Typically, poultry diets contain 1–2 mg I/kg, but higher concentrations are sometimes used to enhance the I content of eggs. In addition to an increased deposition of I in the yolk, other often adverse responses occur, especially at exceptionally high concentrations. Excess I in grower diets can prevent sexual maturation in male and female fowl, and in layer diets will progressively reduce egg production until, by about 2500 mg I/kg diet, ovulation is inhibited and egg production ceases. Most I accumulates in the thyroid gland, and it is likely that the mechanism responsible for these reproductive disorders involves a modification of thyroid hormone activity. Simultaneous with the declining rate of lay, feed intake declines, egg weight and yolk-cholesterol contents decrease and body weight increases. Whereas fertility is unaffected in female breeders, hatch of fertile eggs is reduced, hatch time extended and embryonic mortality and dead-in-shell proportions increased. In contrast, male fertility is decreased because of an increased incidence of dead spermatozoa, although hatchability of eggs from normally fed hens is unaffected. All reproductive variables, together with feed intake and body weight, are normalised within about 7 d of returning to a diet with normal I levels. Excess I suppresses growth in meat-type chickens, but does not affect feed conversion efficiency. There are transient increases in plasma I and cholesterol concentration during excess I intake in all types of bird. The evidence for varying responses to different I sources is equivocal, but the consensus is that source is probably not important.
Relationship of Yolk Cholesterol and Onset of Egg Production
