⬆︎(This blog’s header photo is of a modern 6-wheel tractor tedding the hay field before baling.)⬆︎
In our Facebook group, “The Horse’s Advocate,” a member was concerned about her horse. The “diet” is feeding only pasture and hay, salt and water plus the addition of soybean meal (SBM) to replace the lost amino acids. Here is her post:
My horse just came down with a bad case of grass founder on all four feet for the first time….I have been doing this diet for a year now…got her off of grass and feeding grass hay ( Bermuda & orchard/fescue hay)….she loves the SBM but should i cut it out or maybe decrease?
The following will be a long and scientific answer, but in a nutshell, horses need hormesis. This is the cellular process of resting which helps to clean up cellular debris, remove damaged cells and help the mitochondria switch their fuel source (mitochondrial flexibility). PLEASE read this entirely, even though it will sound too far advanced for most of you. I will summarize along the way in the gold-shaded sections and, at the end, introduce you to a theory of why horses are getting laminitis even though they are off of grain.
The Key Point
The key point of this article is that any animal (humans, horses, dogs, gerbils) who eats glucose in any form (starch, soft drinks, candy, byproducts of grain and sugar beets) in excess of their needs on a DAILY basis will become inflamed at the cellular level, develop metabolic syndrome and become ill in one way or another. Obesity is evidence of inflammation, and chronic protein deficiency is secondary to this (sarcopenia in humans or poor top line/hay belly in horses – same thing).
Current research in humans and lab animals has discovered the development of an enzyme called aldose reductase in people and animals who eat abundant glucose every day of their lives. Many enzymes are developed in animals when certain continuous food intakes require the animal to take action. An example in humans AND IN HORSES is the development of alcohol dehydrogenase when alcohol intake is daily. We did this study on ponies in the 1980s at Cornell because research on liver disease from hepatitis had lots of money. We fed them 100% (200 proof) alcohol in their meals and measured for alcohol dehydrogenase, which was absent at the start of the test. This enzyme is not in children or adults who don’t drink alcohol. Alcohol is a toxin to the body (sorry, folks!), so the body develops this enzyme to turn the alcohol into water. This is observed as “tolerance.” When I drink one cup of my wife’s homemade, hand-whipped egg nog on New Year’s Eve, I become goofy, and with 2 cups, I’m asleep because I don’t drink alcohol any other time.
Aldose reductase is a responsive enzyme developed by the body when glucose intake is daily and non-stop year round. All foods act as signals, and the signal from continuous glucose intake is that winter is coming. Remember, all starch is a chain of glucose molecules (Grazing Not Browsing -Decomplexicating Equine Nutrition Part 1 of 12). Starch is found in growing plants but is gone in dormant plants, especially after rain or melting snow. When consuming food with starch, the signal to animals (in this case, horses) is that winter is coming, and the response is, “We need to store more fat!” The process of making energy within the cell changes, and so does the fuel. Aldose reductase converts glucose into fructose. These are sugars but cause a different pathway in the mitochondria’s metabolic pathway. This alternate route is inflammatory but is necessary as it is usually temporary. Winter is followed by spring, and food becomes abundant once again.
Summary – Glucose is the sugar of starch found in grains and the nonstructural part of plants. Fructose is the sugar of fruit, but it is now discovered that animals can make fructose when they need to add body fat for winter.
The chemical structure of the two sugar molecules.
Glucose And Fructose
First, let’s describe glucose and fructose. Both have 6 carbons, 12 hydrogen and 6 oxygen atoms but the way they are put together is different. Glucose has little sweetness, so the ripe fruit converts glucose into fructose to encourage animals to eat and spread the seed. With aldose reductase, the same is done within animals.
When glucose enters the metabolic pathway (the Kreb’s cycle) it causes ATP (adenosine triphosphate) to lose one of its 3 P (phosphorous) atoms to become ADP (adenosine diphosphate or 2 P). It then does it again to become AMP (adenosine monophosphate or 1 P). This process is conservatively limited by phosphofructokinase, so only about 10% of the total ATP is used. Beyond this point, mitochondrial exhaustion begins (glucose metabolism is turned off, glycolysis is started), and the mitochondrial metabolic pathway is limited. An enzyme called AMP kinase is triggered, which adds back the P atoms so that the AMP becomes ATP again and is ready for the next use. A side note here. The drug metformin enhances this AMP kinase and is used to increase intracellular ATP, thus countering mitochondrial exhaustion.
Summary – When glucose is the fuel, energy is created by the engine inside the cell (the mitochondria). A recycling program then takes over well before it is needed to restore the necessary chemicals to make more energy, so the cell is always ready.
But what happens when fructose is used as fuel? After the ATP converts into AMP with the loss of the 2 P’s and the creation of energy, the path goes in a different direction:
1) The enzyme used to digest fructose (fructokinase) causes up to 50% ATP depletion (greater mitochondrial exhaustion).
2) The loss of ATP causes hunger and thirst. It increases body fat (energy storage) and glycogen (glucose storage) because glucose is no longer metabolized by the mitochondria but rather through glycolysis which does not use oxygen. This is a survival mechanism in all animals facing starvation, resulting in increased body fat and the start of metabolic syndrome. The excess glucose from starch has to go somewhere as it is not being used and the best storage for it is body fat and liver fat (leading to non-alcoholic fatty liver disease in humans).
3) The satiety hormone leptin (not lectin) is blocked by increased glucose intake, further increasing hunger and food intake. The point here is that as the energy factories are shutting down, the continual sugar input needs to be stored because when the food stops (winter), the animal will need to get the energy from somewhere.
4) The last point here is that instead of ATP kinase putting the P atoms back onto the AMP molecule, the enzyme AMP deaminase turns AMP into uric acid (UA). This is significant in humans, and lab animals studied because UA is the cause of inflammation in the kidneys and the islet cells of the pancreas. So what does this do to their health? A lot!
Summary – When fructose is the fuel, energy is still created inside the cell, but supplies’ reserves are greatly reduced, AND the recycling program shuts down. In addition, another chemical is produced (uric acid) that is not normally found. This is OK in a short-term situation such as a season, but when it continues, it affects the health of humans and lab animals and, I presume, horses too (but nobody is researching this in horses).
The islet cells of the pancreas make insulin. When inflamed by uric acid, the islet cells make less insulin with subsequent insulin resistance and type 2 diabetes in humans (from the paper “The association between elevated serum uric acid levels and islet β-cell function indexes in newly diagnosed type 2 diabetes mellitus: a cross-sectional study” – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5846453/ – The conclusion is quoted here: “In our study, insulin resistance and insulin secretion increased with rising serum UA levels in both men and women.”)
UA also inflames the kidney, the regulator of blood pressure (hypertension). A direct correlation exists between high blood UA levels and hypertension in humans and lab animals. This means in humans, and all animals tested that, a continuous glucose intake throughout the year causes higher fructose in the diet. This causes high blood uric acid levels, leading to insulin resistance, high blood triglycerides, fatty liver, obesity, metabolic syndrome, and heart disease associated with hypertension. To drive home this point, when animals are given a medicine that blocks the enzyme that creates fructose from glucose OR when they are placed on a very low glucose and zero fructose diet, hypertension and all the signs of metabolic syndrome are reversed and normalized! Calorie restriction is what this is called in humans and is the leading theory behind increased longevity and, more importantly, an increased health span.
Summary – Reducing the availability of starch and restricting it to only what the horse needs to survive the workload and the seasonal elements will eliminate inflammation, which is at the heart of almost every problem we see in our horses.
Now The Hard Part For Horse Owners
Hay is last summer’s grass. In the 1950s, very few people owned tractors in industrialized nations. The grass was cut with mowers pulled by draft horses, picked up by pitchfork, pulled into barn hay mows with a claw on a rope using pulley systems and finally distributed in the loft by hand and fork (search on YouTube for “making hay with horses”). In the 1960s, the US started the Eisenhower Interstate system of roads (https://www.fhwa.dot.gov/interstate/history.cfm). By 1970 hay was being made into bales and distributed by trucks along high-speed roads to small distribution centers we called farm stores. The concept of horses eating hay then is only about 60 years old. Originally hay was used to feed livestock during the hard times of winter to help them survive. Now horse owners believe hay is a staple and must be fed ad lib every hour of every day. While I have been one of the biggest proponents of feeding horses continuously, as suggested by all horses lacking a gall bladder (very few animals are born without this), I believe I was wrong.
It has been demonstrated by the observations of Dr. Katherine Houpt, VMD (Cornell professor emeritus) that horses chew between 10,000 and 40,000 chews per day. The assumption that one chew equals 1 second means 10,000 to 40,000 seconds per day are used to intake food. There are 86,400 seconds in a day. Using math, a horse is only eating between ⅛ and ½ of the day. While this makes logic for me, I decided to dig deeper. There is science behind what happens when we do not eat. However, we first need to assume that every cell in the body (all animals) requires energy at every moment of life – like a car needs fuel converted into energy to run, or it just stops. We must also assume that all animals don’t take in the raw materials constantly, but they go through a process of taking in a meal. Then, when they are not eating, these raw materials go through the process of digestion into fuels, transport and distribution of these fuels, consumption of the fuels and storage of unused fuel.
Summary – The creation of energy by the cells happens during every moment of life. Taking in the materials (food) needed to make fuel for this process is intermittent both during 24 hours AND during a 365-day year. To buffer this inconsistent intake of food, the body stores fuel as body fat. The more food is consumed beyond daily needs, the more body fat develops. When this occurs every day and year-round, the bad side of things happens, such as disease.
For this part of the discussion, we will call the cell’s mitochondria “the factory.” Fuel goes in, and energy comes out along with the waste. The better the fuel, the less waste and the less work the cell must do to clean up. But with more waste, the clean-up crew starts to complain. With more complaining, management restricts the tools needed to clean up. Why? Because management is too busy worrying that winter is coming. They have too much glucose, so they start to change how energy is created as they look for ways to store the excess. They even begin to convert the amino acids into more glucose because the dangerous signs of a very long winter (an ice age) are coming. Survival is the highest priority, while clean-up, maintenance and repair are low priorities. The means justify the ends. We will die trying to save the ship.
Normally during winter, when glucose availability diminishes to near zero, the cell starts using the more efficient fat fuel (The High Fat Diet – Decomplexicating Equine Nutrition Part 7 of 12). The horse takes fat stored as body fat and converts it to ketone bodies which are 20 to 28 times more efficient in producing energy with a lot less waste. As a result, the clean-up crew goes to work with vigor. After all, if there is no end to cleaning up horse poop with no time left to ride, what is the incentive to keep working? But with less poop, the cleaning becomes fun, right? With less worry, management has time to bring you coffee and food for your morning break! Keep dreaming.
Maintenance and repair become a priority now that there is extra time and energy within the cell. This process is called hormesis. The cell uses many techniques to repair things, and one of those is called autophagy. “Auto” means self, and “phage” means eat. The cells literally eat all the waste material and remove it from the cells. Another process is called apoptosis which is the scheduled death of a cell – like the euthanasia of a very old horse unable to get up off the ground. Many more processes are used every moment to repair damaged proteins (heat shock proteins) and DNA and RNA (sirtuins). But let me stay with the simple explanation of hormesis and horses.
In winter, horses are supposed to lose body fat while maintaining muscle. When we see this fat loss, we must say, “My horse is repairing and maintaining and will remain healthy and sound because I am seeing hormesis at work.” If winter becomes harsh with very low temperatures and unbearable wind and snow, add hay. That is what it is for. Otherwise, being a good horseman requires us to acquire a fine eye for when to add food beyond what they find in the pasture. As good stewards of our horses, we need to recognize the importance of hormesis and know they need this metabolic rest period seasonally.
I can hear all of you say that you have no pasture. I see that. Adding hay is a requirement, but don’t feed it 24 hours a day. Limit it to what the horse needs to maintain their body weight. For all who are competing, use your eye. As the workload increases, then add more energy. About 100 years ago, the work required of horses to plow and harvest for all the people moving to the cities was life-threatening to the horses. They lost too much condition, so farmers started to add grain to compensate. Does your horse work that hard? Then adding grain in the form of whole grains probably won’t bother them as they are consuming the excess glucose and NOT triggering the production of fructose. But if your workload is less, the need to feed glucose 24 hours a day and seven days a week is unnecessary and also harms them at the cellular level.
Summary – Food availability for horses living in nature ebbs and flows. The body needs an abundance of food to prepare for the time when food is scarce. They build reserves with the excess food knowing that tough times are ahead, so they are willing to pay the cost of doing this (inflammation). The cells clean up and repair when food is scarce (winter). This needed repair period is missing in horses in the flow state of abundant food availability – and our horses are becoming ill from it.
Carbohydrate dependency (Carbohydrate Dependency – Decomplexicating Equine Nutrition Part 6 of 12) is the root cause of ills and unsoundness in horses today, with the secondary development of chronic protein deficiency (The Importance of Protein – Decomplexicating Equine Nutrition Part 8 of 12) that I talk so much about. It is very important to understand that if glucose is fed continuously, the amino acid deficiency will be more difficult to restore. In laminitis, feeding soybean meal will help to restore the connections between the hoof and coffin bone. But I think it is more important to eliminate any inflammation first and foremost. Based on current research on humans and what I have said above, I have a hypothesis. There is so little known about uric acid in horses, but we know that the hooves are a vascular bed of fine capillaries. If UA causes inflammation of kidneys with secondary effects on blood pressure, then would it make sense that UA also causes inflammation with the capillary bed of the hooves? The same thought of inflammation of the islet cells and the increase in insulin resistance (IR) may also be associated with this fine mesh of blood vessels. I am sure chronic protein deficiency leads to decreased cystine disulfide bonds in the hooves making their structure and attachments weak. Therefore it is very important to replace this lost amino acid by adding methionine (which converts to cystine and makes up 26% of the hoof). However, in every case of laminitis, there is usually insulin resistance. Therefore, I believe that IR is secondary to the increase of blood uric acid (this may be a new idea in the horse world). High blood UA is directly related to activating AMP deaminase, which converts AMP into more UA. The increase of AMP deaminase is directly related to the increase in fructose made from the conversion from glucose by the enzyme fructokinase developed in animals on a high glucose diet.
Summary – Feeding glucose (starch) every day of the year leads to insulin resistance, metabolic syndrome and hypertension in humans and other mammals tested. This is probably all due to the discovery that glucose is converted into fructose with high uric acid production in the blood. This inflames the kidneys and pancreas with subsequent illness. Testing in horses has not been done, but I propose the possibility that this same process leads to the inflammation of the laminae of the hooves.
Excess glucose > conversion into fructose > increased blood uric acid > IR, diabetes, hypertension, fatty liver, obesity and other signs of metabolic syndrome.
I hope this lengthy discussion will help you understand why your horse foundered on grass. There is so little known about these enzymes and UA in horses and their role in laminitis. I think this will help you look at it from a fresh perspective. For me, these are relatively new findings over the last ten years of research and NOT in my textbooks in the 1980s. We all know there is an epidemic of obesity, diabetes, metabolic syndrome, non-alcoholic fatty liver, dementia and heart disease in humans. We also see obesity and metabolic syndrome in our horses in levels I did not see 50 or even 30 years ago. And it is getting worse.
Read these and blogs from others. Avoid agenda-driven information where they are trying to sell you something. You will find that simplicity works in most cases – that pulling teeth is a last resort.
I hope your horse fully recovers, but you must decrease active inflammation and remove all causes of future inflammation. This will require you to rethink how you feed your horse and throw out all you were taught, as it is not working with this horse. Other horses may be OK with feeding hay daily or grain, but more horses are being pushed to the edge. I hope this long-winded discussion will let you know that, at least in humans, the answers to metabolic syndrome seem imminent. Pfizer is working on a drug to block aldose reductase, which will soon be released. I can see it being used in horses. Allopurinol will block the production of UA from AMP, and metformin will encourage the phosphorylation of AMP back into ATP. Some vets have tried these medicines, but not many qualified studies use them in horses. Be sure to ask your vet about them as you proceed. Thanks for being a part of this group and searching for answers. Doc T