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
  • 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 work in progresses if anyone can (that is however few they are) derive interest from not only on the interesting views of the opposition (Grant Generoux and Dr Garret Smith), but also if they by any remote chance are also diagnosed (defenitely or indefenitely) with Ankylosing Spondyltis.

Strictly work in progress as always. Non-sequitors, mispellings and the like are part of the process.

Live-It-Forward,

AW.


Part 2

Conflicting Sentiments

Despite increasing number of anecdotes concurring with Dr Smith and Grant’s message, there are still many from within forums pro-claiming these views who have tried extensive exclusion protocols as suggested, yet experienced more adverse outcomes. Thus suggesting that Vitamin A depletion or complete “detoxification” as some may relate – is unlikely to be beneficial for everybody.

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.
  • (TBC)

 

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).    

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 in my case ~ 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. Although 100% cure is not going to be a reality, nor would I be aware of such a thing. Furthermore, while I ably manage the condition from one month, to one year and another and the next ~ the unpredictability of another flare episodes still remains 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.

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