Editing Vitamin A (section)

===Secondary causes===
There are causes for deficiency other than low dietary intake of vitamin A as retinol or carotenes. Adequate dietary protein and caloric energy are needed for a normal rate of synthesis of RBP, without which, retinol cannot be mobilized to leave the liver. Systemic infections can cause transient decreases in RBP synthesis even if protein-calorie malnutrition is absent. Chronic alcohol consumption reduces liver vitamin A storage.<ref name="DRI VitA"/> [[Non-alcoholic fatty liver disease]] (NAFLD), characterized by the accumulation of fat in the liver, is the hepatic manifestation of [[metabolic syndrome]]. Liver damage from NAFLD reduces liver storage capacity for retinol and reduces the ability to mobilize liver stores to maintain normal circulating concentration.<ref name="Saeed2017">{{cite journal | vauthors = Saeed A, Dullaart RP, Schreuder TC, Blokzijl H, Faber KN | title = Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD) | journal = Nutrients | volume = 10 | issue = 1 | page = 29 | date = December 2017 | pmid = 29286303 | pmc = 5793257 | doi = 10.3390/nu10010029 | doi-access = free | title-link = doi }}</ref>
Vitamin A appears to be involved in the pathogenesis of anemia by diverse biological mechanisms, such as the enhancement of growth and differentiation of erythrocyte progenitor cells, potentiation of immunity to infection , and mobilization of iron stores from tissues.