Nutritional Secondary Hyperparathyroidism (NSH) – also known as Big Head Disease – is an uncommon problem in horses that stems from a mineral imbalance.
This skeletal condition develops due to a calcium deficiency or an imbalanced ratio of dietary calcium to phosphorus. These minerals play an important role in bone formation and growth.
In horses with chronically low levels of calcium, the parathyroid glands respond by releasing excessive levels of parathyroid hormone.
This hormone causes calcium to be released from bones into the blood, potentially leading to brittle bones over time. The condition can also result in a swollen face, hence the name Big Head Disease.
Studies report that Quarter Horses, Appaloosas, and pony breeds aged two to eight have a higher incidence of NSH.  Pregnant or lactating mares and young colts are also most commonly affected.
Nutritional secondary hyperparathyroidism is a serious disease that can be fatal if left untreated. It is not the disease itself that is typically fatal, but the resulting inability to consume feed can lead to death in some horses. 
The good news is that NSH is easily preventable with appropriate diet balancing. Knowing the causes, symptoms, and treatment for NSH is important for all horse owners.
What is Nutritional Secondary Hyperparathyoroidism?
Big head disease in horses is induced by a diet with a persistent lack of calcium, excess phosphorus levels, and/or imbalanced calcium to phosphorus ratio.
It can also be caused by problems with calcium absorption from the digestive system, including diets with hay that is high in oxalates.
Secondary hyperparathyroidism can also develop due to renal failure or tumour growth, though this is rare in horses. 
Calcium is essential for maintaining many physiological functions including muscle contractions, nerve function, blood clotting, and bone health. When horses have low levels of calcium in their blood (hypocalcemia), the body pulls this mineral from stores in bone tissue. 
Horses with NSH have increased parathyroid hormone levels. The parathyroid glands are two pairs of glands located in the neck behind the thyroid gland. These glands are responsible for regulating calcium levels in the blood.
As calcium levels in the blood fall, the parathyroid glands secrete more parathyroid hormone to resorb calcium from the bones and maintain homeostasis (stable levels) in the blood. 
In horses with hyperparathyroidism, excessive bone mineral loss leads attachment of fibrous tissue to the bone, known as fibrous osteodystrophy. This results in weak and misshapen bones. This is most noticeable in the horse’s head – hence the name Big head disease.
The horse’s limbs can also be affected which results in pain and the reluctance to walk or even stand in some cases. 
History of Big Head Disease
First described in 400 AD, NSH has also been referred to as bran disease, big head, and Miller’s disease.  Though rare in most parts of the world today, this condition was more common in the past when diet balancing and mineral requirements of horses were not well understood.
In South Africa between 1905 and 1909, there were approximately 400 reports of horses suffering from big head disease. In 1931, more than a quarter of the horses at the army hospital in the Philippines presented with NSH symptoms. 
Horses were sometimes fed large quantities of wheat bran which is high in phosphorus and low in calcium.
The condition was often noticed by distillery workers who fed their horses wheat bran and other grain by-products from the brewing process. The distillery workers noticed abnormal bony growths on their horses’ heads and observed that the bridge of the horses’ noses were abnormally wide and misshapen.
Researchers now know that these bony distortions occur in response to bone mineral loss and fibrous growths on the bone. 
Dietary Causes of NSH
There are a few different dietary scenarios that can result in NSH. Ultimately, a poor dietary supply of calcium causes hyperactivity of the parathyroid glands which induces secondary hyperparathyroidism.
Horses should ideally consume a diet with 1.5 – 2 grams of calcium (Ca) for every 1 gram of phosphorus (P). This 1.5 – 2:1 calcium to phosphorus ratio of corresponds to the ratio of calcium to phosphorus found in bones.
For example, if a 500 kg (1100 lb) horse at maintenance consumes 20 grams per day of phosphorus, they should consume a minimum of 30 – 40 grams of calcium per day to maintain a balanced ratio.
The dietary ratio of Ca to P should never be lower than 1:1. If the ratio falls below this level, the absorption of these minerals and levels in the body become imbalanced.
High phosphorus interferes with the absorption of calcium from the small intestine. Phosphorus is primarily supplied in the equine diet in the form of phytate from forages and grains. Phytate binds to calcium and can inhibit the absorption of this mineral.
NSH can result from dietary imbalances or the consumption of high oxalate forages:
- An imbalanced diet: Horses become calcium deficient when they consume too little calcium or when there is an excess of phosphorus in the diet, which blocks the absorption of calcium.  If horses are fed high amounts of phosphorus, absorption of magnesium is also depressed.
- High oxalate forages: Oxalates are molecules that bind calcium in the plant and in the horse’s digestive tract. Once ingested, oxalates prevent horses from absorbing calcium.
Horses grazing exclusively on pastures high in oxalates may develop NSH. These types of grasses are common in tropical regions such as South America, Queensland, Australia, South Africa, the Philippines, and some parts of Florida.
NSH was first clinically diagnosed in Australian horses grazing subtropical pastures in 1974. Since then, it has been widely recognized in horses grazing the following grasses:
- green panic
- purple pigeon
Forages that contain more than 25 g/kg oxalates can reduce calcium bioavailability and lead to NSH. 
This condition is usually seen in spring, summer, and autumn. 
In most parts of the world where high oxalate grasses are not an issue, NSH is rarely found. Many horse owners also feed commercial feeds with added calcium.
However, feeding high amounts of wheat bran or grains can lead to NSH.
What are the Symptoms of NSH?
Symptoms of NSH typically include lameness, weakness, ataxia, and most notably, deformation of the bones in the skull. The nose often appears wider than normal.
Other symptoms associated with NSH include: 
- swollen facial bones (usually symmetrical on each side of the head)
- jaw enlargement
- dental infections
- pain when chewing or inability to properly chew food
- vertebral fractures, potentially resulting in hind end paralysis
- respiratory issues such as nasal collapse, upper airway obstruction, or labored/noisy breathing
- depression or dullness
- shortened stride or stiff gait
- excessive recumbency (lying down and difficulty getting up)
- coarse, stark coat
- pica (eating unusual substances such as soil)
- pain or tenderness in joints
- muscle tremors
In mature horses, NSH usually develops slowly and may not display clinical signs for a long time. Many horses adapt and cope with symptoms fairly well, meaning the condition may go unnoticed for some time.
However, in young growing horses, skeletal calcium cannot be mobilized quickly enough to maintain blood (serum) calcium levels. The result is the rapid development of NSH symptoms. 
How NSH is Diagnosed
Big head disease is usually diagnosed by a veterinarian based on the horse’s history, clinical signs, radiological findings, and laboratory tests.
The most common clinical abnormality is a decreased concentration of ionized calcium in blood plasma in conjunction with increased phosphate levels. Urinalysis may also show normal calcium concentration and increased phosphates.
Increased alkaline phosphatase (ALP) activity, probably caused by increased bone resorption, can also be detected in blood tests.
However, a definitive diagnosis of NSH is usually obtained by measuring serum parathyroid hormone levels. 
Normal levels of parathyroid hormone for a horse without NSH are 4 – 65 picograms per ml. In horses with NSH, levels have been reported at 110 – 518 picograms per ml. 
Dietary Modifications for NSH
Because NSH is caused by dietary calcium to phosphorus imbalance, treatment begins with first correcting mineral balance in the diet. If caught quickly enough in mature horses, most of the damage can be reversed and the bones will remineralize.
The disease is a bigger problem for young horses as their bones have not finished growing and ossifying. The demineralization from inadequate bone calcium can cause permanent damage to young horses even once the diet is corrected. 
Calcium can be added to the diet by feeding alfalfa hay, providing calcium carbonate (agricultural lime), and dicalcium phosphate supplementation. However, calcium supplementation alone may not be sufficient. 
It’s best to remove horses from high-oxalate pastures. If this is not possible, horses need daily calcium supplementation. Calcium carbonate provides more calcium than dolomite (approximately 40% versus 20% calcium).
Feeding chelated minerals is more effective at promoting proper calcium absorption and utilization than providing inorganic sources. Horses on diets containing oxalates and organic minerals had lower levels of parathyroid hormone and higher levels of calcium in bone than horses fed diets containing oxalates and inorganic minerals. 
Dicalcium phosphate is an ideal supplement because it also addresses the phosphorous deficiency that these horses commonly develop. Dicalcium phosphate also helps to keep calcium and phosphorous levels in balance.
The correct feeding rate of calcium depends on levels of oxalate in the pasture as well as the degree of calcium deficiency in the individual horse.
Calcium availability from common feeds and supplements ranges from 67 to 77%. In comparison, phosphorus availability ranges from 34 to 57%. 
Therefore, the level of supplementation must take into account bioavailability, degree of calcium deficiency and presence of oxalate and phytate in the diet.
Up to 100 g of calcium carbonate (limestone) and 200 g of dicalcium phosphate can be fed to a 500 kg (1100 b) horse each day. This is usually tolerated better when mixed with a carrier or flavouring agent such as molasses.
Research suggests that increasing the frequency of supplementation and extending the time of consumption is more effective than increasing the dosage used.  Daily supplementation appears to be more effective than weekly supplementation.
Research shows that a mineral block with a calcium to phosphorus ratio of 3.5:1 and added magnesium and salt was effective in alleviating clinical signs of NSH and also preventing new cases.  This mineral block was used in horses grazing high oxalate pastures.
The effectiveness of your horse’s supplementation program can be determined by the improvement in clinical signs. Supplementation should be continued for six months or indefinitely if the horse is to be kept on high oxalate pasture.
Alfalfa hay should be given in addition to calcium supplements.
Additional Treatments for NSH
In addition to feeding a balanced diet and removing horses from high-oxalate pasture, medications can be used to address cases of big head disease.
The most common treatment for NSH is the administration of tiludronate (Tildren®), a bisphosphonate drug approved for use in horses. This drug works by binding and inhibiting the action of osteoclasts—cells that break down bone.
Horses with NSH benefit from tiludronate administered at the dose licensed for use in horses with navicular disease.  However, NSH symptoms will only improve if this drug is given in conjunction with a balanced diet.
Non-steroidal anti-inflammatories (NSAIDs) are sometimes used to treat bone pain for horses with NSH, but these medications do not cure the condition.
NSH Case Studies
Veterinary case reports provide valuable information to better understand NSH in horses.
In one case study, a 3-year-old male pony was referred to a veterinary hospital for fatigue, severely laboured breathing, and deformity of the skull bones.
The pony received tiludronate given intravenously over a 30-minute period. Thirty days later, follow-up laboratory examinations and radiographs were performed by the attending veterinarians.
They found no noticeable changes except a significant decrease in the pony’s ALP level. Though no bone changes were observed, the pony’s clinical abnormalities were improved and he was discharged from the veterinary hospital. 
In another case study in Queensland, Australia, 33 horses grazing on high-oxalate grasses (13 of which showed signs of NSH) were supplemented once weekly with a 1:2 mixture of Calcium Carbonate and Dicalcium Phosphate. The supplementation was continued for 6 months.
Owners reported that clinical signs including lameness and jaw swelling improved in most of the affected horses. They also reported that horses without symptoms continued to remain symptom-free.
In addition, 7 horses that were introduced to the same pasture and started supplementation right away never developed symptoms.
The results of this study confirmed that appropriately supplementing horses grazing on high oxalate grasses can both combat and prevent symptoms of NSH. 
Nutritional secondary hyperparathyroidism is not common in most parts of the world today.
But dietary imbalances in calcium and phosphorus and high oxalate forages can still produce this condition, which can prove deadly in extreme cases.
Therefore, it’s important to understand what causes Big Head Disease and to take measures to prevent the condition from developing in your horse.
Consult with a nutritionist to determine whether your horse’s diet is providing an appropriate ratio of calcium to phosphorus. You can submit your horse’s diet online for a free evaluation by our nutritionists.
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