Pigment in Hooves

Cheryl Henderson, a US based barefoot trimmer, has a theory that pigmentation increases as the hoof becomes healthier.  She goes as far as saying that the unpigmented inner zone of the stratum medium is 'the enemy of the hoof' because it is more prone to pathogenic action - being less tubule dense and more moisture rich.

Logically, that means Henderson sees the pigment melanin as conferring additional strength to the hoof.

This seems to run counter to formal scientific studies that have concluded the presence of dark melanin pigment does not confer a greater tensile strength or rigidity to the hoof, ie that a 'white' hoof is no weaker than a dark one.

But, Henderson argues that a so-called 'white' hoof (actually creamy coloured) is just as heavily pigmented as a black hoof but just contains pigments of a different colour, ie there are more melanin pigments in the equine hoof than the two that mainstream science has identified.

Some people, in supporting her theory, argue that, just as sunlight stimulates melanogenisis in the skin, a change in the way the hoof meets the ground might stimulate melanin production and, as this increases, the hoof becomes stronger and healthier.

There is no scientific evidence that melanogenisis is triggered by physical stimulation such as ground reaction forces. There is a substance called magnolignan which prevents the formation of melanin - thereby lightening the skin. If that was deficient in unhealthy hooves, a reversal of that deficiency might increase the amount of pigment being produced but that would simply make the hooves darker on the outside - the layer where the pigment naturally occurs.

Coat and hoof pigmentation and skin colour in horses is determined by the presence, the absence or the relative proportions of two melanin pigments  - eumelanin, which is brown/black but thought to always be black in horses, and phaeomelanin, which is reddish and, in humans, found in high quantities in the lips, nipples, genitals and in red hair. 

Most equine skins are black and it seems likely that this is the evolutionary 'default' setting which some humans seek to alter in their ceaseless search for novelty.

If the skin on the pastern is black, the hoof will be black. A 'white' hoof or white part of a bi-coloured hoof always grows from lightly pigmented or unpigmented skin on the pastern.  A horse may grow a black hoof below a white leg but the underlying skin of that leg will be black. 

True albinism (complete lack of melanin) is rare in horses.  I do not know if the 'pink' skin patches found on some horses are completely lacking in pigment or if they contain high levels of phaeomelanin.

Melanin is created in the basal layer of the epidermis by melanocytes. The enzyme tyrosinase plays an important role in melanin production; it is synthesized inside the melanocytes, matures, and transfers into melanosomes, where it produces melanin by binding with the amino acid tyrosine.

The epidermis of the horse has an average thickness of 0.053mm.

Colour, like beauty, is only skin deep -  actually only a fraction of a mm deep.

But in some hooves, most obvious in dark hooves, the pigmented horn seems to flow into the unpigmented layers, ie it does not form a discrete, uniform outer layer. Henderson sees this as evidence that the unpigmented horn has in some way colonised the pigmented layer, or the pigmented layer has in some way degenerated, making the hoof less resistant to pathogens and lacking tensile strength and abrasion resistance.

She does not consider whether the issue is the reverse, ie whether the way a poorly formed hoof meets the ground results in deformations of the superficial pigmented layer.

As the hoof form improves, is what is seen at ground level a more accurate picture of the anatomically normal distribution of tubular and intertubular horn and pigmented and unpigmented horn  - which had been distorted in a forward running / flared / contracted hoof?

The hoof wall proper (the stratum medium) comprises tubules - which are modified hair - around which is intertubular horn that is formed at right angles to the tubules. The bulk of the melanin in the equine hoof is in the intertubular horn and like the pigment of the skin, it lies in a thin superficial layer.

The tubule cortex comprises dense keratinised cells that surround a hollow medulla that contains cellular debris.  The cortex is lightly pigmented or or unpigmented and therefore does not confer colour to the hoof.

The distribution of tubules relative to intertubular horn reduces towards the bone - an arrangement that  is thought to confer a degree of shock absorption. The zones where different types of horn meet and merge are important and actually little understood.   The interface between hoof horn and the highly vascular inner structures close to the bone is arguably the most sensitive to concussive damage - hence the need for an increasing moisture content to the stratum medium. But, the inner structures are also vulnerable to any pathogens that have been able to breach the protective outer layers of horn so, as in all things, there must be a balance.

Pollitt and others argue that it is the intertubular  horn which confers the greatest tensile strength and rigidity to the hoof as the tubules are 3x more likely to fracture than the intertubular  horn.

But, given the need for the outer layers to be more abrasion and pathogen resistant, and the inner layers to be more flexible to help prevent transmission of ground reaction forces to the sensitive structures,  this seems counter intuitive.

What, to my knowledge, has not been tested is the relative abrasion and pathogen resistance of tubular and intertubular horn.  Nor do scientists typically assess the degree and type of deformities present in the specimen hooves they use.

As usual, more questions than answers.

Spring aggression

Just read a post about a horse suddenly becoming aggressive and there possibly being a link to restricted grazing.

Several things may be happening diet wise - what immediately springs to mind are that magnesium uptake may be inhibited by spring grass and the horse may need some extra salt. If there is too much clover it may be short of iodine, so supplementing with iodised salt may be a good idea.

It may be uncomfortable and is anxious because of that or it may simply have too much energy from spring grass and is looking for ways to release it.

Fructans are sugars the horse cannot digest well and the grasses which store sugars in the form of fructans do so in the base of the leaf. Horses forced to graze short, stressed grass may be getting more fructan than is good for them. The havoc this causes in the hind gut may be setting the horse up for laminitis which can have a slow and insidious onset. The horse may be feeling sore long before we realise what the problem is.

The owner may know that the horse doesn't need extra food and in spring, but the animal's instincts are telling it to eat.  When we restrict grass in spring we have to compensate for that with high fibre substitutes to keep the horse's gut and mind happy - and healthy. We do not know enough about the interaction between the neuro-endocrine and peptidergic nervous systems to discount subtle imbalances within and between them as a reason for changes in behaviour.

The horse is instinctually primed to eat 16+ hours a day.  To get the energy it needs from the type of food it evolve to eat, it has to eat little and often. It is a trickle feeder - small stomach, long hind gut.

When it is eating it should be in a calm, relaxed frame of mind, head down, respiration slow and regular, heart rate low - and, producing saliva which contains enzymes that start off the digestion process and buffer the stomach and gut. The hormonal and peptide feed back systems maintain that frame of mind - all is well, keep eating.

If the horse is anxious (feels it is being deprived of food, feels threatened by others, is in discomfort etc) it is in an excited state. The pituitary gland is releasing factors that trigger the adenals to release adrenaline and cortisol in preparation for fight or flight. Heart rate and respiration go up - and critically, the mouth is dry because the horse has a relatively dry mouth when in flight mode.  Never underestimate the importance of saliva to a healthy digestion.

It's our fault that the horse gets access to soft leafed, NSC and legume rich pasture and doesn't get adequate movement so the evolutionarily driven need to eat almost constantly becomes a serious health issue. We need to ensure that the horse has grass substitutes - not fed to our convenience in a big pile of hay, but available in small amounts, almost all the time and in a way that encourages movement.

The basic advice always comes back to this - look to what nature's arrangements are and in what ways and to what extent your management of the horse differs from them. The horse cannot change its nature. It can and does accommodate itself to us to an extraordinary degree and it is a highly adaptable animal, BUT -  all animals have aspects of their physical and psychological being that are non-negotiable ie they are essential to the animal's wellbeing.  The adverse effects of these conditions not being met appropriately may be spectacular and sudden in onset, eg anaphylactic shock; or subtle and slow in onset, eg chronic laminitis, gut imbalances.

There is always a social component in the horse's behaviour because it is a highly social animal. It may be anxious about its place in the herd; it may be driven by its surplus energy to challenge other more dominant horses; it may be a social misfit that is always a nuisance in a large group but fine with one companion.

Horses reestablish herd bonds and hierarchy every day. We impose a huge stress on some horses when we keep them in a constantly shifting herd structure. Some cope very well - usually the calm confident types that every other horse wants to be with; and some go into extremely excited states - which, depending on a number of factors, may manifest as fearful nervous behaviour or overt aggression.

Finally - in trying to establish what the problem is for a given horse, be systematic. Eliminate one possible cause at a time so you can be reasonably certain what the trigger was.

Reading a Hoof

Learning how to 'read' a hoof is a useful skill. These are the severely compromised hooves of a 9 year old 15.2 hh thoroughbred.

 Left fore                    

Long toe;  long walls; stretched white line; long collapsed and contracted heels and bars; bars laying over and fused with sole; flared quarters, worse laterally; very little concavity; thin sole; frog load bearing along inner third; bulbs compressed; central frog sulcus a shallow cleft; no structure to digital cushion. 

                                               

Right Fore 

Medial heel contracted and medial side of P3 narrowed as result; lateral heel much longer, grossly flared and under run; bone loss along distal margins laterally and at medial toe; lateral bar long and fused completely with sole; medial bar wedged under frog; sole corium in medial heel/bar triangle deformed by inward turning heel, in lateral HBT subjected to persistent ground pressure transmitted by overlaid bar and heel horn; rearward third of frog and bulb folded inwards; medial lateral cartilage deformed inwards, lateral pulled under by collapsed under run heel; degenerated digital cushion.

Left hind

Long toe; long, collapsed heels and bars; vertically compressed bulbs and frog sulcus a cleft turned in on itself; weak DC; thin walls. This was the horse's least deformed hoof.

Right hind

Long toe; rotated pedal bone (broken forward HPA); severely contracted medial heel; thin walls, heels and bars; medial bar pushed up and wedged under frog; lateral heel forward and long; gross flare to quarter; bone loss; quarter crack; frog folded in on itself and collapsed forward. (I had already removed a section of medial wall and exposed the frog apex before these shots were taken and sadly there are no lateral or dorsal views of the hinds.)

To shoe or not to shoe ...

To shoe or not to shoe, that is the question.

Whether 'tis better to let the horse

Suffer the hammers and nails of traditional shoeing,

Or to take arms against a sea of convention

And by opposing, end it.

To shoe, to harm – no doubt.

And by that harm to say we reduce the full and natural life the horse is heir to.

‘Tis an consummation devoutly to be avoided.

To shoe - to harm.

To harm, perchance to kill.

Aye there’s the rub.  For in that shod state what ills will come when they have hammered on that metal coil must give us pause.

There’s the understanding that gives form to a trimmer's life.

For who would bear the whips and scorns of the press,

The client’s incomprehension,

The law’s delay,

The insolence of experts,

And the spurns of our patient work the vets may make

When she herself might be popular by doing a paddock trim?

Who would choose to grunt and sweat under a fretful horse

 But that the threat of what the shoe does,

That metalled state in which no horse is whole,

Makes us rather bear those aches and pains than leave the horse to others' care. 

Convention does make cowards of us all and the trimmers' hue of resolution may be diluted by the pale cast of doubt

And this enterprise of great pitch and moment, with this regard, its currents turn awry and loses the name of progress.

The Caudal Hoof

The hoof should land fractionally heel first. As the limb is being retracted, the hoof glides into touch down and begins to accept load. Peak load is reached as the horse’s weight passes over the vertical axis of the limb. The faster the pace, the more fractional any given phase of the load bearing part of the stride is. 

The optimal alignment of the bones of the limb in movement and at rest are critical to the efficiency of the locomotor system – and to hoof health.

The ability of the heels to laterally expand slightly under load and the engagement of the soft horn/tissue complex at the back of the hoof are vital elements of shock absorption and of the optimal circulation of blood.

The attachment of the wall/ bars and sole to the tough but flexible lateral cartilages, combined with the frog/digital cushion/bulbs complex, allows the heel region of the hoof to deform laterally under load and also to displace vertically on uneven ground. The degree to which it can and should do this varies, but either too much or too little expansion under load will have consequences for the health of the hoof and potentially the whole horse.

The Bulbs

The bulbs should be broad and deep.  The hairline, when viewed from the heel, should be more or less level. 

In an inwardly contracted hoof, the bulbs are deformed inwards.




In a shallow hoof that lacks vertical depth at the heel, they may become vertically compressed.

The Frog

The frog is continuous with the digital cushion above it and with the bulbs of the heel.

The frog corium is more like normal dermis than the other coria of the hoof. It produces what should be a tough, leathery pad that can, under certain conditions, degenerate into a soft sometimes, pulpy structure which is easily contused and also easily colonised by pathogens in the ground or in the bedding, if the horse is stabled. (see Canker article)

The frog has two folds in its rearward third and the region between those folds should be a shallow depression. A diseased, weakened frog may lose so much substance in the central sulcus, that the shallow depression becomes a cleft and as such, is a breeding ground for pathogens.

Sometimes, the entire central sulcus degenerates and the frog folds in on itself meaning there is virtually no substance between the top of the cleft and the skin of the pastern.

The photo on the left is of such a hoof; on the right the same hoof a few months later and you can see the extent of the cleft as the hoof has started to open out which allows the central sulcus to regenerate. This heel is still extremely weak and vulnerable to concussive and penetrative injury and infection.

Below - a healthy frog on a soft terrain hoof.

The Digital Cushion

The digital cushion sits above the frog and comprises horizontally arranged bands of fibrocartilage with loose connective tissue in between them. The fibrocartilage attaches to the lateral cartilages and is important in dampening the downward movement of the pastern bones under load and inhibiting the expansion of the heel. 

The DC cannot be seen but the health of it and the frog can be ascertained by placing your thumb on the frog pad in the middle of the central sulcus and your forefinger on the skin of the pastern above the frog, and squeezing. In a healthy hoof this should feel dense and thick and resist the pinch. In a degenerated heel, it feels thin, weak and flabby.  In a severely compressed, underrun and splayed hoof, the thumb and forefinger may almost meet. It is easy to see how inadequate such a structure is to either help dampen the downward load or help inhibit expansion of the heels.

The DC is poorly vascularised and the constant stimulation - from the lateral expansion and return of the heel plus the upward pressure from the ground via the frog pad - is vital for the flow of nutrients that is necessary to maintain cartilage health.  If a horse does not get adequate movement on firm ground in formative years, the digital cushion may never develop properly and will be primarily loose connective tissue.

The Lateral Cartilages

The lateral cartilages with merge with the pedal bone and extend rearward to form the palmar/plantar region. The rear part of the hoof capsule (wall/bars and sole) grows from the laminar and solar corium on the cartilages. They should be dense and strong and curve slightly inwards towards the heel. Without adequate movement and some expansion of the heels, they may be thinner and weaker than is necessary for optimal hoof health.

In a narrow inwardly contracted heel, the LCs are bent inward with the heels; if the hoof is under run, they are pulled under with the heels; if the hoof cannot break over normally the ligamentous attachments of the LCs may be damaged and as a result of long term irritation/damage, they may ossify (side bone).

If the complex of lateral cartilages, fibrocartilaginous DC and dense frog pad is strong and healthy, it not only facilitates the lateral expansion of the heels, it also acts with the bars to control it.

Too little lateral movement reduces shock absorption -> reduces the flow of blood and nutrients ->  reduces tissue and horn health. 

Too much lateral movement or vertical displacement stresses all the structures of the hoof and the coffin and fetlock joints.

A Polemic (aka Rant) on Cup Week

Now that the Melbourne Cup is over, we are waiting with bated breath for the spectacle of Cup Week in Canterbury. 

Can it really be a year ago that one of the silliest women to (dis)grace a race track showed the world her bum and boobs? That really was a comment on our times. 

In 1913 a highly educated suffragette threw herself in front of the king's horse to draw attention to the cause of female suffrage. 

Almost 100 years later, a drunk, half naked woman threw herself in front of a horse to draw attention - to herself!!  All in the hope that someone would take her photo and her bum and boobs would have their 15 minutes of global fame (pun intended).

Every year we have the usual sad collection of boozy bimbos falling over and showing us their bums and skimpy knickers.  (Thought, in the interests of equal opportunities, shouldn't it be bimbo for the male version and bimba for the female?) All too often the bums are of a size and shape that would be best kept hidden inside a large and preferably opaque pair of pants. And as for the boobs, quite often a very good sports bra or two wouldn't go amiss. 

And what about that woman who made a total tit of herself at the Melbourne Cup? She was wearing the skimpiest and tightest of little blue dresses - it was so short, that when she bent over, the numbnuts who was filming her said 'oops I can see her lunch'. The eejit kept falling off her silly heels, then tried to punch anyone who laughed at her. 

Having sobered up and found she had acquired the sort of celebrity that only the truly demented actually want, she now claims to have been drugged.  Hmm, yes, that would be right - alcohol is a drug.

Do any of the boozers, bimbos, bimbas or bettors spare a thought for the horses? That's assuming they have sufficient brain cells to spare a thought for anything other than themselves.

I can already hear the huffing and puffing from the pro-racing lobby. So before anyone starts sending me death threats, I don't think it is wrong to race horses per se - I just hate the hype that is used to cover up some pretty shabby realities. What I am talking about is what happens to the bulk of the horses once they have outlived their usefulness and the rather ugly reality of what the extreme demands of racing do to them before they are surplus to requirements.

But we don't talk about that do we? Nor do we talk about the fact that the raison d'etre for the Sport of Kings is gambling. 

It is not a sport, it is a medium for the placing of bets. 

Yes I know, you can bet on any sort of sport but, in other sports the betting is incidental, it is not the reason most people watch a game of rugby or basketball. In horse racing, the bet is the thing. 

How many people go to the races to watch the horses running purely for the spectacle? Precious few. Most of the plonkers who attend Cup Days go to see, be seen and get drunk.  And let's face it, a horse race is pretty bloody boring unless you've got a bet on and even then it's over so fast it does make you wonder about the average race goer's attention span - and other things.

Of course there's a bit of thrill when a horse falls over, a jockey falls off or some woman with not very much between her ears decides to get her kit off and / or  fall on the ground with her legs in the air.

Those with a vested interest will tell you the horses run for the pleasure of running and that they live better lives than many humans - which, when you think about it, is is a pretty shameful thing to boast about.

Those like me will tell you the horse runs because it has a rider or driver that is making it run and because all the others horses are running ie, that the motive power is fear. Any intelligent and honest horse trainer knows and will admit that the instinctual drive to run away from a threat and to stay with the herd is what is being harnessed. And we force the horse to run further and faster than it ever would in nature. No natural predator chases its prey at 60+kms an hour over a kilometer or longer because the balance between predator and prey rests on the fulcrum of energy conservation.

Boring isn't it, all this talk about the animal's needs?  How dare I intrude on people's fun with my 'boring, animal rights bollocks'. Yes, that's a quote from someone who loves horse racing - and claims to love horses.   

How does the Editor of the Press justify having a whole page devoted to a female reporter being given a 'make over' for Cup Day. And page upon page devoted to race day fashion for men and women. 

Does no-one else find it all utterly tacky and trashy?  Am I alone in seeing it as just another excuse to dress up (why is female race kit identical to modern day wedding guest kit?) or wear as little as is legally permitted, stare and get stared at, have your photo taken, get bladdered, throw your rubbish on the ground, eat lots and puke?  

Equine Canker

An article in The Horse October 29^th on equine canker refers to the fact that the disease has typically ‘frustrated veterinarians’ and refers to a new treatment with a chemotherapy drug.

I’ve collected dozens of photographs of examples of equine ‘canker’ and I have yet to find a case of canker in an otherwise 'normal' hoof.  It is a disease almost unknown in New Zealand where I live, despite some pretty horrendous hoof forms.  

So does the disease cause or result in the pathological hoof form, or vice versa? Are all cankers caused by the same thing? Is infection secondary to an inflammatory condition?

The drawing from Diseases of the Horse by H Caulton Reeks (below left) shows a type of warty growth reminiscent of epidermodysplasia verruciformis which is at its most extreme in the case of Dede Koswara, a Javanese fisherman whose hands are pictured below right. 

This is uncommon these days and there may be a genetic component to the condition in horses as there is in humans, which allows a virus that is normally managed easily by the immune system, to wreak havoc. However, we still have to ask, why would it affect the soft horn and soft tissue of the heel region of hoof?

There are many types of lesion that are described as canker. Most start in the frog but it can involve the solar and laminar coria in the heel region. There are types of lesion that obviously are just extreme degeneration of the frog but others in which the tissue has become hyperactive.  Just as proud flesh on a leg wound is the body's attempt to heal a lesion in an area that lacks underlying muscle and in which the dermis is under a lot of tension, it seems logical that the proliferative form of equine canker is a similar process.

It is necessary to look beyond the symptoms – to the causes  - which very often lie in a pre-existing pathological hoof form, combined with other factors such as stress and possibly diet. 

There are two broad types of hoof that are prone to canker and other degenerative diseases. The narrow, high heeled, inwardly contracted form as typified by the photo on the left below, and the splayed, vertically compressed form, as typified by the photo on the right below.

In both, the highly vascular tissue of the laminar and solar coria, and the less vascularised frog corium are subjected to abnormal persistent pressure and concussion and reduced flow of oxygen and nutrients. As a result, the tissue struggles to survive and in its weakened state, horn production cannot keep pace with the processes of exfoliation and pathogenic action. Contusions and infection exacerbate the situation. The discomfort from this makes the horse even less likely to load its hooves properly with a range of other consequences for overall health and well being.

So what is going on in these hooves that results in such degeneration? Although I have typified two broad types, there are many variations.

The narrow contracted hoof

• The long vertical heels and long high arched bars greatly inhibit or even prevent any normal lateral expansion of the heels. 
• The frog corium is permanently compressed inwards by the heels and bars. 
• The central frog sulcus becomes turned in on itself creating a cleft in which pathogens proliferate.
• The depth of the collateral groove creates a breeding ground for pathogens which eat away at the sides of the frog pad. 
• The arteries that supply the frog corium run along the top of the bars and the pressure from the ground onto the rigid arched bars may impact upon them. 
• The steepened HPA may mimic the arrangement of the foot bones that occurs naturally as the fetlock descends under load in which there is a reduction of blood flow in the hoof and at full pastern extension, flow is cut off entirely. 
• The lateral cartilages are deformed inwards.
• The solar and laminar coria in the heel region are placed under an abnormal persistent pressure. 
• The fibrocartilage in the DC cannot receive stimulation and degenerates. 

The splayed, compressed hoof

• The wall and bars receive load in too shallow a direction resulting in the hoof splaying/flaring. 
• The hoof lacks vertical depth and structure exposing all the volar surfaces to abnormal compressive and concussive force.
• The long but forward running and collapsed heels and bars, sit across and press onto the sole corium.  
• The unpigmented bar horn may fuse with sole horn sometimes overlaying almost the entire sole.
• The bars may also wedge sideways into the base of the frog. 
• Because the frog pad is exposed to abnormal persistent pressure, the digital cushion may displace.  
• Depending on how the heels deform, this sort of hoof may not be able to expand laterally, or it may expand too much resulting in strain on the back of the coffin joint. 
• The lateral cartilages are pulled under and deformed by the underrunning heels.
• The fibrocartilage in the DC cannot receive stimulation and degenerates. 

In both, the balance between the flexor and extensor muscles systems may be disrupted with consequences for correct limb flight and for the stay apparatus.

In either extreme, the horse is unable to either land or stand with comfort. It is a creature of movement; it evolved to be on its hooves for almost its entire existence. It is not anatomically, physiologically or psychologically equipped to be recumbent for any length of time. It needs healthy pain free feet to achieve a balanced frame and it needs a balanced frame to have healthy feet.

There may well be other contributory factors, and it seems logical that stress plays a significant role in the genesis of these conditions.  Diet may also be a contributory factor especially in the horse with weak, splayed feet.

Persistent and abnormal stress impacts on the immune system and a compromised immune system is less able to deal with opportunistic infection. A horse that is in constant pain, or is suffering from a dietary overload or deficiency, is feeling persistently anxious about some aspect of its management etc, may have chronic imbalances in the complex and delicately balanced chemical messengers of the neuro-endocrine and peptidergic nervous systems which are constantly feeding out and feeding back in response to stimuli.  We do not know enough about the way these act and interact and the different ways in which different animals may respond, to discount this as a factor.

There can be no better advice for any owner or vet or other professional involved with horses, than to look to the conditions in which the horse evolved and see how far and in what ways the management of an unwell horse differs from that.   (see post on the essential nature of the horse)

And as for the treatment of canker - as with everything, prevention is far better than cure.  Once there is a high level of damage, veterinary treatment may be necessary to restore something approaching the status quo but the advice I would give both owners and vets is:

• Find someone who knows how to trim to restore hoof form or, or learn yourself. In particular, understand the role of overgrown heels and bars in the genesis and perpetuation of the condition.
• Treat the damaged tissue with the mildest thing first, ie follow the old medical maxim - maximum dilution is the best solution.
• Maintain hygiene and pad / boot to get the horse out into the fresh air with a kind companion to lower stress levels and facilitate self-motivated movement.
• Do not nail or glue on shoes.
• Cut out high carb feed but do not starve; the horse needs to eat almost constantly - our job is to make sure that it eats the right stuff. 
• Feed good quality (spray free if possible) WHOLE food with some salt - iodised if you are in an iodine deficient area and with added selenium if in selenium deficient area.
• Remove possible sources of toxins - including top dressing feeds with supplements. 
• Leave a non-iodised well balanced mineral mix for the horse to help itself to.
• Cut branches of unsprayed, healthy, palatable trees and a range of broadleaf plants for the horse to eat if it wants to.