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Vitamin D, Magic Mushrooms

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  • 3 months later...
We need to reduce our toxin load (less pollution and less consumption of unnatural chemicals, including prescription drugs); stress (which increases free radical production and reduces our immune response); and exposure to infection (wash hands always and beware when eating uncooked food; wear a mask if there is risk of respiratory infection). We need to improve our immune systems by increasing antioxidant intakes (healthy diet and supplements if necessary), and ensure a healthy supply of protective, friendly bacteria in our guts as well as lead healthy lifestyles.


There are many nutrients that are known to increase our immunity that you may want to consider. For example, beta-glucans from mushrooms are known to increase immune cells and also stimulate stem cells. I will elaborate on the anti-inflammatory immune-boosters in future.



■ Dr Amir Farid Isahak is a medical specialist who practises holistic, aesthetic and anti-ageing medicine. He is a qigong master and founder of SuperQigong. For further information, e-mail [email protected]. The views expressed are those of the w[/i]

Rejuvenate me!

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  • 2 months later...
Back to basic: Get vitamins

By The Daily Progress

Published: August 17, 2009


This is almost like the return of tuberculosis or polio.


A health problem addressed long ago has re-emerged to threaten America’s children: a lack of vitamin D.

About 7.6 million children, adolescents and young adults — about 9 percent — have vitamin D levels so low they could be considered deficient.

Another 61 percent — 50.8 million — have levels low enough to be insufficient, according to a new analysis of federal data.


“It’s astounding,” said Michal Mela-med of the Albert Einstein College of Medicine in New York, who helped conduct one of the analyses. “At first, we couldn’t believe the numbers. I think it’s very worrisome.”


Low vitamin levels were especially low among girls, adolescents and people with darker skin, making African-American teenage girls the group at the highest risk.


Anyone with low vitamin D levels is at risk for bone problems, heart disease, diabetes and other problems.


Researchers and others attribute the deficiencies to:

Back to basic: Get vitamins | Charlottesville Daily Progress

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  • 1 month later...


Dear Jane:




The October 4 through 8 conference on Vitamin D in Brugge, Belgium, is mainly for scientists, as it is about 2/3 basic science and test tube research and about 1/3 more general human research. Scientists interested in Vitamin D should not miss it. You can read the scientific program on the above website and decide for yourself. I will be there because of a generous grant from Bill Sardi, who supported the Vitamin D Council beginning in 2003; Bill was our earliest supporter.




Dear Dr. Cannell:




My son has schizophrenia. Will Vitamin D help him? He started hearing voices twelve years ago and our lives have been a nightmare since then. He stayed with us for 8 years but we never knew when he would come home, when he was taking his meds, when he would become paranoid, and when he would lose his temper. He disappeared for weeks at a time and would show up at our door homeless and in trouble with the law. He became increasingly violent when he was home.




My husband and I had to have him arrested after he attacked his sister and he was eventually sent to prison, where he was finally made to take his medications. We feel so guilty about our role in sending him to prison but we were afraid for our lives.




I know he does not get sunlight in prison and the doctors there will not test his Vitamin D levels. They won’t let us send him supplements to take. Can the Vitamin D Council do anything about this?




Joanne, Sacramento, CA




Dear Joanne:




In my experience at Atascadero State Hospital, treating hundreds of patients with schizophrenia, adjuvant Vitamin D does not reduce hallucinations, paranoia, or psychosis but it does improve mood, reduce tremors, may reduce the amount of antipsychotic medications needed and helps prevent diabetes and the metabolic syndrome, which are common side-effects of “modern” antipsychotic medications. Care must be taken however, as the same cytochrome P-450 enzymes that metabolize Vitamin D are many of the same enzymes psychotropic medications utilize. Little or nothing is known about such Vitamin D and psychotropic drug interactions, thus Vitamin D levels are mandatory when treating Vitamin D deficiency in someone taking psychiatric medications.




As you are writing from Sacramento, I assume your son is incarcerated in the California Department of Corrections and Rehabilitation (CDCR). At my hospital, we get hundreds of schizophrenic patients per year directly from CDCR and I have yet to find one who was not Vitamin D deficient (> 50 ng/ml) and I have yet to find one who was prescribed Vitamin D by CDCR physicians. I find this ironic as CDCR is under a federal court mandate to improve the health care of inmates.




For those not familiar with schizophrenia, the course you describe is common, especially the pain and guilt schizophrenia inflicts on families. Schizophrenia is such a debilitating disease (losing your mind while knowing you are losing your mind) that about 10% of schizophrenics cure their disease by committing suicide. Of all the diseases I know, schizophrenia is the most vicious.




Recently, researchers at Harvard published an incredible paper.


Kinney DK, Teixeira P, Hsu D, Napoleon SC, Crowley DJ, Miller A, Hyman W, Huang E. Relation of schizophrenia prevalence to latitude, climate, fish consumption, infant mortality, and skin color: a role for prenatal vitamin d deficiency and infections? Schizophr Bull. 2009 May;35(3):582-95. Epub 2009 Apr 8.


What Drs. Dennis Kinney, Emerald Huang and colleagues did was nothing short of brilliant. I discussed their paper briefly several months ago in a newsletter but this month I want to spend the time this paper deserves.


Like autism, schizophrenia has strong genetic roots. However, just like autism, genetic predisposition is not predestination. That is, for reasons no one has yet understood, one identical twin will get schizophrenia but the other one has a 50% chance of escaping the disease; the identical twin concordance rate is about 50%. This implies an environmental trigger.


We can get a clue to that trigger by looking at identical twins and multiple sclerosis. Although their genes are identical, the identical twin that went out in the sun when young was much less likely to get multiple sclerosis than his or her identical twin. For example the adolescent identical twin who listened to the dermatologists, and avoided sun tanning, was 2.5 times more likely to later get MS than his/her identical sibling who ignored the dermatologists and tanned. (I predict similar studies will be published concerning identical twins in both autism and schizophrenia.)


Islam T, Gauderman WJ, Cozen W, Mack TM. Childhood sun exposure influences risk of multiple sclerosis in monozygotic twins. Neurology. 2007 Jul 24;69(4):381-8.


Unlike autism, schizophrenia takes about 25 years to manifest itself; as Professor Robert Heaney would say, it is a long-latency disease. That is, the average age of onset until recently was about 25, which explains why the incidence of schizophrenia has not yet dramatically increased. In fact, autism used to be called infantile schizophrenia and it seems likely, as the current crop of autistic children ages, some will later be re-diagnosed with schizophrenia.


Recent studies, as compared to studies published in the 1980s and 1990s, show schizophrenia is increasing, especially among teenagers. In fact, all of the studies I could find published in the 21st century, as opposed to earlier studies, show schizophrenia is increasing:


Boydell J, Van Os J, Lambri M, Castle D, Allardyce J, McCreadie RG, Murray RM. Incidence of schizophrenia in south-east London between 1965 and 1997. Br J Psychiatry. 2003 Jan;182:45-9.


Preti A, Miotto P. Increase in first admissions for schizophrenia and other major psychoses in Italy. Psychiatry Res. 2000 May 15;94(2):139-52.


Tsuchiya KJ, Munk-Jørgensen P. First-admission rates of schizophrenia in Denmark, 1980-1997: have they been increasing? Schizophr Res. 2002 Apr 1;54(3):187-91.


(If you want to read something scary, read this article about two large US government autism studies about to be released. In ten years you will be reading the same story about schizophrenia)


Kirby D. Autism Rate Now at One Percent of All US Children? Huffington Post; 08/11/09


Before I describe the remarkable paper from Harvard, I want to compliment researchers at the Saint Barthomew’s Hospital in England for almost saying what most psychiatrists already know; the incidence of schizophrenia is much higher in people with dark skin. In the 1970s and 80s, that was an accepted fact, until charges of racism were leveled against the American Psychiatric Association (APA). The spineless APA promptly did retrospective chart analyses and announced the incidence of schizophrenia is exactly – precisely – the same for Blacks as it is for Whites. The ethnicity question is important as the Vitamin D theory is not tenable unless darker skin means a higher incidence.


Coid JW, Kirkbride JB, Barker D, Cowden F, Stamps R, Yang M, Jones PB.


Raised incidence rates of all psychoses among migrant groups: findings from the East London first episode psychosis study. Arch Gen Psychiatry. 2008 Nov;65(11):1250-8.


Actually, in 2007, a group at Columbia University appears to be the first to break with the APA’s political correctness. Dr. Michaeline Bresnahan and her colleagues followed 12,000 children for up to 28 years after birth. African Americans were 3 (three) times more likely to develop schizophrenia than whites and socioeconomic factors could not explain away their findings.


Bresnahan M, Begg MD, Brown A, Schaefer C, Sohler N, Insel B, Vella L, Susser E. Race and risk of schizophrenia in a US birth cohort: another example of health disparity? Int J Epidemiol. 2007 Aug;36(4):751-8.


Getting back to the Kinney et al paper, they examined 188 studies to find 49 studies that used similar diagnostic methods. The authors were quite strict on only looking at the 49 studies that used similar diagnostic criteria as the authors are aware that most psychiatrists dismiss any latitudinal variation in the prevalence of schizophrenia by saying that doctors around the equator are too stupid to make a correct diagnosis of schizophrenia.


Then, the authors explored the three most common theories for the environmental trigger of schizophrenia:


1. Poor prenatal care,


2. Low omega-3 fatty acid consumption,


3. Prenatal exposure to infections, especially influenza.


First, they found a 10 (ten) fold variance in the prevalence of schizophrenia in the world, from a high of 28 cases per 1000 in Oxford Bay, Canada, near the Arctic Circle, to a low of 1 per 1000 around the equator, confirming Dr. E.F. Torrey’s landmark latitudinal findings published in 1987. Kinney et al confirmed that latitude and cold climate broadly and strongly determine the prevalence of schizophrenia. The majority of the 49 studies the authors reviewed were completed before the sun scare, which has driven many equatorial mothers out of the sun, so I predict the incidence of schizophrenia around the equator will soon be increasing.


Second, if you were born in countries around the equator with high infant mortality (a proxy for poor prenatal care), the incidence of schizophrenia was very low. In other words, around the equator it didn’t matter if you had poor prenatal care, you still did not get schizophrenia. But, at latitudes away from the sun, prenatal care did matter, and it mattered more and more the further you got from the equator. It appears that high maternal Vitamin D levels around the equator overwhelmed the effect of poor prenatal care.


Third, around the equator, it did not matter if mothers ate Vitamin D-containing fish; it only mattered the further you got away from the equator. That is, latitude overwhelmed the effect of fish consumption; consumption of Vitamin D containing fish only began to matter when the sun was not available to make Vitamin D. If omega-3 fatty acid consumption was the cause of schizophrenia, latitude variation in omega-3 consumption would not matter.


Fourth, they found that skin color only mattered away from the equator, that is, in the very dark-skinned equatorial Indians and equatorial Africans, skin color hardly mattered; the prevalence of schizophrenia was quite low. However, the further poleward you live, dark skin preventing maternal Vitamin D production becomes an increasingly significant risk factor for schizophrenia.


The authors could not dismiss the influenza theory of schizophrenia, but as I hope readers are aware, the association between influenza and schizophrenia is probably mediated by vitamin D. That is, influenza is a symptom of Vitamin D deficiency:


“… the characteristic microbe of a disease might be a symptom instead of a cause.”


George Bernard Shaw


(Preface on Doctors, The Doctor’s Dilemma, 1911)


Kinney et al concluded that the Vitamin D hypothesis correctly predicted the associations between prevalence and skin color, fish consumption, infant mortality, latitude and temperature. The Vitamin D effect “overwhelms” the effects of other known risk factors. That is, maternal Vitamin D deficiency is not just “a” cause, but is probably “the” cause of schizophrenia.


I love epidemiological studies like this, and I’m sure Professor John McGrath in Australia does as well. It was McGrath who first hypothesized that gestational Vitamin D deficiency causes schizophrenia. I often despair that I have had to wait two years for the world to learn autism is triggered by gestational and early childhood Vitamin D deficiency. John McGrath has had to wait 10 years for his theory to be accepted and will probably still be waiting 10 years from now.


McGrath J. Hypothesis: is low prenatal vitamin D a risk-modifying factor for schizophrenia? Schizophr Res. 1999 Dec 21;40(3):173-7.


I’d like to add one prediction to McGrath’s theory. The Vitamin D theory of schizophrenia predicts that the age of onset of schizophrenia should be getting younger. That is, as more pregnant women listened to dermatologists, their children are not only more likely to develop schizophrenia, but are more likely to develop more severe cases that present at a younger age. That is exactly what appears to be happening.


Di Maggio C, Martinez M, Ménard JF, Petit M, Thibaut F. Evidence of a cohort effect for age at onset of schizophrenia. Am J Psychiatry. 2001 Mar;158(3):489-92.


Ajdacic-Gross V, Lauber C, Warnke I, Haker H, Murray RM, Rössler W.


Changing incidence of psychotic disorders among the young in Zurich. Schizophr Res. 2007 Sep;95(1-3):9-18. Epub 2007 Jul 16.


If you know any pregnant women, make sure they read our recent newsletter about pregnancy and Vitamin D.


Dear Dr. Cannell:


How much magnesium do you need to allow Vitamin D to work properly?


Sarah, New York


Dear Sarah:


Severe magnesium deficiencies severely impair Vitamin D’s ability to work. What is not known, is how mild to moderate Mg deficiencies, like most Americans have, affect Vitamin D metabolism. The safe thing to do is to eat green leafy vegetables and a handful of sunflower seeds and nuts every day (Trader Joe’s sells a variety of seeds). If you can’t, won’t, or don’t end up doing that, then take a Vitamin D supplement with added Magnesium. Bio Tech Pharmacal now sells such a supplement, Vitamin D3 Plus, and will make a contribution of one dollar to the Council for every bottle sold. Bio Tech’s phone number: (479) 443-9148.


Bio Tech’s new Vitamin D3 Plus formula also contains zinc (the base of the fingers of the Vitamin D Receptor each contains a zinc molecule), Vitamin K2 (Vitamin K helps direct Vitamin D to calcify the proper organs), boron (boron is involved in the rapid, non-genomic action of Vitamin D on the cell wall), a small amount of genestein (about one-half the amount the average Japanese consumes every day), which helps activated Vitamin D stay around longer at the receptor site, and a tiny amount of Vitamin A. Again, the wisest thing to do is to eat green leafy vegetables and a handful of seeds every day as that combination contains the co-factors Vitamin D needs, the co-factors many Americans are deficient in.

John Cannell, MD


Vitamin D Council


This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. Please reproduce it, post it on Internet sites, and forward it to your friends. Remember, we are a non-profit and rely on your donations to publish our newsletter, maintain our website, and pursue our objectives. Send your tax-deductible contributions to:

The Vitamin D Council

585 Leff Street

San Luis Obispo, CA 93422

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Vitamin D seems crucial for the Immune Response to bacteria.

Originally published in Science Express on 23 February 2006

Science 24 March 2006:

Vol. 311. no. 5768, pp. 1770 - 1773

DOI: 10.1126/science.1123933



Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response


In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1–hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D–mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.

Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response -- Liu et al. 311 (5768): 1770 -- Science

The right racial/genetic background helps:-

Vitamin D receptor gene polymorphism: association with Crohn's disease susceptibility J D Simmonsa, C Mullighanb, K I Welshb, D P Jewella


a Gastroenterology Unit, University of Oxford, Radcliffe Infirmary, Woodstock Rd, Oxford, OX2 6HE, UK, b Transplant Immunology, Transplant Centre, Churchill Hospital, Oxford, UK


Correspondence to: J D Simmons, Gastroenterology Unit, John Radcliffe Hospital, Oxford,


Accepted for publication 8 February 2000


BACKGROUND---The vitamin D receptor (VDR) gene represents a strong positional candidate susceptibility gene for inflammatory bowel disease (IBD).

The VDR gene maps to a region on chromosome 12 that has been shown to be linked to IBD by genome screening techniques.

It is the cellular receptor for 1,25(OH)2 vitamin D3 (calcitriol) which has a wide range of different regulatory effects on the immune system. IBD is characterised by activation of the mucosal immune system.

AIM---To determine if polymorphisms in the VDR gene are associated with susceptibility to IBD

SUBJECTS---European Caucasoids: 158 patients with ulcerative colitis, 245 with Crohn's disease, and 164 cadaveric renal allograft donor controls.

, , ,

CONCLUSION---This study provides preliminary evidence for a genetic association between Crohn's disease susceptibility and a gene that lies within one of the candidate regions determined by linkage analysis.



I got so much Vit D today that my back has a warm red glow. B)

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  • 3 months later...

Deep in the radioactive bowels of the smashed Chernobyl reactor, a strange new lifeform is blooming


. . .findings of melanised fungi, happily congregating in the cooling pools of functional nuclear reactors, and by studies of dark, 'radiation-seeking' fungi, purposefully growing towards radioactive particles in soil, particularly around Chernobyl.

. . .

Melanin-containing fungi exposed to the radiation – even when nutrient-starved on purpose – grew significantly larger and up to 2.5 times faster than fungi without melanin and those not exposed to radiation.. . .

. . .results do indeed hint that fungi can live off ionising radiation, harnessing its energy through melanin to somehow generate a new form of biologically usable growing power.


If they're right, then this is powerful stuff, said fungal biologist Dee Carter from the University of Sydney. The results will challenge fundamental assumptions we have about the very nature of fungi, she said.


It also raises the possibility that fungi might be using melanin to secretly harvest visible and ultraviolet light for growth, adds Casadevall. If confirmed, this will further complicate our understanding of these sneaky organisms and their role in ecosystems.


And because the fungi don't actually 'eat' radioactive material, but simply use the energy it radiates, Dadachova said, they're in no danger of becoming radioactive themselves.

Silent spring | COSMOS magazine
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  • 3 weeks later...
Studies show association between high levels of vitamin D and decreased risk of heart disease

16. February 2010 05:41


Middle aged and elderly people with high levels of vitamin D could reduce their chances of developing heart disease or diabetes by 43%, according to researchers at the University of Warwick.


A team of researchers at Warwick Medical School carried out a systematic literature review of studies examining vitamin D and cardiometabolic disorders. Cardiometabolic disorders include cardiovascular disease, type 2 diabetes mellitus and metabolic syndrome.


Vitamin D is a fat-soluble vitamin that is naturally present in some foods and is also produced when ultraviolet rays from sunlight strike the skin and trigger vitamin D synthesis. Fish such as salmon, tuna and mackerel are good sources of vitamin D, and it is also available as a dietary supplement.


Researchers looked at 28 studies including 99,745 participants across a variety of ethnic groups including men and women.


The studies revealed a significant association between high levels of vitamin D and a decreased risk of developing cardiovascular disease (33% compared to low levels of vitamin D), type 2 diabetes (55% reduction) and metabolic syndrome (51% reduction).


The literature review, published in the journal Maturitas, was led by Johanna Parker and Dr Oscar Franco, Assistant Professor in Public Health at Warwick Medical School.


Dr Franco said: "We found that high levels of vitamin D among middle age and elderly populations are associated with a substantial decrease in cardiovascular disease, type 2 diabetes and metabolic syndrome.


"Targeting vitamin D deficiency in adult populations could potentially slow the current epidemics of cardiometabolic disorders."


All studies included were published between 1990 and 2009 with the majority published between 2004 and 2009. Half of the studies were conducted in the United States, eight were European, two studies were from Iran, three from Australasia and one from India.


High levels of vitamin D in older people can reduce heart disease and diabetes


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Studies show association between high levels of vitamin D and decreased risk of heart disease


My family all have low levels of VIt D one severely so. Quite amazing the level of deficiency in a sunny clime.

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Vitamin D. Negative effects on immune system?

Here is some web research i did for a friend. I thought there may be a few here also interested

My comments are in blue


I have highlighted some interesting bits in red.


1,25-Dihydroxyvitamin D3 and Development of Tuberculosis in Cattle



This report describes the presence and activity of 1,25-dihydroxyvitamin D3 (1,25-D3) in experimental bovine tuberculosis.

Animals that went on to develop tuberculous lesions exhibited a rapid transient increase in serum 1,25-D3 within the first 2 weeks following infection with Mycobacterium bovis. 1,25-D3-positive mononuclear cells were later identified in all tuberculous granulomas by immunohistochemical staining of postmortem lymph node tissue. These results suggest a role for 1,25-D3 both at the onset of infection and in the development of the granuloma in these infected animals.

Using a monoclonal antibody to the vitamin D receptor (VDR) as a VDR agonist, we confirmed that activation of the vitamin D pathway profoundly depresses antigen-specific, but not mitogenic, bovine peripheral blood T-cell responses (proliferation and gamma interferon production). Investigation of the mechanism of this suppression showed that the VDR antibody modified the expression of CD80 by accessory cells, such that a significant positive correlation between T-cell proliferation and accessory cell CD80 emerged.


I nursed in a TB unit i the 1970's.

The Hugraian trained doctor would not let us put patients in the sun as he siad it depressed their immune system


Exposure to ultraviolet light, especially UVB wavelengths, can impair immune responses in animals and humans. It is remarkable that this immunomodulation is not restricted to the exposed skin but is also found at other sites, i.e. systemic (distant) immunosuppression. A frequently proposed hypothesis is that UVB exposure inhibits, specifically, T helper 1 (Th1)-mediated immune responses. The major reason for this is that contact hypersensitivity (CHS) and delayed-type hypersensitivity (DTH), both Th1-mediated immune responses, are very sensitive to UVB.

UVB exposure-induced systemic modulation of Th1- and Th2-mediated immune responses

Yet another reason for legislating control (or preferably closure?) of skin tanning salons!





In this study we have shown that the bioactive component of

vitamin D, 1,25-D3, is rapidly mobilized following infection of

cattle with M. bovis.

This mobilization was identified as a tran-

sient increase in serum 1,25-D3 within 2 weeks of infection in

those animals that went on to develop tuberculous lesions. A

similar transient increase in plasma 1,25-D3 (mean increase

from 37 to 118 pM) has been reported for postparturient dairy

cattle (2) coincident with an increased susceptibility to other

infections, such as mastitis, metritis, and paratuberculosis (24).

Interestingly, dietary supplements of vitamin D and vitamin A

(which is known to enhance the effects of vitamin D) are

recommended for postparturient dairy cattle to prevent hy-

pocalcaemia (50).

Whether such supplements, combined with

the increased 1,25-D3 levels in these animals at this time,

contribute to a lowered resistance to infection is an interesting


1,25-Dihydroxyvita]min D3 and Development of Tuberculosis in Cattle

S. G. Rhodes, L. A. Terry, J. Hope, R. G. Hewinson, and H. M. Vordermeier

Clin Diagn Lab Immunol. 2003 November; 10(6): 1129–1135. doi: 10.1128/CDLI.10.6.1129-1135.2003.

PMCID: PMC262436

Full Text | PDF–692K |

Three seems to be a growing realization of the effects of vitamin d on Immunity, usually suggesting a positive effect:-



This review discusses the accumulating evidence pointing to a link between vitamin D and autoimmunity. Increased vitamin D intakes might decrease the incidence and severity of autoimmune diseases and the rate of bone fracture.


Mounting evidence for vitamin D as an environmenta... [Exp Biol Med (Maywood). 2004] - PubMed result


It is a shock that so many Australian in particular have surprisingly low levels of vitamin D when tested.


This, it is thought,e is due to our fear of skin cancer and the over-effectiveness of the slip slop slap campaign

however another reason that seems to be being ignored is the lower levels of vitamin D in mushrooms due to the modern method of growing them --in caves and sunlight free.

Recently it was demonstrated (ref previous post?) that even 3 hours of exposure to sunlight on a growing mushroom increased their vitamin D level quite dramatically. So much so that the USA FDA was contemplating mandating that all mushrooms grown should be given exposure to x(3?) hours of sunlight before picking and deliver to market.

This is something that the Australian medical profession should investigate and lobby for such a law in Australia if this is found to be true here.





Recent studies have shown that 1,25(OH)2D can induce hypo responsiveness to PAMPs by downregulating expression of TLR2 and TLR4 on monocytes.20 In parallel with the induction of antimicrobial agents such as cathelicidin, the suppression of TLR expression in this fashion might act to limit inflamma tory T lymphocyte responses that would otherwise promote autoimmunity mediated by T-helper 1 (TH1) lymphocytes (see below).

Unexpected actions of vitamin D: new perspectives on the regulation of innate and adaptive immunity


Am J Clin Nutr. 2004 Dec;80(6 Suppl):1717S-20S.

So it looks like my old Hungarian doctor was right about TB and maybe also kidney disease:-


Clin Nephrol. 2006 Oct;66(4):275-83.

Immunomodulation by 1,25-dihydroxyvitamin D3: therapeutic implications in hemodialysis and renal transplantation.


Mathieu C, Jafari M.


Department of Endocrinology, UZ Gasthuisberg, Leuven, Belgium.


The active metabolite of vitamin D3, 1,25-dihydroxyvitamin D3, is a secosteroid hormone that regulates calcium and bone metabolism, controls cell proliferation and differentiation, and plays an important role as an immunomodulator. Recent advances in understanding the mechanisms underlying 1,25(OH)2D3 immune actions expand the range of the therapeutic implications of 1,25(OH)2D3 and its analogs. This review will cover the current knowledge on vitamin D-mediated immunotolerance and recent advances in vitamin D-based therapies for the treatment of autoimmune disease and the prevention of graft rejection in renal transplantation. Initiation of vitamin D-based therapies at earlier stages of chronic kidney disease may impact the immune status of patients who progress to require dialysis or transplantation.


PMID: 17063995 [PubMed - indexed for MEDLINE]


Immunomodulation by 1,25-dihydroxyvitamin D3: ther... [Clin Nephrol. 2006] - PubMed result


and is some cancers MB

Increased 1,25-(OH)2D2 concentration in a patient with malignancy-associated hypercalcemia receiving intravenous hyperalimentation inadvertently supplemented with vitamin D2.


Sato K, Imaki T, Toraya S, Demura H, Tanaka M, Kasajima T, Takeuchi A, Kobayashi T.


Department of Medicine, Tokyo Women's Medical College.


A 55-year-old patient with hypercalcemic crisis due to gastric carcinoma with bone marrow metastasis was treated with bisphosphonate (pamidronate) and calcitonin. Urinary excretion of parathyroid hormone-related protein (PTHrP) was increased. When normocalcemia had been attained, intravenous hyperalimentation was started, in which 1,000 U vitamin D2 was inadvertently supplemented on days 5-18, On days 15-18, hypercalcemia rapidly recurred, accompanied by markedly increased serum levels of 25-OHD2 (9.1 ng/dl) and 1,25-(OH)2D2 (161 pg/ml). This clinical course suggests that PTHrP, like PTH, stimulated 1 alpha-hydroxylase activity and produced excessive 1,25-(OH)2D2. Vitamin D should not be administered to patients with malignancy-associated hypercalcemia, particularly that due to PTHrP-producing tumors.

Increased 1,25-(OH)2D2 concentration in a patient ... [intern Med. 1993] - PubMed result[Mesh%20Terms%3anoexp]



And in some infections

Vitamin D3 down-regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen-associated molecular patterns.


Sadeghi K, Wessner B, Laggner U, Ploder M, Tamandl D, Friedl J, Zügel U, Steinmeyer A, Pollak A, Roth E, Boltz-Nitulescu G, Spittler A.


Surgical Research Laboratories, Medical University of Vienna, A-1090 Vienna, Austria.


Toll-like receptors (TLR) represent an ancient front-line defence system that enables the host organism to sense the presence of microbial components within minutes.


As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We report here that vitamin D3 [1alpha,25-dihydroxycholecalciferol, 1,25(OH)(2)D3] suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time- and dose-dependent fashion. Despite 1,25(OH)(2)D3-induced up-regulation of CD14, challenge of human monocytes with either LPS or lipoteichoic acid resulted in impaired TNF-alpha and procoagulatory tissue factor (CD142) production, emphasizing the critical role of TLR in the induction of inflammation. Moreover, reduced TLR levels in 1,25(OH)(2)D3-treated phagocytes were accompanied by impaired NF-kappaB/RelA translocation to the nucleus and by reduced p38 and p42/44 (extracellular signal-regulated kinase 1/2) phosphorylation upon TLR-ligand engagement. Both TLR down-regulation and CD14 up-regulation were substantially inhibited by the vitamin D receptor (VDR) antagonist ZK 159222, indicating that the immunomodulatory effect of 1,25(OH)(2)D3 on innate immunity receptors requires VDR transcription factor activation. Our data provide strong evidence that 1,25(OH)(2)D3 primes monocytes to respond less effectively to bacterial cell wall components in a VDR-dependent mechanism, most likely due to decreased levels of TLR2 and TLR4.

Vitamin D3 down-regulates monocyte TLR expression ... [Eur J Immunol. 2006] - PubMed result


Evidence of the role of vitamin D in the regulation of T and B cells, macrophages, dendritic cells, and keratinocytes continues to accumulate and provides a link between vitamin D and many autoimmune diseases, including Crohn's disease, juvenile diabetes mellitus, multiple sclerosis, asthma, and rheumatoid arthritis. Considering the influence of vitamin D on the immune system, it may have potential as a treatment for immune-mediated diseases, even if additional research is required to better quantify dosage. But the biggest obstacle to its clinical use is its potent hypercalcemic effect. The calcium status of the host may influence the effect of vitamin D on immunity.

Vitamin D and the Immune System. [J Rheumatol. 2010] - PubMed result


The whole issue is far from clear as stated her in this article:-


Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system.


Cantorna MT, Zhu Y, Froicu M, Wittke A.


Department of Nutritional Sciences, Pennsylvania State University, University Park, PA 16802, USA. [email protected]


Vitamin D is an important immune system regulator. The active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to inhibit the development of autoimmune diseases, including inflammatory bowel disease (IBD). Paradoxically, other immune system-mediated diseases (experimental asthma) and immunity to infectious organisms were unaffected by 1,25(OH)2D3 treatment.


There are similar paradoxical effects of vitamin D deficiency on various immune system functions. Vitamin D and vitamin D receptor (VDR) deficiency resulted in accelerated IBD. Experimental asthma was unaffected by 1,25(OH)2D3 treatment and was less severe among VDR-deficient mice.


Vitamin D is a selective regulator of the immune system, and the outcome of 1,25(OH)2D3 treatment, vitamin D deficiency, or VDR deficiency depends on the nature of the immune response (eg, infectious disease, asthma, or autoimmune disease).


An additional factor that determines the effect of vitamin D status on immune function is dietary calcium.


Dietary calcium has independent effects on IBD severity. Vitamin D-deficient mice on low-calcium diets developed the most severe IBD, and 1,25(OH)2D3 treatment of mice on low-calcium diets improved IBD symptoms. However, the best results for IBD were observed when the calcium concentration was high and 1,25(OH)2D3 was administered.


Both the type of immune response and the calcium status of the host determine the effects of vitamin D status and 1,25(OH)2D3 on immunity.


PMID: 15585793 [PubMed - indexed for MEDLINE]



This, not too relevant, but interesting to me.

You are what you chew:-


Vitamin D metabolism in peripheral blood mononuclear cells is influenced by chewing "betel nut" (Areca catechu) and vitamin D status.

CONTEXT: Vitamin D deficiency, common in South Asians, is a risk factor for metabolic syndrome, type 2 diabetes, and ischemic heart disease.

CONCLUSIONS: Betel chewing is a more powerful independent determinant of increased 24(OH)ase expression and of decreased serum calcitriol than serum 25-OHD, supporting the hypothesis that this habit could aggravate the effects of vitamin-D deficiency.


PMID: 16670168 [PubMed - indexed for MEDLINE]

(A pity Betel Nut seems to be good for the heart and circulatory systems)


The whole issue is complex. i am sure with enough time a decent internet connection,open access to the journals, a degree or two in medicine, chemistry, veterinary science and nutrition I might be able to work out something sensible about it.


I would love Vitamin D to be a naturopath's or orthomolecular specialist's "Magic Bullet" but I suspect that life is more complex than that -MB



Histochemistry. 1988;89(3):209-19.

Vitamin D--soltriol the heliogenic steroid hormone: somatotrophic activator and modulator. Discoveries from histochemical studies lead to new concepts.


Stumpf WE.


Department of Cell Biology and Anatomy, University of North Carolina, Chapel Hill 27599.


Evidence from autoradiographic studies with 3H 1,25(OH)2 vitamin D3 (soltriol) about its many sites of nuclear binding and multiple actions suggests that the traditional view of "vitamin D and calcium" is too limited and requires modification.

A new concept has been developed which proposes that the skin-derived hormone of sunshine, soltriol, is a somatotrophic activator and modulator that affects all vital systems. Regulation of calcium homeostasis is only one of its many actions.

Target tissues for soltriol include not only bone, intestine and kidney, but also brain, spinal cord, pituitary, thyroid, endocrine pancreas, adrenal medulla, enteroendocrine cells, thymus, and male and female reproductive organs.


Accordingly, actions of soltriol involve effects on autonomic and endocrine regulation with changes in tissue and blood hormone levels, innervation of skeletal muscle, immune and stress response, digestion, blood formation, fertility, pregnancy and lactation, general energy metabolism, mental processes and mood, and others.


The skin-mediated transduction of short-wave sunlight induces a purposeful modulation of growth, reproduction and other biological activities in tune with the conditions of the sun cycle and season.


Synthesis and actions of vitamin D3-soltriol are dependent not only on the amount of sunlight, but also on the availability of precursor in the skin and access of sunlight, the rate of hydroxylation in liver and kidney, and the modulation of these events by the endocrine status, in particular growth and reproduction.

A concept of a five-level control of soltriol synthesis is proposed, in which the hydroxylation steps provide for a sensitive tuning.


Relationships between the heliogenic skin-derived hormonal system and the helioprivic pineal-derived hormonal system are recognized and a comprehensive concept of the "endocrinology of sunlight and darkness" is pointed out.


PMID: 3042715 [PubMed - indexed for MEDLINE]

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The Vitamin D Newsletter

More Vitamin D Studies of Interest

March 14, 2010


This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you are not subscribed, you can do so on the Vitamin D Council’s website. If you want to unsubscribe, go to the end of this newsletter.


This newsletter is now copyrighted but you may reproduce it for non-economic reasons without prior permission as long as you properly attribute its source.


The mainstream American press is ignoring much of the recent Vitamin D scientific literature. I suspect newspaper editors have decided that too many favorable Vitamin D stories run the risk of repeating the folic acid, beta-carotene and vitamin E affairs, when early epidemiological research was not routinely substantiated by later randomized controlled trials. If the press has made that decision, then this newsletter is your best source of information on new Vitamin D science.


Genetics, as well as dose, determine response to vitamin D supplements.


Your vitamin D blood level depends entirely on how much you take or how often you sunbathe, right? Wrong. Prior studies of identical twins show that about 25 -50% of the variation of Vitamin D levels depends on genetics. In July, researchers at the University of Toronto discovered the heritability of 25(OH)D is probably mediated through the Vitamin D binding protein (VDBP).


Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE. Common genetic variants of the vitamin D binding protein (DBP) predict differences in response of serum 25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation. Clin Biochem. 2009 Jul;42(10-11):1174-7.


One of the common emails I get (and I’m sorry I can’t answer individual emails) is “I am taking 5,000 IU per day but my blood level is only 35 ng/ml.” What should I do? This study helps answer such questions. You probably inherited a tendency to not respond to higher doses of Vitamin D. Simply take a little more and get your blood tested again in 3-4 months.


Also, don’t forget your weight. Does it make sense that if you weigh 300 pounds, you need more vitamin D than a 3 pound baby? If that makes sense to you, congratulations, it has not made sense to any of the five Food and Nutrition Boards (FNB) that have convened and issued recommendations to Americans over the last 60 years; they have all recommended the same 200 IU/day dose for infants and young adults, no matter how much the adults weigh.


More researchers actually recommend that people take Vitamin D and not just give more money to scientists.


Researchers from Austria concluded their review paper on vitamin D and high blood pressure by stating: “In view of the multiple health benefits of vitamin D and the high prevalence of vitamin D deficiency, as well as the easy, safe, and inexpensive ways in which vitamin D can be supplemented, we believe that the implementation of public health strategies for maintaining a sufficient vitamin D status of the general population is warranted.”


Pilz S, Tomaschitz A, Ritz E, Pieber TR; Medscape. Vitamin D status and arterial hypertension: a systematic review. Nat Rev Cardiol. 2009 Oct;6(10):621-30.


Good for Austria! By the way, while vitamin D may improve hypertension, it is not the be all and end all of hypertensive disease. If your doctor can stop your high blood pressure medication after you start taking vitamin D, great, but I doubt that will happen. Most people will have to continue taking their antihypertensive medication even after adequate vitamin D supplementation, albeit sometimes at a lower dose.


While I am on the subject, remember, that vitamin D will not prevent all cancer or heart disease or respiratory infections. True, evidence is accumulating that it will help, but you can still develop cancer, heart disease and respiratory infections with adequate blood levels of vitamin D. That’s why I believe in complimentary, not alternative, medicine.


Professor Michael Holick keeps increasing the amount of vitamin D he recommends.


As readers know, Professor Holick is one of the world’s foremost authorities on vitamin D. However, after being on the 1997 Food and Nutrition Board (FNB), he stuck with the FNB’s 200 IU/day recommendation well into the next century. Then he slowly went to 400 IU, then 800 IU, then 1,000 IU and now he is at 2,000 IU/day. Professor Holick is going in the right direction and is almost there.


Cynthia K. Buccini Sunny Dispositions vitamin D deficiency may be the most common medical problem in the world. BU Today, March 8, 2010


Professor Robert Heaney of Creighton University just discovered that if you take 2,200 IU of vitamin D every day, you only have about 12 days supply of vitamin D in your body.


I love Robert Heaney’s papers. In a previous paper, Dr. Heaney discovered that at blood levels of 35 ng/ml, 50% of people are using up their vitamin D as quickly as they take it, that is, they are not storing any for future use and suffer from chronic substrate starvation. Obviously, one wants to take enough so the body has all it can use, which is why I recommend 25(OH)D levels of at least 50 ng/ml. At that level, no one should have chronic substrate starvation.


In the paper below, Dr. Heaney collaborated with two other Creighton scientists, Dr. Diane Cullen and Dr. Laura Armas, as well as one of the premier experts in measuring vitamin D in the world, Dr. Ron Horst of Heartland Assays. Ron runs tens of thousands of vitamin D samples a year as Heartland Assays performs vitamin D testing for most of the big studies and Dr. Horst is one of the few people in the world who can accurately measure cholecalciferol, and not just 25(OH)D.


Heaney RP, Horst RL, Cullen DM, Armas LA. Vitamin D3 distribution and status in the body. J Am Coll Nutr. 2009 Jun;28(3):252-6.


Anyway, in his latest paper, Dr. Heaney found that if you regularly take 2,200 IU per day, you have about 12 days supply of vitamin D in your body. He explained, “What this indicates is that fat reserves of the vitamin are essentially running on empty and that . . . additional vitamin D inputs are [converted to 25(OH)D] almost immediately.” . . “The currently recommended intake of vitamin D needs to be revised upward by at least an order of magnitude.”


What is not known, at least by me, is what happens when cholecalciferol intake far exceeds the body’s requirement. We know it is stored in the body, mainly in fat and muscle, but what does the body do to control excess cholecalciferol from building up in the body? Professor Reinhold Vieth has written that much of it will simply be excreted unchanged in the bile, but how does that system work exactly, to get rid of excess cholecalciferol? We know it works because the few patients with vitamin D toxicity reported in the literature – almost always due to industrial errors – reduce their vitamin D levels rather quickly by simply stopping the vitamin D and staying out of the sun.


Zocor has no effect on vitamin D levels.


I know several studies have found statins raise vitamin D levels but different scientists report different findings. This paper found Zocor had no effect of vitamin D levels while a previous paper found Crestor almost tripled vitamin D levels. What’s the truth? I don’t know. The above study did find that higher vitamin D levels were strongly associated with better triglycerides and weakly associated with higher HDL (the good cholesterol) levels.


Rejnmark L, Vestergaard P, Heickendorff L, Mosekilde L. Simvastatin does not affect vitamin d status, but low vitamin d levels are associated with dyslipidemia: results from a randomised, controlled trial. Int J Endocrinol. 2010;2010:957174.


Vitamin D lowers statin blood levels


This study makes the point that things are often more complex than they first appear. Almost nothing is known of vitamin D’s drug-drug interactions. That is, how does vitamin D affect the blood level of other drugs? The below study measured the effects of vitamin D on Lipitor levels and cholesterol levels hours after Lipitor was given to patients taking vitamin D. The authors were looking for drug-drug interactions and found them.


Schwartz JB. Effects of vitamin D supplementation in atorvastatin-treated patients: a new drug interaction with an unexpected consequence. Clin Pharmacol Ther. 2009 Feb;85(2):198-203.


The above study found vitamin D not only lowered Lipitor levels, but vitamin D lowered bad cholesterol levels as well. That is, the lowest bad cholesterol levels were found in patients on vitamin D with the lowest Lipitor levels, just the opposite of what one would think. I mean, wouldn’t higher Lipitor levels result in lower cholesterol levels? Not when vitamin D was taken into account. If you think my explanation of this study is confusing, you should read the study.


Intensive treatment with vitamin D, statins, and omega-3 fish oil reverses coronary calcium scores.


The below open study by Dr. William Davis and colleagues studied 45 adults with evidence of calcified coronary arteries, treating them with high dose statins, niacin, fish oil (not cod liver oil) capsules, and enough vitamin D (average of about 4,000 IU/day) to obtain 25(OH)D levels of 50 ng/ml. They found that regimen reduced coronary calcium scores in 20 patients and slowed progression in 22 additional patients. That is, it reversed the coronary calcification process in about half of patients and slowed its progression in most of the rest.


Davis W, Rockway S, Kwasny M. Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults. Am J Ther. 2009 Jul-Aug;16(4):326-32.


Most studies have shown high dose statins on their own do not reverse coronary arthrosclerosis, so we know it was not the statins alone. What would vitamin D levels of 70 ng/ml do? So, if you have coronary artery disease: ask your cardiologist about statins and niacin, take 5-10 fish oil capsules per day, and at least 5,000 IU of vitamin D3 per day.


A word about fish oil is in order. Fish oil means fish body oil, not fish liver oil. And, four or five capsules of omega-3 fish oil a day will do very little if you do not limit your intake of omega-6 oils. Your ratio of omega-6 to omega-3 is the crucial number, your want that ratio at 2 or below, which means no chips, no French fries and no processed foods, a difficult diet. Omega-6 oils are vegetable oils such as corn oil, safflower oil, soybean oil, sunflower oil and cottonseed oil. Read the packages to see what is in them and if they contain the above oils do not eat them. In additions to taking fish oil capsules, try to eat wild-caught salmon three times a week.


Our group’s second paper on influenza is now the most accessed paper in the history of Virology Journal.


I was asked to write the paper by the editor of another journal, who then refused it! I almost decided to scrap the paper but, in the end, submitted it to Virology Journal. I’m glad I did.


Virology Journal: Top 20 most accessed articles for all time


I was glad to see that six other experts recently recommended that the diagnosis and treatment of vitamin D deficiency be part of our national preparedness for the H1N1 pandemic.


Edlich RF, Mason SS, Dahlstrom JJ, Swainston E, Long WB 3rd, Gubler K. Pandemic preparedness for swine flu influenza in the United States. J Environ Pathol Toxicol Oncol. 2009;28(4):261-4.


In addition, I hear through the grapevine that the CDC has discovered that, of the 329 American children who have died so far from H1N1, vitamin D levels in the dead children were lower than in children who survived the swine flu. Maybe something can be done to save our children by next winter? Not to mention the 16,000 adult Americans the CDC thinks died from H1N1.


Reuters. Up to 80-million Americans have been infected with H1N1. 1/15/2010


Low vitamin D levels mean higher death rates in patients with kidney disease.


The below study is the first of its kind; Dr. Rajnish Mehrota and his eight colleagues studied 3,000 of the 28 million U.S. adults who have chronic kidney disease, finding those with vitamin D levels below 15 ng/ml had a 50% increased risk of death compared to those with levels above 30 ng/ml over the nine years of the study. These researchers from UCLA, Harvard, the Los Angeles Biomedical Research Institute, and other institutions concluded: “The broad public health implications of our findings cannot be overemphasized given the high prevalence of vitamin D deficiency among individuals with chronic kidney disease, and the ease, safety, and low cost of maintaining replete vitamin D levels.”


Mehrotra R Mehrotra R, Kermah DA, Salusky IB, Wolf MS, Thadhani RI, Chiu YW, Martins D, Adler SG, Norris KC.. Chronic kidney disease, hypovitaminosis D, and mortality in the United States. Kidney Int. 2009 Nov;76(9):977-83.


These words are music to my ears; these words are strong words, urgent words, and, better yet, they are not my words. This is the first large study looking at a representative group of Americans with kidney disease, before dialysis, finding about 1/3 of them died over the 9 years of the study. Those with low vitamin D levels were more likely to die; in fact, they were more likely to have about every chronic disease you can think of before they died. The average age of those with kidney disease was only 55. This is a very important study, well written and well-conducted.


However, there is a scandal in medicine, a scandal not openly discussed in scientific papers, one not yet reported by the mainstream press. The scandal is this: if you are on dialysis, the chances are very high that your kidney doctor thinks he is giving you vitamin D when he is doing no such thing and some drug companies encourage such ignorance.


Drug companies market very lucrative activated vitamin D drugs to nephrologists as “vitamin D.” The kidney doctors, in turn, think they are giving vitamin D to their dialysis patients when they are doing no such thing. If anything, the activated vitamin D analogs nephrologists use in kidney disease will lower 25(OH)D levels by turning on the enzyme that gets rid of vitamin D.


The ugly secret is that plain old dirt-cheap vitamin D would lower the amount of activated vitamin D analogs needed to treat kidney disease. We used to think it was all or none, the kidneys would either make activated vitamin D to maintain blood calcium or the kidneys would not, as in renal failure. However, it is not all or none; the more vitamin D building blocks available to the diseased kidneys, the more activated vitamin D diseased kidneys can make. And, tissues other than the kidney, such as the skin, pancreas, adrenal medulla, and certain white blood cells, can contribute to serum activated vitamin D levels, and probably would if they had enough of the building block (plain old, dirt-cheap old, regular old, vitamin D).


Just out: Vitamin D administration (plain old vitamin D) to renal dialysis patients reduces the need for expensive vitamin D analogues, reduces inflammation, reduces the need for medication that increases red blood count, and improves cardiac function.


As I was about to finish this tirade about vitamin D and kidney failure, the below open study was published on March 4, 2010 and I ordered it. (By the way, the Council has to pay $11.00 for every paper I get and only one paper in ten is worth reporting on). The study below confirms what the above authors predicted; plain old cheap vitamin D helps patients with kidney disease.


Matias PJ, Jorge C, Ferreira C, Borges M, Aires I, Amaral T, Gil C, Cortez J, Ferreira A. Cholecalciferol Supplementation in Hemodialysis Patients: Effects on Mineral Metabolism, Inflammation, and Cardiac Dimension Parameters. Clin J Am Soc Nephrol. 2010 Mar 4.


Dr. Patricia Matias and colleagues in Portugal gave vitamin D3 to 158 patients on renal dialysis, using a sliding scale of vitamin D3 administration dependent on baseline 25(OH)D levels. Some patients got 50,000 IU per week, some got 10,000 IU per week, etc. Their dosing regimen increased 25(OH)D levels from a mean of 22 ng/ml at the beginning of the study to a mean of 42 ng/ml during treatment, indicating half of patients still had levels lower than 42 ng/ml after treatment. Interestingly, most of the patients who did not increase their 25(OH)D very much had diabetes, suggesting the metabolic clearance (how quickly it is used up) of vitamin D is increased in diabetes. By the way, we know the patients took the vitamin D; the doctors gave it to them when they came in for dialysis.


The results of this study were amazing. After vitamin D administration, parathyroid hormone, albumin, CRP (a measure of inflammation), brain natriuretic peptide (a measure of heart failure), and left ventricular mass index (a measure of heart function) all improved significantly. The dose of activated vitamin D (Zemplar in this case) was reduced, and some patients were able to stop it all together. Also, the dose of two other drugs used in kidney failure, one to bind phosphorus and the other to raise hemoglobin, was reduced.


It is a tragedy that drug companies sell more expensive vitamin D analogs by having their drug salesman assure kidney doctors that the expensive vitamin D analogues are vitamin D, even if it kills their clients. But, with the brand new knowledge that kidney failure patients live much longer on vitamin D, the drug companies might want to do some simple math. They might make even more money if they kept their patients alive longer. True, they will need less vitamin D analogues and other expensive kidney drugs every day, but the patients may live many more days.


John Cannell, MD


This newsletter is now copyrighted but may be reproduced for non-economic reasons as long as proper attribution to its source is clearly stated in the reproduction. Please reproduce it, post it on Internet sites, and forward it to your friends.


Remember, we are a non-profit and rely on your donations to publish our newsletter, maintain our website, and pursue our objectives. Send your tax-deductible contributions to:


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1241 Johnson Ave., #134

San Luis Obispo, CA 93401

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Supplementing vitamin D in people with low levels may have different effects based on patient race

15. March 2010 02:46


Vitamin D is quickly becoming the "go-to" remedy for treating a wide range of illnesses, from osteoporosis to atherosclerosis. However, new evidence from a Wake Forest University School of Medicine study suggests that supplementing vitamin D in those with low levels may have different effects based on patient race and, in black individuals, the supplement could actually do harm.

Supplementing vitamin D in people with low levels may have different effects based on patient race

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An interesting show on the Australian mushroom Industry; including a bit on quick pulsing with intense UV light to increase Vit D levels

ABC iView



Medicinal Mushrooms - Readings and References

Medicinal Mushrooms - Readings & References



International Journal of Medicinal Mushrooms


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ARS research physiologist develops preliminary model that predicts individual's vitamin D requirements

ARS research physiologist develops preliminary model that predicts individual's vitamin D requirements

19. June 2010 04:16


Your skin tone and the amount of sunshine you receive--in addition to what foods you eat--all can influence the amount of vitamin D that your body has on hand for optimum health. In a preliminary and apparently first-of-its-kind study, Agricultural Research Service (ARS) research physiologist Charles B. Stephensen and colleagues have developed a preliminary model that predicts an individual's vitamin D requirements.


Stephensen is based at the ARS Western Human Nutrition Research Center at the University of California-Davis.


Scientists have known since the early 20th century that our bodies are stimulated to make vitamin D when ultraviolet rays from the sun reach our skin. But the amount of direct sunlight that a person receives is affected not only by the amount of time spent in the sun, but also by latitude, season, skin pigmentation, and even the amount of protective clothing that one wears.


Some vitamin D comes from food, including salmon and some other fish; milk and breakfast cereals fortified with this essential nutrient, and nutritional supplements such as multivitamin tablets.


The current recommended daily allowance of vitamin D for U.S. adults who are less than 50 years of age is 200 international units.


To develop the preliminary model, Stephensen and co-investigators worked with 72 young adult volunteers who provided intermittent records of what they ate and, for 7- to 8-week stints, wore photosensitive badges from 7 a.m. to 7 p.m. so scientists could determine their level of sun exposure.


Data from the volunteers--either African-American or of European ancestry--who had relatively low amounts of sun exposure suggest that they may need additional vitamin D to reach a target blood level of 75 nanomoles of vitamin D per liter of plasma.


Stephensen cautions, however, that some vitamin D levels indicated by the model exceed the level currently considered safe. More research, with a larger number of volunteers, may refine the predictive power of the model, he reports.


The research was published earlier this year in the Journal of Nutrition.


Source: United States Department of Agriculture-Research, Education, and Economics

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It seems the incidence of BPH (prostate problems and LUTs) is also dependent on latitude like so many diseases, those Canadians must be a crook lot!.

So a Vitamin D connection here too.


Any chemists about ?

Apparently Vit D is very hard to find in stuff. The test used is to give a rat rickets then give him something you think has Vit D in it, and see what happens.

So it is hard to find in plants, but a recent study found a little in spoiled hay!

Is there cheap quick away of analyzing plant material for Vit D?


To the same chemists– Do short chain fatty acids have a connection/relationship with Vit D?

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