Supplementation with
thyroxine (thyroid hormone) is commonplace among racehorse trainers, and
recently this practice has been accompanied by a swirl of confusion. Like so many other typical racetrack
practices, the supplementation with thyroxine has been demonized in some
corners, from being used to “cover up” cobalt abuse to being responsible for sudden
deaths on the track. Like so many other typical
racetrack practices, thyroxine supplementation is defended by its proponents as
making the horses “feel better and do better,” with no real explanation of how
it might work.
So, let’s start this
discussion by reviewing what thyroxine actually does. Thyroxine is normally produced in the thyroid
gland, a paired gland on either side of the neck, just behind the head. Thyroxine affects every cell in an animal’s
body, affecting everything from normal growth to normal muscle development in
response to exercise. You can consider
that thyroxine is the hormone that permits everything else in the body to
function properly. The basic metabolic
rate, including heart rate and temperature are determined by thyroxine. In fact, veterinarians recommend that horses
which suffer from metabolic syndrome, a disease not dissimilar to type 2
diabetes in humans, be supplemented with thyroxine to increase their metabolism
for the purpose of weight loss, which requires a dose 3 – 6 times the typical
amount supplemented to the average racehorse.
Remarkably, these horses don’t seem to have a higher than average risk
of sudden death and unquestionably have had no out of the ordinary exposure to
cobalt, despite this large dose of thyroxine.
Most have minimal, transient signs or no signs at all of thyrotoxicosis
(dangerously high levels of thyroxine in the blood).
What are the signs of
thyrotoxicosis in horses? There are no
published reports…actually there are only a few published reports about thyroid
hormone in horses at all. This leaves us
with a large hole in the scientific literature to assess whether our horses
need extra thyroxine at all.
Thyrotoxicosis in other species is associated with increased heart
rates, increased body temperatures, weight loss and diarrhea. In fact, most veterinarians will tell you
that nervousness and diarrhea accompany excessive thyroxine use, and can be
seen occasionally in the first few days after starting the very high dose used
in metabolic disease (Type 2 Diabetes-like) horses with high doses of thyroxine. In humans, extremely high levels of
thyroxine, such as those seen with thyroid gland tumors, are associated with
cardiac arrhythmias and death, which is clearly the far-reaching source of the
supposition made by racing officials when they posited a correlation between
extra thyroxine and racetrack deaths.
Based on the fact that many racehorses are supplemented with thyroxine,
and the spikes of sudden death were only observed in one jurisdiction,
suggestions that there is a relationship between thyroxine supplementation and
sudden death is irresponsible at best.
So, the next question
is, why do so many trainers supplement racehorses with thyroxine, and is it a
legitimate practice? In actuality, while
the scientific literature is sparse on the subject in horses, the only studies
that exist clearly demonstrate that racehorses tend to be low in thyroxine1,2. These old studies are likely the original
source of the idea. Luckily, there is a
lot of good scientific evidence in other species. Like the Thoroughbred racehorses in those two
early studies, humans undergoing intense exercise can experience a low
thyroxine3, which significantly impairs the individual’s ability to
perform4. Additionally, there
is a lot of good scientific evidence in people5 and some limited
data in horses6 that low thyroxine is associated with rhabdomyolysis
(tying up).
Are there other causes
besides intensive exercise that can cause low thyroxine in a race horse? The test for thyroxine in horses measures
both active (free) and inactive (protein bound) forms of thyroxine, and many
exogenously administered substances, including estrogens and antibiotics can
displace thyroxine from its protein binding sites, causing a falsely low
thyroxine reading, without actually affecting the thyroid function in the
horse. Other exogenously administered
substances can actually drop both the active and inactive forms of thyroxine in
the blood. For example, 5 days in a row
of bute causes a profound drop in both forms of thyroxine7, which
lasts 2 days for the active form and 10 days for the inactive form.
Cobalt chloride also
interferes with normal thyroid function.
While a critical and necessary mineral in trace amounts, cobalt has been
used in higher than normal quantities for a variety of reasons in horses. At levels exceeding daily requirements,
especially many orders of magnitude above required amounts, cobalt activates
and upregulates over 300 genes, of which a number might influence
performance. At modest amounts cobalt
has been administered to racehorses to counteract low red blood cell counts,
although there is no evidence that it works for this purpose, and has been used
as a preventative for rhabdomyolysis8. Very high persistent levels of cobalt in the
blood interfere with the iodine uptake by the thyroid gland resulting in
hypothyroidism, which is clearly the source of the rumored association between
the two. However, in addition to
dropping the thyroxine level, injudicious use of cobalt causes heart and liver
damage9. Simple thyroxine
supplementation does not counteract these adverse effects. Additionally, the implementation of
regulations limiting cobalt levels renders the exogenous administration of cobalt
obsolete.
The veterinary community
has not invested a lot of research on thyroxine in racehorses, but clearly the scientific data that do exist support limited use of
this therapeutic substance in racehorses.
At the dosages typically used in racehorses, toxicity is unlikely, but
the best method to determine if your horse needs supplementation is to have a
baseline thyroxine test, and only supplement if your horse actually has a low
thyroxine. The best method to determine
a reproducible level of thyroxine is to have the blood test drawn in the morning
before training, when the horse has not received other medications within 10 days.
Conclusions? The use of thyroxine supplementation is
clearly an appropriate therapeutic treatment for horses, but it is critical to
test for a low blood thyroid before starting on therapy, rather than indiscriminately
treating all horses. Has overuse of
thyroxine been responsible for sudden deaths among racehorses? Highly unlikely. Is it good to investigate all possible
variables when there is an unexpected number of deaths or other incidents
involving animals? Absolutely. Is it irresponsible to suggest a cause
without solid scientific evidence?
Yes. Both regulators and horsemen
are under pressure to have an answer whenever injuries or deaths occur, but
kneejerk responses without science to back it up doesn’t get us any closer to
solving the problems in our industry. At
the same time, it is critically important that we understand every therapy we
institute in our athletes and apply each of them appropriately.
