Genetic variation in mineral metabolism of ruminants

Abstract

The occurrence of disorders of mineral metabolism in cattle and sheep, for example hypocalcaemia, hypomagnesaemia or swayback, suggests that some individuals are unable to meet their mineral requirements. The question arises whether such differences among individuals are inherited and can be affected by a breeding policy. The incidences of most of the metabolic disorders are low and sporadic, even though costly. Generally, under these circumstances little progress can be expected in reducing the incidence of these metabolic disorders in future generations by removing, or allowing nature to remove, only the clinically affected animals from the breeding population. Even such little change as might be expected from natural selection is counteracted by normal husbandry and veterinary practices which preserve deficient individuals by rescuing them from the consequences of disorder or by preventing its manifestation (an example relating to swayback is discussed by Wiener (1971)). Genetic progress in reducing metabolic disorders is most likely to be made if the underlying biochemical variation is understood, is measurable in apparently healthy animals and is inherited. More urgency is given to finding answers to the appropriate questions if the disorders are expected to increase in frequency as higher production and intensive husbandry systems impose additional stresses on the animals or, conversely, as ruminants are expected to make increasing use of the extensive, more ‘deficient’ areas of the world, and of plant and industrial by-products. Suboptimal performance has also been associated with mineral deficiency or imbalances (Underwood, 1966) and reports in the literature are not uncommon of favourable responses to dietary additions of, for example, cobalt, copper or selenium where no clinical symptoms of deficiency were detected. If genetic variation is demonstrated at the level of clinical disorder, it must also be sought at other points in the scale from disease at one end to optimum performance at the other. This paper reviews the evidence to date for genetic variation in disorders of mineral metabolism, and in the mineral concentrations in blood, milk, excreta and tissues of sheep and cattle. Some of the results from cattle blood are presented for the first time.