This could be the key. Thanks.
Retinoic acid is a form of vitamin A. It may help the ever present inflammation, improve collagen and my scaling psoriasis.
Vitamin A palmitate is a form of vitamin A. It’s found in animal products, such as liver, eggs, and cheese. It’s also called preformed vitamin A and retinyl palmitate. Vitamin A retinyl palmitate is available as a manufactured supplement and vitamin A palmitate is a retinoid (retinol). There’s a common misunderstanding that beta-carotene found in fruits and vegetables is the same thing as vitamin A. Beta Carotene can be converted to retinol by the enzyme β-carotene 15,15′-monooxygenase (BCMO1 gene) and is then used by the body in the same way as preformed vitamin A from animal products is used or stored, but almost half of everyone have variants (two common mutations) on the BCMO1 gene which cause a 30% to 70% decrease in the amount of vitamin A that we can convert from beta-carotene. This means that contrary to popular wisdom, vegetables like carrots and red peppers may not be adequate food sources of vitamin A for many. This may be quite normal in some people however as your body has individual genetics that help to balance inflammation/immunity and the levels and so have genes in different areas modified that help with that. Retinol however then needs to be converted by enzymes into other active metabolites such as retinoic acid, and I found that both zinc and cytochrome P450 enzymes that require magnesium as a cofactor are involved in these additional conversions and also prevent excessive levels, Perhaps a low ceruloplasmin level is among ways to note if there are problems converting to the active forms.
Zinc and Vitamin A are both lowered from inflammation and infection, especially with fever. Episodes of acute infection deplete body stores of vitamin A. We have found that significant amounts of retinol and retinol-binding protein (RBP) were excreted in the urine during serious infections, whereas only trace amounts were found in the urine of healthy control subjects. Subjects with fever (temperature > or = 38.3 degrees C) excreted significantly more retinol (geometric mean = 1.67 mumol/d) than did those without fever.
https://pubmed.ncbi.nlm.nih.gov/8074070/ Severe infections in adult patients (i.e., sepsis and pneumonia) result in excretion of large quantities of Vitamin A retinol in the urine and depletion of vitamin A stores.
https://www.ncbi.nlm.nih.gov/pubmed/1152102/ https://www.ncbi.nlm.nih.gov/pubmed/7762530/ Retinol levels decline rapidly as part of the acute phase response
https://www.ncbi.nlm.nih.gov/pubmed/11063445/ and this translates into increased susceptibility to infection, creating a “vicious circle” difficult to break
https://www.ncbi.nlm.nih.gov/pubmed/10466190/ Vitamin A insufficiency is associated with increased mortality to lung infections and immune responses to infection were compromised upon loss of Vitamin A.
https://www.medicalnewstoday.com/articles/219513#1
Vitamin A is involved in zinc metabolism and vice versa. For example, Zinc deficiency is thought to interfere with vitamin A metabolism in several ways: (1) Zinc deficiency results in decreased synthesis of retinol-binding protein (RBP), which transports retinol through the circulation to peripheral tissues for its utilization by the body and protects the organism against potential toxicity of retinol; (2) zinc deficiency results in decreased activity of the enzyme that releases retinol from its storage form, retinyl palmitate, in the liver; and (3) zinc is required for the enzyme that converts retinol into retinal. Zinc is involved in that conversion of retinol to retinaldehyde (retinal) and retinal to retinoic acid, respectively - The zinc metalloenzyme ADH is required for this oxidative process. Zinc uptake is lowered and also becomes less available to utilize during chronic inflammation/infection.
The gene encoding alcohol dehydrogenase-1 (Adh1) (which requires Zinc.) greatly facilitates degradative metabolism of excess Vitamin A retinol into retinoic acid which may help protect against toxic effects of high dietary vitamin A intake or supplementation. and also helps convert to the active forms.
https://portlandpress.com/biochemj/...lular-retinol-binding?redirectedFrom=fulltext
Since there are no known enzymes that can reduce retinoic acid to retinal, excessive or unneeded retinoic acid is not recycled back to retinol/retinyl ester and must be catabolized and eliminated from the body. This catabolism is catalyzed by one of several cytochrome P450 (CYP) enzymes which require magnesium. Any factor that lowers magnesium or cytochrome P450 enzymes can lead to excessive retinoic acid.
https://www.jlr.org/article/S0022-2275(20)42124-8/fulltext
Over 600 enzyme systems require Magnesium as a cofactor to function optimally, including the cytochrome P450 enzymes (CYP450
https://www.liebertpub.com/doi/abs/10.1089/pai.1994.8.7
I just mention that as it may require lowering of inflammation beyond just taking supplements sometimes to restore function due to the impact inflammation and infection has on zinc and cytochome p450 enzymes.
