Trace mineral feed additives

Trace minerals are supplemented because forages and grains are variable and often deficient in zinc, copper, manganese and selenium. The nutritional question is never the analysed concentration in the ration. It is how much of the element crosses the intestinal epithelium in a usable form, and that depends on the chemical species the element is presented in and on what else is competing with it.

Why form matters#

Inorganic salts — sulphates, oxides, carbonates — dissociate in the gut and release the free ion. A free divalent cation in intestinal contents is chemically promiscuous: it precipitates with phosphate, binds to fibre and phytate, and takes part in the same competitive interactions as every other divalent cation present. Oxides in particular are poorly soluble and their relative bioavailability is markedly lower than sulphates.

Organic and chelated forms — amino acid complexes, proteinates, hydroxy analogues — are designed so that the metal is held in a coordination complex stable enough to survive the upper gut and not release the free ion into that chemistry. The claimed benefit is a matter of degree, not of kind, and it is usually expressed as a relative bioavailability against sulphate; the honest reading of the literature is that differences are real, are often modest, and are largest exactly where antagonists are high or requirement is high, which is where the trials that show the clearest effects have been run.

Antagonism is the reason for all of this#

The absorptive routes are shared. Zinc, copper and iron interact at the level of the divalent metal transporters and at the level of the metallothionein induced in enterocytes, so an excess of one suppresses uptake of another. High dietary zinc induces metallothionein, which binds copper with high affinity and holds it in the enterocyte until the cell is sloughed — copper deficiency produced by zinc excess is a textbook case of an antagonism rather than a shortage. Iron uptake is likewise suppressed by high zinc, and in ruminants the dominant antagonism is different again: sulphur and molybdenum form thiomolybdates in the rumen, which bind copper into unabsorbable complexes, which is why a copper requirement in cattle is only meaningful when stated alongside dietary sulphur and molybdenum.

Phytate, the plant seed’s phosphorus store, adds a further layer. Its six phosphate groups chelate divalent cations, and the resulting complexes are largely unavailable to monogastrics, which lack sufficient endogenous phytase. Supplemental phytase releases phosphorus and simultaneously releases the bound zinc — the mineral effect of a phytase is not a side note.

The upper limit is in the manure#

What is not absorbed is excreted, so mineral supplementation is directly a soil loading question. Copper and zinc accumulate in soils receiving repeated applications of manure, do not degrade, and are toxic to soil organisms and to sheep grazing the land at concentrations well below those that trouble the pigs and poultry the manure came from. High pharmacological doses of zinc oxide, formerly used against post-weaning diarrhoea in piglets, were withdrawn in the EU on this basis and on antimicrobial co-selection grounds. This is why higher-bioavailability forms are argued for on environmental as much as on nutritional terms: the same performance from a lower inclusion means less excreted metal.