This is a discussion of some principles underlying a common field problem. Pasture-fed livestock are at risk of nutritional imbalance for many reasons including availability and composition of the pasture on the one hand and the animal's requirements for maintenance, growth and production on the other. Both sides of the equation can be affected by environment and management. As appetite is limited by feed digestibility and rumen capacity, the animal may be unable to eat enough pasture to supply sufficient nutrients to balance input with output without drawing on body reserves, which, like rumen capacity, are finite. This is exacerbated when pasture quality (composition relative to the requirements of the animal both for rumen function and tissue metabolism) declines. Animal breeders, using phenotypic methods of selection (that is, selection for observable characteristics of the animal), have increased, and are continuing to increase inherent milk, wool and meat yield. If genotypic methods of selection (that is, selection for the gene(s) associated with the desired characteristic) are employed alone and in the absence of adequate live animal testing, negative balances are likely to become more common as will any undesirable consequences.
Negative nutrient balance and frank deficiency affect the metabolism of all cells but mostly those of the more active tissues and systems: nervous, reproductive, immunological, lactation, and structural tissues undergoing rapid growth. The malnutrition syndrome is therefore very complex, with diverse input factors and diverse outcomes.
While chronic malnutrition causes poor condition and emaciation, lesser degrees of (and acute or short-term) nutritional deficiency or imbalance also result in clinical diseases. Reproductive performance is commonly considered to be related to condition score and condition score is a useful clinical indicator of the state of nutrition. However, the relationship is casual (coincidental), not causal. Low condition score is not the cause of reproductive failure. Both low condition score and reproductive performance are caused independently by cellular dysfunction with at least the reproductive system being affected before body condition. Conception can be affected within three days after change of pasture quality, especially a change to pasture low in readily available carbohydrate (McClure 1994). This is a potential problem especially where reproduction is synchronised, as is the case for AI and embryo transfer programmes and for dairy herds.
It is important to understand the pathogenesis of the diseases caused by malnutrition: first to confirm the nature of the putative agent involved, secondly to determine how it affects the metabolism of the critical tissues and thirdly to help develop control measures. The experimental evidence (McClure 1994, McClure 2009a), together with general principles and the rapidity with which clinical signs can develop after change in diet suggests that cellular energy supply is the first to be affected, regardless of which nutrient is deficient. This hypothesis also allows for the inclusion of vitamins and minerals which act as co-enzymes or cofactors in the glycolytic pathways and of other agents such as toxins decreasing the supply of cellular energy. This may cause physiological failure of the tissues and systems, predisposing them to stresses (the precipitating causes of disease). These can arise from the environment, infection, lactation, reproduction, weaning, growth, physical performance and chronic mental/emotional stress. Such a failure of cellular energy metabolism thus predisposes animals, including humans, to a wide range of diseases. These include infertility, change in demeanour, metabolic disease for example ketosis in dairy cows, post-weaning diarrhoea in lambs, and reduced milk and wool quality. Thus there may be an 'hour-glass' effect, with a number of input factors, a number of outcomes, and but a single mechanistic 'stem' (the glycolytic pathway).
The critical substrate for cellular energy, glucose, is in the ruminant normally derived mainly from rumenal propionate and glucogenic amino acids, but when necessary is mobilized from the limited body reserves of glycogen without significant loss of liveweight or body condition. Later, the glucose is obtained from glycerol released from the catabolism (breakdown) of fat reserves and from glucogenic amino acids by the catabolism of muscle protein. Both of these cause loss of condition and liveweight. Catabolism of fats and proteins also provide triglycerides and ketogenic amino acids which are used as alternative sources of energy by some non-neurological tissues. Low dietary carbohydrate can be mimicked experimentally. For example, the experimental administration of the glucose metabolic inhibitor 2-deoxy-D-glucose at prooestrus will cause developing follicles to regress and inhibit ovulation in cows, and in rodents, embryonic death before implantation.
Thus the hypothesis is that malnutrition predisposes ruminants and monogastric animals, including humans, to 'stress'-induced diseases by causing cellular metabolic dysfunction via a limited number of biochemical pathways, possibly only one. If this hypothesis is correct, then we need to determine the next step in the pathogenesis. The first possibility is that the metabolic dysfunction occurs in cells of the nervous system, which is known to affect the function of other systems directly or hormonally. Negative energy balance is also known to impair immunity and increase susceptibility to infection, and the immune system affects many other systems and their responses to stress. It is possible that the altered regulation of the immune response which underlies diverse chronic inflammatory diseases has as a common mechanism the sub-optimal supply of energy in critical cells. The third possibility is that the cellular dysfunction occurs directly in the target system, as may be the case in the neurodegeneration accompanying aging. When we know which cells are involved, and what cell processes are affected, specific intervention strategies will become possible.
Diseases are best controlled and prevented by eliminating or reducing their predisposing causes. Adverse climate and economic pressures encourage overstocking and the feeding of immature or over-mature grass-dominant pastures. Competition from feral and native pests, and in some cases ignorance, also contribute to poor pasture management. In practice, commercial livestock production must always operate in an economic environment but balancing welfare and environmental considerations. However, for optimal health and production, ruminants need to be offered unlimited access to palatable highly digestible pasture or crop, balanced for all nutrients essential both for rumenal digestion and for systemic cellular metabolism. Even then the intake of essential nutrients may be insufficient for high-producing animals at critical times, that is late pregnancy, parturition and early lactation until mating and implantation. In the event that deficiency or imbalance is likely, and the identification or prediction of such requires skill on the part of the manager, animals can be supplemented with concentrates balanced for essential nutrients or in the case of dairy animals, the milk yield dampened over the critical period.