Metabolic debate...food for thought?

The perfect hoof club forum is great for learning about true foot function and proper barefoot hoofcare.  Below is a post I left today which is in a thread about different opinions about the cause of metabolic disease.  I recently believed some of my horses were metabolic and maybe insulin resistant (IR).  Blood tests were send to an IR in the US (Dr Thomas-from 'for love of the horse') and I am discussing the company view on metabolic disease in response to a reply from KC LaPierre from a previous post....

ME: I, like you guys seem to have spent years on the merry go round of metabolic disease and it is also the reason I am 'here' and become a DAEP. After holding the rope of several precious horses whilst they face the gun is a truly heart breaking experience and I will not give up the fight for answers The more I research, the less questions are actually answered...in fact the endless research ploughs up more and more questions! I am keen to hear about experiences from DAEP's and horse carers and owners who have used FLOTH products.

I too looked up the chinese herbs in the various products, and over the years I have formulated my own herbal blends and have had some results at making the symtoms go away for a while. But Chinese medicine is very complex and requires a deep understanding of the pathologies of the disease process and when a Chinese herbalist makes a blend, it may include many herbs and in very carefully chosen amounts and from specific parts of the plant. Also they use 'carrier' herbs which alter the path and effect of other herbs and while I considered making my own blend, I decided to stop experimenting and just accept that herbology is NOT my area and to stick with podiatry and consultations!

Those who know me know that I rave about thunderbrook feeds and Dr debbie has her own Cushings and laminitis blends which several clients have used with success....but if I dont try, I guess I will never know! i accept too that other paths of healing are successful (homeopathy, etc) and that all horses are individual.

But I have a nagging suspicion that a lot of the EDE I am seeing is related to problems with insulin levels (and other metabolic problems and their side effects), especially given that the tissues in the soft tissues in the foot are so easily affected by vasoconstriction (one effect of raised insulin levels). There is a lot of focus on laminitis as a result of IR and metabolic issues but I think EDE comes first and can maybe be a more accurate precursor to IR related laminitis.

Thoughts anyone? KC RESPONCE:

Another perspective that you should consider is the reduction in glucose consumption in peripheral tissue, known to accompany acute metabolic stress. The purpose is to maintain proper glucose levels, and therefore energy supplies, to vital organs. Reductions in glucose consumption have been associated with connective tissue degradation (Elastosis). This may appear to be the complete opposite of the symptoms associated with the IR or Cushing’s horse, but observations may be deceptive. Metabolic syndrome/disease often associated with lack of exercise, improper diet, and stress may present high glucose blood levels, but in fact the horse's peripheral connective tissue may be starved of glucose. Food for thought, no pun intended..

My response:  I think Dr Thomas' metabolic progression curve theory acknowledges that a lack of elasticity in the body reduces potential for correct physiological function (and his model I think would have more credibility if he acknowledged EDE in the pathology of laminitis).  However he talks about laminitis occurring as an end result of a metabolic process in which IR is the cause.  The way in which he presents his theory/findings is strongly based on blood work and symptoms.  He says that IR is identified when “a normal quantity of insulin does not produce a normal response in the cells of glucose uptake”.  So IR would show in bloods as raised serum insulin and normal glucose levels.  But the appearance of normal serum glucose however is only accounting for extracellular glucose levels and does not account for intracellular glucose. 

We know that insulin’s role; aside from ‘pushing’ glucose into cells for cellular function, is to act as a vasoregulatory hormone.  So as the cells do not somehow receive enough glucose, more insulin is released by the pancreas, thus causing more vasodilation and so on.  Hence the ability for Dr Thomas to map the path of a progressively more IR horse towards more raised blood insulin levels until the pancreas can no longer support the continued demand for insulin and the horse becomes clinically diabetic (with raised blood glucose levels and low insulin levels).  He says that as the horse becomes more progressively IR, the risk for laminitis increases; which is also due in part to raised inflammatory factors (due to cellular wall breakdown and raised insulin levels) and their negative effect directly on the lamellae.  We know that the dilation of blood vessels could restrict the capacity for a cell to receive nourishment, including oxygen and glucose, which could very conceivably result in EDE; particularly as the peripherals would be affected first (i.e.; the foot).  So I guess I can see his connection clearly with increasing risk of laminitis as the horse becomes more IR

However, I have been thinking along the very same lines as you mention in your reply, KC.  I filled in a detailed questionnaire and sent to ‘for love of the horse’ staff to evaluate.  I was told my horse had IR which explained his low level laminitis (EDE).  Herbal Products and dosages were then discussed.  However, Dr Thomas replied in person a few days later to say that if the blood work was correct, then he didn’t have IR as his blood glucose and insulin levels were within normal ranges.  He also had normal cortisol levels and the only signs of ill-health were some abnormal liver enzyme results and WBC anomalies.  So that doesn’t fit his model for IR and risk of laminitis.  I have another 3 horses with metabolic concerns and their tests were similar.  One other horse is footy but no signs of EDE and another gets EDE and laminitis when stressed; usually if injured, (which seems to be a frequent occurrence with this horse!). 

So KC, are you saying that in acute metabolic stress, blood flow can get restricted, particularly to peripheral tissues, (as a result of vasoconstriction presumably as a result of high cortisol levels or improper cortisol balance) which reduces health of the cells as they cannot receive vital nutrients (including glucose) or get rid of waste products.  And that this leads to systemic EDE (and laminitis potentially)?

In our recent experience, the outward signs were fitting the IR horse model, but detailed blood work showed otherwise.  I could have spent huge resources on products aimed at rebalancing insulin levels and could have potentially caused more harm if I just completed a questionnaire and didn’t send blood work results.  It doesn’t explain what caused recent deterioration in health and I may never know.

Which leads me right back to where I was prior to recent research and experiences:  that EDE and metabolic issues, if not explained by the ‘normal route’ of IR development (too high carb diet coupled with genetic predisposition), it could be explained by chemical damage to the pituitary causing a faulty endocrine system and so called peripheral Cushings disease.  One theory by Dr Debbie from Thunderbrook feeds (who closely studies human endocrine research and related diseases) is that neuro toxins and other chemicals (from crop spraying, wormers, vaccinations and modern horse food production techniques-basically unhealthy environmental stimulus!) enters the horses blood stream and the blood/brain barrier.  This then damage the cell’s mitochondria in the pituitary and other brain glands responsible for maintaining said cortisone levels and other signalling hormones and therefore body metabolism or homeostasis.  This causes the cell to malfunction and hyperplasia results.  As the mitochondria have in essence their own DNA, therein lays the challenge in healing the damage in these horses.  The horse’s body either has to identify and expel the damaged cell or heal the faulty mitochondria and both are difficult due to the nature of the fault and position of the damaged cells.  The result is the horse has difficulty in maintaining a healthy endocrine system and as cellular health is dependent at a very basic level on proper hormonal signalling; every cell in the body can have challenges to its health.  Elastosis would be one such health challenge.  With such damage, the horse would be much more sensitive to trigger factors such as stress (and resulting raised levels of cortisol/cortisone) in a similar way in which the IR horse become increasingly sensitive to the trigger factors including eating carb rich food such as spring grass.

One system particularly challenged is the barrier defence system made up of the cell wall of the digestive system, respiratory system and the skin (including the lamellae).  As the lining of the gut is only one cell thick, it is easily damaged from an unhealthy metabolism (as already described) and from ingested toxins (which are surprisingly common in the vast majority of domestic horses-mostly from so-called ‘healthy’ horse feeds).  If this defence mechanism fails, the potential for further insult on the endocrine system and other body tissues is immense.  Another way to think of it is this; the cells which line the entire digestive system form a continuous ‘skin’ both in the lungs and the outer skin.  It stands to reason that these form one continuous barrier and the health of one part impacts on the health in another.  In other words, insult and damage to the gut wall has a direct impact on the health of the lamellae and soft tissues in the horse feet (as the ‘skin’ at the bottom of the legs!).  Damage to the gut wall can be permanent but given proper environmental stimulus, it stands a chance of healing (by removing the causes of damage and supporting the bodies own healing process).  Unfortunately there is no equine related concrete scientific evidence supporting this theory.  Dr Debbie believes that in 5 to 10 years time all horses will become metabolic as a result of damage resulting from improper environmental stimulus.  And maybe the drug companies know something of this?  A huge sum of money was recently spent developing and licensing a horse pergolide drug.  If there wasn’t going to be an increase in demand and in turn; profits, why bother?

So I ask myself; are my horses stressed; probably not, in fact they are pretty chilled.

Are they exercised enough; probably not but they do have 24/7 turnout which is better than most.

Do they have classic IR; no (not according to test results)

Do they have proper diet; as much as I can provide with safe, healing, chemical free supplementary feed, herbs and naturally occurring supplements such as rosehips and nettles, but they do not get organic hay until I can source it!

Are they healthy; not really.  I believe at least 4 out of my 7 horses have had unhealthy stimulus in the past via chemicals and toxins in their diet, vaccination and worming programme which had led to metabolic problems.  They get great foot care (AEP) and their owner (me!) does the very best they can for them.  At least two have signs of EDE and another gets laminitis when injured.

How do I FEEL about that as a DAEP; pretty embarrassed!  Despite best intentions, and fervent research I still cannot help my horses heal themselves properly and all I can do is manage the symptoms as best I can with the time and resources I have and keep on asking questions.

Any more food for thought (or will I become obese?)

 Mmmmmm???

Another perspective that you should consider is the reduction in glucose consumption in peripheral tissue, known to accompany acute metabolic stress. The purpose is to maintain proper glucose levels, and therefore energy supplies, to vital organs. Reductions in glucose consumption have been associated with connective tissue degradation (Elastosis). This may appear to be the complete opposite of the symptoms associated with the IR or Cushing’s horse, but observations may be deceptive. Metabolic syndrome/disease often associated with lack of exercise, improper diet, and stress may present high glucose blood levels, but in fact the horse's peripheral connective tissue may be starved of glucose. Food for thought, no pun intended..