Maternal Metabolic Status and the Occurrence of OCD in Thoroughbred Foals.

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7th May 2008

Maternal metabolic status and the occurrence of OCD in Thoroughbred foals.


Dr Caroline Foote, Equine Consulting Services


Equine Consulting Services, in association with the University of Queensland has commenced a major project funded by the Rural Industries Research and Development Corporation investigating the effect of maternal nutrition and metabolism on skeletal disease in growing foals. In a 1998 publication, skeletal disease, collectively referred to as Developmental Orthopaedic Disease (DOD) was estimated to cost the Hunter Valley Thoroughbred breeding industry approximately $10 million each year. This figure included costs associated with diagnosis and treatment, increased labour, loss of sale value, and training fees. If these figures were applied Australia wide, the costs to the Thoroughbred industry alone are estimated to be as much as $60 million per year [1]. DOD is not exclusively a Thoroughbred problem, and is commonly seen in other breeds including Standardbreds, Quarter Horses and Warmbloods. OCD, or Osteochondritis Dissecans refers to thickening, cracking and tearing of the joint cartilage of growing horses. Loose fragments of cartilage or bone may be present in the joint space, causing swelling, pain and lameness. It has been estimated that 10% of foals will not be sold as yearlings due to these conditions.

OCD has been the subject of research interest for many years and while it is regarded as a multifactorial condition, nutrition is generally considered to be one of the major causes. Mineral deficiencies, excesses or imbalances, protein deficiencies and excessive dietary energy have all been implicated as causative factors in equine OCD. More recently, feeding diets high in soluble carbohydrates (such as grains and lush pastures) to growing horses has been implicated in the development of orthopaedic diseases and it has been suggested that glucose intolerance caused by insulin resistance may be associated with OCD in young horses. Both insulin and insulin-like growth factor-1 (IGF-1) play a role in chondrocyte maturation and perturbations of these hormones as a result of chronic hyperinsulinaemia caused by high carbohydrate diets may be manifested by OCD [2, 3].

The majority of studies conducted to investigate nutritional causes of OCD in growing foals have focused on nutritional strategies from weaning age (approximately six months) onwards. However, several studies have identified the highest incidence of OCD and other skeletal disorders to be at a younger age than this. In one study, the average incidence of DOD in Thoroughbred foals evaluated between 4 through 18 months of age was 16.1% (range 12.9 – 28.8%) and the highest incidence was recorded at 4 months of age [4]. While nutritional strategies during the growing period may reduce the incidence of OCD, it is possible the causative factor exists prior to this time, either during early lactation, or during gestation.

Few studies have evaluated the contribution of the mare’s ration to the incidence of skeletal disease in growing foals. Some studies have suggested that a reduced copper intake/absorption during gestation could possibly either initiate the development of DOD under certain conditions or may reduce the ability to repair lesions [5, 6]. However in another study, copper supplementation had no statistically significant effect on the frequency of lesions in 160 day old foals [7]. More recently, data from other species suggests that nutrition of the dam and stress on the dam during gestation and lactation could precipitate endocrine responses that would alter neonatal physiology. It has been suggested that nutrition during gestation and/or lactation turns on different genes in the foetus/neonate, essentially preparing the offspring‘s endocrine and metabolic systems for an appropriate response to the expected energy intake [8]. There have been numerous studies conducted in human nutrition to examine this hypothesis which describe a relationship between adiposity, and higher glucose and insulin concentrations in offspring of diabetic mothers [9-11].

The influence of maternal insulin status in mares and its effect on the development of insulin resistance in offspring is unknown. The first question is: what is the insulin status of our mares? We know that insulin sensitivity is approximately 80% lower (i.e. more insulin resistant) in obese horses than in nonobese horses and in horses consuming meals rich in starch and sugar [12]. Many of our mares (who are often good-doers grazing lush pastures) fall into these risk categories. As such, the relationship between the metabolic status of mares and their likelihood of producing hyperinsulinaemic foals, and its effect on OCD warrants investigation.

The current study will investigate the role of insulin resistance in the mare on skeletal development in the foal. Briefly, mares have been recruited from Thoroughbred stud farms and the relationship between their metabolic status (i.e. insulin resistance) with foal skeletal development and growth will be determined. These studies will be conducted in conjunction with detailed studies of the nutritional intake and status of mares throughout pregnancy and lactation. The incidence of OCD will be determined from survey and sale radiographs and from farm veterinary records. The key objectives of the proposed research will be an increased understanding of the pathogenesis of skeletal disease in foals and a reduction of wastage in the breeding industry through the identification of key nutritional risk factors associated with this disease. Furthermore, it has been suggested that skeletal failure in horses during training may be due to weaknesses linked to these developmental lesions and as a result, this work may also have the potential to financially impact insurance companies as well as trainers and other industry members associated with racing. Moreover, as the research will concentrate on the role of the dam in the development of OCD it will provide insights into mare nutrition and metabolism.

This work is fully funded by the Rural Industries Research and Development Corporation and being carried out by Equine Consulting Services and the University of Queensland. Equine Consulting Services is an independent nutritional advisory service for the horse industry. We consult to trainers, breeders, spelling properties and individual horse owners with the objectives of improving performance, optimising growth and reducing the risks disease through improved health and nutrition. For further information on the OCD project or nutritional services available, please contact us on 0418 488 718 or by email: Further information on nutrition and OCD is available on our website:


1. Aldred, J., Developmental Orthopaedic Disease in Horses. RIRDC Publication No. 97/79., 1998.

2. Henson, F.M., et al., Effects of insulin and insulin-like growth factors I and II on the growth of equine fetal and neonatal chondrocytes. Equine Veterinary Journal, 1997. 29: p. 441-447.

3. Ralston, S.L., Hyperglycaemia/hyperinsulinemia after feeding a meal of grain to young horses with osteochondritis dissecans (OCD) lesions. Pferdeheilkunde, 1996. 12: p. 320-322.

4. Jelan, Z., et al., Growth rates in Thoroughbred foals. Pferdeheilkunde, 1996. 12: p. 291-295.

5. Knight, D.A., Weisbrode, S.E., Schmall, L.M., Reed, S.M., Gabel, A.A., Bramlage, L.R., Tyznik, W.I., The effects of copper supplementation on the prevalence of cartilage lesions in foals. Equine Veterinary Journal, 1990. 22: p. 426-432.

6. Pearce, S.G., Firth, E.C., Grace, N.D., Fennessy, P.F., Effect of copper supplementation on the evidence of developmental orthopaedic disease in pasture-fed New Zealand Thoroughbreds. Equine Veterinary Journal, 1998. 30: p. 183-185.

7. Gee, E., et al., Osteochondrosis and copper: Histology of articular cartilage from foals out of copper supplemented and non-supplemented dams. The Veterinary Journal, 2007. 173: p. 109-117.

8. Hales, C.N. and D.J.P. Barker, Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia, 1992. 35: p. 595-601.

9. Krishnaveni, G.V., et al., Anthropometry, glucose tolerance, and insulin concentrations in Indian children: relationships to maternal glucose and insulin concentrations during pregnancy. Diabetes Care, 2005. 28: p. 2919-2925.

10. Pettitt, D.J., et al., Congenital susceptibility to NIDDM. Role of intrauterine environment. Diabetes, 1988. 37: p. 622-628.

11. Hillier, T.A., et al., Childhood obesity and metabolic imprinting: The ongoing effects of maternal hyperglycemia. Diabetes Care, 2007. 30: p. 2287-2292.

12. Hoffman, R.M., et al., Glucose clearance in grazing mares is affected by diet, pregnancy, and lactation. Journal of Animal Science, 2003. 81: p. 1764-1771.