VIII. VITAMIN' A DEFICIENCY IN HUMAN lUOINGS 137 



cytologist who, llirough application and extension of cj'tochemical metliods, 

 may blaze trails for the biochemist and geneticist. 



VIII. Effects of Vitamin A Deficiency in Human Beings 



KAUr. E. MASON 



A. GENERAL CONSIDERATIONS 

 1. "Primary" and "Secondary" Deficiency 



\"itamin A deficiency, or avitaminosis A, is termed "primary" when it 

 results from an inadequacy of vitamin A or its precursor, carotene, in the 

 diet. It is called "secondary" or "conditioned" when it occurs as a result of 

 (1) disorders which interfere with the absorption or storage of the vitamin 

 or provitamin, as represented by celiac disease, cystic fibrosis of the pan- 

 creas, sprue, giardiasis, congenital absence or obstruction of the bile duct, 

 cirrhosis of the liver, ulcerati^'e colitis, and prolonged, severe diarrhea; (2) 

 disorders interfering with the conversion of carotene to vitamin A, such as 

 may occur in diabetes mellitus and hypothyroidism; and (3) factors causing 

 unusuall}^ rapid utilization or loss of vitamin A in the body, such as acute 

 or chronic infections with associated high and sustained fever. These con- 

 ditioning factors exert their effect not so much by depleting body stores of 

 vitamin A, of which 90 to 95 % is represented by liver storage, as by dimin- 

 i.shing vitamin A levels in the circulating plasma, and consequently in body 

 tissues generally, either by inhibiting its release from storage depots, by 

 depressing the vitamin A carrjang capacity of the plasma, or by inactivat- 

 ing vitamin A after its release into the circulation. States of "conditioned" 

 deficiency rarely lead to outspoken manifestations of avitaminosis A. They 

 may, however, account for variations in incidence and severity of mani- 

 festations of "primary" vitamin A deficiency in groups or populations 

 existing on marginal levels of vitamin A intake, and also for differences in 

 responses to comparable levels of vitamin A therap}'. 



The vitamin A storage in well-nourished individuals is of such magnitude, 

 and the vitamin so tenaciouslj'' held by tissues, that at least 2 to 3 years 

 of severe deprivation would be required to bring about clear-cut deficiency 

 symptoms and pathologic lesions. For this reason, avitaminosis A occurs 

 but rarely in adult man and usually in association with a very prolonged 

 intake of generally inadeciuate and un])alanced diets deficient to a variable 

 degree in dietary essentials other than vitamin A; in other words, avitamino- 

 sis A is usually a more or less predominant phase of a "multiple deficiency" 

 state, except when induced in human volunteers by careful dietetic manage- 



