months of low magnesium intake reduced trabecular bone volume significantly. 

They also found that low magnesium intake reduced levels of activated vitamin D, i.e. 1,25 dihydroxyvitamin D, aka calcitriol, by 50%!   This suggests that magnesium deficiency profoundly impairs activation of vitamin D.  This would mean that people who do not get adequate magnesium would show signs of vitamin D deficiency despite adequate sun exposure or vitamin D intake.  Conversely, people who consume more magnesium-rich foods, such as my paleo-dieting patient, require less vitamin D, and may more easily suffer from vitamin D excess. 

Finally, Rude et al also found that magnesium deficiency increased markers of bone inflammation (cytokines) and RANKL, also favoring bone resorption.

I exchanged a few emails with Dr. Stephan Guyenet (Whole Health Source) discussing this and he graciously shared a few other studies of interest here.

First, Batchelor and Compston studied the effects of cereal fiber on vitamin D pharmacokinetics in humans, following up on a study by Ford et al which “demonstrated biochemical improvement in ten patients with rickets or osteomalacia following the substitution of white leavened bread for chappattis in the diet”  (4).  They gave healthy volunteers bran supplying 20g of cereal fiber daily.   They demonstrated that the high intake of cereal fiber reduced the plasma half-life of 25-hydroxyvitamin D from 27.5 days to 19.2 days.  Since vitamin D appears in bile and cereal fibers may bind bile, Batchelor and Compston suggested that this may explain the loss of vitamin D in the cereal-fiber-supplemented individuals. 

This suggests conversely that people not consuming cereal fiber have a superior retention of vitamin D and would not require the same high doses as people consuming cereal-based diets.  Again, people on paleo diets would then have a greater susceptibility to adverse effects of high dose vitamin D.

Another study by Zanchi et al looked at bone metabolism in children suffering from celiac disease compared to controls (5).  Among the untreated celiacs, 40% had low blood calcium, 11% low blood magnesium, more than 50% had hyperparathyroidism, and 35% had blood 25(OH)vitamin D below 20ng/mL (frank deficiency).  The untreated celiacs had an average 25(OH)vitamin D less than half of healthy control subjects.  Ten of 20 patients who had at least two positive laboratory tests had osteopenia, which resolved after 6 months on a gluten-free diet.  Unfortunately, adults with late-diagnosed celiac do not have the same pattern of recovery of bone mineral density on gluten-free diets.


This shows that ingestion of gluten can reduce vitamin D levels in celiac patients.  Since at least two studies (6, 7) have shown that gliadin increases intestinal permeability of non-celiacs as well as celiacs, I suspect that gluten may affect vitamin D status in non-celiacs.  If so, a gluten-free paleo diet may increase the effectiveness of vitamin D, reducing the required dose and making paleo dieters more susceptible to vitamin D overdose.

By the way, Jorde et al gave 324 overweight or obese subjects either 40K IU or 20K IU weekly (5714 or 2857 IU daily) of vitamin D for a year.  They found no reduction in levels of markers of inflammation over that time, compared to unsupplemented subjects.

It could very well turn out that elevated vitamin D levels don’t themselves confer all the benefits linked to vitamin D status.  Higher vitamin D levels linked with lower risks of some chronic diseases (e.g. skeletal and autoimmune in particular) may turn out to only serve as a marker for the beneficial effects of outdoor activity, better micronutrient status (e.g. magnesium above), or lower intake of or susceptibility to the effects of gluten.

Urashima et al reported this month that school children given 1200 IU of vitamin D daily had nearly half the incidence of influenza and one-sixth the incidence of asthma found in unsupplemented children.  Thus, it appears that improved vitamin D status does improve innate immunity against infectious disease and reduce susceptibility to asthma.

For now I recommend keeping your serum vitamin D level between 40 and 60 ng/ml (edited 3/26/10) and not making an effort to obtain the higher levels (50-80ng/mL) recommended by the Vitamin D Council.  I still recommend using 10K IU for 1-3 days at the onset of symptoms of a cold or flu, to enhance the innate immune response and terminate the infection.    

In short, it seems likely that paleo dieters probably require less vitamin D supplementation than people on grain-based diets, and might have a higher risk of side effects from chronic high dose supplementation.  



1. Earl S. Ford and Ali H. Mokdad.  Dietary Magnesium Intake in a National Sample of U.S. Adults. J. Nutr. 133:2879-2882, September 2003

2. K. J. Morgan, G. L. Stampley, M. E. Zabik and D. R. Fischer. Magnesium and calcium dietary intakes of the U.S. population. Journal of the American College of Nutrition, Vol 4, Issue 2 195-206

3. Robert K. Rude, MD, Frederick R. Singer, MD and Helen E. Gruber, PhD. Skeletal and Hormonal Effects of Magnesium Deficiency. Journal of the American College of Nutrition, Vol. 28, No. 2, 131-141 (2009)

4. Batchelor and Compston.  Reduced plasma half-life of radio-labelled 25-hydroxyvitamin D, in
subjects receiving a high-fibre diet. Br. J. Nutr. (1983). 49, 213.

5. Zanchi et al.  Bone Metabolism in Celiac Disease. J Pediatr 2008;153:262-5.

6.  Drago et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac
intestinal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology, 2006; 41: 408-419.

7. Bernardo et al. Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides. Gut 2007;56;889-890.


 

Sunday, March 21, 2010

Paleo Protest: The Great American Meat-Out.

From the Detroit News:

Jerry Schneble, the Michigan director of the Great American Meatout, asked Michigan Governor Jennifer Granholm to proclaim a Michigan Meat-Out, an "eat meatless meals" day in Michigan. This sparked a protest from Michiganders , many of whom produce beef, pork, or other meats for a living.  Schneble responded to the controversy like a typical misinformed vegetarian:
"I would point out that two-thirds of all Americans are either overweight or obese, and I can guarantee you they did not get that way by overeating fruits and vegetables," he said.
"Meat has no fiber, no phytochemicals, or antioxidants -- all critical for good health."
These vegetarians continually attack meat because it contains fat, cholesterol, and animal protein, but no fiber, phytochemicals, or antioxidants.  My response to Schneble and all the other meat-bashers:

1. Fiber has never been proven “critical” for good health–mother's milk doesn't have any fiber either–but in case you didn't notice, no one prevents a meat-eater from also eating vegetables rich in fiber. 

2.  Meat contains CLA, which is an antioxidant and has anticancer potential: “...studies on mice and rats show encouraging results in hindering the growth of tumors in mammary, skin, and colon tissues.”   Grass-fattened meat contains larger amounts of CLA than grain-finished.  Meat also contains vitamin E, and more if grass-finished.

Meat also contains cholesterol, which may also act as an antioxidant.

Again, nothing prevents a meat-eater from also eating vegetables and fruits rich in antioxidants. 

3.  Even grain-finished meat contains some carotenes and vitamin E, which are phytochemicals, and grass-fattened beef contains twice as much carotene and nearly three times as much vitamin E as grain-finished meat.

Again, nothing prevents a meat-eater from also eating vegetables and fruits rich in phytochemicals. 

4.  Meat contains vitamin B-12, critical for good health.   Plant foods contain very little if any functional cobalamin (B-12), but that doesn't mean you shouldn't eat plant foods.

5.  I can guarantee people in American did not get overweight by overeating meat, which is actually a bit difficult to do because of the satiating power of protein and fat. 


According to the USDA (page 15), in 2005 meat, fish, and poultry altogether contributed only 15% of all energy (calories) to the US food supply, dairy products only about 8%, eggs only 1.3%, and animal fats (lard, tallow, and butter) only 2.5%, whereas grain products contributed 23%, sweeteners 17%, and plant-sourced oils and fats 23%. 

Hence all animal products contributed only 27% of energy to the U.S. food supply, which means that plants provide 73% of energy in the U.S. food supply.  Plant oils and sweeteners form 40% of the energy supply, 50% greater than all animal products together, and the grain products, sweeteners, and plant fats sum total 63% of total energy, more than double the contribution of all animal products. 

6.  I don't recall any one ever proving that humans must eat only foods that contain fiber, or only foods that contain vitamin B-12.

Finally, human mother's milk contains lots of fat, lots of saturated fat, lots of cholesterol, animal proteins (lactalbumin and casein), and no fiber.  Shall we stage a "breast milk out" also?

Now sugar, that has no fiber, phytonutrients, or antioxidants.  Plant oils have almost no micronutrient value.  So how about a "sugar and vegetable oil out"?

I hope they get their facts straight some day.  I wonder if B-12 deficiency causes delusions?

 

Friday, March 19, 2010

My Practically Paleo Meals 3/19/10

Today I decided to do a nutrition analysis of my meals in addition to posting photos.

Breakfast


Very rare beef rib steak, two soft boiled eggs, and a sauteed medley of onion, garlic, kale, and red pepper using olive oil.


About a cup of kabocha squash with coconut oil.



Frozen blueberries with Thai Kitchen coconut milk. When you put the coconut milk on top of the frozen fruit and stir them together a bit, the coconut milk freezes, creating a texture I enjoy.

Lunch


Same beef (larger portion), a whole avocado with salsa, same vegetables, an apple, and an orange.

Nutrition Analysis

I don't do this very often on my own meals.  Here's the breakfast food list and macronutrient totals:


This gives the macronutrient ratios for breakfast in pie chart form:

 This has the entire food list for the day:


This gives the pie chart representation of the macronutrient ratios along with fatty acid analysis (SFA, PUFA, MUFA), cholesterol content, and fiber content:


You can see that this menu supplied 59% of calories as fat, 26% as protein, and 16% as carbohydrate, with 35 grams of fiber.  This program calculated that saturated and monounsaturated fat each supplied 24% of calories (48% total), and polyunsaturated only 4%, but I suspect these may not be correct because the grass-fed meat and omega-3 eggs I used probably have proportions of fatty acids different from the items in the database.   On the days I eat walnuts instead of coconut it will vary with a higher proportion of polyunsaturated fats.

This gives the micronutrient analysis in tabular form with quantification:



This one depicts the nutrient contents in percents of the RDA in graphic form:

These meals fell slightly short of the 150g/d carbohydrate recommendation but this does not concern me since carbohydrate is not a required nutrient.  Vitamin D I get from sun and a supplement, and fish on the days I consume it, so it does not concern me either. 

Calcium fell short of the RDA about which we have a debate.  Recent research by USDA scientists indicates that that people may require only ~750mg of calcium daily (See Hunt and Johnson, full text here), rather than the 1000 mg RDA used by the FitDay calculator.  My food still fell short of that by about 300mg.  On the other hand, compared to other species on a pound for pound basis, we would predict humans requiring more like 2000mg daily; obviously these meals fell far short of that.

These meals also fell short of the RDA for magnesium by 30%, and 21% short of the RDA for thiamin.

I already knew that my meals do not typically meet the RDA for calcium or magnesium. Since I don't always eat fish bones or use bone broth daily, I currently take a calcium-magnesium supplement daily (in addition to vitamin D).  The thiamin level does not concern me because it fluctuates according to my food selections.

I might do another of these on a day that I eat less coconut and more walnuts to see what comes up.  

Practically Paleo: Storing Stock

To make eating grass-fed meat more economical, I buy it frozen in large quantities.  I just got about 100 pounds of grass-fattened beef and 50 pounds of wild Kodiak salmon from Kenny Aschbacher, the Fishhugger.

I have a chest deep freezer in one corner of my office:

 

Atop the contents I put this insulation to keep them very cold:

 

This box contains grass-fed ground beef:




This bag holds 50 pounds of wild salmon bellies in five pound packages:



Two more boxes of beef steaks and roasts:


One of the shrink-wrapped steaks; notice the yellow color of the grass-fed fat:


I had a couple of the steaks today.  I enjoy buying in bulk and saving myself money and shopping time.  I won't need to purchase meat for almost 6 months now.

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

My Meals 3/16/10


Breakfast:  Roast beef, stir fried bok choy, scallions, and red pepper, kim chee, and sweet potato with coconut butter. All leftovers.



Lunch:  Same beef, freshly cooked stir-fry, and two slices of bacon.  Also had an orange and a blend of 1/2 cup coconut milk with 1 cup blueberries.

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.