Vitamin A: How Much Causes Liver Toxicity?
By Michael Mooney
October 30, 2011

One of the most misunderstood issues in the world of natural foods is vitamin A's potential for toxicity. Over the last half dozen or so years some of the most popular manufacturers of dietary supplements have taken real vitamin A (retinol) out of their multivitamins and replaced it with the vitamin A precursor, beta carotene.

This is mistake, as several studies confirm that beta carotene does not absorb or convert into real vitamin A well enough to adequately substitute for vitamin A for a majority of people.

When I hear people talk of vitamin A toxicity, as if it's common, I know they don't understand the concept of dosing.

Vitamin A is completely safe in its effective dosage range AND there are no multivitamins sold in the United States that have even close to a dose that could cause toxicity.

Realize that the safe, effective dosage range for vitamin A is between 2333 IU, as the lowest recommended daily dose for women and 10,000 IU, which is the Institute of Medicine's No Observed Adverse Effect Level (NOAEL).

The NOAEL is a conservative dose where healthy adults can take this much vitamin A long-term with no potential for toxicity.

This also applies to pregnant women, with the World Health Organization saying, "It is safe to give fertile women 10,000 IU of vitamin A at any time during pregnancy."

However, the Lowest Observed Adverse Effect Level (LOAEL) for vitamin A is 21,600 IU. The LOAEL is a dose where toxicity may occur "...rarely, but for some sensitive subgroups is does occur..." when taken over a period of time, such as three months.

This means that doses under 21,600 IU might cause no problems. Additionally, the potential for toxicity at the LOAEL only happens if a person takes 21,600 IU of vitamin A over a period of time, such as three months.

So, what do published studies say about what doses of vitamin A have been documented to cause liver toxicity?

The study below said that the lowest dose of vitamin A that caused severe liver toxicity was 25,000 IU over a period of six years. It also said that similar toxicity occured with dosages of 100,000 IU or more over a period of 2 1/2 years.

So, vitamin A at supplemental doses, which are typically no greater than 5,000 IU, can not be toxic to normally healthy adults.

Geubel AP, et al. Liver damage caused by therapeutic vitamin A administration: estimate of dose-related toxicity in 41 cases. Gastroenterology. 1991 Jun;100(6):1701-9.

Clinical presentation, changes in liver function test results, and liver morphology were examined in 41 consecutive patients with vitamin A hepatoxicity. The cause of liver disease was suspected at initial interview in only 13 instances, whereas histological evidence of fat-storing cell hyperplasia with fluorescent vacuoles led to the diagnosis in the remaining cases. Cirrhosis was found in 17, mild chronic hepatitis in 10, noncirrhotic portal hypertension in 5, and "increased storage" alone in 9 cases. During a mean follow-up period of 4.6 years, 6 patients died of causes related to the liver disease. A precise appraisal of drug consumption was obtained in 29 cases. Among them the total cumulative intake was the highest in patients with cirrhosis (423 +/- 103 x 10(6) IU) and significantly lower in those with noncirrhotic liver disease (88.5 +/- 41; P less than 0.02). The smallest continuous daily consumption leading to cirrhosis was 25,000 IU during 6 years, whereas higher daily doses (greater than or equal to 100,000 IU) taken during 21/2 years resulted in similar histological lesions. It was concluded that at least in some western countries chronic vitamin A consumption might represent an appreciable cause of chronic liver disease, the recognition of which mainly relies on expert liver biopsy interpretation. The data also indicate that prolonged and continuous consumption of doses in the low "therapeutic" range can result in life-threatening liver damage.