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. Hindgut microbes need 1–2 weeks to adapt to a new feed.

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.

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 the first limiting amino acid.

Minerals split into macrominerals (calcium, phosphorus, magnesium, sodium) needed in grams and microminerals (copper, zinc, selenium) needed in milligrams. Vitamins come largely from fresh forage and sunlight; hay-fed, stabled horses often need supplementation. Fibre is both a nutrient and the physical substrate that keeps the gut moving.

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. A horse holding condition on its current ration needs no change, whatever a calculator says.

A 500 kg horse at rest drinks around 25–30 litres a day; 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. Horses drink more from water around 5–15°C than from near-freezing water; heated buckets or warm top-ups raise intake.
• 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.

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 — the safest, calmest fuel, and the one the horse is built for. 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), “cool” and slow-release, with no starch load. 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.

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 the first limiting amino acid — if it runs short, the horse can't build tissue no matter how much total protein is present. Threonine and methionine come next. 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 — often need more, and more digestible, protein as efficiency declines.

Mature horses at maintenance rarely lack protein on decent forage. Excess isn't directly harmful but is wasteful, raises water intake and stable ammonia, and is an expensive way to buy energy.

With several minerals it's the ratio between them, not the absolute amount, that matters most. The headline example is calcium and phosphorus.

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), which is why a regular “bran mash” is poor practice.

Others worth knowing

• Salt (sodium) — the one mineral almost every horse needs supplemented; offer a salt lick and add 1–2 tablespoons to feed, more in heat or hard work.
• Magnesium — works with calcium in nerve and muscle function; deficiency is linked to tension and tying-up in some horses.
• Selenium — deficient in many regions but toxic in excess; one of the few minerals where over-supplementing is genuinely dangerous.
• 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.

Healthy horses on good fresh forage and sunlight make or obtain most vitamins themselves. The gaps open up with hay-based diets, limited turnout, hard work, and old age.

• Vitamin A — from beta-carotene in green forage. Plentiful on pasture; declines in hay stored for months.
• Vitamin D — made in skin from sunlight and present in sun-cured hay; deficiency is rare except in fully stabled horses.
• 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. Demand may exceed supply in hard work, illness, or after antibiotics.
• Vitamin C — horses make their own; supplementation is rarely needed except in some sick or aged animals.

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, free-choice salt plus good forage is enough.
• 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.

• 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; avoid more than ~2–2.5 kg of concentrate per meal for an average horse.
• 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.

• “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. The single most common source of accidental over- or under-feeding.
• Weekly bran mashes. They upset the diet's consistency and invert the Ca:P ratio; the gut prefers steadiness.
• 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.

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 (%) — water-soluble and ethanol-soluble carbohydrates (the sugars). Key for laminitis-prone horses.
• Starch (%) — usually low in forage but adds to the sugar load.
• NSC (%) — non-structural carbohydrate, broadly WSC + starch (or ESC + starch). The number metabolic horses live and die by; aim under ~10–12% for those at risk.
• NDF (%) — neutral detergent fibre; total fibre. Higher NDF means lower intake (the horse fills up sooner) and coarser, more mature forage.
• ADF (%) — acid detergent fibre; the least digestible fraction. Higher ADF means lower digestibility and energy.
• Ca, P, Mg, K, and trace minerals — the basis for balancing the rest of the diet around what the forage already supplies.

Non-structural carbohydrate (NSC) — simple sugars 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 choose hay under ~10–12% NSC for at-risk horses.
• Soak hay 30–60 minutes to leach some water-soluble sugar (discard the water; it's sugary).
• Mind the pasture clock. Grass NSC peaks on sunny afternoons and after frosts; restrict grazing at those times.
• Choose low-NSC bucket feeds — high-fibre, oil-based, beet-pulp-based — over cereal mixes.

For the first two trimesters, a mare in good condition needs little more than maintenance — the foetus is small, and overfeeding just makes her fat, complicating foaling.

Demand rises in the final trimester (months 9–11), when about two-thirds of foetal growth occurs. Energy climbs modestly (roughly 10–20% over maintenance), but the bigger story is protein and minerals — calcium, phosphorus, copper and zinc — for skeletal development. Trace-mineral status in late gestation influences the foal's lifelong joint soundness, because the foal stores minerals in the liver to draw on while nursing.

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.

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.

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.

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.
• Reduced digestive efficiency means seniors often need more, and more digestible, protein and energy to hold condition.
• 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.

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. Don't drop below about 1.5% of body weight in forage dry matter; 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.

A growing share of leisure horses and ponies are “easy keepers” prone to obesity, Equine Metabolic Syndrome (EMS), or PPID (“Cushing's”). For them, the priority flips from supplying energy to restricting it — particularly sugar and starch.

Core strategies

• Low-NSC forage — aim for hay under roughly 10–12% combined sugar plus starch; soaking helps.
• Restrict, not starve — keep forage at or above ~1.5% body weight; use slow-feeders.
• 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.

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 — a small fibre meal (a couple of handfuls of chaff) before work creates a physical mat that limits acid splashing onto the squamous mucosa.
• Alfalfa/lucerne — its calcium and protein give extra buffering; a useful component for ulcer-prone horses.
• Cut starch and sugar — keep cereal meals small and split; replace energy with oil and digestible fibre. High starch increases stomach acidity and volatile fatty acid production against the squamous lining.
• Turnout and trickle feeding — grazing posture and constant intake are protective.

“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

• Replace starch with fat. Oil-based energy avoids the glucose/insulin surges that worsen glycogen-storage myopathies.
• Consistent daily exercise and turnout are non-negotiable — stall rest with full feed provokes episodes.
• Adequate forage, electrolytes and vitamin E/selenium support muscle health.
• Change gradually and reintroduce work slowly after an episode.

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 is an underappreciated cause of poor performance, loose droppings, mild recurrent colic, and behaviour change.

How it goes wrong

When starch or fructan overwhelms small-intestinal digestion and reaches the hindgut, rapidly fermenting (amylolytic) bacteria proliferate and produce lactic acid, dropping hindgut pH. The fibre-digesting (cellulolytic) bacteria, which prefer a near-neutral pH, die off — reducing fibre digestion and releasing toxins and vasoactive amines as the gram-positive populations turn over. This is the same cascade that, at the extreme, triggers 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) has reasonable evidence for stabilising hindgut pH and fibre digestion; broader probiotic claims are weaker. Treat them as support, not a fix for a high-starch diet.

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

When excess starch or fructan reaches the hindgut, amylolytic bacteria (Streptococcus, Lactobacillus) ferment it rapidly to lactic acid, dropping pH. The pH-sensitive cellulolytic bacteria die off; their lysis and the proliferation of gram-positive organisms release endotoxin and vasoactive amines. This drives hindgut acidosis and, at the extreme, the classic carbohydrate-overload model of laminitis (experimentally reproduced with oligofructose).

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.

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 first-limiting, then threonine and methionine. 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 raises 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, and why high-protein diets show up as ammonia smell and increased drinking.

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)

Several trace minerals compete for absorption, so balance — not just amount — determines status:

• Copper ↔ zinc ↔ iron: high zinc or iron suppresses copper uptake; excess of one induces functional deficiency of another.
• Copper ↔ molybdenum & sulphur: high molybdenum and sulphate form thiomolybdates that lock up copper (a classic ruminant problem, milder but real in horses).
• Iodine homeostasis is narrow at both ends — deficiency and excess both impair thyroid hormone synthesis and cause goitre.

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. Sources are sun-cured forage and dermal synthesis under UV; deficiency is rare outside fully housed animals.
• 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. Demand can outstrip supply in hard work, illness, or after antibiotics disrupt the microbiome. Biotin supplementation has reasonable evidence for improving hoof horn quality over months.

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

Insulin dysregulation and endocrinopathic laminitis

The dominant cause of laminitis in practice is endocrinopathic, not carbohydrate-overload. In Equine Metabolic Syndrome, tissues become insulin-resistant and the pancreas compensates with hyperinsulinaemia. 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 3–5 days in.

• Reintroduce small, frequent meals — good-quality forage (lucerne is often used) — and build up slowly over 7–10 days.
• 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.