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University
Joe
Equine Musculoskeletal Development and Performance: Impact of the Production System and Early Training . . . . . . 83
Chris Rogers, PhD
Massey University
Effect of Mare Nutrition and Management on the Development and Sports Career of Offspring and the Role of Epigenetics
Pascale Chavatte-Palmer, DVM, PhD
Université Paris-Saclay, France
Sport-Specific Musculoskeletal Injuries: Differences and Similarities
Chris Kawcak, DVM, PhD
Colorado State University
Omega-3 Index: Relevance for Human Health and Disease
William Harris, PhD
Fatty Acid Research Institute
Omega-3 Index: An Equine Perspective
Joe Pagan, PhD
Kentucky Equine Research
Introduction
Welcome to the 28th Annual Equine Health and Nutrition Conference, presented by Kentucky Equine Research. We are delighted you could join us!
True to tradition, we have assembled an outstanding lineup of cutting-edge topics and world-renowned speakers for the next two days. Kentucky Equine Research has followed the equine health and nutrition landscape for 38 years and understands well how dramatically it has transformed. Events like this conference keep our feed-manufacturing partners as well as industry leaders, farm managers, and veterinarians informed of important trends.
These proceedings serve as a conference companion, a curated collection of accessible Q&As. We asked our speakers targeted questions about their expertise, and they responded with their candid insights. We are deeply grateful to all speakers for their participation both at the conference and in creating this valuable resource.
About the Speakers
Pascale Chavatte-Palmer, DVM, PhD
Dr. Pascale Chavatte-Palmer earned her veterinary degree in France and specialized in equine reproduction and neonatology through internships, residencies, a doctorate, and postdoctoral fellowships in the United Kingdom, United States, and France. In 1998, she became a lecturer at AgroParisTech and studied fetal and postnatal development of cloned cattle at the National Institute of Agronomical Research (INRA). Since 2006, she has led the research team Placenta, Environment and Programming of Phenotypes, focusing on both agricultural and biomedical objectives. Her work aims to evaluate and improve the effects of maternal environment alterations on fetoplacental and postnatal development, using large animal species, including horses, as models. Dr. Chavatte-Palmer served on the board of the International Society for Embryo Transfer from 2009 to 2014 and was elected a member of the French Academy of Veterinarians in 2016.
Laurent Couetil, DVM, PhD, Diplomate ACVIM-LAIM
Dr. Laurent Couetil is a professor of large animal medicine at Purdue University. He obtained his veterinary degree from the French National Veterinary School of Alfort and subsequently worked for several years in private equine practice in France. Dr. Couetil completed a residency in large animal medicine at Tufts University and earned a doctorate in respiratory physiology from the University of Liège, Belgium. He has been a faculty member at the Purdue University College of Veterinary Medicine since 1995, where he serves as director of the Equine Research Program and the Donald J. McCrosky Equine Sports Medicine Center. He is the current president of the Large Animal Internal Medicine specialty of the American College of Veterinary Internal Medicine (ACVIM). His research focuses on the causes and treatment of poor performance in athletic horses, particularly equine asthma.
Aaron Ericsson, DVM, PhD
Dr. Aaron Ericsson earned his veterinary degree with honor from the University of Missouri College of Veterinary Medicine in 2006. After completing a three-year residency in the University of Missouri Comparative Medicine Program, he pursued a doctorate investigating interactions between the innate immune system and gut microbiota using mouse models of inflammatory bowel disease and colitis-associated colorectal cancer. He is the director of the University of Missouri Metagenomics Center and serves as lead scientist for microbiota research at the NIH-funded University of Missouri Mutant Mouse Resource and Research Center and Rat Resource and Research Center. His expertise includes animal models, metagenomics, mucosal immunology, and microbiology.
Carrie Finno, DVM, PhD, Dipl. ACVIM
Dr. Carrie Finno is an equine internist and associate professor of veterinary genetics, as well as the Gregory L. Ferraro Endowed Director of the Center for Equine Health at the University of California, Davis. She earned her veterinary degree from the University of Minnesota in 2004 and completed a three-year residency in large animal internal medicine at UC Davis. Dr. Finno focuses on translational genetic research, particularly inherited neuromuscular diseases. Her work investigates the interaction between vitamin E and neural development in naturally occurring equine diseases, using a well-established mouse model.
William S. Harris, PhD, FAHA
Dr. William Harris is an internationally recognized expert on omega-3 fatty acids and their benefits for cardiovascular health. He earned his doctorate in human nutrition from the University of Minnesota and completed postdoctoral fellowships in clinical nutrition and lipid metabolism with Dr. Bill Connor at Oregon Health Sciences University. His interest in omega-3s began during his postdoctoral work, when in 1980 he published his first study on the effects of salmon oil on serum lipids in humans.
Since then, he has received several NIH grants to study the effects of EPA and DHA on human health and has authored more than 300 publications on fatty acids. He is also a co-author of two American Heart Association scientific statements on fatty acids, “Fish Consumption, Fish Oil, Omega-3 Fatty Acids and Cardiovascular Disease” (2002) and “Omega-6 Fatty Acids and Risk for Cardiovascular Disease” (2009), both published in Circulation. Dr. Harris is a professor in the Department of Medicine at the Sanford School of Medicine, University of South Dakota, and serves as president and CEO of OmegaQuant.
Christopher Kawcak, DVM, PhD, DACVS,
DACVSMR
Christopher Kawcak received his veterinary degree and doctorate from Colorado State University. He is currently professor of orthopedics at Colorado State University and serves on a team of researchers working to find ways to prevent and treat catastrophic injuries in equine athletes. His work includes evaluating threedimensional imaging techniques, particularly MRI and CT, to detect early joint disease and microscopic injuries before they progress. In collaboration with biomedical engineers, his team has developed biomechanical models to assess individual risk factors, with implications for both equine and human bone and joint health. Dr. Kawcak specializes in equine orthopedics and sports medicine.
Rosanna Marsella, DVM, DACVD
Dr. Rosanna Marsella graduated from the University of Milano in Italy. After several years in private practice, she pursued specialty training in dermatology and became a board-certified dermatologist in 1996. She has been a faculty member at the University of Florida since 1997, where she is currently a professor. A horse lover and owner, Dr. Marsella has a special interest in equine dermatology. She has published extensively on equine allergies, particularly their diagnosis and treatment, and was the first to describe skin barrier defects in equine atopic dermatitis. Her research continues to focus on developing new therapeutic and preventative strategies.
Joe Pagan, PhD
Dr. Joe Pagan is the founder and president of Kentucky Equine Research, an international equine nutrition and exercise physiology company. He earned his master’s and doctorate degrees from Cornell University in equine nutrition and exercise physiology. Shortly after graduation, he formed Kentucky Equine Research and has been conducting innovative research for over 35 years at the flagship facility in Versailles, Kentucky, and at the Kentucky Equine Research Performance Center in Ocala, Florida. Kentucky Equine Research served as equine nutrition consultants for the last seven Olympic Games and several World Equestrian Games. He received the American Feed Industry Association (AFIA) Award in Equine Nutrition Research in 2005, an honor that recognizes excellence in equine nutrition research and the contributions of an individual to equine feeding management practices and the equine feed industry. In 2025, Pagan was named a Fellow of the Equine Science Society.
Chris Rogers, MAgrSc, PhD
Dr. Chris Rogers is a professor at Massey University, where he teaches and conducts research spanning veterinary science, equine science, agricultural production systems, and sport science. He earned his doctorate in equine biomechanics from Massey University and was a Huygens postdoctoral fellow at Utrecht University, in the Netherlands, before returning to Massey University as faculty. His research interests mirror his interdisciplinary teaching, with a focus on how environmental and training stimuli influence tissue development and career longevity in racehorses and sport horses.
Stephanie Valberg, DVM, PhD, DACVIM, DACVSMR
Dr. Stephanie Valberg is a pioneer in understanding and managing equine neuromuscular disorders in horses. Her research has transformed equine clinical practice and has led to the discovery of previously unknown muscle disorders, the identification of their genetic basis, and the development of nutritional strategies to minimize muscle pain. She worked with Kentucky Equine Research to develop the first feed used to reduce the incidence of tying-up and was a member of the team that sequenced the equine
genome. She was named the Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University’s College of Veterinary Medicine in 2015 and remained in that position until she retired in 2022. She mentored more than 60 graduate students, interns, residents, and postdoctoral students. She is widely published and is a recipient of numerous awards for teaching and mentorship. In 2012, she became the first woman to be inducted into the University of Kentucky Equine Research Hall of Fame and twice received the Pfizer Research Excellence Award.
Muscle Atrophy in Horses: Causes and Cures
Stephanie Valberg, DVM, PhD
Can you give a brief biographic sketch, especially as it pertains to your experience with this topic?
My initial experience with the importance of muscle mass came as a three-day eventer. Our horses needed to build the right muscles to achieve self-carriage for dressage, strength and coordination for show jumping, and balance and stamina for cross-country courses. There were few specifics for monitoring or measuring this when I was a young rider.
My introduction to muscle atrophy came from treating horses in veterinary practice. While some causes of atrophy were straightforward, many required in-depth research to identify their origins and determine the most effective management strategies. My philosophy has always been this: you have to understand the cause and pathophysiology to develop targeted treatments.
How do you define muscle atrophy?
We often think of muscle as a permanent structure. However, after 10–14 days, about 50% of the original contractile proteins have been replaced with new proteins. Muscle atrophy is a decrease in muscle size that occurs when muscle protein breakdown surpasses new protein production, leading to reduced muscle mass.
How do you diagnose atrophy?
Muscle atrophy is diagnosed by visually inspecting a horse standing square and comparing the symmetry from right to left side and the amount of muscle a horse has relative to either what was there previously or what one would expect from a horse of that breed at that level of performance.
What disorders cause muscle atrophy?
Muscle mass is maintained by constant nerve stimulation of muscle fibers, which creates muscle tone and contractions. Both the nerve connection and muscle fiber must be healthy to prevent atrophy.
Neurogenic causes of atrophy can include a focal loss of muscle from damage to a specific nerve due to trauma or compression of the nerve. Equine protozoal myeloencephalitis (EPM) can cause focal atrophy due to damage to the nerve’s origin in the spinal cord. Generalized muscle loss due to diseases within the central nervous system also affect muscle mass. One example is equine motor neuron disease (EMND), similar to amyotrophic lateral sclerosis (ALS) in humans.
Muscle atrophy can also be due to myogenic causes, e.g., alteration in the muscle’s ability to produce enough protein to maintain a normal muscle mass. Myogenic causes include:
1. Disuse: constant contractions are needed to maintain muscle mass.
2. Nutrition: insufficient caloric or protein intake; vitamin E deficiency can cause a reversible vitamin E-responsive myopathy.
3. Malabsorption: horses with intestinal malabsorption may not absorb adequate calories and vitamin E, even when supplied in adequate amounts in the diet.
4. Metabolic: Pars pituitary intermedia dysfunction (PPID) due to excessive production of corticosteroids, which reduces type 2 muscle fiber size and potentially number; any disease that increases metabolic rate such as severe systemic disease or cancer can cause atrophy.
5. Immune mediated: Quarter Horses inheriting myosin heavy chain myopathy.
6. Older horses homozygous for type 1 polysaccharide storage myopathy.
7. Myofibrillar myopathy.
8. Severe muscle damage that results in scarring rather than muscle fiber regeneration.
9. Rare congenital myopathies.
Does chronic administration of corticosteroids cause atrophy?
This very much depends on the dose and the method of administrations (inhalation, intraarticular, oral). It is not usually an issue in clinical practice.
What is sarcopenia? Is it treatable?
Sarcopenia is a progressive loss of muscle mass, strength, and function, commonly occurring with aging. To avoid sarcopenia, exercise and proper nutrition are important. High-quality nutrition with adequate protein and vitamins, particularly vitamin E, is important but exercise, particularly exercise that requires strength training, is essential.
Are atrophy and myotonia the same? If not, explain the difference.
Atrophy is the loss of muscle mass; myotonia is a disorder of the electrical conduction system in the muscle that causes abnormal sustained muscle contractions. One form, myotonia dystrophica, is seen in young foals with large and often dimpled muscles, and these foals, if they live long enough, can subsequently develop muscle atrophy.
How is atrophy treated?
Atrophy is treated by identifying the underlying cause of the atrophy and then targeting treatment for that specific cause. Diet has an impact in that horses need adequate calories to prevent them from breaking down muscle for fuel. In addition, horses need adequate amino acids to synthesize the proteins that they turn over every day. Branched-chain amino acids such as leucine are particularly important because they are major activators of the mTOR signaling pathway, which stimulates muscle protein synthesis.
It is also important that diets provide adequate amounts of the most limiting proteins in the diet such as lysine. Vitamin E plays a key role in maintaining muscle mass.
Chronic deficiency can lead to EMND, which disrupts the connection between nerves and muscles, and results in significant generalized atrophy. Shorter term vitamin E deficiency impacts mitochondria in muscle and potentially gene transcription, resulting in weakness and muscle atrophy that can be reversed by providing adequate levels of vitamin E.
What happens when an athlete is affected?
It is extremely important to monitor muscle mass in athletes. If we see horses every day, we may miss subtle signs of muscle atrophy, which impacts their strength. For example, a 5–10% reduction in muscle mass usually produces measurable decreases in strength, even if not clinically obvious. A 10–20% reduction in muscle mass clearly impairs strength.
If the specific muscles needed to perform a specific movement are weak, then other muscles may take over and become strained. The lack of strength and pain from muscle strains impacts the ability to perform.
Do you use any scoring system when evaluating muscle atrophy? If so, can you explain it? If not, how do you determine if treatment is working?
There are several scoring systems that are used for research studies. We developed a handheld three-dimensional scanner that accurately assesses muscle mass. Although muscle mass strongly influences performance, there is currently no effective means to measure the three-dimensional muscle mass of horses. We evaluated a three-dimensional scanning methodology for its ability to quantify torso and hindquarter volumes as a proxy for regional muscle mass in horses. We set out to determine the repeatability of three-dimensional scanning volume measurements and their correlation to body weight, estimated body volume, and muscle/fat ultrasound depth.
Handheld three-dimensional photonic scans were performed on 16 Quarter Horses of known body weight 56 days apart (n = 32 scans) with each scan performed in duplicate (n = 32 replicates).
Tailhead fat, gluteal, and longissimus dorsi muscle depths were measured using ultrasound. Processed scans were cropped to isolate hindquarter (above hock, caudal to tuber coxae) and torso (hindquarter plus dorsal thoracolumbar region) segments and algorithms used to calculate volume.
The handheld three-dimensional scan provided a rapid repeatable assessment of torso and hindquarter volume strongly correlated to body weight and estimated volume. Superimposition of regional scans and volume measures could provide a practical means to follow muscle development when tailhead fat depth remains constant.
Here is the entire citation: Valberg, S.J., A.K. Borer Matsui, A.M. Firshman, L. Bookbinder, S.A. Katzman, and C.J. Finno. 2020. 3 dimensional photonic scans for measuring body volume and muscle mass in the standing horse. PLoS ONE 15(2): e0229656. https://doi.org/10.1371/journal.pone.0229656
Others use various systems for scoring muscle atrophy, such as:
Herbst, A.C., M.G. Johnson, H. Gammons, S.E. Reedy, K.L. Urschel, P.A. Harris, and A.A. Adams. 2022. Development and evaluation of a muscle atrophy scoring system (MASS) for horses. Journal of Equine Veterinary Science 110:103771.
Pallesen, K., K. Gebara, C. Hopster-Iversen, and L.C. Berg. 2023. Development of an equine muscle condition score. Equine Veterinary Education 35(8):e550-562.
Urbanek, N., and Q. Zebeli. 2023. Morphometric measurements and muscle atrophy scoring as a tool to predict body weight and condition of horses. Veterinary Sciences 10(8):515.
Does regular photographing of horses help?
In practice, photos of horses taken with them standing square from several angles including front and sides can be of help to regularly monitor horses, but photos often do not often capture the degree of atrophy because of shadows.
The Role of Vitamin E in Equine Neuromuscular Disease
Carrie Finno, DVM, PhD
Can you give us a brief biographical sketch, especially as it relates to your work with vitamin E?
I am an ACVIM-boarded equine internist who pursued a career in comparative genetics and genomics. I have a strong commitment to biomedical research in the field of inherited neuromuscular disorders in the horse. The focus of my research is the interplay of vitamin E and neurodegeneration in the horse, and I also use mouse models to understand how vitamin E is neuroprotective across species.
Why is vitamin E so critical to muscle health in horses?
Vitamin E is a potent antioxidant that protects muscle membranes from free radical damage and supports muscle mass maintenance. While providing high doses of vitamin E will not necessarily aid in muscle repair after intense exercise, a vitamin E deficiency can have detrimental effects on performance in some horses.
What muscle disorders are associated with vitamin E deficiency? Can you differentiate these: neuroaxonal dystrophy/degenerative myeloencephalopathy, vitamin E responsive myopathy, and equine motor neuron disease? Are there other important vitamin E-related diseases?
Equine motor neuron disease (EMND):
1. Age of onset: adult, median age 10 years
2. Clinical signs: muscle wasting and fasciculation, abnormally low head carriage, prolonged recumbency
3. Effect of treatment with vitamin E: 40% of cases improve, 40% of cases stabilize but remain disfigured, 20% progress
3. Effect of treatment with vitamin E: supplementation will not improve affected horses but can prevent eNAD/EDM in susceptible horses
Vitamin E responsive myopathy (VEM):
1. Age of onset: adult
2. Clinical signs: muscle wasting and fasciculation, abnormally low head carriage
3. Effect of treatment with vitamin E: affected horses can recover within three months
Why are horses today at higher risk for vitamin E deficiency?
Most horses today do not have at least 12 hours/day access to green pasture for at least 6 months out of the year. This is how horses naturally maintain normal vitamin E concentrations. The potency of vitamin E declines very quickly once forages are harvested and dried (i.e., hay). Additionally, the vitamin E that is found in grain is synthetic (all-rac-alpha-tocopherol), and therefore very poorly bioavailable in horses.
How is vitamin E status assessed?
A deficiency of whole-body vitamin E is typically assessed by measuring blood (serum or plasma) concentrations of vitamin E, with normal equine concentrations >2 µg/mL at most laboratories.
Whether or not a deficiency of vitamin E has an impact on health depends upon individual genetic factors, the temporal occurrence of deficiency during development, and the duration of deficiency.
Why are foals and young horses particularly vulnerable?
Across species, there is a need for vitamin E early in life for normal development of the nervous system. Specific neural tracts require vitamin E early in life.
When is vitamin E supplementation necessary?
For any horse with a deficient serum/plasma vitamin E level, vitamin E supplementation is recommended whether the horse has signs of neuromuscular disease or not.
Are all vitamin E supplements equally effective?
The type and formulation of vitamin E supplements have a major impact on their bioavailability. Natural vitamin E, RRR- or d-alpha-tocopherol, is more bioavailable than synthetic vitamin E and therefore many equine supplements now strongly market the “natural” (i.e., RRR or d) form. Natural formulations are available as esterified forms (d-tocopheryl acetate) to prolong shelf life (i.e., powder or pellet) or water dispersible (i.e., liquid) formulations with higher biopotency.
The natural powder/pellet form of vitamin E may have less bioavailability because the ester must be removed, and the alpha-tocopherol made water-dispersible by the action of bile salts (micellization). In contrast to the natural powder/pellet vitamin E, the liquid formulation leads to a more rapid increase (within 24 hours) in serum vitamin E concentrations in horses. Both formulations are useful for equine practice and selection of the appropriate formulation will depend upon whether vitamin E supplements are being used to prevent deficiency, to treat a deficiency, or to treat a disease associated with vitamin E deficiency.
How much vitamin E should be supplemented?
The amount of vitamin E supplemented will depend on the type used and the baseline serum/plasma level of vitamin E in that horse. In general, for horses with one of the aforementioned disorders, 5,000 IU for a 500-kg horse per day is appropriate in either the natural liquid or natural powder/pellet formulation,
but rechecking vitamin E concentrations is strongly recommended after starting a supplementation program.
Why do some horses fail to respond to supplementation?
There are some horses that may not absorb fat-soluble vitamins well and these horses could have a treatment failure. It is important to have a veterinarian involved in establishing what the underlying cause could be.
Can horses receive too much vitamin E?
In humans, high doses of vitamin E interfere with vitamin K metabolism and can lead to prolonged bleeding (i.e., failure to clot). It is unclear whether the same phenomenon occurs in horses, but we are currently doing a study to investigate this.
What is the most effective long-term strategy for maintaining adequate vitamin E status?
Maintain horses on irrigated pasture for at least 12 hours a day for at least 6 months out of the year, if possible. This would be a top priority for broodmares and foals. For competition horses that do not receive this type of turnout, monitoring vitamin E concentrations and supplementing appropriately is warranted.
Can you explain what nutrigenomics means in simple terms?
What are some established examples of nutrigenomics in horses?
Nutrigenomics is a term that defines the interaction between the genome, nutrition and overall health. Put simply, it is how each of us responds to our diet.
In horses, there are currently two genetic diseases for which the phenotype is strongly influenced by diet. These are hyperkalemic periodic paralysis (HYPP) and type 1 polysaccharide storage myopathy (PSSM1). In horses affected with HYPP, which is due to a missense mutation in a sodium channel gene, a diet low in potassium can prevent episodes of cramping and muscle fasciculations. With PSSM1, diets low in carbohydrates and high in fat have been shown to decrease episodes of exertional rhabdomyolysis.
Why focus on vitamin E specifically regarding nutrigenomics?
In humans and in horses, there appears to be wide variability in the response of an individual to vitamin E supplementation. In humans, they have identified many DNA changes that explain this, and we are just starting to investigate this in horses.
Can you walk us through a case study?
To highlight the impact of individualized nutrition as it relates to vitamin E intake, let’s discuss an 8-year-old Percheron gelding that was presented to University of California Davis School of Veterinary Medicine for severe muscle wasting, weight loss, and inability to back up. Muscle wasting extended to all muscle types but was most pronounced along the topline and hindquarters. There was no evidence of ataxia, or incoordination, on the neurologic examination. However, the gelding displayed lower motor neuron weakness, with tremoring of the thoracic and pelvic limbs, which worsened when he was asked to pick up a foot or move backwards.
What were the diagnostic findings?
Blood was collected for serum vitamin E assessment, and muscle biopsies of the tailhead and gluteal muscles were collected and evaluated by Dr. Stephanie Valberg. The tailhead muscle had microscopic changes supportive of a diagnosis of vitamin E responsive myopathy (VEM). Serum vitamin E concentrations were 2 µg/mL, which is considered the low end of the normal reference range (2-6 µg/mL).
What was the treatment approach?
The gelding was started on 10 IU/kg of water-dispersible vitamin E orally once daily for three weeks. Dramatic improvements in his coat color, muscling, and gait were noted. The gelding was able to pick up his feet and walk backwards without trembling.
Did you try adjusting the dose?
A repeat serum vitamin E concentration revealed a very high vitamin E concentration (8 µg/mL). The dose of vitamin E was reduced to 5 IU/kg orally once daily; however, within 3 days, clinical signs of trembling returned. The dose of vitamin E was promptly increased to 10 IU/kg (i.e., the original dose) and the gelding’s trembling resolved within two days.
What is the broader significance of this case?
This case is an example of a horse that requires a higher serum vitamin E concentration to prevent neuromuscular disease. Horses with VEM often have normal to high serum vitamin E concentrations, yet their muscles are deficient in vitamin E and dramatically respond to supplementation. This gelding likely has an underlying genetic cause for this higher requirement of vitamin E that has yet to be identified.
Beat the Heat: Nutrition and Heat Stress
Joe Pagan, PhD
Can you lay the groundwork for understanding heat stress in horses?
All performance horses have one thing in common: locomotion. All locomotion involves muscle contraction, and all muscle contraction produces heat. Eighty percent of the energy consumed by most performance horses is released as metabolic heat; other performance horses, such as racehorses, have even greater heat loss, as much as 7% more.
When a horse is exercising, its body is initially most concerned with delivering oxygen to the muscles and not with removing heat. As a result, muscle temperature rises rapidly. Once a horse’s muscle temperature exceeds about 108° F (42° C), problems begin to occur. Bottom line: exercising horses generate large quantities of heat in their muscles. Once the exercise stops, the horse can start to cool itself.
How does a horse cool itself?
The horse uses several mechanisms to cool itself. Some heat is lost through convection as air moves past the body.
Convection and evaporation also occur in the lungs as hot air is exhaled and cooler air is inhaled. Increased respiratory rate means heated air (as hot as 100-105° F, or 38-41° C) is expelled more quickly and replaced by cooler air. A high respiratory rate can dissipate up to about 25% of the metabolic heat produced during normal exercise. This is relatively low compared to some other mammals; for example, dogs dissipate most of their excess heat through panting.
Horses rely on sweating as their main natural cooling strategy. In fact, horses are the grand champions of sweating, with some performance horses losing 10-15 liters per hour during longduration exercise.
Surprisingly few other species sweat significantly. Horses are heavy and, relative to their mass, do not have a large surface area, so they need an efficient way to move heat from the blood to the skin and then from the skin to the environment.
About 70-75% of the heat produced by an exercising horse can be lost through evaporation of sweat when humidity is low. As humidity increases, the effectiveness of sweating as a cooling mechanism diminishes.
Why are horses such good sweaters?
Horses actively pump electrolytes into their sweat glands, and water follows passively via osmosis. The more electrolytes secreted, the more water follows, and the more profusely the horse sweats. Unlike humans, who also cool through sweating, horses do not resorb electrolytes in their sweat glands. This strategy has trade-offs. The primary advantage is the ability to produce large volumes of sweat for efficient cooling, whereas the disadvantage is the substantial concurrent loss of electrolytes.
Explain the importance of electrolytes in the horse.
Electrolytes are minerals that dissociate in solution into electrically charged ions. The primary ones in equine sweat and blood are sodium, chloride, and potassium. Equine sweat is higher in electrolytes compared to human sweat.
Horses “turbocharge” sweating by sacrificing electrolytes, but this creates a significant problem: horses need electrolytes for far more than sweating. Electrolytes help maintain osmotic pressure, fluid balance, nerve function, and muscle contraction.
When horses sweat heavily during exercise, sodium, chloride, and potassium are lost in large quantities, which can cause fatigue, muscle weakness, and decreased thirst response. Evolution prioritized exceptional sweat production over electrolyte conservation.
Key problems with equine sweat include (1) remarkable electrolyte loss reduces critical physiological functions; (2) salty sweat evaporates less efficiently than pure water, and (3) combined water and electrolyte loss suppresses thirst, potentially worsening dehydration.
Sweat only cools effectively when it evaporates. Evaporation removes tremendous amounts of heat from the body. When sweat merely drips off, cooling is minimal.
If you see sweat dripping off a horse, consider it a red flag, as the horse has failed to cool itself properly. Dripping sweat provides only 5-10% of the heat loss achieved through skin evaporation.
However, horses have a sophisticated adaptation to prevent this: a protein called latherin creates a bubbly foam on the coat that acts as a surfactant, dramatically enhancing evaporation efficiency. Latherin breaks the surface tension of the water so the sweat spreads out over the hair in a thin film rather than staying in droplets. This increases surface area for evaporation.
How do you determine how much sweat and electrolytes are lost?
Three key factors determine sweat and electrolyte losses.
1. Exercise intensity and duration: Harder, longer work equals greater losses.
2. Environmental conditions: Higher temperatures and higher humidity equal more sweating.
3. Acclimatization status: Unadapted horses sweat more and lose more electrolytes initially; as acclimatization increases, horses sweat more efficiently.
When horses sweat heavily, electrolyte replacement is essential. How do you replace lost electrolytes?
The simple answer is targeted electrolyte feeding. We developed products that mimic equine sweat composition. Our latest allpurpose formula adds a key innovation: encapsulated sodium chloride.
Electrolytes are rapidly excreted in urine, but encapsulation slows sodium release, ensuring longer-lasting absorption and efficacy. This delivers optimal electrolyte replenishment for performance horses.
Moving on to managing hot horses, what are the most effective ways to cool a horse?
Equine heat stress research surged in the leadup to the 1996 Olympic Games. Set for July in Atlanta’s sweltering heat and humidity, the Games reignited concerns first raised at the 1992 Barcelona Olympics, where horses struggled in similar conditions. This massive research effort yielded critical insights into managing equine thermoregulation. The topic resurfaced for the 2020 Tokyo Olympics, another hot, humid venue.
To add to this research, the Japan Racing Association’s research branch conducted a key treadmill study, exercising horses until muscle temperature reached 107° F (42° C). They then tested five cooling methods: a control with no additional cooling; two fans placed 4 meters ahead creating a 3 m/s backward airflow; intermittent cold-water (50° F, 10° C) application every three minutes over the body (excluding head and neck) with scraping; the same intermittent cold-water application but without scraping; and a continuous 30-minute “standing wash” or “mega-shower” with 79° F (26° C) tap water.
The horses cooled fastest with the standing wash, followed by intermittent cold water without scraping, then cold water with scraping, fans, and finally the control group, which was slowest to recover.
How do you measure muscle temperature?
Understanding heat production and dissipation rates is crucial for managing performance horses. Until recently, studying this was impractical due to invasive instrumentation needed to measure muscle or core body temperature.
Thermal-sensing microchips have changed the game. These chips are no larger than standard ID microchips, which are typically implanted in the nuchal ligament.
Thermal-sensing microchips track real-time muscle temperature. A University of Queensland research group validated thermalsensing microchips by implanting them in various muscles and correlating readings with core body temperature. They found the gluteal muscle (along the croup) and pectoral muscle (chest) provided the most accurate measurements.
We implanted thermal-sensing microchips into 28 Thoroughbreds used in exercise studies at our Florida and Kentucky farms. With a simple wand scan, we obtain real-time temperature readings from both muscle sites, even during racetrack exercise and high-speed treadmill work.
These microchips have enabled us to investigate multiple factors affecting post-exercise cooling rates: total accumulated heat load, ambient temperature, relative humidity, fitness level, nutrition, sweat production, and cooling methods.
We monitor heart rate and respiratory rate in addition to muscle temperatures to gain a comprehensive understanding of equine thermoregulation.
Has this work with microchips yielded any surprises?
Yes. One surprise was how slowly muscle temperature declines following exercise. We expected muscles to cool rapidly after exercise, but peak temperature occurred after maximal effort, during the treadmill cooldown. Even after hand-walking, muscle temperature remained elevated one hour after exercise, higher than pre-exercise levels. This was shocking.
These findings prompted us to test cooling methods in a series of trials. Water proved dramatically superior to air. Water conducts heat away from a horse’s body 25 times more effectively than air. In one Ocala study comparing walking alone versus hosing and walking, five minutes of hosing significantly accelerated cooling, as measured by muscle temperature.
In another study, also performed in Ocala, we compared three cooling protocols: five minutes of hosing followed by 10 minutes of walking, 10 minutes of walking followed by five minutes
of hosing, and 15 minutes of walking with no hosing. Hosing proved effective regardless of whether it preceded or followed walking, but respiration rate dropped fastest with the initial five-minute hosing followed by walking.
We followed up in Kentucky by sponging horses with 7.5 gallons of water over five minutes and comparing this to standard hosing plus walking. Sponging large water volumes proved equally effective for cooling.
To add to our knowledge, in an Ocala study, we compared cooling techniques for eight two-year-old Thoroughbreds after a onemile training gallop on a day that was 73° F (23° C) with 67% relative humidity, when heart rates peaked at 200 bpm. We tested four protocols: hosing for five minutes followed by 10 minutes of walking, then stalling with a fan and water; 10 minutes of walking followed by five minutes of hosing, then stalling with a fan and water; 15 minutes of walking followed by stalling with a fan and water; or immediate stalling with a fan and water access but no walking.
Hosing made a tremendous difference in cooling speed, causing muscle temperature to drop three times faster than walking alone. Timing did not matter, as hosing before or after walking was equally effective.
How does body clipping affect cooling?
Body clipping makes a huge difference in cooling. A long winter coat acts as insulation, trapping heat against the horse’s body. In a Kentucky study with unclipped horses during cool weather (30–40°F, -1-4°C), reasonably fit horses performed a standardized exercise test. Coolers made little difference because the thick hair coat prevented effective cooling regardless.
When we repeated the study with hosing and scraping, it helped somewhat, but recovery remained slow. The insulative hair coat fundamentally limited heat dissipation.
Have you tried cooling in any other ways?
Yes, we tested misting water, specifically on horses cooling out on an automated walker equipped with built-in irrigation nozzles. Walking alone dissipated 15% of heat, but hosing followed by misting on the walker increased heat loss to 40%.
This is not new, as misting fans debuted at the 1996 Atlanta Olympics and have since become standard at major international equestrian venues.
In short, what’s the most effective way to cool a horse?
1. Continual hosing (moving water is best, tap water or cold water)
2. Misting fans
3. High-velocity fans
Stale air is the enemy of the hot horse. The air needs to get away from the horse.
What about acclimatization of horses to heat?
An interesting study done in the Netherlands right before the last Olympics studied the effect of a 14-day period of heat acclimation on horses using heated indoor arenas. At that time of year, the average temperature in the Netherlands is 65° F (18° C). Three Olympic event horses and one Paralympic horse participated in the study. The horses were worked in an indoor arena with a temperature of 90° F (32° C) for 90 min/day.
The researchers found that after 14 days, the horses had lower heart rates, rectal temperatures, and lactate concentrations, plus delayed peak rectal temperatures. They showed that it is possible to acclimate horses, but they must train in the heat.
What are some beneficial nutritional recommendations while acclimatizing a horse to a hotter environment?
Start on a high-quality electrolyte supplementation right away. Check vitamin E status and aim for a serum level of 4 µg/mL (normal is considered 2-5 µg/mL). If low, supplement with a
natural-source, highly bioavailable source of vitamin E. Perform daily exercise in heat for two to three weeks before peak performance.
What nutrients affect cooling?
One of the great things about research is that we occasionally stumble onto unexpected findings. This is a perfect example. We designed an exercise study to look at a polyphenol product in which eight fit horses that were all fed the same amount of vitamin E and selenium performed a standardized exercise test on a high-speed treadmill. Importantly, this exercise test was more intense than we usually conduct (an hour-long test that included a 10 m/s gallop), and the horses got quite hot. We then assessed how well they cooled.
While the polyphenol positively affected some parameters related to oxidative stress, we also discovered something unrelated to the polyphenol. Seven of the eight horses fell into two distinct groups, which we termed the HOT phenotype (three horses) and the COOL phenotype (four horses). Not only did the HOT horses accumulate more muscle heat, but they also had higher heart rates, lactate, and glucose concentrations following exercise compared to the COOL horses. The HOT horses also took longer to recover. Surprisingly, the HOT horses had much lower serum vitamin E levels both before and after exercise. Additionally, HOT horses had significantly less whole blood selenium than cool-phenotype horses.
Since the HOT horses also had elevated blood biomarkers related to oxidative stress, we concluded that horses in the HOT group used more vitamin E than those in the COOL group because their muscles became hotter and produced more reactive oxygen species (ROS), thereby placing greater demand on antioxidant stores, including vitamin E and selenium.
A year later, we revisited these horses and supplemented the horses in the HOT group with 5,000 IU of vitamin E for 70 days. They completed the same standardized exercise test.
Environmental conditions were cooler and drier, so the horses did not get as hot overall as in the first study, but we still detected differences in muscle temperature between the two groups. Although the HOT group still got hotter than the COOL group during exercise, their recovery kinetics improved after vitamin E supplementation compared to the COOL group.
Restoring vitamin E does not necessarily keep hot-phenotype horses from getting hotter during exercise, but it does help them cool more quickly following exercise.
What explains the “hot phenotype”?
The exact mechanism remains elusive. At the mitochondrial level, hot-phenotype horses might generate excessive heat per ATP produced, possibly due to greater anaerobic metabolism, which is supported by their higher post-exercise lactate, or reduced mitochondrial efficiency. However, when we supplemented vitamin E and horses still reached similar peak temperatures, the improvement occurred during recovery, not during exercise.
This points to impaired heat dissipation. Effective muscle cooling requires redirecting blood flow from muscle to skin following exercise. We hypothesize oxidative stress from low vitamin E impairs vasodilation, trapping heat in the muscles.
The core mystery persists: Why do hot-phenotype horses accumulate heat initially? Poor cutaneous perfusion during exercise might prevent heat removal as it builds, creating a vicious cycle. Vitamin E supplementation appears to restore this heat-dissipation mechanism during recovery.
Research in other species has shown that oxidative stress disrupts this pathway. Nitric oxide is rapidly degraded by reactive oxygen species. This potentially explains impaired heat dissipation in HOT horses. Chronic vitamin E supplementation for 70 days in our study may have protected nitric oxide bioavailability. It also may have repaired oxidatively damaged endothelium, restoring efficient cutaneous perfusion.
What other nutritional interactions affect cooling?
We investigated different fat sources through isocaloric amounts of soybean oil, canola oil, and stabilized rice bran using standardized exercise tests. Horses fed rice bran generated less gluteal muscle heat during exercise and produced significantly lower lactate compared to the other groups. This aligns with our 1990s findings showing rice bran outperformed corn oil for lactate clearance.
These results are preliminary. We maximized standardization but could not use the same horses due to the study’s longitudinal design. Statistically significant differences in lactate and muscle temperature warrant further investigation.
Possible mechanisms include rice bran’s antioxidant properties, from gamma-oryzanol, for example, or effects on cutaneous perfusion during or after exercise. Rice bran affected heat production during exercise, unlike vitamin E, which facilitated post-exercise cooling.
Where will the research lead now?
More research is certainly needed to determine vitamin E’s role in improving cooling after exercise. Does nitric oxide play a role and how does oxidative stress affect long-term performance?
We also plan to develop vitamin E dosing guidelines based on heat production and create more appliable field recommendations. We hope to repeat the rice bran study in a switchback design with identical horses, though long washout periods and seasonal variation present challenges.
Additionally, we continue evaluating vitamin E product bioavailability, especially under heat stress conditions and with different levels of oxidative stress. No one currently recommends heat-adjusted vitamin E dosing, and this work could change that practice.
The Role of the Gut Microbiome in Horse Health and Disease
Aaron Ericsson, DVM, PhD
Can you give us a brief biographical sketch, highlighting your work with the gut microbiome?
After obtaining my veterinary degree, I pursued a residency in comparative medicine and a doctorate in veterinary pathobiology focused on the influence of gut microbes on inflammatory bowel disease and colorectal cancer. As a junior faculty member at the University of Missouri, I joined the NIH-funded Mutant Mouse Resource and Research Center (MMRRC) as a co-investigator, overseeing applied research investigating the gut microbiome as an independent and dependent variable in animal models used in biomedical research. I also established the University of Missouri Metagenomics Center in 2014, providing collaborative and fee-for-service molecular microbiology services to internal and external researchers. Lastly, research performed in my own lab is focused on the intergenerational effects of the parental gut microbiome on offspring development.
As part of the Equine Gut Group, you were involved in a landmark study that involved thousands of equine fecal microbiome samples. Can you tell me how this project came about, especially the multiregional nature of it, and its objectives?
The project began very organically as a collaboration with Dr. Philip Johnson, then head of the equine internal medicine service at University of Missouri. We were initially interested in colic, but soon realized that we would need a considerable sample size to produce meaningful data. Along with factors like diet and use, we were concerned about more subtle variables that might influence the microbiome, such as breed, geography, or season.
Rather than controlling for these variables, we decided to throw out all exclusion criteria and simply collect as many samples as possible, from horses admitted to the MU Veterinary Health Center (VHC) for any reason.
When possible, we also collected samples daily during their stay in the VHC.
To address the question of geography, we first reached out to several clinicians at other U.S. veterinary teaching hospitals, inquiring whether they would be willing to provide samples and patient data as part of a collaboration. Eventually we would receive samples from Dr. Heidi Banse (then at Louisiana State University, now at Arkansas State University), Dr. Kara Lascola (Auburn University), Dr. Emily Barrell (University of Minnesota), and Dr. Anthony Blikslager (North Carolina State University). At the end of 2019, I reached out to several clinicians at veterinary teaching hospitals in other countries.
Somehow, during the height of the pandemic, we were able to arrange shipment of multiple boxes of equine feces from the Universities of Queensland and Sydney in Australia, and the University of Liverpool in the U.K. Ultimately, we have now collected over 2,400 samples from over 1,200 individual horses. The objectives are to identify reliable markers of health and specific conditions in the equine microbiome, and to provide the foundation for a growable database that can be used by the research community.
Briefly describe the demographics of the horses involved and a layman’s perspective of study methods.
The horses in the study were admitted to one of eight veterinary teaching hospitals, between 2015 and 2022. There are roughly equivalent numbers of mares and geldings, and much fewer fillies, colts, and stallions, plus one or two jenny and jack samples. We have samples from week-old foals, seniors in their 30s, and everything in between; samples from over 50 different horse breeds; and samples from healthy horses, and horses affected by gastrointestinal, orthopedic, respiratory, or one of 10 other disease categories.
In layman’s terms, we analyzed and compared the fecal DNA from horses affected with colic and other conditions, and healthy controls, to identify features of the microbiome that can be used as diagnostic, prognostic, or therapeutic tools.
Let’s dig into the findings. What were some environmental factors that influenced the microbiome?
Collectively, the data indicate that country, age, and diagnosis (i.e., health condition) had the greatest overall effects on microbiome composition, while month of the year and breed type also had detectable effects. Within the healthy horses, we were able to isolate the effect of each variable on specific bacterial families, often replicating findings from prior studies.
Explain the idea of leveraging microbiome data to predict gastrointestinal disease? What connections were made between the microbiome and high-interest diseases like colic and gastric ulcers?
Ultimately, I envision a clinical assay based on the fecal microbiome that could help diagnose colic and other gastrointestinal conditions or provide information on the severity of disease.
The methods we used to analyze the fecal microbiome are not amenable to routine use in the clinics, but a subset of marker species within the microbiome can be exploited as targets for more rapid qPCR-based assays. This approach has been successfully implemented to diagnose and monitor canine and feline inflammatory bowel disease (IBD), and recent work from a group in Finland suggests it could work in equine IBD as well.
There were several interesting findings from the horses affected with colic in our study. First, while many horses admitted for colic showed different degrees of dysbiosis (changes in the microbiome associated with disease), many appeared completely normal. However, for horses remaining in hospital with unresolved colic, the richness and diversity of the microbiome (positively associated with health) decrease steadily over time. Lastly, we found that the degree of change over time depends on the type of colic, with inflammation or impaired motility both being associated with more severe dysbiosis.
Are there any other findings from this study that you would like to discuss?
It is worth mentioning that several other health conditions were also associated with significant changes in the microbiome.
For example, horses admitted for respiratory conditions or dental procedures both showed evidence of dysbiosis. The exact cause is unclear, but we speculate that the changes are associated with reduced dietary intake.
Can you provide the reference for this study?
McAdams, Z.L., E.J. Campbell, R.A. Dorfmeyer, G. Turner, S. Shaffer, T. Ford, J. Lawson, J. Terry, M. Raju, L. Coghill, L. Cresci, K. Lascola, T. Pridgen, A. Blikslager, E. Barrell, H. Banse, L. Paul, A. Gillen, S. Nott, M. VandeCandelaere, G. van Galen, K.S. Townsend, L.M. Martin, P.J. Johnson, and A.C. Ericsson. 2025. A novel dataset of 2,362 equine fecal microbiomes from veterinary teaching hospitals across three countries reveals effects of geography and disease. Animal Microbiome. 7(1):124. doi: 10.1186/s42523-025-00493-x.
You also created a full microbial map of the equine gastrointestinal tract rather than focusing solely on fecal samples. What prompted that?
Prior work in other species gave us very strong reason to believe that there would be differences between the upper and lower gastrointestinal tract (GIT) in microbial composition. Given the size and anatomy of the equine GIT, we wanted to assess the value of fecal material as a representative sample of the gut. For the same reason, matched samples were collected from the lumen and tissue mucosa at each site, including the dorsal and antral stomach, jejunum, ileum, cecum, and ventral and dorsal colon. Fecal material only gives part of the picture, and we wanted to characterize and highlight other regions of the gut, each with its own physiological relevance.
Why is understanding the healthy equine gut microbiota so important for clinical practice and disease prevention?
The gut microbiota has a significant influence on digestion and metabolism, immunity and colonization resistance against pathogens, cardiovascular health, neurodevelopment and cognition, and other physiological processes. Accordingly, disease is often associated with changes in the composition of the microbiota, either as a cause, consequence, or co-occurrence.
Depending on the relationship between the microbiota and the phenotype, it can be used as a diagnostic tool, biomarker, or target for preventative strategies.
Can you tell us about the differences in the microbiota of the upper and lower gastrointestinal tract. What factors do you think account for this difference?
The upper GIT is characterized by greater relative abundance of lactic acid bacteria (LAB), including Lactobacillus and Streptococcus, and Actinobacillus, a gram-negative genus within the family Pasteurellaceae. All of these are facultative anaerobes.
The hindgut is dominated by obligate anaerobes in the families Lachnospiraceae, Rikenellaceae, Oscillospiraceae, and an uncultured family of microbes named WCHB1-41 (phylum Kiritimatiellaeota), related to Akkermansia in humans and mice.
In our experience, the upper GIT microbiome shows much less inter-horse variability than the lower GIT microbiome. The microbiome of the upper and lower GIT differs markedly in most vertebrates, likely due to multiple factors reflecting the different functions of each region of the gut. One good example is glucose and other simple sugars, which are present at high levels in the upper GIT postprandially. LAB are highly efficient at fermenting simple sugars, as well as tolerating the slightly higher oxygen tension of the upper GIT. After absorption of glucose in the jejunum, the hindgut microbiome performs fermentation of complex polysaccharides that have reached the cecum and colon. Add to this the effects of pH, bile salts, innate immunity, and motility, and the differences become understandable.
Why do you think microbial populations in the stomach, jejunum, and ileum were so variable between horses?
That also likely reflects distinct functions associated with each compartment. The differences between the stomach and upper GIT are obvious, but the more subtle differences between duodenum, jejunum, and ileum likely reflect distinct features in each region such as Brunner’s glands in the duodenum and enhanced mucosa-associated lymphoid tissue and Paneth cells in the ileum.
In contrast, what might explain the remarkably consistent microbial communities observed in the cecum and colon?
This is speculation, but I believe the uniformity of the hindgut across healthy horses may reflect, at least partially, the much slower transit through the hindgut, giving microbial communities more time to reach a similar equilibrium.
Based on your experience, how reliable are fecal samples as indicators of microbial composition in the stomach or small intestine?
Fecal samples give limited information on the composition of the upper GIT. Feces may be useful in detecting the presence or absence of DNA from a specific taxonomy in the upper GIT, but it provides minimal information about the overall composition of the upper GIT microbiome.
What does this mean for clinicians who rely heavily on fecal testing for diagnosing GI disorders?
It underlines the importance of considering other regions of the gut in disease mechanisms. Feces are easy samples that can be collected noninvasively, but they don’t tell the whole story.
Work from other groups comparing the effects of high-fiber and high-starch diets on the microbiome in different regions of the horse gut showed more pronounced effects of diet on the upper GIT microbiome compared to the cecal and colonic microbiome. A surprising amount of fermentation occurs in the upper GIT and the hindgut-centric view of the gut microbiome needs to be expanded.
How could this mapping inform future approaches to diagnosing diseases such as colic, colitis, or metabolic syndrome?
Like the study mentioned above, the upper GIT should be included in outcomes, when possible. That being said, collection of such samples is incredibly challenging and typically requires postmortem collection. There are alternative capsule-based methods that have been developed for collection of upper GIT microbiome samples in adult humans, and I am eager to investigate their utility in horses or other large animals. The drawback is cost and the challenge of timing recovery of the capsule from the voluminous feces.
What potential do you see for microbiome-targeted therapies in horses—such as fecal microbiota transplantation (FMT)?
I think FMT has tremendous potential for specific conditions. FMT is typically indicated by some adverse health condition in the context of reduced microbial richness, often due to a known instigating factor (e.g., antibiotics, removal from pasture) but sometimes with no known cause. Assuming the causative factors have been removed, FMT can effectively restore the microbiome. Of course, if changes in the microbiome occur coincidentally with some adverse health condition due to some other primary etiology, FMT may provide transient benefit or no benefit at all.
Given the strong hindgut uniformity, what risks or benefits might occur when altering the hindgut microbiota with antibiotics or supplements?
We have found that even seemingly small doses orally of certain compounds can have immediate devastating effects on the entire hindgut microbiome. It almost seems impossible that such a large volume of biomass could be depleted so quickly and thoroughly, but certain antibiotics and other compounds (e.g., clioquinol) can do just that to the equine gut. Placed on pasture, horses will eventually return to something close to their original composition, but it can take time to rebound. During that time, colonization resistance is reduced, and horses are much more susceptible to pathogens in the environment. This may be inconsequential in a clean barn with only a couple horses, but can be problematic in the clinic or heavily populated barns. Regarding supplements, I am less concerned about deleterious effects.
What major questions remain unanswered regarding the upper GI microbiota in horses?
One of the greatest challenges is improved methods of noninvasively sampling the upper GIT microbiome. As mentioned above, there are multiple innovative methods developed in humans that could be translated to horses.
What would you most like to explore next—seasonal effects, geographic variation, or functional metagenomics?
Functional genomics are certainly of interest and something we have performed in rodent studies. Our lab has also begun developing comparable methods for the characterization of eukaryotic DNA, similar to environmental DNA (eDNA) analysis. I am particularly interested in greater resolution of the protozoal and fungal communities present in the equine gut. Several studies have found significant relationships between the protozoal and bacterial compartments of the microbiome in other hosts, and I would like to begin incorporating these different kingdoms in the equine gut.
Equine Asthma: New Insights in Origin and Management
Laurent Couetil, DVM, PhD
Can you give a brief biographical sketch, especially as it pertains to your experience with this topic?
I grew up on a small farm in Normandy, France, where my father bred, trained, and rode racehorses for steeplechase racing. Naturally, I began riding racehorses at an early age and later developed a strong interest in English riding, particularly show jumping and three-day eventing.
I completed my veterinary training at the École Nationale Vétérinaire d’Alfort and subsequently worked with Thoroughbred racehorses for six years at a veterinary clinic in Chantilly, France. During that time, I became fascinated by scientific publications originating from American universities. After working with a colleague who had recently returned from an internship in the United States, I decided to apply for a large animal medicine residency.
I was fortunate to match with Tufts University, where I worked with world-class investigators focused on equine sports medicine. Later, I worked with Dr. Andrew Hoffman, who introduced me to respiratory physiology and lung function testing. From that point on, I caught the “respiratory bug.”
Subsequently, I joined Purdue University to help establish its Equine Sports Medicine Center and completed a doctorate at the University of Liège in Professor Pierre Lekeux’s laboratory. My research has focused on identifying improved methods to diagnose and manage mild airway disease. I have been at Purdue University for over 30 years and continue to investigate respiratory causes of poor performance in horses, with a particular emphasis on equine asthma.
Can you provide a definition of asthma in horses? How does it differ from chronic obstructive pulmonary disease?
“Heaves” has been recognized for centuries as a cause of dyspnea and severe coughing in stabled horses fed poor-quality hay. In the 1970s, Sasse in Europe used the term chronic obstructive pulmonary disease (COPD) after demonstrating that affected horses exhibited neutrophilic airway inflammation and airway obstruction, similar to people with COPD. However, subsequent research showed that airway obstruction in affected horses could be markedly improved with bronchodilator or corticosteroid therapy.
In contrast, COPD in humans is primarily associated with tobacco smoke exposure and is characterized by nonreversible airway obstruction and a progressive decline in lung function over time. Consequently, Derksen and Robinson proposed the term recurrent airway obstruction (RAO) in the mid-1980s to describe horses with heaves.
Later, clinicians and researchers recognized that athletic horses were commonly affected by a milder form of chronic lower airway disease characterized by intermittent coughing, excess airway mucus, and poor performance. In the 1990s, the term inflammatory airway disease (IAD) was introduced to describe these horses, which typically have normal breathing at rest.
As knowledge of asthma pathophysiology evolved, it became clear that multiple asthma phenotypes existed, with striking similarities between some human and equine forms. In 2015, the term equine asthma was introduced to standardize terminology and define a spectrum of chronic airway diseases ranging from severe asthma (heaves or RAO) to mild–moderate asthma (IAD).
How prevalent is asthma?
Severe asthma (heaves or RAO) affects approximately 14% of horses in countries with a northern temperate climate. Mild–moderate asthma (IAD) affects horses worldwide, with the highest prevalence observed in racehorses, where up to 80–90% may be affected by mild, often subclinical, airway inflammation.
What are the clinical signs of asthma?
Horses with severe asthma exhibit markedly increased respiratory effort (dyspnea) and frequent coughing during disease exacerbations. Clinical signs typically resolve with therapy or appropriate environmental management, sometimes to the point that horses appear clinically normal. However, signs often recur following re-exposure to triggering allergens, and affected horses are considered susceptible for life.
Horses with mild–moderate asthma do not exhibit increased respiratory effort at rest but may present with intermittent coughing, excess airway mucus, and/or poor performance. Racehorses with mild asthma often do not cough, and negative effects on performance may not be appreciated until airway inflammation is treated. Other athletic horses may show poor performance manifested as prolonged recovery times, increased respiratory effort during or after exercise, or reluctance to work or run (e.g., “gate issues” in barrel racers). It is important to rule out other common causes of poor performance, such as musculoskeletal disease, upper airway obstruction, or exerciseinduced pulmonary hemorrhage (EIPH).
Horses may also present with serous or mucoid nasal discharge, particularly after exercise. Excess tracheal mucus is best detected by endoscopy approximately one hour after exercise or racing. Mucus accumulation may be graded using Gerber’s scale (0–5) (Gerber et al., 2004). Racehorses with scores ≥2 and sport horses with scores ≥3 are more likely to be poor performers.
What is the difference between asthma and mild asthma?
Mild asthma refers to horses with mild airway inflammation and no overt clinical signs, a presentation commonly observed in racehorses. Horses with mild airway inflammation accompanied by poor performance, intermittent coughing, or prolonged recovery are classified as having moderate asthma. Horses with moderate to severe airway inflammation and increased breathing efforts at rest are classified as having severe asthma or heaves.
The degree of airway inflammation is best categorized by evaluating bronchoalveolar lavage fluid (BALF) cytology. Normal BALF cytology is characterized by total nucleated cell count <600 cells/ul, and differential cell count with <5% neutrophils, <2% mast cells, and <1% eosinophils. Horses with mild-moderate asthma have >5% neutrophils, >2% mast cells, and/or >1% eosinophils and total nucleated cell count may be elevated. Horses with severe asthma have >25% neutrophils, but some severe cases may have lower neutrophil proportions that is likely due to poor BALF return secondary to severe airway obstruction (Couetil et al., 2016).
What causes asthma? Is it purely dust-related, or is mold involved as well?
Severe asthma is strongly associated with exposure to high levels of organic molds, particularly those found in moldy hay and poorly ventilated stables. Clinical signs may develop within hours to days of exposure. Even good-quality hay contains molds that may trigger clinical signs in susceptible horses. Hay from round bales has been associated with more severe clinical presentations, likely due to increased dust exposure or environmental contamination from field storage.
Outdoor airborne pollens and molds also appear to contribute to summer-associated severe asthma, and some horses suffer from both summer and winter (hay-associated) forms of the disease.
There is strong evidence supporting the role of dust and inhaled molds in the pathogenesis of mild–moderate asthma. Exposure of healthy horses to moldy hay or endotoxins results in bronchoalveolar lavage (BAL) neutrophilia and airway hyperresponsiveness.
The importance of small dust particles (respirable dust ≤4 µm and particulate matter ≤10 µm [PM10] and PM2.5) has been demonstrated in racehorses, where increasing exposure correlates with elevated BAL inflammatory cells—eosinophils in younger horses (1–2 years old) and neutrophils or mast cells in older horses (3 years old and older).
Atmospheric pollutants such as ozone, nitrogen dioxide, carbon monoxide, and sulfur dioxide, as well as noxious stable
gases including ammonia, hydrogen sulfide, and methane, may also contribute to airway inflammation. Many of these compounds have been shown to cause airway disease in humans and animals, and emerging data in horses demonstrate negative effects on race performance.
The role of bacterial infection remains controversial. Tracheal inflammation and bacterial isolation are common in racehorses, and bacterial culture positivity correlates with inflammation severity. However, bacteria may represent sampling contamination or transient colonization of proximal airways. In up to 54% of horses with mild asthma, no bacteria are cultured from tracheal wash samples. While tracheal inflammation is associated with coughing in racehorses, it is not associated with decreased performance.
Respiratory viruses do not appear to play a significant role in mild asthma. Multiple studies have failed to identify viral infection based on serology or virus PCR for equine herpesvirus, influenza, adenovirus, and rhinovirus.
How is asthma diagnosed?
Diagnosis relies on a detailed history, physical examination, and targeted diagnostic testing to rule out alternative causes of cough, increased respiratory secretions, and poor performance. Fever suggests infectious respiratory disease such as viral infection, bronchopneumonia, pleuropneumonia, or pulmonary abscessation.
Hematology may help rule out infection. Leukocytosis with neutrophilia, often with a left shift, is common in bacterial infections. Neutrophilia may also occur in noninfectious inflammatory conditions, neoplasia, mycotic, or parasitic disease. Viral infections often produce normocytic, normochromic anemia, lymphopenia or lymphocytosis, and sometimes neutropenia, followed by neutrophilia during secondary bacterial infection. Most horses with asthma have normal hematologic findings.
Inflammatory biomarkers such as serum amyloid A (SAA) or fibrinogen are typically elevated in cases of infectious respiratory disease, but are normal in horses with asthma.
Horses with severe asthma typically show exercise intolerance and increased respiratory effort during exacerbations, though signs may be subtle during remission. In such cases, pulmonary function testing or response to therapy aids diagnosis. BAL fluid cytology is a highly sensitive test and identifies three inflammatory profiles in mild–moderate asthma:
• Neutrophilic (>5%)
• Mast cell–predominant (>2%)
• Eosinophilic (>1%), or combinations thereof
Regional variation in BAL phenotypes has been observed based on geographic and climatic factors. Severe asthma typically exhibits more pronounced neutrophilia (>25%), although overlap exists between moderate and severe disease. Eosinophilic inflammation may also be associated with parasitic pneumonitis, hypersensitivity pneumonitis, fungal pneumonia, or cutaneous habronemiasis. Dictyocaulus arnfieldi infection is typically non-patent in horses, making Baermann fecal flotation unreliable. Increased mast cells have been described in equine asthma but are not associated with other respiratory diseases.
How do you measure breathing effort?
Direct measurement of airway obstruction requires specialized equipment available only at referral centers. However, transpulmonary pressure can be measured in the field using an esophageal balloon catheter constructed from a foal nasogastric tube and condom attached to a pressure gauge. In horses with severe asthma, transpulmonary pressure decreases by at least 20% within 5–10 minutes following bronchodilation (e.g., Buscopan). Visual assessment of respiratory effort alone before and after bronchodilator administration is insufficiently sensitive.
How do you measure dust in a horse’s breathing zone?
Can you describe “Black Beauty”?
We demonstrated that dust exposure measured around the horse’s nose (i.e., within the breathing zone) is closely associated with the severity of airway inflammation, whereas dust measurements taken elsewhere in the barn are not. It is also essential to quantify particles capable of penetrating deep
into the lungs. Particles larger than 100 µm in diameter cannot pass beyond the upper airways (for reference, a human hair is approximately 50–100 µm in diameter). Only particles small enough to reach the lower airways (≤10 µm) are associated with airway inflammation.
Historically, exposure to airborne irritants has been measured using size-selective samplers designed to collect inhalable (≤100 µm), thoracic (≤10 µm), or respirable (≤4 µm) particulate fractions. These samplers are connected to a pump aspirating air at a constant flow rate approximating that of a resting person, with dust particles collected on a filter. Gravimetric analysis is performed by weighing the filter before and after sampling. Accurate measurement of small particles, particularly respirable dust, requires prolonged sampling periods (typically 6–8 hours in a horse stall). Advantages of filter-based sampling include the ability to perform microscopic examination and elemental analysis (e.g., endotoxin and ß-glucan content). Disadvantages include cost, extended sampling time, bulky equipment, and the technical expertise required.
More recently, compact devices capable of measuring particle size and number in real time using light-scattering technology have become commercially available. We developed a wearable device that attaches to the horse’s halter to measure dust exposure directly in the breathing zone, known as the “Black Beauty” (BB) monitor. The BB monitor is equipped with temperature and humidity sensors, GPS, and an LED display panel.
We demonstrated that horses tolerate the BB monitor for extended periods without discomfort and that measurements obtained correlate strongly with gold-standard dust-sampling methods (Ivester et al., 2024). In addition, the BB monitor can be fitted with a miniature video camera, allowing recording of horse activity during dust sampling.
How do you manage mild equine asthma?
The cornerstone of managing mild equine asthma is environmental control aimed at reducing exposure to respirable dust. Two primary strategies are effective. The first, and most effective, is the use
of low-dust feedstuffs and bedding. The second, which is less effective, is increasing the removal of airborne particles by improving ventilation within barns or stalls.
Multiple studies have shown significant reductions in dust exposure when horses are fed haylage or soaked or steamed hay instead of dry hay. Feeding method is also important; for example, hay fed from a net in a stall results in a three- to fourfold increase in respirable dust exposure compared with hay fed on the ground.
A second important management strategy is supplementation with omega-3 polyunsaturated fatty acids (PUFAs). In particular, supplementation of racehorses with mild asthma using eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) derived from fish oil reduces airway neutrophilia and improves performance. These anti-inflammatory effects are thought to be mediated through the metabolism of EPA and DHA into specialized pro-resolving mediators (SPMs), including resolvins (E-series and D-series), maresins, and protectins.
Can you explain how omega-3 supplementation emerged as a management strategy?
After years of research on pharmacologic therapy and dustreduction strategies in horses with mild–moderate to severe asthma, it became evident that clinical signs often returned within days of discontinuing medications and re-exposing horses to dusty environments. Additionally, achieving clinical remission in horses with severe asthma required months of strict environmental management.
At the same time, growing evidence from human medicine and animal models suggested that omega-3 PUFA supplementation was beneficial for chronic inflammatory diseases, including asthma. When a company approached our team to evaluate their supplement (Aleira) in asthmatic horses, we conducted a double-blind, randomized, controlled trial. The results demonstrated that horses with moderate to severe asthma transitioned to a low-dust diet (complete pelleted feed) showed improvement within 5–8 weeks; however, supplementation with a DHA-rich product (Aleira) led to marked improvement within two weeks and complete clinical
resolution by five weeks (Nogradi et al., 2015).
Subsequently, we conducted a clinical trial in Thoroughbred racehorses with mild asthma and found that supplementation with fish oil rich in EPA and DHA for four weeks—without reducing dust exposure—was sufficient to resolve airway neutrophilia. Notably, supplementation did not affect airway eosinophils or mast cells.
Can you help us understand Resolvin D2 and its importance in lowering airway inflammation?
As part of a clinical trial evaluating the effects of low-dust forages (steamed hay and haylage) on BAL cytology in racehorses, we investigated potential associations between selected SPMs and BAL neutrophil proportions. Using ELISA kits, we quantified Resolvin D2, Resolvin E2, Maresin 1, and Protectin D1 in plasma samples collected before and six weeks after the feeding trial.
Resolvin D2 was the only SPM demonstrating a modulatory effect on BAL neutrophil proportions: higher plasma concentrations were associated with attenuation of the increase in BAL neutrophils in response to rising dust exposure. Evidence from rodent models of airway inflammation suggests that DHA-derived resolvins (D1 and D2) inhibit neutrophil and macrophage recruitment to the lung.
Can you explain recent innovations in equine asthma, such as dust masks and wearable technology?
We recently developed a respirator (“dust mask”) for horses and conducted pilot testing demonstrating marked reductions in dust exposure while horses were eating hay. The patented design covers only the nostrils, allowing horses to eat and drink while breathing filtered air. We hope to make this product commercially available soon.
Much of your work with omega-3s has focused on racehorses. How do you plan to study sport horses?
We are currently conducting a clinical trial in barrel racing Quarter Horses comparing two omega-3 PUFA supplements.
Both supplements provide the same omega-3/omega-6 ratio, but only one contains EPA and DHA. We are evaluating the effects of supplementation on blood lipid profiles, BAL cytology, and clinical signs, while monitoring dust exposure.
Is there anything new on the cytology front?
We are actively investigating improved methods for preserving BALF cell morphology during shipping to enhance diagnostic yield from samples collected in the field. In addition, we are using machine learning and artificial intelligence approaches to improve the diagnosis of airway inflammation based on BAL cytology compared with traditional microscopic evaluation.
Will you continue investigating pro-resolving lipids?
Pro-resolving lipids are challenging to quantify because they are present in extremely low concentrations in biological fluids such as blood and BAL fluid. Thus far, we have been unable to detect SPMs in plasma using highly sensitive mass spectrometry methods. Although ELISA kits are commercially available, none have been validated for use in horses. We are currently pursuing methods to detect SPMs directly in lung cells.
Are there findings from human medicine that may translate to horses?
Our recent clinical trial on fish oil supplementation provides strong evidence supporting the benefits of omega-3 PUFA supplementation for neutrophilic airway inflammation in asthma. Previous human studies yielded inconsistent results, largely due to small sample sizes (often fewer than 20 patients per trial). In contrast, our study included 81 racehorses and used a robust design, providing compelling evidence for the efficacy of EPA and DHA in mitigating airway inflammation.
It has been 10 years since “Inflammatory Airway Disease in Horses— Revised Consensus Statement” was published. Would you revise anything?
We recently submitted a systematic review of the equine asthma literature for publication. Stay tuned!
References
1. Couetil, L.L., J.M. Cardwell, V. Gerber, J.-P. Lavoie, R. Léguillette, and E.A. Richard. 2016. Inflammatory airway disease of horses—Revised consensus statement. Journal of Veterinary Internal Medicine 30(2):503–515. https://doi. org/10.1111/jvim.13824.
2. Gerber, V., A. Lindberg, C. Berney, and N.E. Robinson. 2004. Airway mucus in recurrent airway obstruction—Short-term response to environmental challenge. Journal of Veterinary Internal Medicine 18(1):92–97.
3. Ivester, K.M., J.-Q. Ni, L.L. Couetil, T.M. Peters, M. Tatum, L. Willems, and J.H. Park. 2024. A wearable real-time particulate monitor demonstrates that soaking hay reduces dust exposure. Equine Veterinary Journal:14425. https://doi.org/10.1111/ evj.14425.
4. Nogradi, N., L.L. Couetil, J. Messick, M.A. Stochelski, and J.R. Burgess. 2015. Omega-3 fatty acid supplementation provides an additional benefit to a low-dust diet in the management of horses with chronic lower airway inflammatory disease. Journal of Veterinary Internal Medicine 29(1): 299–306. https://doi.org/10.1111/jvim.12488.
Allergies in Horses and Food Allergy Testing
Rosanna Marsella, DVM
Could you provide a brief biographical sketch, particularly on the topic at hand?
I am a veterinary dermatologist with a strong interest in equine allergic skin diseases. I have worked to identify mediators of inflammation and itch in horses and have demonstrated that IL-31 is a powerful mediator. Thus, I have developed an antibody to block it. My goal is to provide this antibody as a new steroid-free biological treatment to provide relief to itchy horses. I have served as the chair of the international committee on equine allergic skin diseases, and I am the lead author of the 2023 consensus guidelines on this topic. These guidelines reflect the current level of knowledge on equine allergies, including food allergies.
As a jumping-off point, what is an allergy?
Allergy is commonly defined as an aberrant or extreme response of the immune system against stimuli that should otherwise be innocuous and tolerated in healthy individuals. Once that response is developed, even minute amounts of stimulation can trigger severe responses. In many cases, this is an immediate immune response (within minutes) but it can also be delayed (hours or days) after exposure.
Before we learn more about allergies, please define “pruritus.”
Pruritus is simply itch, which is an unpleasant sensation leading to the desire to scratch an area of the skin to provide relief from such sensation. Sometimes itch can be abrogated by the development of pain as the two sensations share common pathways.
Insect bite hypersensitivity, particularly involving Culicoides midges, seems to be the most common and best understood atopic disease in horses. Can you provide a brief overview of that?
The most common triggers for allergic skin diseases in horses are insects, with Culicoides being the most studied. For this reason, when people refer to insect bite hypersensitivity, they frequently use it to describe Culicoides allergy (hypersensitivity). Culicoides hypersensitivity involves a combination of immediate (type I, IgE mediated hypersensitivity) and delayed (cell-mediated hypersensitivity). Mixed mechanisms make it challenging to manage since some treatments that are effective for immediate hypersensitivities (e.g., antihistamines) are ineffective for delayed types of hypersensitivity.
Much work has been done to identify the main components in the saliva of the Culicoides (salivary allergens) that trigger the allergic response. We know that most Culicoides allergic horses react to nine main identified salivary allergens. This information is important for developing both diagnostic tests and new targeted therapies.
Do you recommend the use of omega-3 supplements as part of a treatment plan for horses with insect bite hypersensitivity? If so, which have proved most likely to help?
Essential fatty acids have been tried both topically or systemically as treatments for insect bite hypersensitivity, but the clinical improvements are only moderate. This incomplete clinical response is probably due to mixed pathogenesis and the fact that this approach is probably best suited as adjunctive therapy rather than as a monotherapy.
The published studies used these options as monotherapy; thus, it is not surprising that the results were not always significant. Consequently, essential fatty acids are not routinely recommended as treatment to manage Culicoides hypersensitive horses. It is important, however, to note that there is preliminary evidence that skin barrier defects play an important role in insect allergic horses.
This discovery justifies the need to further investigate formulations of topical ceramides and essential fatty acids to improve skin barrier function in affected horses.
I believe it is also beneficial to further explore sources of essential fatty acids that are best incorporated in the skin of horses and the optimal ratio between omega-3 and omega-6 to provide the strongest anti-inflammatory benefits.
What is atopic dermatitis?
Atopic dermatitis is the term used to describe environmental allergies to pollens such as grasses, trees, and weeds. Other common triggers for atopic dermatitis are mites and molds. Atopic disease has a range of clinical manifestations including skin disease (atopic dermatitis or eczema) and respiratory signs (asthma). In people, there is a progression from cutaneous to respiratory disease (atopic march). In horses, such progression is not well documented, but we certainly see horses that have a combination of cutaneous disease and respiratory issues.
Preliminary evidence in horses suggests that the skin of atopic individuals has skin barrier defects that increase the risk of allergic sensitization to pollens. In people and dogs, it is well established that skin plays a key role in both the sensitization and the elicitation of clinical signs of atopic dermatitis. In horses, the evidence is still preliminary.
Many atopic horses are also insect allergic thus there is an overlap between atopic dermatitis and insect bite hypersensitivity.
Researchers understand far less about food allergies than insect hypersensitivity or atopic dermatitis. In fact, food allergies are given short shrift in the scientific literature. Is this because they are not important or because researchers know so little?
Food allergies in horses are minimally understood or described. The most documented food allergy in horses is urticaria when horses develop hives within minutes after ingesting a certain supplement or hay.
There are, however, no well-documented reports of food being the cause of pruritic atopic dermatitis-like syndrome.
The truth is that, for horses, grasses and weeds are both food allergens and inhalatory allergens, thus the line between what is a food allergy and what is an environmental allergy caused by pollen is blurred in horses. In other species like dogs, there is an obvious separation between pollen and foods, separate atopic dermatitis from food allergy.
What is the prevalence of food-induced skin allergies in horses?
As mentioned above, the prevalence is unknown at this time. Food induced urticaria has been described, but it is considered uncommon.
How do food-related skin allergies present?
What are the clinical signs?
In other species, food allergies manifest with pruritic skin disease sometimes associated with gastrointestinal signs. In horses, we have no documented cases of pruritic dermatitis caused by foods.
How are food-related diagnostics performed?
In other species, food trials are recommended as the most reliable way to diagnose a food allergy as there is evidence not to support the use of blood test or skin test to diagnose a food allergy.
In horses, one publication confirmed that blood test for food allergy is unreliable and does not predict any clinical relevance (Dupont et al., 2016).
When you suspect a food allergy, how do you design and structure an elimination diet in practice, and how strict does it need to be to be meaningful?
Generally, when food trials are implemented, the key part is to feed a novel diet. Practically speaking, what it means is to switch the horse to a type of hay that has not been fed before and either stop feeding commercial concentrates or switching to a simplified source of grain, without additives.
This choice needs to be made based on the age and the nutritional requirements of the horse. It is also important to note that some hays are more allergenic than others. For example, peanut and alfalfa hays are more likely to be triggers in atopic horses than others, thus are usually eliminated from the diet of a horse that is worked up for food allergy. This choice needs to be made based on the age and the nutritional requirements of the horse. It is also important to note that some hays are more allergenic than others. For example, peanut and alfalfa hays are more likely to be triggers in atopic horses than others, thus are usually eliminated from the diet of a horse that is worked up for food allergy.
Owner compliance can make or break an elimination trial. What communication strategies or tools do you use to help owners stick to the plan?
Yes, compliance is key as it can take exposure to minute amounts of allergens to trigger allergic responses in severely allergic individuals. I encourage people to keep things simple and to remember that for a peanut allergic person, even a few peanuts can lead to a severe response, thus they need to be strict in their avoidance.
I have personally seen horses flare when the horse in the next stall was fed peanut hay or was fed another hay that had been stored in the same room with the peanut hay. Thus, even the dust from a certain hay can cause major issues when the horse is very sensitive. Performing a food trial or any kind of avoidance when horses are kept in a boarding facility with a variety of horses with different feeding needs and preferences can be a real challenge.
How do you know if an elimination diet makes a difference? Do the clinical signs disappear completely? How do you know when you’ve “solved the puzzle”?
I have never had a horse where dietary restrictions alone were able to completely solve the issue. The fact that allergic individuals are typically polysensitized makes it more complex to completely resolve problems with just eliminating a specific hay or food.
Most of the time, allergic horses have many different components to their disease, ranging from insect to environmental allergens, and require a plan of desensitization. That is accomplished with
subcutaneous immunotherapy, which involves the injection of increasingly higher doses of allergens to retrain the immune system to go from allergic to tolerant so that the aberrant response is manageable and maintained below a threshold of clinical significance.
Many owners use blood or hair tests marketed for “food allergies.” What are the main limitations and pitfalls of these tests in horses? Are these tests efficient?
Currently there is no evidence to recommend such tests. Matter of fact, there is evidence to indicate that they are not reliable and their ability to predict clinically significant allergies is unsatisfactory.
How does a horse owner decide to do allergy testing? Is it the presence of hives? What prompts most owners?
In my experience, horse owners decide to do allergy testing, whether blood or skin test, to identify triggers for the disease of their animal. Most tested horses are itchy horses and not horses with hives, although some of them have also have recurrent urticaria. These owners have tried the symptomatic therapy of steroids and antihistamines, and realized that treatments either did not work (antihistamines) or are not sustainable (steroids), so they want to get to the root of the problem.
Would you ever recommend a blood test to find the source of an allergy?
No. I prefer intradermal skin test as it tests for cutaneous IgE rather than circulating IgE. Those do not always correlate, and many blood tests are unreliable. Thus, I prefer skin test.
What are the most common misdiagnoses you see, i.e., situations where pruritus or skin disease is attributed to food allergy but the true cause is something else?
The common situation is people miss skin infections. Allergic horses frequently also develop secondary bacterial skin infections, which are missed. Once those infections are diagnosed and properly treated, itch becomes much easier to manage.
The second most common issue is the use of ineffective fly sprays that are not true repellents. Statistically speaking, insect bites are
the single most common trigger for equine allergic skin disease, thus not having an effective fly prevention is a common cause for treatment failure.
In your experience, how often are presumed food allergies adverse reactions to storage mites, molds, or contaminants rather than the primary feed ingredient?
In dogs, that is a common issue. In horses, we see reactivity to storage mites very often on intradermal skin test. This may be cross-reactivity to dust mites, and we desensitize toward mites as part of the allergen specific immunotherapy.
Are there particular life stages or conditions (e.g., young horses, seniors, horses with PPID or EMS) where you see food-related allergic disease more or less frequently?
We have no data about any of that.
Do you see any emerging feed ingredients, processing methods, or trends (e.g., insect protein, novel fiber sources) that might change the landscape of food-related allergies in horses?
Currently there is no hydrolyzed feed for horses. That could be important in horses to address type I hypersensitivity and may be a tool to diagnose true food allergies.
How do pasture components—grasses, weeds, trees—fit into the picture of “food” allergens, and how often are they part of the problem?
As mentioned before, in horses, grasses and weeds are both food allergens as well and respiratory environmental allergens which cannot be separated. There are certainly horses that have worse skin or respiratory issues when they are on pasture and have increased exposure to all those triggers.
Do concurrent conditions—like insect bite hypersensitivity or atopic dermatitis—complicate the diagnosis and management of food allergies, and how do you untangle overlapping triggers?
Yes, all these triggers are cumulative and can make diagnosis and management difficult. A simple way to start is to treat the treatable, starting with the allergy for which we have no ability to desensitize, which is insect allergy.
Insects are the most common and severe trigger for allergic skin disease in horses, so it is critical to educate people on what fly spray is an effective repellent and how to use it to get the biggest benefit. Once insect bites are decreased, then we can work on what is left. The next step is typically an intradermal skin test and based on those results, both management changes are implemented in conjunction with the beginning of allergen specific immunotherapy.
What role, if any, do you see for microbiome-targeted therapies (prebiotics, probiotics, fecal transplants) in horses with suspected or confirmed food allergies?
In other species we have data to support the link between dysbiosis and atopic dermatitis as well as the link between increased intestinal permeability and the development of both food allergies and atopic dermatitis. I am not aware of any study in atopic horses that has evaluated the role of the gut microbiome. In dogs and people, atopic individuals have dysbiosis and decreased microbial diversity, but there still debate on whether these changes are primary or secondary. This would be a very interesting area to explore in horses.
Based on current evidence, what are the most important myths about equine food allergies that you wish owners and trainers would let go of?
Please stop relying on blood tests. There is no evidence that a blood test can help you decide whether your horse is allergic to carrots or apples.
Can you recommend three to five seminal references (articles, book chapters, books, etc.) on equine feed allergies written by you or someone you admire in the field?
1. Marsella, R., S. White, V.A. Fadok, D. Wilson, R. Mueller, C. Outerbridge, and W. Rosenkrantz. 2023. Equine allergic skin diseases: Clinical consensus guidelines of the World Association for Veterinary Dermatology. Veterinary Dermatology 34(3): 175-208. doi: 10.1111/vde.13168.
2. Pali-Schöll, I., M. De Lucia, H. Jackson, J. Janda, R.S. Mueller, and E. Jensen-Jarolim. 2017. Comparing immediate-type food allergy in humans and companion animals-revealing unmet needs. Allergy 72(11):1643-1656. doi: 10.1111/all.13179.
3. White, S,D. 2023. Approach to the pruritic horse. Journal of the American Veterinary Medical Association 261(S1):S66-S74. doi: 10.2460/javma.22.10.0444.
Reference
1. Dupont, S., A. De Spiegeleer, D.J. Liu, L. Lefère, D.A. van Doorn, and M. Hesta. 2016. A commercially available immunoglobulin E-based test for food allergy gives inconsistent results in healthy ponies. Equine Veterinary Journal. 48(1):109-113. doi: 10.1111/ evj.12369.
Modeling Growth in Thoroughbreds
Joe Pagan, PhD
Can you explain how your interest in growth arose?
I became interested in the growth and development of Thoroughbreds when I came to Kentucky in the late 1980s. Since Kentucky is home to the American Thoroughbred breeding industry, growth and health of young horses were focal points for breeders and farm managers. The only substantive data at that time came from a comprehensive 1970s study by Dr. Skip Hintz. He described Thoroughbred growth and development at a single, large-scale operation in Canada. Although the paper covered several years of growth data, I wondered if those data were applicable to foals born in the United States, especially in Kentucky, given the differences in climate and environment.
I began weighing foals in Kentucky. One of the most progressive farm managers to recognize value in the weighing program was Steve Caddel, who at the time worked for Mickey and Karen Taylor and Jim Hill, co-owners of Triple Crown winner Seattle Slew. Steve began weighing mares and foals that resided at Slew’s Nest Farm. His motivation to gather this data fueled our motivation to collect more data. A few years later, Steve transitioned from his farm manager post to Hallway Feeds, one of Kentucky Equine Research’s longstanding Brand Partners. Steve carried his interest in weighing young horses to his work at Hallway, creating a weighing service for regional Thoroughbred farms.
This turned out to be a game-changer. Steve traveled to many central Kentucky farms, weighing young horses, measuring height, and assessing body condition. One key element to this service was the regularity of the data reporting. He visited most farms monthly.
We very rapidly developed a large dataset of information about how Thoroughbreds grow. While data collection began in Kentucky, we have expanded the program worldwide through our partner-
ships with feed manufacturers. Because of these collaborations, we have extensive information on how Thoroughbreds grow in different environmental conditions.
In studying growth and development, numbers count, so a large population of foals is necessary. Because we followed thousands of young horses across many farms and over multiple years, we have been able to answer important questions about how growth affects incidence of skeletal disease and ultimately racing performance.
When did you first publish this data in a scientific journal?
We initially published two papers. The first, published in 1996, was titled “A Summary of Growth Rates of Thoroughbreds in Kentucky,” with Steve Jackson and Steve Caddel as coauthors. This paper reported on growth and development in general, such as the effect of gender and season, so it was a follow-on to Hintz’s paper that detailed the Canadian Thoroughbreds, but our paper focused specifically on foals in central Kentucky.
The second detailed data from a specific farm. This farm had adopted a weighing program of its own before we approached the managers about a collaboration. We eventually worked with this farm, collecting data for four consecutive years, from 1991 to 1994, and ending up with over 200 foals in the study. That farm also had a resident veterinarian. We worked in collaboration with the veterinarian to catalog and quantify the incidence of developmental orthopedic disorders. This was the first paper to identify relationships between growth rate and the incidence of skeletal issues.
When does Gro-Trac come into the picture?
We became a victim of our success. The success of the Hallway weighing program created a data-management problem. In the beginning, we used a spreadsheet that we designed to collate and graph growth data. The program grew so much that we had an employee who spent half of her time entering growth data. At that time, we reached out to our software designer, who had already designed MicroSteed, our ration evaluation software, for us. He created a program to make it easier to enter and report growth data.
Most importantly, the reason these data are so different from others is that we have a way to compare how a foal is growing relative to similar foals in a population. Gro-Trac, our growth-tracking software, was born around 2000 out of necessity, allowing us to have a more automated, specialized software program to track growth and development.
At present, we are working with University of Kentucky statisticians on a huge statistical analysis project using our global Gro-Trac population of about 69,000 individual growth records. Again, these are all Thoroughbred foals, and data have been gathered from all over the world. The foundation, however, remains the Hallway dataset, because of the uniqueness of its weighing program.
In most other parts of the world, the horses are weighed by farm staff. The farms have their own scales and an outside technician does not come in. While we value all the growth data, farms get busy, and occasionally the weighing becomes deprioritized. The regularity of the Kentucky data keeps it more robust than data obtained in some other places.
Further, the Kentucky data is multigenerational because Steve has retired from Hallway. He mentored a former Kentucky Equine Research intern, Megan McFaull, who is now running the program.
How do farm managers use the Gro-Trac reports?
Gro-Trac provides easy-to-understand references for foal size relative to the overall population (same gender, same age). Because foals are born over a span of months, how do you decide if a foal is small, average, or big compared to an entire crop?
Having that reference information based on thousands of other foals gives the farm manager an idea of the foal’s relative size. We have now discovered that the relative size of the foal, particularly early in its life, is somewhat predictive of its susceptibility to developmental disorders.
Starting with that information, a farm manager might modify management—such as feeding and turnout decisions—based on
the information that the foal might have a higher susceptibility. When you are looking at weights of young horses, there is a lot of confusion because there are two related but distinct measures.
The first is size. Size is a static number, taking a body weight and a withers height at a single point in time. Think of it as a snapshot. How either of those measurements changes over time is growth, the second measure. These are two different things.
We discovered both measures are important, but they are important for different reasons. Originally, the concept was that rapid growth was the culprit that led to developmental problems. We have subsequently modified that view.
Absolute size, particularly when young, influences their susceptibility to skeletal disease. If you have a foal, especially one that is smaller than normal, that gets big with rapid growth, called compensatory growth, that rapid growth may predispose the horse to different issues. Our data indicate that sesamoiditis is one of those issues. Osteochondritis dissecans (OCD), which is what everyone focused on in the 1990s and 2000s, has a higher relationship with how big the foal is at birth, in that big foals are more susceptible to OCD than small foals, according to our data.
Going back to the question of how farm managers look at Gro-Trac reports, because they have access to normal growth curves, they are looking for abnormal growth patterns. It could be the foal is growing too fast, not paralleling the reference curve, or the foal has stopped growing altogether.
In some instances, we see changes in growth curves but do not understand why initially. After further evaluation, the herd may have a problem, like Lawsonia infection (causing proliferative enteropathy), or in the United Kingdom, parasite resistance, which is a hot topic there.
We have seen farms where growth slows in many horses at once, which highlights another benefit of Gro-Trac. With the software, you can look at an individual foal or look at the entire crop of foals. Sometimes, looking at the entire crop is more instructive. If all the foals slow down, there is something happening to the entire
group—it is more than an individual problem. This could be an environmental issue, such as forage quality and weather, or some external factors. These issues are often picked up in growth rates before being identified as a specific problem on the farm.
From all this work, years and years of data collection and analysis, what factors affect growth?
We can classify growth using three specific factors: geographic region, month of birth, and parity.
The first factor goes back to the top of this Q&A: was the Canada data appropriate for Kentucky? We found growth is quite different in Canada and central Kentucky. As it turns out, that could be for a few reasons, including the fact Thoroughbreds are changing in size. We have even seen that in our own span of time studying this. So, the region in which the horse is raised is very important, whether it’s Kentucky, England, Japan, Australia, or New Zealand. This is a direct reflection of the environmental conditions to which the horse is subjected.
The second factor is month of birth. In the Northern Hemisphere, foals are born from January to May, a span of five months. When the foal is born determines when it is exposed to more nutrients, typically through higher-quality pastures. In the U.S. and England, pastures are rich in the spring, slow to grow in the summer with the heat, and then flush again in the fall. Subjecting foals to these environmentally-influenced nutritional differences at different ages—and how they deal with that—varies depending on how old they are. The birth month is a huge factor.
The third factor is parity, though we initially did not appreciate it. When we first started weighing, we didn’t record if this was the first foal out of a mare or even ask how many foals the mare had produced. One of the things that got me thinking about it was that we knew foals born in January and February in Kentucky were a lot smaller than foals born in March and April, for instance. I had always been completely focused on this being an environmental effect. We discovered the number of foals that are first foals is disproportionately higher in January and February than later in the season.
Explain more about the importance of parity. We looked specifically at the size of first foals—foals out of primiparous mares (those having their first foal). They are significantly smaller than foals of mares that have had at least two foals. Foals from mares with two previous foals are bigger than those of firsttime dams. When you get to three foals or more, there is a big difference. Those first foals are about 15% lighter than foals out of multiparous mares (those that have foaled more than once). Throw in all these primiparous foals with their lighter birth weights and that skews how big the foals are born that month.
In a subpopulation of about 1,000 foals born in Kentucky, we saw that over half of the foals born in January are out of primiparous mares, and in February about 40% are from primiparous mares and 60% are from multiparous mares.
In reflection, this should not have surprised me. What happens when you have a maiden mare? Thoroughbred breeders typically want to breed maiden mares when the shed opens in February because you want to make sure she gets in foal early. A multiparous mare gets bred depending on when she is due to foal unless she is barren. So, these data are extremely skewed toward early foals.
By the time the primiparous foals are yearlings, they have caught up almost entirely. This suggests to me that the uterine environment of the first-foal mare is restricting the development of the foal and probably its early growth. The milking ability of a primiparous mare is probably limited, too. Once the foals escape those restrictions, they get into a compensatory growth pattern by eating grass and grain. Our data have shown that primiparous foals have a different incidence of disease. They tend to be protected against OCD, and I think it is because they are born small, but they have a higher tendency toward developing sesamoiditis, which has to do with them catching up.
One of the things we are doing with the University of Kentucky’s statistics team is to take a deep dive into the differences in growth between primiparous and multiparous foals to understand if there is a window of vulnerability for sesamoiditis when they are playing catch-up.
How important are birth weights?
In the weighing program spearheaded by Hallway, the foals are weighed monthly. This is great because it gives us extremely uniform data. However, we rarely get a birth weight, simply because weighing is done on a fixed day of the month. Further, for biosecurity reasons, the weighing crew does not usually go into foaling barns. Because so many farms appreciate that birth weights are important, we have a lot of birth weight information. I would say if you’re going to take any weight of a foal, birth weight is one of the most important ones.
Because foals are only 50-60 kg (110-132 lb) at birth, farms do not have to have such a robust scale, so they can get by with pet scales. Reviewing birth weights reveals the importance of parity. There was once a vague rule of thumb that stated if a Thoroughbred foal was less than 45 kg (100 lb) when it was born then it is probably not going to amount to much. This deserves a huge asterisk and that asterisk needs to say “unless it’s a primiparous foal.”
As we have looked at birth weights, we have evaluated them in the context of the incidence of skeletal disease of the foals but also their racing success. We typically use as a proxy for racing success whether foals are stakes race winners. Though there are many ways to quantify success, this is an easy designation for people to understand. We observed there is a narrow range between 44 kg (97 lb) and 64 kg (141 lb) for birth weight that can be useful in predicting likelihood for success. Most foals that are successful— that is, stakes winners—fall into that range except for primiparous foals. Some of those can be below 40 kg (88 lb). In fact, we have weights from a filly in Australia that was 39 kg (86 lb) that ended up being a Group 1 winner. Further, one of the leading stallions in Kentucky was a primiparous foal and was 45 kg (100 lb) when he was born. By the time he was a yearling, though, you could not tell a difference between him and multiparous foals.
In the past, I have tried to pick out primiparous foals at Keeneland yearling sales based on physical characteristics, but I found the exercise hard. First, many of them were born in January or February so they are three or four months older than April or May foals, and they are usually well-grown.
Current data do not suggest that primiparous foals fail to reach their mature size.
When we looked at the birth weights of a large group of foals in Kentucky, for which we also had their medical records regarding whether they had OCD that required surgery, we found if the foal was 64 kg (141 lb) or heavier, it was twice as likely to have OCD surgery. So, we have taken that as our upper bumper, as the beginning of the danger zone. The incidence of OCD in an entire population is 10%; for foals over 64 kg (141 lb), the incidence was 20%. Sometimes, we overemphasize the notion of increased risk. In this case, 80% of foals born over 64 kg (141 lb) will not have a problem.
I recently saw a stallion ad for a farm that was crowing about the fact it had a 66-kg (146-lb) foal born, the implication being it will grow to be a big horse and potentially a successful racehorse. Our data does not support that. In other words, a very high birth weight does not predict either soundness or superior racing performance.
If you look historically at the data, it seems there are more big foals. Perhaps it is genetics, breeding bigger stallions to bigger mares, or perhaps it is an environmentally rooted change. I suspect genetics as the reason for big foals.
Why might bigger foals have more problems with OCD?
Data from Scandinavian researchers studying horses and pigs could explain it. The skeleton of very young animals consists largely of cartilage. For cartilage to ossify into bone, adequate vascularization is essential. This blood supply can be compromised by excess weight. Once ossification occurs, vasculature is no longer needed, but during the process, it is critical. If disrupted, cartilage fails to convert to bone, potentially forming an OCD lesion. These lesions often aren’t visible until yearling radiographs.
Spring survey radiographs may reveal lesions that originated when the foals were much younger. Most lesions in Thoroughbred yearlings are found incidentally on survey radiographs, not due to clinical signs like joint swelling or lameness.
Many early abnormalities self-resolve. If survey radiographs are taken too early—at weaning, for instance—you may see changes initially classified as OCD. When rechecked as yearlings, many lesions have disappeared. Only persistent lesions that form cartilage flaps cause ongoing problems.
Large sample sizes are essential for studying growth-disease relationships. With low-prevalence conditions like OCD (10% incidence), small studies lack statistical power. In a group of just 10 foals, you would expect only one case, insufficient for meaningful analysis. Our weighing program succeeded because farms contributed enough animals over years to identify patterns.
A recent analysis examined growth, skeletal disease, and racing records from Kentucky foals. We reviewed medical records from participating farms and obtained public racing data. We focused on spring yearling survey radiographs, standard for public auction horses. These are taken in February or March to allow time for surgery and healing before sales, with results disclosed to buyers.
We analyzed spring survey data from 1,047 foals across 11 central Kentucky farms over four years. Lesions were categorized into two main groups: sesamoiditis (sesamoid bone inflammation) and OCD (failed cartilage ossification). OCD cases were subdivided by joint (fetlock, hock, stifle) and sometimes specific location within joints.
Growth was expressed in population percentiles by age and sex, rather than raw measurements. Monthly weighing means foals vary by ±15 days in age within a given month, a significant difference at rapid growth stages. Percentiles standardize these variations for accurate comparisons.
We found that the early months were the most important in identifying OCD, particularly the first 30 days. The birth weight or a weight taken within the first 30 days tended to be the most highly correlated to the incidence of a surgical OCD.
When survey radiographs are taken, the radiologist looks at them and says, “I think that is a clean joint or I think that is an OCD lesion.” Then, the radiologist must make another decision:
“Is it concerning enough to operate or is it minor enough to resolve or not affect the sale?” If we look at the radiographic incidence, about 15% had radiographic evidence of OCD, but only about 10% had surgery.
For the next stage of the research, we focused on the foals deemed surgical candidates, about 104. We found that the ones that were big when they were foals had a higher likelihood of having OCD surgery. Once they got to the weanling and yearling stages, those requiring surgery were no longer distinguishable from those that did not, so our data showed OCD seemed to be an early-onset problem.
As I mentioned before, sesamoiditis seemed to happen in initially lighter foals that got heavier, especially through compensatory growth. Sesamoiditis occurred in about 20% of these lightturned-heavy foals during spring survey radiographs. Almost all the sesamoiditis was described as “mild.” Very few foals had both sesamoiditis and OCD, so it looked like those problems occurred in separate populations of foals, which is a unique finding.
Are there differences in growth patterns regionally?
Yes, those differences take two different forms. One of them is the environment in which the foal is raised. Countries that have pastures like Kentucky (temperate, cool-season pastures that tend to grow best in the spring and autumn) have similar growth rates (average daily gain). These foals tend to slow down in the winter and then grow more rapidly when the grass comes back in late April and early May. The interesting point is that all of them increase their growth rate regardless of how old they are (earlier age if born in May, later age if born in January). Pasture quality is one thing that causes disparity of growth rates regionally.
You see the same growth pattern in the United Kingdom and Ireland with one exception. The growth surge in the spring happens one month later in the United Kingdom and Ireland than it does in Kentucky. If you look at the environmental temperatures and when the soil warms sufficiently for grass to grow, those regions are about a month behind.
Another country experiences the same growth pattern but on steroids. Most of the Thoroughbreds in Japan are raised in Hokkaido, the northern island. They have nice pasture in spring and autumn, but a severe winter, so they have a much bigger dip in the winter followed by a much more intense compensatory growth phase in the spring. The grass comes back nicely in the spring, and the yearlings grow fast. If you look at other places in the world without that pasture growth pattern, they may use irrigation, as in Australia. Pastures do not get the big spring surge that they get in the U.S. or England. India tends to be the same way and foals are not quite as big, potentially because they do not have exposure to lush pastures for much of the year.
We did an interesting comparison. We looked at yearlings sold at Keeneland (Lexington, Kentucky) and Tattersalls (Newmarket, England). We considered only the elite horses sold in both locations, choosing those that sold in the top 10% based on sale price. We recorded their size, expressed not as percentile but as quartiles. A quartile is taking percentiles and splitting them into four parts (first quartile: lowest 25%; second quartile, next 25%, etc.).
In Kentucky, 50% of the expensive yearlings were in the fourth quartile, and 25% were in the third quartile. Therefore, 75% of the top-selling foals were in the third and fourth quartile. At Tattersalls, the same type of prestigious sale, the ones that were most expensive were dominated by the second quartile, followed by the third quartile. If you look at height, the third quartile was preferable in both. Based on racing records (stakes winners and top 10% by career earnings), we saw the same pattern for sale price. The top 10% of U.K. horses came from the second quartile as yearlings; the top 10% of U.S. horses came from the fourth quartile as yearlings.
The size of the yearlings in the U.K. probably represented the American Thoroughbred 30 or 40 years ago. Virtually all the foals born in the U.K. are turf horses but, in the U.S., they are mostly dirt horses. There has been selectivity for horses of a different phenotype, including those with conformation traits that better suit shorter race distances, including larger hindquarters and straighter hindlimbs. That regional difference is likely a genetic one.
Where is the research going?
With the help of the University of Kentucky, we are creating more complex models of growth, considering all these factors: gender, month of birth, parity, region. Our aim is to create a custom reference curve for an individual foal. Right now, we are comparing general reference curves for different regions, like the U.S. or the U.K., but we would like to create a specific curve—for example, one for a U.K. filly born in February to a multiparous mare. This would provide a much better comparison for farm managers.
Most of this data we have, and all I mentioned here in this Q&A, is from Thoroughbreds. We are beginning to assemble similar datasets for other breeds, such as Warmbloods, and expect to compare Thoroughbred and Warmblood growth patterns as these databases mature.
Equine Musculoskeletal Development and Performance: Impact of the Production System and Early Training
Chris Rogers, PhD
Can you give us a brief biographical sketch, especially regarding the topic at hand?
I grew up in the Waikato, New Zealand’s epicenter of equestrian sport and racing, and was involved in competitive showjumping and racing from a young age. After completing a master’s in equine genetics, I pretrained jumpers for a couple of years before starting a doctorate in equine kinematics.
During the completion of my doctorate, I was involved in the running of an intervention trial examining the tissue response associated with the training of two-year-old racehorses. This study ended up providing a large volume of data that formed the basis of our knowledge on tissue response to early race training.
After the completion of a postdoctoral fellowship at Utrecht University, I returned to New Zealand and ran a large international trial (the GEXA project) in which we provided extra exercise to foals and then followed these horses through to the end of their three-year-old racing season. We then completed several epidemiological studies examining what happens within the breeding and racing industry and the association of early exercise (everything from preweaning management to two-year-old training and racing) on racing career success and injury.
As result of this industry-focused research program, I was recruited to hold the New Zealand Equine Trust Chair in Equine Health, Welfare and Performance at Massey University.
Can you provide some background information about the welfare issues that surround Thoroughbred racing that led you to begin thinking about this topic?
The Thoroughbred racehorse is an athlete, and as such the largest reason for involuntary loss of training days or loss of horses from racing are injuries to the musculoskeletal system. Many of these injuries are subtle. Some, such as race-day fractures, may result in euthanasia. The incidence of race-day fractures is low in most racing jurisdictions. However, the images of these events may be the only images of racing observed by people outside the industry, and they can severely compromise the racing industry’s social license.
There are two approaches to reducing the risk of injury: improving methods to identify injuries before they become significant or optimizing early life experiences so that the risk of injury is reduced. As a country that exports Thoroughbreds (approximately 40% of the annual New Zealand foal crop is exported), a focus on optimizing early-life experiences was the most logical path. In conjunction with this, there were several research groups within New Zealand at the time working on the developmental origins of health and disease (DoHaD) hypothesis.
The rapid growth and development of the horse clearly signaled that it was highly receptive to environmental prompts early in life. The GPS tracking of foals demonstrated this, with foal play activity (osteoinductive exercise) perfectly overlying the theoretical ideal of type and frequency of load to stimulate bone growth and development.
Can you explain the “rule of one-third” when it comes to foal crops in racing and other sports?
The rule of one-third is an observation across several equestrian sports (racing, showjumping, dressage). It provides an indication of what proportion of horses progresses through the production system from birth to sport.
Of the annual foal crop, approximately a third of these foals will not be registered for sport. Of the horses entering sport, a third will be retired due to lack of talent, often called voluntary
retirement in the epidemiology literature. Another third of those entering sport will retire in relation to an injury, often referred to as an involuntary retirement.
In most Thoroughbred industries, there is now a greater proportion of the foal crop entering sport, with an increased focus on breeding the right type of animal and less loss in the production system. However, the relative proportion of voluntary and involuntary losses has remained remarkably consistent over the years.
Why are racehorses put into training so young?
The concept of “putting racehorses into training so young” reflects anthropomorphism, as our frame of reference is often human growth and development. We often struggle to appreciate how quickly and rapidly a horse grows and develops. Within the human literature, maturity is often cited to occur at 18 years of age, when most individuals have reached 98% of mature height. In the horse, this occurs by the time the horse is 24 months old. The interesting thing is, irrespective of breed, most horses achieve 98% mature height by 24 months of age.
In humans, we often describe growth as consisting of three phases: rapid infant growth, childhood phase, and puberty and postpuberty growth spurt. In the horse, the rapid infant growth phase could describe the period from birth to weaning. The childhood phase represents the period from weaning to the horse’s first spring, when about 10 months old. In most situations, puberty in the horse will occur during the first spring and summer, before the horse is 18 months old. In human sports, athlete development and education often begins well before the athlete’s eighteenth birthday. Therefore, from a musculoskeletal developmental and athlete development perspective, the question should be this: why do we wait so long before we start the education process with horses, when earlier, appropriate loading reduces injury risk later?
What is the primary reason for lost training days or retirement from racing? Do different injuries affect horses of different ages?
The major reason for lost training days and (involuntary) retirement from racing is due to musculoskeletal injury. Within this category, lameness has the highest incidence rate (IR)
(approximately 0.9/1,000 training days) followed by dorsal metacarpal disease (DMD, bucked shins) (IR approximately 0.5/1,000 training days).
If examined across age categories, two-year-old horses have more lost training days than other age categories. Part of this is a healthy horse effect, as horses in the older age categories tend to only have horses that are relatively robust, and two-year-old horses have a musculoskeletal system generally naive to the loads of race training.
DMD represents a major reason for lost training days in two-yearolds (IR approximately 1.2 and prevalence of 16-70%). The large variability in prevalence of DMD represents differences in how the gallop load cycles are applied relative to the bone’s ability to respond to novel strain. Bone only needs a few loads (i.e., few strides) at the high microstrain to elicit a response. DMD represents either a delay in the introduction of gallop work or an imbalance between canter and gallop volume.
In older horses, injuries are typically associated with the accumulation of load cycles and the relatively finite life of some tissue, such as cartilage and tendons. Tendon and ligament injuries typical increase with age, having a low incidence in two-year-olds (IR 0.05/1,000 training days) increasing to IR 0.55 with horses five years old and over.
Can you give us a brief explanation of epigenetics?
Traditionally, we believed that the phenotype of the horse was rigidly determined by the genes that the foal received from its parents. Now we recognize that the maternal environment during pregnancy can alter what genes are expressed and how strongly they are expressed. In mammals, including horses, such diverse external stimuli, such as exercise of the dam or the diet of the dam, can alter how the resultant offspring’s metabolic pathways react.
Within the human literature, there is even evidence that if the mother exercises when pregnant the offspring will have greater musculoskeletal health. In human health, this in utero priming is referred to as “DoHaD” or developmental origins of health and disease.
Describe the interplay between epigenetics and plasticity.
Epigenetics represents the in utero priming of gene expression. In mammals, including the horse, it has become apparent that for musculoskeletal tissue there are developmental windows of plasticity. If the horse is provided with sufficient stimuli during these sensitive periods, then the phenotype can be changed (either positively or negatively). A classic example of this in the horse is the “blank joint.”
The articular cartilage in the fetlock joint of the horse starts life as a blank joint and functionally develops according to the loads it receives in the developmental phase before weaning. Application of load, such as that experienced with free exercise at pasture, promotes biochemical heterogeneity. Without loading, irrespective of any epigenetic priming, the cartilage will fail to develop the heterogeneity required to tolerate the loads it will experience later in life.
Explain receptivity of tendons, cartilage, skeletal muscle, and bone. These tissues have differing windows of developmental or adaptive response. Evidence from laboratory animals indicates that it may be possible to alter the development potential of tendons if the appropriate load is applied within seven days of birth. In horses, there has not been any conclusive data indicating an ability to alter the size or morphology of the superficial digital flexor tendon.
Cartilage appears to have an immediate window of receptivity to stimuli immediately after birth and up to weaning. Data from Warmbloods indicate it may still be possible to stimulate cartilage up to when the horse is a year old, though the response is much less than that observed in the preweaning period.
Skeletal muscle and bone are highly responsive during growth and when horses are racing. In human sport science, it is common to talk about the “bone muscle unit” as increases in muscle mass increase microstrain on bone and thus increase bone mass. Most of the longitudinal growth of the bones in the limbs is completed by the time the horse is 24 months old. Appositional growth (increase in bone cross-sectional area)
continues in response to mechanical load via increases in muscle mass, body weight, and osteoinductive exercise.
What is the turnover time for each of these tissues, and at what age is there increased susceptibility to injury?
Tissue turnover time provides an indication of the tissue’s capacity to repair. Tissues such as muscle and bone are highly vascular and respond dynamically to exercise and load. As such it is estimated that in a 10-year period the equivalent of the entire skeleton is replaced.
In horses entering race training, DMD is an example of how dynamic the bone response can be in relation to a new load. To increase the resistance to bending strain associated with galloping, new bone is rapidly deposited on the dorsal periosteal surface of the third metacarpal bone to increase cross-sectional area, which may be sore on palpation. During high-speed exercise (race training), remodeling of bone is often inhibited or downregulated. When the gallop exercise is removed (such as during a spell or a break in training due to injury), there is an immediate increase in remodeling to repair microcracks. The new bone deposited is less mature and in the short term is not as strong as the bone it replaced. This rapid response of bone is one of the reasons for a greater risk of fracture being reported in the literature after a spell or break in high-speed events.
In contrast to muscle and bone, cartilage and tendon have limited capacity for repair. During a horse’s lifetime, there is gradual loss of capacity with these tissues. Within the human literature, it is estimated that the tissue turnover time for cartilage is about 150 years, effectively nonrenewing over the horse’s lifetime, and this reinforces the need to focus on priming the tissue and minimizing wear and tear via abnormal forces on these tissues.
It is a similar situation with tendons, which with increasing load cycles have a loss of crimp and structural integrity. The effect of accumulated cyclic load on susceptibility to injury is reinforced with the increase in the IR of tendinopathy for racehorses five years old or older.
Can you explain tissue “priming” in young horses?
Tissue priming can be either in the form of a direct change in the phenotype or a change in how the tissue will respond to load later in life. The nature and the type of tissue priming depends on the tissue type and when the priming exercise is applied.
An example of a direct response is the greater biochemical heterogeneity of cartilage observed with foals with additional exercise. At six months of age, there were quantifiable differences in biochemical heterogeneity and increased chondrocyte viability.
In the same cohort of foals provided additional pasture exercise, the response of the bone in the first phalanx and third metacarpal bone provided an example of an upregulating response. In the exercised foals, the increased bone mass and strength, which persisted throughout life, was not observed until the foals were 12 months old.
What work has been done in the exercise of foals?
The initial work by the team at Utrecht University compared stall-raised foals with pasture-reared foals. This study demonstrated greater musculoskeletal development in foals reared at pasture, and this advantage persisted even when all cohorts had access to pasture up to yearling age. Data were then reported using GPS to track mare and foal activity at pasture. This work demonstrated that paddock (field) size altered the distance covered by mares and foals per day and that optimal or maximal distance covered appeared to be 7 km/day. A subsequent GPS study demonstrated that maximal osteoinductive activity in foals occurs preweaning and that this play behavior overlays with the theoretical ideal for promotion of bone development.
In a controlled intervention study, foals were provided 30% more activity than pasture-managed controls, and this resulted in upregulation of most musculoskeletal tissues. More recently, an epidemiological study in the U.K. reported fewer injuries and greater racing success in commercially reared foals managed in larger field sizes.
What about yearlings?
From the literature, it appears that the greatest response of tissue to priming is during the preweaning period. However, for many tissues there is still some capability to be stimulated/primed even as a yearling. Epidemiological data from commercial breeding farms indicate that yearlings provided with greater ability to exercise (more time at turnout and greater field size) had fewer interruptions in their first race preparation.
Describe briefly how two-year-old Thoroughbreds are managed and trained?
There are subtle differences across racing jurisdictions in the training and management of two-year-old racehorses. Data on the time from entry into a racing stable to first barrier trial or race demonstrate that two-year-olds take longer than older horses to achieve these milestones. This is in part because training two-year-olds requires education and learning how to train as well as the task of becoming fit enough to race.
In Australasia, most two-year-olds have a lower volume of training (both pace work and breeze ups) than older horses and will often have several short-duration preparations during their two-year-old year. In New Zealand, only 18% of horses will have a start as a two-year-old (though most will have a barrier trial) and will have a median of two (IQR 1–3 starts) as a two-year-old.
Can you describe the relationship between the amount of physical activity performed early in life or early in a training regimen and success as racehorses? Is this why two-year-olds that train and race have longer, more successful careers?
Cross-sectional studies of foal crops from a few racing jurisdictions (U.K., Australia, and New Zealand) have produced very consistent results with a clear exercise dose response of two-year-old exercise and racing success and longevity. In the New Zealand dataset, the level of exercise was able to be graded based on the milestones of being registered with a trainer (having basic race training), having a barrier trial (a qualifying or preparatory race with no gambling), or an official race start. There was a clear increase in the odds of a longer career and
greater prize money with the progression from registered with a trainer, to trial start, and to an official race start.
These epidemiological studies used career length as a proxy for musculoskeletal health. Direct epidemiological evidence for the benefit of racing as a two-year-old can be found in the reduced odds of race-day fracture in horses that raced as two-year-olds. This result has been consistently reported across several racing jurisdictions even though they had subtly different methods of preparing and training two-year-olds.
Other factors come into play. Can you describe how training and racing surfaces affect injury rate?
The racing surface alters the load the limb experiences. There are differences between track surfaces (dirt, all weather/synthetic, and turf) in the type and location of injuries observed. Racing on firm (less compliant) tracks irrespective of surface type increases the risk of injury and race-day fracture. Most jurisdictions and track managers actively manage tracks to avoid racing on this type of surface. Horses can adapt to certain surfaces and type of going (how soft the track is) and “tune the tension in the limb” in relation to previous experience on surfaces. This tuning requires consistency of the surface, and lack of consistency in a racing surface is probably one of the major risk factors on which we still require metrics.
How does training load affect injury risk?
The relationship between injury risk and training load or training duration (preparation length) is nonlinear. As the horse accumulates load cycles, the risk of injury compounds, resulting in an inflection point and rapidly increasing injury risk relative to extra load cycles, or days in training. Where this inflection point is in relation to accumulated load cycles and the magnitude of the slope depends on the capability of the tissue. The capability of the tissue is the cumulation of positive (early priming and development), cyclic load, and periods of rest or recovery. Early priming of the tissue cannot only improve the initial set point for injury risk but can also alter the slope by moderation of how the tissue responds to load.
Do you have any final thoughts on the idea that the challenge is not “too much exercise too soon” but “too little exercise too late”?
If we use feral or wild horses as an indication of the ecological niche occupied by the horse, then we underestimate the locomotor capability of the horse. Most management systems restrict exercise, either due to climatic or spatial constraints, or to reduce the risk of injury. Pasture exercise may be desirable, but an additional 30% more high-speed activity has been shown to generate positive results on the musculoskeletal system of foals. GPS data demonstrates that horses chose to cover 7 km/day when grazing, and this includes foals as young as one week old. To achieve this as free exercise in a paddock requires a paddock of approximately 4 hectare. This paddock size is greater than the largest paddock size category recently reported for foals reared on commercial Thoroughbred farms in the U.K.
How can the racing industry improve training practice and optimize welfare?
The coming decade will see a dramatic change in the ability to monitor horses and interpret data to prevent injury. The potential for trainers to record stride-by-stride training information on horses
with wearable technology for every workout permits a high level of monitoring sensitivity. Greater data-processing capacity and the use of AI will permit greater identification of variables that could contribute to injury.
However, these tools are only assisting with the horses once they are in training. As an industry, we need to examine how we can provide the optimal rearing environment to generate a phenotype that is best prepared for a life as an equine athlete.
Can you recommend three to five seminal references (articles, book chapters, etc.) on muscular development written by you or someone you admire in the field?
1. Rogers, C.W., and K.E. Dittmer. 2019. Does juvenile play programme the equine musculoskeletal system? Animals 9(9):646. https://doi.org/10.3390/ani9090646.
2. Rogers, C.W., E.K. Gee, C.F. Bolwell, and S.M. Rosanowski. 2020. Commercial equine production in New Zealand 2: Growth and development of the equine athlete. Animal Production Science 60(18):2155-2163. https://doi.org/10.1071/an16752.
3. Rogers, C.W., E.K. Gee, and K.E. Dittmer. 2021. Growth and bone development in the horse: When is a horse skeletally mature? Animals 11(12):3402. https://doi.org/10.3390/ ani11123402.
Effect of Mare Nutrition and Management on the Development and Sports Career of Offspring and the Role of Epigenetics
Pascale Chavatte-Palmer, DVM, PhD
Can you give us a brief biographical sketch, especially regarding the topic at hand?
Initially trained as a veterinarian with specialization in equine reproduction (veterinary degree at Alfort, France; internship at Rossdale’s, U.K.; residency at University of Florida; doctorate at Cambridge University, U.K.), I currently lead the INRAE BREED research unit focusing on the developmental origins of health and disease (DOHaD) in model and domestic species and in humans. My own work focuses on how the maternal environment, including nutrition, metabolic health, age, parity, reproductive biotechnologies and management, influences embryo development, placental function, and long-term offspring health, possibly affecting athletic performance, in horses.
Over the past two decades, our team has developed equine models that allow us to separate genetics from maternal environment, particularly through between-breed embryo transfer. These models have helped demonstrate how profoundly the uterine and overall maternal environment can shape growth, metabolism, and orthopedic risk for the offspring. More recently, we have turned our attention to epigenetics, seeking molecular markers that explain how early-life conditions become biologically embedded in the foal.
What is developmental origins of health and disease?
Developmental origins of health and disease (DoHaD) is the concept that conditions during early development, especially around conception, gestation, and early neonatal life, influence long-term health. The fetus adapts to its environment to maximize immediate survival. However, those adaptations may predispose the individual to metabolic disease later in life.
In humans, this has been linked to obesity, diabetes, cardiovascular disease, and osteoporosis, among other noncommunicable diseases. In horses, we are seeing similar patterns involving insulin dysregulation, inflammation, and altered skeletal development that could affect performance outcomes.
What is epigenetics, and how does it relate to DoHaD?
Epigenetics refers to modifications that regulate gene expression without altering the DNA sequence. These include DNA methylation, histone modifications, and RNA-based mechanisms such as noncoding RNAs. These epigenetic marks act as a kind of biological memory. They are especially plastic during early embryonic development. Some of these marks become permanent, whereas others are transient depending on the environment of the individual.
Nutrition, inflammation, and metabolic state can modify these marks, permanently influencing gene expression patterns. Epigenetics provides the mechanistic explanation for how maternal environment can shape long-term phenotype under the DoHaD framework.
Can you explain predictive adaptive response?
Predictive adaptive response is the idea that the fetus uses maternal cues to “predict” the postnatal environment. For example, if nutrient availability appears limited during gestation, the fetus may adapt by becoming metabolically efficient. If the postnatal environment matches that prediction, the adaptation may be beneficial. However, if a nutrient-restricted fetus is born into a nutrient-rich environment, that same adaptation may increase the risk of obesity or insulin resistance. The mismatch is where problems arise.
How do these adaptive mechanisms sometimes lead to health problems?
Adaptations are not inherently harmful, as they are survival mechanisms. But when environmental conditions change, or when metabolic stress persists, those adaptations may become maladaptive.
In horses, this can manifest as insulin dysregulation, chronic low-grade inflammation, altered cardiovascular regulation, or orthopedic disease such as osteochondrosis. One important point is that birth weight alone does not necessarily reflect programming; metabolic alterations can occur even when growth appears normal.
How does this relate to recipient mares in an embryo transfer program?
Recipient mares provide the uterine environment for nearly a year and then the lactational environment for months afterward. In embryo transfer, the size, metabolic health, and nutrition of the recipient mare can dramatically alter fetal growth, even though the foal’s genetics remain unchanged. This makes recipient mare selection critically important. Ideally, the recipient should match the donor mare in size and breed to minimize unintended enhancement or restriction of growth. The mare should be fed correctly at all stages of pregnancy, ensuring the maintenance of a body condition score of around 5 (on the familiar 1-9 scale).
Can you explain the proof of concept using different-sized horses?
We used between-breed embryo transfer models. For example, transferring pony embryos into large draft mares or transferring large-breed embryos into pony recipients. This allowed us to separate genetic potential from maternal uterine capacity.
The results clearly show that maternal size and uterine environment can either enhance or restrict fetal growth beyond what genetics alone would predict and affect metabolism and the incidence of osteochondrosis before the age of 18 months.
Can you describe a model that shows increased fetal growth?
When pony embryos are carried by draft mares, fetal growth is significantly enhanced by as much as 30 to 57 percent in some measures. Importantly, this growth is described as harmonious, meaning body proportions remain balanced through at least 18 months of age. However, metabolic differences are present early in life, including temporary insulin resistance and cardiovascular differences.
Were there health differences in these “enhanced” foals?
Yes, pony-in-Thoroughbred foals demonstrated elevated arterial blood pressure and altered baroreflex (a rapid, short-term mechanism that maintains stable blood pressure) sensitivity shortly after birth. Pony-in-draft foals showed early insulin resistance around weaning. Although some of these metabolic differences diminished by 18 months, the findings show that early programming effects are measurable.
Can you describe a model of restricted fetal growth?
In contrast, when large-breed embryos such as American Saddlebreds are transferred into pony recipients, fetal growth is restricted. These foals are born lighter and grow more slowly until weaning, after which they often exhibit disharmonious catch-up growth.
Were there health differences in restricted foals?
Yes, restricted foals were initially more insulin-sensitive than controls until weaning, but that difference disappeared by 18 months. Importantly, they had an increased risk of osteochondrosis at around six months of age, although this difference was no longer evident at 18 months when animals were managed adequately to lower the incidence of osteochondrosis.
How does broodmare nutrition affect offspring health?
Both undernutrition and overnutrition influence fetal programming. Even moderate undernutrition—about 80 percent of energy requirements—may not change birth weight but does induce placental adaptations, including increased vascularization and nutrient transport. Overnutrition and obesity are associated with
insulin resistance and inflammation in offspring. The key message is that metabolic state, not just calorie level, matters.
How does mare nutrition affect osteochondrosis risk?
High-starch cereal diets produce repeated postprandial hyperglycemia and hyperinsulinemia. Chronic hyperinsulinemia can disrupt cartilage development and bone maturation. Maternal metabolic dysfunction, including insulin dysregulation, increases the risk of osteochondrosis lesions in offspring.
How did you study pregnant mares fed diets with and without cereals?
We compared mares receiving cereal-based concentrates to those on forage-based diets and measured postprandial glucose and insulin responses. Mares receiving cereals had significantly higher postprandial glucose and insulin peaks. These metabolic shifts are consistent with mechanisms that could influence fetal cartilage and bone development.
What were the differences in mares and placentas?
In metabolically stressed mares, placental inflammation and vascular changes were observed at the molecular level. Some models showed changes in placental gene expression without obvious gross morphological changes. This reinforces that placental function can be altered even when size appears normal.
What effects does mare undernutrition have on foals?
Moderate undernutrition did not significantly affect birth size. However, long-term outcomes included delayed testicular maturation in males, reduced insulin sensitivity in adolescence, and reduced cannon bone width late in the study period. These findings highlight subtle but meaningful programming effects.
What effects do mare overnutrition and obesity have?
Obesity beginning early in gestation led to offspring insulin resistance, low-grade inflammation, and increased osteochondrosis risk at about 12 months. Birth weight was not significantly different, which again demonstrates that metabolic programming can occur independently of visible growth differences.
How does mare obesity accompanied by insulin dysregulation and inflammation affect foals?
This metabolic state amplifies programming effects. Offspring show prolonged inflammatory signals, increased insulin resistance at 6 and 18 months, and higher risk of orthopedic lesions. Early gestation appears to be a particularly sensitive window.
What is primiparity in mares, and how does it affect foals?
Primiparous mares are carrying their first foal. These mares tend to produce smaller, lighter foals. Placental exchange surface may be reduced, and maternal metabolic adaptation may be less efficient. Offspring may show delayed metabolic and reproductive maturation.
How does parity affect sport success?
Data suggest that offspring of primiparous mares may have slightly reduced performance in racing and show jumping compared to those from multiparous mares, regardless of genetic merit. Yearling size correlates positively with racing performance. Performance is multifactorial, but maternal factors contribute.
What effects does mare age have?
Older mares produce embryos with altered gene expression suggestive of delayed development, which is partly responsible for their reduced fertility. Placental gene expression shifts in pathways related to inflammation, transcription, and angiogenesis.
Gross birth morphology may appear similar, but molecular differences are present. Interestingly, regardless of age, lactation at breeding shortens gestation length and alters placental gene expression, with reduced long-term postnatal growth, due to reduced milk production at the end of lactation. Nutritional support to the foal after four months may be required to maintain preweaning growth.
Does postnatal management affect metabolic status?
Yes, feeding practices influence insulin dynamics. In our study comparing two meals per day versus eight meals per day, there were no major differences in glucose metabolism or osteochondrosis incidence, but differences in intestinal flora and metabolome were
observed. This suggests gut biology may be sensitive to feeding distribution even when overt metabolic markers are not.
What are you working on now?
We are focusing on identifying epigenetic biomarkers in embryos and placentas that can predict long-term outcomes. By integrating transcriptomics and molecular profiling, we aim to develop tools that breeders and veterinarians can use to optimize broodmare management.
When you compare racehorses and sport horses, what are the most common musculoskeletal injury patterns you see in each discipline?
Horses in both disciplines suffer mainly from “repetitive stress injury” which means that most injuries result from the chronic, repetitive nature of the exercise. For racehorses, the stress comes early, and the tissues typically respond quickly to strengthen. For the sport horse, the stress comes later but the tissues are still naive and need to adapt. But for some horses the ability to adapt to the work is compromised and the processes that lead to injury begin.
For the racehorse, the bone is the most sensitive of tissues, and “stress” fractures can result. This can occur most anywhere in the body, but the fetlock is the most susceptible. Tendon and ligament injuries are also common. For the sport horse, foot, fetlock, and suspensory ligament injuries are common. Advanced imaging such as MRI shows many of these to be chronic in nature. We know from the western performance disciplines that the bone-ligament interface at the suspensory origin adapts and remodels with training, and that injuries are likely due to repetitive stress.
Which injuries would you consider truly “sport-specific” (i.e., rarely seen outside a particular discipline)?
Catastrophic injuries in racehorses, whether they be in the axial or appendicular skeleton are truly unique. The application of high-speed work induces that problem. Condylar fractures and proximal sesamoid fractures are unique to racehorses, again due to the nature of the sport.
Collateral ligament injuries and fetlock bone bruising appear unique in nonracing horses. The landing from jumps or the unique gaits of dressage horses likely create that cascade of events. It is interesting that some acute damage to tissues can go unnoticed—the horse shows no lameness, but can be the inciting cause of a cascade of events that lead to subchondral bone damage.
Are there specific anatomical “hot spots” (e.g., fetlock, suspensory apparatus) that consistently differ by sport, and what loading patterns cause those differences?
Fetlocks in racehorses are certainly the “hot spot.” Carpal joints are also a concern. But the entire skeleton is a concern since stress fractures can occur just about anywhere. In sport horses, the feet (coffin joint, navicular apparatus, etc), fetlocks, and suspensory apparatus are always a concern.
Conversely, which musculoskeletal injuries are essentially universal across all athletic horses regardless of discipline?
Injuries that have a predisposition from developmental orthopedic diseases are common to all disciplines. Hock and stifle osteochondritis dissecans (OCD), subchondral cystic lesions in the stifles, some ankle chips. Those don’t seem to discriminate among disciplines.
How do training surfaces (dirt, turf, synthetic, grass, arena footing) influence the type and frequency of injuries in each sport?
Years of research has shown that certain injuries are more common on specific footing. Changes in footing have resulted from that work. High-speed work on dirt tracks has the highest injury rate. Although better on turf, it is more susceptible to weather effects. Track maintenance practices now are making tracks safer and more consistent.
Arena footing is a growing concern. We are now seeing more first phalanx (P1) fractures in sport horses lunged on modern footing. Something is happening with the hoof-footing interface that might be causing the problem.
Can you talk about how discipline-specific training regimens (high-speed gallops vs. collected work vs. repeated jumping efforts) shape bone and soft-tissue adaptation. When does adaptation tip into pathology?
Musculoskeletal tissues adapt to the stresses and direction of stresses they see. This starts at birth. When high-speed work or collected work with change in balance begins, the musculoskeletal tissues have time to adapt to those changes. Unfortunately, that required time varies between individuals due to a lot of factors. When the specific stress volume and magnitude exceed the rate of adaptation, then tissue damage begins. This is normal and stimulates local tissue remodeling. This builds resilience in the tissues. But when the tissues cannot adapt fast enough, then progressive damage occurs to the point of injury.
In your experience, how does age at training onset and early career workload differ among these sports, and how does that relate to later injury risk?
Early exercise, when brought on thoughtfully, is protective. We have shown experimentally and we know from horse-rearing practices that early exercise is critical. In racehorses, especially those intended for breeze-up sales, the early, intense speed is high. But it creates high resilience. So, it’s a double-edged sword. The benefit now is that most trainers know this and are aware of the subtle signs of exercise-related problems. Sport horses tend to be brought on slower, but the push for young-horse events is growing, and likely leading to more early injury.
Are there notable differences in forelimb versus hindlimb injury distribution between racing and sport horses such as jumpers and dressage horses?
The fetlocks and carpi are the highest focus for racehorses, and the general thinking was that sport horses had comparatively higher hindlimb issues. But as sport horses go higher and faster, the incidence of forelimb issues is fairly high. They all seem to get chronic tarsal and stifle issues. Those are typically higher in sport horses. But there is a lot of overlap in injury distribution between disciplines. Now, they can look different.
Tarsal slab fractures are a good example. They occur in horses of all disciplines, but they are different in bone affected and fracture configuration between disciplines.
How does conformation interact with discipline choice? For example, are there conformational traits that are relatively well tolerated in one sport but high-risk in another?
Any major conformational issue will have impact regardless of sport type. We also know that some minor flaws are acceptable, as the horse likely adapted the tissues within that area over time. We also know that some conformational appearances can be protective, like mild carpal valgus (knock-kneed) in racehorses.
Straight hocks, hyperextended fetlocks and long-toe, low-heel conformation predispose sport horses to hind suspensory issues. So conformation does play a role. We also have to keep in mind the length of an athletic career. Some racehorses might be able to tolerate a mild hock issue because of a relatively short athletic career compared to a sport horse meant to compete into their teens.
For catastrophic injuries in racehorses versus chronic, performancelimiting injuries in sport horses, what similarities and differences do you see in underlying pathology and risk factors?
The basic molecular, biochemical, and structural tissue changes are similar. Tissues undergo stress, they remodel, and they try to adapt or heal. But when the stress magnitude or volume exceeds a threshold, progressive damage occurs to the point of injury and pain. Since racehorse catastrophic injuries primarily occur in bone, the outward appearance of the horse might not change much before the injury. Now that is changing with the use of wearable sensors, which could help in detecting subtle movement changes at speed.
This is similar for sport horses. A lot of performance-limiting injuries show no outward signs. The horse just does not work to expected levels, or shows behavioral issues or other signs. Ironically, it’s the same for human athletes. All athletes in all disciplines work with pain. Some deal with it better than others. Working through that resiliency makes identifying the horse at risk of injury very difficult.
How has advanced imaging (e.g., standing CT, MRI, nuclear scintigraphy) changed your ability to detect discipline-specific injury patterns early, before they become catastrophic?
This has been key to identifying the horse at risk of injury. PET, CT, MRI, and nuclear scintigraphy have been key to optimizing health and welfare in athletic horses in all disciplines. A horse that shows changes in behavior or performance now has a solution paradigm for identifying the problem. Advanced imaging has shown the common locations and patterns of injury. They have improved our ability to give a more accurate prognosis and thoughtful rehabilitation program. The last 30 years has really brought the greatest changes in our understanding of disease.
Are there particular “red flag” clinical signs or subtle performance changes that trainers or veterinarians should watch for in each discipline to catch injuries earlier?
Any change in movement is key, whether it’s seen by the grooms and trainers or felt by the riders. Not that a horse can’t be sore from a hard work. But vigilance is key. Same with changes in behavior and performance. Daily palpation of the limbs is vital as, in my opinion, any subtle pain or swelling of a tendon or ligaments needs to be addressed immediately, regardless of discipline. Some issues, like navicular pain, can manifest more at a walk than a trot. That always is concerning.
How do shoeing and farriery practices differ between racehorses and sport horses, and what impact do those choices have on injury patterns?
In racehorses, the effects of things like toe grabs are known and managed well. I think the role of farrier practices has more to do with the effectiveness of the team than any one particular practice. The trainer, vet, and farrier working together to optimize health and performance is most effective. That team knows the nuances of shoeing Thoroughbred racehorses whose feet adapt to specific work on specific footing.
The same is true of sport horses. Knowing how balanced and strong a dressage horse is, for instance, will give them insight on how best to support the suspensory apparatus with shoeing.
Many eventers cross-train in dressage and jumping. Does that multimodal workload increase risk, or can it be protective compared to more single-discipline horses?
I think its protective. Giving the tissues multiple directions and intensity of forces can build resiliency and neuromuscular plasticity, and makes the horses better balanced and able to overcome subtle imbalances.
Do you see differences in reinjury rates or return-to-sport outcomes among these disciplines for similar injuries (e.g., suspensory desmitis, proximal suspensory injury, fetlock osteoarthritis)?
I think some horses can continue with things like suspensoryorigin injuries, at least in some level of work. Osteoarthritis has no cure, so there must be a management approach in which continued work is critical. Fractures and any injury requiring surgical repair needs time off, which is dictated by the type of injury. Tendons are the real difficult ones to deal with. It takes a long time to bring a horse back from a significant tendon injury, and reinjury rates are relatively high. This is where I think the racehorse has a disadvantage due to the volume of high-speed work needed to compete. Suspensory injuries too, but a lot of those are chronic, nagging injuries, similar to a high ankle sprain in people. The chances of return to sport are sometimes dictated more by the athlete’s resiliency and the thoughtfulness of training. You hear some jumper trainers say that good jumpers often don’t need to see a lot of jumps, depending on the level, so keeping them fit without a lot of jumping is sometimes used.
How do management practices (e.g., turnout, rest periods, competition schedules) modulate musculoskeletal injury risk differently in each discipline?
There is growing concern that a lot of racehorses are not getting a break in their training because of global and national racing stress. That downtime is often critical but must be handled carefully to properly condition when coming back from layoff. The injury rate in racehorses does go up after layoff, so thoughtful reintroduction of high-speed work is needed.
For sport horses, rest and turnout are great if they are available. Competition schedules and constant transport make that difficult. Consequently, a lot of the training occurs at the competition venues. Long hacks are very useful from a rest, rehab, and conditioning standpoint, but this is often limited by availability of land and schedules.
Are there evidence-based conditioning or rehabilitation strategies you recommend that are particularly effective in reducing injury risk for specific sports?
For racehorses, short bursts of high speed are critical. Bone does not need to see much high-speed volume to adapt. The industry has known this for decades and best practices are based off of that knowledge. For sport horses, neuromuscular training is critical to be able to handle the various movements needed. This includes gymnastics and training on various surfaces.
Layering rehabilitation techniques onto regular training is helpful, but not a replacement. Swimming and underwater treadmill exercise are often advantageous, but the body needs to see vertical loading to adapt.
From a research perspective, what are the biggest knowledge gaps in sport-specific musculoskeletal injury epidemiology or biomechanics?
We are much better at understanding the factors associated with injury. Those practices that are helpful and hurtful. The difficult part now, and it’s the same in human sport performance, is characterizing injury susceptibility in an individual athlete. Answering why injury occurs in one individual and not in another. It is easy to say genetics, breeding, footing, and other factors.
All of those factors do play a role. But really homing in on factors that affect a particular athlete are critical. Given the advancements in multisource data analytics, we are closer to getting to athlete-specific monitoring and management.
How can sport-governing bodies and competition organizers use what we know about discipline-specific injury patterns to improve safety (e.g., course design, surface standards, rule changes)?
Some federations and governing bodies are very proactive. HISA is working hard to develop strategies and, most importantly, is working with researchers and clinical practitioners to develop solutions for racehorses. The United States Equestrian Federation (USEF) is working with the American Association of Equine Practitioners (AAEP) on sport horse practices. Some governing bodies lag due to many issues, some cultural between countries. I feel that the best way to manage welfare, health, and safety is for governing bodies to engage with those involved on a regular basis.
If you could give one practical, discipline-tailored injury-prevention message to trainers and owners in racing, show jumping, dressage, and eventing respectively, what would those four messages be?
Well, for all four, it is to work with your team on a regular basis.
Racing: monitor closely prior to and after breezes. Consider using sensors and working with your vet.
Show jumping: look at workload volume and make sure the horse is getting fitness and proprioception-type work, i.e., grids and gymnastics, to get the horse to really think about its feet.
Dressage: watch closely during times of moving up the levels. Again, try and prepare for the body soreness that can come with balance and core strengthening.
Eventing: consider training with movement and cardiac sensors. There is a lot of work emerging that are better informing conditioning and training practices.
Can you recommend three to five seminal references (articles, book chapters, books, etc.) on equine sports injury written by you or someone you admire in the field?
1. Garcia-Lopez, J.M., and T.J. Divers. Equine Sports Medicine. 2018.
2. Hinchcliff, K.W., A.J. Kaneps, R.J. Geor, and E. Van ErckWestergren. Equine Sports Medicine and Surgery. 2022.
3. Ross, M.W., and S.J. Dyson. Diagnosis and Management of Lameness in the Horse. 2011.
Omega-3 Index: Relevance for Human Health and Disease
William Harris, PhD
Can you give us a brief biographical sketch, especially regarding the topic at hand?
I earned a doctorate in nutritional biochemistry and have been studying omega-3 fatty acids for over 45 years. I have over 360 omega-3-related publications and have been the recipient of eight National Institutes of Health grants on omega-3 fatty acids. In 2004, I codeveloped an omega-3 blood test called the “Omega-3 Index,” and in 2009, I formed OmegaQuant Analytics, LLC, to offer the test to researchers, clinicians, and consumers. In 2020, I created the Fatty Acid Research Institute to accelerate the discovery of fatty acid and health relationships. I have been on the faculty of three state medical schools and am currently a professor in the Department of Medicine at the Sanford School of Medicine, University of South Dakota.
Can you give us an overview of fatty acids, with special emphasis on the polyunsaturated fatty acids EPA and DHA?
Fatty acids are chains of carbon atoms ranging from 3 to 35 or more carbons. Those in our diets and the predominant ones in our tissues are between 10 and 22 carbons long. The carbons are connected to each other by single or double bonds. If all the bonds are single bonds, the fatty acid is considered saturated (i.e., with hydrogen atoms, two per carbon). Fatty acids with one double bond in the chain are called monounsaturated and those with two or more double bonds are called polyunsaturated fatty acids (PUFAs).
The PUFAs are subdivided into two families: omega-3 and omega-6. The difference is where the first double bond counting from the methyl end (as opposed to the acid group on the other end) is located.
If the first double bond is on the third carbon, you have an omega-3; if it is on the sixth carbon, it is an omega-6. The “omega” term refers to the end of the chain; the acid group is the “alpha” carbon.
The omega-3 fatty acids come in two subclasses: plant-derived (alpha-linolenic acid, ALA) found in flaxseed oil, soybean oil, chia seeds, and black walnuts, and the marine-derived (EPA and DHA), which are found primarily in seafoods. ALA is the principal omega-3 fatty acid in our diet (mostly from soybean oil), and EPA and DHA are the main omega-3 fatty acids from fish/krill/algal oils. Chemically, ALA is called C18:3n-3, which means it is made up of 18 carbon atoms; it has three double bonds; and the first one from the methyl end is in position three. EPA is C20:5n-3 and DHA is C22:6n-3.
Can you tell us where humans get EPA and DHA, what foods?
Fish can provide a lot or very little EPA and DHA depending on the species. Those particularly rich in EPA/DHA include the “SMASH” fish: salmon, mackerel, albacore tuna (or anchovies), sardines, and herring.
Can you explain why omega-3s are more appropriately labeled important for life but not essential?
In nutrition, “essential” means a nutrient cannot be made by the body. ALA is the essential omega-3 fatty acid, and from it, EPA and DHA can be made. But they are made in very low quantities, so high blood and tissue levels cannot be reached with ALA alone. Much research has shown that high levels of EPA and DHA have distinct health benefits, and these levels can only be reached by eating (or supplementing with) “preformed” (or actual) EPA and DHA. These are considered “bioactives” and important for optimal health but not “essential” in the strict biological sense.
What happens to ALA if it is not converted to EPA and DHA?
ALA is mostly burned for energy like most fatty acids we eat or stored in adipose tissue. EPA and DHA are mostly spared these fates and are incorporated into cell membranes all over the body. They are essential for making membranes “work” properly and are the starting materials for the synthesis of a very wide variety of other “bioactive” molecules like prostaglandins, leukotrienes, resolvins, and protectins.
Do people become deficient in omega-3s, as they can with other nutrients, or is there a preferred level for optimal health?
People like vegetarians (and especially vegans who eat no animal products at all) can have very low levels of omega-3 fatty acids (by which from now on I mean EPA+DHA), but they are not incompatible with life like being deficient in vitamins or minerals. There are preferred levels for optimal health, however, and that is what the Omega-3 Index is trying to get at.
Can you explain how you came up with the Omega-3 Index? What is it?
The Omega-3 Index is a blood test that assesses whole-body omega-3 status. It is the EPA+DHA content of red blood cell (RBC) membranes expressed as a percentage of the total fatty acids in the membrane. Typical levels are <4% (e.g., vegans), 5-6% (typical Americans), >8% (optimal; typical of cultures like Japan and Korea where lots of fish is eaten throughout life). I came up with it in 2004 with a colleague (Dr. von Schacky) based on research others had done showing that people with a low RBC EPA+DHA level (a low Omega-3 Index) are at increased risk for sudden cardiac death, or primary cardiac arrest, or more simply, a heart attack that kills within a few minutes (about 40% of heart attacks). In 2004, we published a paper (Harris and von Schacky, 2004) proposing the Omega-3 Index as a new risk factor for heart disease, and we recommended the cutpoints noted above for “low or undesirable,” “intermediate,” and “high or optimal” based on literature available at the time. These cutpoints continue to be supported by subsequent studies.
Why were red blood cells (RBCs) chosen as the measurement site, and how does it differ from serum or plasma measures?
RBC membranes are generally reflective of cell membranes throughout the body. Since omega-3 fatty acids operate or exert their influence ultimately at the membrane level, it is only reasonable to measure the enrichment there. The Omega-3 Index is much like hemoglobin A1C (HbA1c) as a measure of glycemic control: measured in RBCs, expressed as a percent, and serves as a longer-term stable marker of status than plasma glucose. The same is true for the Omega-3 Index. Plasma and serum (which are similar from a fatty acid composition standpoint) are more labile and reflect recent changes in omega-3 fatty acid intake.
Is the Index a percentage or a raw numerical value?
Percentage of total fatty acids in the membrane. The membrane has a fixed number of fatty acids (carried as phospholipids) so “concentration” terms do not make any sense, and are rarely used in scientific studies. PUFA percent composition has been shown to be a better reflection of dietary intake than plasma concentrations, which are highly influenced by lipoprotein concentrations since these are the carriers of virtually all fatty acids in the plasma.
Why is this considered a “long-term” marker rather than a “snapshot” in time? Is it because of the 120-day lifespan of the RBC?
Yes. Although RBC membrane fatty acid composition can be changed while in circulation, composition is primarily determined in the bone marrow.
Explain how omega-3s foster cell membrane flexibility and what that means for the human body. Why should cell membranes be flexible?
Imagine comparing the “flexibility” of butter versus olive oil. Obviously, the latter is more fluid than the former. Even at refrigeration temperatures where butter is quite solid, olive oil begins to cloud up as some of the saturated fatty acids begin to coagulate.
Olive oil has mostly oleic acid (a monounsaturated fatty acid), and the “kink” put into that molecule makes them harder to “stack” together than the completely straight chains of saturated fatty acids (in butter). Fish oil is even more flexible because there are up to six double bonds—or kinks—in these fatty acids, so fish oil will not even solidify in the freezer.
Cell membranes are essentially a “sea” of phospholipid molecules through which millions of protein pores (receptors, channels, etc.) are inserted. If the membrane is stiffer, these protein pores are more “locked down,” unable to move and change shape very well. When the membrane is more fluid, these proteins have “elbow room” and can much more easily carry out their functions without the constraints of a stiff membrane.
My favorite metaphor is this: if you picture the millions of protein pores as “doors” on the membrane, some opening in and some opening out. The in door is for bringing food into the cell and the out is for the garbage. For a cell to be healthy, the doors must swing smoothly on their hinges. What the omega-3s do is “oil the hinges” on both kinds of doors. They make each cell healthier by optimizing the functions of the in and out doors. This has broader effects on important functions of cells and tissues and organs: reducing chronic inflammation, lowering blood lipid levels, making the artery walls more flexible to enhance blood flow, and slowing the heart rate, among other functions.
Can you tell us about omega-3 and heart health?
There is a long history of omega-3 fatty acids and heart health. Beginning with observations in the 1970s that Greenland Inuits had very few heart attacks despite eating a high-fat, highcholesterol, low-vegetable diet. It was discovered that the EPA and DHA levels in their food and blood were very high (compared to Westerners), and years of research since has shown that both giving omega-3 fatty acids in randomized trials and measuring blood omega-3 fatty acids (e.g., the Omega-3 Index) in observational trials is virtually always linked with better heart health.
Another important aspect of omega-3 is brain health, including mental health. What can you say about that?
The two most prominent fatty acids in the brain are DHA and arachidonic acid (AA), DHA’s omega-6 cousin. Studies have shown that omega-3 treatment can improve depression and can slow cognitive decline with age. We have shown in several studies that a high Omega-3 Index is strongly linked with a lower risk for Alzheimer’s disease. Maintaining a high Omega-3 Index throughout life is important for forestalling the onset of mental disorders and decline.
Athletes often have lower index numbers than nonathletes. Why? Is it just diet? Does work intensity matter?
This observation is likely related to the intensity of work. The omega-3 fatty acids, in this high demand setting, are probably being burned for energy instead of stored in membranes.
Can people feel the effects of upping omega-3 consumption?
In general, no, but people have noticed an improvement in dry eye symptoms with omega-3 treatment, and it is common that people given high doses of omega-3 pharmaceutical products to treat high blood triglycerides report a lessening of joint pain.
Is it all salmon and sardines, or do supplements work well?
The SMASH fish (salmon, mackerel, albacore tuna or anchovies, sardines, and herring) all will raise the Omega-3 Index, and so will supplements. I always recommend fish first, but many people just will not eat enough of the right kinds of fish, so supplements are plan B.
Reference
1. Harris, W.S., and C. von Schacky. 2004. The Omega-3 Index: A new risk factor for death from coronary heart disease? Preventive Medicine 39:212-220.
Omega-3 Index: An Equine Perspective
Joe Pagan, PhD
For a thorough introduction to omega-3 and omega-6 fatty acids in equine nutrition, see the 2024 Equine Health and Nutrition Conference proceedings. The PDF is available at www.ker.com/library/2024proceedings/, with “Omega-3 and Omega-6 Fatty Acids in Equine Nutrition” starting on page 105.
Kentucky Equine Research has been studying fatty acid chemistry for more than a dozen years. What has accelerated this work in recent years?
We have partnered with OmegaQuant, a laboratory that offers assays that measure 24 fatty acids in different materials, not only blood, but also feeds, oils, pastures, and hays. This has allowed Kentucky Equine Research to make large-scale measurements of multiple fatty acids. OmegaQuant was founded by Dr. Bill Harris and is now headed by his daughter, Dr. Kristina Harris Jackson.
Initially, because of sample collection logistics, we only made measurements on our resident research horses. To measure the composition of red blood cells (RBC), we had to very quickly preserve the RBCs by freezing them and then ship them frozen to a lab for analysis. We did that successfully, even harvesting other tissue samples, such as gastric lining, for analysis.
More recently, in collaboration with OmegaQuant, we have developed a commercial dried blood spot (DBS) test specifically for horses. This test has allowed us to take samples from lots of horses because it is easy to do. It requires little blood, just a couple drops, and the DBS card contains a preservative that allows for it to be stable at room temperature. The cards can be shipped by ordinary postal service with no fear of instability.
We now have over 800 horses that we have sampled. Most of these horses are from the U.S. and Australia. The reason we have so many from Australia is that Dr. Peter Huntington, the director of nutrition at Kentucky Equine Research, is well connected in the racing and breeding industries. He has collected a lot of samples there, so we have strong data from several sectors in Australia. Additionally, we have collaborated with multiple veterinarians in the U.S. and have collected samples from many breeds and disciplines.
Overall, we have a much clearer understanding of what is going on with a larger population. This has really opened our eyes about what we are measuring.
For over 40 years, researchers have studied the use of fat as an energy source for horses, but they rarely focused on the fatty acid composition of these fats. Today, we recognize that specific fatty acids play a key role in the structure and function of cell membranes. They also act as precursors for bioactive lipid mediators such as prostaglandins, leukotrienes, and resolvins. Many of these mediators either promote or resolve inflammation.
What are the most important fatty acids to measure in humans?
In humans, Dr. Harris decided that the most meaningful measure in RBCs was the sum of two fatty acids, EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid). The sum of EPA and DHA is called the Omega-3 Index. EPA and DHA are both long-chain omega-3 polyunsaturated fatty acids (LC-PUFAs).
In humans, DHA is typically much higher than EPA; DHA can be around 3–6% of total RBC fatty acids, whereas EPA is usually closer to 0.5–1.5%. This pattern is thought to be evolutionary. DHA is the key polyunsaturated fatty acid in neural tissue (brain and spinal cord) and the retina, where it has a crucial structural role. Species with large brains tend to have RBCs dominated by DHA, which is why humans need substantial DHA. DHA is also important in cardiac membrane structure and is predictive of cardiac health.
Does the Omega-3 Index hold true for horses?
We initially expected EPA and DHA in horses to behave similarly to human samples. When we started to measure them, this was not the case.
A third omega-3 LC-PUFA is important here: docosapentaenoic acid (DPA). EPA is 20 carbons long with 5 double bonds; DPA is 22 carbons with 5 double bonds; and DHA is 22 carbons with 6 double bonds, making DHA the most highly unsaturated of the three.
In humans, DPA can be converted to DHA, and there is some reciprocity in that pathway. In horses, however, DHA does not appear to be efficiently produced from DPA. Horses synthesize DPA as an interchangeable pool with EPA. In essence, DPA becomes a buffer that can help replenish EPA but does not significantly contribute to DHA synthesis.
Horses evolved to consume plant material, primarily pasture. Pasture plants are reasonably high in two short-chain polyunsaturated fatty acids (SC-PUFAs): the omega-3 fatty acid alpha linolenic acid (ALA) and the omega-6 fatty acid linoleic acid (LA). Horses have a limited ability to convert ALA to EPA by a series of desaturase and elongase enzymes, and they appear to have poor capacity to convert EPA (or DPA) onward to DHA. The pathway from ALA to DHA in horses seems markedly constrained.
To understand this limitation, we first examined horses on pasture. Using the DBS test, we sampled many horses consuming predominantly pasture with minimal hay or concentrate. In these horses, EPA and DPA can reach relatively high levels, about 0.3% of total RBC fatty acids each, while DHA remains surprisingly low, around 0.1–0.15%. Therefore, a mature horse on pasture (nonpregnant, nonlactating) tends to have reasonable EPA and DPA but very low DHA, along with high ALA. Pasture-derived ALA accumulates in cell membranes and can be modestly converted to EPA and then DPA. The final desaturation step from DPA to DHA, however, is inefficient in horses. In RBCs of adult horses eating pasture, DHA is therefore a minor component, which is markedly different from the human pattern.
This brought about the question of whether the Omega-3 Index, defined as the sum of EPA and DHA, is as important in horses as it is in humans.
We concluded that it is probably not as important. In most horses, excluding mares and foals, it is probably the sum of EPA and DPA that is the more meaningful number.
The red blood cells of horses have a lot of LA, the predominant fatty acid, about 37-45%. Pasture contains a lot more ALA than LA, about three times as much ALA than LA. Why then is the cell membrane not full of ALA?
Several factors likely explain why ALA does not accumulate in cell membranes as much as one might expect. First, ALA is preferentially used as an energy source and is oxidized, so a portion of dietary ALA is simply burned for fuel. Second, membrane remodeling enzymes favor LA over ALA. Third, some ALA is converted to EPA, which removes additional ALA from the pool available for direct incorporation into membranes. Finally, LA is conserved because it is an essential structural fatty acid, playing an important structural role in membranes and skin barrier lipids.
Although LA and ALA are both SC-PUFAs, LA has two double bonds whereas ALA has three, making ALA more unsaturated and more susceptible to oxidation. Cell membranes in horses seem to prefer maintaining a somewhat lower degree of unsaturation, so they incorporate more LA than ALA. This pattern contrasts with humans. The proportion of LA in human RBCs is about one-half that in horses, and humans have substantially more AA, a longchain omega-6 fatty acid, in their cell membranes. Humans also have higher levels of long-chain omega-3 fatty acids (EPA and DHA) than horses, along with considerably more AA.
Horses on pasture have polyunsaturated fatty acids as their predominant membrane fatty acids, with LA as the dominant type by a wide margin, followed by ALA and then the long-chain omega-6 fat AA and the long-chain omega-3 fats EPA and DPA. The AA content of horse RBC membranes is roughly one-tenth that found in human RBC membranes. Human cell membranes therefore contain
much more AA and much less LA than equine membranes. Considering what the two species eat from an evolutionary perspective—horses as herbivores and humans as omnivores— these differences are logical.
What happens when you remove a horse from pasture and feed it a diet of hay and grains?
When you take a horse off pasture and put it on cereal grains and vegetable oils, you dramatically increase LA intake. LA goes up and ALA goes down, so you end up with even more LA and less ALA. Remember that LA in equine RBC membranes starts quite high, around 37% of total fatty acids, whereas in humans RBC LA is
typically in the teens. Human cell membranes are more enriched with longer chain, highly unsaturated fatty acids such as AA, EPA, and DHA, which is a fundamental species difference.
There is an important distinction here that I have learned to appreciate. As fatty acid science entered popular nutrition, it was quickly oversimplified. We ended up with the mantra “omega-3 good, omega-6 bad,” and similarly “all omega-3s are anti-inflammatory; all omega-6s are pro inflammatory.” Omega-3, omega-6, and omega-9 are three distinct families of fatty acids with different structures and functions. Omega-9 fatty acids, rarely discussed in equine nutrition, are monounsaturated fats such as oleic acid.
That dichotomy is far too simplistic. Inflammation is an essential physiological process in both horses and humans. It is the first line of defense against insults, whether exercise-induced tissue damage or pathogens. Without inflammation, the body cannot mount an effective response. The key is balance. You absolutely need a certain amount of AA. Our work with DBS testing suggests there is a “floor” level of AA required in the RBC membrane. If AA falls too low, the horse may be unable to mount an adequate inflammatory response. At the same time, sufficient long-chain omega-3 fatty acids, particularly EPA, are needed to act as a functional counterweight to AA so that inflammation does not become excessive or chronic.
Short-term, targeted inflammation is both beneficial and necessary. Chronic, unchecked inflammation arises when pro-inflammatory signals are not balanced by anti-inflammatory and pro-resolving mediators derived from omega-3 fatty acids, allowing the response to run away rather than resolve.
We want enough AA to support a normal inflammatory response, but we also need an appropriate AA:EPA balance, so that ratio (AA:EPA) is of particular interest.
Striking the right balance between initiating inflammation and resolving it is critical.
If we assume that a horse grazing pasture has, through evolution, arrived at a specific AA level—narrow, relatively low compared to humans, but sufficient to support necessary inflammatory responses—while also maintaining EPA and DPA levels that act as a “brake,” we are essentially assuming that nature has tuned this system well. That is a substantial assumption, but a reasonable working premise.
Using that premise, the AA:EPA ratio in pasture-fed horses typically is about 4–6:1.
Let us now consider horses that are not kept on pasture full time. Racehorses represent the extreme case. They are typically fed hay rather than pasture and have high energy requirements, so they receive substantial supplemental energy. Modern racehorse feeds are often high in fat. These diets are low in ALA. Hay contains much less ALA than pasture. In fact, we have measured that even during the short window after cutting, hay loses about half its ALA content. ALA is highly unsaturated and oxidizes easily, so the curing process degrades it. Cereal grains and vegetable oils, meanwhile, provide abundant LA.
To convert ALA to EPA requires a series of desaturase and elongase enzymes. The first desaturase—delta-6 desaturase—is shared by both the omega-3 (ALA to EPA) and omega-6 (LA to AA) pathways. When LA intake overwhelms the system, it outcompetes ALA for this enzyme, shunting conversion toward AA rather than EPA.
We first noticed this pattern in our research horses fed high-grain diets and trained moderately hard: ALA dropped sharply. When we tested actual racehorses, EPA and DPA levels fell to nearly undetectable levels. These intensely working horses are also likely oxidizing whatever little ALA they consume.
With LA overwhelming the delta-6 desaturase enzyme, the horses cannot produce enough EPA. The AA:EPA ratio escalates into double digits, not because AA levels drop, but because EPA plummets.
One of our dietary strategies is to feed EPA directly, such as through fish oil. Horses did not evolve to consume marine products, but they efficiently incorporate EPA and DHA into cell membranes. The response is predictable: you can feed just 2–3 g of EPA per day to a 500-kg horse to meaningfully restore cell membrane composition and return the AA:EPA ratio to pasture-like levels (4–6:1). Early fish oil research overestimated requirements, assuming large doses were needed. Modest amounts work effectively.
As I mentioned, fish oil also contains DHA, which is typically low in horses regardless of diet. DHA levels don’t differ much between pastured horses and racehorses. However, when fed directly, DHA levels rise predictably.
DHA generates specialized pro-resolving mediators (SPMs) that actively resolve chronic inflammation. DHA appears particularly important for resolving equine asthma and other respiratory issues. When fish oil raises both EPA and DHA, researchers believe DHA drives much of the asthma benefit. Asthma represents chronic airway inflammation, and its resolution hinges on SPMs counteracting that process.
With fish oil, EPA restores the AA:EPA balance, while DHA serves as a compliance marker. Horses efficiently incorporate DHA into cell membranes, so elevated DHA confirms consistent feeding. If a horse has been on fish oil for weeks but shows no increase in EPA or DHA, the horse likely hasn’t received it consistently (forgotten doses, underdosing, or refusal). DHA provides a reliable check on both feeding compliance and membrane incorporation.
DHA plays a special role in adult performance horses, particularly for asthma, which appears to be the most responsive condition.
DHA has a very different role in foals and young, growing horses. As fetuses and neonates, they grow rapidly and require substantial DHA for nervous system development. Once incorporated into neural tissues like the brain, DHA is not freely exchangeable and does not function as a “rinse-and-replace” pool that can be easily mobilized or replenished.
DHA is extremely important in foals. We sampled day-old foals and their dams immediately after birth, before the mares began significant lactation and with no fish oil supplementation. The foals already had high DHA and AA levels, while the mares showed the typical pasture-horse profile. This suggests pregnant mares can selectively prioritize DHA delivery to the fetus, ensuring adequate neural development.
During early lactation, foals continue receiving DHA through milk. In some cases, supplementing the mare with DHA during lactation becomes valuable to maintain milk transfer. When targeting DHA, focus especially on pregnant and lactating mares and potentially young foals during rapid growth. By weaning, however, the foal’s blood profile resembles that of an adult, with DHA levels normalized as most has been deposited into neural tissue.
Stallions may also benefit from DHA to a lesser degree. When intentionally adding DHA (through fish oil supplementation), owners must monitor antioxidant status. Vitamin E becomes equally or even more critical than DHA itself. Supplement vitamin E to gestating mares, lactating mares, and stallions regardless of fish oil use.
Explain how fatty acids affect gastric health?
This is another area where the oversimplified “omega-3 good, omega-6 bad” mantra falls apart. Consider the omega-6 pathway: LA is converted to gamma-linolenic acid (GLA), then efficiently to dihomo-gamma-linolenic acid (DGLA). DGLA is a long-chain fatty acid that can be further converted to AA but only by delta-5 desaturase, which adds one more double bond. Hors-
es can regulate delta-5 desaturase activity, favoring either DGLA accumulation or AA production.
We demonstrated this in an intriguing Florida study before we validated the use of DBS testing. We used eight Thoroughbreds in this study. They had been on a long-term exercise study, so we gave them a summer “vacation,” feeding them bahiagrass pasture, timothy hay, and a fortified concentrate and requiring no work. At summer’s end, we assessed fatty acids in plasma and RBCs, performed gastroscopies for ulcer grading, and collected stomach biopsies.
Despite the rest period, all horses had squamous ulcers (seven grade 2, one grade 3), which was not unexpected. More surprising, though, four horses had no glandular ulcers, while four had grade 3 glandular ulcers, despite identical management. Grade 3 glandular ulcers are considered the most severe.
This prompted closer scrutiny. We knew these horses well from prior studies, including sweat response through terbutaline testing. Of the glandular ulcer cases:
• Two were borderline anhidrotic (poor sweating);
• One was a high-stress horse unsuitable for treadmill work due to anxiety;
• One was heavily muscled and prone to heat stress.
Summer in Ocala is notoriously hot and humid. No prior studies have explicitly linked environmental heat stress to glandular ulcers, but these observations suggest it may contribute.
All the glandular ulcers occurred in the pyloric region, a common site for this pathology. We biopsied both the squamous (nonglandular) stomach and two glandular regions: cardia and pylorus. Fatty acid profiles revealed key differences.
Squamous tissue fatty acids matched RBC composition. However, glandular regions (particularly pylorus) showed elevated DGLA and AA compared to RBCs. Most strikingly, horses with pyloric ulcers had lower AA and higher DGLA than ulcer-free horses.
This initially seemed counterintuitive. Conventional wisdom holds DGLA as anti-inflammatory and ulcer protective, while AA fuels pro-inflammatory eicosanoids. Why the elevated DGLA in ulcer cases?
Apparently, when faced with a localized gastric insult, the horse downregulates delta-5 desaturase at that specific site. This blocks DGLA conversion to AA, favoring DGLA accumulation. DGLA produces anti-inflammatory prostaglandin E1 (PGE1), while AA generates pro-inflammatory eicosanoids. At this very local level, the horse actively shifts the fatty acid balance to promote healing. I thought this was fascinating!
This demonstrates the remarkable complexity of these interactions. Red blood cell membrane data provides a whole-body dietary snapshot. Tissue-specific profiles, however, can differ dramatically based on local needs.
The findings also validated the rationale behind our product ReSolvin EQ, an oil blend containing EPA, DHA, and GLA.
By feeding GLA, we increase DGLA levels, favorably shifting the AA:DGLA ratio to support gastric health.
These data taught us a valuable lesson. Those four horses with glandular ulcers were actively taking matters into their own hands—upregulating DGLA and downregulating AA locally at the insult site. There is a critical distinction between prophylactic (preventive) and resolving (therapeutic) strategies, and we often conflate them.
Looking back at the ReSolvin EQ development data, the most striking finding was not preventing ulcers in healthy horses. Rather, grade 3-4 ulcers resolved to grade 0.
ReSolvin EQ excels as a “resolution product,” helping horses recover from active gastric insults rather than preventing new ones.
Now, let’s take a moment to discuss practical application with DBS testing. How does it work?
In addition to taking a DBS sample, a complete horse history is important: performance level (racehorse, youngstock, breeding), diet (forage/concentrate details), and current supplements.
Then evaluate:
• LA:ALA ratio (SC-PUFAs): Low ratio = pasture/forage phenotype (little to no grain or oil); high ratio = grain or vegetable oil dominant.
• EPA + DPA (long-chain omega-3 status): New gold standard (vs. human Omega-3 Index). Low levels + high LA:ALA = supplement fish oil. Pasture horses with adequate EPA/DPA often need no intervention. Track changes over time to confirm compliance. Overshooting is possible due to overgenerous dosing.
• DHA: Target for asthma/ulcers (resolution role) and pregnant/ lactating mares or young foals (neural development).
DBS reveals dietary compliance and guides precise supplementation.
Can you provide any news insights into omega-6s?
Interestingly, AA serves essential gastric-protective functions beyond its pro-inflammatory role. In the stomach, AA produces prostaglandins of the 2-series (PG2) that reduce gastric acid secretion, increase mucus production, and support barrier function. Horses require a minimum of approximately 1% AA in RBC membranes. Levels below this threshold warrant investigation.
Excessive ALA feeding can depress AA synthesis. Feeding 100 g/ day of ALA, equivalent to 6–7 oz of flax oil, can lower AA levels. This may compromise gastric protection and is undesirable.
Can you provide some guidelines for practical DBS interpretation and supplementation decisions?
Horses with moderate AA, lower LA, and moderate-high EPA + DPA typically exhibit a pasture phenotype. Feeding additional
ALA will not meaningfully increase EPA levels in these horses. Consuming pasture naturally boosts ALA and allows endogenous EPA production.
Horses training on high-LA diets with low EPA respond poorly to ALA megadoses. Abundant LA overwhelms delta-6 desaturase, blocking ALA to EPA conversion. Excess ALA can further depress AA synthesis. The optimal approach is to feed 2–3 g EPA directly (via fish oil), reduce LA intake (switch oils), and maintain AA above 1%.
Protocol for horses with low AA:
1. Do not feed fish oil, as EPA competes with AA synthesis.
2. Modify ALA intake to allow AA rebound to approximately 1%.
3. Once AA threshold is achieved, introduce fish oil to optimize the AA:EPA ratio.
Both the absolute AA threshold (~1%) and the AA:EPA ratio (4–6:1) must be optimized for health.
Where is this research going in the future?
We are continuing to gather fatty acid data from horses in the field using the DBS cards and are building a more robust population database, which will refine our ability to make more precise dietary recommendations.
We are also studying the effect of various vegetable oils on fatty acid metabolism in horses and the interaction between LC-PUFAs and antioxidant status during exercise. We have learned a tremendous amount about fatty acids in horses over the past five years, but I suspect we have just scratched the surface of their importance for equine health and performance.
