“Is Navicular Disease in Horses Curable Using Gallium Nitrate?”

Written by George Eby, Copyright 1996-2015

From our experimental results, with appropriate gallium treatment, absolutely yes for the early stages of the disease. Even the most severe and otherwise lethal cases respond to gallium nitrate treatment by going sound within a few months. However, from a historical (and veterinarian) perspective, it has not been. For example, steel egg bar shoes, more upright shoeing (but not too much), and possibly corrective shoeing were the best bets in the early stages, with nerving performed in the later stages. Correct farrier techniques remain indispensable. There are some who say that incorrect shoeing causes navicular disease. Although this is likely true, I think navicular disease is more of an environmental degradation problem.

However, without appropriate gallium nitrate treatment, the disease is degenerative, worsens progressively, and eventually, the navicular diseased horse becomes no longer useful, remains a cripple for the rest of its life, is nervetomized, or is euthanized. Appropriate gallium nitrate treatment, as described below, is the only known means of restoring most navicular-diseased horses to health. For example, after 8 years of treatment with gallium nitrate, my horse Don Dee has responded by having no further degradation observed in 2004 than he had in 1997. See the 2003 letter from his latest veterinarian here.

The navicular bone of a horse acts as a fulcrum over which flexor tendons from the back of the leg attach to the coffin bone in the foot. This fulcrum is subject to both compressive and surface shear forces, perhaps not exceeded by any other bone in the horse. That navicular disease (osteomalacia) of the navicular bone in horses starts as a result of trauma, over-exertion, malnutrition, and combinations thereof, which is generally accepted as causal. The navicular bone is also the least vascularized bone in the horse. Often, blood thinners are given supposedly to improve circulation; however, evidence has been published that these blood thinners do little or nothing for the disease. There is typically much swelling of the flexor tendon.

NOTE: The following text (down to FAQs) was written between 1996 and about 2002, and it mainly shows the theoretical reasons why I first tested gallium nitrate against navicular disease. It was based upon a relationship between gallium (beneficial to bone/joints) and aluminum (harmful to bone/joints). The theory was simple. Add enough gallium to displace aluminum, an effect that would occur due to their extremely close physical and chemical properties; thus, if aluminum was the problem, it would be displaced, and benefits would occur. In about 2002, the notion that gallium nitrate was a “bone resorption inhibitor” was added. Yet, neither of these two effects can explain the full benefits clearly observed using gallium nitrate to treat navicular disease. It was not until people convinced me in about 2003 that gallium nitrate was good for human arthritis that I made a diligent search for more reasons to explain the full spectrum of benefits of gallium nitrate for bone/joint benefit. Since navicular disease is a bone/joint problem very similar to arthritis, I believe that the benefits are the same. Actually, navicular disease is a bit more difficult to treat than arthritis. Rather than describe these benefits fully on this page, they are explained in my medical journal article on gallium and arthritis. Veterinarians, physicians, and scientists will want to examine the list of benefits and effects of gallium nitrate in the Discussion section and see the thorough discussion of the effects of gallium by Larry Bernstein (Mechanisms of Therapeutic Activity for Gallium). Also, in the FAQs of this current article, there is a list of other benefits of gallium nitrate, which is very broad and is likely to increase further. 

On the other hand, hundreds of recent reports from cancer research show that positively charged, trivalent aluminum ions (AL (III)) are one important, previously unrecognized cause of bone resorption and osteomalacia (bone softening, crushing, and breaking), and in particular, they are the cause of surface bone loss. This change occurs in all mature vertebrates, not associated with vitamin D deficiency.

AL (III) in bone causes bone pain and proximal myopathy (disorders of adjoining muscles and tissues) in all vertebrate species tested. (REF. 1)

In blood chemistry experiments at Cornell Veterinary Clinic with mature ponies, a basal amount of 336 parts per million (ppm) aluminum was naturally found in feed consisting of one third each of oats, beet pulp, and a commercial pelleted, complete horse ration. Between the basal amount of aluminum and the diet supplemented to 1370 ppm aluminum, there was little difference in effect on absorption, retention, and pathway excretion of calcium, phosphorus, magnesium, zinc, iron, and copper. (REF. 2)

However, the ponies fed the same diet containing 4500 ppm aluminum were in negative phosphorus balance because phosphorus absorption was greatly suppressed. Calcium absorption was unaffected by 4500 ppm aluminum intake from their food, but the ponies were in negative calcium balance due to their greater urinary excretion of calcium. Presumably, calcium was excreted in urine because it was not being utilized in the formation of bone crystals because of the lack of phosphate. Plasma calcium was always elevated, and plasma phosphorus was always depressed when ponies were fed the 4500 ppm aluminum diet. Plasma hydroxyproline concentration was increased with high aluminum intake, showing that bone turnover was increased due to aluminum effects on phosphorus and calcium metabolism. Magnesium, zinc, iron, and copper metabolism were unaffected by aluminum intake. (REF. 2)

The similarities between bone disorders caused by AL (III) ion in man, laboratory animals, and ponies, and navicular disease in horses sound strikingly similar and offer, for the first time ever, real hope for either stopping the degenerative process or possibly even a cure (restoration of the navicular bone to normalcy).

Why aluminum now? Aluminum is the third most abundant element on the surface of the Earth. It has been held captive in rock, biologically unavailable for 3 billion years. Now, industrialization has resulted in acid rains that have decreased the pH of lake waters to the point where AL (III) ions are leached out of rocks and soil. The Al (III) ion is so toxic that fish can live in acidic water, but not in equally acidic water with 5 micromol/L of aluminum ion. (REF. 3)

All vertebrate species, including man and horses, can pick up biologically available AL (III) ions from plants and grasses contaminated with aluminum leached from rock by acid rain. In humans, tea from plants grown in acidic soil is believed to be a prime cause of osteoporosis and dementia ranging from Parkinson’s disease to Alzheimer’s disease, but only when citric acid (lemon or lime juice) is added and consumed regularly over a number of years. Adding milk to tea detoxifies aluminum. Aluminum (III) ion has no biological role in vertebrate life forms and is always considered to be a cytotoxin, bone toxin, and neurotoxin. Clinical signs of AL (III) ion toxicity in humans are vitamin D-resistant osteomalacia, iron-adequate microcytic anemia, and dialysis dementia. (REF. 3)

In horses, a symptom of AL (III) neurotoxicity has been suggested by Henry Heymering, RJF of Cascade, MD, to be an intolerance to gentle petting or rubbing while tolerating well hard slaps on the neck. This symptom has been reported by others and is also my observation. I have found it to reverse after about a year of treatment with gallium nitrate. Henry has found toxic levels of aluminum in hair samples of several navicular horses, but also in several non-navicular horses. (REF. 4) It is suggested that a finding of toxic concentration of aluminum in hair samples taken near the base of the hair in non-navicular horses should be interpreted as a necessary precondition for the development of aluminum ion-induced navicular disease.

Aluminum is a group IIIa element under boron in the periodic table of the elements. In some complex boron-containing biomolecules, boron prevents bone resorption in laboratory animals, exactly the reverse of aluminum, and similar to gallium, although no testing has been done in treating navicular disease.

Below Aluminum in the periodic table is Gallium, a liquid metal at room temperature. Gallium, in considerable excess over aluminum, effectively competes with aluminum for absorption in bone and beneficially displaces aluminum, similar to the way that immunoregulatory zinc replaces carcinogenic cadmium from tobacco smoke in lung tissue.

According to Raymond P. Warrell, Jr., M.D., previously of the Memorial Sloan Kettering Cancer Center in New York City, elemental Gallium and its various compounds are potent inhibitors of bone resorption that act to maintain and restore bone mass in all vertebrate species. By virtue of these biological effects, Gallium compounds (mainly gallium nitrate) are useful treatments for a variety of human diseases that are characterized by accelerated bone loss, including cancer-related hypercalcemia (including multiple myeloma, and breast cancer), bone metastases, Paget’s disease, and postmenopausal osteoporosis. (REF. 5) See his 1987 on-line article here. A web site for nurses concerning uses of intravenous gallium nitrate (Ganite^R) administration as an antihypercalcemic agent suggests that it produces its hypocalcemic effect by inhibiting calcium resorption from bone, perhaps by reducing disease produced increased bone turnover. Information from Med Line Plus Health Service concerning gallium nitrate injectable is also available. Based upon our pioneering work with oral gallium nitrate in horses, Dr. Warrell has started an oral program of gallium nitrate (Ganite^R) for humans.

Another inhibitor of bone resorption, tiludronate has been used somewhat effectively to treat recent onset navicular disease in horses (symptoms began within 2 to 6 months of treatment), but not for chronic navicular disease (symptoms for more than 6 months prior to treatment). Tiludronate is one of the bisphosphonates. See the full article here (10 MB PDF). Dr. Warrell tested another bisphosphonate, (etidronate), and found gallium nitrate superior. Consequently, there is precedent for using agents that restore calcium to bone in the treatment of navicular disease. Unfortunately, tiludronate has been reported as toxic and is administered only in a veterinary hospital, and it is less effective than gallium nitrate. Gallium nitrate is also a potent anti-inflammatory also, making it vastly superior. Dr. Warrell also tested another bisphosphonate, pamidronate; APD, and found similar results to tiludronate.

Injected gallium nitrate in appropriate dosages is considered a highly effective agent in reducing accelerated bone loss in both cancer and metabolic bone disease and in restoration of lost bone mass in humans when administered by qualified physicians, usually oncologists. Gallium nitrate lowers blood hypercalcemia into the normal range, resulting in a marked reduction in urinary calcium. It causes a higher accretion rate of radio-labeled calcium into bone, showing that gallium nitrate enhances mineralization of newly forming bone rather than simply acting to decrease physiologic resorption. Gallium concentrates in the metabolically active metaphysis (bone end), and notably in the epiphyseal region of bones, along with calcium, restoring bone strength. (REF. 5)

Although Dr. Warrell was unfamiliar with navicular disease in horses, he suggested to me by telephone in August of 1995 that any species with bone calcium loss would likely benefit from 0.2 mg to 2.0 mg anhydrous gallium nitrate per pound of body weight, with the high dosage used to initiate treatment and a lower dose being used for maintenance. (We use 5.0 mg per pound in horses.)

Pure (anhydrous) gallium nitrate is an oxidizer and corrosive and, like potassium nitrate, could be used as an oxidizer in making an expensive gunpowder. Even so, I have soaked cotton rags in strong gallium nitrate aqueous solutions and found that either wet or dry, the rags were no more combustible than untreated rags. Since pure gallium nitrate is an oxidizer (like potassium nitrate), it is unlikely that gallium nitrate can be successfully and safely added to commercial feeds without microencapsulation and stored for long periods of time. I have placed a few crystals of pure gallium nitrate in nitric acid in an aluminum foil container, and they promptly melted a hole in the aluminum and fell through. The crystals are hazardous to both people and animals, plants, and aluminum metal.

Extending human and laboratory animal findings to horses is a significant step. No horse, to my knowledge—other than my 14-year-old, dearly loved 17-hand thoroughbred gelding, Don Dee (severe navicular disease with lollipops and cones in the left front foot and other changes, and the beginning of navicular changes in the right front foot)—had previously been treated with gallium nitrate for navicular disease. Starting May 15, 1997, he was treated for one year with improvement in bone density on X-ray examination in the first year. He became increasingly sound after the first few weeks of treatment and was fully sound in a few months. In the fall of 2004, he remains sound. However, over the past 7 years, there have been several relapses, which vanished using a standard dose for two weeks and no further treatment of any kind other than proper shoeing. He always becomes lame when farriers fit him with aluminum shoes. Many owners of navicular horses report to me that their horses became lame when fitted with aluminum shoes. In our previous 7 years of experience with gallium nitrate, no horse has gone sound until the aluminum shoes had been removed for 3 to 6 weeks.

By spring of 2004, treatment with 500 ml of 1.0% gallium nitrate solution for navicular disease had been tried by about 2500 horse owners (plus 500 others using crystalline gallium nitrate previously supplied by others) with great success, and only a few people have told me of failures. This comes out to more than 50,000 daily doses used with no reported evidence of toxicity. There is every reason to believe that this treatment will become the standard by which all other treatments for navicular disease are measured. In my opinion, judging from the results observed, all other drug treatments for navicular disease are fool’s play.

Consequently, I ran a research trial using 500 ml of the 1.0% gallium nitrate in water, which is now over.

Our (100 owners and myself) research appears to be the first to document the effects of oral gallium nitrate in horses. Consequently, until this trial was complete, no data using gallium nitrate for navicular disease had been collected.

Doses were not given for longer than 14 days each month because high, prolonged, continuous doses for over a year have been associated with kidney damage in humans from the use of IV administration. On the other hand, those side effects may have resulted from concurrent use of strong chemotherapeutic drugs for lymphoma. Therefore, a theoretical possibility for side effects exists in treating horses, but no side effects of any kind have been observed, except for excessive exuberance during turnout. Also, the human drug was administered intravenously, which caused it to be nearly immediately excreted via the kidneys, resulting in reversible damage to the kidneys, which was repaired with rehydration.

Using the oral route, very little gallium shows up in urine, according to scientists using gallium maltolate to study several cancers in humans by Titan Pharmaceuticals. According to Titan, most, if not all, is excreted via the feces, thus avoiding to a great extent any possible kidney damage. Gallium preferentially settles in inflamed tissues that we want to treat with gallium and not in healthy tissues. Our pilot study results do not show a significant lessening of effect during the 14 days off treatment.

X-ray exams of the navicular bone in all navicular horses were suggested to be performed before beginning treatment to provide a baseline point. Again, X-rays at day 365 of treatment were proposed, with the objective of determining increases in bone density, not repair of diseased navicular bone, which may occur later, as in the observed case of a filled-in cyst. However, recent observations by veterinarians show that if the injury is not old and consolidated, bone restoration is occurring. Even so, the navicular bone is similar to human skull bone, and neither mends like leg bones. On the other hand, early navicular bone changes usually disappear completely after three months of therapy with gallium nitrate. This response might not be explained by the repair of bones by gallium nitrate and is most likely explained by an anti-inflammatory effect of gallium nitrate on flexor tendons under and around the navicular bone and in the navicular bursa, reducing injury to bone and allowing bone to heal.

Remember: “AL (III) in bone causes bone pain and proximal myopathy (disorders of adjoining muscles and tissues) in all vertebrate species tested. (REF. 1)”

Experience over the last 10 years confirms that lameness disappears much sooner than complete bone recalcification (as per the human model); consequently, training and work should be limited until the horse has been sound for a few months. Experience with Don Dee suggested that dressage work while on gallium nitrate is not injurious. Other riders have jumped their gallium nitrate-treated navicular horses four feet six inches in professional jumper contests after a few months of treatment with no lameness being observed before, during, or after the jumping. However, I consider that risky!

Considering the encouraging human clinical, in vitro, laboratory animal, and pony evidence, the big question now is: Will gallium nitrate stop the progression of navicular disease? Yes, of this I am absolutely certain. I am certain it is by far the best bet ever, or I would not have tried it on my own beloved horse, Don Dee, first. Gallium nitrate seems to work as hypothesized for navicular problems without apparent side effects. It seems to prevent and reverse (in early-stage navicular syndrome) this miserable and devastating affliction. Not everything is understood about this disease or gallium nitrate treatment. Some horses have, for many years, had horrible navicular X-rays and remained completely sound with no treatment. Others show navicular lameness with no observable changes on X-ray. Gallium nitrate does not, within a year, and perhaps not within two years, repair well-established, old navicular bone lesions. Regardless, gallium nitrate may increase navicular bone density, has eliminated early-onset navicular changes, and has terminated lameness in most cases observed to date when properly used. In one case, a cyst completely disappeared.

It is emotionally and financially attractive to stop treatment once the horse goes sound. If this results in a mistake and lameness reoccurs, starting full-dose gallium nitrate treatment for three months followed by half-dose daily gallium nitrate for many months or years usually is sufficient to terminate—again—the lameness.

As previously stated, gallium nitrate treatment in early navicular syndrome usually appears curative, reversing the early changes seen on X-ray. With advanced navicular bone disease, there may be no cure, but complete relief from lameness and life extension and normalized utility are usually possible with gallium nitrate treatment given for many years.

Gallium III ions, from gallium nitrate, at sufficiently high dosage, appear to be extremely powerful anti-inflammatory agents having many uses beyond the elimination of toxic aluminum ions. It may be the most anti-inflammatory substance ever tested. Radioactive Gallium citrate has been used to locate malignant tumors and inflamed tissues for over 25 years in nuclear medicine. It preferentially accumulates and remains for a long time in those tissues. Gallium ions are also known to affect some T-cell lymphocyte subpopulations and the cytokines released during inflammation. However, the exact mechanism of its anti-inflammatory effects in horses remains the subject of laboratory research. When used in much higher doses than the tiny microgram amounts used in nuclear medicine for diagnostic purposes, gallium ions appear to have an extremely strong anti-inflammatory action. An inflamed tendon beneath the navicular bone has been shown to be reduced very rapidly by gallium nitrate treatment of navicular disease. The anti-inflammatory effect and long residence time in inflamed tissues are very useful in treating most, but not all, inflammatory disorders in animals and humans. Doses identical to those used to treat navicular disease have also been useful in treating laminitis, coffin bone separation, and founder in several cases each. Additionally, fourteen percent gallium nitrate solutions as a topical rub have been used to reduce both equine and human leg inflammation (tendonitis) due to impact injury by about 80% within 30 to 45 minutes. With four additional 30-minute gallium nitrate rubs, all visible tendonitis swelling was eliminated within several days.

One may wonder if aluminum horseshoes contribute to navicular disease. The answer is unproven and is a question that only research will be able to answer—but I think yes—absolutely YES! For example, if the horse with aluminum shoes stands in water with a pH of less than 6 (a clearly possible, mildly acidic pH for ground and lake water, as well as urine-soaked (salty and acidic) stall floors), metallic Al (III) ions can form and will be harmful to bone. Considering the evidence, I decided to shoe my horses with aluminum shoes and not knowingly permit aluminum contamination of the ground they walk on or use aluminum feed or water containers. It occurs to me that steel horseshoe nails in contact with aluminum shoes create an aluminum-iron battery, creating an electrical field capable of moving Al (III) into the foot. This is not conjecture, and the biophysics is totally sound and absolutely correct.

What does lasagna have to do with Navicular disease? NOTHING! But there is something called a “Lasagna Cell,” according to Wikipedia, which is the battery that forms when one cooks salty lasagna in a steel pan and covers it with aluminum foil. The electrical current that is formed eats holes in the aluminum foil where the lasagna touches the aluminum foil. This occurs in about an hour, attesting to the high voltage occurring in the aluminum-iron battery. The lasagna ends up with aluminum deposition in it. This is exactly the same idea as I propose to be the principal cause of navicular disease.

We do know from our trial results that navicular horses shod with aluminum shoes did not become sound until 3 to 6 weeks after the aluminum shoes were removed.

Since Don Dee has lived his last 9 years in the alkaline (pH 9+) soils of the Texas hill country, and he is not exposed to wet stall conditions, formation of aluminum ions in his feet is considered unlikely. Consequently, I foolishly elected in 2003 to use Aluminum wedge shoes to improve hoof angles on the strong advice of Don Dee’s highly experienced farrier. Don Dee became moderately lame after several weeks, and I replaced the Aluminum wedge shoes with flat steel shoes immediately. Lameness disappeared within 3 weeks of gallium nitrate treatment, even though the steel shoes are flat and do not have the optimal angle theoretically needed by Don Dee. My strong feeling is that most horses with navicular disease, but without symptoms, are hypersensitive to Aluminum, and they will develop navicular disease pain. In my opinion, aluminum shoes should never be used in a navicular-diseased horse, regardless of whether the horse has foot pain. If wedge shoes are needed, I recommend finding a farrier who will custom-make steel wedge shoes and not use aluminum shoes.

Remember: “AL (III) in bone causes bone pain and proximal myopathy (disorders of adjoining muscles and tissues) in all vertebrate species tested. (REF. 1)”

Another principal concern of mine about shoes is that the horse not land toe-first. Toe-first landing can be evidenced by watching for dirt being kicked up. Horses that land toe-first will develop foot problems. These problems must be addressed by your farrier.

Feeds based primarily upon oat and wheat bran can result in calcium deficiencies and a loss of bone mass, particularly in young horses. A number of bone disorders result, as well as tendon contraction. Why? Each contains phytate or phytic acid, which binds calcium and some other minerals, thus making many ingested minerals biologically unavailable. Consequently, the calcium/phosphate balance is damaged, and bone diseases develop. (6) In areas where adequate calcium can be obtained from soils such as limestone, the problem should not be as severe or may not occur. The British Horse Society book warns, “Oats have a poor calcium to phosphorus ratio, so if fed alone, it must be supplemented by ground limestone to balance the minerals.” (7) Leslie Law, a top British horse trials competitor, writes in the book CROSS-COUNTRY MASTERCLASS compiled by journalist and event rider Debby Sly concerning feeding, “All the horses in our yard have certain supplements in their evening feed, namely a half teaspoon of limestone flower, …” My attitude about feeding horses a diet primarily of oats is clear and simple. DON’T DO IT.

The best soils for horses’ feet are limestone soils such as those found in the Bluegrass region of Kentucky, the hill country of Texas, Tennessee, Arkansas, Ireland, and other places where these ancient sea beds are now exposed. Limestone is a sedimentary rock that consists primarily of calcium carbonate from the exoskeletons, skeletons, and shells of ancient sea life. Also, caliche is an accumulation of soft calcium carbonate in dust to gravel size at or near the soil surface. It also may contain dolomite (calcium magnesium carbonate) and other minerals (especially magnesium) in trace to low amounts. Recovery from navicular disease requires (in addition to gallium nitrate) an adequate supply of these vital skeleton-forming minerals (especially balanced amounts of calcium and magnesium).

Incidentally, I have experimented with another horse with zinc dietary supplements to treat anorexia (no appetite to the extent of loosing significant weight), and magnesium for emotional instability. Don Dee never had these problems, but his full brother Sharpe did. Update, the anorexia was vanquished using 120 mg zinc daily from zinc gluconate. Recently, we started to supplement our horses’ diets with flaxseed, which greatly increased their appetites. The health benefits of flaxseed are known to be enormous, and apparently the horse recognizes flaxseed as important due to their ravenous appetite for it.

To eliminate ammonia from urine soaked stall bedding use sodium bicarbonate sprinkled over the bedding (baking soda) – never use lime. Lime is extremely caustic and useful mainly to dissolve flesh from bone in rendering plants, and to disinfect outhouse waste. Limed stall floors will cause injury to the horse’s feet. Long term use of sodium bicarbonate on stall floors usually results in stalls that have no (zero) foul odor.

Cited References:

(1) Alfrey Allen C., MD. (1995) Toxicity of detrimental metal ions – Aluminum. (Guy Berthon, editor), Handbook of Metal-Ligand Interactions Biological Fluids – Bioinorganic Medicine, Volume 2, Marcel Dekker, Inc., New York, pages 735 – 742.

(2) H.F. Schryver DVM, D.L. Millis DVM, J. Williams DVM, and H.F. Hintz DVM. Metabolism of some essential minerals in ponies fed high levels of Aluminum. Cornell Vet. 1986:76;354-360.

(3) Martin R. Bruce., Ph.D. Aluminum: a neurotoxic product of acid rain. Accounts of Chemical Research. 1994:27;204-210.

(4) Paolo Zatta, Tamas Kiss, Mario Suwalsky, Guy Berthon. Aluminum (III) as a promoter of cellular oxidation. Coordination Chemistry Reviews. 2002:228;271-284.

(5) Henry Heymering RJF, (personal communication) e-mail: horseu at earthlink.net.

(6) Warrell Raymond P., MD. (1995) Gallium for Treatment of Bone Diseases. (Guy Berthon, editor), Handbook of Metal-Ligand Interactions in Biological Fluids – Bioinorganic Medicine, Volume 2, Marcel Dekker, Inc., New York, pages 1253 – 1265.

(7) O.R. Adams, Lameness in Horses, Third Edition, Lea & Febiger.

(8) The British Horse Society, Manual of Stable Management, Book 7 (Watering and Feeding), page 59.

Dr. Raymond Warrell has published many medical journal articles on gallium nitrate and bone. Access PubMed (a library retrieval service of the National Library of Medicine, National Center for Biotechnology Information, National Institutes of Health) here, Search for “gallium nitrate” and “Warrell” for his published articles.