Vitamin D Facts:
The National Health and Nutrition Examination Survey 2005 to 2006 data were analyzed for vitamin D levels in adult participants (N = 4495). Vitamin D deficiency was defined as a serum 25-hydroxyvitamin D concentrations ≤20 ng/mL (50 nmol/L). The overall prevalence rate of vitamin D deficiency was 41.6%, with the highest rate seen in blacks (82.1%), followed by Hispanics (69.2%).
[Further breakdown of deficiency shows the following demographic:
32% of doctors and med school students are vitamin D deficient.
40% of the U.S. population is vitamin D deficient.
42% of African American women of childbearing age are deficient in vitamin D.
48% of young girls (9-11 years old) are vitamin D deficient.
Up to 60% of all hospital patients are vitamin D deficient.
76% of pregnant mothers are severely vitamin D deficient, causing widespread vitamin D deficiencies in their unborn children, which predisposes them to Type 1 diabetes, arthritis, multiple sclerosis and schizophrenia later in life. Many vitamin D deficient persons are more likely to contract infections. And then have autoimmune disease shortly after, that in turn causes attack on Islets of Langerhans Beta cells that produce insulin due to similarity of markers on the beta cells and streptococcus, these cell membrane surface markers are called antigens. When those cells are killed off, the insulin production is diminished or entirely destroyed and lifelong insulin injections are required and creates potentially greatly reduced life expectancy.]
81% of the children born to these mothers were deficient as well.
Up to 80% of nursing home patients are vitamin D deficient.(4)
We see the huge amount of cases of Infection in those housed in nursing homes.
Given that vitamin D deficiency is linked to some of the important risk factors of leading causes of death in the United States, it is important that health professionals are aware of this connection and offer dietary and other intervention strategies to correct vitamin D deficiency, especially in minority groups.(1)
Vitamin D3 is a secosteroid hormone produced in the skin in amounts estimated up to 25,000 international units (IUs) a day by the action of UVB radiation on 7-dehydrocholesterol.(2)
Vitamin D deficiency is common due to both lack of adequate sun exposure to the skin, and because vitamin D is present in very few food sources.(2)
All patients in a hospital had been routinely screened on admission for vitamin D deficiency since July 2011, and offered supplementation to either correct or prevent deficiency. During this time, they admitted over 4700 patients, the vast majority of whom agreed to supplementation with either 5000 or 10,000 IUs/day. Due to disease concerns, a few agreed to larger amounts, ranging from 20,000 to 50,000 IUs/day. There were no cases of vitamin D3 induced hypercalcemia or any adverse events attributable to vitamin D3 supplementation in any patient. Three patients with psoriasis showed marked clinical improvement in their skin using 20,000 to 50,000 IU’s/day.(2)
In another study that took place in a Graz, Austrian Hospital, a randomized, double-blind, placebo-controlled pilot study in a medical ICU at a tertiary care university center was conducted. Twenty-five patients (mean age 62 ± 16 yrs) with vitamin D deficiency [25-hydroxyvitamin D (25(OH)D) ≤ 20 ng/ml] and an expected stay in the ICU >48 hours were included and randomly received either 540,000 IU (corresponding to 13.5 mg) of cholecalciferol (VIT-D) dissolved in 45 ml herbal oil or matched placebo (PBO) orally or via feeding tube.
Results: The mean serum 25(OH)D increase in the intervention group was 25 ng/ml (range 1-47 ng/ml). The highest 25(OH)D level reached was 64 ng/ml, while two patients showed a small (7 ng/ml) or no response (1 ng/ml). Hypercalcemia or hypercalciuria did not occur in any patient. From day 0 to day 7, total serum calcium levels increased by 0.10 (PBO) and 0.15 mmol/L (VIT-D; P < 0.05 for both), while ionized calcium levels increased by 0.11 (PBO) and 0.05 mmol/L (VIT-D; P < 0.05 for both). Parathyroid hormone levels decreased by 19 and 28 pg/ml (PBO and VIT-D, ns) over the seven days, while 1,25(OH)D showed a transient significant increase in the VIT-D group only.(3) These results show positive shifts in metabolic processes and physiology.
The pilot study shows that a single oral ultra-high dose of cholecalciferol corrects vitamin D deficiency within 2 days in most patients without causing adverse effects like hypercalcemia or hypercalciuria.(3)
Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increasing concentrations of anti-inflammatory cytokines.(5)
that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d.(5)
Dr Zahid Naeem, MBBS, MCPS, DPH, FCPS, Professor has described the Vitamin D Deficiency as An Ignored Epidemic.
His study states:
Vitamin D3 deficiency can result in obesity, diabetes, hypertension, depression, fibromyalgia, chronic fatigue syndrome, osteoporosis and neuro-degenerative diseases including Alzheimer’s disease. Vitamin D deficiency may even contribute to the development of cancers, especially breast, prostate, and colon cancers. Current research indicates vitamin D deficiency plays a role in causing seventeen varieties of different cancers as well as heart disease, stroke, autoimmune diseases, birth defects, and periodontal disease.
Vitamin D3 is believed to play a role in controlling the immune system (possibly reducing one’s risk of cancers and autoimmune diseases), increasing neuromuscular function and improving mood, protecting the brain against toxic chemicals, and potentially reducing pain.(6)
Although it’s recommended, To prevent vitamin D deficiency, one should spend 15 to 20 minutes daily in the sunshine with 40% of the skin surface exposed.(6)
Who do we know that gets 40% skin exposure let alone 40% skin exposure to sunlight? Especially during the fall and winter!
When folks say they did, did they take these additional factors into account:
High concentration of melanin in the skin slows the production of vitamin D; similarly aging greatly reduces skin production of vitamin D. Use of sunblock, common window glass in homes or cars and clothing, all effectively block UVB radiation – even in the summer.(6)
VITAMIN D FOR TREATMENT AND PREVENTION Of INFECTIOUS DISEASES: A SYSTEMATIC REVIEW OF RANDOMIZED CONTROLLED TRIALS was Published in final edited form as: Endocr Pract. 2009 Jul–Aug; 15(5): 438–449.
Studies from 1948 through 2009 have been conducted to determine vitamin D in the treatment and prevention of infectious disease.
Due to its immunomodulating effects and importantly, strongest evidence supports further research into adjunctive vitamin D therapy for tuberculosis, influenza, and viral upper respiratory tract illnesses.
That was from 2009! The results have trickled in, sometimes in waves.
It’s clear now that, even the average untrained person can see: the seasonal influenza is strictly periodic based vitamin D levels! Summertime sunlight boosts daily Vitamin D levels, thus reducing and nearly eliminating influenza virus of all types. Fall and wintertime reductions in sunlight absorption creates a decrease in seasonal Vitamin D levels to acute and subacute deficiency and this causes an increase in influenza, and more severe illness.
These studies combined create the argument, significantly, that we must boost vitamin D3 levels, to greatly reduce the pandemic D3 deficiency with the supplementation of significant D3, initially 10,000iu’s or higher initially for the short term, and then consistently at 5000iu permanently.
An overall study reveals As the vitamin D receptor is expressed on immune cells (B cells, T cells and antigen presenting cells) and these immunologic cells are all are capable of synthesizing the active vitamin D metabolite, vitamin D has the capability of acting in an autocrine manner in a local immunologic milieu. Vitamin D can modulate the innate and adaptive immune responses.
Deficiency in vitamin D is associated with increased autoimmunity as well as an increased susceptibility to infection. As immune cells in autoimmune diseases are responsive to the ameliorative effects of vitamin D, the beneficial effects of supplementing vitamin D deficient individuals with autoimmune disease may extend beyond the effects on bone and calcium homeostasis.
The immune system defends the body from foreign, invading organisms, promoting protective immunity while maintaining tolerance to self. The implications of vitamin D deficiency on the immune system have become clearer in recent years and in the context of vitamin D deficiency, there appears to be an increased susceptibility to infection and a diathesis, in a genetically susceptible host to autoimmunity.
As vitamin D is cutaneously produced after exposure to UV B light, its synthesis is influenced by latitude, season, use of sunblock and skin pigmentation.
Melanin absorbs UVB radiation inhibiting the synthesis of vitamin D from 7-dihydrocholesterol. This promotes deficiency in those darker pigment.
The Liver and Kidneys and their proper function is essential to the production, sequentially, to the active form of vitamin D. This reflects the elegant beauty of the nature of physiology.
The initial vitamin D compound 7-dihydrocholesterol is inactive and it is next hydroxylated in the liver to form 25 OH vitamin D3 (25 D). 25 D is also an inactive compound, but is the most reliable measurement of an individual’s vitamin D status. It is converted in the kidney to the active compound 1,25 dihydroxy vitamin D (1,25 D) or calcidiol by 1-α-hydroxylase (CYP27B1), an enzyme which is stimulated by PTH . 1,25 D may be further metabolized to the inactive 1,24,25 vitamin D by 24-hydroxylase (CYP24). 1,25 D levels are tightly regulated in a negative feedback loop. 1,25 D both inhibits renal 1-α-hydroxylase and stimulates the 24-hydroxylase enzymes, thus maintaining circulating levels within limited boundaries and preventing excessive vitamin D activity/signaling.
There are specific vitamin D receptors that are activated by Vitamin D, these occur in various cells across the spectrum, Many tissues other than the skeletal and intestine express the VDR including cells in the bone marrow, brain, colon, breast and malignant cells and immune cells suggesting that vitamin D may have functions other than calcium and bone homeostasis.
Some of the more recently recognized non-classical actions of vitamin D include effects upon cell proliferation and differentiation as well immunologic effects resulting in an ability to maintain tolerance and to promote protective immunity. As antigen presenting cells (macrophages and dendritic cells), T cells and B cells have the necessary machinery to synthesize and respond to 1,25 D, vitamin D may act in a paracrine or autocrine manner in an immune environment. This information is reported in this over arching report over 8 years ago, yet the research compiled was reports in some cases years older, as this is prospective research study.
Liu PT, et al. Studied as far back and reported that there were Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. These reports occurred as far back as 2005 and 2006.
Science. 2006;311(5768):1770–3. [PubMed]
One recent well-designed prospective, double blind placebo study using an objective outcome, nasopharyngeal swab culture (and not self report), and a therapeutic dose of vitamin D showed that vitamin D administration resulted in a statistically significant (42%) decrease in the incidence of influenza infection.
toll like receptors (TLR). Vitamin D Engagement of TLRs leads to a cascade of events that produce peptides with potent bacterialcidal activity such as cathelocidin and beta defensin 4. These peptides colocalize within phagosomes with injested bacteria where they disrupt bacterial cell membranes (lysis) and have potent anti-microbacterial activity .
Vitamin D inhibits the production of inflammatory cytokines (IL-1, TNFα) by monocyes. Cytokine production by monocytes from both normal controls and from patients with autoimmune diabetes (type 1 or latent autoimmune diabetics) is significantly diminished by vitamin D.
With research that was developed in the early 1970’s There was evidence as far back as the late 1990’s and more so in the early 2000’s that vitamin D deficiency may confer increased risk of influenza and respiratory tract infection. Vitamin D deficiency is also prevalent among patients with HIV infection. Cell culture experiments support the thesis that vitamin D has direct anti-viral effects particularly against enveloped viruses. Though vitamin D’s anti-viral mechanism has not been fully established, it may be linked to vitamin D’s ability to up-regulate the anti-microbial peptides LL-37 and human beta defensin 2. It is learned that the same anti microbial effects create antiviral beneficial effects as well. This study states Additional studies are necessary to fully elucidate the efficacy and mechanism of vitamin D as an anti-viral agent.
As far back as 2011 research results support the hypothesis that vitamin D induced LL-37, and to a lesser extent human beta defensin 2, may play a major role in the inhibition of viruses.
Patients with levels of vitamin D3 of less than 10 ng/ml had a 55% risk of infection when compared to controls.