What is Cobalt?

What is Cobalt?

By:  Clara Fenger, DVM, PhD, DACVIM and Pete Sacopulos, JD

Cobalt is a mineral which is present in animal systems predominantly as part of Vitamin B12, which is a key cofactor in DNA synthesis. It is a nutritionally required element with the lowest dietary requirement of all of the required trace minerals.   Recommended daily allowances for humans is about 0.1 µg/day in the form of Vitamin B12 (Unice et al., 2012).  The National Research Council, which determines daily requirements of nutrients for animals, has determined a dietary cobalt requirement of 0.5 to 1.1 mg/day in horses and 1.2 to 2.4 mg/day for a cow, depending upon weight and metabolic state (Lawrence et al., 2007).  Maximum tolerable amount is 25 mg/kg of dry matter of feed or forage (Lawrence et al., 2007).

Cobalt concentrations in drinking water typically range from 0.1–5 ng/mL, and daily cobalt intake ranges from 11–580 µg/day in humans (Unice et al, 2012; Schroeder, 1967). Legumes like alfalfa and clover are the principle sources of cobalt in the natural diet of horses, and there can be widely varied concentrations of cobalt in these forages across different geographical locations in the United States and internationally (Kubota et al, 1987, Herbert, 1996). Deficient soils can result in profound deficiencies in cattle and sheep, resulting in anemia, weight loss and general unthriftiness.  Deficiencies in these species are likely under identified, but readily corrected by supplementation (Merck Veterinary Manual, accessed 1/22/15).  In contrast, deficiency has not been identified in horses.

Oral absorption of cobalt salts in humans varies depending on the dose, compound, nutritional status of the individual and proximity in time to a meal (Tvermoes et al., 2013).  For example, less than 5% of an oral dose of cobalt oxide is absorbed, compared with 30% of an oral dose of cobalt chloride, as determined from rodent studies. Increasing the dose of cobalt does not tend to cause significant accumulation as increasing doses result in a smaller proportion of the dose being absorbed. In humans, approximately 80% of cobalt is excreted in the urine and about 15% in the feces (Lison, 2007).  No studies evaluating the oral absorption of cobalt have been done in horses.

Why is cobalt used in athletes?

Human recombinant erythropoietin (EPO) became available in the 1990’s, and rapidly became adopted into covert doping programs for human athletes.  EPO stimulates the bone marrow to produce red blood cells, increasing the oxygen carrying capacity of the blood.

The ability to test for EPO was developed in the early 2000’s, curbing its abuse, but it was pointed out in the medical literature (Lippi et al., 2005, 2006) that cobalt, the original treatment used to increase human hematocrits in the treatment of anemia, also had potential to be used/misused in athletics in much the same way as administration of EPO. The potential illicit use of cobalt to improve athletic performance is based on the cellular actions of cobalt, leading to its recent and reportedly widespread use in horse racing (Paulick, 2014; Merkeberg, 2013).

A high dose of cobalt triggers a series of events which increases endogenous blood concentrations of EPO. Cobalt increases a protein in the cell called Hypoxia Inducible Factor (HIF-1α).  High intracellular HIF-1α causes direct activation of the erythropoietin gene resulting in increased plasma concentrations of erythropoietin, which would then drive the increase in red cell formation and an equivalent increase in the animal’s hematocrit (Semenza, 2014).  In addition to its EPO effects, other effects include increased blood supply to the muscle, and increased efficiency of energy utilization.

The theory is interesting but does this really work in horses?  The hematological effects at high levels of cobalt can be impressive:  in laboratory animals (Gluhcheva et al., 2011), dogs (Fisher, 1959) and humans (Lippi et al., 2006) chronic daily administration of large quantities of cobalt chloride have resulted in significant increases in red blood cell counts and hemoglobin.  Lower doses appear to have no hematological effect.  In horses, single doses of 22 mg or 49 mg of Co2+  (Kynch et al., 2014), or up to 449 mg of Co2+  (pers. Comm. Mary Scollay) had no effect on red blood cell parameters.   The consensus from the literature including multiple studies in multiple species is that chronic blood concentrations of 300 ppb and less are not associated with hematological or toxicological effects, whereas chronic concentrations in excess of 300 ppb are associated with both hematological and toxicological effects (Finley et al, 2012).

In racehorses, cobalt is typically administered a day or two before racing.  It seems unlikely that cobalt directed changes in EPO gene transcription or capillarity of muscles could be in effect at the time of the race if cobalt is administered only a few days before competition.  However, a small subset of horses, specifically among Standardbreds, seem to have impressive racing performances pursuant to Co²⁺ administration two days pre-race.  One possible mechanism of action of this cation is its effect as a calcium channel blocker (Simonsen et al., 2012).  Standardbreds are unique among the racing breeds in that they are susceptible to “tying-up” during racing (Isgren et al., 2010).  Other racing disciplines do not suffer this condition during racing, but may “tie-up” before or after racing.  The underlying mechanism of tying-up is unclear, except that it is probably a heritable condition (Collinder et al., 1997), and likely mediated by calcium channels in the muscles (Lopez et al., 1995).  Certainly some of the preventative therapies for tying-up involve calcium channel blockers, such as Dantrolene (Lopez et al., 1995) or another divalent cation, magnesium (Fenger, unpublished observation).  Since tying-up is prevalent among Standardbreds, and other preventative treatments for this condition are banned on raceday, the purported performance enhancing effect of Co²⁺ administration two days before racing may simply be prevention of tying-up.   

Why should cobalt be regulated?

Other than a possible mechanism to prevent tying-up, or muscle cramping in some horses, there appears to be no effect of cobalt on horses in the doses most commonly used.  On the other hand, there are many reports of cobalt toxicity in people.  In a mining town in Peru, excessive exposure caused chronic excessive red blood cell production in miners to the point of sludging of blood (Jefferson, 2002) and the US Environmental Protection Agency has set safety levels for cobalt for the protection of workers at high risk, such as mining and some industrial jobs. 

Typical adverse reactions to chronic cobalt administration in humans include nausea, vomiting, heart failure, low thyroid hormone levels and goiter, with neurological symptoms being reported less frequently (Jelkmann, 2012).  Large circulating concentrations of cobalt interfere with the uptake of iodine into the thyroid gland, resulting in low thyroid hormone levels.  In the late 1960’s, cobalt was added to beer as an anti-foaming agent, and resulted in a number of cases of heart failure. Cobalt is taken up in high concentrations into the heart muscle, likely in its role as a calcium channel blocker, and has been linked to an epidemic of heart failure in a group of heavy beer drinkers from the cobalt-containing beer (Alexander, 1972).  This specific syndrome was clearly multi-factorial, as the specific disease syndrome did not match any others associated with excessive cobalt.

It is likely that these chronic high doses which are required to cause thyroid dysfunction or cardiac failure are not achievable in horses.  However, at the extremely high doses that are suspected of being in use, horses can exhibit impressive adverse effects, such as tremors, sweating and colic (pers. comm Mary Scollay).  All of these effects are transient, and the horses appeared to be completely normal within a few hours.  Nonetheless, there has been suspicion that some incidents of sudden death on the racetrack have been associated with high serum cobalt levels, suggesting that there may be a relationship.

What are current regs?

Hong Kong has had a cobalt threshold longer than any other jurisdiction, and the ‘in-house’ urine cobalt threshold is 100 ng/mL.  A recent paper out of Hong Kong suggests 2 ppb as an appropriate threshold in plasma (Ho et al., 2014).  Among the criticisms of this threshold by the Hong Kong authors is that one of the study populations was a group of 109 horses in the Emirates.  This population races under strict security and yet 6 horses were considered to be outliers and had to be eliminated from the population before the balance of the group would fit the 2 ppb threshold.  Thresholds for naturally occurring substances must be carefully considered, and elimination of data must be done only where considerable investigation is performed. 

In Australia, Harness racing officials have introduced a urinary threshold of 200 ng/mL after samples in certain harness horses there reportedly exceeded 3,500 ng/mL (Bartley, 2014).  Similar to the Hong Kong analysis, Hibbert (2014) examined a group of post-race samples and identified a “natural break” in the data, ultimately requiring the researchers to eliminate 17 horses from a population of 80 in order to make the proposed threshold fit.  Again, the elimination of 20% of the population without further investigation into alternative explanations, such as feed or hay sources is inappropriate for establishing a threshold for which the penalty is on par with erythropoietin.

Indiana is the first US jurisdiction to regulate and implement a cobalt rule.   Indiana’s rule regulating cobalt establishes a threshold of 25 ppb.   The regulation that was implemented, by way of emergency rule, became effective October 1, 2014, for horses in competition and January 1, 2015, for out-of-competition testing.   Indiana’s cobalt rule states:  “Cobalt – not to exceed twenty-five (25) parts per billion of cobalt in serum or plasma.  A sample from a horse tested and found by the Commission’s primary lab to have cobalt in excess of this threshold shall be placed and remain on the veterinarian’s list until the concentration of cobalt in serum or plasma has fallen below the designated threshold.”   71 IAC 8-1-9(a)(3)   Indiana’s rule regulating cobalt makes a positive test a category “A” penalty, as established by the Recommended Penalties and Model Rule, regardless of its presence in a post-race or out-of-competition sample.    71 IAC-8-1-7(b). 

Interestingly, the Indiana Horse Racing Commission has issued a supplemental notice relative to the new emergency rule on cobalt that suggests leniency for those receiving a positive test for cobalt wherein the positive detected level is more than 25 ppb but less than 50 ppb. 

Indiana’s cobalt rule for in-competition testing became effective during Indiana’s 2014 season and, significantly, with only weeks left in that season.   Despite that being the case, there have been positive test results for cobalt all of which, as of this date, have been/are for in-competition testing.

Several other states have been closely observing Indiana’s lead to regulate cobalt.   The State of California is one of those states.   In fact, the State of California’s Horse Racing Board recently discussed a proposal by its Medications and Track Safety Committee to add Board rules to regulate the use of cobalt.   In October of last year, California’s Equine Medical Director, Dr. Rick Arthur, addressed the issue before the State of California Horse Racing Board.   In doing so, Dr. Arthur noted a study that the Board had performed at Maddy Laboratory that examined the results of Cobalt Chloride at low doses.   Dr. Arthur reported that: “. . .  what was found is that after the first elimination where probably 80% of it is eliminated in the first 48 hours . . . it takes weeks to get rid of the rest of it . . . that’s actually good news because it allows us to set a threshold that would eliminate its use . . . .”   (State of California Horse Racing Board Meeting Minutes for October, 2014)   Based on Dr. Arthur’s report and other considerations, the Executive Director of the State of California’s Horse Racing Board,  Rick Baedecher, stated that the Board would pursue a rule regulating cobalt at: “ . . . the 25 nanogram level.   And if a horse is above that level (the horse) will be placed on the vet’s list until . . . it tests lower than the threshold . . . .”  (State of California Horse Racing Board Meeting Minutes for October, 2014)    Dr. Arthur, at the October, 2014 meeting of the Board, also recommended the proposed rule regulating cobalt include out-of-competition testing.

Another state contemplating a rule regulating cobalt is Minnesota.   In the Fall of last year the Minnesota Racing Commission discussed the status of cobalt regulation in racing.    The chief veterinarian of the Minnesota Racing Commission, Dr. Lynn Hovda, provided a briefing to the Commission.  Dr. Hovda discussed both Indiana and California’s efforts in this regard and the reason for needed regulation.   The reasons given are those that are normally cited with regard to regulating cobalt, being the potential for toxicity to equine athletes if Cobalt Chloride is administered at high levels and a second reason being that it is believed that excessive amounts  of Cobalt Chloride may be performance enhancing.  The Minnesota Racing Commission has been and continues to move forward with adopting a rule for regulating cobalt.   It will likely closely follow the Indiana rule.   One exception may be the threshold level.    Discussions have included setting the threshold level for cobalt between 50 and 70 ppb, slightly higher than Indiana’s current threshold of 25 ppb.   (Minnesota Horse Racing Commission Meeting Minutes for September and October, 2014)

On March 4, 2014, the California Horse Racing Board (CHRB) issued a notification that they were about to commence monitoring cobalt concentrations, and they implemented a regulatory threshold of 25 ppb.  California, similar to the Hong Kong and Australian studies performed preliminary survey studies, which also excluded outliers in order to achieve their threshold.  The trend is clear:  in order to set the regulatory thresholds, horses with higher cobalt levels must be eliminated from the study data because they fall outside what looks “right.”  This is hardly appropriate science, nor the appropriate method of regulating a multi-million dollar industry.

On May 20, 2014, the Maryland Racing Commission decided that Maryland will begin testing horses for cobalt. The chairman of the board indicated that there was ‘no definitive threshold’ concentration for cobalt at that time. There are also no specific rules in place in Maryland relating to cobalt, and no comments were made on how a horse presenting with high concentrations of cobalt might be addressed (Vespe, 2014). 

In the absence of a state regulation, the Meadowlands Racetrack owner, Gural implemented a “house rule” regarding cobalt, using the current Hong Kong threshold of 10 ppb, as an out of competition threshold.

There is marked confusion over the regulation of cobalt, because experts disagree on an appropriate thresholds (Popot, 2014).  Surveys of horses have resulted in the wholesale elimination of “outlier” horses based on the assumption that these horses must have been treated with exogenous cobalt.  In a study where different laboratories across the globe tested the same samples, the variation between testing laboratories was as high as 82% for the testing in serum and 23% in urine.  Because of the greater agreement between lab testing methods using urine, the international community has settled on a urine threshold of 100 mcg/mL raceday threshold for uniformity.

No dose-response studies have been performed to determine at what level cobalt has any effect on horses.  However, a review of the literature in the animals which have been studied indicates that a sustained cobalt level above 300 ppb is required for cobalt to exert its hematopoietic and other effects (Finley, 2012).  Current regulatory focus on thresholds have sought levels which reflect likely exogenous administration of a naturally occurring substance which may or may not have been with intent, and not levels which actually reflect any performance enhancing effect.  This lack of valid scientific basis for the cobalt thresholds which have been adopted has led to headlines and career-threatening accusations across the turf media.

Conclusions

The regulation of cobalt in North America has come about with great fanfare and headlines, but the science has yet to catch up.  The thresholds adopted fail to hold up to scientific scrutiny, and, like so many other regulations in this day and age, are more likely to trap innocent horsemen than those actually cheating.

1. Unice, K.M., Monnot, A.D., Gaffney, S.H., Yvermoes, B.E., Thuett, K.A., Paustenbach, D.J., Finley, B.L.., 2012.  Inorganic cobalt supplementation: prediction of cobalt levels in whole blood and urine using a biokinetic model. Food and Chemical Toxicology 50:2456-61. 
2. Lawrence, L.M., Cymbaluk, N.F., Freeman, D. W. et al.  2007.  Nutrient Requirements of Horses.  Chapter 5.  Minerals.  The National Academies Press.  pp 87-88. 
3. Schroeder, H.A., Nason, A.P., Tipton, I.H.  1967.  Essential Trace Minerals in Man:  Cobalt.  Journal of Chronic Disease.  20:869-890.
4. Kubota, J., Welch, R.M., Van Campen, D.  1987.  Soil-related nutritional problem areas for grazing animals.  Advances in Soil Science.  Ed. B.A. Stewart.  P 193.
5. Herbert, V., 1996. Vitamin B-12. Present knowledge in nutrition, 7th edition. Washington, D.C. ILSI p 191-205.
6. http://www.merckmanuals.com/vet/management_and_nutrition/nutrition_cattle/nutritional_requirements_of_beef_cattle.html?qt=cobalt%20&alt=sh (accessed Jan 15, 2015)
7. Tvermoes, B.E., Finley, B.L., Unice, K.M., Otani, J.M., Paustenbach, D.J., Gailbraith, D.A., 2013.  Cobalt whole blood concentrations in healthy adult male volunteers following two weeks of ingesting cobalt supplement. Food and Chemical Toxicology 53:432-39.
8. Lison, D., 2007. Cobalt. In Handbook on the Toxicology of Metals, 3rd edition.  Nordberg, G.F., Fowler, B.A., Nordberg, M., and Friberg, L.T., Eds., Amsterdam: Elsevier Science Publishers. Pages 511-28.
9. Lippi G, Franchini M, Guidi GC., 2005. Cobalt chloride administration in athletes: a new perspective in blood doping. British Journal of Sports Medicine 39(11):872
10. Lippi, G., Franchini, M., Guidi, G.C., 2006.  Blood doping by cobalt. Should we measure cobalt in athletes? Journal Occupational Medicine and Toxicology. 1:18-20.
11. Paulick, R., 2014.  Is cobalt a killer in horses? The Paulick Report. http://www.paulickreport.com/news/ray-s-paddock/is-cobalt-a-killer-in-horses/ (accessed June 1, 2014)
12. Merkeberg J.  2013  Blood manipulation: current challenges from an anti-doping perspective. Sports Medicine in Hematology 2013:627-31.  doi: 10.1182/ asheducation-2013.1.627.
13. Semenza, G.L.  2014., HIF-1 and human disease: one highly involved factor. Genes and Development 14:1983-1991.
14. Gluhcheva, Y., Madzharova, M., Zhorovab, R., Atanasov, V., Ivanovac, J., Mitewa, M., 2011. Cobalt(II)-induced changes in hemoglobin content and iron concentration in mice from different age groups. Biotechnology & Biotechnological Equipment 26:126-128
15. Fisher, J.W., 1959.  The effects of cobalt injections on total circulating red cell volume and bone marrow cytology in normal and adrenalectomized dogs. Endocrinology 64(4):522
16. Knych, H.K., Arthur, R.M., Mitchell, M.M. et al.  2014.  Pharmacokinetics and selected pharmacodynamics of cobalt following a single intravenous administration to horses.  Drug Testing and Analysis.  DOI 10.1002/dta.1737.
17. Finley, B.L., Monnot, A.D., Gaffney, S.H. et al.  2012.  Dose-response relationships for blood cobalt concentrations and health effects:  A review of the literature and application of a biokinetic model.  Journal of Toxicology and Environmental Health, Part B:  Critical Reviews 15(8):493-523.
18. Simonsen, L.O., Harbak, H., Bennekou, P., 2012. Cobalt metabolism and toxicology—a brief update. Science of the Total Environment 432:210-15.
19. Isgren, C. M., Upjohn, M. M., Fernandez-Fuente, M., Massey, C., Pollott, G., Verheyen, K. L. P., and Piercy, R. J. 2010. Epidemiology of Exertional Rhabdomyolysis Susceptibility in Standardbred Horses Reveals Associated Risk Factors and Underlying Enhanced Performance. PLoS ONE, 5(7), e11594. doi:10.1371/journal.pone.0011594.
20. Collinder, E., Lindholm, A. and Rasmuson, M.  1997.  Genetic markers in standardbred trotters susceptible to the rhabdomyolysis syndrome.  Equine Veterinary Journal. 29:117-20.
21. López, J.R., Linares, N., Cordovez, G. and Terzic, A. Elevated myoplasmic calcium in exercise-induced equine rhabdomyolysis.  Pflugers Arch. 1995 430:293-5.
22. Jefferson, J.A.  2002.  Excessive erythrocytosis, chronic mountain sickness and its relation to serum cobalt levels. Lancet 359:407-8.
23. Jelkmann, W., 2012. The disparate roles of cobalt in erythropoiesis, and doping relevance. Open Journal of Hematology 3-6.  DOI: http://dx.doi.org/10.13055/ojhmt_3_1_6.121211
24. Alexander, C.S.  1972.  Cobalt-beer cardiomyopathy.  A clinical and pathologic study of 28 cases.  American Journal of Medicine 53(4):395-417.
25. Ho, E.N.M., Chan, G.H.M., Wan, T.S.M. et al.  2014.  Controlling the misuse of cobalt in horses. Drug Testing and Analysis.  DOl 10.1 002/dta.1719.
26. Bartley, P., 2014. Cobalt Chloride taking over from EPO?  Thoroughbred Village.  http://forum.thoroughbredvillage.com.au/cobalt-chloride-taking-over-from-epo_topic48586.html  (accessed June 1, 2014)
27. Hibbert, D.B.  2014  Cobalt in Equine Urine.  Presented at The 20^th International Conference of Racing Analysts and Veterinarians, September 20-27, Mauritius.
28. Popot, M.A., Ho, E.M.N., Wan T.S.M. et al.  2014 An international collaboration on cobalt for setting up a threshold value.  Presented at The 20^th International Conference of Racing Analysts and Veterinarians, September 20-27, Mauritius.

Wandering Withdrawal-Times and the Racing Medication and Testing Consortium Model Rules: Time for the RMTC to get days

Clara Fenger, DVM, PhD, DACVIM; Andy Roberts, DVM; Jim Casey, DVM, MS

The ARCI Controlled Therapeutic Medication Rules have gone into effect in a number of new states, coming on line rapidly in the last few months.  The regulatory authorities have promised that providing a stringent and well defined set of uniform medication rules would make racing cleaner and safer for all participants.  Gone would be the days of supposed rampant cheating and we could all compete on a level playing field.  In fact, we have known for some time that operating outside the lines of legal and ethical competition in horse racing is extremely rare…representing only 0.015%  of horses passing through the test barn (1).  Clearly, the playing field has been quite level and well regulated for some time.  Nonetheless, it is human nature to suspect “that guy (or gal)” who is winning at a 40% clip must be using something, so we ought to all welcome the ever increasing oversight by our regulatory bodies.  Besides, even the horsemen agree that uniform rules would make racing across state lines easier.

Enter RMTC.  In an effort to produce National uniform medication rules, the RMTC has come up with a plan.  First, limit the number of medications that can be used therapeutically in race horses, and regulate them.  Have uniform National thresholds based on scientific studies which provide valid and realistic withdrawal time guidelines for trainers and veterinarians.  The Executive Director of the RMTC has suggested that adopting these rules actually reduces positive tests(2).  However, recent issues cropping up across the country seem to dramatically refute that claim.

The first uniform medication rule to be implemented across the country was to drop the acceptable phenylbutazone level from 5 µg/mL to 2 µg/mL.  Even though all of the pain relieving effect
of phenylbutazone is eliminated at the 5 µg/mL level(3), racing commissions in various jurisdictions felt that this threshold allowed levels at the time of the pre-race exam that interfered with their ability to determine if a horse was sound.  Nonetheless, at the time the change was made, the recommended withdrawal in many jurisdictions remained 2 g IV at 24 hours(4).  This, despite having data collected at the University of Florida showing that only 95% of the horses that received the original 2 g IV dose were below the regulatory threshold(5).  Which is akin to routinely giving a speeding ticket to one in 20 cars going 55 mph in a 55 mph zone.  Although the 24 hour 2g dose recommendation was continued in several states after the threshold change, the RMTC changed the dose to 9 cc (1.8 g) IV at 24 hours for the model rule, and state recommendations vary from the model rule recommendation to 1 g IV at 24 hours (KY)(6), 2 g IV at 28 (VA) or even 2 g IV at 36 hours (WV)(4).  You have no way of knowing for sure until you get back a positive test.  So much for uniformity.

Flunixin (aka Banamine®) is another example where the RMTC has been flat wrong in their withdrawal recommendations.  The manufacturer’s recommended dose is 500mg, or 10 cc to a 1,000 pound horse.  Originally the RMTC recommended that this dose be administered no closer than 24 hours pre-race(4).  Somehow, the decision was made that the cutoff for a positive test was going to be 20 ng/ml in blood(5).  This, despite the unhappy fact that when you actually read the studies, the science indicates that many 24 h post-race samples will exceed the 20 ng/ml threshold(7).  When post-race samples came up positive in droves, confirming this already-known detail, the RMTC backtracked.  In their meeting this spring at Gulfstream Park, they heard the “positives” message; their solution was to leave the sacred 20 ng/ml threshold in place but to move the withdrawal time out to 32 hours(8).

The RMTC doesn’t seem to be any more clued in with Ketoprofen.  When they set the original 10 ng/ml level, they had minimal “positives.”  So, since they couldn’t believe NO ONE was “cheating” (because there were no positive tests) with this drug, at the same Gulfstream Meeting, the RMTC reduced the threshold to 2 ng/ml(8).  Still no problem with cheating (no positive tests), so surely a further reduction is coming.  Seems like every five minutes, the RMTC and subsequently various regulators are changing a rule or a recommendation, all without real, publicly reviewable substantive scientific evidence to support their “new” position.  If you can’t dazzle the horsemen with brilliant science, baffle them with confusing and ever-changing …well you know.  Somehow, the idea of getting the facts straight with scientifically sound research before implementing rules that profoundly affect the lives of the people and horses you regulate has escaped them.

Next, Methocarbamol:  Robaxin is a mainstay of the prevention of muscle cramps (i.e. “tying up”) in training, a painful condition that plagues many racehorses and mostly fillies.  It is an important therapeutic medication to have available to horses in training.  And a rash of methocarbamol positives at Delaware Park(9) has further underscored the problems with both the RMTC studies and the implementation of changes in regulatory procedures.  Firstly, the studies were performed on only 20 horses(10), and when the results are applied across thousands of racehorses with varied management, different metabolism and under a myriad of different specific circumstances across the country, the outcomes are not so clean.  Secondly, medication interactions were apparently not taken into consideration.  The RMTC Executive Director has recently explained in great detail(11) that methocarbamol and phenylbutazone are metabolized by the same pathway in the horse and phenylbutazone is preferentially eliminated, slowing the metabolism of methocarbamol, and thereby resulting in the positive tests.   Except there is no published scientific data to support that statement(8).  And if there were, the RMTC should have been aware and done the studies to provide guidelines for the practitioners and horsemen.  Dr. Rick Sams, Director of LGC Sports Science, the lab that runs the Delaware post-race tests responded:  “While the guidelines that are in place were well thought out and researched, there will, I’m sure, be adjustments made as time goes on.(11)”  Sounds like the horsemen are guinea pigs in a high stakes game of chicken:  let’s figure out the rules as we go, and if you try to adhere to the rules and guess wrong, the penalty is harsh.  This is no way for an industry to act.  The stakes are too high for all concerned, including the horse and rider, to base medication regulations on questionable science.  

“There will, I’m sure, be adjustments made…:” not surprising when one considers the history of the RMTC threshold for Methocarbamol, which goes like this: First, RMTC commissioned a study at University of Florida using their 20 exercised horse herd and a 15 mg/kg methocarbamol dose(10)…a typically used dose(12). This study came up with a 20 ng/ml threshold and a 24 hour withdrawal time.  Unfortunately, Pennsylvania already had in place a 1 ng/ml threshold, based on studies with a REALLY low, below any clinical effect, 2.2 mg/kg dose of methocarbamol(5,12).  What to do??  Simple! Just leave the cutoff for a positive test at 1 ng/ml but arbitrarily, and without performing the necessary scientific study to back it up, move the withdrawal time out to 48 hours, and trust that it works.  If it doesn’t work out, come up with something convenient to blame, in this case apparently phenylbutazone.  At the same time tell horsemen that THEY have to move the withdrawal time out again.  The only problem is those pesky horsemen who actually got Methocarbamol positives during this “educate the regulators” “adjustment making” period.

In deflecting the blame towards a heretofore unidentified drug interaction with phenylbutazone, the RMTC is also directing attention away from the simple fact that Methocarbamol has long been known to show dose dependent kinetics.  In other words, as the dose increases, Methocarbamol is eliminated more slowly and tends to accumulate, increasing the likelihood of a positive(13).  Both the RMTC and the University of Pennsylvania studies were single IV dose studies.  We would therefore be not in the least surprised if it turns out that many of the numerous recent positives reported for Methocarbamol are more closely associated with a normal multi-dose therapeutic schedule of Methocarbamol than just with the concomitant administration of phenylbutazone.  The end result of the confusing withdrawal guidelines is to make a safe and effective therapeutic medication, Robaxin, essentially illegal and out of reach for those horses that may get muscle cramps.  

For many months preceding the adoption of the RMTC Model Rules regarding uniform medication, racing officials went around the country and were quoted in the press about the new rules regarding joint injections.  Low grade joint inflammation is an extremely common outcome of strenuous exercise, and joint injections are a useful and widely used therapeutic approach to handling this concern.  Modern human sports medicine has included the use of therapeutic joint injections for years, and studies have shown no long term ill effect from repeated injections(14).  Which fits very well with the experiences of racetrack practitioners:  Judicious joint injections are therapeutic and preserve the long term health of the athlete, not just for its racing career, but for the career that follows.  Nonetheless, the racing officials and proponents of the RMTC “driven” Uniform National Model Rule have, perhaps less than logically, insisted that veterinarians should have sufficient time after a joint injection to assess response to therapy.  They argued that horses should not be raced within 7 days of injection with a relatively quick acting corticosteroid like triamcinolone (Vetalog) or betamethasone, or 14 days of injection with a long acting corticosteroid like methylprednisolone (Depo-Medrol).  Veterinarians and horsemen have long agreed that assessing response to therapy should be part of any therapeutic intervention, but felt that the time periods set forth in the Model Rules were well beyond the time frame necessary.  Nonetheless, we were prepared to go along with it.  Unfortunately, we and other practitioners were not prepared for the outcome of the first few weeks of the new medication policy which have resulted in numerous alleged positives in at least 2 jurisdictions (IN,WV).

The uniform medication rules have put in place a 100 pg/mL blood threshold level of methylprednisolone (Depo-Medrol®), and a withdrawal of 7 days, nominally based on an RMTC sponsored report, where 100 mg was injected into a single knee(15).  And yet in the Controlled Therapeutic Medication Schedule recommendations(16), right next to the recommended 7 day withdrawal, it states that the withdrawal for 100 mg (2.5 cc) Depo-Medrol is actually 21 days…so which is it?  7 days or 21 days?  Given this uncertainty in the published guidelines, the states have varied from 10 days (IN) to 21 days (WV) for recommended withdrawal times linked to this threshold.  Faced with these ambiguities, practitioners, in an abundance of caution, have adhered doggedly to the recommended withdrawals.  And, despite this care, “cloudy” or possible positives have been coming up at a frightening rate in the first few weeks of the new rules, such as has been seen in WV(17).  It turns out, if you put the Depo-Medrol in a stifle, the clearance time is one thing.  If you put it in a hock, it is something else.  God forbid the horse moves while you inject it, because then all bets are off.   A racing official stated, off the record, that the purpose of the Depo rule was to discourage the use of Depo at all…hey wait, what happened to “so you could assess the response to therapy”?  A little deceptive to say the least.  And another, safe and effective, FDA approved therapeutic medication relegated to being essentially illegal.

To further complicate matters, Veterinarians, trainers and owners are anxiously awaiting the results of their post-race tests, which are taking an inordinate amount of time [a month or more] as a result of a laboratory backlog.  The new Uniform Model Rules mandate that a Depo Medrol positive requires purse redistribution and a fine(18).  All while the racing officials cannot even provide useful practical guidelines for withdrawal times.  As this article goes to press, even the racing commissions are unsure of their own final decision(17).  We all remember Brass Hat’s impressive effort to finish second in the 2006 Dubai World Cup.  The trainer and veterinarian tried to contact the appropriate authorities to identify the withdrawal time for methylprednisolone, and then added 5 days in order to inject the horse’s hocks well outside of those guidelines.  When the horse was disqualified for the positive test, the trainer and veterinarian protested, but to no avail.  After the trainer and veterinarian did everything possible, there was nothing that could be done: surely this can’t happen in America.

Other problems with the Controlled Therapeutic Medication Schedule (April 17, 2014), the cornerstone of the RMTC Model Rules have not yet reared their ugly heads. The recommendations on a common tying up preventative, dantrolene (Dantrium) is 48 hours.  This is based on a study performed with a single dose of 1 mg/kg, which is well below the therapeutic dose of 2-4 mg/kg(12,16).  Xylazine, a common tranquilizer, used to sedate horses for procedures, including dental work, veterinary procedures and some grooming procedures like clipping is listed as permissible at 48 hours with a published threshold level (cutoff for a positive test), but NO recommended dose and NO research paper to explain where the recommendation came from is listed(16).  Can I use the whole bottle?  Mepivacaine (Carbocaine) has a withdrawal recommendation of 72 hours, and represents a class B penalty i.e., a minimum of a 60 day suspension, loss of purse and fines (RMTC website).  And the RMTC recommendations are based on 1.5 mL of Carbocaine in a 1000 pound horse(16).  This is an amount which is below ANY usual therapeutic use of the product, which would be at least 10 mL for a Caslicks procedure or 5 -10 mL for a typical diagnostic nerve block.  So the actual RMTC recommendations appear to be at best a complete lack of understanding of how therapeutic medications are applied and at worst an intentional set up of any trainer or veterinarian who even thinks of using a therapeutically appropriate amount of mepivacaine.

This seems to be a common theme among the “permitted medication” list:  no good faith effort was made to determine how these medications are correctly and appropriately used as therapeutics before the withdrawal studies were performed or recommendations were made.  As a further matter of interest, the mepivacaine threshold is based on confidential data generated by the European Horseracing Scientific Liaison Committee [EHSLC] and therefore subject to EHSLC non-disclosure requirements apparently signed by all members of the RMTC Scientific Advisory Committee(8); so much for industry-wide transparency and independent scientific review.  Further, the cloak of secrecy does not end there:  a number of other US medications rules, such as acepromazine, albuterol, betamethasone, clenbuterol, dexamethasone, firocoxib, furosemide, isoflupredone, lidocaine, omeprazole, prednisolone, procaine penicillin and xylazine are based on secret data that has never
been subjected to independent review, and is currently unavailable to the horsemen or their racetrack vets(19). 

Drugs outside the magic “26” list of therapeutic substances are a no man’s land.  There is only one antibiotic, procaine penicillin, on the list.  States differ from 24 hours to 96 hours4 to “zero tolerance” (infinite in IN?20) on withdrawal for “sulfa drugs,” like Trimethoprim-sulfadiazine, probably the most commonly used antibiotic in horses, which is not even in the magic “26.”  Within the word “race horse” is the word “horse,” and this word is attendant with all the day to day things that might befall any animal.  In addition to scrapes and infections, a horse may get stung by an insect, necessitating an injection with an antihistamine, or scratch his cornea necessitating atropine or other therapeutic medication.  These conditions are not life threatening, but the varied therapeutic medication rules could prevent this otherwise completely healthy horse from competing, depending upon which jurisdiction you are in.  Imagine:  there are likely more than 26 over the counter medications in your bathroom medicine cabinet at home, but the most elite of athletes are prevented from benefitting from modern day sports medicine under the misnomer of “clean racing”. 

In 1900, infant mortality among humans was 30% and life expectancy was less than 50 years 21.   Much of the reason for the improvement in health of humans is the advent of modern medicine.  And yet we want to send our most precious charges, horses who have no voice for themselves, back to the dark ages.  Modern equine sports medicine is NOT a crime.  It has been developed to give the athlete the best possible quality of life and as a result to perform to the best of their abilities.  There are substances which may potentially enhance performance, and these are and should be banned.  Severe penalties should be in place and vigorously enforced.  But, folks, let’s get it right.  The rush to implement the RMTC rules has had a mountain of unintended consequences.  Shouldn’t we first and foremost get the science right, perform studies which reflect real world and appropriate uses of therapeutic medications and then establish dosage, thresholds, and withdrawal times.  Finally we should implement an appropriate phase in period allowing us to identify gaps in our scientific knowledge before imposing strict and onerous penalties.   Appears that it is the RMTC that needs to get “days.”

1. Association of Racing Commissioners International.  Drugs in US Racing – 2010:  the Facts.  2011. 
2. KAEP meeting, February 
3. Hu HH, MacAllister CG, Payton ME, Erkert RS. Evaluation of the analgesic effects of phenylbutazone administered at a high or low dosage in horses with chronic lameness J Am Vet Med Assoc. 2005 Feb 1;226(3):414-7.  4. http://www.rmtcnet.com/withdrawal_show.asp , accessed 8/12/2014
5. Summary of Medication Recommendations: Pennsylvania Horse Racing Commission Updated September 8, 2010. 6. http://www.khrc.ky.gov/Documents/24%20Therapeutic%20Medications-TB.pdf, accessed 8/12/2014
7. Sams, R.  Scientific Rationale for Establishing a Regulatory threshold for flunixin.  College of Veterinary Medicine, The Ohio State University.  2006.
8. Personal communication, Thomas Tobin 9. http://www.theracingbiz.com/2014/07/21/delaware-horsemen-concerned-positive-drug-tests/, accessed 8/12/2014
10. Rumpler MJ, Colahan P, Sams RA.  The pharmacokinetics of methocarbamol and guaifenesin after single intravenous and multiple-dose oral administration of methocarbamol in the horse. 2013 J Vet Pharm Therap 37:25-34. 11. http://www.drf.com/news/drug-combination-sets-rash-positives, accessed 8/12/2014
12. Hagyard Equine Medical Institute Formulary
13. Muir WW, Sams RA, Ashcraft S.  Pharmacologic and pharmacokinetic properties of methocarbamol in the horse. Am J Vet Res. 1984 Nov;45(11):2256-60.
14. Raynauld JP, Buckland-Wright C, Ward R, Choquette D, Haraoui B, Martel-Pelletier J, Uthman I, Khy V, Tremblay JL, Bertrand C, Pelletier JP. Safety and efficacy of long-term intraarticular steroid injections in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trial.  Arthritis Rheum. 2003 Feb;48(2):370-7.
15. Knych HK, Harrison LM, Casbeer HC, McKemie DS.  Disposition of methylprednisolone acetate in plasma, urine, and synovial fluid following intra-articular administration to exercised thoroughbred horses. 2013  J Vet Pharm Therap  37:125-132.  16. http://www.rmtcnet.com/resources/Controlled%20Therapeutic%20Medications%20April%202014.pdf, accessed 8/12/2014 17. http://www.bloodhorse.com/horse-racing/articles/86515/wv-hires-new-lab-purse-money-still-in-limbo, accessed 8/12/2014 18. http://www.rmtcnet.com/resources/RCI%20Uniform%20Classification%20Guidelines-December%202012.pdf, accessed 8/12/2014
19. http://arcicom.businesscatalyst.com/assets/arci-controlled-therapeutic-medication-schedule---version-2.1.pdf 
20. Joe Gorajec quoted during a meeting with the Indiana Standardbred horsemen on 8/12/2014 regarding the positive tests  21. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4838a2.htm, accessed 8/12/2014

To Salix or Not to Salix

In the wake of the PETA videos, which portrayed our majestic sport in a most unflattering light, we are left reeling from the backlash.  While most of what was shown in the video was either legal (the use of Salix and thyroxine) or just edited to the extreme (video of the state veterinarian drawing a post-race blood sample for drug testing, while the commentary implied that something illicit was taking place), certainly there were things that were offensive (the non-stop stream of profane language) and things that were clearly illegal, such as forging documents for illegal workers.  The unfortunate ramifications from this video seem to be taking the form of a rallying cry against raceday medication, which, of course, means no Salix.  The clip of the track vet telling the PETA girl that Salix is performance enhancing because of the weight loss is damning.  He failed to explain the repercussions to the animal of bleeding in the lungs, how scar tissue builds up over time, impairing the horse’s long term respiratory health…or perhaps he did explain it and it just didn’t make the video.  However, if Salix is performance enhancing, oughtn’t it be banned?

  Not so fast.  The scientific paper that first suggested performance enhancement by Salix was published in 1990¹.  It showed only that geldings raced faster on furosemide with no statistically significant difference among fillies and colts.  (Meaning that any performance enhancement is negligible.)  Geldings also race longer than fillies and colts, and hence are more likely to have the effects of chronic bleeding. A previous study² showed improved performance associated with Salix, but this study was performed with known “bleeders”  so the obvious conclusion is that is that any difference in performance is exactly the difference between how well the horse would have raced had it not bled, irrespective of the furosemide (ie Salix is performance enabling).  In fact, a well designed study in 1996³ looking at horses in treadmill exercise tests showed no difference whatsoever between a horse’s exercise performance with Salix and without Salix.

 The same 1996 study mentioned above is oft quoted in the vernacular of the anti-Salix contingent, as supportive of their position.  However, the truth lies in the actual details of the study.  When calculated on a weight for weight basis, the horses had higher oxygen consumption (meaning they performed more efficiently), however, the actual oxygen consumption was unchanged.  Which is exactly what we would expect if Salix had no effect on performance, despite the change in weight.  The vet caught so ominously on video saying they run faster because they are lighter should be embarrassed, not for saying what he obviously believed, but for not carefully reading the very paper he was quoting.

What about the case for the use of Salix?  Certainly racing occurs all over the world without it, which is the primary driving argument for the naysayers.  So let’s again go to the scientific literature and investigate the facts.  A series of studies^4-11 published in 1987 carefully investigated the clinical, diagnostic and necropsy findings of a group of 26 horses retired from racing in Hong Kong.  This group of horses were almost all known bleeders.  The findings were of severe, permanent pulmonary damage.  Clearly, horses are not immune from bleeding in Hong Kong, and more importantly, bleeding was proven unequivocally to cause permanent and severe pulmonary pathology. So, what is to be done?  We look again to the published scientific literature.  The ultimate placebo controlled, cross-over study on the efficacy of furosemide was finally performed by Hinchcliff et al, in 2009¹², funded by the Jockey Club.  As a scientist who has designed and performed many studies, this was the Holy Grail of all study designs, a rare opportunity in Veterinary Science.  This paper showed beyond a shadow of a doubt that furosemide ameliorates in all and prevents in some, EIPH.  In this study, NO horses bled a grade 3 or 4 on furosemide, which answers the question of:  is this the right thing to do or not.  Clearly, yes.

 So, the scientific literature concludes that racing on Salix is beneficial to the health and welfare of the individual horse, and Salix is just as likely (or more likely) to enable normalized performance rather than enhance performance.   The states obviously came to an agreement a long time ago that, just in case it IS performance enhancing (an infinitesimally small effect, if there), we should identify horses that race on furosemide with an L in the program, in order to provide transparency to the public.  This is an effective model, and, according to the Jockey Club’s own sponsored research, should remain.  We should not aspire to the model of foreign lands, many of which have restrictive medication rules for the purpose of human food safety.  Rather than base our reactions on arguments, such as “everyone else does it,” we should rely on the facts and science to guide our future.  Should we react to the PETA video?  Yes.  Should our reaction be to eliminate raceday medication?  I think not.

 

 

1.     Sweeney CR, Soma LR, Maxson AD, Thompson JE, Holcombe SJ, Spencer PA. Effects of furosemide on the racing times of Thoroughbreds. Am J Vet Res. 1990 May;51(5):772-8.

2.     Soma LR, Laster L, Oppenlander F, Barr-Alderfer V.  Effects of furosemide on the racing times of horses with exercise-induced pulmonary hemorrhage.  Am J Vet Res. 1985 Apr;46(4):763-8.

3.     Hinchcliff KW, McKeever KH, Muir WW, Sams RA. Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion. J Appl Physiol (1985). 1996 Oct;81(4):1550-4.

4.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. I. Clinical profile of horses. Equine Vet J. 1987 Sep;19(5):384-8.

5.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. II. Gross lung pathology. Equine Vet J. 1987 Sep;19(5):389-93.

6.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. III. Subgross findings in lungs subjected to latex perfusions of the bronchial and pulmonary arteries. Equine Vet J. 1987 Sep;19(5):394-404.

7.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. IV. Changes in the bronchial circulation demonstrated by C.T. scanning and microradiography. Equine Vet J. 1987 Sep;19(5):405-10.

8.     O'Callaghan MW, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations.  Equine Vet J. 1987 Sep;19(5):411-8.

9.     O'Callaghan MW, Pascoe JR, O'Brien TR, Hornof WJ, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations.  Equine Vet J. 1987 Sep;19(5):419-22.

10.  O'Callaghan MW, Hornof WJ, Fisher PE, Pascoe JR. Exercise-induced pulmonary haemorrhage in the horses: results of a detailed clinical, post mortem and imaging study. VII. Ventilation/perfusion scintigraphy in horses with EIPH.  Equine Vet J. 1987 Sep;19(5):423-7.

11.  O'Callaghan MW1, Pascoe JR, Tyler WS, Mason DK. Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Conclusions and implications.  Equine Vet J. 1987 Sep;19(5):428-34.

12.  Hinchcliff KW, Morley PS, Guthrie AJ. Efficacy of furosemide for prevention of exercise-induced pulmonary hemorrhage in Thoroughbred racehorses.  J Am Vet Med Assoc. 2009 Jul 1;235(1):76-82.

 

Eulogy for my Friends

On Sunday morning, my husband and I awoke to a conflagration in one of my barns.  The barn was already engulfed in flames and all we could do was call 911 and watch in horror as our horses and lives went up in smoke.  I have had an incredible outpouring of support from my friends and colleagues, which is strengthening during a time in which I am paralyzed with grief.  I have plenty of work to do, and need plenty of sleep, but whenever I sit to work on the computer or close my eyes, I imagine all my horses burning alive. 

 

It wasn't just a barn full of horses, or Thoroughbreds.  These were my children in some cases the third generation that has been in my family.  I hear so much negativity about the Thoroughbred and racing industry and I can't understand it, because I live this industry and it is wonderful. The greatest highs and now the lowest lows of my life have come from these incredible animals.  When you hear of a tragedy like this one, you think, how awful a bunch of animals perished.  And then the story passes on to something else.  Well, this is a eulogy for my animals.  They were not just animals, some raised to race, some raised to sell, some destined to be riding horses and some just retired: all cherished.  They deserve for the world to know that each one was an individual, and carried one veterinarian's hopes and dreams for their futures.

My first thoroughbred Broodmare, Miss Red, was in that barn.  Her first foal, a colt named Warm Courage (Howard) got loose from my help as a weanling with a chain hanging from his halter.  He freaked out, and ran around the farm, flipped over a fence and fractured his pelvis into a thousand pieces.  Two surgeons recommended euthanasia.  A third said to stall rest him for four months (after all, "you can always euthanize them later").  For over a month, you could walk into that stall and gently rock his pelvis from side to side and the bits of fractured bones made a sound like a bag of potato chips crunching. 

After four months of stall rest, he gradually made it to turnout and never took another lame step.  On the racetrack, he was a two year old workmate for a Canadian Champion, and regularly trained with good horses as a racehorse.  However, in two starts, he bled so much in his lungs that it streamed out his nose.  We turned him out for 6 months to recover.  Back then, I rode the racehorses, so when it came time for him to start back into training as a four year old, I tacked him up and rode him down to the arena on a loose rein.  He was perfect and quiet, walk, trot and canter like a seasoned show horse.  Thus he began his second career.

Howard went on to be a successful Dressage horse with my highest score on him at first level, 68.  He was a successful show hunter and jumper (3'6") on the A circuit, usually in the ribbons, and competed at Novice in eventing.  He was schooling at third level Dressage when he died, and I even bought new white breeches with the plan of starting back into my own show career this spring.  Most of his show career was with 12 and 13 year old girls.  While he had spurs in his hocks, and needed those injected occasionally, his pelvic fracture as a weanling never bothered him.  Never let anyone tell you an OTTB can't be a wonderful, talented and quiet kid's horse.  And don't give up on a pelvic fracture in a young horse, because you can always euthanize them later.  RIP Howard.

Miss Red, a Red Ransom mare,  went on to an unremarkable career as a broodmare.  During the "Tent Caterpillar Crisis"  of 2001-2002 in Kentucky, she developed pericarditis, an inflammation of the specialized membrane covering the heart.  I drained the pericardial sac, and treated her with antibiotics and anti-inflammatories and she recovered.  She went on to have a number of foals, but after they all excelled as show horses and NOT as racehorses, I decided to breed her to a Showhorse stallion in 2008 and get myself a fancy showhorse.  In the last month of pregnancy with that foal, she went into heart failure.  She was diagnosed with restrictive pericarditis, a sequela of the original pericarditis.  We nursed her along and I got my fancy showhorse (although a little small), Sweet Southern Style.  The mare's heart was fine as long as she was not pregnant, so she was retired at the age of 14.  RIP Miss Red and Sweetie.

A 23 year old Exceller mare who was a multiple graded stakes producer had been unable to have a foal for several years and the owners decided to give her up.  I took her on and got two foals out of her, before retiring her at the age of 25.  I spent the next four years of her life pampering her and nursing her through arthritis and other conditions of aging, with the help of other experts.  RIP Excedent at the age of 29.  Never thought something like this would take you.

My husband is a Thoroughbred horse trainer, but we met in graduate school.  He has a Master's Degree in Genetics.  He spends hours researching pedigrees to come up with the best matches for our broodmares.  For the first time in years, we had several commercial yearlings that we could expect a payday at the sales.  Despite the likeliness that they would go to the sale, he would watch them run and play and talk about how he hoped we could afford to keep them and put them in training when the time came, because they looked like great prospects. 

One yearling was a Proud Citizen colt out of a homebred mare.  We raced the granddam of this colt.  She won her first start and ran through her conditions easily in Kentucky, not an easy thing to do.  As a four year old, she was starting to develop marked arthritis of her hock joints:  a condition that would ultimate resolve with time, but it became difficult to keep her sound, so rather than wait out the joints to fuse, we bred her (She was a half to a Champion).  The first foal out of the mare was by Proud Citizen and was gorgeous.  He sold as a weanling for $140,000.  She went on to produce some beautiful foals, of which we raced several.  One day in the spring, when she was in foal to the stallion, Malibu Moon and had another Proud Citizen by her side, I was walking down my farm lane to feed the horses, and I heard her nickering to me.  This was not a usual thing, especially since she had a foal by her side.  I ran to her paddock to find her with a fractured cannon bone.  No, they don't just do this on the racetrack, they can do this in a paddock.  The foal by her side had a femur fracture.  I had to euthanatize them where they stood. 

We still had a filly out of the mare, whom we promptly retired from racing and bred.  Her first foal was a Flatter colt whom we sold for $160,000.  Her second is a Tiz Wonderful filly (3 yo) who is in training, and the third is a Flatter filly (2 yo) who is also in training.  The fourth was a Proud Citizen colt, as beautiful as his 3/4 brother.  RIP Proud Citizen - Saint Savior 2013. 

One of the yearlings was a Pure Prize filly out of one of our own homebred mares.  The mare, Veiled Vow, had been a hard knocking race horse, winning four of 19 starts, all in gutty fashion.  As a seven year old, she was in the lead by 5 lengths in a wide open 5 claimer (which is actually a very tough race, as many old class horses race in these), suddenly stopped, finishing third.  It was completely out of character for her.  She had torn in impressive fashion a ligament in her pastern.  While the mare's pedigree was not really strong enough to breed her in Kentucky, I looked around for someone in a different state market to give her to as a broodmare.  I could find no one I felt would take care of her, and give her the rehab needed to recover from her injury, so we decided to go ahead and breed her ourselves.  If she throws her heart, she will be a great broodmare, despite not being a producer for the commercial market.  So we found a season to Pure Prize and got a beautiful filly.  RIP Pure Prize - Veiled Vow 13.

The third yearling was the first foal out of a young mare we claimed for a broodmare.  As the industry looks to be turning around, we thought it was time to get a commercially viable mare.  She was a beautiful Successful Appeal filly that my husband was desperately hoping we could afford to race instead of sell when the time came.  RIP Successful Appeal - Miss Hanky Panky 2013.

There are always cats and dogs being dropped off in the country by people who realize that they are unable to care for them.  The local small animal clinic identifies them as "Fenger Barn Cat #x"  when I bring them in for FeLV/FIV testing.   A few months ago, a black kitten showed up and adopted us.  We named him Spooky II, since our farm is Spooky Hollow, and we always have to have a Spooky.  We kept him locked in the tack room at nights to protect him from the coyotes, who get pretty bold this time of year.  RIP Spooky II.

 

Thank you for allowing me to write a long eulogy for my friends and livelihood.  I love my farm and the business I am in, but am having a hard time seeing how I can continue in it.  I keep having to meet with adjusters and fire marshalls and walk through the burned out hull of death, and just felt like I had to express what those burnt carcasses meant to my husband and I.  I'm sure time will heal, but having a hard time right now seeing how.