The intensive nature of modern poultry production has led researchers to reconsider the folic acid requirements of poultry for optimum nutrition. Although there is still uncertainty over these requirements, recent research suggests a need for dietary supplemental levels greater than National Research Council requirements. The goal is to permit optimum performance rather than just prevent signs of clinical deficiency.
Like other species, poultry rely on both feed sources and microbial synthesis in the intestine to meet their folacin (folic acid) requirements (Roche, 1989). In feedstuffs, folacin occurs mainly in polyglutamate forms, which must be converted via hydrolysis into monoglutamate derivatives before they are absorbed, primarily in the duodenum and jejunum. These derivatives are then transported in plasma to the cells, where they are built up again in steplike fashion as pteroylpolyglutamates.
At the cellular level, folacin is essential to the transfer of single carbon units in various reactions, much as pantothenic acid is essential to the transfer of two-carbon units. Among these reactions are purine and pyrimidine synthesis, and the transfer of methyl groups for such compounds as methionine, choline and thymine.
Because purine bases and thymine (a pyrimidine base) are constituents of nucleic acids, folacin plays a key role in cell formation and function. Indeed, it appears necessary for mitosis, and requirements are greatest during periods of rapid growth and in rapidly dividing cells and tissue, such as epithelia, epidermis and bone marrow. Thus, breeders and newly hatched birds have greater folacin requirements than other poultry.
One of the first signs of folacin deficiency is severe macrocytic anemia due to megaloblastic arrest of erythrocyte formation in bone marrow. In hens, folacin deficiency appears to affect embryonic development, hatchability and chick viability more than egg production. NRC requirements are higher for hatchability than for egg production.
Folacin deficiency in chicks is characterized by poor growth, very poor feathering, an anemic appearance and perosis. The birds become lethargic, and feed intake declines. As anemia develops, the comb becomes waxy white and the mucous membranes of the mouth pale. Wong et al. (1977) reported that folacin deficiency in Japanese quail also led to high mortality, leg weakness and cervical paralysis.
Apart from the effects of severe deficiency, folic acid insufficiency may have a more routine cost for producers through less than optimum production. In recent research by Whitehead et al. (1995) with practical wheat- and corn-based diets, weight gains and feed conversion in the study were significantly enhanced in birds whose dietary supplementation brought total folacin intake to three to four times the NRC requirement of 0.50 g per ton of complete feed.
In the first part of this study, chicks received an unsupplemented wheat-based diet formulated to contain 0.18 g of folic acid per ton of complete ration. The birds also received supplemental folic acid at 0, 0.91, 1.4 or 1.8 g/ton. The chicks fed 1.4 or 1.8 g/ton had significantly greater (P<0.5) average body weights and better feed conversion than the control birds at three weeks of age (Figure 1).
