Tag: laminitis

Trimming laminitic horse is success

Posted on: November 3, 2013

Robin sore at the walk on July 21, 2013

Horses with low-grade laminitis can be made comfortable and taken off bute while still having an active case of the disease. I didn’t believe that before this year. I thought the laminitis cascade had to be stopped before the horse would find any degree of comfort. I also thought the owner needed to find the trigger that caused the laminitis and remove it, or it was hopeless to waste time on the feet. I was wrong. The fact is that I may never find the trigger of my horses’ laminitis.

Success with my gelding Robin Hood has taught me that trimming the horse according to farrier Pete Ramey’s principles can help the coffin bone return to a better position and keep the toes from getting stretched out, even as low grade laminitis continues. Stretched toes put painful pressure on the front of the foot and lead to abscess after abscess, tearing the foot apart further.

Robin Hood's left front foot on May 18, 2013

Robin Hood’s left front foot on May 18, 2013.

I’m still learning how to trim, but my beginner attempt has transformed the life of my gelding, Robin Hood. He has gone from almost needing a vet to put him down at low points in April, June and July 2013 to galloping across a field with his brother (with no help from anti-inflammatories) in November 2013.

Robin's left front foot on Nov. 3, 2013

Robin’s left front foot on Nov. 3, 2013.

Robin Hood always seems to have chronic low grade laminitis, as evidenced by the continuously growing rings around his hoof and the steady, strong digital pulse that never goes away.

And, yet, I took him off bute in October 2013, and he didn’t get sore; he just continued to improve. My previous attempt to wean him off bute in July 2013 ended badly. He was in so much pain, he was shaking when he tried to get up. Success this time around has been from the trim.

Robin actually was doing fairly well in January and February 2013, but his toes got longer in the spring, and I failed to see it. One day in April, he couldn’t get up, and he was lying down, grunting and moving his feet in a circular motion as if he couldn’t stand the pain. It was heartbreaking.

I spent years trying to understand equine feet but never caught on enough to try to trim one.

As I noted in my previous post on this topic, a kind farrier named June started helping me by email in May 2013. Read the previous post to review the easy principles she provided for understanding the equine foot.

In this post, I want to show you the result.

When I look back at images of my trimming over the year, I see how slow I was to follow June’s directions. I was really scared. But once I did, Robin came around very quickly.

I also have to fess up to the fact that my farrier tool of choice is a belt sander. Think electric nail file. It’s a piece of sand paper that is looped around a machine that spins it.

It has its drawbacks. Sometimes, I sand things unintentionally. If I accidentally hit my pants with the sand paper, that section of my pants disappears, and I’m looking at my leg.

That speed and power are also the sander’s strength. With a laminitic horse that can’t hold up a foot for long, speed and power are a big plus.

The sum total of my life-changing trim on Robin has been sanding around the outside of the foot to remove the damaged hoof and then sanding the bottom of his foot at the toe, or beveling it, so his toe doesn’t touch the ground in front of the point of breakover.

 

Robin walking Oct. 20, 2013

Robin walking barefoot Oct. 28, 2013

Robin trots briefly on lungeline on Nov. 3, 2013

Robin galloping in lower field with Kurt on Nov. 3, 2013

 

My other post talks about marking up the foot with a marker to have guidelines. When I first started trimming Robin in May 2013, he was mostly lying down, and you’ll see in the video below that the lines I drew weren’t straight because I was kneeling and leaning over his feet. Still, I had some target for how long I wanted the hoof to end up when finished.

Robin's left front toe after a trim on July 23, 2013

Robin’s left front toe after a trim on July 23, 2013.

At the front of the hoof, I wanted to get rid of the stretched white line area. I put the sander on the outside of the front of the hoof at the toe and pressed as I moved the sander around the toe. Rasping would have accomplished the same thing. At times, the hoof “wall” that was left looked really scary, but I just had to believe that all that bad wall would go away eventually.

On the sides of the hoof, I wanted to get rid of the flare. What is flare? If a laminitic horse has a groove, or gutter, around the bottom of the hoof where the white line used to be, the wall outside that gutter is flare. That detached wall is hitting the ground and likely feeling about as comfortable as a loose fingernail. It needs to go.

Robin’s whole hoof got noticeably smaller. Because I was so timid and Robin so sore, I did a teeny bit every night. Now, I work on him once a week to maintain what I’ve accomplished. He can stand on each foot for a long time.

As for the bottom of the foot, I left it alone.

As I described in my other post, the principle behind this is to allow the sole to become much thicker and put the horse’s weight on that sole, not on what’s left of the compromised wall. The loading of the sole pushes the dropped coffin bone back up in the skeleton. Sounds crazy, but it works.

Of course, when you make a horse walk on its sole, the horse pretty much has to be booted and given padding inside the boot or fitted with some sort of styrofoam taped to the feet.

The change in Robin’s feet has been remarkable. If I didn’t take the photos in the video below, I wouldn’t believe this was the same horse.

If I use the grooves next to the frog as a measurement for where the coffin bone is, as farrier Ramey suggests, it’s easy to see that the coffin bone has moved higher in the foot relative to the ground and the sole is actually starting to slough off some of the extra thickness as it works to become concave again.

Watch the video below of his foot transforming. The video is less than 90 seconds and rolls through photos of Robin’s left front foot from May 18, 2013, to October 12, 2013. I’m amazed.

 

Robin’s left front foot evolves from May 18, 2013, to October 12, 2013

How to trim a laminitic horse

Posted on: August 3, 2013

Proper hoof trimming has been my weakest area over the years.

A kind and generous farrier named June contacted me in May 2013 and not only helped me see the flaws in Robin’s trim but also helped me locate some resources for getting up to speed quickly on hoof anatomy.

I have been riding since I was 6 and owned a horse continuously since I was 9, and it’s embarrassing to realize how little I’ve known about horse feet. But not for a lack of trying.

My main resources now, in addition to June, are the websites of farriers Gene Ovnicek and Pete Ramey. These names are not new to anyone. These two farriers are highly regarded resources for providing instruction to others.

Using their concepts, I’ve tried to assemble what I hope is a quick guide to understanding the healthy hoof, as well as the laminitic one, and I will update this with additional information as I learn it. For more information, click the links within the text to go to the original material.

Ovnicek’s Hoof Mapping Protocol

Ovnicek’s ELPO (Equine Lameness Prevention Organization) Hoof Mapping Protocol provides guidelines for assessing the foot. I am shortening his guidelines to give you some very simple principles, but you can find the full protocol by downloading the PDF.

elpoprotocol

This is a screen grab of Ovnicek’s mapping protocol. Click it to go to the full protocol.

I found it helpful to mark the bottom of Robin’s feet with a marker to learn all of these principles.

A properly trimmed hoof should have the same amount of hoof ahead of the widest part of the hoof as it has behind the widest part (or even 60 percent behind the widest part). Sadly, most horses have 60 percent in front of the widest part. When I started this, Robin had at least 60 percent of his foot in front of the widest part. This would put too much pressure on his toe.

To evaluate your horse’s foot:

Step 1: Find the widest part of the hoof.

For me, the following instruction has been the easiest way to do this:

Measure the length of the central sulcus, the dimpled area inside the frog, with a tape measure. Double that measurement along the frog to get the true apex, or tip, of the frog. So, for example, if the central sulcus is 1 1/2 inches, measure from the front tip of the central sulcus 1 1/2 inches forward on the frog to arrive at the true apex. Mark the true apex.

From the true apex, measure 1 inch toward the heel to get the widest part of the hoof. Draw a line across the hoof at this point.

Step 2: Find the tip of the coffin bone:

The tip of the coffin bone is approximately 1 3/4 inches in front of the widest part of the hoof. Measure from the line you drew for the widest part of the foot 1 3/4 inches toward the toe and draw a new line across the foot.

Step 3: Find the approximate point of breakover:

This is 1/4 inch in front of the tip of the coffin bone. Draw another line for the point of breakover.

If you’re looking for shortcuts when you’re working on your horse, you can find the point of breakover by measuring 1 inch in front of the true apex of the frog.

Step 4: Draw a line where the toe should end:

I was mistaken earlier in saying this is one gloved finger width in front of the point of breakover. The toe should fall just beyond the point of breakover. There doesn’t seem to be a fixed measurement here, but one gloved finger width might be a good maximum. Since we want the white line area to be tight, it’s counterproductive to let the toe get long and stretched.

Step 5: Analyze your horse’s hoof:

If you have a lot of hoof in front of the line where the toe should end, you likely have some work to do.

Ramey’s theories on the dissent of the coffin bone

Ramey has assembled a page on understanding how and why the coffin bone drops in the foot.

He says the coffin bone often drops in horses, particularly sport horses, due to shoeing practices that force the hoof walls to bear all of the force of impact, creating more constant stress than the laminae were ever intended to withstand. Ideally, the hoof walls, soles, bars and frogs are supposed to work together to support the horse. Thus, the descent of the coffin bone is not just a problem for laminitic horses.

Ramey says the coffin bone can return to the proper position by moving higher in the hoof relative to the coronary band if the sole is allowed to grow properly.

Here are some of his concepts:

The sole grows from the bottom of the coffin bone. That’s it. The term sole is used inappropriately in reference to other parts of the hoof. Any hard material in front of the tip of the coffin bone is “intertubular hoof horn produced from cells migrating down from the coronet with the epidermal laminae.” It’s not sole. That intertubular horn should not be there. The coffin bone should be attached to the hoof wall.

Ramey says all horse hooves are very consistent in their distance from the bottom of the collateral grooves (along the frog) to the bottom of the coffin bone, so we can use the grooves to judge where the coffin bone is inside the hoof without radiographs.

He says to put a rasp or ruler across the bottom of the hoof. Using another measurement tool, measure from the rasp or ruler to the bottom of the collateral groove at the tip of the frog and again from the rasp or ruler to the bottom of the groove near the heel.

In healthy hooves, this measurement should be around 3/4 inch at the tip of the frog and 1 inch toward the heel.

If this measurement is only 1/16th of an inch at the tip of the frog, the coffin bone is very close to the ground.

I personally find this measurement technique almost impossible to pull off, but I do study my horses’ grooves, particularly in photos over time, and I grow more confident as the grooves get deeper.

For more about sole thickness, visit Ramey’s page on understanding the horse’s sole.

So, what to do about a dropped coffin bone? Don’t touch the sole when trimming. Especially, don’t remove any lumps in the sole. Ramey says the hoof will build calluses around the coffin bone as the horse tries to grow healthy sole, and farriers who trim this lumpy area in trying to create concavity are actually thinning the sole and causing the coffin bone to drop even more. The sole needs to be loaded and unloaded with weight to grow, so it needs to come in contact with the ground. When the sole becomes thick enough, it will drive the coffin bone higher relative to the coronary band. As this happens, the sole will become concave on its own, and this concavity will be appear all the way to the edge of the wall. The sole creates its own concavity. You cannot do this for it.

If there is flare in the wall, or a gap between the sole and hoof wall, this flared wall should be rasped off and the bottom of the hoof beveled, or sloped, from inside to out at 30 degrees, so only the inside of that bevel is touching the ground. If the hoof doesn’t have irreversible damage, this trim should allow the hoof wall to grow in with a tighter attachment. In the meantime, the horse needs to carry its weight on the sole rather than the wall and should be provided with boots with neoprene foam (according to Ramey) or insulation-type foam taped to the hoof (according to Ovnicek) to make it comfortable.

Ramey says he follows one big rule on how much to trim the hoof in the laminitic horse: He trims the walls and bars to 1/16th inch above healthy sole (assuming there’s healthy wall to trim), and lets the sole grow out.

Where I run into challenges is finding an appropriate heel height in Ramey’s principles.

I do understand that, in the perfect foot, the heels are low enough to allow the frog to touch the ground and expand and contract. Getting there is more challenging, since the laminitic horse often grows a ton of heel. How much can you take off and when, particularly if the coffin bone is dropped? I noticed over the summer of 2013 that every time I took Robin’s heels down a little bit, he was sore again, and this wasn’t due to the pull of the deep digital flexor tendon. What I believe is needed is the heel needs to be longer while you’re leaving the sole alone to push the coffin bone back into position. The hoof needs to be relatively level front to back. If you take the heel down, you’re lowering the heel too much and inflicting pain. You must wait until the sole becomes concave and then you can lower the heel to once again maintain a level foot.

With my new and still evolving understanding of the hoof under way, I now think passing a hoof quiz should be mandatory for anyone who wants to buy a horse.

Also, I should add, as I put all this knowledge into practice in the summer of 2013, I thought it was interesting, but Robin was too far gone to save. Nonetheless, I trimmed up his feet over several months and got them looking more normal. By November 2013, he was off bute and trotting and cantering. I am a convert. And, if I can do this, anyone can.

 

Slow-feed hay nets help laminitic horses

Posted on: April 15, 2013

These are two slow-feed hay nets send to me by a reader named Angie. They are put together quite professionally.

These are two slow-feed hay nets sent to me by a reader named Angie. They are put together quite professionally.

I avoided the slow-feed hay net trend for a long time because my gelding, Kurt, has a history of putting his front feet where they don’t belong. I was convinced I’d come home from work to find him hanging from the wall.

One of my readers, Angie, convinced me that Kurt couldn’t get his foot through the slow-feed nets, and she sent me two that she made from hockey netting. She also showed me a video of her horse eating from a similar net. In the video, the horse shakes the net to drop some hay on the ground and then cleans it up before repeating the process. And his weight looks absolutely perfect.

After seeing that, I was on board. Angie mentioned that I might need to put some hay on the ground even while putting some in the nets until the horses got used to eating that way, so I did.

Kurt caught on to the slow-feed nets right away. Robin thought they were too much work. Eventually, Kurt soured on them, too, and the hay in the nets didn’t get eaten.

I asked Angie if I could cut some diamonds out of the nets to create bigger holes. That worked. The horses started eating the hay again. But it allowed the horses to pull out a lot more hay than they could from the original mesh. We needed a happy medium.

I thought I’d try larger mesh.

Thus, began my education on sports netting. There’s a lot of sports netting out there.

hay net penny comparison

Angie’s netting appears to be 1 1/4-inch mesh. A penny almost fills the opening.

The best way to judge netting size is with a penny. This is what all the websites use.

Angie’s hockey netting appeared to be about a 1 1/4-inch mesh in a diamond shape. There is also squared-shaped netting.

We thought 3-inch mesh might be better, but no one makes an affordable 3-inch mesh.

We found a 2-inch mesh on the Gourock website, but it was in a square pattern, and I wasn’t sure if a square pattern would be as easy for a horse to eat through; Gourock had a 1 3/4-inch mesh in a diamond pattern, and the website said it stretched. I emailed Gourock to ask if the store had an opinion on which would be better.

#36 x 1 and 34 diamond

This is how Gourock displays its mesh.

Gourock responded that its 1 3/4-inch diamond mesh was a very popular mesh for hay feeders.

Another consideration was knotted or knotless. Knotted sounded like it would be more heavy duty.

I ordered the 1 3/4-inch diamond-shaped knotted netting with a 381-pound breaking strength at 50 cents a square foot. I asked for a width of 60 inches so I could fold the width over, making each hay net 30 inches deep. I’d say 30 inches is almost right for a depth. A few inches shorter would have been better with the stretchy material. I figured my nets would be 2 feet across, so I would need a length of 12 feet for six nets. I ordered a few more feet so I could make mistakes.

I don’t think I ordered the right thing. The mesh size is fine, though the horses still prefer Angie’s nets with the cutout holes to having to pick the hay out of this larger mesh without the holes.

The Gourock rep warned me that the diamond pattern would be harder to work with than a square pattern. Yep, the diamond material is all over the place when you try to cut it. Speaking of which, my tip for cutting diamond-patterned netting is to cut left, then right, then left, then right in zig-zag pattern. If you do that, you will actually cut straight across.

Angie's seam

Angie’s seam

I did not order my hay mesh with borders, but that’s an option, and I think the border would have helped tremendously in attaching the sides together. I’m still struggling with this. Angie was able to wrap thin twine around the seams of her nets and make the seams perfect. I have not been able to do that. I’ve tried twice, and I give up. I have been tying knots along the sides with tarred Seine twine in a size 12 that I bought on Amazon. The tar is unnoticeable, if that seems off-putting. It’s suppose to keep the twine secure. Kurt untied some of the knots in my first model; my latest model has somewhat obsessive knotting, and it has survived.

If I were to reorder the netting from Gourock, I would get knotless, 2-inch square netting with borders on the netting, mostly likely the rope border unless I were to take up sewing and would be able to work with the nylon webbing border. The rope border would allow me to create a smooth and more secure seam.

My slow-feed net is black with a pink cord.

My slow-feed net is black with a pink cord.

For the cord around the top, I used a 3/16-inch twine that I bought at Lowe’s and cut it at a length of 84 inches. I tried 72 inches, but that length didn’t allow me to pull the net as wide as I wanted when I filled it. The extra 12 inches means I have to wrap the cord an extra time around the post I’m using to hang the net, but that’s OK. I used a contrasting color, hot pink, so I’d be able to find the cord better when trying to fill my black netting, but it looks a little tacky. Angie used a white cord with her white netting, and that looks nice.

I used the cheapest snap I could find at Lowe’s. The snap needs to have a snap at one end and a circle at the other. After threading my twine through the snap and making a knot, I wrapped electrical tape below the knot, taping the twine ends to the twine, to secure the knot.

Electrical tape keeps my snap secure.

Electrical tape keeps my snap secure.

I am convinced that slow feeder nets are our best asset yet in overcoming the problems with today’s high-calorie and high-sugar hay.

The equine feed class that I took online through the University of Edinburgh recommended these nets, or at least using two of the regular nets, which would put more barriers in the way of the horse.

There are many small net products on the market. One Facebook reader suggested hay pillows, which her horses love, and I think these are really nice. I would say that mesh size is too small for my horses, given their demonstrated laziness, but maybe not, because they could push against the pillow to get the hay out. And the pillows allow the horses to move around to get some exercise.

This is where we come to my first concern about the nets. Once I put them up during the winter and got them adjusted to meet my horses’ approval, the horses didn’t move much. They stood in their shed all day pulling the hay out of the net. That’s not what I want to see happen. I want them moving. And a little less poop in the shed would not be a bad thing.

My second concern, or observation, is that my horses don’t bother eating hay from the nets if the horses are not madly in love with that bale. If I put the same hay on the ground, the horses will pick through it. Since we didn’t have a good hay year last year, not every bale is perfect.

Still, I am a fan. I’m a big fan. I’m kicking myself for being opposed to the idea in the early going.

Thank you, Angie.

What is the link between laminitis and horse smegma?

Posted on: April 14, 2013

This article was reviewed and updated April 5, 2023.

Horse smegma is not a topic that gets a lot of press.

I went on a mission in 2013 to find the definitive study on smegma and laminitis and came up empty. None seemed to exist.

Horse smegma is the stuff that builds up inside the male horse’s sheath.

I found a few desperate forum postings by horse owners requesting help in dealing with horses with an itchy sheath, as well as references on less established sites to excessive smegma production in horses with insulin resistance. But I didn’t find one university or medical site that had waded into the conversation, as of 2013.

Kurt has what I would describe as excess smegma. And he used to itch a lot. He was backing into me, sometimes at a trot. Sometimes, he would see me come out of the house and run to me from across the driveway, then spin around and back into me.

My vet made a renewed effort to tackle this issue in February 2013 when I pointed out the problem had existed for five years, and I felt like a terrible owner.

Luckily, I now have a female vet. My previous male vets just sort of sighed when I brought up the topic. I think their take on it was that Kurt should take a little itch like a man. It wasn’t a “little” itch, and Kurt preferred to fix it.

In the past, the female vet tried cleaning Kurt herself, as well as approving the idea of me trying various feminine hygiene products on Kurt. None worked.

Kurt tumor 2 17 2013

Kurt’s biggest tumor in his sheath on Feb. 17, 2013.

This time, she suggested we put Kurt on Tagamet, or cimetidine, commonly used as an antacid in horses and people because it blocks the action of histamine on certain cells in the stomach. Maybe it would block a similar allergic reaction in the sheath. The drug also has been shown in some studies to benefit cancer patients. Kurt has several tumors in his sheath. The idea was to reduce the itching and shrink the tumors.

Note that my own search of these tumor studies found more research that says the drug doesn’t help than does. However, there are a lot of forums with horse owners reporting that Tagamet prevented regrowth of a tumor that was removed. I would consider inhibiting growth of tumors worth using it. Mostly, I cared about the itching.

Kurt started taking the Tagamet on March 5, 2013, and he was on it for a month. 

The experiment looked good in the early going. He didn’t back into me very much. We went days without him bothering me. I think he was distracted by the snow. Once the weather warmed to 70 degrees, Kurt became itchy again. I’m not recommending Tagamet as a treatment for the itch. We stopped using it.

After hearing some local radio broadcasters rave about a mixture of water, mouthwash and vinegar as a foot wash, I decided to try that on Kurt’s sheath. It turned out to be a great concoction for cleaning a sheath, and I added baking soda to the mix because I thought it helped reduce the itch even more. Kurt became much less frantic. And the cleanings reduced the smell considerably.

I later removed the vinegar from the mixture because I didn’t think it was needed.

I clean Kurt every two weeks in a process that I describe here.

Silvia Kornherr, an equine nutritionist from Canada, read my original post on this topic and commented that insulin resistance and Cushing’s disease deal with metabolic dysfunction, which leads to many hormonal imbalances, not just inbalances in insulin and ACTH. Logically, there are going to be secondary changes in many areas affected by the hormonal imbalances.

She said many owners of horses with Cushing’s report increased smegma production and a change in the consistency of the smegma. The smegma becomes very thick, glue-like and abrasive against the sensitive sheath skin, causing inflammation, itching and infection, as well as blockage.

Based on her experience in treating horses with this problem, she suggested I try Animal Legends’ Tea Tree Oil enriched with vitamins A, D and E in the spray formulation. So we did in July 2013. We don’t use it currently because the washing alone seems to solve the problem.

So what is the contents of smegma?

There’s an amusing article on ScienceBlogs that discusses the content. The article says smegma is a waxy, oily secretion from skin cells. It consists of about 71 percent fatty acids and 18 percent cholesterol and cholesterol esters.

The article looks at a study published in 1947 by top research institutions that applied horse smegma to mice (poor mice) to see if the smegma produced cancerous tumors. It did not.

I’m not trying to blame Kurt’s tumors on the smegma. The mice study did say that horse smegma was used because penile cancer is frequent in the horse. But, technically, Kurt has sheath tumors. And that study was done in 1947. There are other statements in the study that are not backed up by current science.

Another interesting study is one published by a veterinary school in Turkey in 2006 that looked at the immune function of the reproductive tract of stallions, including their sheaths, and it concluded that the reproductive tract does likely “contribute to the immune surveillance” of the horse. I suspect the fact that Kurt’s sheath has been having an immune system reaction is not helping the insulin resistance.

I hit the jackpot when I did a Google search of “diabetes” and “itch,” because Google suggested several additional terms and one was “groin.” A forum on the site of the American Diabetes Association is full of people, both male and female, with anguished stories about groin itch related to their diabetes. And the ADA’s page on skin disorders says: “As many as 33 percent of people with diabetes will have a skin disorder caused or affected by diabetes at some time in their lives. In fact, such problems are sometimes the first sign that a person has diabetes. … These include bacterial infections, fungal infections, and itching.”

If your laminitic horse has jock itch, and your vet rolls his eyes or sighs, this is one condition that you can help on your own with products found easily. Click this link to read a tutorial on cleaning an itchy sheath. Your horse will thank you.

University of Edinburgh pulls out all stops with online equine nutrition course

Posted on: March 5, 2013

The equine nutrition course that I took online through the University of Edinburgh was excellent, and I have compiled all the information to share with you.

This course was a massive open online course, or MOOC, offered through the education site Coursera. It was free, but don’t let the price fool you. The University of Edinburgh pulled out all the stops.

Dr. Jo-Anne Murray

Dr. Jo-Anne Murray

This was so well done that some of the students who took the course asked for the school to put up a link where they could donate money in appreciation, and people are being quite generous, according to the latest email we received.

The course was taught by Dr. Jo-Anne Murray, senior lecturer in animal husbandry and nutrition at the Royal (Dick) School of Veterinary Studies at the University of Edinburgh. Before the course started, she sent out an email welcoming us and mentioned that 260,000 students had signed up. I’m not sure if that was a typo. She said in a video mid-course that 23,000 were actually taking the class.

The course ran five weeks, and online students worked through a dashboard.

We watched two or three videos each week on our own. These were accompanied by a PDF  that we could use to follow along for spellings and such. Once we went through the material, we took a review test for practice and then a real test.

There were several instructors involved in this, and they all monitored the forum that was provided. The idea was that we should learn on our own, but the instructors were very hands on and helpful. I’m sure they were ready to collapse once it was over, because horse people can be quite enthusiastic when it comes to forums.

After each week, the instructors posted another video on our dashboard to respond to trending topics and questions.

Once we had watched the material for Week 5, there was a final assessment test, which was challenging, even though it was open book.

I specifically asked in the forum how much of this material we could share with others. Dr. Murray said it was all open source. Share it all.

I downloaded all the videos because it was easier for me to play them on my software than through the dashboard. And I wrote down everything Dr. Murray said. I’ve included all the material I have.

Week 5 addresses laminitis a lot, but all weeks are relevant for understanding how a horse can get into trouble eating sugar and starches. For me, it’s just important to finally learn more about what and how horses should be eating.

However, now that I understand all this better, it makes me sadder that we are so ill-equipped to feed horses properly, given how their systems are designed to eat.

I was going to try to edit down my notes and present a summary, but there’s too much material. Just editing my notes to make sure you could read them took forever.

The one thing I do want to post here is this interesting tidbit. In Week 5, Dr. Murray discussed the idea of putting a horse on pasture only some of the time. Here’s the little problem she pointed out, and I had never read this:

“There have been studies done that when we remove horses or ponies from pastures for half a day, they will actually do compensatory eating. They can actually eat as much in 12 hours as they can in 24 hours if brought inside part of the time. There has been some work done that ponies can eat up to 40 percent of dry matter intake in a period of three hours. So, bringing them into a stable and then turning them out for limited periods may not be as effective as we think.”

I hope you get as much out of this as those of us who took the course did. I stand in awe of this team of equine nutrition instructors at the University of Edinburgh. We owe them big time.

Here is the course material.

University of Edinburgh’s online equine nutrition course

Posted on: March 5, 2013

This is the open-source course material that accompanied the University of Edinburgh’s equine nutrition course in January and February 2013. I have tried to arrange it in a way that is clear.

The course was five weeks in length. Each week’s material includes video files, PDFs provided by the school and notes typed by me. I would call the notes transcripts, but I did some rewriting.

INTRO

Video: Introduction to the course
Slides: Introduction to Equine Nutrition
List: Abbreviations used in videos

WEEK 1

Video: Week 1 Digestive Tract Part 1
Video: Week 1: Digestive Tract Part 2
Notes: Week 1
Slides: Week 1

WEEK 2

Video: Week 2: Nutrient Digestion Part 1
Video: Week 2: Nutrient Digestion Part 2
Notes: Week 2
Slides: Week 2

WEEK 3

Video: Week 3: Nutrient Sources Part 1
Video: Week 3: Nutrient Sources Part 2
Video: Week 3: Nutrient Sources Part 3
Notes: Week 3
Slides: Week 3

WEEK 4

Video: Week 4: Diet Part 1
Video: Week 4: Diet Part 2
Video: Week 4: Diet Part 3
Notes: Week 4
Slides: Week 4
Slides Full Page: Week 4

WEEK 5

Video: Week 5: Clinical Nutrition Part 1
Video: Week 5 Clinical Nutrition Part 2
Notes: Week 5
Slides: Week 5
Slides Full Page: Week 5

Another horse owner questions role of iron in laminitis

Posted on: November 28, 2012

A drinking glass with a three-month buildup of iron from the well water

This drinking glass shows a three-month buildup of iron from the well water. CLR removes the iron, and the glass looks clear for a few days before the process starts over again.

 

I have two reasons to revisit the topic of iron and laminitis.

One is an email I received Nov. 26, 2012, from a woman whose 6-year-old mare has been suffering from laminitis since February 2011. The mare was on supplements for a long time, including expensive laminitis supplements, and she still was chronically lame. A month ago, the owner went against conventional wisdom and turned the mare out on a 100-acre pasture with a stream running through it. The horse is now sound and bucking and playing like a foal. Needless to say, the owner has been pleasantly surprised. She’s investigating if the culprit may have been her well water, since the mare is now drinking exclusively from the stream. The owner describes her well water as I would mine: It turns everything orange and tastes bad.

The owner asked me about testing her mare for iron overload.

I suggested she do what I failed to do: a serum ferritin test.

I had Robin Hood tested for iron overload on Oct. 12, 2012, but I believe I asked for the wrong test. I did a serum iron test, which tested the amount of iron currently in Robin’s blood. A local zoo did the test. Robin’s serum iron level is 2.9, with normal being up to 2.6 and the toxic level being 4.6. These numbers are specific to the zoo’s lab. I can’t compare these numbers to the results of other labs.

At any rate, it would be more productive to know the amount of iron stored in Robin’s organs, and this requires a serum ferritin test, which is on our to-do list.

According to veterinarian and author Eleanor Kellon, the higher the serum ferritin, the more iron is stored in the body tissues. Primary storage sites are the liver and the spleen. Kellon says some horses are so heavily loaded with iron that their livers are found to be black on postmortem examinations.

When I first brought up iron overload as a possible cause of my horses’ problems, one prominent laminitis researcher told me iron was studied as a possible cause of laminitis and failed to produce laminitis in study subjects.

However, the human world is completely on board with iron being linked to diabetes. I’ve been hearing this from journalism friends with good sources, but I’m also seeing it in clinical research, which leads me to the second reason I’m revisiting this topic. I just stumbled over a study published September 10, 2012, in the Journal of Clinical Investigation that leads off with the sentence: “Iron overload is associated with increased diabetes risk.”

The study notes that other recent studies have found a negative correlation between serum ferritin and adiponectin, which is an insulin-sensitizing adipokine (a cell-to-cell signaling protein).

“Negative correlation” always makes my head hurt. Adiponectin would be lower in subjects with high serum ferritin levels.

The study says “the hypothesis that adiponectin links iron and insulin resistance is appealing, as decreased adiponectin levels are associated with obesity and type 2 diabetes and are causally linked with insulin resistance.”

The study suggests that serum ferritin levels could predict the presence or absence of metabolic syndrome in humans and that iron reduction may be a possible treatment for diabetes.

I wonder if the problem with the previous iron research in horses was it tried to overload horses’ iron levels in their bloodstream, whereas the destruction may occur over the long haul through iron buildup in organs. Under this scenario, an iron study would have to go on for a long time, which would be very expensive if it required housing horses for an extensive duration.

My three laminitic mares took two to three years to develop laminitis once living at my farm and drinking my well water.

I walk away from this iron theory from time to time as other things grab my attention, but I always seem to come back. What makes me look elsewhere is the fact that not every foundered horse is on well water.

But a lot of people provide trace mineral blocks for their horses, and many of these blocks are 25 percent iron. And a lot of feed makers are putting iron in the feed, too.

Some horses simply may be more sensitive to iron overload.

And horses that get additional iron in the water may be doomed.

Looking for the thrifty gene in laminitic horses

Posted on: November 18, 2012

Kurt and Robin are substantially overweight, whereas their nephew was skinny for years on a nearby pasture.

Kurt and Robin are substantially overweight (in mid-October 2012), whereas their similarly built cousin was skinny for years on a nearby pasture that was by all standards very green and lush.

I have often heard researchers refer to a “thrifty” gene in horses that develop laminitis.

Researchers say this gene may be the reason that some horses founder and some don’t. My farm is surrounded by pastures far larger than my own that are dotted with horses — some relatives of my horses — that haven’t foundered, so I’m skeptical of this thrifty gene, but it would explain some things.

I’ve heard a couple of laminitis researchers theorize that horses that traveled from Europe to America by boat as America was colonized had to be able to get by on little food to survive. The researchers suggested we owe the birth of our country to those horses’ thriftiness.

The website of the International Museum of the Horse paints a grim picture of Spaniards shipping their horses to the New World in the 1600s, and let’s remember that this was only 400 years ago. Hard to believe.

Apparently, horses were shipped in slings. This took their weight off their feet and allowed them to swing with the roll of the ship. The dark, damp atmosphere in the boats and lack of exercise often killed half the horses, and the dead animals were buried at sea. Some say this is how the section of the Atlantic Ocean named the Horse Latitudes got its name, though others say this is folklore.

Getting the horses off the ship was hazardous, as well. They were lowered by sling into the water and made to swim ashore by people in row boats.

Laminitis researchers suggest that the same thrifty genes that served horses well in hardship are now killing them because the improved grass and hay created for cows is too rich for the systems of these horses, and they develop laminitis (as do cows).

I would buy the thrifty gene theory more if I could explain why none of my parents’ Connemaras (the ancestors of my horses) foundered. Similarly, I don’t know of any siblings of my horses that have foundered, though many live on pasture. My mare Angel moved to my current farm as a 3-year-old in 1997 and got very fat in a year. I sent her to Ohio for three years as a broodmare, and immediately she dropped a tremendous amount of weight, even though she got pregnant. She was stalled some of the time but she also got out on pasture each day. I don’t think her access to grass there was much different than her life at my farm, because, here, she had almost no grass, sharing a 2-acre pasture with four other horses round the clock. One could argue she got more grass while away. She was very thin when she returned home from Ohio at the end of 2001. She got fat and foundered by February 2004, a little over two years later, in the middle of winter even as I worried about laminitis from having problems with my other horses and tried to maintain an appropriate diet for all of the horses.

At any rate, I’ve been searching online for this equine thrifty gene. Mostly, it seems like the thrifty gene is a theory, and scientists are trying to find which gene is the culprit.

I saw a few references to a likely thrifty gene in an article by laminitis researcher Philip Johnson at the University of Missouri’s vet school. He wrote the article in 2009 for the Journal of Diabetes Science and Technology.

Johnson’s article covers the fact that horses that evolved naturally would go through the process of putting on excess weight during the fall in the form of stored fat to get through harsh winters.

He says herbivores, including horses, contain a critical survival mechanism — increased secretion of proopiomelanocortin (POMC) peptides in the fall — that stimulates the appetite and leads to other changes that result in fat storage in preparation for winter, when food tends to be relatively scarce.

This short-term addition of fat was fine historically. Johnson says it’s the chronic persistence of fat that leads to problems, and owners today generally keep their horses too fat.

He talks about how wild horses survived by covering a great distance daily to find little grass that was relatively low in sugar. He says today there is good evidence that providing higher sugar rations leads to diminished insulin sensitivity.

Higher sugar combined with less exercise and “grossly excessive” feed rations is what is getting horses in trouble today, he says. And he points out that today’s forage is designed to make farm animals gain weight quickly.

He says there are few statistics on current horse obesity, but one study found 45 percent of 319 randomly selected horses to be fat or very fat. That compares to 25.8 percent rate of obesity in cats and 25.2 percent rate in dogs, he says. I’ve seen other numbers that put cat and dog obesity much higher in 2012.

Johnson points out that laminitis is seen in two forms: one that leads to separation of the hoof lamellar interface, the tissue that connects the hoof to the bone inside the foot; and one due to chronic remodeling of the foot resulting from endocrine disorders (others have compared this remodeling to cancer-like growth).

Johnson says the endocrine abnormalities that are most often seen in horses with chronic laminitis are insulin resistance and excessive levels of corticosteroids. He says insulin resistance is likely an important component of thriftiness — horses with insulin resistance can survive on far less food.

As for corticosteroids, the corticosteroid named cortisol, a glucocorticoid due to its role in sugar metabolism, is secreted by the adrenal glands. Its primary roles are to increase blood sugar, suppress the immune system and aid in metabolism. Stress can lead to elevated cortisol levels, which can lead to weight gain.

Johnson said that an enzyme called 11-hydroxysteroid dehydrogenase-1 (11-HSD1), which converts inactive circulating cortisone to cortisol in localized tissue, is an important component of human metabolic syndrome and it is seen in increased amounts in the hoof lamellar interface (the connective tissue between the hoof and the bone) in laminitic hooves as well in the cresty necks of horses with equine metabolic syndrome. He said this enzyme is likely one of these thrifty genes.

Johnson also reviews the fact that insulin itself is toxic to the hoof lamellar interface, and raising a horse’s insulin level can result in laminitis.

My feeling is that, yes, all of these thrifty genes may behave in a way that leads to laminitis, but something has to trigger them to behave in that manner. If horses of similar genetic background can live on grass nearby, what is triggering these thrifty genes to behave in a problematic manner in my horses? What is triggering them in the horses of others?

Laminitis researchers provide huge volume of free information

Posted on: November 11, 2012

Equine Veterinary Journal

Screen shot of the Equine Veterinary Journal’s new release of laminitis research.

The laminitis research community has released a huge volume of free work intended to set the record straight on all things laminitis, as of 2012.

Science papers released online often cost $35 per paper, beyond the budget of many a laminitis-poor horse owner. This “virtual” collection of papers released through the Equine Veterinary Journal is a gift. A big thank you to this publication and all those researchers who contributed their time and knowledge.

The release includes the full text and references of these papers and costs nothing. You don’t even have to log in or leave an email address, though no one would mind, I’m sure.

The material is written by all the big names in laminitis research: James Belnap, Chris Pollitt, Philip Johnson, James Orsini, etc.

Note that this is a very large body of work. I downloaded the provided PDFs (as far as I can tell, you have to download each individual PDF, as opposed to downloading the whole thing in one take — compiling all the papers into one PDF might have made it too large to download). I then made the mistake of printing the PDFs, and I used up maybe half a ream of paper.

Also, note that this material is written using a lot of scientific language, even though the editor states upfront that the purpose of this release is to combat the fact that much of the freely available material published online for horse owners “lacks rigor and quality.” So, these papers are for the average horse owner, but many words will be unfamiliar.

I’ve been reading science papers since 2007, and my first attempt seemed hopeless. I stopped at every new word to look it up, and it took me several days to get through one paper written by someone whom I consider very easy to understand in person. But this is how laminitis researchers write. My advice to anyone who wants to read these papers is perhaps to skip over something at first if it’s causing you great difficulty, because the more you read the material, the more familiar you will get with the terms. When you go back to a paper a second time, it will make more sense.

The takeaway message I see in the early going of my reading is as follows:

Scientists now consider there to be three forms of laminitis. The disease can be caused by sepsis (gastrointestinal injury), endocrine disease (insulin-resistance and Cushing’s disease) or excessive weight bearing. There may be some overlap between the forms based on the horse’s situation, but the changes in the foot are different for each.

There is much work to be done in studying each form. However, there is also a small glimmer of hope on the treatment front.

The paper titled “Progress toward effective prevention and therapy for laminitis” says these differences in the various forms of laminitis make it hard to target a failed process in the hoof and come up with a therapeutic intervention.

However, it also raises the possibility of reversing laminitis. It says new evidence suggests that the laminae do attain the ability to remodel, but this has been absent in the laminitic hoof, and it may be caused by reduced activity of p63, a regulator of epidermal stem cells. It suggests that transplantation of these stem cells from unaffected regions of the horse may have regenerative therapeutic potential for laminitic horses.

I talked to someone in the stem cell lab at Rood & Riddle Equine Hospital in Lexington, Ky., in May 2011 right before I put down my mare Angel, and, at that time, the rate of success for stem cells was not good, and I felt as if the trip alone would kill Angel, and the success rate at the time didn’t warrant trying, even if the monetary challenges could be overcome. I do not have any details on what the lab was using in terms of stem cells at that time. I’m guessing that this new development may bring stem cells to the forefront as a treatment.

As for new details on those various laminitic models:

The sepsis model includes carbohydrate overload and excess fructan scenarios. In the paper titled “Sepsis-related laminitis,” it gives a good explanation of the process: Excess starch arrives in the large intestine and is digested by intestinal bacteria, which results in a severe drop in intestinal pH, an ensuing die off of Gram-negative organisms and a moderate to severe enterocolitis, or inflammation of the colon and small intestine. This leads to injury to the mucosal barrier and absorption of numerous substances, including bacterial toxins. For years, people thought the bacterial toxins, called endotoxins, were the culprit. But this paper says experimental infusions of endotoxins did not result in lamellar failure, so investigators are looking for other trigger factors absorbed from the compromised gastrointestinal tract.

For the endocrine form of the disease, the paper titled “Endocrinological aspects of the pathophysiology of equine laminitis” raises some interesting points. Inducing laminitis in horses and ponies results in serum insulin concentrations much higher than those commonly associated with Cushing’s disease and some cases of pasture-associated endocrine-related laminitis, and it says “similarly high serum insulin concentrations have been documented in recurrently laminitic ponies in the absence of clinical signs of laminitis, such that very high serum insulin concentrations alone are not necessarily laminitis-inducing.” And, even more interesting to me, the feet of the ponies induced with the insulin form of laminitis showed a lack of basement membrane disintegration. Instead, the feet showed apoptosis (programmed cell death) and mitosis (cell division). Thus, these feet do not fall apart in the same manner as in the carbohydrate overload model or the naturally occurring disease. The paper says that debate continues over whether insulin resistance is associated with increased or decreased blood flow in the feet, and insulin resistance’s association with inflammation in the laminitic horse is also unclear. It says studies suggest that excess glucose does not play a role in insulin-induced laminitis.

It talks about identifying horses with insulin resistance. One study on a group of ponies combining five diagnostic tests did not result in higher diagnostic accuracy than individual tests of insulin or leptin. Leptin is a peptide secreted by adipose tissue. I’m not aware of ever having a leptin test done on my horses. The mention of that as a test was a surprise to me.

It says that phenomenal efforts by scientists have increased knowledge about this form of the disease dramatically over the last few years, but those efforts have probably generated as many questions as answers. And it closes with an interesting summary: “It should be remembered that not all laminitis-prone animals are obese and/or insulin resistant, not all obese animals are insulin resistant and not all insulin resistant animals are laminitis-prone.”

Perhaps the opening line of the support limb laminitis paper says a mouthful: “Supporting limb laminitis is a veritable dark hole when it comes to our goal of completely understanding the pathogenesis and therefore the prevention of all types and clinical presentations of laminitis.” However, if you read further, progress is being made on understanding how the laminae fail in this model. That is good news.

There is much to explore in these papers, and a quick study on my part can’t begin to cover the research included. Hopefully, the release of this information will move research forward in a meaningful way. Again, we should all be grateful for this information being given to us online at no charge. Thank you, Equine Veterinary Journal.

 

I fear fertilizer more than sugar for my laminitic horses

Posted on: October 27, 2012

The upper pasture by my house

The upper pasture by my house.

The question on my mind for weeks has been whether to fertilize my two upper pastures.

I’ve been digging online for information on grass content and sugar levels in trying to quell my fear of fertilizer.

I keep finding more laminitis researchers who believe fertilizer is a good thing for laminitic horses because it keeps grass from getting stressed, thus preventing sugar levels in the grass from spiking. But I am not convinced that this is the right strategy.

I have dug up some interesting statistics on horses eating grass that have helped me come to a conclusion for my own horses. I’m not suggesting that others follow my lead. Each of us has to make decisions for our own horses.

Numerous environmental factors — cool temperatures, short day length, intense sunlight, drought, and limited nutrients — raise the sugar levels of grass.

Finding a definitive number for how much these factors stress the plant and increase sugar levels is difficult, but Australian researcher Chris Pollitt suggests the sugar levels in grass can triple under stress.

Modern grasses have more sugar content than their predecessors, according to plant experts, who say this is intentional. Grass companies have “improved” grass to beef up cows, not to feed horses. The higher sugar content allows grass to recover faster after grazing, as well as to grow in cooler temperatures and to stand up better in drought.

Fertilizing a pasture can lower the sugar levels in the grass, because the grass uses its sugar to grow, but fertilizing also creates more grass, possibly giving the horse more sugar in the end and certainly more calories.

The prevailing advice these days appears to be fertilize the grass so you have healthy grass but limit your horse’s time on the grass.

That seems completely backward to me. I want my horses out all the time, moving, keeping busy, exercising and looking for food. But I want them to have less grass with lower sugar, and no one is providing that product. How is it that some enterprising person has not made a low-calorie, low-sugar grass for horses yet?

Ray Geor, the chairman of Large Animal Clinical Sciences at the College of Veterinary Medicine at Michigan State University, looked at the calorie intake and exercise of horses on pasture in an article on thehorse.com in 2003.

While the data is not new, Geor provides some interesting statistics, and I can’t think of any reason why these numbers wouldn’t hold up today:

— Horses spend about 10 percent of their time walking when on pasture.

— Horses spend more time walking on pasture if the pasture is of poorer quality or the horse is alone.

— Horses graze approximately 70 percent of the time when they are on pasture, so, if a horse has 24-hour access to pasture, it will spend up to 17 hours grazing.

— Grazing time is inversely proportional to the quality and amount of pasture forage, as in a horse will spend less time grazing a lush pasture compared to a dry pasture with lower forage availability (still, I would suggest the horse likely takes in far more food on the lush pasture).

— The amount of exercise depends on the amount of time in pasture. Horses grazing for 17 hours per day have been measured traveling 8 to 9.5 miles, while those out for seven hours have gone 2.5 to 3 miles.

— A 1,000-pound horse eats about 1 to 1.4 pounds of grass per hour (dry matter) if the grass is not limited.

— Orchard grass contains about 1,000 calories per pound.

Doing a little math based on Geor’s numbers, I believe that if a horse were out for 10 hours and grazed 70 percent of the time, or seven hours, on good grass, it may consume 7,000 to 9,800 calories per day. The National Research Council suggests that a 1,000-pound horse out of work should have about 15,000 calories per day, so a horse stuffing its face on grass for seven hours would still need some hay at the end of the day.

A horse on sparse grass — which some would shun as “stressed grass” higher in sugar — would get fewer calories and walk more, but the sugar level might be three times higher.

I’m thinking that three times the amount of sugar in a lot of grass equals a lot of sugar, but three times the amount of sugar in sparse grass is not so much sugar.

Beyond the sugar levels being affected by stress, they also fluctuate at different times of the day, spiking in the late afternoon.

Given the countless variables, I think it’s safe to say that trying to monitor or even guess the sugar levels in grass is a futile exercise for the average horse owner.

What I can control is the amount of grass I create, and, given the statistics I read in Geor’s article, I feel like having the horse walk more to eat less grass, stressed or not, is the better deal. It’s highly unlikely that I’m going to fertilize my pastures.

 

Persimmons pose threat for all horses, not just those with laminitis

Posted on: September 11, 2012

One of my horses got an abscess in September 2012, and it turned out to be a stroke of good luck for a change.

Thanks to the abscess, the horses were confined to the two upper pastures.

This was Robin’s first abscess. I closed the gate to the lower fields to keep Kurt from getting too far away from Robin, who couldn’t put any weight on the sore foot but was still trying to follow Kurt around. It seemed like a temporary inconvenience to Kurt, but he would live. Little did I know that it probably saved both horses’ lives.

One night after work, I took my stray cats for a walk around my lower fields and noticed some persimmons on the ground. I have two persimmon trees that I have to keep an eye on every fall.

A bucket this size holds about 550 persimmons, a lethal amount for a horse to consume.

A bucket this size holds about 550 persimmons, a lethal amount for a horse to consume.

In 2011, I didn’t remember seeing any persimmons, and I made no notes on the topic in my horse journal.

I guess we made up for it in 2012.

On this night, the ground was blanketed with persimmons. By the time I finished trying to pick them all up, I had gathered three buckets’ full, and it was dark.

In less than a week, I picked up 4,140 persimmons.

A persimmon with a diameter of 2 1/2 inches has 118 calories. Most of mine are 1 1/2 inches in diameter, or three-fifths of that size, so the calorie count would be more along the lines of 71 calories per persimmon.

And the average persimmon has 10.6 grams of fructan, so these would be closer to 6.36 grams. Excess fructan in significant amounts can induce laminitis in a horse.

All totaled, these collected persimmons represent an estimated 293,940 calories and 26,330 grams of fructan.

A horse out of work should have no more than maybe 15,000 calories a day.

In April 2010, Equine Science Update reported on a presentation by Dr. Teresa Hollands at the Laminitis Awareness 2010 seminar in which she described how much fructan it takes to induce laminitis.

Hollands, a nutritionist at Dodson and Horrell, said the amount was 5 grams to 12.5 grams of fructan per kilogram of bodyweight, or about 3.75 kilograms of fructan for a 500-kilogram (1,100-pound) horse. The 26,330 grams of persimmon fructan that I collected would equal 26 kilograms, a tad above the 3.7 kilograms needed to induce laminitis.

Beyond my concerns for the horses developing laminitis, there’s the little problem of impaction.

An online search turns up plenty of entries for persimmon and acorn impactions in horses.

Basically, horses will eat persimmons until they die.

I was expecting not to worry about the persimmon trees in 2012 because of the drought. Low and behold, persimmon trees can be quite drought resistant, according to several sources.

Is deworming horses leading to chronic inflammation and metabolic syndrome?

Posted on: September 1, 2012

Editor’s note: When I wrote this post, I was looking for all possible factors that might be causing my horses’ laminitis. I no longer think lack of worms plays a role. But the post is still interesting, and I am leaving it up for now.

In the span of one week, I read two articles in which medical professionals praised the power of worms to regulate inflammation in humans. Experts in “The New York Times” and on “The Huffington Post” say the lack of worms in people in developed nations may be what is causing chronic inflammation, and this inflammation may be the source of such baffling diseases as autism, asthma, rheumatoid arthritis, inflammatory bowel diseases, multiple sclerosis and metabolic syndrome.

They point to the fact that these diseases don’t exist in undeveloped nations where worms and infections are the norm.

It appears the worms are well-known for limiting inflammation.

“The Huffington Post” suggests that a lack of worms leads to “immune system idleness,” resulting in the immune system going on the offense, leading to automimmune disorders that account for “a huge portion of the disease burden in modern societies.”

According to “The New York Times,” at least a third of autism cases are attributed to inflammation, and a Denmark study indicates that inflammation in the mother is to blame for autism in these children. Experts theorize that, if they can fix the inflammation in the womb, they can get rid of those cases of autism because the inflammation won’t interfere with fetal brain development. A Swiss study using mice backs up that theory.

While some doctors are looking at drugs and probiotics as a therapy, Dr. William Parker at Duke University is simply restoring parasites in people, according to the article. These are worms developed solely for the purpose of correcting the wayward, postmodern immune system. And a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine in New York testing a medicalized parasite called Trichuris suis in autistic adults.

Dr. David Katz, M.D., wrote the article in “The Huffington Post,” and he says the use of probiotic bacteria in capsule form as a therapy for conditions such as irritable bowel syndrome is increasingly routine, and he makes extensive use of probiotics in his office. He says the use of therapeutic parasites is not yet routine, or even routinely accessible, but there might be some movement in that direction.

Where does that leave us with horses? I immediately searched for some sort of scientific revelation in the horse world that our endless deworming was doing more harm than just making worms resistant to the dewormer. What I found was well-written papers by top vet schools in the last few years still encouraging people to deworm, though in a more organized fashion.

But what is this deworming doing?

We know that horses that won’t gain weight often are examined for worms. Now I’m wondering if that inability to gain weight is a bad thing. The wormy horse’s body may be working perfectly.

Maybe worms aren’t the enemy.

Still, a recent study in the UK indicated that deworming reduced the risk of a horse developing laminitis. According to The Horse, which quoted Claire Wylie, PhD, MSc, BVM&S, a veterinary epidemiologist at Rossdales Equine Hospital, in Newmarket, England: “Compared to horses wormed every one to six months, horses that had been dewormed in the past four weeks had a reduced risk of laminitis; horses that had not been dewormed in the past six months to a year were 2.5 times more likely to founder; and horses that had not been dewormed in over a year or never were 11.3 times more likely to founder. ‘We don’t know why this is,’ Wylie said, ‘but it could be due to many things, such as a novel effect of anthelmintic drugs, an association between laminitis and gut function, or maybe it indicates better-cared-for horses (are less likely to develop laminitis).'”

Advice on pasture management for laminitic horses is often conflicting

Posted on: August 12, 2012

Kurt picks through ragweed on Aug. 11, 2012.

Kurt picks through ragweed in the field by the house on Aug. 11, 2012.

For years, I was caught in the middle an argument over whether owners of laminitic horses should fertilize their pastures. On one side of the argument was my veterinarian, who specialized in laminitis and was opposed to fertilizer; on the other side was a plant scientist with laminitic horses of her own who had been studying the sugar content of grasses under various conditions and was in favor of fertilizer. She worked with my vet and at one point visited my farm.

The plant specialist said that fertilizing a stressed horse pasture would keep the plants healthier and the sugar level lower, making it safer for a laminitic horse.

The vet insisted that the fertilizer would increase grass production so much that the horse would get far more sugar from the extra plant growth than it would from an unfertilized pasture that had higher sugar levels due to stress.

My current vet agrees with the previous vet’s view: the less grass, the better, whether the grass is stressed or not.

My research over the past month suggests that there’s no right answer for pasture management for the laminitic horse. There is much conflicting advice. And doing nothing is not a good option, either.

The plant scientist was not shy in her assessment of the poor condition of my overgrazed, unfertilized pastures when she visited in 2007; she felt the pastures needed help. If I remember her instructions correctly, she wanted me to fertilize my pastures and fence them off into smaller pastures to rotate my horses on the grass as opposed to letting them have access to the full pastures all the time. I decided against dividing the pastures into smaller areas since their original purpose was to allow the horses to run; with each field being about 2 acres, the horses had limited ability to gallop already. I had four pastures; thus, I had the capacity to rotate the horses, if I wanted to rest each field. Plus, I was so laminitis-poor by that point that I had no money to add fencing anyway. A lot of decisions are made simply based on a lack of money.

These were not the only opinions about grass that I was weighing.

In 2004, after Angel foundered, a prominent laminitis veterinarian from Sweden visited my farm on a ride-a-long with my vet and said after hearing about my multiple laminitis cases: “I think you should move.” His rationale was that someone had put something in the soil over the years, whether through fertilizer or by planting a certain crop, that had created a condition that was ripe for a horse to develop laminitis, and it might take years for the makeup of the soil to change. Don’t I wish I had listened to him?

And, at the end of 2008, another prominent laminitis veterinarian from the Midwest came to my farm and said I should get rid of the grass completely. Since my whole farm slopes downward, and Missouri is prone to what we call “gully washer” storms, removing the grass cover seemed like a bad idea for that reason alone.

Getting back to the plant scientist’s advice — since I had one founder case after the next with my horses, the idea of adding fertilizer to any of the grass seemed too scary, so I wasn’t inclined to go that direction. I applied fertilizer only once in 2008 when trying to bring back a patch of pasture that had died after builders removed some dirt to erect my hay shed elsewhere. I applied fertilizer and grass seed to that stripped area with no results; it’s still brown. At the same time, I stupidly put the leftover fertilizer and grass seed on my septic area in the pasture by my house because the septic drain field was getting bare. Perhaps, not surprisingly, that summer was the first year that Robin Hood truly foundered.

According to Donna Foulk, former senior agriculture program coordinator at Rutgers Cooperative Extension, if you are going to fertilize your pasture, your horses should be removed. She says: Nitrogen fertilizer is toxic, and horses should not be allowed to graze pastures until rain has completely removed all of the fertilizer from the leaf surfaces and carried it into the soil. As a general rule, horses should be removed from fertilized pastures and not returned until at least a half inch of rainfall has occurred and the fertilizer is no longer visible on the soil surface. Best management practices dictate that after fertilizing pastures, horses should not be returned to the pastures for two to three weeks to provide ample time for the pasture grasses to grow and recover from grazing.

I didn’t pull the horses off the pasture when I put out the fertilizer. I didn’t put out much, but I didn’t remove the horses, either.

I have never applied weed killer to any of my pastures. I considered it in 2011, but, the vet mentioned at the top of this article cautioned that he wasn’t willing to put weed killer down in his own pastures out of concern for what it may do to the laminitic horses in his care. I’ve been basically paralyzed with fear and, hence, have done nothing about the continuing decline of my pastures.

As a result, I have a truly magnificent stand of ragweed that comes up every July now.

Five horses kept this field bare year-round in the early 2000s, yet three of the horses -- the mares -- foundered.

The five horses that grazed the field by the house in the early 2000s kept it bare, yet three of the horses — the mares — foundered at the time.

Oregon State University has a guide for pasture management on its site that says grass cutting, seeding, fertilizer and horse rotation are the main tools for maintaining quality pastures. Use of herbicide on a regular basis indicates that you are managing your pastures poorly, it says.

OK. So, I shouldn’t use herbicide. Then, what should I do?

Many university websites decry overgrazed pastures. But there’s no shortage of laminitis experts who say laminitic horses should be on dry lots, and even the university websites say horse owners should have a “sacrifice” area where the horses can hang out when the pastures are wet or overgrazed, lessening the damage to the pastures. I personally think there’s a very fine line between a dry lot and an overgrazed pasture. Would the pasture in my photo with the five horses grazing be considered a dry lot? Can you have less vegetation than that and not have considerable soil erosion?

Speaking of soil erosion, the pasture maintenance guide by the Oregon State University extension office is particularly harsh about keeping your horses on mud. It recommends sacrifice areas have an all-weather surface such as gravel or sand. On mud, it says: “Mud harbors bacteria and fungal organisms that cause health problems. Mud fever (or scratches) is a common condition that usually affects horses’ lower limbs. It is marked by inflammation of the skin and the appearance of crusty scabs. It usually is caused by bacteria that penetrate the skin following either damage or softening from exposure to wetness or mud. The bacteria thrive in wet, muddy conditions. On the upper body, the same condition is referred to as rain scald.”

At the end of all this research, I know nothing.

Should laminitic horses get a thyroid supplement?

Posted on: June 9, 2012

Kurt's sides are lumpy despite years of taking thyroid supplements to boost his metabolism.

Kurt’s sides are lumpy despite years of taking thyroid supplements to boost his metabolism.

Editor’s note on June 15, 2015: I wrote this post before reading Juliet Getty’s post on treating the insulin resistant horse. Thyroid supplement may help the laminitic horse lose a little weight, but I think it’s a poor substitute for helping a horse restore balance in its diet and life. Even before I read Getty’s post, I had taken Kurt off thyroid powder because it was making him break out in a drenching sweat. It took me a while to figure out the cause of the sweat. The day I stopped the thyroid powder, the sweat went away. Giving thyroid powder to a laminitic horse may cause unintended consequences. I’m leaving the article up, because the reporting of the research is accurate.

Laminitic horses often are put on the thyroid supplement levothyroxine sodium (commonly sold under the brand name Thyroid-L).

While it can be an effective component for treating the insulin form of laminitis, the reasons for using it have fluctuated over the years.

The thyroid is located in the neck of all mammals. The gland secretes the hormone thyroxine, or T4, and to a lesser extent triiodothyronine, or T3. These hormones predominantly affect metabolism, but they also influence growth, development and body temperature.

The pituitary gland and hypothalamus in the brain also play a role in regulating thyroid levels. The anterior pituitary gland releases thyrotropin, a thyroid stimulating hormone referred to as TSH. The hypothalamus releases thyrotropin releasing hormone, or TRH, which affects thyrotropin.

Low thyroid levels may be the result of problems in the thyroid, hypothalamus or pituitary gland, or all three.

According to Nat Messer, DVM, at an AAEP meeting in December 1998, hypothyroidism is uncommon in horses, but widespread misdiagnosis of thyroid dysfunction results in more than $750,000 worth of thyroid hormone supplement being sold for use in horses annually.

So, why have we been using thyroid supplements for laminitic and foundered horses? There was a time when laminitic horses that were “easy keepers” were presumed to have hypothyroidism because their body condition, particularly regional fat deposits, mirrored that of dogs with hypothyroidism, plus the horses had low or low-normal resting serum T3 and T4 concentrations.

But, in a 2006 proceedings paper for the AAEP, Nicholas Frank, DVM, admitted that scientists had come to realize that low thyroid levels were a consequence rather than a cause of the horse’s metabolic issues and may even be the result of use of phenylbutazone, or bute.

That surprised me. In more than 15 years of treating laminitic horses with bute, I was never told that bute might be lowering my horses’ thyroid levels.

Still, many owners of laminitic horses, including me, have been told to try thyroid supplement because it may help speed up the horse’s metabolism so the horse can lose weight, which hopefully will lower the horse’s risk for having a relapse of laminitis. Losing weight is often a battle for foundered horses because they are too lame to exercise and their food needs drop off dramatically due to the fact that they don’t move much.

I can tell you from personal experience that Thyroid-L doesn’t always help a horse lose weight — my horses got 2 grams of Thyroid-L a day for years, and they both were obese.

Where levothyroxine sodium does appear to help is with controlling insulin levels, though insulin’s role in laminitis was only solidified by research in 2007, so Thyroid-L may have been silently doing some good on the insulin front for years while being prescribed as a weight-loss treatment.

In a study published in 2008 in the American Journal of Veterinary Research, Frank said administration of levothyroxine sodium led to weight loss and increased insulin sensitivity in adult horses with healthy thyroid gland functioning. He also said levothyroxine sodium significantly increased the rate of insulin disposal.

Note that the amount of T3 and T4 in the bloodstream regulates the release of TSH by the pituitary gland, so low levels of T3 and T4, for whatever reason, make the pituitary release more TSH. There is no shortage of studies that talk about the link between a high TSH level and insulin resistance in humans.

In a German study published in 2000 in Clinical Endocrinology, researchers concluded that study subjects with normal thyroid function (euthyroidism) but elevated TSH were more obese, had higher triglycerides and an increased likelihood for metabolic syndrome, also known as insulin resistance syndrome.

The concern with the insulin form of laminitis is how much insulin and glucose is circulating in the horse’s bloodstream. If Chris Pollitt’s Australian research team is correct, elevated insulin levels in a horse can lead to the excess insulin in the blood errantly binding with the wrong receptors in a horse’s feet (insulin-like growth factor 1 receptors, rather than insulin receptors, which don’t appear to exist in horses’ feet), leading to out-of-control hoof growth, not unlike cancer, destroying the structure of the hoof wall, coffin bone and laminae.

If Thyroid L can lead to faster disposal of insulin, that alone might be a reason to add it to the diet of the laminitic horse.

At the same AAEP meeting in 1998, Messer addressed some additional factors that may affect thyroid levels, including nutrition. He said short periods of food deprivation can lower thyroid levels, as can diet composition.

Messer and associates conducted a study at the University of Missouri (published in 1995) in which food was withheld from six adult horses with normal thyroid function for four days. Hormone levels decreased more than 50 percent over that time. When the horses returned to a normal eating schedule, their thyroid levels returned to normal.

In a laminitic horse, thyroid levels might be lowered by bute and food deprivation, which are normal treatments for laminitis, and the resulting elevated TSH levels may increase insulin resistance. Elevated insulin would cause even more damage to the feet than had happened already. Given this scenario, it’s easy to see why owners might see some improvement giving a thyroid supplement to a laminitic horse.

Are phthalates in hoses a problem for laminitic horses?

Posted on: May 6, 2012

Garden hose

Garden hose.

The “Los Angeles Times” released a report May 4, 2012, titled, “Garden hoses often contain phthalates and lead, study says.”

It includes a lot of information worth discussing in the horse world because many people give their horses water through garden hoses that sit out in the sun, which apparently leads to more phthalates contaminating the water.

I was interested in whether phthalates, which mimic estrogen in the body, could alter the endocrine system of a horse enough to lead to laminitis. Like many of my theories, this one cannot be proved, at least not by me from my farm.

And there may not be one thing leading to laminitis. There may be many things that push a horse over the edge into having elevated insulin and developing laminitis — from getting just a little too much iron though trace mineral blocks to developing elevated estrogen through water ingestion of phthalates to taking in too much sugar and starch by eating grass or hay designed to fatten cows quickly.

The “Times” article on garden hoses says the nonprofit environmental research group HealthyStuff.org in Ann Arbor, Mich., found that the lead and phthalates in water hoses exceeded allowable levels set by the Consumer Product Safety Commission, and the lead in brass fittings for garden hoses exceeded standards for brass fittings in residential water fixtures as set by the federal Safe Drinking Water Act.

The study tested other gardening products, as well, but Jeff Gearhart, research director for HealthyStuff.org, said garden hoses were the one that raised the most concern. Tests indicated that phthalates and bisphenol A migrated out of the hose and into water sitting inside.

“I was surprised at the levels of chemicals and some of the chemicals we found,” Gearhart told the “Times.” “But I was even more surprised that there’s a lot of better choices in the marketplace.”

Gearhart recommended that consumers buy lead-free garden hoses, which he said are often white with a blue stripe and found at marine and RV stores.

For people who use hoses with lead and phthalates, Gearhart suggested letting the hoses run before using them and storing them in the shade to prevent the sun from heating the hose and releasing plastic chemicals into the water.

There are groups of scientists who dispute whether phthalates are a cause for concern at all. Animal studies using phthalates apparently have not cleared up the controversy.

However, the U.S. Department of Health and Human Services has a posting on its website from Dr. John Bucher, associate director of the National Toxicology Program, which summarizes his group’s investigation to the topic in 2008. The report describes bisphenol A, or BPA, the phthalate in garden hoses, as a high-production industrial chemical used to manufacture polycarbonate plastics and epoxy linings of tin cans.

Bucher says BPA “has been known since 1938 to mimic estrogen when given in large amounts to experimental animals. More recently, it has also been studied for its ability at very much lower doses to affect hormonal processes involved in development, when an animal is exposed as a fetus or during infancy.”

He says a CDC study from 2003 to 2004 found detectable levels of BPA in 93 percent of 2,517 urine samples from people 6 years and older in the United States.

He went on to say: “We express ‘some concern’ that current estimated exposures of BPA to fetuses, infants, and children could cause neural and behavioral effects, effects on the prostate and mammary gland, and an earlier age at which females attain puberty. We express “negligible concern” or “minimal concern” that current exposures to BPA could cause adverse health effects in other segments of the population.”

I did a previous post on young girls developing earlier if you want to read more on that topic.

Bucher said there are a number of uncertainties in the scientific information on BPA. The literature from experimental animal studies is large but conflicting, and human studies are insufficient.

So, where does this leave horse owners?

A lead-free hose won’t solve the phthalate problem.

My water well is so far from my shed that I can’t get water from one place to another without a hose unless I want to invest a lot of money in piping. Actually, if I had the money, I’d do it.

I have always noticed that the water had a bad taste to it in summer that wasn’t there in the winter, and new hoses have a bad taste, as well. So, the “Times” article more confirms my suspicions than surprises me. The hose is tainting the water. And the water is more tainted in the summer, when horses drink more water.

Is this enough to change a horse’s estrogen level to a level that effects the horse’s insulin level? We know estrogen can effect insulin levels.

I find no studies on hose water and horses on Google Scholar. There are so many unanswered questions that it’s maddening for those of us who need answers now to save our laminitic horses. Where are we going to get these answers?