exposure had lower rates of IBD-related admissions. Another United States based study similarly concluded that the rate of IBD-related hospitalization was found to conform to this geo- graphical pattern, with significantly more admissions in northern compared to southern states. In another study, a greater propor- tion of individuals living at latitudes of 35° north or higher were diagnosed with celiac disease or elected to eat a gluten free diet compared to those residing in more southern latitudes. Similarly, studies not only demonstrate that lower vitamin
D levels correlate with worsened disease activity, relapse rates, and clinical severity in Crohn’s disease, multiple sclerosis (MS), psoriasis, systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA), but vitamin D sufficiency is associated with im- proved symptomatology and lower frequency of disease onset in autoimmune conditions such as IBD.
Vitamin D: A Master Immunoregulatory Hormone
Vitamin D is critical to immune cell homeostasis, prolifera- tion, apoptosis, and the process of self tolerance, or the failure to mount an immune response against self-antigens present on bodily constituents. It similarly exerts regulatory effects on both first line innate, or non-specific immune responses, as well as secondary adaptive immune responses that are deployed later on in an infectious scenario.
As previously noted, vitamin D levels have been demon-
causes any STRUCTURE to break down Pain
Numbness/Tingling Dizziness Arthritis Headaches
The body’s foundation is the head and
starts to break down.
Logical. Simple.
Effective.
Triad Upper Cervical Clinic 432A W. Mountain St.,
Kernersville
336.992.2536
www.TriadUpperCervical.com M. Chad McIntyre, D.C. offers Orientation Classes at his office twice per month
22
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upper cervical spine. When it shifts out of balance, the body
Ignoring the FOUNDATION
strated to be compromised in autoimmune disease, and circulat- ing levels of 25-hydroxy vitamin D3 are inversely related to autoimmune disease activity. This is due in part to the fact that vitamin D promotes expression of toleragenic FoxP3+ regula- tory T cells, a subset of immune cells which prevent dominance of either the Th1, Th2, or Th17 arms of the immune system, all of which can perpetuate autoimmunity. Moreover, vitamin D inhibits activation and differentiation
of pathogenic T cells, which are intimately involved in the etiol- ogy of autoimmunity. According to Finamor et al. (2013), “In- tracrine and paracrine action of 1,25(OH)2D3 synthesized within immune cells may control inappropriate activation of interleukin-17-producing cells—the Th17 aberrant response, which may play a major pathogenic role in multiple inflamma- tory and autoimmune disorders”. Pivotally, vitamin D serves as an essential component in maintenance of gut integrity, prevent- ing both the intestinal hyper-permeability or ‘leaky gut’ that precedes autoimmune disease and the dysbiotic changes in the gut microbiota that can also mediate gut barrier compromise and initiation of autoimmune mechanisms. Vitamin D supplementation results in significant reductions
in inflammatory mediators such as C-reactive protein, an inflam- matory acute phase reactant, and matrix metalloproteinases (MMPs), which are proteolytic enzymes that inflict damage by degrading the extracellular matrix. Vitamin D also down-regu- lates, or decreases, expression of pro-inflammatory cytokines— inflammatory cell signaling molecules such as IL-1, IL-17, and IFN-gamma. This hormone also inhibits nuclear factor kappa beta (NF- kB), a master transcription factor that leads to expression of downstream mediators of inflammation. Lastly, vitamin D supple- mentation leads to an increased production of anti-microbial peptides such as beta defensins and cathelicidin, which improve
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