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Journal of equine veterinary science2026; 159; 105816; doi: 10.1016/j.jevs.2026.105816

Fragile foal syndrome: manifestations, heterozygous advantage and the future of breeding policies.

Abstract: Scientific interest in relation to Fragile Foal Syndrome (FFS) has proliferated in the last decade, but before this, many clinical cases were attributed to other similarly presenting equine neonatal disorders. It was thought that FFS-affected foals were mainly miscarried throughout gestation, but recent study results suggest that often, foals are born alive and die shortly after birth. FFS is proposed to have originated as long ago as the Godolphin Arabian, but the definite derivation of the mutant allele is unconfirmed. The discovery that FFS is present in 11-30% of Warmbloods and 2-3% of Thoroughbreds is likely due to balancing selection because of human interference in equine breeding. However, the discovery has catalysed research and resulted in the formation of hypotheses proposing that heterozygous horses have an athletic advantage. Now, studbooks face a novel era of balancing the demand for successful competition horses, whilst actively promoting positive equine welfare.
Publication Date: 2026-02-20 PubMed ID: 41724255DOI: 10.1016/j.jevs.2026.105816Google Scholar: Lookup
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Summary

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Overview

  • Fragile Foal Syndrome (FFS) is a genetic disorder in horses causing affected foals to be fragile and often die shortly after birth.
  • Recent research has found that heterozygous carriers may have an athletic advantage, influencing breeding policies and equine welfare decisions.

Introduction to Fragile Foal Syndrome (FFS)

  • FFS is a genetic disorder affecting foals, leading to fragile skin and connective tissues.
  • Previously, many symptoms of FFS were confused with other neonatal equine disorders.
  • It was once believed that FFS mainly caused miscarriages, but newer studies show foals often survive birth but die soon afterward.

Genetic Origins and Prevalence

  • FFS is thought to date back to the Godolphin Arabian, one of the foundation stallions of modern horse breeds, although this origin remains unconfirmed.
  • The mutant allele responsible for FFS is present in 11-30% of Warmblood horses and 2-3% of Thoroughbreds.

Heterozygous Advantage and Balancing Selection

  • The presence of FFS mutation at relatively high frequencies suggests a balancing selection mechanism influenced by human breeding practices.
  • Heterozygous horses (carrying one copy of the mutant allele) may have an athletic performance advantage, which potentially explains why the allele persists.
  • This phenomenon is referred to as heterozygous advantage, where carriers gain benefits despite homozygous individuals (two copies) experiencing severe disease.

Impact on Breeding Policies and Equine Welfare

  • Studbooks and horse breeding organizations are now challenged to balance competitive breeding success with ethical equine welfare.
  • Breeding decisions must now consider genetic testing to avoid producing affected foals while maintaining desired performance traits.
  • This new era of breeding requires integrating scientific knowledge of genetics with responsible animal welfare practices.

Conclusion and Future Directions

  • The recent advances in understanding FFS have transformed both the scientific approach to the disorder and practical breeding strategies.
  • Further research is required to clarify the exact origin and influence of the mutant allele and to optimize breeding policies that promote healthier foals without sacrificing competitive qualities.

Cite This Article

APA
Gartland KL, Leśniak K, Twigg-Flesner A. (2026). Fragile foal syndrome: manifestations, heterozygous advantage and the future of breeding policies. J Equine Vet Sci, 159, 105816. https://doi.org/10.1016/j.jevs.2026.105816

Publication

ISSN: 0737-0806
NlmUniqueID: 8216840
Country: United States
Language: English
Volume: 159
Pages: 105816
PII: S0737-0806(26)00052-3

Researcher Affiliations

Gartland, K L
  • School of Hartpury University, Hartpury Gloucester, Gloucestershire, GL19 3BE, England, UK. Electronic address: gartlandkirsty@hotmail.com.
Leśniak, K
  • School of Hartpury University, Hartpury Gloucester, Gloucestershire, GL19 3BE, England, UK.
Twigg-Flesner, A
  • School of Hartpury University, Hartpury Gloucester, Gloucestershire, GL19 3BE, England, UK.

MeSH Terms

  • Horses
  • Animals
  • Horse Diseases / genetics
  • Horse Diseases / pathology
  • Breeding
  • Heterozygote
  • Genetic Predisposition to Disease

Conflict of Interest Statement

Declaration of competing interest None of the authors has any financial or personal relationships that could inappropriately influence or bias the content of the paper.

Citations

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