The many guises of vitamin D deficiency

Posted on August 25, 2012 by John Cannell, MD



Vitamin D deficiency may be on its way to being known in medicine as a grand deceiver, presenting in various guises and imitating different diagnoses. Take a recent case report on rickets mimicking the incurable arthritic disease, ankylosing spondylitis.

Demirbilek H, Aydoğdu D, Ozön A. Vitamin D-deficient rickets mimicking ankylosing spondylitis in an adolescent girl. Turk J Pediatr. 2012 Mar-Apr;54(2):177-9.

Dr. Huseyin Demirbilek and colleagues of the Hacettpe University Faculty of Medicine in Turkey report on a 14-year-old African girl with generalized bone aches referred to their clinic when her symptoms did not improve with treatment. Ankylosing spondylitis was her diagnosis, a disease of the skeleton with variable involvement of other joints. It is a chronic, inflammatory autoimmune disease, which mainly affects joints in the spine and the pelvis, and can cause eventual fusion of the spine.

However, the good doctors noticed she was heavily clothed, had very black skin, and had severe pain on pressure to her sternum. Sure enough, her 25(OH)D was literally 1 nmol/L, her alkaline phosphatase was 2312 (very high), her blood calcium was low with normals between 8.6 and 10.5 (quite different than American normals which often call a calcium of 10 as elevated). Her PTH was 923 (very high). X-rays of her wrists confirmed rickets.

Her disease and her suffering disappeared a month after treatment with a one-time dose of 300,000 IU of vitamin D and 1000 mg/day of calcium. After the one time dose, they very conservatively maintained her on 800 IU/day of vitamin D.

Besides ankylosing spondylitis, vitamin D deficiency may present as frequent infections, chronic pain, heart disease, stroke, multiple autoimmune diseases, fibromyalgia, osteoporosis, gingivitis, diabetes, and in my opinion, sun sensitivity, to name but a few. Vitamin D deficiency is now the grand deceiver.

http://blog.vitamindcouncil.org/201...n-d-deficiency/

I have been taking Vit D but only 900 iu. The area where I live is dry and very cold so I haven't got outside in what seems like forever. My car is broke down and I have been just a hermit. My friend told me about Vit D but I just bought some cheap 400 iu capsules to go with the multi-vitamins I take. I have tried to stick to the CAD/CALP but have serious cravings after dinner which is unlike me. I even cut out the reward dessert and yet I still wanted to nibble. I know I'm bored and lonely after my divorce but I realized I must be experiencing SAD to go with it. I can't afford a more quality Vit D supplement but I will try increasing the dosage. It couldn't hurt. Thanks again for not only this power of suggestion but the facts and links that go along with this thread.

Sun exposure: Is just a little bit enough?

Posted on January 16, 2013 by John Cannell, MD


Some experts opine that brief sun exposure will supply all the vitamin D that one needs. However, there has never been a study of how much vitamin D such exposure generates.

Recently, researchers in Korea decided to find out. Dr. Sang-Hoon Lee and colleagues from the Ajou University School of Medicine in South Korea studied the effect of brief sun exposure on vitamin D levels in 20 young women for four weeks.

Lee SH, Park SJ, Kim KM, Lee DJ, Kim WJ, Park RW, Joo NS. Effect of sunlight exposure on serum 25-hydroxyvitamin d concentration in women with vitamin D deficiency: using ambulatory lux meter and sunlight exposure questionnaire. Korean J Fam Med. 2012 Nov;33(6):381-9.

The study was conducted between October and November at latitude 37 degrees north, about the latitude of Washington DC. Initial mean 25(OH)D levels were 11 ng/ml and no woman had levels greater than 20 ng/ml to begin the study. The women were told to get 20 minutes of midday sun exposure on their hands, forearms and face every weekday for four weeks. Facial sunblock and sunglasses were permitted.

Guess how much 25(OH)D levels increased after a month of daily sun exposure? Vitamin D levels did not increase at all; in fact, they were a little lower than when the study began!

Why? I think four reasons may explain the finding.

Perhaps the women did not go outside as often as required. Second is the latitude; I think less UVB is available in October and November than many people think at such latitudes. Perhaps the vitamin D winter begins in the fall at latitude 37 degrees. Third, perhaps forearms, face and hands are just not enough skin surface to make meaningful amount of vitamin D. And four, such brief sun exposure may not be long enough to make meaningful amount of vitamin D.

Our hunter-gatherer equatorial ancestors had very dark skin but wore no or little clothing and were outside most or all of the day. Recent studies indicate such people had vitamin D levels around 50 ng/ml. This indicates a vitamin D input of about 5,000 to 10,000 IU/day.

Vitamin D status in indigenous populations: Part 1. Posted on August 27, 2012 by John Cannell, MD

That’s why the Vitamin D Council recommends full body sunbathing, not incidental sun exposure. Make sure your shadow is shorter than you are so you know you are making vitamin D. Also, since most people can’t sunbath every day, and because the vitamin D winter is so severe, we recommend 5,000 IU/day on the days you don’t sunbathe.

http://blog.vitamindcouncil.org/201...lations-part-1/

Does vitamin D prevent formation of blood clots?

Posted on January 17, 2013 by John Cannell, MD


A venous thrombosis is a blood clot that forms within a vein. A classical venous thrombosis is in a deep vein thrombosis, usually deep in a vein in the leg. These can break off, go to the lungs, and become a life-threatening pulmonary embolism. Complications of pulmonary embolism include coughing up blood, heart failure or shock, heart palpitations, pulmonary hypertension, severe breathing difficulty, severe bleeding (usually a complication of blood thinner treatment), and sudden death.





Venous thromboembolism is a major health problem. The average annual incidence of venous embolism among Whites is about 700,000 cases per year. The incidence appears to be higher among Blacks. Pulmonary embolism is predominantly a disease of older age as rates go up steeply with age. The incidence rates are also somewhat higher in women during their childbearing years. Birth control pills are a major risk factor for blood clots. An Italian study showed pulmonary embolism peaked in December.

Does vitamin D play a role in venous thrombosis? Dr. P. Brøndum-Jacobsen and colleagues of the Copenhagen University Hospital in Denmark obtained vitamin D levels on more than 18,000 patients and then followed them for up to 30 years to find out.

Brøndum-Jacobsen P, Benn M, Tybjaerg-Hansen A, Nordestgaard BG. 25-hydroxyvitamin D concentrations and risk of venous thromboembolism in the general population with 18,791 participants. J Thromb Haemost. 2012 Dec 29.

The mean follow up time was 13 years for this cohort, which averaged 57 years of age. Nine hundred and fifty patients ended up with a blood clot; the average time to a blood clot was 13 years. When the authors split baseline vitamin D levels into tertiles (one-thirds), they found those with the lowest vitamin D levels were 37% more likely to have a blood clot. After statistical adjustment, the relative risk increased to 106% for those with the lowest levels.

The authors postulated three mechanisms by which higher vitamin D levels were protective. First, vitamin D deficiency may lead to a decrease in the gene expression of anti-blood clot proteins (antithrombin in the liver and of thrombomodulin in the aorta) leading to more blood clots.

Second, vitamin D deficiency may lead to an increase in the gene expression of a protein (tissue factor) in the liver and kidneys, which will lead to more blood clots.

Finally, in human aortic smooth muscle cells, vitamin D like drugs have been shown to reduce the production of certain blood clotting factors (plasminogen activator inhibitor-1, thrombospondin-1, and thrombomodulin) leading to an overall anti-thrombotic effect. It turns out that atherosclerotic cardiovascular disease and blood clots may not be as separate a disease, as the two diseases share some common risk factors. It may be that reduced plasma vitamin D could be an independent and common risk factor for both conditions.

The authors concluded,


“The consistent and stepwise increasing risk that we found may tempt to suggest causality; however, one cannot infer causality from the present study. Therefore, randomized intervention trials are needed to test the question of causality, and randomized trials with vitamin D supplementation are needed before implementing supplementation in the general population or in selected patient groups to reduce the risk of venous thromboembolism.”

I disagree in that the time to act is now. Treatment of vitamin D deficiency cannot wait for further science. While scientists are required to wait, physicians caring for patients are ethically required to act on what is known now; they cannot patiently wait to find out what may be discovered in the future. Physicians have always been required, both ethically and legally, to preform risk benefit assessments of treating or not treating vitamin D deficiency. We know there are potentially huge benefits and simply no significant risks of treating deficiency.

http://blog.vitamindcouncil.org/201...of-blood-clots/

Vitamin D deficiency prevalent in autoimmune skin disorder

Posted on January 15, 2013 by Kate Saley


Researchers in Egypt report a link between vitamin D deficiency and vitiligo, an autoimmune skin disease characterized by loss of pigmentation (brown color) from areas of the skin.





Vitiligo may appear at any age, affecting about 1 out of every 100 people in the United States. Vitiligo is often associated with existing autoimmune conditions including lupus, type 1 diabetes, hypo and hyperthyroidism, and rheumatoid arthritis.

Hanan M Saleh and colleagues at the Department of Dermatology and Venereology in Cairo set out to evaluate vitamin D status in vitiligo patients with and without systemic autoimmune diseases.

The researchers conducted a case-control study, randomly selecting 40 vitiligo patients; 20 with systemic autoimmune disease, 20 without autoimmune disease. The authors included 40 age, gender, and skin type matched control participants.

After assessment of 25(OH)D status, physical examination, and medical history, the authors found:
■No statistical difference between age, gender, skin type, or reported vitamin D intake.
■There was a highly statistical significance between occupations of the vitiligo vs control groups. Eighty-seven percent of control participants worked outdoors.
■There was a significant difference between both groups regarding duration of vitiligo (p=0.008). Participants with vitiligo, without autoimmune disease had the disease for an average of 5.5 years compared to 2 years for those with vitiligo and autoimmune disease.
■97.5% of vitiligo participants were vitamin D deficient, while only 12.5% of controls were deficient (p=0.0001).
■There was no statistical difference between vitamin D status of patients with vitiligo and autoimmune diseases (group 1) and patients without autoimmune diseases (group 2), although slightly lower levels were found in group 1.

The authors conclude,


“The key question is whether low 25(OH)D levels in vitiligo patients confer greater risk of developing secondary autoimmunity or autoimmune inflammatory processes consumes excess vitamin D…Whether low 25(OH)D levels are the consequence or the cause of autoimmune disease, 25(OH)D screening may be a worthwhile screen for vitamin D deficiency and hence vitamin D supplementation to control autoimmunity. Given its relative safety in conjunction with its beneficial immunomodulatory effects, there is optimism that correcting vitamin D deficiency will lead to better outcomes for vitiligo patients.”

The authors recognize several limitations of the study, including the failure to match occupation of patients and controls, which could explain the significant difference between vitamin D blood levels between the two groups. The researchers call for future trials with larger sample size and matching patients and controls with similar sun exposure habits.

Source

Saleh HMA, Abdel Fattah NSA, Hamza HMM. Evaluation of serum 25-hydroxyvitamin D levels in vitiligo patients with and without autoimmune diseases. Photodermatology, Photoimmunology & Photomedicine. Feb 2013.

http://blog.vitamindcouncil.org/201...-skin-disorder/

Dr. Holick on Vitamin D

Free Webinar

Dr Michael Holick: What does the sun do for me?
January 22, 2013
Are you ready for the second Grassroots Health webinar?

Today at 10am PST Dr Michael Holick will be discussing the question: "What does the sun do for me?"

Register here for today's webinar! Have a vitamin D question? You can submit your questions for Dr Holick when you register

http://www.grassrootshealth.net/webinars

Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis1,2,3


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3349454/

A 12-week double-blind randomized clinical trial of vitamin D3 supplementation on body fat mass in healthy overweight and obese women

CONCLUSION: Among healthy overweight and obese women, increasing 25(OH) D concentrations by vitamin D3 supplementation led to body fat mass reduction.

This trial is registered at clinicaltrials.gov as NCT01344161.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514135/

Cholecalciferol (Vitamin D3) Improves Myelination and Recovery after Nerve Injury



http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669361/

Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease.

Suzuki M, Yoshioka M, Hashimoto M, Murakami M, Noya M, Takahashi D, Urashima M.


Source

Department of Neurology, Katsushika Medical Center and the Division of Molecular Epidemiology, Jikei University School of Medicine, Tokyo, Japan.


Abstract


BACKGROUND:

In our previous study, higher serum 25-hydroxyvitamin D [25(OH)D] concentrations and the vitamin D receptor (VDR) FokI CC genotype were associated with milder Parkinson disease (PD).

OBJECTIVE:

We evaluated whether vitamin D3 supplementation inhibits the progression of PD on the basis of patient VDR subgroups.

DESIGN:

Patients with PD (n = 114) were randomly assigned to receive vitamin D3 supplements (n = 56; 1200 IU/d) or a placebo (n = 58) for 12 mo in a double-blind setting. Outcomes were clinical changes from baseline and the percentage of patients who showed no worsening of the modified Hoehn and Yahr (HY) stage and Unified Parkinson's Disease Rating Scale (UPDRS).

RESULTS:

Compared with the placebo, vitamin D3 significantly prevented the deterioration of the HY stage in patients [difference between groups: P = 0.005; mean ± SD change within vitamin D3 group: +0.02 ± 0.62 (P = 0.79); change within placebo group: +0.33 ± 0.70 (P = 0.0006)]. Interaction analyses showed that VDR FokI genotypes modified the effect of vitamin D3 on changes in the HY stage (P-interaction = 0.045), UPDRS total (P-interaction = 0.039), and UPDRS part II (P-interaction = 0.021). Compared with the placebo, vitamin D3 significantly prevented deterioration of the HY stage in patients with FokI TT [difference between groups: P = 0.009; change within vitamin D3 group: -0.38 ± 0.48 (P = 0.91); change within placebo group, +0.63 ± 0.77 (P = 0.009)] and FokI CT [difference between groups: P = 0.020; change within vitamin D3 group: ±0.00 ± 0.60 (P = 0.78); change within placebo group: +0.37 ± 0.74 (P = 0.014)] but not FokI CC. Similar trends were observed in UPDRS total and part II.

CONCLUSION:

Vitamin D3 supplementation may stabilize PD for a short period in patients with FokI TT or CT genotypes without triggering hypercalcemia, although this effect may be nonspecific for PD. This trial was registered at UMIN Clinical Trials Registry as UMIN000001841.

http://www.ncbi.nlm.nih.gov/pubmed/23485413

Vitamin D, Mitochondria, and Muscle

http://jcem.endojournals.org/content/98/3/961.long

W V Med J. 2013 Jan-Feb;109(1):22-5.

Antibiotic-like actions of vitamin D.

Shuler FD, Hendrix J, Hodroge S, Short A.


Source

Joan C. Edwards School of Medicine, Marshall University, Huntington, USA.


Abstract


Vitamin D is a secosteroid hormone that has expanding importance for a healthy lifestyle and disease prevention. A multitude of studies have highlighted that vitamin D acts not only in bone and calcium homeostasis but is critically important for human immunity. The discovery that the storage form of vitamin D (25-hydroxyvitamin D3) can be locally converted to the active form (1,25-hydroxyvitamin D3) in immune cells, epithelial cells and numerous other non-renal tissues highlights the importance of maintaining sufficient stores. When responding to a specific external stimulus, like bacterial invasion, intracrine synthesis of active vitamin D has the ability to regulate gene expression providing a specific response and directing cellular actions. These responses include the generation of antimicrobial peptides with production of these peptides dependent on vitamin D status. Vitamin D deficiency is associated with an increased rate of infection. This paper highlights the antibiotic like actions of vitamin D and importance of vitamin D sufficiency.

http://www.ncbi.nlm.nih.gov/pubmed/23413544

Am J Alzheimers Dis Other Demen. 2013 Mar;28(2):126-36. doi: 10.1177/1533317512473196. Epub 2013 Jan 15.

The role of vitamin D in Alzheimer's disease: possible genetic and cell signaling mechanisms.

Lu'o'ng KV, Nguyen LT.


Source

Vietnamese American Medical Research Foundation, 14971 Brookhurst St. Westminster, CA 92683, USA. Lng2687765~aol.com


Abstract


Alzheimer's disease (AD) is the most common form of dementia in the elderly individuals and is associated with progressive memory loss and cognitive dysfunction. A significant association between AD and low levels of vitamin D has been demonstrated. Furthermore, vitamin D supplements appear to have a beneficial clinical effect on AD by regulating micro-RNA, enhancing toll-like receptors, modulating vascular endothelial factor expression, modulating angiogenin, and advanced glycation end products. Vitamin D also exerts its effects on AD by regulating calcium-sensing receptor expression, enhancing amyloid-β peptides clearance, interleukin 10, downregulating matrix metalloproteinases, upregulating heme oxygenase 1, and suppressing the reduced form of nicotinamide adenine dinucleotide phosphate expression. In conclusion, vitamin D may play a beneficial role in AD. Calcitriol is the best vitamin D supplement for AD, because it is the active form of the vitamin D3 metabolite and modulates inflammatory cytokine expression. Therefore, further investigation of the role of calcitriol in AD is needed.

http://www.ncbi.nlm.nih.gov/pubmed/23322908

HI everyone. I'm sure this has been answered somewhere along the way in these years, but I'm hoping someone has it at the tip of their brains.
If Vitamin D is stored in fat, why do we need to take it every day? I've seen discussion about people taking it once a week, but do we really know how often we have to take it to avoid deficiency again?

Thanks!

Good question. I wonder about this too. Hope this thread is still active?