Should Vitamin A be avoided? (A Self-Meta draft Part 2)

From the previous part we covered:

  • Introduction, rationale and context behind this Self-Meta
  • Brief history, metabolism, and toxicology of Vitamin A
  • Highlights and summaries of the (2) opposition views against Vitamin A as an essentiality.

In this part two:

  • Conflicting sentiments (as further Questions)
  • How this concern relates to Ankylosing Spondylitis

For the next part (3) I will get to cover

  • Other confounding factors
  • Conclusion

Once again, this is Live Draft preview, that which I am willing to share all writing as WIP (work-in-progresses). Non-sequitors, mispellings and the like are all laid on the table.

Live-It-Forward,

AW.


Part 2

How does this relate to my condition (Ankylosing Spondylitis / “AS”)

For context, Ankylosing Spondylitis (literally meaning ~ “Fusion” [Ankylosing], “Spine” [Spondy] and Inflammation “litis”) affects overall mobility amongst individuals with a confirmed HLA-B27 genetic expression. In granular explanation, it is an autoimmune condition upon which

In my case, I have been diagnosed, although not a 100% guarantee as there is still some ambiguity surrounding HLA-B27, with pathophysiological symptoms of AS. We’re not talking about mere effects of aging. But believed to be an auto-immune response affecting overall disc health. Particularly susceptibility  to injury along lower / lumbar spine regions L4/5/S1. These can also be exacerbated with heavy compound exercises ~ particularly the annulus disc tearing event(s) that usually follows from such training movements, especially under repetitive.  

This is not just affecting the spine. Uveitis / eye inflammation, gut health malaise, and psoriasis have all been documented to have close implications to those with AS. 

It also beckons as one of the most less-respected illnesses, at least in well-developed nations. Due to their lack of symptomatic visibility and the stigma surrounding their difficult diagnosis – social support circles remains to this day far and few.

So far, I had a decade worth of N=1 self interventions surrounding nutrition, that from SKD, CKD to now CKD+IF ~ I am very happy thus far to have managed this. While accepting that 100% cure is not going to be a reality and that the unpredictability of another flare episodes still remains as just that – unpredictable.

Following from my last (major and big) Self Meta on Vitamin D ~ convinced me with the research collected thus far (see here, here, here and here) ~ suggesting that Vitamin D with Calcium, despite mixed concerns on auto-immunity ~ seems to be more protective. I concluded there is a need nevertheless to cycle everything inbetween none, low and high intakes on not just Vitamin D, but their synergists ~ including but not limited to Magnesium, and Vitamin K2. Besides I have never once experienced any “major” depressive or adverse health outcomes from megadosing Vitamin D, up to 10k IU during winter seasons counting to almost half a decade, as I’m writing this.

However in this Vitamin A debacle ~ I am met with more, albeit interesting confusion given the more research I’m willing to dig into.

  1. Vitamin A appears to have an antagonistic relationship to Vitamin D (Deanna Minich, 2018). This trial (S. Johansson &H. Melhus, 2009) looking at daily livers intake amongst Scandiavian males likewise finds reduced Calcium intestinal absorption.
  2. Hypercalcemia is also suspected to be linked with serum vitamin A. This case study (Hammid D et al. 2014) examining a modest amount of Vitamin A (7,000 IU “supplementation”, note – not dietary) daily for 10 years on 67 year old senior female ~ appears supportive to this hypothesis. But noteworthy that this is within the context of impaired kidney function. Mechanism behind this is inconclusive but suspected that due to “osteolytic” effect in response to the prolonged frequency of the vitamin A supplementation.
  3. Serum retinol levels were compared between healthy controls and those with AS (O’Shea, FD, et al. 2007). Interestingly, the researchers noted a decrease in the AS group.
  4. Similarly, a study (Dougados M et al. 1988) comparing multiple conditions (hyperostosis, AS and rheumatoid polyarthritis) found that serum retinol decreased on AS and Rheumatoid polyarhtritis. Interestingly, serum retinol levels increased on the Hyperostosis.
  5. A single + double blind trial on subjects with AS supplementing with Vitamin E and A found that only Vitamin E appears to be helpful for pain relief (Mahmud Z & Ali SM 1992).  Vitamin A interestingly, was found to be as “not effective”.
  6. A Harvard article on Vitamin A suggests correlation between Retinoic Acid status with increase risk of fractures due to more osteoclast (the “erosion” of bone) activity over osteoblast (the “building”) activity in response to Vitamin A status. This further suggests that calcium is being eroded off the bones, and transfers into the serum.

April May 2024 Update: thoughts Vitamin D exclusion and reinclusion

There is some degree of confidence that, throughout the two months, there was indeed a change on overall quality of life /QOL did. Adversely, that is, in subtle but noticeable ways throughout the two months of :

  1. Experimental increase of Vitamin A intake from bioavailable sources (DIY chicken liver pate) OVER Vitamin D. In other words, Vitamin A intake/supplementation: increase. Vitamin D intake/supplementation: decrease.
  2. Reinclusion of Vitamin D supplementation (of 10k IU with K2). In other words,  Vitamin D intake / supplementation: increase. Vitamin A intake/supplementation : decrease

Chiefly among factors This Author(AW) felt compromised were : dry tired eyes / lack of moisture, overall stress resilience, sleep quality and psychological composure. These were noted when Vitamin D supplementation was drastically reduced whilst Vitamin A increased.

Firstly with eye health, those unaccustomed with Anklyosing Spondyltis (AS) is advised that any pinks or redness around the sclera (or whites of the eyes) may indicate sign of inflammation thought to be associated with the AS. A study reviewing eleven sources seem to indicate a correlation with lowered Vitamin D intake with severity of the disease. Overall eye tiredness, but not its cosmetic redness seemed to be helped with increasing Vitamin D, OVER Vitamin A intake.

Stress resilience, sleep quality and composure wise also seem to indicate, throughout the two months update above; as supportive towards more Vitamin D intake and/or supplementation, over Vitamin A intake.  Sleep quality seemed felt less in terms of overall rejuvenation, leading to noticeably increased sense of fatigues upon awakening  ,lingering hours on end until afternoons. Upon supplementing Vitamin D (10k IU per day) these effects seemed to decrease or lessen to a degree that is quite noticeable. Whether or not Vitamin A affects the complex cortisol / stress hormones dynamics remains a complex subject.

This two (months) of introspective exclusion and reinclusion is by no means a “definitive” suggestion for prescribing complete elimination of Vitamin A sources. The copper content from most potent wholefood source (chicken livers chiefly among them) does nonetheless serve to regulate the immune system, alongside also dietary choline status for overall methylation health.

Nevertheless, readers should prompt for their ownselves enough time, should they likewise embark on similarly concentrated – exclusion and reinclusion surrounding Vitamin D to A ratio.

Conflicting Sentiments as Further questions.

So here are a curation of snippets, or should we say, unasnwered questions which may prove noteworthy as each have been debated fervently, yet still leaving little to no room for any resolution.

Vitamin A interaction with Vitamin D ~ which one is which?

One of many questions pertaining health optimizations, surrounding which key vitamin deficiency(s) play a bigg(er) role to mortality risks, within the nuances of individual (N=1) genomics, is likely always an on-going mystery that is likely not going to be resolved overnight.

Vitamin A appears to have antagonist processes to Vitamin D. Several papers (here and here) demonstrated these both in mechanistic and animal based models. Hence a question that remains undoubtedly difficult to answer is ~ is it the Vitamin A or the Vitamin D ~ the failure of the utilization somewhere or somehow in the biology, that predisposes one to develop symptoms of excess of one vitamin vs the other (and/or vice versa)?

Not everybody appears to gain benefit in complete dietary Vitamin A restriction.

Despite increasing # of anecdotes concurring with Dr Smith and Grant’s message, so too a few who, despite trialling these extensive exclusion protocols as suggested ~ experienced adverse outcomes. Obviously no names need mentioning, but several insights can be found here.

(minor offtrack) but Important disclaimer: there are many forums whose members do use exact same “handle” or “user names” as my own shortened name and identity ~ be it “Andrew W” or “AW”.  I can assure everyone that I am not currently affiliated NOR am I proclaiming I am such-and-such individual(s) residing in these forums. Unless I explicitly declare that I am such a member. My presence here remains clear for everyone to identify~ be it (thus far) in this website, my own website, and obviously – my youtube channel. I hope this clears any confusions. ~ AW.

Understanding why behind these conflicting outcomes, are obviously difficult to translate for lay reading. Presuming within the safest conclusion that everyone bears an unique response to any exclusion protocols; perhaps the following can derive further reading(s) that may assist at putting things to perspective.

  • Eliminating all Vitamin A foods can and may predispose deficiencies or inadequacies in another.
  • Vitamin A still remains throughout history a nutrient praised amongst indigenous and ethnic cultures for centuries.

Eliminating Vitamin A foods can and may also prove challenging as such may invite more problems than they are constructive, or worse – may pose further confusions as a cascading array of unknowns unless one is prepared and very thoroughly patient to assess such a repercussion. For instance foods that are rich in Vitamin A, notably those in animal form (retinyl esters) contain many other non-obligatory essentials. Chiefly among them, eggs ~ containing the much needed pre-methylated choline, are considered vital as it helps in the packaging of Retinol into the RBP / retinol binding protein (48:50).    

 


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