Why is my Vitamin A high when I don't eat high vitamin A foods or take supplements?

[ironfist]

65.4 Range 20.1-62

Other related things. Calcium 10.1 Range 8.7-10.2. Vitamin D 84.6 Range 30-100.

 

[Highserotonin90]

@ironfist Why is it pouring into the blood?

 

[youngsinatra]

Poor bile flow & chronic constipation could cause a build up.

Or a cofactor deficiency in the cascade of vitamin A clearance / activation into retinoic acids. (NAD, FAD, Molybdenum)

 

[Weak Yet Strong]

Here are the possible causes for high vitamin A without supplementing or eating high vitamin A foods

1. STRA6 pore dysfunction. I think the number one issue here is lack of magnesium uptake into cells. This could be from losses of magnesium in urine from being in acidosis or competition with ionized calcium that occurs in acidosis. This could also be from high zinc intake. If blood zinc levels are high, that competes with the same transporter that transports calcium and magnesium. The STRA6 pore that allows the carrier for vitamin A to doc, requires activation by calmodulin. Calmodulin needs to be loaded with calcium, but it also has an arm on it that requires magnesium so that calmodulin isn't always in the "ON" position. If magnesium is low in the cell, then calmodulin stays "ON". This leads to the preference of the STRA6 pore for apo RBP4 (empty RBP4 that can take retinol out of cells). This causes vitamin A to efflux from the cells onto RBP4 and stay in serum. Biotin deficiency might play a role here because biotin is a component of the STRA6 pore, but this is still being studied.

2. High oxalate diet or making oxalate in the body due to a block at pyruvate dehydrogenase complex from loss of thiamine or other cofactors. These leads to a low NAD state which slows vA metabolism

3. VDR receptor dysfunction causing low calcium uptake and struggles with calcium regulation. This could cause low calmodulin activity resulting in less uptake of vitamin A through STRA6 pore. This could also be caused by low active vitamin D (1,25 OH D) which isn't usually tested.

4. Magnesium deficiency causing low calmodulin activity and same cascade as above. (Needs some magnesium). I honestly have been thinking about this a bunch and I believe that high serum A could be caused by dysfunctional EF-hand control of calmodulin due to acidosis and also candida overgrowth (consumes magnesium) plus overactive TCA cycle (those with anhydroretinol toxicity) causing a cellular magnesium deficiency resulting in calmodulin staying ON. If calmodulin is ON then vitamin A effluxes from cells back onto RBP4 and vitamin A does NOT enter cells. This causes a cellular retinol deficiency (could lead to poor function of energy metabolism) and also retinoic acid deficiency. This would cause high serum A levels.

4. PAPS deficiency resulting in the inability to control cellular levels of alcohol leading to the production of anhydroretinol. This leads to anhydroretinol taking the place of retinol in the PKC Delta signalosome. A cascade occurs which results in an overactive TCA cycle and eventually a build up of citrate. Citrate chelates calcium and keeps it from binding to calmodulin. This prevents Stra6 pore from allowing vitamin A into the cells. Serum A goes up, cells become deficient in retinoic acid.
PAPS deficiency could also be the cause of high vitamin E. We need PAPS and SULT activity to clear excess vitamin E from the body (vitamin D, too but she may just actually have a vitamin D deficiency)

Inhibitors of SULT - quercetin, salicylates (aspirin, but foods too)

Inhibitors of PAPS production - chlorate and perchlorate in tap water, arsenic (needs massive amounts of methyl groups to clear; rice is a huge source), selenate versions of selenium (check supplements)

Too much vitamin D orally won't help because it could tie up PAPS further. But some may be needed if unable to get sunlight.

5. High citrate from supplements or from making citrate in TCA cycle, but due to oxidative stress or low iron status, aconitase is not working. This leads to high citrate levels. Citrate chelates ionized calcium which causes low calcium uptake into cells. This causes vitamin A to stay in the blood. I would like to say that if you HAVE calcium oxalate stones, citrate actually binds to the CALCIUM and stops the formation of calcium oxalate stones. It doesn't bind to oxalate that I know of. So please do NOT stop your citrate supplements without talking to your own provider due to this could be problematic for kidney health.

6. Hyperlipidemia is causing a first pass competition for LPL which must clear triglycerides first before accessing vitamin A from chylomicrons. This leads to the brain sensing low vitamin A state. The vitamin A from a meal is then taken to the liver. The brain tells the liver to make more RBP4 to send it back into the blood for a second pass.

7. Candida or aspergillus or e coli or other gut dysbiosis causing high alcohol levels which ties up alcohol metabolism enzymes and uses up NAD and also directly competes with retinol.

8. Alcohol. Lower NAD availability for retinol metabolism.

9. Melatonin (high doses) causes low NAD state. Also can cause impaired insulin release leading to poor postprandial uptake of lipids from chylomicrons and need for more second pass vitamin A distribution.

10. High dose vitamin C...becomes hydrogen peroxide (or oxalate ....see #11)

11. Gluten Free diet....or diet low in betaine (TMG) this causes a functional B6 deficiency that causes a mess of things. This is because low betaine intake forces the body to make betaine using the enzyme ALDH7A1 which moonlights in lysine metabolism and lipid peroxidation detoxification. Bad lysine metabolism results in a build up of P6C which leads to inactivation of B6 by binding to it. Low functioning B6 slows de novo NAD production. Low B6 also slows GABA production through the GABA shunt. GABA typically upregulates enzymes such as GPX, catalase, and SOD to help control reactive oxygen species. If cellular H202 goes high, this leads inhibition of ALDH enzymes leading to increase levels or retinaldehyde and low levels of retinoic acid. In the brain, if retinoic acid isn't made, the brain will send a message to the liver to make more RBP4 and send out MORE vitamin A into serum. This will make serum levels go up because the brain thinks there isn't enough vitamin A available.

 

[Weak Yet Strong]

On your calcium being on the higher side of normal, when serum vitamin A goes up it aggravates osteoclasts which causes more calcium to be mobilized from bones. Normal serum A should be between 30 mcg/dl and 60 mcg/dl fasting. Definitely your levels seem high.

 

[DanDare]

There is a lot of doubt about serum levels being reliable indicators of tissue ( and liver) levels.

I think if you have serum levels of zero after avoiding as much A as possible ( like Grant Genereux) then that's different.

 

[Peater]

65.4 Range 20.1-62

Other related things. Calcium 10.1 Range 8.7-10.2. Vitamin D 84.6 Range 30-100.

What is your previous vit A consumption history?