The charts alone make it crystal clear: lack of sun exposure, low D levels and a host of diseasesi [19] result. Critical for all of us living in northern climates, but especially true for people of African descent with dark skin. It's apparent from his presentation that even 2000 units a day is not enough for the elderly, African Americans, and those of us with illness. 4000 units a day is more like it.
http://wildhorse.insinc.com/directms13oct2005/ [20]
Just ran across this fairly easy to read recent review article on Vit D3 and thought others might be interested:
The Complex Role of Vitamin D in Autoimmune Diseases [21]
It's well worth a read...
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Gotta love this one.
[Note: the full text of this open-access article, outlining evidence that sun/vitamin Di [26] status could have "profound implications for the prevention of influenza" is available free at http://www.virologyj.com/content/5/1/29 [27] ]
The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson [28]. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns."
Recent discoveries indicate vitamin D upregulates the endogenous antibioticsi [29] of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums:
1. Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?
2. Why are the epidemics so explosive?
3. Why do they end so abruptly?
4. What explains the frequent coincidental timing of epidemics in countries of similar latitude?
5. Why is the serial interval obscure?
6. Why is the secondary attack rate so low?
7. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?
8. Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers?
9. Why has influenza mortality of the aged not declined as their vaccination rates increased?
We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies.
We hypothesize that two factors explain the nine conundrums:
• Vitamin D's seasonal and population effects on innate immunity,
•And the presence of a subpopulation of "good infectors."
If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.
Source: Virology Journal, Feb 2008, 5:29; DOI:10.1186/1743-422X-5-29 by Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Department of Psychiatry, Atascadero State Hospital, California; Departments of Surgery and Pediatrics, Georgetown University, Washington, DC; Department of Family and Preventive Medicine, University of California San Diego, La Jolla, California; Department of Epidemiology and Biostatistics, University of Auckland, New Zealand; Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.
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CAPi [23]i [23] for Cpni [30]i [30] 11/04. Dx: 25yrs CFSi [31]i [31] & FMSi [32]i [32]. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii [33]i [33] 1000mg/day pulses; Vit D2000 units, T4 & T3
Most prescription D is D2 rather than the more effective D3. This article has an excellent review of the state of the science and why D3 is preferred for supplementation.
http://www.ajcn.org/cgi/content/full/84/4/694 [34]
A lot of people coming to the site here have questions about the Marshall Protocol and the Cpni [30] CAPi [23], where we recommend Vitamin Di [26] supplementation in contrast to MPi [35]. The most detailed analysis of the MP in relation to what is known in the scientific literature about Vitamin D occurs in this link:
http://stuff.mit.edu/people/london/universe.htm [36]
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Since so many on the site are dealing with thyroid issues, I thought I'd pass this along...
First, here's a little news blurb on the study:
Modern Medicine: Vitamin D Directly Affects Thyroid Function in Mice [38]
Below is the full study article. While the article focuses on Graves' hyperthyroidism, the discussion and conclusion sections list some interesting findings of recent research on Vitamin D3's importance for proper thyroid function in general. It's well worth a read:
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Posting this one as a whole, seems "fair use" for an informational web site, because it includes a useful discussion of the limitations of the methodology of the study not found in the abstract. Still, it behooves those of us with pain to consider Vitamin Di [26] levels as at least a variable that either modulates pain itself or contributes to other factors, like infection, that generate pain and inflammationi [40].
Low Vitamin D Levels Linked to Chronic Pain in Women
Medscape Medical News 2008. © 2008 Medscape
August 18, 2008 — Women with low vitamin D levels have more chronic widespread pain, a new study has found. The modest findings do not support the use of vitamin D status as a key determinant for chronic pain, researchers suggest, but they do raise interesting questions about the possible influence of endocrine or immunological factors. The work is published online August 12 in the Annals of the Rheumatic Diseasesi [19].
Chronic widespread pain is thought to be a multifactorial condition. To date, the focus has been on psychosocial influences, note the study investigators, led by Kate Atherton, MD, from the University College London Institute of Child Health, in the United Kingdom. Although associations between chronic pain and general psychological distress, depression, somatization, and other factors have been consistently reported, translating these observations into management strategies has been fairly unsuccessful, they note.
Vitamin D deficiency has been suggested as a new modifiable risk factor for chronic pain. Vitamin D is a hormone precursor, which is obtained either through diet or skin synthesis. Using a nationwide population sample of white British adults, the researchers wanted to examine the link between vitamin D and chronic pain.
Women With Vitamin D Levels of 75 to 99 nmol/L Had Less Pain
"To our knowledge, this study is the largest population-based examination of the association between vitamin D status and chronic widespread pain to date," write the researchers. The work is also the first to consider related variations in lifestyle factors or to focus on white ethnic groups, they add.
The study included more than 9300 participants in England, Scotland, or Wales born during 1 week in March in 1958 who had completed a biomedical assessment at age 45 years. Of these, 6824 participants had data on 25-hydroxyvitamin D and pain.
Investigators found that chronic pain levels varied by 25-hydroxyvitamin D concentration in women, but not in men. "In our study, the lowest prevalence of chronic widespread pain was observed for women with 25-hydroxyvitamin D 75 to 99 nmol/L," Dr. Atherton and her team report. "This is intriguing given that 25-hydroxyvitamin D 75 nmol/L has been previously suggested as the cutoff point for optimal bone health."
Prevalence of Chronic Pain in Relation to Vitamin D Concentrations in Women
| 25-Hydroxyvitamin D (nmol/L) | Women with Chronic Pain (%) |
| < 25 | 14.4 |
| 25 – 49 | 14.8 |
| 50 – 74 | 11.6 |
| 75 – 99 | 8.2 |
| > 100 | 9.8 |
The investigators report there was an interaction between vitamin D concentration and sex in relation to chronic pain (interaction P = .006), which was not fully explained by differences in lifestyle or social factors (adjusted interaction P = .03).
The researchers point to a number of limitations of the work. They note the vitamin D status of participants was obtained during the study and may not represent the patient's status during the time that chronic pain developed, which may have been years earlier.
They also suggest that given the cross-sectional design of the study, it is not possible to establish whether suboptimal vitamin D status results in an increased risk for pain or whether changes in the behavior of subjects with pain result in reduced vitamin D concentrations.
"The lack of a stronger association between vitamin D and chronic pain in our general population sample may suggest that pain is primarily indicative of a severe vitamin D deficiency rather than a more gradual response to varying concentrations," the researchers write.
Dr. Atherton and her team report that it is unclear why an association between vitamin D and pain was observed in women but not in men. They suggest that since the women in the cohort are still mostly premenopausal, perhaps the influences of hormonal vitamin D on the regulation of estrogen activity may at least partly contribute to this sex difference.
"Nevertheless," they add, "given the observational nature of these data, we cannot exclude the possibility that our finding of an association between vitamin D status and chronic pain in women (or the lack of any association in men) is confounded by unmeasured factors.
"Follow-up studies are needed to evaluate whether higher vitamin D intake might have beneficial effects on [chronic widespread pain] risk," they conclude.
The researchers have disclosed no relevant financial relationships.
Ann Rheum Dis. Published online August 12, 2008. Abstract [41]
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CAPi [23] for Cpni [30]i [30] 11/04. Dx: 25yrs CFSi [31]i [31] & FMSi [32]i [32]. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii [33]i [33] 1000mg/day pulses; Vit D2000 units, T4 & T3
Following are some new Vitamin Di [26] abstracts by Holick. With 1,25-dihydroxyvitamin D involved in regulating more than 200 genesi [42], you would think it might not be such a good idea to formulate treatment around Vitamin D starvation...
Jim
Mol Aspects Med. 2008 Sep 2. [Epub ahead of print]Click here to read Links
The vitamin D deficiency pandemic and consequences for nonskeletal health: Mechanisms of action.
Holick MF.
Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, MA, United States.
Vitamin D, the sunshine vitamin, is important for childhood bone health. Over the past two decades, it is now recognized that vitamin D not only is important for calcium metabolism and maintenance of bone health throughout life, but also plays an important role in reducing risk of many chronic diseasesi [19] including type I diabetes, multiple sclerosis, rheumatoid arthritis, deadly cancers, heart diseasei [43] and infectious diseases. How vitamin D is able to play such an important role in health is based on observation that all tissues and cells in the body have a vitamin D receptor, and, thus, respond to its active form 1,25-dihydroxyvitamin D. However, this did not explain how living at higher latitudes and being at risk of vitamin D deficiency increased risk of these deadly diseases since it was also known that the 1,25-dihydroxyvitamin D levels are normal or even elevated when a person is vitamin D insufficient. Moreover, increased intake of vitamin D or exposure to more sunlight will not induce the kidneys to produce more 1,25-dihydroxyvitamin D. The revelation that the colon, breast, prostatei [44], macrophages and skin among other organs have the enzymatic machinery to produce 1,25-dihydroxyvitamin D provides further insight as to how vitamin D plays such an essential role for overall health and well being. This review will put into perspective many of the new biologic actions of vitamin D and on how 1,25-dihydroxyvitamin D is able to regulate directly or indirectly more than 200 different genes that are responsible for a wide variety of biologic processes.Curr Diab Rep. 2008 Oct;8(5):393-8.Links
Diabetes and the vitamin d connection.
Holick MF.
Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Boston University School of Medicine, 715 Albany Street, M-1013, Boston, MA 02118, USA. mfholick@bu.edu [45]
Vitamin D deficiency, which is common in children and adults, causes rickets, osteomalacia, and osteoporosis. Most organs and immunei [46] cells have a vitamin D receptor, and some also have the capacity to metabolize 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. 1,25-Dihydroxyvitamin D is a potent immunomodulator that also enhances the production and secretion of several hormones, including insulin. Vitamin D deficiency has been associated with increased risk of type 1 diabetes. Glycemic control and insulin resistance are improved when vitamin D deficiency is corrected and calcium supplementation is adequate. 25-Hydroxyvitamin D (measure of vitamin D status) of less than 20 ng/mL is vitamin D deficiency and 21 to 29 ng/mL is insufficiency. Children and adults need at least 1000 IU of vitamin D per day to prevent deficiency when there is inadequate sun exposure.
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CAPi [23] for Cpni [30]i [30] 11/04. Dx: 25yrs CFSi [31]i [31] & FMSi [32]i [32]. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii [33]i [33] 1000mg/day pulses; Vit D2000 units, T4 & T3
Reports describing Vitamin D3's benefits by Oliver Gillie, a freelance medical researcher and writer, are available online.
Here's the latest. Note the recommendations by Drs Vieth, Holick, Holis, etc on pages III and IV. It's a very interesting article, and one well worth the 30 minutes it takes to skim:
Scotland's Health Deficit: An explanation and a plan [47]
His older books can be viewed from here:
The Health Research Forum: Reports [48]
About the Author:
Oliver Gillie is a freelance medical researcher and writer. Formerly he was medical correspondent of The Sunday Times, then medical editor and later special correspondent of The Independent newspaper. He has a BSc and PhD degrees from Edinburgh University where he studied geneticsi [42] and developmental biology under Professor C.H. Waddington at the Institute of Animal Genetics, Edinburgh. He also undertook research at the National Institute for Medical Research, Mill Hill, under Sir Peter Medawar.
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The tolerability and biochemical effects of high-dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insufficiency.
Leventis P, Kiely PD.
Department of Rheumatology, St George's Healthcare NHS Trust, London, UK.
Objectives: To investigate the practicality and tolerability of high-dose intramuscular (i.m.) vitamin D2 or oral vitamin D3 replacement in vitamin D-insufficient patients, and to evaluate the biochemical efficacy of each formulation.
Methods: Sixty-nine patients with vitamin D insufficiency [25-hydroxyvitamin D (25(OH)D) <40 nmol/L] were recruited from the Rheumatology Outpatient Department of St George's Hospital, London.
In study 1, 50 patients received 300 000 IU i.m. vitamin D2 (ergocalciferol).
In study 2, 19 patients received 300 000 IU oral vitamin D3 (cholecalciferol) under observation.
Biochemical response was measured at baseline, and at 12 and 24 weeks. Results: Bolus i.m. vitamin D2 or oral vitamin D3 was well tolerated.
The change from baseline in serum 25(OH)D was significantly greater at 6 and 12 weeks in study 2 (p<0.0001 and <0.0001, respectively).
In study 1, a modest increase in mean serum 25(OH)D at 6, 12, and 24 weeks was observed but no patients achieved a serum 25(OH)D concentration >/=50 nmol/L. PTH remained elevated in 42% of patients with secondary hyperparathyroidism at 12 weeks.
In study 2, 100% and 89% of patients had serum 25(OH)D>50 nmol/L at 6 and 12 weeks, respectively.
All patients with elevated baseline PTH were fully suppressed at 12 weeks. No cases of hypercalcaemia were observed in either group.
Conclusion: The 300 000-IU bolus of vitamin D2 or D3 was practical, well tolerated, and safe.
Vitamin D3 had greater potency than equimolar vitamin D2, with a higher, sustained serum 25(OH)D response and efficacious PTH suppression.
To adequately treat vitamin D insufficiency we would recommend administering 300 000 IU oral vitamin D3 approximately three times per year.
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Daisy - Husband on CAPi [23]i [23] 5/07. "When Going Thru Hell, Just Keep Going", Winston Churchill
Veterans Affairs Medical Center, San Francisco, California 94121, USA. Daniel.bikle@ucsf.edu [52]
PURPOSE OF REVIEW: The role of vitamin Di [26] extends well beyond that of regulating calcium homeostasis. One of these areas is immunei [46] function. Immunity is both adaptive and innate, and vitamin D signaling is operative in both. This review will examine these actions of vitamin D, in particular the role of vitamin D in host defense against infection. RECENT FINDINGS: This review will consider two examples of vitamin D-regulated innate immunity that have been recently explored: the role of vitamin D signaling within macrophages to enable them to respond to and kill Mycobacterium tuberculosis organisms, and the role of vitamin D signaling in the keratinocytes of the epidermis to enable them to respond to disruption of their barrier function. Potential application to periodontal disease will then be considered. SUMMARY: Both adaptive and innate immune processes are two edged: beneficial and harmful. Although suppression of adaptive immunity may be beneficial in a number of self-destructive diseasesi [19], such suppression may predispose to infection. Enhancement of innate immunity is clearly beneficial in diseases like tuberculosis, but potentiation of proinflammatory processes can increase tissue destruction as in bone loss in periodontal disease. The balance, however, favors adequate vitamin D nutrition in host defense against infection.
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CAPi [23]i [23] for Cpni [30]i [30] 11/04. Dx: 25yrs CFSi [31]i [31] & FMSi [32]i [32]. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii [33]i [33] 1000mg/day pulses; Vit D2000 units, T4 & T3
The Vitamin Di [26] Council is an excellent source of information on Vitamin D, health and science (thanks Reenie:).
http://vitamindcouncil.org [53]
Their research page is a useful listing of all the conditions in which insufficient Vitamin D has been linked to, including cancer, MSi [54] and autism. http://vitamindcouncil.org/research.shtml [55]
Of interest to sarcoidosis patients looking to cautiously increase Vitamin D as part of a CAPi [23] for Cpni [30]:
Hypersensitivity, Not Toxicity
Vitamin Di [26] hypersensitivity syndromes are often mistaken for vitamin D toxicity. The most common is primary hyperparathyroidism. Other syndromes occur when abnormal tissue subverts the kidney's normal regulation of endocrine calcitriol production. Aberrant tissues, usually granulomatous, convert 25(OH)D into calcitriol causing high blood calcium. The most common such condition is sarcoidosis, oat cell carcinoma of the lung and non‑Hodgkin's lymphoma but other illness can cause the syndrome and they can occur while the patient's 25(OH)D levels are normal or even low. For that reason, while rare, it is advisable to seek a knowledgeable physician's care when repleting your vitamin D system, especially if you are older, have sarcoidosis, cancer or other granulomatous diseasesi [19]i [19]. In such high‑risk patients, periodic monitoring of 25(OH)D levels and serum calcium will alert the physician to the need to do more tests, such as calcitriol or PTH, and take further action.
However, it seems clear that restoring physiological serum levels of 25(OH)D will help many more patients that it will hurt. In fact, living in America today while worrying about vitamin D toxicity is like dying of thirst in the desert while worrying about drowning.
http://www.vitamindcouncil.org/vitaminDToxicity.shtml [56]
Although this is with a different intracellulari [57] pathogen than Cpni [30], it suggests one of the possible protective mechanisms that Vitamin Di [26] gives against intracellular pathogens. Like Cpn, Mycobacterium tuberculosis infects the immunei [46] cells (macrophages) themselves, and this study describes the inhibition of cell invasion by Vitamin D.
J Microbiol Immunol Infect. 2008 Feb;41(1):17-25.
Synergistic action of vitamin D and retinoic acid restricts invasion of macrophages by pathogenic mycobacteria. Anand PK, Kaul D, Sharma M. Molecular Biology Unit, Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India. BACKGROUND AND PURPOSE: Phagosomal maturation arrest is known to play a central role in the survival of pathogenic mycobacteria within macrophages. The maturation arrest of mycobacterial phagosome results from the retention of tryptophan-aspartate-containing coat protein (TACO) on this organelle, enabling successful replication of the pathogen. We have shown earlier that vitamin D(3) and retinoic acid (RA) down-regulate TACO gene transcription in a dose-dependent manner. METHODS: In this study, we analyzed the promoter region of TACO gene using bioinformatics tools and observed that the vitamin D receptor (VDR)/retinoid-X-receptor (RXR) response sequence was highly functional. We also evaluated the effect of treatment with vitamin D(3)/RA on Mycobacterium tuberculosis entry and survival in cultured human macrophages. RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Treatment of macrophages with vitamin D(3)/RA allows maturation of mycobacterial phagosome, leading to degradation of the pathogen. CONCLUSIONS: Our results elucidate the mechanism of TACO gene down-regulation observed with vitamin D(3)/RA. Furthermore, the results revealed that vitamin D(3)/RA treatment inhibits mycobacterial entry as well as survival within macrophages, possibly through rescue of phagosome maturation arrest. The developing knowledge in this area suggests that vitamin D(3)/RA may be of importance in the treatment of intracellular infection, particularly tuberculosis.
Here's another interesting area to keep an eye on, namely the apparent importance of IL-15 for bioconversion of 5-hydroxyvitamin D3 (25D3) into bioactive 1,25D3 and the downstream induction of cathelicidins:
"In this study, we found that TLR2/1-induced IL-15 was required for induction of CYP27b1, the VDR and the downstream antimicrobial peptide cathelicidin. Although both IL-15 and IL-4 triggered macrophage differentiation, only IL-15 was sufficient by itself to induce CYP27b1 and subsequent bioconversion of 25-hydroxyvitamin D3 (25D3) into bioactive 1,25D3, leading to VDR activation and induction of cathelicidin"
Here's another study along these lines:
"Together, these results demonstrate that IL-15 plays an important role in antigen-induced neutrophil migration during inflammationi [40], triggering a sequential OVA, IL-15, IL-18, MIP-2, MIP-1alpha, TNF-alpha, LTB4 and neutrophil migration signaling cascade"
There are quite a few other studies in pubmed showing the importance of IL-15 in fighting infectionsi [60]. Here are a couple:
Unfortunately, some drugs seem to inhibit IL-15, and researchers are on the hunt for additional IL-15 inhibitors to treat "inflammatory" diseasesi [19]:
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Links:
[1] http://www.cpnhelp.org/vieth_slide_show_vitamin_0
[2] http://www.cpnhelp.org/another_good_article_on_v
[3] http://www.cpnhelp.org/are_influenza_epidemics_a
[4] http://www.cpnhelp.org/d2_vs_d3_supplementation_
[5] http://www.cpnhelp.org/detailed_info_on_vitamin_
[6] http://www.cpnhelp.org/great_video_on_importance
[7] http://www.cpnhelp.org/interesting_study_importa
[8] http://www.cpnhelp.org/low_vitamin_d_levels_link
[9] http://www.cpnhelp.org/more_and_more_vitamin_d
[10] http://www.cpnhelp.org/oliver_gillies_reports_vi
[11] http://www.cpnhelp.org/sunlight_uv_radiation_vit
[12] http://www.cpnhelp.org/the_tolerability_and_bioc
[13] http://www.cpnhelp.org/vitamin_d_and_skin_physio
[14] http://www.cpnhelp.org/vitamin_d_and_immune_syst
[15] http://www.cpnhelp.org/vitamin_d_council_and_bri
[16] http://www.cpnhelp.org/vitamin_d_inhibits_entry_
[17] http://www.cpnhelp.org/vitamin_d_pathways_import
[18] http://www.cpnhelp.org/vitamin_d_status_measurem
[19] http://www.cpnhelp.org/taxonomy/term/34
[20] http://wildhorse.insinc.com/directms13oct2005/
[21] http://www.blackwell-synergy.com/action/showFullText?submitFullText=Full Text HTML&doi=10.1111/j.1365-3083.2008.02127.x
[22] http://www.cpnhelp.org/taxonomy/term/142
[23] http://www.cpnhelp.org/glossary/term/168
[24] http://www.cpnhelp.org/chlamydia_pneumoniae/supp
[25] http://www.cpnhelp.org/glossary/term/177
[26] http://www.cpnhelp.org/chlamydia_pneumoniae/vita
[27] http://www.virologyj.com/content/5/1/29
[28] http://en.wikipedia.org/wiki/Robert_Edgar_Hope-Simpson
[29] http://www.cpnhelp.org/taxonomy/term/38
[30] http://www.cpnhelp.org/glossary/term/167
[31] http://www.cpnhelp.org/glossary/term/163
[32] http://www.cpnhelp.org/taxonomy/term/24
[33] http://www.cpnhelp.org/chlamydia_pneumoniae/an_0
[34] http://www.ajcn.org/cgi/content/full/84/4/694
[35] http://www.cpnhelp.org/glossary/term/174
[36] http://stuff.mit.edu/people/london/universe.htm
[37] http://www.uvadvantage.org/portals/0/pres/
[38] http://www.modernmedicine.com/modernmedicine/Endocrinology/Vitamin-D-Directly-Affects-Thyroid-Function-in-Mic/ArticleNewsFeed/Article/detail/562611
[39] http://endo.endojournals.org/cgi/rapidpdf/en.2008-1191v1.pdf
[40] http://www.cpnhelp.org/taxonomy/term/67
[41] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=18697776&dopt=Abstract
[42] http://www.cpnhelp.org/taxonomy/term/60
[43] http://www.cpnhelp.org/taxonomy/term/29
[44] http://www.cpnhelp.org/taxonomy/term/15
[45] mailto:mfholick@bu.edu
[46] http://www.cpnhelp.org/taxonomy/term/64
[47] http://www.healthresearchforum.org.uk/reports/scotland.pdf
[48] http://www.healthresearchforum.org.uk/reports.html
[49] http://www.cpnhelp.org/javascript%3AAL_get%28this%2C+%27jour%27%2C+%27Curr+Opin+Nephrol+Hypertens.%27%29%3B
[50] http://www.cpnhelp.org/javascript%3APopUpMenu2_Set%28Menu18660668%29%3B
[51] http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term="Bikle DD"[Author]&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus
[52] mailto:Daniel.bikle@ucsf.edu
[53] http://vitamindcouncil.org
[54] http://www.cpnhelp.org/taxonomy/term/6
[55] http://vitamindcouncil.org/research.shtml
[56] http://www.vitamindcouncil.org/vitaminDToxicity.shtml
[57] http://www.cpnhelp.org/glossary/term/114
[58] http://www.ncbi.nlm.nih.gov/pubmed/18981132?dopt=Abstract
[59] http://www.ncbi.nlm.nih.gov/pubmed/17979156?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
[60] http://www.cpnhelp.org/taxonomy/term/58
[61] http://www.ncbi.nlm.nih.gov/pubmed/18653461?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
[62] http://www.ncbi.nlm.nih.gov/pubmed/18086532?ordinalpos=32&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
[63] http://www.ncbi.nlm.nih.gov/pubmed/11817607?ordinalpos=67&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
[64] http://www.ncbi.nlm.nih.gov/pubmed/17984577?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum