Vitamin A deficiency is common in developing countries but rarely seen in the United States. Approximately 250,000 to 500,000 malnourished children in the developing world become blind each year from a deficiency of vitamin A.1

In the United States, vitamin A deficiency is most often associated with strict dietary restrictions and excess alcohol intake.2

Severe zinc deficiency, which is also associated with strict dietary limitations, often accompanies vitamin A deficiency. Zinc is required to make retinol binding protein (RBP) which transports vitamin A. Therefore, a deficiency in zinc limits the body's ability to move vitamin A stores from the liver to body tissues.3

Night blindness is one of the first signs of vitamin A deficiency. In ancient Egypt, it was known that night blindness could be cured by eating liver, which was later found to be a rich source of the vitamin.4 Vitamin A deficiency contributes to blindness by making the cornea very dry and damaging the retina and cornea.5

Vitamin A deficiency diminishes the ability to fight infections. In countries where such deficiency is common and immunization programs are limited, millions of children die each year from complications of infectious diseases such as measles.6 In vitamin A-deficient individuals, cells lining the lungs lose their ability to remove disease-causing microorganisms. This may contribute to the pneumonia associated with vitamin A deficiency.7 8 9

There is increased interest in early forms of vitamin A deficiency, described as low storage levels of vitamin A that do not cause obvious deficiency symptoms. This mild degree of vitamin A deficiency may increase children's risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness.1011 Children in the United States who are considered to be at increased risk for subclinical vitamin A deficiency include:

  • toddlers and preschool age children;
  • children living at or below the poverty level;
  • children with inadequate health care or immunizations;
  • children living in areas with known nutritional deficiencies;
  • recent immigrants or refugees from developing countries with high incidence of vitamin A deficiency or measles; and
  • children with diseases of the pancreas, liver, or intestines, or with inadequate fat digestion or absorption.

A deficiency can occur when vitamin A is lost through chronic diarrhea and through an overall inadequate intake, as is often seen with protein-energy malnutrition. Low blood retinol concentrations indicate depleted levels of vitamin A. This occurs with vitamin A deficiency but also can result from an inadequate intake of protein, calories, and zinc, since these nutrients are needed to make RBP.12 Iron deficiency can also affect vitamin A metabolism, and iron supplements provided to iron-deficient individuals may improve body stores of vitamin A and iron.13

Excess alcohol intake depletes vitamin A stores. Also, diets high in alcohol often do not provide recommended amounts of vitamin A.14

It is very important for people who consume excessive amounts of alcohol to include good sources of vitamin A in their diets. Vitamin A supplements may not be recommended for individuals who abuse alcohol, however, because their livers may be more susceptible to potential toxicity from high doses of vitamin A.15 A medical doctor will need to evaluate this situation and determine the need for vitamin A supplements.

Related Links: What is vitamin A? | What foods provide vitamin A? | How much vitamin A do I need? | What happens if I do not get enough vitamin A? | Do I need extra vitamin A? | Can vitamin A be harmful? | What are some of the current issues and controversies about vitamin A?

Disclaimer

Reasonable care has been taken in preparing this document and the information provided herein is believed to be accurate. However, this information is not intended to constitute an "authoritative statement" under Food and Drug Administration rules and regulations.

About Source: ODS

The mission of the Office of Dietary Supplements (ODS) is to strengthen knowledge and understanding of dietary supplements by evaluating scientific information, stimulating and supporting research, disseminating research results, and educating the public to foster an enhanced quality of life and health for the U.S. population.

General Safety Advisory

Health professionals and consumers need credible information to make thoughtful decisions about eating a healthful diet and using vitamin and mineral supplements. These Fact Sheets provide responsible information about the role of vitamins and minerals in health and disease. Each Fact Sheet in this series received extensive review by recognized experts from the academic and research communities.

The information is not intended to be a substitute for professional medical advice. It is important to seek the advice of a physician about any medical condition or symptom. It is also important to seek the advice of a physician, registered dietitian, pharmacist, or other qualified health professional about the appropriateness of taking dietary supplements and their potential interactions with medications.

Email This Page Email This Page Print This Page Print This Page

Footnotes

  1. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001. [↩]
  2. Rodrigues MI, Dohlman CH. Blindness in an American boy caused by unrecognized vitamin A deficiency. Arch Ophthalmol 2004;122:1228-9. [↩]
  3. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001. [↩]
  4. Gerster H. Vitamin A-functions, dietary requirements and safety in humans. Int J Vitam Nutr Res 1997;67:71-90. PubMed abstract [↩]
  5. Sommer A. Nutritional Blindness: Xeropthalmia and Keratomalacia. Oxford University Press, London and New York, 1982. [↩]
  6. Ross AC. Vitamin A status: Relationship to immunity and the antibody. Proc Soc Exp Biol Med 1992;200:303-20. PubMed abstract [↩]
  7. Gerster H. Vitamin A-functions, dietary requirements and safety in humans. Int J Vitam Nutr Res 1997;67:71-90. PubMed abstract [↩]
  8. Ross AC. Vitamin A and retinoids. In: Modern Nutrition in Health and Disease. 9th Edition (edited by Shils ME, Olson J, Shike M, Ross AC). Lippincott Williams and Wilkins, New York, 1999, pp. 305-27. [↩]
  9. Ross AC, Stephensen CB. Vitamin A and retinoids in antiviral responses. FASEB J 1996;10:979-85. [PubMed abstract [↩]
  10. Stephens D, Jackson PL, Gutierrez Y. Subclinical vitamin A deficiency: A potentially unrecognized problem in the United States. Pediatr Nurs 1996;22:377-89. PubMed abstract [↩]
  11. Butler JC, Havens PL, Sowell AL, Huff DL, Peterson DE, Day SE, Chusid MJ, Benning RA, Circo R, Davis JP. Measles severity and serum retinol (vitamin A) concentration among children in the United States. Pediatrics 1993;91:1176-81. PubMed abstract [↩]
  12. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001. [↩]
  13. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001. [↩]
  14. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press, Washington, DC, 2001. [↩]
  15. Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene: Adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr 1999;69:1071-85. PubMed abstract [↩]

Comments are closed, but trackbacks and pingbacks are open.