Vitamin A deficiency

Short answer

The first symptom of vitamin A deficiency is night blindness; if it continues, xerophthalmia, that is, involvement of the cornea and conjunctiva, and eventually permanent blindness can develop. Deficiency is rare in the US and is still common in many developing countries; a blood level alone does not make the diagnosis. ^[1] This page does not recommend personal doses.

How does vitamin A deficiency develop?

Most of the vitamin A in the body is stored in the liver; deficiency therefore appears after low intake or malabsorption has continued for a long time and the stores are depleted. The NIH reports that xerophthalmia develops after retinol in the blood has remained low for a long time and the eye’s vitamin A reserves are depleted. ^[1] According to the NIH, in many countries where deficiency is still common in the world, the cause is limited access to foods containing animal-source preformed vitamin A and provitamin A because of poverty or traditional dietary patterns. ^[1]

What are the symptoms?

In the eye: night blindness and xerophthalmia

The NIH reports that the most common clinical finding of deficiency is xerophthalmia. The first symptom is night blindness, being unable to see in low light or darkness because rhodopsin in the retina is reduced; xerophthalmia also affects the cornea and can eventually lead to permanent blindness. Deficiency is one of the leading causes of preventable blindness in children. ^[1] In the Cochrane 2022 review, night blindness and Bitot spots were among the outcomes whose frequency decreased with vitamin A supplementation (night blindness RR 0.32, Bitot spots RR 0.42; moderate certainty; children). ^[3]

Difficulty with night vision does not on its own mean vitamin A deficiency; the cause is distinguished by eye examination. In addition, in a case report (a woman in her early 40s), sudden vision loss, Bitot spots, and progressive keratomalacia were found 8 years after biliopancreatic diversion with duodenal switch surgery; deficiencies of vitamins A, D, E, and K1 were found and were attributed to nonadherence to bariatric follow-up and vitamin supplementation. The authors report that deficiency can appear years after surgery; this is a single case and gives no information about prevalence. ^[6]

Infections, respiratory disease, and anemia

Chronic deficiency has been associated with impaired lung development, respiratory diseases (such as pneumonia), anemia, and an increased risk of death; the severity of infections and the risk of death increase, particularly in measles and diarrhea. ^[1] According to 2013 data reported by the NIH, in low- and middle-income countries 94,500 children died of diarrhea and 11,200 children of measles attributable to deficiency; more than 95% of deficiency-related deaths occurred in sub-Saharan Africa and Asia. ^[1] These figures are global estimates of child deaths; no inference can be made for a healthy adult in Türkiye.

Who is at high risk of deficiency?

The groups the NIH lists are as follows:

• Premature infants: Liver stores are low at birth and plasma retinol levels can remain low throughout the first year; in those with deficiency, the risk of eye and chronic lung disease is higher. In high-income countries, clinical deficiency in infants is rare and is seen only in those with malabsorption. ^[1]
• Infants, children, and pregnant and lactating people in low- and middle-income countries: According to the WHO, about 190 million preschool children (one-third of this age group) have deficiency; in people with deficiency, the vitamin A in breast milk may not adequately protect the stores of an exclusively breastfed infant. ^[1]
• People with cystic fibrosis: Pancreatic insufficiency, in up to 90%, impairs fat absorption. In studies in Australia and the Netherlands, deficiency was found in 2–13% of children and adolescents with cystic fibrosis; standard care (US and Australia) includes lifelong vitamin A, other fat-soluble vitamins, and pancreatic enzymes. ^[1]
• Digestive system diseases: About one-quarter of children with Crohn’s disease and ulcerative colitis have deficiency; it can also be seen in newly diagnosed celiac patients, and a gluten-free diet does not always correct the deficiency. There are studies that show and do not show benefit of supplementation in these diseases. ^[1]
• People using orlistat: By reducing vitamin A and beta-carotene absorption, this medicine, which reduces fat absorption, can lead to low blood levels in some patients. ^[1]

Deficiency has also been reported after bariatric surgeries that reduce absorption (the case report above).

Treatment of deficiency is under physician management: fat-soluble vitamin A accumulates, and high amounts can cause birth defects in pregnancy and chronic toxicity. ^[1]

Detailed guideWhat is vitamin A? Pregnancy, upper limit, and excess→

What do serum retinol thresholds say?

The NIH reports that in clinical practice, plasma retinol can be used to document significant deficiency: 20 µg/dL (0.70 µmol/L) or below often indicates moderate deficiency, and 10 µg/dL (0.35 µmol/L) or below indicates severe deficiency. The same source also states that these levels are not always a reliable indicator of status: they do not fall until the liver and other stores are nearly depleted, and acute or chronic infections can reduce serum retinol. ^[1]

The WHO’s 2011 document uses the same 0.70 µmol/L threshold at the community level: in children aged 6–71 months, if the proportion with serum retinol of 0.70 µmol/L or below is 2–9% it is considered a mild, 10–19% a moderate, and 20% or more a severe public health problem (these thresholds are not valid for infants under 6 months). The document also states that infections without clinical findings can lower serum retinol by up to 25%, and that zinc deficiency and protein-energy malnutrition can also lower serum retinol by reducing retinol-binding protein synthesis. ^[2] That is, the threshold is an indicator for populations, not an individual diagnostic rule; a single low result is interpreted together with symptoms, history, and infection status.

What is the situation in Türkiye?

The two studies below are local and concern children.

• Izmir, 6–59 months (Kurugöl et al., Paediatr Perinat Epidemiol 2000): In 160 healthy children selected by cluster sampling, serum retinol measured by HPLC ranged from 9.8 to 59.2 µg/dL (mean 29.3 ± 9.5); the level was below the lower limit of the normal range in 15.6% of children. In stunted children, deficient and borderline levels were found at 16% and 42%; the relationship between low serum retinol and stunting was significant (P < 0.05). The authors reported that clinical findings were rare, but that subclinical deficiency was a public health problem in Izmir. ^[4]
• Ege University, hospitalized children (Tosyali et al., 2025): A retrospective review of 360 children aged 2 months to 18 years, hospitalized in the general pediatrics unit in 2017–2020, in whom vitamin A level was measured. Those below the study’s own threshold of 316 µg/L numbered 89 children (24.7%); of these, 62 (69.6%) were in the borderline range and in 27 (30.4%) the level was below 200 µg/L. 98 of the children (27.2%) had malnutrition. ^[5]

Both studies concern only children. The Izmir study was conducted in a single province and with an old measurement; the second is a hospital sample and does not represent the general child population. These findings cannot be carried over to adults or to Türkiye as a whole. The “low” threshold of the Tosyali study (316 µg/L, that is, 31.6 µg/dL) is higher than the WHO’s 0.70 µmol/L (about 20 µg/dL = 200 µg/L) threshold; the group close to the WHO threshold is the 27 children with a level below 200 µg/L (about 7.5% of the 360 children), whereas the abstract of the Kurugöl study says “lower limit of the normal range.” The percentages therefore cannot be compared directly with each other or with the WHO classification.

When should a physician be consulted?

In people with difficulty seeing at night, dry eyes, or vision loss, a disease that impairs fat absorption or a surgery that reduces absorption, or recurrent infections, evaluation is done by an ophthalmologist and the relevant specialty. The treatment regimen (amount, duration, route) is determined by the physician; this page does not give a treatment scheme. In pregnancy or when planning pregnancy, the preformed vitamin A content of any additional vitamin A supplement is evaluated together with a doctor or pharmacist.

Detailed guideVitamin A benefits: evidence in deficiency and in healthy people→ Detailed guideWhich foods contain vitamin A?→