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You CAN get vitamin A toxicity from beta-carotene

Ippodrom47

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Joined
Jun 7, 2021
Messages
56
We have all been told that only preformed vitamin A in the form of retinol, which is found in supplements, liver, eggs, can be toxic. However, beta-carotene seems to have a very good rep because it is not supposed to give you toxicity due to the fact that the body is able to tightly regulate its conversion to retinol, and, in any case, that conversion rate is reportedly pretty low.

I personally got apparent vit A toxicity from eating too much beef/chicken liver and canned cod liver, as well as eggs and dairy on top of that. Then I continued to have all the classic debilitating vitamin A toxicity symptoms from high beta-carotene foods (slowed metabolism, dry skin, eyes, and mouth, high calcium and cholesterol, irritability, fatigue), and it was only a week ago that I realized that vitamin A/carotene might be the cause.

Here's a case study I found a couple of days ago:
Refractory hypercalcemia owing to vitamin A toxicity in a 4-year-old boy

I understand that a 4 yo boy has a bit different bodily processes and mechanisms than an adult, but the case is still very unusual.

A 4-year-old, previously healthy boy presented to the emergency department with a 2-day history of polydipsia, fatigue, irritability, cheilitis and a refusal to bear weight.
He appeared pale, with significant cheilitis, xerotic skin, diffuse alopecia and periorbital and pedal edema (Figure 1). Initial investigations were significant for severe hypercalcemia, hyponatremia, hypokalemia, mildly elevated creatinine, elevated C-reactive protein, leukocytosis and normocytic anemia (Box 1).

He also had elevated liver enzymes, a prolonged international normalized ratio and hypoalbuminemia. A liver ultrasound showed hepatomegaly, and abnormal sheer wave elastography was suggestive of fibrosis.

...the vitamin A level was significantly elevated at 4.1 (reference 1.0–1.6) μmol/L. Because of his elevated vitamin A level, we carefully reviewed his diet and supplement intake. He was on a predominantly plant-based diet, and we estimated his vitamin A intake to be between 1528 μg and 3304 μg of retinol activity equivalents (RAE) per day, or 31 087–63 507 international units (IU) per day (recommended intake for children at the age of our patient is 400 μg/d RAE). We referred to the US Department of Agriculture to provide the levels of vitamin A in the foods (FoodData Central) and the conversion of factors for RAE and IU from the US National Institutes of Health (Box 2). The patient’s main sources of vitamin A included 1–2 cups of kale, 2–3 cups of green vegetables, 2–3 cups of fruit and 4 oz of meat per day (nonliver), plus a multivitamin containing vitamin A as β-carotene (28 μg RAE). He had previously been taking cod liver oil supplements (276 μg/day RAE) for more than 1 year, but had stopped many months previously.

We managed the patient’s hypercalcemia with IV hyperhydration, multiple doses of subcutaneous calcitonin and IV bisphosphonates and a low vitamin A diet (Figure 2). We discharged him home with a normal ionized calcium, and 1 month after discharge, his hypercalcemia and bicytopenia had resolved. His papilledema improved and he was tapered off acetazolamide. His liver markers remain mildly elevated, with ongoing evidence of fibrosis on liver ultrasound.

Basically, the child used to take cod liver oil in a safe dose several months prior to the admission, but stopped and continued to eat a plant-based diet with lots of carotene-rich products. Most of his issues were resolved or improved in a short period of time on a low-A diet.
The initially consumed amount of beta-carotene was enough to cause vit A toxicity, even though his body should have stopped converting it to retinol once its liver stores were full in order to prevent hypervitaminosis.
Also, note that his skin is a healthy color, even "pale" as mentioned in the article, with no signs of carotenemia. Once again, in a normal "defense mechanism" against vit A toxicity, the body should have stopped the conversion and started to direct it to the subcutaneous fat and cause apparent carotenemia (which I also had and thus was anything but "pale". In fact, I was so yellowish that my docs all asked me about any liver issues).

Would like to hear your thoughts!
 

Tim Lundeen

Member
Joined
Feb 19, 2017
Messages
296
This is correct, I've seen a few other people reporting the same. I suspect the problem is that we can up or downregulate beta-carotene conversion within some range, but can't shut it down altogether.
 

aliml

Member
Joined
Apr 17, 2017
Messages
240
Genes Associated With Beta-carotene Levels:

BCO1 (beta-carotene oxygenase 1) gene produces the enzyme responsible for converting beta-carotene into vitamin A (retinoid).

BCO2 (beta-carotene oxygenase 2) is a key enzyme that prevents oxidative stress by breaking down beta-carotene in the mitochondria.

BCO2 breaks down beta-carotene in a different way than BCO1, without producing vitamin A. Mutations in these two gene increase beta-carotene levels.
 

Birdie

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Joined
Aug 10, 2012
Messages
3,408
Location
USA
Ray has been pointing this out for years. He even advises rinsing carrots to remove part of the beta carotene as well as limiting the amounts or avoiding such high beta carotene foods as sweet potatoes.
 
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