The Week's Links

A London specialty ice cream shop starts serving the ultimate primal ice cream today, made from human breast milk.  From the Reuter's article:

The breast milk concoction, called the "Baby Gaga," will be available from Friday at the Icecreamists restaurant in London's Covent Garden.

Icecreamists founder Matt O'Connor was confident his take on the "miracle of motherhood" and priced at a hefty 14 pounds ($23) a serving will go down a treat with the paying public.
The breast milk was provided by mothers who answered an advertisement on online mothers' forum Mumsnet.

Victoria Hiley, 35, from London was one of 15 women who donated milk to the restaurant after seeing the advert.

Hiley works with women who have problems breast-feeding their babies. She said she believes that if adults realized how tasty breast milk actually is, then new mothers would be more willing to breast-feed their own newborns.

"What could be more natural than fresh, free-range mother's milk in an ice cream? And for me it's a recession beater too -- what's the harm in using my assets for a bit of extra cash," Hiley said in a statement.

Duo Li presents the evidence that vegetarians and vegans can have increased platelet stickiness and higher risk of thrombosis due to dietary deficiencies of vitamin B12 and omega-3 fatty acids in his article "Chemistry Behind Vegetarianism" in the Journal of Agricultural and Food Chemistry online.

"Collagen- and adenosine-5′-diphosphate (ADP)-stimulated ex vivo whole blood platelet aggregation were significantly higher in both vegetarian and vegan groups than in both high- and moderate-meat-eater groups. The vegan group had a significantly higher mean platelet volume (MPV) than the high- and moderate-meat-eater and ovo-lactovegetarian groups (35). Increased MPV in vegans suggests the presence of larger, activated platelets. Evidence from case control studies has indicated that an increased MPV is an independent risk factor for acute myocardial infarction (MI) (39) and for acute and/or nonacute cerebral ischemia (40). Large platelets, in such cases, have been shown to have increased reactivity. When platelets become activated, they change from their normal resting disk-like structure to assume a spherical shape and their volume increases substantially, leading to the potential for thrombus formation. In a multiple linear regression analysis, after controlling for potential confounding factors such as dietary group, age, exercise, body mass index, and dietary PUFA and saturated fat, cholesterol, carbohydrate, and fiber intake, the MPV was still strongly negatively correlated with platelet PL 20:3n-6 (p = 0.003) and 22:5n-3 (p =0.001). The data suggest that 22:5n-3 and 20:3n-6 may play a role in the structural function of the platelet membrane (41). This, in conjunction with the increased platelet aggregability, suggests what should be an increased thrombosis tendency in vegans, and in the case of the platelet aggregation is associated with low dietary intake of n-3 PUFA. " (emphasis added)

Ronda Bokram, a nutritionist with Olin Health Center in Lansing, Michigan, proves herself ignorant of the biochemistry of eating disorders in this article in the Lansing State Journal online.  Bokram is quoted as endorsing an MSU program that distributed Twix candy bars to students as part of National Eating Disorders Awareness week:

"Students found miniature Twix bars all over campus and were encouraged to eat them without guilt.

It's one of several campus activities in recognition of National Eating Disorders Awareness Week.


The message behind the Twix bars?

"Eating disorders are not about food," said Ronda Bokram, a nutritionist with Olin Health Center. "Students come to my office and they say, 'My problem is I like food.' The problem isn't that you love food.

"The problem is you feel guilty about it ... and that leads to a distorted relationship with food. We label food as good or bad, and then when we eat the food, we put that label on ourselves: 'I'm bad if I eat this.' "

I'm sure this is a bonanza for Mars, Inc, but Bokram clearly has not read the research showing that eating refined carbohydrates like Twix bars will elevate insulin and activate dopamine centers of the brain, leading to transient hypoglycemic reactions, sugar addiction, and chronic insulin resistance, all of which can distort appetite.   Anorexia nervosa occurs only in civilization, i.e. it is a disease of civilization, and includes metabolic dysfunction, namely loss of appetite combined with inability to store fat in fat cells.  Most likely we have something like fat cell insulin resistance.  We don't have the details yet but I know that guilt has nothing to do with it.   I suggest Bokram and her colleagues take some time to read Good Calories Bad Calories, particularly Part 3, especially page 440, and also brush up on her human biology.  Its not about whether food is "good" or "bad," its about whether humans have adapted to an item or not.  If chimps developed anorexia nervosa while on a diet of refined carbohydrates, we wouldn't blame it on "distorted relationships with food" and guilt about eating "bad" foods, we would immediately suspect the food.  Why this escapes human nutritionists I don't understand.


Last but not least, new research shows that children with low vitamin D levels have a higher risk of allergies.

Institute Of Medicine Vitamin D Panelist Has Conflicts of Interest

On November 30, 2010, the Institute of Medicine release its "Consensus Report" suggesting updated Dietary Reference Intakes for Calcium and Vitamin D, in which it "reviewed" the evidence on vitamin D and health and came to the conclusion:

The IOM finds that the evidence supports a role for vitamin D and calcium in bone health but not in other health conditions. Further, emerging evidence indicates that too much of these nutrients may be harmful, challenging the concept that “more is better.”

The IOM decided that the "evidence" indicates that people do not require more than 600 IU of vitamin D daily, and that 4000 IU is the "Upper Level Intake" which we should not .  This conclusion could have come about only by ignoring the research of vitamin D experts,  which has determined that the average person uses about 4000 IU of vitamin D daily, and produces 10,000 IU by endogenous synthesis stimulated by 20-30 minutes of mid-day summer sun exposure [check here].  

If you were wondering what happened, the Alliance for Natural Health may have an answer for you:

A pharmaceutical company is developing a patentable man-made vitamin D analog—yes, a synthetic drug version of vitamin D. And Glenville Jones, PhD, one of the committee members who determined the new vitamin D guidelines and who is quoted as saying that under these guidelines, most people “probably don’t have vitamin D deficiency” and “We think there has been an exaggeration of the public’s interest in vitamin D deficiency,” is an advisor for that same pharmaceutical company.

4000 IU Vitamin D Daily Cuts Preterm Birth Risk in Half

A new study by researchers from Medical University of South Carolina has found that women taking 4000 IU of vitamin D daily during pregnancy cut their chances of a preterm birth in half compared to women taking only 200-400 IU.  The women taking 4000 IU of vitamin D also has a reduced risk of infections.  There were no adverse effects found for this level of supplementation.  

If you think you live in a sunny environment and don't need vitamin D, consider this:

"All the women taking part in the study were living in Charleston — in sunny South Carolina. Overall, 85 per cent were either insufficient, or "frankly deficient" in vitamin D when the study began."

This adds to the list of studies indicating that the vast majority of urbanites are deficient even if they live in sunny places.  

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.

8. Jorde et al. No effect of supplementation with cholecalciferol on cytokines and markers of inflammation in overweight and obese subjects.

9. Urashima et al. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am J Clin Nutr (March 10, 2010).

 

Islam deprives women of vitamin D

Acharya S has an excellent post on her blog Truth Be Known, titled Muslim Women, Vitamin D, and Osteomalacia. I highly recommend taking a look at it. She quite rightly states:

"In the global debate regarding the dress codes for Muslim women, one important factor is often overlooked: The fact that depriving a human being from live-giving sunlight and air represents physical torture. Indeed, this form of torture has been used for centuries in prisons."

Acharya has written several excellent books on the solar myth that forms the basis of Christianity, including The Christ Conspiracy, Suns of God, and Who Was Jesus? I recommend all of them to anyone who wants to understand the roots of Christianity.

Grassroots Health Vitamin D Study Seeks Participants

Before I get on with the other nine problems people have when implementing paleo diet, I wanted to pass along a link to the website of Grassroots Health, an organization that has organized an open study of vitamin D and health under the auspices of leading vitamin D scientists. From the site:

GrassrootsHealth has launched a worldwide public health campaign to solve the vitamin D deficiency epidemic in a year through a focus on testing and education with all individuals spreading the word.

Everyone is invited to join in this campaign! Join Daction and test two times per year during a 5 year program to demonstrate the public health impact of this nutrient.

$40 and a quick health survey allows everyone to

• get a vitamin D blood spot test kit to be used at home (except in the state of New York)
• have the results sent directly to them
• take action to adjust their own levels to get to the desired ranges with whatever help is needed from their healthcare practitioners.

With only 100 people joining up today, and getting 2 friends to join in 2 weeks (and those 2 friends getting 2 more), by week 42, there could be 400,000,000 people who are vitamin D ‘replete’! (more than the United States population)

I signed up. As a participant, you pay $40 every 6 months to receive a vitamin D lab test delivered to your door, and you agree to fill in some surveys along the way, over a 5 year period. You can't beat the price for the vitamin D test, and your participation will contribute greatly to our understanding of the health protective effects of vitamin D.

Perils of Indoor Living: Skin Cancer

Aaron Hicks just sent me a copy of this paper from Medical Hypotheses:

Increased UVA exposures and decreased cutaneous Vitamin D3 levels may be responsible for the increasing incidence of melanoma

This paper may enlighten, or upset, dermatologists mired in the "sunlight causes cancer" myth. It also has the potential to damage the sunscreen industry, also based on the myth that sun exposure causes skin cancer.

The authors, Dianne E. Godar, Robert J. Landry, and Anne D. Lucas propose that intermittent, intense exposure to UVB initiates cutaneous malignant melanoma (CMM), but that promotion of CMM requires increased UVA exposures and inadequately maintained cutaneous levels of vitamin D3.


Some interesting facts cited in support of their hypothesis:

• "Although outdoor workers get much higher outdoor solar UV doses than indoor workers get, only the indoor workers’ incidence of cutaneous malignant melanoma (CMM) has been increasing at a steady exponential rate since before 1940."

• "Outdoor workers have a lower incidence of CMM compared to indoor workers."

• People who use UVB-absorbing sunscreens have a significantly increased risk of melanoma and these sunscreens promote the growth of melanoma in mice.

• People who maintain an all-year-tan have a reduced risk of melanoma, and outdoor workers, who receive three to nine times the erythemally effective UV dose of indoor workers have a significantly lower incidence of melanoma.

• Excluding sunburns, outdoor activities in childhood decrease the incidence of melanoma and research has failed to find a ‘‘critical period,” such as childhood, where intense exposures contribute more towards the induction of melanoma.

• Sunburns throughout life increase the risk of melanoma, while low level solar UV exposures reduce the risk.

• Melanoma patients who receive regular sun exposures live longer than those who do not.

• UVA not only promotes skin tumor growth in mice after initiation by artificial sunlight, but also causes twice as many tumors to form .
  

• UVA increases melanomas in a mouse model after initiation by UVB.

• People can get considerable UVA exposure from windows, but windows do not allow passage of adequate UVB to stimulate vitamin D production.

• UVA exposure, absent UVB exposure, leads to degradation of vitamin D; and UVA also causes DNA damage.
  

• "High-rise office buildings, needing many large windowpanes, became increasingly popular around the mid 1910s, about 20 years prior to the first observed increase in the incidence of CMM. The time-line for the industrial revolution fits the CMM observations, unlike the introduction of fluorescent lights in the mid-1940s [80] or any other events that occurred after the mid- 1930s. Thus, the industrial revolution caused many workers to stay indoors during the day reducing their cutaneous vitamin D3 levels and, the UVA entering their offices caused photodegradation of vitamin D3 and mutations to the DNA of their skin cells."

Finally:

"In the early 20th century, people went against evolution by going indoors during the day to work, which drastically decreased their daily amount of cutaneous vitamin D3 and, along with it, their blood levels. With the addition of larger buildings and sky scrappers, people created an unnatural UV barrier when windows were developed and used in abundance. The UV barrier created by window glass divided UVB from UVA, so that the vitamin D making UVB was excluded from our indoor working environment; only the vitamin D-breaking and DNA-mutating UVA was included. Because this unnatural UV environment existed for decades in buildings and cars, CMM began to steadily increase about 20–30 years later in the mid-1930s."

In short, a boat-load of evidence that avoiding the full-spectrum UV light provided by old Sol and hiding inside drives the production of CMM. This paper shows how elegantly the theory of evolutionary adaptation can explain all of the known facts about CMM and provide the basis for uncovering the cause of a degenerative process.