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PSSM in horses: understanding feeding with PSSM1 and PSSM2

What distinguishes PSSM1 from PSSM2, which tests support a diagnosis, which feeding principles are evidence-based and why vitamin E and selenium belong in the ration only in line with requirements.

A calm, powerful horse walks relaxed across a grass paddock; in the foreground lie a bundle of hay, an unlabelled bottle of golden vegetable oil and a feed bowl.
Explanatory illustration · Equivora

The short answer

PSSM is a muscle disease with impaired glycogen storage. PSSM1 can be detected with a GYS1 genetic test, PSSM2 only with a muscle biopsy 1. The specialist literature recommends forage as the basis, little starch, energy from fat instead of cereals and daily, gradually increased exercise 2. Diagnosis and feeding plan belong under veterinary supervision.

What is PSSM – and what distinguishes PSSM1 from PSSM2?

PSSM stands for polysaccharide storage myopathy. It is one of the exertional myopathies, in which muscles tire, hurt or cramp during or after work. Based on muscle biopsies and genetic tests, the specialist literature distinguishes, among others, PSSM type 1 and type 2 2.

PSSM1 is caused by a dominantly inherited mutation in the GYS1 gene and occurs in more than 20 breeds 1. In a large analysis using the stricter biopsy criteria, 87% of draught horses with PSSM carried this mutation, 72% in Quarter Horse-related breeds and 18% in warmbloods 3. The cause of PSSM2 is unknown. Many earlier PSSM2 cases in Arabians and warmbloods are now regarded as myofibrillar myopathy (MFM), a separate muscle disease 24.

FeaturePSSM1PSSM2
CauseDominantly inherited GYS1 mutation 2Unknown 1
DetectionGenetic test from blood or hair 2Muscle biopsy with a negative GYS1 test 2
Common inDraught horses and Quarter Horse-related breeds 3Light breeds such as warmbloods, Arabians and some Quarter Horses 2
Feeding evidenceGood response to a low-starch, high-fat ration plus exercise described 1Improvement reported, but incomplete 5

PSSM1 and PSSM2 compared – simplified from the sources reviewed.

How is PSSM diagnosed – and how useful are genetic tests?

PSSM1 can be detected with a genetic test from blood or hair. PSSM2 is diagnosed with a muscle biopsy if the GYS1 test is negative and the sample shows abnormal glycogen deposits 2.

For PSSM2, commercial genetic tests are offered for variants such as P2, P3 and P4 6. Independent studies in warmbloods and Arabians found no association between these variants and biopsy-confirmed PSSM2 or MFM; the authors advise against using the tests for breeding, pre-purchase examinations or diagnosis 6. In Quarter Horses, the tests would have wrongly classified 57% of healthy horses as affected and missed 40% of horses with PSSM2 7.

Which feeding principles are evidence-based?

For PSSM1 and the PSSM2 form in Quarter Horses, the review describes a good response to a ration low in non-structural carbohydrates and high in fat, combined with regular exercise 1. The specialist overview gives as a framework: forage at 1.5–2% of body mass, more than 15% of digestible energy from fat and less than 10% from starch. Cereals are limited or replaced with a fat source for this purpose 2.

The underlying data are partly small. In a trial with four mares, muscle enzyme activity after exercise was lowest on the lowest-starch, highest-fat of four rations with equal energy content 8. This supports the principle but does not provide a dosage for your horse.

  • Forage forms the basis of the ration 2.
  • Starch-rich cereals are limited 2.
  • Fat replaces energy from cereals instead of simply being added on top 2.
  • Feeding and exercise are implemented together 9.

Why does hay matter so much with PSSM?

With PSSM, forage is not only the basis but also a source of sugar in its own right. In a small crossover study, hay with 17% non-structural carbohydrates triggered considerably stronger rises in glucose and insulin in PSSM horses than hay with 4%. The authors consider these rises potentially detrimental for PSSM horses 11.

Sugar and starch in hay cannot be recognised by appearance. A hay analysis shows what you are working with. Only then can you judge whether concentrates should be reduced, hay changed or energy redistributed via fat 10.

What role does exercise play?

The specialist overview is clear: improvement in PSSM requires both the change of diet and gradually increased daily exercise and turnout 2. In an owner survey of 40 Quarter Horses with PSSM, all horses whose owners implemented both recommendations improved; where there was no improvement, they had not been implemented 9. These are owner reports without a comparison group, but they are consistent with the specialist recommendation.

Vitamin E and selenium: in line with requirements rather than high doses?

Vitamin E and selenium are often discussed in connection with PSSM. The specialist overview names a deficiency of vitamin E or selenium as a possible contributor to sporadic exertional myopathies, not as a cause of PSSM 2. We have not found any evidence that amounts above requirements improve the course of PSSM.

Vitamin E comes mainly from fresh pasture grass; hay contains only little after longer storage 12. Vitamin E status can be measured in the blood 13. With selenium, caution matters more than generosity: horses are more sensitive to selenium poisoning than cattle 14, and chronic excess damages mane, tail and hooves 15. The legal maximum level of 0.5 mg selenium per kg complete feed applies to all sources together 16.

What is different with PSSM2 – and what remains uncertain?

For PSSM2, the recommendations for PSSM1 were adopted without their benefit having been documented. In an owner survey of warmbloods with PSSM2, 80% reported overall improvement on a low-starch, fat-supplemented ration and exercise. Nevertheless, 53% of the horses did not develop as expected; on average, their muscle glycogen was not higher than in healthy warmbloods 5.

If a horse with PSSM2 does not respond sufficiently to the ration, the specialist overview considers a six- to eight-week trial with a ration for myofibrillar myopathy appropriate after veterinary investigation. For this it names cysteine-rich whey-based amino acid supplements, further antioxidants and an adequate vitamin E supply 2. In warmbloods with MFM, pain behaviour and reluctance to engage the hindquarters are often the main signs, with normal muscle enzymes 4. Your vet decides which direction fits based on the findings.

Key takeaways

  • PSSM1 is detected with a GYS1 genetic test, PSSM2 only with a muscle biopsy; commercial PSSM2 variants do not support a diagnosis 16.
  • Little starch, energy from fat instead of cereals, forage as the basis and daily exercise go together 29.
  • Vitamin E and selenium belong in the total ration in line with requirements; selenium has a narrow safety margin 1615.

Frequently asked questions

What should a horse with PSSM not eat?

The specialist literature does not name blanket bans, but it does give a framework: limit cereals or replace them with fat, starch below 10% of digestible energy 2. Hay high in sugar and starch also triggered considerably higher rises in glucose and insulin in PSSM horses than low-sugar hay 11.

How much oil does a horse with PSSM need?

There is no universal amount of oil. The specialist overview gives a framework of more than 15% of digestible energy from fat 2. How much that is for your horse depends on hay, weight, work and the other feeds and belongs in a ration calculation with veterinary supervision.

Can PSSM be cured?

PSSM1 is hereditary 1. The literature therefore describes permanent management through feeding and exercise, not a cure. In an owner survey, owners reported improvement in all horses in which both recommendations were implemented; there was no comparison group 9. For warmbloods with PSSM2, most owners reported improvement, yet many horses still did not develop as expected 5.

Does a horse with PSSM need extra selenium and vitamin E?

We have not found any evidence that amounts above requirements help in PSSM. The specialist overview names vitamin E and selenium deficiency as a possible contributor to sporadic exertional myopathies 2. So check the supply; selenium has a legal upper limit for the total ration 16.

Sources & studies

The content is based on the references listed below. It does not replace individual veterinary or feeding advice.

Show list of sources (16)
  1. Firshman AM, Valberg SJ (2025): Polysaccharide Storage Myopathy. Veterinary Clinics of North America: Equine Practice 41(1):125–137Review, abstract checked (PMID 39893126, Europe PMC): PSSM1 autosomal dominant, more than 20 breeds, detected by genetic test or muscle biopsy; PSSM2-ER in Quarter Horses by biopsy, genetic basis unknown; both forms respond well to a ration low in non-structural carbohydrates and high in fat plus regular exercise. Full text not checked.
  2. Valberg SJ (2026): Exertional Myopathies in Horses. Merck Veterinary ManualSpecialist overview, as of July 2026, checked on 30 September 2026: PSSM1 caused by a dominantly inherited GYS1 mutation, detected by genetic test from blood or hair; PSSM2 without GYS1 mutation by muscle biopsy, many PSSM2 cases in Arabians and warmbloods reclassified as myofibrillar myopathy (MFM); dietary framework for PSSM: forage 1.5–2% of body mass, more than 15% of digestible energy from fat, starch below 10% of digestible energy, limit grain or replace it with fat; in addition, gradually increased daily exercise and turnout; if response is inadequate in PSSM2, 6–8 weeks of MFM diet; acute signs and kidney risk with myoglobinuria. Vitamin E/selenium deficiency mentioned only as a possible contributor to sporadic exertional myopathy.
  3. McCue ME, Valberg SJ, Lucio M, Mickelson JR (2008): Glycogen synthase 1 (GYS1) mutation in diverse breeds with polysaccharide storage myopathy. Journal of Veterinary Internal Medicine 22(5):1228–1233Abstract checked (PMID 18691366, Europe PMC): 831 PSSM horses diagnosed by biopsy from 36 breeds; GYS1 mutation in 17 breeds; with grade 2 criteria, the share with the mutation was 87% in draught horses, 72% in Quarter Horse-related breeds, 18% in warmbloods and 24% in other light breeds. Shares refer to PSSM cases, not the general population.
  4. Valberg SJ, Williams ZJ (2025): Myofibrillar Myopathy. Veterinary Clinics of North America: Equine Practice 41(1):139–150Review, abstract checked (PMID 39880730, Europe PMC): MFM, previously thought to be a glycogen storage disease, is now regarded as a distinct myopathy; in warmbloods mostly pain-associated behaviour, exercise intolerance, reluctance to engage the hindquarters and normal muscle enzymes; indications of reduced cysteine-based antioxidants. Full text not checked.
  5. Williams ZJ, Bertels M, Valberg SJ (2018): Muscle glycogen concentrations and response to diet and exercise regimes in Warmblood horses with type 2 Polysaccharide Storage Myopathy. PLoS ONE 13(9):e0203467Open-access study, abstract checked (PMID 30183782, Europe PMC): the benefit of PSSM1 recommendations for PSSM2 had not previously been documented; retrospective owner survey, 36 PSSM2 warmbloods with muscle samples; 80% of owners reported overall improvement on a low-starch, fat-supplemented ration plus exercise, yet 53% of horses still did not progress as expected; glycogen content not higher than in controls.
  6. Valberg SJ, Finno CJ, Henry ML, Schott M, Velez-Irizarry D, Peng S, McKenzie EC, Petersen JL (2021): Commercial genetic testing for type 2 polysaccharide storage myopathy and myofibrillar myopathy does not correspond to a histopathological diagnosis. Equine Veterinary Journal 53(4):690–700Open-access cross-sectional study, abstract checked (PMID 32896939, Europe PMC): commercially offered variants P2, P3a, P3b and P4 not peer-review validated; in warmbloods and Arabians no significant association with a histopathological PSSM2/MFM diagnosis, sensitivity of all tests below 0.33; the authors advise against using them for breeding, pre-purchase examinations or diagnosis.
  7. Valberg SJ, Henry ML, Herrick KL, Velez-Irizarry D, Finno CJ, Petersen JL (2023): Absence of myofibrillar myopathy in Quarter Horses with a histopathological diagnosis of type 2 polysaccharide storage myopathy and lack of association with commercial genetic tests. Equine Veterinary Journal 55(2):230–238Open-access study, abstract checked (PMID 35288976, Europe PMC): 229 healthy and 163 PSSM2 Quarter Horses; P2/P3/P4 not associated with PSSM2; the tests would wrongly classify 57% of healthy horses as affected and miss 40% of horses with histological PSSM2.
  8. Ribeiro WP, Valberg SJ, Pagan JD, Gustavsson BE (2004): The effect of varying dietary starch and fat content on serum creatine kinase activity and substrate availability in equine polysaccharide storage myopathy. Journal of Veterinary Internal Medicine 18(6):887–894Abstract checked (PMID 15638274, Europe PMC): 4 mares of Quarter Horse-related breeds, 4×4 Latin square, four isocaloric diets with 21.2 to 3.9% starch and 7.2 to 12.7% fat as a share of digestible energy; CK activity after exercise was lowest on the lowest-starch diet; authors' conclusion: below 5% starch and above 12% fat as a share of digestible energy can reduce exertional myopathy. Very small number of animals; no dosage for individual horses.
  9. Firshman AM, Valberg SJ, Bender JB, Finno CJ (2003): Epidemiologic characteristics and management of polysaccharide storage myopathy in Quarter Horses. American Journal of Veterinary Research 64(10):1319–1327Abstract checked (PMID 14596472, Europe PMC): retrospective owner survey on 40 Quarter Horses with PSSM and 37 controls; 40% of owners implemented the diet and exercise recommendations together, and signs improved in all of these horses; where there was no improvement, the recommendations had not been implemented. Survey data without a control group for the intervention.
  10. Bayerische Landesanstalt für Landwirtschaft (LfL): Gruber Tabelle zur PferdefütterungPractical reference table with requirement and feed values based on the GfE recommendations; the basis of many ration calculations in German-speaking countries. Chapter 9.3, Table 39: most common poisonous plants for horses with habitat, toxicity and risk level (after Kamphues et al. 2014)
  11. Borgia L, Valberg S, McCue M, Watts K, Pagan J (2011): Glycaemic and insulinaemic responses to feeding hay with different non-structural carbohydrate content in control and polysaccharide storage myopathy-affected horses. Journal of Animal Physiology and Animal Nutrition 95(6):798–807Abstract checked (PMID 21198966, Europe PMC): crossover with 7 PSSM and 5 control horses, hay with 17%, 10% or 4% non-structural carbohydrates without grain; PSSM horses showed a markedly higher glucose and insulin response to the 17% hay than to the 4% hay; the authors consider the insulin rises on NSC-rich hay as possibly detrimental for PSSM horses. Small number of animals, short-term measurement.
  12. Verein Futtermitteltest (VFT) e.V.: Neuerungen zum Mineralstoff- und Vitaminbedarf und zur Versorgung in der Pferdefütterung (Merkblatt MB 287)Summary of the GfE 2014 changes; contains the mineral requirement per work level (600 kg) according to Coenen/Vervuert 6th ed. and GfE 2014, the sweat electrolyte losses (3.1 g Na and 5.5 g Cl per litre) and the GfE 2014 daily vitamin supply (600 kg warmblood: vitamin E 610–1,220 mg maintenance, 1,220–2,420 mg work), and the note that forage has only low vitamin contents, especially after prolonged storage. Secondary source; primary works are listed separately in the source list.
  13. Finno CJ, Valberg SJ (2012): A Comparative Review of Vitamin E and Associated Equine Disorders. Journal of Veterinary Internal Medicine 26(6):1251–1266Peer-reviewed review (PMID 22925200): structure, absorption and metabolism of vitamin E in horses, higher bioavailability of the natural (RRR) form, antioxidant function during exercise, need for supplementation with little access to pasture, and the neuromuscular diseases associated with persistent vitamin E deficiency (incl. eNAD/EDM, EMND, vitamin E-responsive myopathy).
  14. Liburt NR (2026): Nutritional Diseases of Horses and Other Equids. Merck Veterinary ManualSpecialist overview, as of February 2026: energy surplus, non-specific signs of deficiency and risks of oversupplementation; no basis for a remote diagnosis.
  15. Merck Veterinary Manual: Selenium Toxicosis in AnimalsStandard veterinary reference work (toxicology): chronic selenosis/alkali disease with hair loss and breakage in the mane, tail and neck, plus coronary band swelling, separation of the hoof wall and horizontal hoof cracks; notes that the neurological disease “blind staggers” historically attributed to selenium is more likely polioencephalomalacia due to high sulphur intake. The horse-specific acute single dose is documented by the primary study Miller and Williams (1940).
  16. Durchführungsverordnung (EU) 2020/2117Renewal of the authorisation of selenium yeast from Saccharomyces cerevisiae CNCM I-3399 (identification number 3b812) for all animal species; total maximum content of selenium 0.50 mg/kg complete feed (12% moisture) and at most 0.2 mg/kg of added organic selenium. Authorisation expires according to the Annex on 6 January 2031. Other selenium sources with the same total value: Implementing Regulations (EU) 2019/49, 2019/804 and 2024/3168.