Trust Your Gut – the importance of nutrition for health, performance and longevity

Article by Dr. Richard McCormick, M.V.B., Dip. Eq.Sc., M.R.C.V.S. 

The science of equine nutrition is really quite simple – The horse is a flight animal and in the wild, needs to be able to escape from predators using a short burst of energy. Nutrition and subsequent ‘energy’ for survival is all provided by grass which has the required balance of vitamins, minerals, immune supportive nutrients and  fiber to maintain a healthy gut microbiota and keep the horse in adequate health for reproduction. Proper functioning of the gastro-intestinal tract (GIT)  in horses is dependent on a broad range of micro-organisms and more than half of the energy requirement for their survival comes from the microbial fermentation occurring in their enlarged caecum and colon (Chaucheyras-Durand et al 2022). The bacterial populations resident in the various compartments of the horses intestinal tract vary greatly (Costa et al 2015) and there is more DNA in the bacteria located in the gastro-intestinal tract  than there is in the entire body. Because of this, having a healthy gut flora is critical to having a healthy immune system.

In modern times, our demands of horses for performance for our pleasure rather than their survival has led to their need for increased energy that cannot be provided from grass alone. Because of this, the intricacies of diet (in particular the consumption of starch, fiber and fat) has come under scrutiny. Equine feed manufacturers have looked for additional sources of starch, a carbohydrate and a natural component of grass that is ‘essential  to provide energy, fiber and a sense of fullness’ (Seitz 2022). Today, most horses and rapidly growing foals are commonly fed diets with >50% of total ration by weight in the form of grain ‘concentrates’ and carbohydrates from oats, maize, soya, barley and wheat. These grain based feeds contain high concentrations of soluble, easily fermentable starches but can be deficient in certain minerals and vitamins so getting an optimally balanced feed ‘right’ is difficult.

Too much of a good thing  

With advances in scientific knowledge, we now know that when a horse is exposed to surplus starch, the hydrogen ion concentration of their gut increases promoting  the production and absorption of lactic acid, acetate and propionate through the activity of fermentation (Ralston 1994). The process is quick, with lactic acid entering the bloodstream within 3 hours of feeding and calcium subsequently being excreted in the urine.  In order to combat this nutrient loss, the horses’ hormone system triggers the release of parathyroid hormone into the bloodstream, activating the release of stored calcium (to maintain optimal blood levels) but unfortunately causing  bone demineralisation. Clinically, the horse experiences health consequences of varying degrees including digestive diseases (eg: gastric ulcers, diarrhea, colic or colitis), muscle dysfunction (eg: rhabdomyolysis (known as ‘tying up’), defective bone mineralization (expressed as increased incidence of stress fractures and developmental orthopedic diseases), systemic diseases (such as laminitis, equine metabolic syndrome and obesity (Chaucheyras-Durand et al 2022) as well as potential causes of fatigue.

The ideal equine diet 

There is little equine focused research available on the benefits of individual nutrients (due to limited numbers in trials and their subsequent evaluation) of grain ‘concentrates’. But we do know that ingredient availability and quality is regularly influenced by market pressures. 

The table (fig 1) below outlines the sugar, starch and fiber components of the various ingredients commonly found in horse feeds. The optimal grain for equine nutrition with its efficient energy source through lower starch content (relative to other grains) and its high level of soluble fiber (relative to other grains) are oats.

The healing power of omegas and short chain fatty acids 

While grass provides optimal equine nutrition in its own right, the ‘curing process’ when making hay depletes the valuable omegas 3 and 6 intrinsic in grass. These ‘healing’ nutrients naturally protect the lining of the gastro-intestinal tract by increasing mucous production and alleviating ‘auto digestion’ (via hydrochloric acid). For horses, bacterial fermentation in the hind gut also results in the production of Short Chain Fatty Acids (SCFAs), namely acetic, proprionic and butyric acids. These SCFAs ‘cross talk’ with the gut immune system providing local immunity in the gut as well as protection of the respiratory system, the brain and other tissues against disease. In human medicine, it has been repeatedly established that a dysfunctional gut microbiome is associated with respiratory problems. This is evidenced by the fact that when gut disorders such as Irritable Bowel Syndrome  (IBD) or Coeliac disease exist in humans, they are commonly associated with a higher incidence of respiratory infections and related asthmatic like conditions. Barragry (2024) explores the relationship (Fig 2) between gut microbiome and the immune system's ability to support health and combat disease in cattle. A scenario mirrored in the equine.

The stabled horse should be provided with SCFAs daily to support proper functioning gut microbiome. This critical dietary consideration should ideally be provided in the form of flaxseed which has the highest ratio of omegas 3 and 6 (in the ideal ratio 4:1) in the plant world and is most suitable for the equine herbivore.

The health benefits of flaxseed for both humans and equines has been recognized as early as 3,000 BC. Flaxseed was used for various medicinal purposes such as the treatment of gastric disorders, as a soothing balm for inflammation and as a laxative (Judd, 1995). Horsemen (who relied heavily on their equines) and trainers (who sought optimal performance from their charges through natural means) also used flaxseed as a way to supplement the diet with omega-3’s and fiber to produce high quality proteins. Now, thirteen centuries later, we have research to substantiate the knowledge of our ancestors. The renowned German researcher of ‘fats’ and pioneer in human nutrition, Dr. Joanna Budwig, as early as the 1950’s reported that “the absence of highly unsaturated fatty acids causes many vital functions to weaken". Dr. Budwig’s life’s work focused on the dietary ‘imbalance’ between omega-3 and omega-6 fatty acids in humans has been a cornerstone to the exploration of the role of inflammation and the development of many diseases of the coronary, respiratory, metabolic and immune system.

The small seed of the flax plant is also an excellent source of high-quality protein (exceeding that of soybeans and fish oils) and potassium (a mineral that’s important for cell and muscle function). But, the true power of flaxseed lies in three key components: 

Omega-3 essential fatty acids – Also known as "good" fats, omegas enhance the oxygen usage of cells and in combination with alpha-linolenic acid (ALA) are anti-inflammatory in their effect within the body.

Lignans – Flaxseed contains 750 - 800 times more lignans than other plant foods (McCann 2007, Yan 2014). Lignans are a group of compounds with antioxidant properties which also contain plant estrogen. Lignans are linked to a reduced risk of developing osteoporosis, heart disease and cancer.

Fiber - Flaxseed contains both the soluble and insoluble types of fiber essential for maintaining ‘gut’ health.

In equines, adding flaxseed to the diet has the immediate benefits of a shiny, healthy coat and fewer skin allergies. Consistent use of flaxseed has multiple long term benefits including strong hoof quality, improved joint health, reduced muscle soreness, faster healing of ulcers (Sonali et al 2008) and significantly impacts inflammation associated with chronic skin conditions (commonly known as ‘sweet itch’). In breeding stock, increased Omega-3 levels in mares’ milk leads to boosted immunity in foals with higher stallion fertility and improved conception rates in broodmares documented (Holmes, 2015).

How diet can influence performance 

It is easy to think that ‘providing more is better’ when it comes to using nutrition to support performance. But having excess levels of essential vitamins and minerals being processed by the horses’ sensitive gut has a direct impact on their behavior and willingness to perform. Today, we have greater ‘choice’ at the feed store with a broad range of commercial feeding offerings available including mixes, mashes and supplements but the discerning horse owner can be forgiven for being overwhelmed by the range of diet options for every ailment and stage of life.

In modern times, despite advances in nutrition offerings, we have seen a falloff in performance (Fig 3). During the late 1960s, the U.S. Jockey Club stats noted that racehorses averaged 12 starts per year – a far cry from today's horses racing in the U.S. where the average of 3 ‘starts’ was highlighted by leading US Trainers in 2020 (www.ownerview.com). Unfortunately, this is not just a U.S. based problem, but a phenomenon noted worldwide.

The first equine pelleted feed was formulated in the US by the Cistercian  monks in Gethsemani, Kentucky in 1957. Prior to this, all horses were fed ‘straights’ (primarily oats as their energy source and flaxseed as their protein source). My own understanding of the link between modern feeding practices and compromized performance since the 1960s has been curated off an understanding of “what was different” then, as well as a career of observations, clinical practice and scientific review. Fact is, the equine diet of the 1960s was lower in starch and high in fiber. It consisted of oats, minerals, and flaxseed as the “norm”. Hay was the preferred forage (Fig 4).

Today, soya (with one fifth of the omega 3 content of flaxseed) has practically replaced flaxseed as the protein source in equine nutrition. This small change has seen a significant drop in omega-3 and 6 (needed for prostaglandins) in the diet with consequential gastro-intestinal and joint issues. Other dietary changes include those recommended by the National Research Council (NRC) in 1978, who suggested doubling the recommended calcium levels for horses with a subsequent increase in levels of Osteochondrosis (OCD) and Osteopetrosis in the equine population (Krook and Maylin, 1989). Additional moisture in the diet too has led to excess mould formation in convenience feeds and with severe exposure causes liver damage (Buckley et al 2007). Stabled racehorses today mostly lack the nutritional protection afforded a previous generation of horses. The impact has been noted clinically in the widespread increase in equine gastric issues and as stated by J.E. Anthony “Racing fans are missing about half of what they once enjoyed in racing.”

The role of the gut bacteria in the prevention of disease

The gut microbiome begins populating and diversifying from the moment of birth. Though ‘sterile’ in utero, gut derived DNA immediately drives immune health with exposure to nutrition. Recent research suggests that the gut microbiome can be stimulated by using proven probiotics with a track record in enhancing gut health (Barragry 2024). But it is the protective power of SCFAs to allow ‘cross talk’ between the lungs and the gut microbiome that is critical to supporting horses through their life span. 

Nutrition using grain ‘concentrates’ is currently at approximately  99% saturation in today’s equine population so a return to feeding ‘straights’ is a swim against the tide of modernity. But, knowing the influence of nutrition on health, performance and longevity it falls on horse owners to be mindful of the consequential  impacts  such convenience feeds have on the gut microbiome and immune system. Random supplementation and high starch feeds are leading to dietary health issues such as gastric ulcers, hyperinsulinemia and  hyperlipaemia (obesity) as well as increased risk of laminitis . So trust your gut and keep it simple – a diet of oats, flaxseed, a multi-vitamin balancer and ad lib hay will not only meet your horses’ energy needs but will keep them happy and healthy too.

REFERENCES

Barragry. TB (2024) WEB https://www.veterinaryirelandjournal.com/focus/254-alternatives-to-antibiotics-probiotics-the-gut-microbiome-and-immunity

Buckley T, Creighton A, Fogarty (2007)  U. Analysis of Canadian and Irish forage, oats and commercially available equine concentrate feed for pathogenic fungi and mycotoxins. Ir Vet J. 2007 Apr 1;60(4):231-6. doi: 10.1186/2046-0481-60-4-231. PMID: 21851693; PMCID: PMC3113828.

Budwig, Dr. J (1903-2008) WEB https://www.budwig-stiftung.de/en/dr-johanna-budwig/her-research.html

Chaucheyras-Durand F, Sacy A, Karges K, Apper E (2022). Gastro-Intestinal Microbiota in Equines and Its Role in Health and Disease: The Black Box Opens. Microorganisms. 2022 Dec 19;10(12):2517. doi: 10.3390/microorganisms10122517. PMID: 36557769; PMCID: PMC9783266. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9783266/

Holmes, R (2015) Feeding for stallion fertility. WEB 

https://www.theirishfield.ie/feeding-for-stallion-fertility-172113/

Judd A (1995) Flax - Some historical considerations. Flaxseed and Human Nutrition, S C Cunnane, L U Thompson. AOCS Press, Champaign, IL 1995; 1–10 [Google Scholar]

Martinac, P (2018) What are the benefits of flaxseed  lignans?  WEB https://healthyeating.sfgate.com/benefits-flaxseed-lignans-8277.html

National Research Council. 1989. Nutrient Requirements of Horses. Washington D.C.: National Academy Press.

Ralston, S VMD, PhD, ACVN (1994) The effect of diet on acid-base status and mineral excretion in horses in the Journal of Equine Practice. Vol 16 No. 7. Dept of Animal Science, Rutgers University, New Brunswick, NJ 08903

Seitz, A  (2022) What to know about starch_Medically reviewed by Seitz, A - MS, RD, LDN, Nutrition — WEB https://www.medicalnewstoday.com/articles/what-is-starch#benefits

Sonali Joshi, Sagar Mandawgade, Vinam Mehta and Sadhana Sathaye (2008) Antiulcer Effect of Mammalian Lignan Precursors from Flaxseed, Pharmaceutical Biology, 46:5, 329-332, DOI: 10.1080/13880200801887732

Orthopaedic problems in young Thoroughbreds

Helping these future athletes achieve a protective conformation is vital with respect to their welfare, athletic career and sales potential: Orthopaedic conditions have the potential to blight a promising athletic career and prevent young horses reach their full potential. Early diagnosis and management are critical if horses are to be given the best chances of a successful and long career. And this, of course, depends on horsemen being able to pick up on problems as early as possible so they can be dealt with effectively. The Beaufort Cottage Educational Trust is a charity that aims to help disseminate knowledge in the Thoroughbred breeding and racing communities with the ultimate goal of improving horse welfare.

Each year, the charity organizes the Gerald Leigh Memorial lectures which are fantastic resources for horsemen. The lecture series is supported by the Gerald Leigh Trust in honor of Mr. Leigh's passion for the Thoroughbred horse and its health and welfare. Most years, the lectures are presented in person in an event at the UK’s National Horseracing Museum in Newmarket; but for 2021, an in-person gathering was not possible and instead, the lectures are available online. For 2021, the charity chose the theme of orthopaedic problems, which are such a common challenge in young Thoroughbreds.

Angular Limb Deformities: Evaluation and treatment in foals and yearlings

Recognizing, diagnosing and understanding angular limb deviations in young Thoroughbreds are critical skills for horsemen and an important part of both stud management and veterinary care. Angular limb deformities (ALD) refer to deviation of the limb in its frontal plane, or side to side when evaluating the individual from the front or back. A varus deformity is a medial deviation of the limb below the location of the problem (e.g., toeing in), whereas a valgus deformity is a lateral deviation of the limb below the location of the deformity (e.g., toeing out). Angular limb deformities must be distinguished from a flexural limb deformity, which is in the sagittal plane, i.e., from front to back when evaluating the individual from the side.  

How do ALD occur?

ALD can be both congenital and acquired. Congenital means the condition has been present from birth and causes include incomplete ossification or immaturity of the small cuboidal bones, which make up the hocks and knees as well as weakness of the ligaments supporting the joints and periarticular laxity. These issues tend to result in valgus knees and hocks. We also know that ALD can be inherited and that as a breed, Thoroughbreds tend to be varus (toe in). 

Acquired ALD develop after birth and come about through overloading of the physis (growth plate), which is usually caused either from hard ground, an over-conditioned foal or a combination of the two. The biomechanics of equine limb lead horses to bear more weight through the inside of the leg; therefore, the inside of the growth plate, which is inhibited more than the outside and when there is overloading the net effect is that the foal will toe in.

How do ALD impact a foal’s future career?

Carpal and fetlock injuries in racing Thoroughbreds account for a large majority of the reasons racehorses spend time out of training. Intervening while foals are growing and developing to help them achieve a protective conformation gives them the best chance of maximizing their potential and enjoying their racing career. 

Diagnosis of ALD

Evaluating young stock is certainly best achieved using a team approach involving owners/managers, farriers and veterinarians. Regular evaluation from a young age is key, as is examination of the foal while static and while walking. Severe deviations should also be evaluated radiographically.

Treatment of ALD

Conservative treatment options can include exercise restriction, corrective farriery and nutritional management. Hoof correction and toe extensions can be extremely helpful in managing foals and yearlings with minor deviations; and farriery can often correct such issues without needing to resort to surgical treatment options.

The surgical treatment of choice for correcting ALD is the transphyseal screw. In general, it achieves the most effective and cosmetic outcome of the surgical options. The procedure involves placing a screw across the growth plate on the side of the leg that is growing too fast. For example, for a foal that is toeing in, the screw is placed on the outside of the leg. This allows the inside of the growth plate to grow faster and so correct the deviation. The screws are placed under a short general anesthetic. The screw does need to be removed to avoid over-correction, but often they can be removed with the horse standing using a mild sedative once the desired correction is achieved.

Osteochondrosis – recent advances and diagnosis

Osteochondrosis is one of the most important developmental diseases in young athletic horses. It occurs in young, large-breed horses, including Thoroughbreds, and can cause a variety of clinical signs. The age at which the disease starts to cause clinical signs varies from a young foal to horses over 10 years old. This is because lesions can remain silent and only cause clinical signs later on in life. But even in the absence of any clinical signs, the pathological lesions will have been present since the horses reached skeletal maturity. 

How does osteochondrosis affect athletes?

Osteochondrosis often starts to cause problems when the horse is put into training—when they are athletically challenged. This age will differ for different populations, starting earlier in Thoroughbred racehorses than in Warmbloods destined for sports horse disciplines. Often the horse will be sound, or can experience different degrees of lameness and may present with joint effusion. This disease affects more than one joint in an individual in over 50% of cases, and it usually occurs in the same joint on the contralateral limb; but it can also affect multiple different joints. 

How does osteochondrosis develop?

In foals, areas of growth cartilage within the joints will continue to ossify (become bone) after birth. When this process is complete and the animal is skeletally mature, a thin layer of normal articular cartilage will remain supported by subchondral bone. Osteochondrosis is caused by a “failure of endochondral ossification,” which simply means the growth cartilage fails to become healthy bone. A defect, with or without a fragment, is then created in the articular surface of the bone. This dynamically changing area is susceptible to trauma or high biomechanical loads. Recent advances in research, carried out in Norway by Dr. Olstad, suggest that failure of endochondral ossification is likely caused by loss of blood supply to these areas of growth cartilage, which prevents it from ossifying. This has been linked to a heritable predisposition, among other factors such as rapid growth, dietary imbalance, exercise, environment and prior joint sepsis.

Diagnosis of osteochondrosis

Thorough clinical examination and radiography remain at the forefront of osteochondrosis diagnosis. This disease occurs at joint-specific predilection sites as a result of site-specific biomechanical forces and differences in the age at which that site becomes skeletally mature. For example, in the femoropatellar joint (pictured), the most common site of osteochondrosis is the lateral trochlear ridge of the femur. This is predilected by the thick cartilage surface, later age of maturation/ossification, and by the shear forces the patella exerts on the ridge as the stifle flexes and extends. Ultrasonography can also be very sensitive in detecting osteochondrosis in the stifle. Research performed by Dr. Martel in Canada suggests early detection of subclinical lesions in the stifle have been found in foals aged 27-166 days old.  

Management of osteochondrosis

Lesions can spontaneously resolve, and the majority will have done so by 12 months old. Otherwise, management recommendations to limit lesion development include keeping horses exclusively at pasture up to 1 year old, not using rough terrain, in large group sizes (>3 brood mares) or in a large pasture size (large pasture size > 1 hectare before 2 weeks old and > 6 hectare before 2 months old). Strict box rest is discouraged, and a convalescence paddock of 33ft x 56ft (10m x 17m) for 60-90 days may help stabilize lesions. 

Conclusion

Gerald Leigh was an incredibly successful Thoroughbred breeder and owner based in the UK. The 2021 lectures honoring his passion for the Thoroughbred provide a useful update for horsemen on two common conditions of the young Thoroughbred and add to the contribution the charitable trust established by Mr. Leigh’s family, which continues to make in supporting the Thoroughbred industry.

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Osteochondrosis - genetic causes and early diagnosis

By Celia M. Marr

Osteochondrosis (OC) is a common lesion in young horses affecting the growing cartilage of the articular/epiphyseal complex of predisposed joints at specific predilection sites. In the young Thoroughbred, it commonly affects the stifles, hocks and fetlocks. As this condition has such important impact on soundness across many horse breeds, it is commonly discussed in Equine Veterinary Journal. Four recent articles covered causes of the disease, its genetic aspects, and a new and very practical approach to early diagnosis through ultrasound screening programs on stud farms.

OC is a disease of joint cartilage. Cartilage covers the ends of bones in joints, and healthy cartilage is central to unrestricted joint movement. With OC, abnormal cartilage can be thickened, collapsed, or progress to cartilage flaps or osteochondral fragments separated from the subchondral bone leading to osteochondrosis dissecans (OCD). OC and OCD can be regarded as a spectrum rather than two discrete conditions.

Certain joints are prone to OC and OCD, and there is some variation between breeds on which joints have the highest prevalence. In Australian Thoroughbreds, 10% of yearlings had stifle OC, 8% had fetlock OC, and 6% had hock OC. The prevalence data may seem very high, but Thoroughbred breeders may take some comfort in learning that similar, and indeed slightly higher prevalences, are reported in the warmblood breeds, Standardbreds, and Scandinavian and French trotters. Heavy horse breeds have the highest prevalences.

In an article discussing progress in OC/OCD research, Professor Rene Van Weeren concludes that the clinical relevance of OC is man made.  In feral horses, where there is no human influence on mating pairings, OC does occur but at much lower prevalence than in horse breeds selected for sports or racing. Similarly, in pony breeds where factors other than speed and size are desirable characteristics, OC is also rare. These facts suggest that sports and racehorse breeders have inadvertently introduced a trait for OC along with other desired traits. There is a strong link between height and OC, suggesting that one of the desired traits with unintended consequences is height. This is of particular relevance in sports horses: the Dutch warmblood has become taller at a rate of approximately 1 mm per year over the past decades, which might not seem much but it is still an inch in 25 years. Van Weeren points out that if the two-hands tall Eohippus or Hyracotherium and the browsing forest-dweller with which equine evolution started some 65 millions of years ago had evolved at this speed, the average horse would now have stood a staggering 40 miles at the withers.

Drs. Naccache, Metzger and Distal, based at the Institute for Animal Breeding and Genetics in Hannover, Germany, have worked extensively on heritability and the genetic aspects of OC in horses. Their work has shown that there is not one single gene involved. In fact, genes located on not less than 20 of the 33 chromosomes of the horse are relevant to OC.

These researchers use whole genome scanning—otherwise known as genome-wide association studies, or GWAS. This approach has only been possible since the equine genome was mapped. GWAS look at the entire genetic map to detect differences between subjects with and without a particular trait or disease. Millions of genetic variants can be read at the same time to identify genetic variants that are associated with the disease of interest. Based on the number of genetic markers already found in warmblood OC, it is unlikely that a simple single-gene test will prove to be useful for screening young Thoroughbreds for OC.

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