Feed the horse in front of you.

A horse evolved to graze for 16-18 hours a day, taking in small amounts of fibrous forage almost continuously. Its tract reflects that: a relatively small stomach that empties quickly, a modest small intestine for enzymatic digestion of starch, sugar, protein and fat, and a very large hindgut (caecum and colon) where billions of microbes ferment fibre into the volatile fatty acids that supply much of the horse's energy.

What this means in the feed room

• Forage first, always. Fibre is the fuel the system is built to run on, and it keeps the microbial population stable.
• Little and often. The stomach secretes acid continuously whether or not the horse is eating, so long empty gaps raise ulcer risk.
• Small starch meals. The small intestine has limited capacity to digest starch; overload spills it into the hindgut, where it ferments rapidly, drops the pH, and kills fibre-digesting microbes - the cascade behind grain-associated colic and laminitis.
• Change slowly. A 7-14 day transition is a practical starting convention; adaptation varies with the feed change and the individual.

Evidence and limitations: [1] · [22] · [44] · [47]

Water is the most important and most overlooked nutrient. A horse drinks roughly 5 litres per 100 kg of body weight per day at rest - far more in heat, work or lactation. Clean, unfrozen water must always be available.

The six conventional nutrient classes are water, carbohydrate, fat, protein, vitamins and minerals. Fibre is predominantly carbohydrate; energy is supplied by nutrients rather than being a separate nutrient class.

Energy is measured as Digestible Energy (DE) in megacalories (Mcal) per day. It comes from fibre (fermentation), starch and sugar (grains), and fat (oils). It's the number that most often drives weight gain or loss.

Protein supplies amino acids for muscle, hooves, coat and milk; quality matters as much as quantity, with lysine commonly limiting.

Minerals split into macrominerals (calcium, phosphorus, magnesium, sodium) needed in grams and microminerals (copper, zinc, selenium) needed in milligrams. Vitamins come from the diet and, for some vitamins, synthesis within the horse or its microbes. Assess the full ration before supplementing. Fibre is both a nutrient and the physical substrate that keeps the gut moving.

Evidence and limitations: [1] · [24] · [25]

The scale only tells you weight. Body condition scoring (BCS) tells you whether that weight is right. The Henneke system rates fat cover from 1 (emaciated) to 9 (extremely fat), assessed by feel over six places: neck, withers, behind the shoulder, ribs, loin, and tailhead.

Targets

• 4-6 - ideal for most horses; ribs easily felt but not sharply seen.
• 5 - a common target for breeding mares entering the season.
• 7+ - overweight; a real welfare and laminitis risk, not cosmetic.

Score every 2-4 weeks and let the trend, not a single reading, guide changes. Stable condition helps judge energy supply, but cannot establish adequate protein, vitamins or minerals.

Evidence and limitations: [2] · [3] · [7]

A 500 kg horse at rest may drink around 25-30 litres a day, but intake depends on forage moisture and conditions; this is never a water allowance or limit; in hard work or hot weather that can double, and a lactating mare needs far more again. Dehydration is a leading trigger of impaction colic, and reduced drinking in winter (cold or frozen water) is a common hidden cause.

Practical points

• Always available, always clean. Scrub troughs and buckets; horses drink less from fouled water.
• Take the chill off in winter. Cold-weather pony research supports offering warmed water, but does not establish a universal optimal temperature. Keep water unfrozen and monitor individual drinking.
• Salt drives thirst. Adequate salt keeps horses drinking and replaces what's lost in sweat.
• Watch intake around travel and competition - many horses drink poorly away from home; flavouring water at home first can help.

Evidence and limitations: [4] · [51]

All three raise DE, but they behave differently, and the choice shapes temperament, ulcer risk and metabolic health.

Fibre (forage)

Fermented slowly in the hindgut into a steady supply of energy - an important energy source alongside its role in chewing and gut function. Behaviour depends on more than fuel choice. Good hay or haylage can meet the full energy needs of a horse at maintenance or light work.

Starch & sugar (cereals)

Energy-dense and fast-releasing. Useful for hard work, but large cereal meals overwhelm small-intestinal digestion, spill starch into the hindgut, and can trigger acidosis, “fizzy” behaviour and laminitis. Keep starch meals small - a common guide is under ~1-2 g starch per kg body weight per meal - and split across the day.

Fat (oils)

Very energy-dense (about 2.25× the energy of carbohydrate by weight), with no starch load. Fat can replace some cereal energy, but does not guarantee a calmer horse or improved performance. Vegetable oil or high-oil feeds add condition to a hard keeper or fuel endurance work. Introduce gradually over several weeks so the horse adapts to using fat efficiently.

Evidence and limitations: [5] · [16] · [43]

Horses need amino acids, not crude protein as such. Crude protein (CP) just measures nitrogen; it says nothing about whether the limiting amino acids are present.

Lysine is commonly a limiting amino acid - if it runs short, the horse can't build tissue no matter how much total protein is present. The next limiting amino acid depends on the ration; a fixed threonine-then-methionine ranking is not established for every horse. A quality source (soybean meal, alfalfa/lucerne) therefore outperforms a larger quantity of a poor one.

Who needs more

• Growing youngstock - building new tissue; quantity and amino acid quality both critical.
• Lactating mares - milk is protein-rich; requirements roughly double in early lactation.
• Hard-working horses - a moderate increase for muscle repair.
• Senior horses - need changes based on teeth, intake, health and condition, rather than age alone.

Mature horses at maintenance rarely lack protein on decent forage. Unnecessary excess wastes nitrogen and can increase urine output, water needs and stable ammonia. Effects vary with the diet; disease may alter protein tolerance.

Evidence and limitations: [19] · [20] · [21]

Mineral adequacy depends on absolute intake and balance. A suitable calcium:phosphorus ratio cannot compensate if both amounts are too low.

This is a real risk on cereal-heavy diets, because grains are high in phosphorus and low in calcium, while forages - especially alfalfa/lucerne - are calcium-rich. Wheat bran is a notorious offender (over 1% phosphorus), so bran must be included within a ration with adequate calcium and phosphorus. Its presence alone does not make a ration harmful.

Others worth knowing

• Salt (sodium) - often needs supplementation; weigh the dose and account for the whole ration and sweat losses. Salt-block consumption varies.
• Magnesium - works with calcium in nerve and muscle function; behaviour or muscle signs alone do not diagnose deficiency, and routine calming benefits are not established.
• Selenium - deficient in many regions but toxic in excess; avoid overlapping supplements and assess the total dose.
• Copper & zinc - important for coat, hoof and (in youngstock) sound bone; their ratio to each other matters too.

A well-formulated commercial feed or a broad-spectrum balancer is the simplest way to get micromineral balance right when forage alone falls short.

Evidence and limitations: [1] · [40]

Fresh forage, stored feed, fortified products and internal synthesis all contribute differently to vitamin supply. Assess the whole ration and health status; age or workload alone does not prove a deficiency.

• Vitamin A - from beta-carotene in green forage. Plentiful on pasture; declines in hay stored for months.
• Vitamin D - dietary supply, including forage-derived D2, matters. Equine studies found absent or minimal skin synthesis of D3, so the human sunlight model should not be applied to horses. This does not justify indiscriminate supplementation.
• Vitamin E - abundant in fresh grass, but falls sharply once grass is cut and stored. Hay-fed, hard-working and breeding horses are the classic candidates for supplementation; E works alongside selenium as an antioxidant.
• B vitamins & vitamin K - synthesised by the hindgut microbes, so a healthy gut on adequate fibre usually covers them. Evidence does not establish routine supplementation for every working or sick horse; assess specific circumstances.
• Vitamin C - horses make their own; routine supplementation solely for age or work is not established; individual illness requires veterinary assessment.

Evidence and limitations: [24] · [25] · [26] · [27]

Horse sweat is hypertonic - it carries more electrolytes than blood does - so heavy sweating drains sodium, chloride and potassium faster than water alone. Replacing only water actually dilutes the blood further and can blunt the thirst response.

Practical approach

• Sodium and chloride (plain salt) are the main losses; potassium is usually well covered by forage but matters after very heavy sweating.
• For light sweating, assess forage and actual salt consumption; free-choice access does not establish an adequate dose.
• For heavy or prolonged sweating (endurance, hot competition), use a balanced electrolyte that mimics the proportions lost - and always alongside, not instead of, free water.
• Give electrolytes after work with water available; concentrated doses on an empty stomach can irritate it.

Evidence and limitations: [46] · [51]

• Feed by weight, not by scoop. Weigh hay and hard feed. A “scoop” of two feeds can differ by 50% in mass.
• Little and often. Split concentrates into at least two, ideally three, small meals; calculate starch per meal using the actual analysis and body weight; concentrate weight alone cannot establish suitability.
• Forage around the clock. Avoid gaps longer than ~4-6 hours without forage. Slow-feeder nets stretch a fixed amount of hay to mimic grazing.
• Make changes gradually over 7-14 days to protect the hindgut microbes.
• Don't work hard immediately after a large grain meal.
• Keep it clean and fresh; mouldy or dusty forage causes colic and respiratory disease.

Evidence and limitations: [5] · [44]

• “He needs a hard feed.” Many leisure horses in light work need little or no concentrate - just forage plus a balancer for vitamins and minerals.
• Feeding by scoop, not weight. A preventable source of inaccurate feeding.
• Weekly bran mashes. Bran is high in phosphorus. Assess its amount and the whole-ration Ca:P balance; an occasional meal is not equivalent to chronic dietary imbalance.
• Sudden feed or forage changes. A leading avoidable cause of colic.
• Treating “low sugar” as automatically safe. NSC is sugar plus starch; a low-sugar feed can still be high in starch.
• Over-supplementing. Stacking multiple supplements can unbalance minerals and, with selenium, become toxic. One well-chosen balancer usually beats a shelf of buckets.
• Ignoring the forage. Forage is 50-100% of the diet, yet often the part no one analyses.

Evidence and limitations: [40]

Because forage is most of the diet, analysing it is the highest-value test you can run. A typical report (dry-matter basis) includes:

• DE (Mcal/kg) - energy density. Drives how much weight forage alone will hold or add.
• Crude protein (%) - total protein; pair with the horse's stage to judge sufficiency.
• WSC & ESC (%) - different laboratory fractions. WSC includes more fructans; ESC predominantly includes simple sugars but can include short fructans. They are not interchangeable.
• Starch (%) - usually low in forage but adds to the sugar load.
• NSC (%) - confirm the lab definition, commonly WSC + starch. ESC + starch is a different sum. Interpret any clinical target with its assay, dry-matter basis, total intake and insulin response.
• NDF (%) - neutral detergent fibre; total fibre. Higher NDF often accompanies maturity and can constrain intake, but it is not a precise predictor across all forages.
• ADF (%) - acid detergent fibre; the least digestible fraction. Higher ADF often accompanies lower digestibility and predicted energy; the relationship varies with forage.
• Ca, P, Mg, K, and trace minerals - the basis for balancing the rest of the diet around what the forage already supplies.

Evidence and limitations: [11]

Non-structural carbohydrate (NSC) - commonly WSC (including fructans) plus starch - is the dietary lever most tied to laminitis. Two distinct mechanisms matter:

• Hindgut overload. A large starch meal that escapes small-intestinal digestion ferments rapidly in the hindgut, crashing the pH, killing fibre microbes, and releasing toxins that can trigger laminitis. This is the “grain founder” pathway.
• Insulin dysregulation. In metabolic horses (EMS/PPID), high sugar and starch drive large insulin spikes, and persistently high insulin itself damages the laminae. This is the more common modern pathway, and it's why sugar, not just starch, is the target.

Controlling NSC

• Test the forage and agree an assay-specific dry-matter target with the clinician. A figure around 10-12% is sometimes used, but its meaning depends on the assay and does not guarantee safety.
• Hay soaking can reduce soluble carbohydrate, but effects vary and 30-60 minutes is not a safety guarantee. It also changes nutrient content and can worsen microbial hygiene. Use fresh water, discard soak water safely, feed promptly, and assess analysed forage against the clinical plan.
• Mind the pasture clock. Sunlight, temperature and plant growth affect carbohydrate. Time of day or a muzzle cannot guarantee safe intake for an insulin-dysregulated horse; grazing access needs an individual plan.
• Choose low-NSC bucket feeds - high-fibre, oil-based, beet-pulp-based - over cereal mixes.

Evidence and limitations: [7] · [8] · [9] · [10] · [11] · [12]

Pregnancy requirements remain near maintenance early on, then rise progressively from about month 5. Use the specific month, prepregnancy weight, forage analysis and condition trend.

Demand rises in the final trimester (months 9-11), when about two-thirds of foetal growth occurs. Energy rises progressively (the model gives about 16-28% above average maintenance in months 9-11), but the bigger story is protein and minerals - calcium, phosphorus, copper and zinc - for skeletal development. Foals accumulate mineral stores before birth, but prenatal supplementation does not guarantee later joint soundness. Copper studies have differing results, and developmental orthopaedic disease is multifactorial.

Lactation is the single most demanding state in the equine calendar. In early lactation a mare can produce 3% of her body weight in milk daily; energy needs can approach double maintenance and protein needs rise even more steeply. Underfeeding shows up first as rapid weight loss, not poor foal growth - the mare sacrifices her own reserves to protect the milk.

Evidence and limitations: [1] · [28] · [29]

Young horses have high requirements relative to size because they're building tissue, but the goal is steady, moderate growth - not maximum growth. Pushing youngstock with energy-dense feed for early size is linked to developmental orthopaedic disease (DOD): conditions such as OCD and physitis that damage joints and growth plates.

Priorities

• Energy matched to growth rate - enough for condition, not so much as to force rapid gain or fat.
• Quality protein with adequate lysine for tissue building.
• Correct mineral balance - calcium, phosphorus, copper and zinc in the right ratios are central to sound bone; a youngstock-specific feed or balancer really earns its place here.

Monitor growth and condition closely; a smooth curve beats a spiky one, and sudden growth spurts after restriction are a particular DOD risk.

Evidence and limitations: [1] · [20] · [28] · [29]

Working horses need more energy, and the temptation is to pour in cereals. Better practice is to match the fuel to the work and lean on forage and fat as far as possible.

• Endurance and steady work favour fat and fibre - slow-release, sparing of muscle glycogen, gentle on the gut.
• Short, intense, explosive work (sprinting, jumping efforts) draws on glycogen, so some starch has a place - still in small, split meals.
• Electrolytes lost in sweat must be replaced after hard or hot work.
• Hydration and gut health underpin performance; chronic low-grade ulceration from too much grain and too little forage quietly erodes results.

Evidence and limitations: [16] · [43]

Older horses are individuals, but several changes are common and call for tailored feeding.

• Worn or lost teeth reduce chewing of long forage. Offer soaked, easy-to-chew fibre - hay replacers, soaked beet pulp, short chops, grass meal - so fibre intake doesn't collapse. Quidding (dropping balls of half-chewed hay) is the classic warning sign.
• Age alone does not establish reduced digestibility. Healthy older horses may digest feed similarly to younger adults; investigate teeth, disease, intake and weight trend before changing nutrient density.
• PPID (Cushing's) is common in old horses and overlaps with laminitis risk; many seniors therefore need a low-sugar/starch approach even while needing more calories - best met with oil and highly digestible fibre rather than cereals.
• Dental and weight checks become more frequent: regular dentistry, body condition scoring, and prompt response to weight loss.

Evidence and limitations: [18] · [19]

Putting weight on a thin horse

• Rule out the cause first - teeth, worms, pain, or disease - with your vet before simply feeding more.
• Build up gradually to avoid overwhelming the gut. Start with maximising good forage.
• Add calories with oil and highly digestible fibre (beet pulp, alfalfa) before reaching for cereals.
• Expect slow, steady gain; aim to move condition score over weeks, not days.

Slimming an overweight horse

• Restrict, but never starve. Use about 1.5% of body weight in forage dry matter as a conservative owner-facing starting minimum. A clinician may prescribe a lower amount with monitoring; severe restriction risks dangerous hyperlipaemia, especially in ponies and donkeys.
• Use low-NSC forage, soak hay, and stretch it with slow-feeder nets.
• Replace fortified hard feed with a low-calorie balancer so vitamins and minerals stay covered.
• Increase exercise where health allows, and limit lush grazing with a muzzle or track system.
• Re-score every 2-4 weeks and adjust; aim for gradual loss.

Evidence and limitations: [7] · [42] · [50]

A growing share of leisure horses and ponies are “easy keepers” prone to obesity, Equine Metabolic Syndrome (EMS), or PPID (“Cushing's”). Obesity, PPID and insulin dysregulation are distinct. Restrict energy when weight loss is needed; a lean horse may need more calories while still controlling sugar and starch. PPID treatment does not reliably correct insulin dysregulation, which needs separate assessment.

Core strategies

• Low-NSC forage - use an assay-specific dry-matter target and actual analysis. Soaking is variable and does not certify safe forage.
• Restrict, not starve - use ~1.5% body weight in forage dry matter as a starting minimum; more restrictive or replacement diets need a monitored clinical plan.
• Limit grazing at high-risk times (lush spring/autumn, frosty sunny mornings) with a muzzle or track system.
• A low-calorie balancer supplies vitamins and minerals without the calories of a fortified feed.

Evidence and limitations: [7] · [13]

Equine gastric ulcer syndrome is really two distinct conditions, and the distinction changes the plan.

• Equine squamous gastric disease (ESGD) affects the unprotected upper (squamous) stomach lining. It is largely an acid-splash problem - driven by empty stomachs, high-starch meals, and exercise (which pushes acid up against the squamous mucosa). It responds well to feeding management.
• Equine glandular gastric disease (EGGD) affects the acid-producing lower stomach, where defence mechanisms have failed. It behaves more like a mucosal-defence/inflammatory problem, is less responsive to diet alone, and stress and individual factors weigh heavily.

Feeding strategies that genuinely help (mostly ESGD)

• Continuous forage - a fibre mat plus near-constant chewing buffers acid with saliva (which is bicarbonate-rich and only produced while chewing). Avoid fasts over ~4-6 hours.
• Feed forage before exercise - forage access before work is a practical strategy, but a couple of handfuls is not a validated universally protective dose. It does not replace treatment.
• Alfalfa/lucerne - its calcium and protein give extra buffering; a useful component for ulcer-prone horses.
• Cut starch and sugar - for ulcer-prone horses, commonly used limits are 1 g starch/kg body weight per meal and 2 g/kg per day, alongside forage and treatment. These are risk-management guides, not safety guarantees; replace energy as appropriate with fibre or fat. High starch increases stomach acidity and volatile fatty acid production against the squamous lining.
• Turnout and trickle feeding - may support management, but turnout alone is not a guaranteed prevention or treatment.

Evidence and limitations: [5] · [6] · [52]

“Tying-up” (exertional rhabdomyolysis - muscle stiffness, pain, reluctance to move, dark urine in severe cases) is an umbrella term for several distinct disorders. Diet matters most for the chronic, heritable forms.

Principles common to the dietary forms

• Match the diet to the diagnosis. Selected RER and PSSM1 cases benefit from low-starch approaches; add fat only as needed for energy and condition. This is not established treatment for every PSSM2/MFM case.
• Long-term exercise programmes can be important once the diagnosis and recovery plan are established. During an acute painful tying-up episode, stop exercise and seek veterinary care; do not force the horse to move.
• Adequate forage, electrolytes and vitamin E/selenium support muscle health, but do not increase selenium without assessing total intake and status.
• Change gradually and reintroduce work slowly after an episode.

Evidence and limitations: [14] · [15] · [16] · [17]

Most of a forage-fed horse's energy comes from microbial fermentation in the caecum and colon. That microbial population is a delicate ecosystem, and subclinical hindgut acidosis may occur with dietary disruption. Poor performance, loose droppings, colic or behaviour change are nonspecific and do not diagnose it.

How it goes wrong

Starch escaping small-intestinal digestion and fructans (which mammalian enzymes do not digest like starch) can be rapidly fermented in the hindgut. Excess substrate promotes lactate accumulation and a fall in pH, disrupting fibre-digesting microbes. Gram-positive acid producers are distinct from Gram-negative sources of lipopolysaccharide endotoxin. Inflammatory and vascular pathways in carbohydrate-overload laminitis are complex and differ from endocrine laminitis.

Protecting the hindgut

• Maximise forage, minimise large starch meals - the single biggest lever.
• Keep meals small and split so starch stays within small-intestinal capacity.
• Make all changes slowly to let microbial populations adapt.
• Pre/probiotics - live-yeast (Saccharomyces cerevisiae) findings vary with strain, dose, diet and outcome. Some trials show effects; others do not show improved digestibility. Broad product claims cannot be inferred from one strain or trial. Treat them as support, not a fix for a high-starch diet.

Evidence and limitations: [22] · [23] · [47]

The equine tract runs two digestion systems in series: enzymatic digestion in the foregut and small intestine, then microbial fermentation in the hindgut.

Foregut & small intestine (enzymatic)

The stomach and small intestine digest and absorb sugars, a portion of starch, protein (to amino acids) and fat. Crucially, equine pancreatic amylase activity is low relative to omnivores, so the small intestine has a limited capacity to break down starch. Processing (rolling, micronising, extruding, cooking) raises pre-caecal starch digestibility; raw whole cereals and large meals leave more starch undigested.

Hindgut (microbial fermentation)

Whatever isn't digested in the small intestine - structural fibre (cellulose, hemicellulose, pectin), fructan, and escaped starch - passes to the caecum and colon, where billions of microbes ferment it into short-chain (volatile) fatty acids (VFAs): chiefly acetate, propionate and butyrate.

• Acetate & butyrate are oxidised for energy or used to synthesise body fat.
• Propionate is glucogenic - the liver converts it to glucose by gluconeogenesis. In a forage-fed horse absorbing little dietary glucose, propionate-driven gluconeogenesis is a major source of blood glucose. This is a key reason fibre delivers such steady, “cool” energy.

The acidosis cascade

Rapid fermentation of excess starch or fructan can lower hindgut pH and disrupt microbial populations. Fructans are not substrates for mammalian amylase. Gram-positive lactate producers and Gram-negative lipopolysaccharide endotoxin must be distinguished; carbohydrate-overload laminitis involves multiple pathways and is not identical to insulin-associated laminitis.

Evidence and limitations: [22] · [47]

The energy cascade: DE → ME → NE

Equine systems are usually expressed in digestible energy (DE) for simplicity, but energy is progressively lost at each step:

Fermentation produces more heat than enzymatic digestion, so fibre has a higher heat increment - relevant in hot climates (extra metabolic heat to dissipate) and useful in cold (fibre fermentation helps keep a horse warm). DE values overstate the relative usefulness of forage slightly, which NE systems correct for.

Fuel for work

• Muscle glycogen is the primary fuel for intense, anaerobic effort. Equine glycogen replenishes slowly (days, not hours), so back-to-back hard sessions can deplete it.
• Fat oxidation dominates low-to-moderate aerobic work and is glycogen-sparing. Fat adaptation over several weeks upregulates the enzymes of fat metabolism, improving endurance and reducing reliance on starch.
• Phosphocreatine covers the first seconds of maximal effort.

Glucose & insulin dynamics

A large starch/sugar meal produces a glycemic and insulin spike; a forage/fat ration produces a flatter curve. Avoid a big cereal meal immediately before intense work - the insulin response suppresses fat mobilisation and can blunt performance. This same glycemic behaviour underlies the dietary management of metabolic and muscle disorders.

Evidence and limitations: [43]

Dietary protein is digested to amino acids and absorbed in the small intestine. Microbes in the hindgut do synthesise microbial protein, but the horse cannot meaningfully absorb amino acids from the colon - so, unlike a ruminant, the horse depends on the quality of protein digested before the hindgut.

Consequences

• Amino acid quality matters, not just crude protein. Lysine is commonly limiting; threonine or other amino acids may also matter depending on the diet. A small amount of high-quality protein (soybean, good lucerne) outperforms a large amount of poor-quality protein.
• Non-protein nitrogen is of little use and potentially harmful in quantity - horses can't exploit it the way ruminants do.
• Excess protein is deaminated; the nitrogen is excreted as urea in urine. This can increase water intake, urine output and stable ammonia, and wastes energy on the deamination and excretion process.

This is why “more protein” is rarely the answer for energy or performance, although increased drinking is not a consistent response in every study or horse.

Evidence and limitations: [19] · [20] · [21]

Calcium: regulated at the gut and kidney

Horses absorb dietary calcium efficiently and somewhat passively, and regulate calcium balance mainly through renal excretion - which is why normal horse urine is alkaline and cloudy with calcium carbonate crystals. Blood calcium is held in a tight range by hormones:

• PTH (parathyroid hormone) raises blood Ca: bone resorption, renal Ca reabsorption, and activation of vitamin D to calcitriol, which increases intestinal absorption.
• Calcitonin lowers blood Ca.

Nutritional secondary hyperparathyroidism (“big head”)

Chronic low calcium, excess phosphorus, or high oxalate forage (oxalate binds calcium, blocking absorption) drives sustained PTH. Persistent bone resorption replaces bone with fibrous tissue - osteodystrophia fibrosa, most visibly enlarging the facial bones. The blood calcium may look normal throughout, because that is exactly what the PTH response is protecting.

Trace-mineral antagonisms (at the gut wall)

Assess absolute intakes and potential mineral interactions; quantitative equine evidence varies:

• Copper ↔ zinc ↔ iron: high zinc or iron suppresses copper uptake; excess of one induces functional deficiency of another.
• Copper ↔ molybdenum & sulphur: thiomolybdate antagonism is established mainly in ruminants. An equine experiment did not show the expected copper interference under its conditions, so it should not be presented as an established routine equine mechanism.
• Iodine homeostasis is narrow at both ends - deficiency and excess both impair thyroid hormone synthesis and cause goitre.

Evidence and limitations: [30] · [40]

Fat-soluble (A, D, E, K) - stored, slower to deplete

• Vitamin A from forage beta-carotene; stored in the liver, so deficiency takes months of carotene-poor (long-stored) hay to appear.
• Vitamin D is unusual in the horse - circulating concentrations are naturally low, and horses appear relatively insensitive to it. Dietary sources, including forage-derived D2, appear important. Equine studies found absent or minimal cutaneous D3 synthesis under UVB; sunlight exposure alone cannot establish adequate status.
• Vitamin E (alpha-tocopherol) is a membrane (lipid-phase) antioxidant, abundant in fresh grass but lost rapidly once forage is cut and stored. Hay-fed, hard-working and breeding horses are the classic candidates for supplementation. Chronic deficiency is linked to specific neuromuscular diseases (equine motor neuron disease; equine degenerative myeloencephalopathy).
• Vitamin K from forage and microbial synthesis.

The vitamin E–selenium antioxidant system

The two work in tandem on the same problem - oxidative damage - in different compartments:

Deficiency of either leaves muscle and other tissues vulnerable to oxidative injury - the basis of nutritional myodegeneration (white muscle disease) in foals and tying-up/poor recovery in adults.

Water-soluble (B-complex, C) - mostly made in-house

Hindgut microbes synthesise the B-vitamins, and the horse makes its own vitamin C, so a healthy horse on adequate fibre rarely needs supplementation. These circumstances warrant individual assessment, but do not establish a routine benefit from B- or C-vitamin supplements. Biotin supplementation has reasonable evidence for improving hoof horn quality over months.

Evidence and limitations: [24] · [25] · [26] · [27]

Nutritional status is rarely read off a single blood value. Each marker has a window and a caveat.

Evidence and limitations: [13] · [32] · [41]

Insulin dysregulation and endocrinopathic laminitis

The dominant cause of laminitis in practice is endocrinopathic, not carbohydrate-overload. Insulin dysregulation can involve abnormal insulin secretion, clearance or tissue sensitivity; it should not be reduced to insulin resistance alone. Persistently high insulin is itself laminitogenic: it is thought to act on IGF-1 receptors in the lamellar tissue, driving dysregulated epidermal cell behaviour and lamellar failure. This is why controlling dietary sugar and starch (and obesity) - which control the insulin response - is the central preventive lever.

PPID (pars intermedia dysfunction)

In PPID, age-related loss of dopaminergic inhibition of the pituitary pars intermedia leads to overproduction of POMC-derived peptides (including ACTH). The clinical picture - long curly coat (hypertrichosis), muscle loss, laminitis, infections, often overlapping insulin dysregulation - is managed with the dopamine agonist pergolide, alongside a low-sugar/starch diet. Many PPID horses need more calories (from oil and fibre) while still avoiding NSC.

Refeeding syndrome (the starved horse)

Reintroducing feed to a severely malnourished horse too quickly is dangerous. A carbohydrate load triggers an insulin surge that drives phosphate, potassium and magnesium into cells, producing acute hypophosphataemia, hypokalaemia and hypomagnesaemia - with risk of cardiac and neuromuscular failure during early refeeding. Timing varies and requires close clinical monitoring.

• Reintroduce small, frequent meals - good-quality forage (lucerne is often used) - and increase intake according to a veterinarian-led plan with electrolyte monitoring; no fixed timetable guarantees safety.
• Limit starch/sugar early; monitor electrolytes, especially phosphate.

Hyperlipaemia

In ponies, donkeys and pregnant/lactating mares, a negative energy balance can spiral into massive fat mobilisation and triglyceride accumulation that overwhelms the liver - a life-threatening emergency requiring veterinary management and prompt restoration of energy intake.

Evidence and limitations: [7] · [8] · [13] · [42]

Evidence and limitations: [28] · [29]

Evidence and limitations: [31]

Evidence and limitations: [32] · [33] · [49]

Evidence and limitations: [34] · [35] · [36]

Evidence and limitations: [37]

Manganese supports enzymes and skeletal metabolism. Equine evidence for specific age-linked deficiency syndromes is limited, so limb, reproductive or coat changes should not be used to diagnose manganese deficiency.

Available supplementation studies include blood-concentration outcomes, which do not establish clinical benefits or a diagnostic syndrome. Assess the whole ration and investigate clinical signs with a veterinarian.

Evidence and limitations: [48]

Evidence and limitations: [40]

Evidence and limitations: [40]

Evidence and limitations: [38]

Evidence and limitations: [46] · [51]

Evidence and limitations: [39] · [45]