(Self-Meta) Vitamin D ~ For and Against (Part 3 of 4)

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**Draft WIP / Work in progress Part 3 of 4**
**Undergoing writing & readibility amends December 2023**

In this third section reserves a separate discussion Auto Immunity condition specific to This Author’s (AW) concern (Ankylosing Spondlyitis).




Vitamin D and Calcium intake relations to Ankylosing Spondylitis and autoimmunity.

Preface & Context

The first beginning preface here begins as a brief summary of This Author’s (AW) context and condition; mainly surrounding his partial diagnosis of a possible autoimmune  condition known as Ankylosing Spondylitis.

Ankylosing Spondylitis” or AS for short ¬ is recognised as an “rheumatoid” and/or “osteoarthritis” related group of skeletal and physiological declines resembling disc degeneration disorders. There appears to be a growing call  for concern that such condition may yet indeed be relative to that as autoimmune related (Arabi S et al. 2019).

Typical symptoms manifest as high levels of pain on lower regions of the lumbar spine, particularly upon rising during mornings but does not resolve for many hours until at least some fitness or exercise routines is surpassed. Ankylosing Spondylitis first and foremost is characterised by unexpected bone growth in areas or in extents where such growth causes bone infusion; thereby inciting risk of nerve impingement. This is accompanied by markedly high C-RP readings or C-reactive proteins, although not all patients affected exhibit this.

Affecting mostly male adults, AS is often diagnosed firstly as serum presence of “HLA-B27″ ~ a white blood cell antigen specifically grouped under “Human Leukocite Antigens”. However, reliance on this genetic testing alone remains  widely contested as both severity and final diagnosis of AS appears to be defenite only within 10% of all who tested positive. This Author (AW)’s own initial diagnosis in 2014 indeed confirmed positive for HLA-B27, despite reassurance that this only implied a 10% certainty for defenite illness.

“The association of HLA-B27 with AS is well established and occurs in 85–90% of patients. HLA-B27 is seen in 5–15% of the general population, with some variability associated with ethnic background, but only 5% of HLA-B27 positive people develop AS. As such, HLA-B27 in the patient with clinical features of SpA can support the diagnosis but has no role as a general screening test for spinal pain.” ~ RACGP.org.au

However,  the many years that followed after initial diagnosis manifest an intermittent though thankfully infrequent inflammation flare(s) along the lumbar disc region L4/5/s1. The immobility and pain experience(s) throughout each of episodic flare strongly resemble the above typical diagnosis for AS.

Whilst symptomatically manageable, it is the degree of unknown(s) for recurrences that are yet to be reconciled or understood; as is typical of many autoimmunity conditions. Thus the very rationale behind why this section was written and prepared for readers whom are affected and thereby keenly interested at pursuing further research on the possible etiology.

General view of Vitamin D & Auto Immunity

Vitamin D and Calcium has been raised noteworthy by many literatures to date (De Martinis M. 2021) & (Athanassiou IK et al 2019) for auto immune related conditions. The following cliff notes represents a summary of insights based on research reviews and meta-analysis gathered. As follows:

  • (Diao M et al 2022)  ~ According to this meta-analysis there appears to be no significant correlation between active 1,25 OHD with severity of AS compared to healtthy controls. But suggests nonetheless that the inactive / plasma 25OHD correlates with a protective effect. This is despite  AS patients seem to have lower 1,25 OHD readings; but they too are usually accompanied with higher C-reactive Protein and Erythrocyte Sedimentation Rate.
  • (Guoqi C. et al. 2014) ~ There appears to be protective effect of plasma reading of Vitamin D 25OHD against severity of AS.
  • [Talotta R et al. 2020) ~ there appears to be mechanistic appraisal of Vitamin D and Calcium on subjects with AS.

The above are only cliff summary findings and certainly does not and should not substitute full top-to-bottom obligatory reading. 

In addition to the above there appears to be very few suggestive objective recommendation or hypothetical dosage protocol of 25OHD or any Vitamin D substrate is deemed beneficial. Except one (1) research (Charoenngam N, 2021) suggests a plasma reading up to 150 NMOL ~ appears to be the limit of what is deemed “maximal” benefit; as quoted from the abstract:

“Although the optimal level of serum 25(OH)D is still debatable, it is advisable it is advisable that patients with rheumatic diseases should maintain a serum 25(OH)D level of at least 30 ng/mL (75 nmol/L) to prevent osteomalacia, secondary osteoporosis, and fracture, and possibly 40-60 ng/mL (100-150 nmol/L) to achieve maximal benefit from vitamin D for immune health and overall health.” ~ Charoenngam N. 2021.

This Author’s own experience (Vitamin D depletion & repletion)

In May 2020, upon a much delayed blood panel test This Author (AW) witnessed a markedly high 25(OHD) readings at 179 nmol/L ~ despite normal readings in both Calcium (corrected), PTH, and C-reactive protein markers. However for a three week period ~ he decided to trial abstaining all Vitamin D supplementation and interestingly noted a markedly reduced QOL / surrogate quality of life markers ~ from digestion, overall psychology, outlook and resilience. From what was 179 NMOL came down to 132 NMOL in a matter of three weeks.

Upon restoring maintainance Vitamin D supplementation of at averaging 5K IU daily (during summers / warmer seasons) to 15K IU intermittently during winters ~ brought him back the homeostatic “defaults” of overall surrogate QOL markers.

Calcium intakes and AS severity.

As brief preface ~ Calcium, next to Phosphate remains in general consensus essential  for bone integrity, strength, density, muscle contraction, nerve transmission / conduction, enzymatic reactions including that of insulin release, and homeostatic cell proliferation, division and programmed apoptosis. So far there are three types of calcium bound within human physiology (note: not exogenous / supplemental form) has been identified (teachmephysiology.com) at least within the serum level ~ 

  • Free-ionised 
  • Anion-bound
  • Protein-bound

Two (2) factor(s) taught to be essential behind these tight regulation is Vitamin D and PTH (Parathyroid hormone). 

Dietary calcium associations or correlation research to AS or rhteumatoid / arthritic groups of autoimmunity remains interestingly mixed given the diverse essence of calcium to both enzyematic and endocrinological roles beyond than bone mineralisation. There nonetheless appears to be a few, though limited evidences ~ at questioning whether high calcium, be it dietary or supplemental may warrant caution for those with AS.

“In this systematic review, we have determined, from a relatively small number of studies, that the evidence on the relationship between diet and AS is extremely limited and we have highlighted important methodological weaknesses in the studies reviewed.” Macfarlanne, TV et al. 2017
“Calcium supplements may be disadvantageous for entheseal calcifications, but so far there are no clear data confirming that such an association exists.” ~ Talotta, R. 2020

What can we learn from here?

In light of the above view, it remains strongly suggestive that BOTH decline of Vitamin D or Calcium input status ~ seems very likely detrimental.

At best, on a general widespread view there seems to be more or less concur towards a favourable stance to Vitamin D supplementation.  Upon which examining these further suggests there are healthful markers which may warrant contemplative further research:

  • First and foremost ~ is the need to maintain the key inflammatory CRP or C reactive protein.
  • Next, whilst there appear to be equivocal / mixed stances when it comes to parathyroid hormone PTH to severity of AS ~ it nevertheless appear to be pragmatic to manage this at a lower rate as PTH is generally associated an inflammatory contributing risk to various mortality.


This concludes the third of the fourth ongoing work in progress of this Self Meta. Please meanwhile proceed into reading the public open/transparent draft on the fourth and final part where This Author (AW) shall disclose overall pragmatism and N=1 course of actions.

<personal message> May I hope you find the above and this entire concept initative ~ both lateral and broad in its branching interest. Please forward any comments and or thoughts surrounding this work in progress, not for profit, and entirely self-initiated academia interest to demonstrate scientific self-enquiring. Thank you. Live-it-forward, AW. 

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