Vitamin D and the human immune system generally; Part 2 of a series
Vitamin D is essential to human immune function and for adequate production of many of the body’s hormones. So it is a vitamin, by definition, because we need it in order to survive.
Vitamin D’s role against pathogenic microbes has been known for a century. [1]
Vitamin D is capable of entering not only the cell but the nucleus as well, and can affect transcriptional change, including to the point of interfering with viral replication. Viruses sicken us when their numbers multiply to such an extent that wellbeing and homeostasis are disrupted and temporarily overwhelmed. Vitamin D helps prevent this. It is known to interfere with transcription of RNA, which keeps the viral load smaller.
Vitamin D deficiency is common in autoimmune patients. [2] Vitamin D has an essential role in immune regulation, [3] and has been preventive to helpful to even curative in some of the most common and serious auto-immune diseases, such as inflammatory bowel disease (IBD) [4] and even Type 1 diabetes, [5] and rheumatoid arthritis, were 100% of studied RA-induced mice were cured after administration of vitamin D. [6] Immune dysregulation and chronic inflammation are characteristic of the above conditions, and Vitamin D seems to re-regulate the immune system and suppress inflammation, by decreasing NF kappa B, [7] [8] [9] [10] which in turn decreases pro-inflammatory cytokines. [11] Vitamin D was also shown to improve immune tolerance of transplanted organs. [12] Vitamin D cured a polio condition in 100% of laboratory mice. In laboratory mice infected with a polio condition, autoimmune encephalomyelitis (AE), 100% showed evidence of AE, which is one of the many synonyms of polio, as the polio virus has not yet been isolated. The researchers mentioned the AE connection with multiple sclerosis, another disease of vitamin D deficiency. [13] [14] In their study, after supplementing 1,25-dihydroxy D3, zero percent of those mice showed AE at 6 days post inoculation, although all had been determined to have the condition earlier in the study. [15]
Vitamin D deficiency (and severe D deficiency such as in rickets) has long been correlated with increased respiratory tract infections, [16] [17] including in this 15-year observational study. [18] In the Martineau-Joliffe study, vitamin D blood levels had statistically significant inverse correlation with mortality from respiratory tract diseases. Darker skin color [19] and advanced age [20] have both been shown to inhibit vitamin D production in the skin. Obesity is inversely correlated with vitamin D levels, because too little of bodily reservoir of vitamin D is available outside adipose tissue. [21] So certain populations are more prone to vitamin D deficiency, and need adequate sun exposure and / or supplementation, particularly in winter.
1, 25 (OH)2 cholecalciferol is the active form of vitamin D. Eggs, fish and meat are dietary sources, and high fructose corn syrup is an anti-source in the sense of interfering with active vitamin D. Sunlight is the optimal and universally available source for us to produce Vitamin D. This is likely a key and underappreciated aspect of why respiratory viruses have such strong seasonality, and are problematic for humans primarily in the winter and early spring, after the year’s fewest hours and lowest angle of sunlight at the winter solstice in each hemisphere respectively. This event corresponds with the time of least endogenous vitamin D production. Humans spend an average of 7 to 8% of our time outdoors. [22] However, for those living north of the 35th parallel in the northern hemisphere, or south of the 35th parallel in the southern hemisphere, our winters expose us to only low angled, indirect rays of sunlight, and residents of those regions are generally not able to acquire enough sunlight to rely on sun exposure alone for adequate production of vitamin D. That is, to have enough vitamin D in those regions of the earth in their respective winters, vitamin D must be supplemented or obtained through diet. Sunlight exposure is further limited by staying inside during harsh weather, and dressing to minimize exposed skin while venturing outdoors. Further, since mid-2020, mask-wearing is popular, which further reduces the little available skin to sun exposure and vitamin D production. This may contribute to the finding that masked populations have been found to have higher rates of COVID than unmasked populations. [23] Vitamin D vs COVID is explored later in this series of articles, now that much research has been done during 2020 and is available on this topic.
Sanatoriums were the treatment of choice in pandemic tuberculosis treatment. Regular sunlight exposure was a daily component of the treatment there. Vitamin D was gradually reasoned and understood to be essential to conquering the pathogenesis of tuberculosis in these settings. What is now better understood about this effect is as follows: The presence of the Mycobacterium tuberculosis upregulates a key enzyme, CYP27B1 and the vitamin D receptors in macrophages. This has been found to lead to downstream production of the peptide cathelicidin, which is anti-microbial toward the Tuberculosis bacterium, [24] as well as Influenza A, [25] and other bacteria and viruses. [26] However, the association was not observed to hold for Hepatitis B or C, even though all of those patients had lower vitamin D levels than controls. [27] Cathelicidin is able to kill pathogenic viruses and bacteria directly, and it is able to bind to endotoxin, by forming ion channels and increasing membrane permeability. [28] Vitamin D has been established to be key to this process. [29] [30] [31] [32]
Vitamin D and the innate immune system
Vitamin D is active in the innate immune system, [33] Vitamin D interacts with the immune system as it connects with receptors on white blood cells. If the location and function of adaptive immunity can be considered primarily systemic, the location and function of the innate immune system is local everywhere throughout the body. The innate immune system is the first to encounter infection. 1,25 (OH) vitamin D hydroxylase has been found in dendritic cells and macrophages, which are present at the site of first inflammation. [34] In its active form, 1,25 di-hydroxy-vitamin D3, or calcitriol, has receptors in every tissue in the body where it was searched.
In the innate immune system, vitamin D is essential to the maturing of macrophages. Vitamin D was found to cause precursor cells, promyelocytes to differentiate into monocytes. [35] [36] These are precursor cells to macrophages. Activated macrophages influenced by vitamin D produce hydrogen peroxide, which is an important pro-oxidant molecular weapon against pathogenic microbes, including viruses. [37]
Vitamin D receptors have been found throughout the innate immune system in these cellular components: monocytes and macrophages, dendritic cells [38] as well as in the adaptive immune system, in T cells and B cells. [39] The cells in the innate immune system, epithelial cells in the respiratory tract, as well as monocytes, macrophages and dendritic cells were also found to have the enzyme CYP27B1, which is required to convert inactive vitamin D to the active form, 1,25-OH-vitamin D. [40] [41] Vitamin D stimulates a variety of anti-microbial peptides that appear in natural killer cells and neutrophils in respiratory tract epithelial cells, where they have a protective role in lung tissues against the ravages of infection and inflammation.
Inflammatory cytokines are a double-edged sword for the severely ill. While acting as overwhelming forces against pathogenic invasion, the results of cytokine storm can be so overwhelming for the frail patient that they become the immediate cause of death. In these situations also, vitamin D plays a necessary role in prevention of excessive inflammatory cytokines.
The next article in this series will address the adaptive immune system, T cells and B cells, and vitamin D’s versatility and immune-enhancing function in that system, and will delve deeper into how vitamin D defeats viral infections.
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[13] L McLaughlin, L Clarke, et al. Vitamin D for the treatment of multiple sclerosis: a meta-analysis. Neurol. Dec 2018. 265 (12). 2893-2905. https://pubmed.ncbi.nlm.nih.gov/30284038/
[14] J Matías-Guíu, C Oreja-Guevara, et al. Vitamin D and remyelination in multiple sclerosis. Neurología. Apr 2018. 33 (3). 177-186. https://pubmed.ncbi.nlm.nih.gov/27321170/
[15] M Cantorna, C Hayes, et al. 1,25-dihydroxyvitamin D3 reversibly blocks the progression of relapsing encephalomyelitis, a model of multiple sclerosis. Pro Natl Acad Sci. Jul 23 1996. 93 (15). 7861-4 https://pubmed.ncbi.nlm.nih.gov/8755567/
[16] A Martineau, D Joliffe, et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. Feb 15 2017. 356:i6583. https://pubmed.ncbi.nlm.nih.gov/28202713/
[17] S Esposito, M Lelii. Vitamin D and respiratory tract infections in childhood. BMC Infect Dis. 2015. 15:487. https://bmcinfectdis.biomedcentral.com/track/pdf/10.1186/s12879-015-1196-1.pdf
[18] H Brenner, B Holleczek, et al. Vitamin D insufficiency and deficiency and mortality from respiratory diseases in a cohort of older adults: potential for limiting the death toll during and beyond the COVID-19 pandemic? Nutrients. Aug 18 2020. 12 (8): 2488. https://pubmed.ncbi.nlm.nih.gov/32824839/
[19] O Gutiérrez, W Farwell, et al. Racial differences in the relationship between vitamin D, bone mineral density, and parathyroid hormone in the National Health and Nutrition Examination Survey. Osteop Intl. 2011. 22. 1745-1753.
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[20] J MacLaughlin, MF Holick. Aging decreases the capacity of human skin to produce vitamin D3. J Clin Invest. Oct 1985. 76 (4): 1536-8. https://pubmed.ncbi.nlm.nih.gov/2997282/
[21] J Wortsman, L Matsuoka, et al. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 72 (3). Sep 2000. 690-693. https://academic.oup.com/ajcn/article/72/3/690/4729361
[22] N Klepeis, W Nelson, et al. The National Human Activity Pattern Survey (NHAPS): a resource for assessing exposure to environmental pollutants. J Expo Anal Environ Epidemiol. May-Jun 2001. 11 (3): 231-252. https://pubmed.ncbi.nlm.nih.gov/11477521/
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[24] P Liu, S Stenger, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. Feb 22 2006. 311 (5768). 1770-1773. https://europepmc.org/article/MED/16497887
[25] P Barlow, P Svoboda, et al. Antiviral activity and increased host defense against influenza infection elicited by the human cathelicidin LL-37. PLoS One. Oct 20 2011. https://europepmc.org/article/PMC/3198734
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[27] S Iacob, E Panaitescu, et al. The human cathelicidin LL37 peptide has high plasma levels in B and C hepatitis related to viral activity but not to 25-hydroxyvitamin D plasma level. Rom J Intern Med. Jun 30 2012. 50 (3). 217-223. https://europepmc.org/article/MED/23330289
[28] B Ramanathan, E Davis, et al. Cathelicidins: microbicidal activity, mechanisms of action, and roles in innate immunity. Microbes Infect. 2002. 4 (3). 361-372. . https://europepmc.org/article/MED/11909747
[29] J White. Vitamin D as inducer of cathelicidin antimicrobial peptide expression: past, present and future. J Steroid Biochem Mol Biol. 2010. 121 (1-2). 234 – 238. Mar 16 2010. 121 (1-2). 234 – 238. https://europepmc.org/article/MED/20302931
[30] S Yim, P Dhawan, et al. Conduction of cathelicidin in normal and CF brochial epithelial cells by 1,25-dihydroxyvitamin D3. Cyst Fibros. Apr 26 2007. 6 (6). 403-410. https://europepmc.org/article/PMC/2099696
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[34] R Chun, P Liu, et al. Impact of vitamin D on immune function: lessons learned from genome-wide analysis. Front. Physiol. Apr 21 2014. 5 (151). https://pubmed.ncbi.nlm.nih.gov/24795646/
[35] E Abe, C Miyaura, et al. Differentiation of mouse myeloid leukemia cells induced by a 1alpha,25-dihydroxybitamin D3. Proc Natl Acad Sci. Aug 1981. 4990-4994. https://pubmed.ncbi.nlm.nih.gov/6946446/
[36] H Tanaka, E Abe, et al. 1alpha, 25 di-hydroxycholecalciferol and a human myeloid leukaemia cell line (HL-60). The presence of a cytosol receptor and induction of differentiation. Biochem J. Jun 1982. 204 (3). 713-719. https://pubmed.ncbi.nlm.nih.gov/6289803/
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Polio
Ah! Your heart just started racing. You heard that taboo word... and now you are suddenly very afraid!😱 But why?
It seems you've bought into the propaganda spewed by the government and mainstream media hook, line, and sinker. Unfortunately, it's all bullshit.
Since you mentioned polio first, let's take a look at history and polio!
1824: Metal workers had suffered for centuries from a paralysis similar to polio caused by the lead and arsenic in the metals they were working with. English scientist John Cooke observed: 'The fumes from these metals, or the receptance of them in solution into the stomach, often causes paralysis.'
1890: Lead arsenate pesticide started to be sprayed in the US up to 12 times every summer to kill codling moth on apple crops.
1892: Polio outbreaks began to occur in Vermont, an apple growing region. In his report the Government Inspector Dr. Charles Caverly noted that parents reported that some children fell ill after eating fruit. He stated that 'infantile paralysis usually occurred in families with more than one child, and as no efforts were made at isolation it was very certain it was non-contagious' (with only one child in the family having been struck).
1907: Calcium arsenate comes into use primarily on cotton crops.
1908: In a Massachusetts town with three cotton mills and apple orchards, 69 children suddenly fell ill with infantile paralysis.
1909: The UK bans apple imports from the States because of heavy lead arsenate residues.
1921: Franklin D. Roosevelt develops polio after swimming in Bay of Fundy, New Brunswick. Toxicity of water may have been due to pollution run-off.
1943: DDT is introduced, a neurotoxic pesticide. Over the next several years it comes into widespread use in American households. For example, wall paper impregnated with DDT was placed in children's bedrooms.
1943: A polio epidemic in the UK town of Broadstairs, Kent is linked to a local dairy where cows were washed down with DDT.
1944: Albert Sabin reports that a major cause of sickness and death of American troops based in the Philippines was poliomyelitis. US military camps there were sprayed daily with DDT to kill mosquitoes. Neighboring Philippine settlements were not affected.
1944: NIH reports that DDT damages the same anterior horn cells that are damaged in infantile paralysis.
1946: Gebhaedt shows polio seasonality correlates with fruit harvest.
1949: Endocrinologist Dr Morton Biskind, a practitioner and medical researcher, found that DDT causes 'lesions in the spinal cord similar to human polio.'
1950: US Public Health Industrial Hygiene Medical Director, J.G. Townsend, notes the similarity between parathion poisoning and polio and believes that some polio might be caused by eating fruits or vegetables with parathion residues.
1951: Dr. Biskind treats his polio patients as poisoning victims, removing toxins from food and environment, especially DDT contaminated milk and butter. Dr. Biskind writes: 'Although young animals are more susceptible to the effects of DDT than adults, so far as the available literature is concerned, it does not appear that the effects of such concentrations on infants and children have even been considered.'
1949-1951: Other doctors report they are having success treating polio with anti toxins used to treat poisoning, dimercaprol and ascorbic acid. Example: Dr. F. R. Klenner reported: 'In the poliomyelitis epidemic in North Carolina in 1948 60 cases of this disease came under our care... The treatment was massive doses of vitamin C every two to four hours. Children up to four years received vitamin C injection intramuscularly... All patients were clinically well after 72 hours.'
1950: Dr. Biskind presents evidence to the US Congress that pesticides were the major cause of polio epidemics. He is joined by Dr. Ralph Scobey who reported he found clear evidence of poisoning when analyzing chemical traces in the blood of polio victims.
Comment: This was a no no. The viral causation theory was not something to be questioned. The careers of prominent virologists and health authorities were threatened. Biskind and Scobey's ideas were subjected to ridicule.
1953: Clothes are moth-proofed by washing them in EQ-53, a formula containing DDT.
1953: Dr. Biskind writes: 'It was known by 1945 that DDT was stored in the body fat of mammals and appears in their milk... yet far from admitting a causal relationship between DDT and polio that is so obvious, which in any other field of biology would be instantly accepted, virtually the entire apparatus of communication, lay and scientific alike, has been devoted to denying, concealing, suppressing, distorting and attempts to convert into its opposite this overwhelming evidence. Libel, slander, and economic boycott have not been overlooked in this campaign.'
1954: Legislation recognizing the dangers of persistent pesticides is enacted, and a phase out of DDT in the US accelerates along with a shift of sales of DDT to third world countries.
(Note that DDT is phased out at the same time as widespread polio vaccinations begin. Saying that, polio cases sky rocket only in communities that accept the polio vaccine, as the polio vaccine is laced with heavy metals and other toxins, so the paralysis narrative starts all over again. As the polio vaccines cause huge spikes in polio, the misinformed public demand more polio vaccine and the cycle spirals skyward exponentially)
1956: the American Medical Association mandated that all licensed medical doctors could no longer classify polio as polio. All polio diagnosis would be rejected in favor of Guillian-Barre Syndrome, AFP (acute flaccid paralysis), Bell's Palsy, Cerebral Palsy, ALS, (Lou-Gehrig's Disease), MS, MD etc etc. This sleight of hand was fabricated with the sole intent of giving the public the impression that the polio vaccine was successful at decreasing polio or eradicating polio. The public bought this hook, line and sinker and to this very day, many pro vaccine arguments are ignited by the manufactured lie regarding the polio vaccine eradicating polio.
1962: Rachel Carson's Silent Spring is published.
1968: DDT registration cancelled for the US.
2008: Acute Flaccid Paralysis (AFP) is still a raging in many parts of the world where pesticide use is high, and DDT is still used. AFP. MS, MD, Bell's Palsy, cerebral palsy, ALS (Lou Gehrig's Disease), Guillian-Barre are all catch basket diagnosis, all similar in symtpoms, tied to heavy metal poisoning and high toxic load.
2008: WHO states on its website: 'There is no cure for polio. Its effects are irreversible.'
Conclusion: Modern belief that polio is caused by a virus is an ongoing tragedy for the children of the world. Public funds are wasted on useless and dangerous vaccines when the children could be treated with antitoxins. A call into failing vaccine mythology is warranted, as is a complete investigation of the real agenda being executed against humanity involving science, chemicals, vaccines, the medical field in general, and the government.
Outstanding review! Thank you.