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Archive for the ‘horse research’ Category

Reading through some of my posts it is pretty obvious that I lean towards research topics. I have no scientific background and can’t pronounce most of the terminology used in scientific reports, but my mind tends to always be asking questions and that runs it into the world of research papers. Through scientific endeavors we know a lot more about horses these days then we knew in the past, but there are still an awful lot of topics left on desktops with no funding to initiate.

Research on horses is expensive and most horse studies use a very small population because of the expense. Think about it; it is pretty expensive to have a hundred or more horses around for a research project: land, feed, labor–– Cha-ching, cha-ching. There are also rules that have to be abided by. Most research is done through academic organizations and they have ethics boards on how the animals can be handled or treated and they are very susceptible to lobby groups. So if you wanted to do a study where you tested the reaction of a horse to a tap on the nose by your finger, you might not be able to get that approved. A finger tap could be defined as cruel in some interest group’s vocabulary. And there are things that we, as a society in the West, just won’t tolerate. You can do all sorts of nutrition tests on pigs because pigs are a food source. You test protein and you can put the pig down and necropsy it and look for findings. The pigs life is limited anyway. You can’t really do that with horses, certainly not on a research scale.

Yet, it is through research that we find stuff out, learn to eliminate harmful things and incorporate beneficial things for our animals. Just doing chemistry equations doesn’t really work; if it did we would have an answer to all the world’s diseases. Just play a game of chemical bonds between the bad-guys-disease-makers and the medicines. The pharmaceutical libraries are full of papers on what should happen, but what in fact did not happen.

But now we have the Internet. My son has his extra CPU power harnessed by Stanford for a gnome project, gamers are connecting and creating whole fantasy societies and people are connecting to share ideas around the world. What if we all could share a research project?

I first started thinking about this when I heard a podcast by the Science Times (New York Times) on Moebius Syndrome. A researcher connected into that particular population affected by this syndrome and asked for volunteers to take a survey. She got a really good response. Cornell is doing a study on skeletal variations of the horse and they put ads in horse publications and sent packets to horse owners for measurements. And just this week I received a survey from a Ph.D. candidate doing a project on horse personalities. (You can participate through a link below)

Now putting surveys in the hands of untrained scientists can be a can of worms. But let’s be optimistic and say you could develop a survey that allowed you to detect the outliers and wild cards. Going to the masses might give enough information that would make a follow-up project much more informative and meaningful because you would have already narrowed down a focus through those survey results.

I’ll bet every vet has a few clients in his or her practice that they feel confident in. They are the clients that the vet knows really follow the instructions: the wound is hosed twice a day for 20 minutes-really. The eye drops are put in every three hours around the clock- really. The horse is walked 1 hour a day for 10 days – really. Why couldn’t these individuals be asked to join a “survey army”?  We are talking about basic research, but let’s say you want to do research on horses drinking after work in hot weather. Wouldn’t it be great to get 300 inputs to that question instead of 15? It could be done. Yes, lots of work and effort to come up with a standardization procedure, but think of the payouts. And once a procedure has been developed it can become an industry standard and used throughout. Think of the potential world-wide. There is a lot of information and a lot of variances that could be discovered.

The fact of the matter is that we really are at a point where this is being done by researchers. We just need to expand our horizons and get more equine researchers thinking this way. We can participate in helping to discover the magic that makes up a horse.

If you have 20 minutes why not try your hand at being part of a research army. Rachel Kristiansen at the University of Mississippi is conducting a survey about horse personalities. Take Ms Kristiansen’s survey and become an active member in helping to help your horse.

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David W. Horohov Ph.D., Maxwell Gluck Equine Research Center, University of Kentucky

I love the “wow” factor in associations and reminded myself of that experience when I reviewed the tape I made of Dr. David Horohov at the 2010 Mid-Atlantic Nutrition Conference.

Horohov reminded us of the complexities of disease and the circumstances of fact-finding. He gave a talk on rhodococcus equi, a nasty foal disease, but he wove in stories of HIV, the hygiene theory, and the wire walk of how to jump-start one system while leaving another alone.

Rhodococcus equi (RE) is a disease that plagues foals, usually under 2 months, and is known for its distinctive diarrhea and its production of pneumonia. It has veterinary, time, labor and worry costs associated with it and it can kill. Just like the human population, diarrhea and dehydration go hand in hand and little bodies dehydrate pretty quickly; and if the runs don’t get them the lungs drowning in fluid might. Pneumonia is always serious.

The little bugger that causes this disease is ubiquitous. It is everywhere in the ground. Yup, you too are stepping on RE somewhere on your farm. It’s just like ants, if you don’t have them, chances are nothing around you is breathing, including you.

Some farms are plagued more than others and for years the general direction has been cleanliness is akin to healthiness.

Taking a look at RE the first thing that jumps out is that this everywhere-in-the-air disease doesn’t much affect adults. In fact, it is pretty unusual to have an adult with RE.  Turns out the adult horse population has immunity to this little bugger. So the thinking was that the younger horse population had no immunity. And so the thought went until the medical community identified rhodococcus equi in AIDS patients. Huh? The medical community thought the same thing so they started looking into this. (told you the bug was ubiquitous) Human medicine has funding and the results found in that sector were scooped up by the equine medical community.

It was discovered that the foals had immunity, but the immunity just wasn’t kicking in yet. Their bodies had to be “sensitized” to the bacteria, rather like the act of a vaccine. To take a sentence from Horohov’s extract “While most cellular components of the immune system are present at birth, in many cases these cells can be considered immature or lacking full functional capability.”

How do you get an immune system to “grow-up”? One theory (I always want to make sure that people realize we are talking about the discovery phrase, not the we-know-it-for-sure phase.) is that the immature immune cells grow-up to be productive members of the organism by being challenge. This gives some strong meaning to the aphorism, “What doesn’t kill us makes us stronger.”

How do you sensitize a foal? They actually “challenged” their immune system by bringing them into a less than pristine barn for four hours everyday (with mom). This is a scary thing to say because I always worry how others interpret the statement. The foals were getting good management, nutrition, and the barn didn’t have 3 feet of manure in the stalls with no ventilation. It was just dirty, maybe not all the manure and urine out of the stalls, maybe not all the dirt swept from the aisles.

The findings were that these foals didn’t get the disease at the same rates their pasture counter parts did. A lot more work needs to go into this, a lot more blood pulled, conditions researched, etc. But it took the first step in saying maybe these foals need a little challenge in their life. (Horohov discussed the pivotal immunity thruster, interferon gamma, and how it kicks in, but you need lots of cups of coffee to deal with that story.)

It also makes sense in light of the “hygiene” theory.  Human studies that show kids who aren’t exposed to animals, flora and fauna early on in life are much more susceptible to developing allergies later. I see this in the Icelandic horse population where a horse imported from pristine Iceland has a 30% chance of developing summer eczema (allergy) when it hits the states; yet, the domestic-bred Icelandics don’t show this propensity.

If further research confirms these initial findings and theories, the equine community can look into how to beef up immunity faster. It is there, just start the engine earlier. Is there an intra-nasal spray that can be used, a vaccine, a probiotic to feed? But in interfering with a foal’s immunity system can you end up damaging the immunity that mom has passed on? Questions that won’t be answered for a while. But the first step is taken- knowing a bit more about the little bugger and the system it attacks.

Meanwhile, I am starting to see the value in the adage “ you need to eat a pound of dirt before you’re 12.” There just might be something to that.

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Raymond Geor, BVMS, College of Veterinary Medicine, Michigan State University

Dr. Raymond Geor, a veterinarian and researcher at the College of Veterinarian Medicine at Michigan State University, gave one of the first presentations I heard at the Mid-Atlantic Nutrition Conference.  His talk had big 6-syllable scientific terms- all delivered with the measured pace of a scientist. He packs a lot of information in his talk, and as a layperson I usually come away thinking, “What was he talking about?”

I am fortunate to have a tape recorder to help me keep track of the stuff I miss. The more I listen to his talk, the more I can skate around the moguls of language and studies: And the more I can see the landscape he is describing. There were no bunny slopes in sight; the good doctor took us to the top of the Matterhorn and it was an hour’s speed race the whole way down to the end.

The verbal description of his talk was only two paragraphs long. It stated that there are anecdotal impressions by veterinarians of a relationship between obesity, insulin resistance, equine metabolic syndrome and laminitis. The second paragraph stated Geor would review the current diet and nutrition management for reducing the risk of laminitis in these animals.

ah, the miracles of photoshop

We start with a wee background from last year where Dr. Nicholas Frank gave a presentation that I summarize as “ Obesity in a horse is a good clinical sign that you are courting problems.” This is where Geor picks up and in a nice way says- it has been noted that the observable characteristic of obesity often indicates a predisposition for pasture-induced laminitis in horses. This, then, would be the laminitic phenotype. These horses seem to respond to changes in dietary and environmental conditions differently than other members of their herd.

We were also reminded of the fact that at the heart of laminitis is inflammation that disrupts life in the laminae resulting in its death and, in some cases, severe coffin bone rotation and the demise of the horse as well. Furthermore, there is a pretty good hunch that there is a connection between a pasture-induced laminitis episode and disturbance in the animal’s hind-gut brought on by rapidly fermenting carbohydrates that in some way (death of microbes, toxin release, gut leakage?) causes an inflammatory response in the horse that takes it over the threshold into laminitis.

Currently there are three main theories scientists are working on.

  1. there is an underlying inflammatory condition in these horses and ponies.
  2. Insulin toxcity
  3. A perfect storm of multiple colliding factors

Why would a fat horse or pony be more susceptible to laminitis? Ah-ha. That’s a good question that has no answers. But, there have been some recent discoveries in other species (us humans for one) that merit consideration (and therefore research) for the equine species.

It would seem that fat, once thought of as a simple collection of  storage cells, actually is ALIVE! ( the monster within- I sense a movie in all of this.) Adipose tissue is very metabolically active. It regulates things like pro-inflammatory cytokines, which makes the scientist wonder if the obese horse is in a constant metabolic state of systemic inflammation. If so it would be easy enough to understand why anything that would contribute more inflammation would tip the horse over the laminitic threshold.

Wondering what insulin looks like?

In other species fat seems to have a pretty strong affect on insulin. Interestingly insulin actually has two pathways, one is use (sensitivity) and the other is production. Fat appears to decrease the use of insulin while increasing the production of it with the result that there ends up being a large concentration of insulin in the blood stream (hyperinsulinemia.) That’s a very bad thing for the circulation and results in vaso-constriction: in other words tissue (such as the laminae) starvation and death.

Then there is the perfect storm theory, fat, inflammation, insulin, gut mobility, gut bio-environment, gut motility, gut permeability, forage composition factors other than carbohydrates, genetics, climate, life-style. Whew. Oh, and what about the obese mom that predisposes her foal to metabolic disorders? Happens in humans – could the same be true in horses?

And here’s my own wild card questions. How about how the whole digestion process works in these laminitic phenotypes.  Does their system empty slower or faster than their healthy counterparts? There is always talk of the role of  GI micro-organisms in creating laminitis.

coprophagia: foal eating mom's manure

Well, perhaps the genetic pre-disposition component is the foal eating mom’s bacteria laden feces.Mom could have “laminitis-making-bacteria” in her GI track. Maybe it’s not a gene, maybe it’s being in a stall with predisposed, obese, laminitic mom and the foal’s natural and needed coprophagia.

So many of these conditions are tightly intertwined that it will be a galactic challenge to investigate. And, of course, there is very little money to support this research.

I have an insulin resistant horse and another overweight pony. After listening to Geor’s presentation I renewed my efforts to reduce their weight as I have seen and heard the devastation of laminitis.

And, personally, I’m going on a diet lest I become even more inflammatory in my remarks.

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new research on livestock nutrition

One of my annual March sojourns is to partake of the Mid-Atlantic Nutrition Conference. I come away filled with adrenaline and excitement: my brain neurons firing away at all the paths those little research tidbits lead me down. None of my conjectures  have any scientific backing, but they are still worth a moment  or two of wonder. I noticed some interesting directions from the conference this year.

It might help for you to understand what this conference is all about–– livestock nutrition. Primarily dairy cattle, poultry and equine. This is where the academic researchers, feed mills, veterinarians and large livestock producers go to find out what are the newest research studies and theories on animal nutrition. You are not going to get razzle-dazzle slides here; you are going to get charts and ugly photos. But you walk out with a good sense of what isn’t known, what needs to be studied and a few sentences of something that has finally been proven.

It always reminds me the road to knowledge is a long one and that the body is blessedly complex.  I hope to post a number of entries over the next several weeks on specific topics covered at the conference along with my thoughts and questions. But for now I am still cogitating on a number of overall directions and impressions from my time in Maryland.

  • There was a new word thrown around quite liberally phenotype. Phenotype refers to the OBSERVABLE characteristics of an organism that has resulted from the interaction of its genotype and environment. It is an old word, but is being picked up and used more regularly in the scientific community. One might say that I am a phenotype for heart attacks; I have a chicken physique. (we’re using silly examples here, folks.) All fat lands in a plumb Buddha belly with nary an ounce going into my legs or butt. Observable characteristics are the belly fat. My mother and father had the same structure. This predisposition is most likely a genetic code of where my family line should store fat. Environment characteristics are the incessant putting of a full fork into my mouth. And now we have research to show that belly fat is hormonally active and a leading cause of heart attack. So I could stand as a phenotype for humans courting heart attacks. Or I could be a fat horse and the phenotype for laminitis.

There was a lot of discussion of the laminitic, IR and obese horse phenotype.

  • I think this word is being used more often because of another trend- the researchers are looking really small. Better technology has helped here as well as directions in human medicine. And in looking really small they are finding that the organism is REALLY connected. A cure for laminitis isn’t going to come by just looking at the inflammation of the feet. That is a sign, but now they are realizing that there are a lot of things on the cellular level that might cause inflammation in a body structure that might send hormone signals to other parts of the body that might start another cascade of seemingly unrelated events that end up in the feet. In looking really small, researchers are broadening their horizons.
  • Researchers are starting to whisper in the hallways about the failures. No one studies the failures in a research project. Part of that is due to the “system” of publishing papers where talking about failures is likely to result in a failure of the paper to get published. One of the speakers mentioned that in a clinically induced challenge of horses with genetic predispositions for laminitis, 20% of them never get laminitis. Their results are left in the paper trail that hits the circular file. Yet, this researcher had the strength to pause and say, folks someone should study these failures- what have they got in their systems that the other horses don’t have. (Please remember a failure is what does not prove the hypothesis. So if the hypothesis is that lush green grass will produce laminitis and these predisposed horses didn’t get it. Well, they “failed” in that they did not prove the point where as the other 80% did get it and proved the hypothesis.- Okay, okay- it’s a very simplistic explanation to help get across a very complex point.)

I’m not a scientist, but I find this thrilling stuff.  Finally the research industry is connecting the smaller dots that make up the larger ones. I also find it overwhelming- the amount we now know we don’t know. Dr. Raymond Goer from the University of Michigan School of Veterinary Medicine said it nicely,

“I know a lot less than I did a year ago. And I know a whole lot less than I knew two years ago.”

We are having to step back to go forward, but it is putting us on a better path.

Oh, and that word “phenotype” bet you see it everywhere now.


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Viewing where the horses go

The holidays are here and, in New Jersey, the festivities are going to be heralded with cold and snow. Relatives in the South assure me that “normal” has stopped for them as well. Most riding activities consist of a carrot and a promise, if there is a visit to the barn at all.

Come January 2, a line of horse trailers starts to form at the Delaware Memorial Bridge; the Northeast portal to highways leading to Aiken, Southern Pines, Ocala, and Wellington. Last year that line was identifiably smaller and a fair number of Southern horse shows, dependent on the snow-birds, were canceled. I am wondering what this year will be like. Friends who have played in the Southern winter circuits calculate it runs them about 10 grand a month- travel, training, board, turnout, grooms, show fees, their own housing and amusement.

What interests me in this disruption of the annual trek south is the soundness issue of show horses. I wish the AAEP would run a survey or study on this matter. Here is what I suspect- sounder horses next spring in the North.

It is only 20 years ago that winter in the North meant trail riding in the snow or three months of R & R for the horses. Whatever the choice it was slow work. The landscape saw only a few indoor rings. The ground being frozen, people just walked their horses undersaddle on sunlit days and left the animals to their own games in the field the rest of the time.

hanging out with friends

Rest is the operative word here. I had an opportunity to listen to some of the nations leading equine leg surgeons. They all stated, the number one cause for an unsuccessful surgery is lack of time to heal. The horse is a performance animal and everyone wants it back in work ASAP. Being an animal whose survival depends on flight, horses may get a quick, low-level of heal. Enough to get them out of the cougar’s path. But everything is knitted together with bailing twine at that point and the breakdown comes faster and harder or the top performance never comes at all if the horse is put back into serious work at this stage.

There is also the question of what structures  are compromised that we are unaware of and heading for a catastrophic breakdown with no rest. And what about the sour attitudes and vices that appear with all work and no play. Surely there has been 12 month show schedules for centuries in warm climates- but I’m talking about a Northern life cycle, here. But it does beg the question of comparison studies in soundness issues of horses in no-rest warm regions and imposed time off in frigid climates.

winter grazing

Offer a cup of coffee to your older vet (someone who has seen the half-a-century mark) and start a conversation of equine R & R. He/She will probably concur: limbs, backs and minds healed during the winter solstice. Even now, some older vets might confide to you that many leg injuries and ailments just need time. You may think it was the last shock-wave session that healed the injury, but, in fact, that session occurred at the injury’s six-month anniversary, a time frame it would have healed on its own anyway.

Before the 12-month show season your farrier would tell you to treat the thrush, but not to worry, standing in the winter snows would clear it up. It would help the foot bruise, the crabby attitude, the tense muscles, sensitivity to touch, girth sores, saddle hot spots. There might be a lot of mud and dirt on the animals, but skin afflictions due to constant washing and stripping of natural oils wasn’t on the vet’s treatment list during this solstice.

Smokin Mokes having some winter fun

This is not a diatribe against showing. Just some assurances to those staying home, that the time really isn’t lost or wasted if they let their horses rest and have some snow time. They might have sounder, happier horses to perform in the spring. The only way to know would be to do a study- now who’s going to pay for that?

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Earlier this week I attended the Rutgers Equine Science Update and got a peek into some of the research they are doing on horses. I have to hand these people a lot of credit for exposing themselves before a research project is complete. They are one of the few groups I know who really do try to be transparent, to use a word-of-the-moment.

The Equine Science Center looks at ways to prevent disease, as opposed to a veterinary hospital, which researches ways of treating and curing a disease. Throughout the years I’ve seen the Center produce some valuable information, and since they discuss the projects while “in progress” it gives the layperson, like myself, a better in-sight as to the complexity of research. A while back they did some research on the efficacy of supplements for joint pain. It took them a year to identify specific blood markers that would accurately predict joint inflammation.

Then they spent considerable time on sourcing specific ingredients in their pure form. After all, you may think it’s the yogurt in your daily dose of strawberry yogurt that makes you break out, when in fact, it may be the strawberries! Same with a supplement, you want to test the active ingredient by itself to eliminate the possibility that it really is the alfalfa meal that is providing all the benefit.

No wonder some medical cures take so long to come about.

So I was intrigued by one of the research studies the Center is sponsoring. Dr. Janet Onishi is actually a plant biologist with a pharmaceutical background. Doesn’t know a thing about horses and I wonder how she came out of the woodwork. How she came upon laminitis as an equine pathology and why it peeked her curiosity remains a mystery to me.

Janet Onishi, Mike Fannell, Dr. Michael Fugaro

Her interest is in the chronic laminitic situation. Chronic laminitis differs from the acute form in that the horse is never really free form it. The disease continually flares up in the horse’s life. An acute case can turn chronic, but many acute cases are one time events, are treated and the horse remains free from it afterward.

She also approached the question in a different light. The traditional thinking on causes of laminitis involve a carbohydrate overload killing-off bacteria and creating endotoxins, which churn up inflammation with a result of  laminitis in the hoof. Endotoxins are a structural component of the wall of gram-negative bacteria and are only released when the bacteria die.  What caused a big ‘Hmmm” from Onishi is that injecting the endotoxins directly in the horses blood stream does not create the same scenario. In fact, injecting these endotoxins in the blood stream doesn’t cause any laminitic conditions at all.

Coming from the outside, Onishi had no preconceived notions about the disease and her ponderings gave her wings. Looking at human literature she found evidence that microbes (bacteria) can cross out of the gastro-intestinal track into the lymph system and from there cross into the blood stream and have full access to the body. So she had a thought “What if the microbes were playing a different role in the disease then we imagined? Perhaps it is not the products of the microbes that are causing the problem, but the bacteria itself.”

So she got initiated into the world of animal research protocol, ethics and oversight and is working closely with area veterinarians on a current study. She has some initial findings that are showing there might be merit in her hypothesis. Lamina taken from horses who were euthanized due to causes other than laminitis had no, or very minute, bacteria counts in their hoof lamina. Horses euthanized due to chronic laminitis had significantly high bacterial counts in their hoof lamina.

There are over 77,000 horses suffering from chronic laminitis in the U.S. and I suspect there are an equal number of horse owners who are praying for a way to prevent or control this havoc in the lives of their animals.

The study has just started and even if the results prove the hypothesis, there is still the question of identifying the bacteria, what causes the movement, and how do you affect or interrupt the cascade. But, I find this project replicates one of the purposes of this blog. Talking to people in different mind-sets, careers, and experiences; crossing sectors of science, art, and sociology; going away from horses to bring back to them the best thoughts from other sectors, and not being afraid to say,  “I wonder, what would happen if…”

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Mares are looking at the stallion, looking at the dog, and we're looking at the dog, not what's about to happen

Mares are looking at the stallion, looking at the dog, and we're looking at the dog, not what's about to happen

We see a scene and then we focus on a specific element and miss some really important stuff. I took my dog to a trainer and at one point, while the dog was barking hysterically, and I was focused on calming her down, the trainer pointed out that the dog was afraid, “Look at the ear position and her eyes are dilated.” Her eyes were dilated! I missed all that; turns out it’s really important.

Same with my horses. I can sense they are getting tense before an explosion comes, but then my focus goes to control and calming and I miss all the other body signals and instigations.

Inside of a Dog by Alexandra Horowitz

Inside of a Dog by Alexandra Horowitz

So it made me take an afternoon in thought when I read in the doggy book, Inside Of A Dog, by Alexandra Horowitz, about eyes. (it’s a really interesting book if  you’re into your dogs.) It seems, on a cellular level, rods and cones in the retina take up the “picture” of the world and send that to the brain. But then the cell has to get rid of that picture and take up the “new” picture in front of it, otherwise our view would never change. The cell refreshes on routine, not just when something in the picture has changed and this takes time. A miniscule amount of time, but time just the same. Horowitz called this the “Flicker-fusion” rate although I’m betting there is some other super long scientific name we can’t pronounce. The book, after all, was written for real folks, not the scientific community.

Well, the flicker-fusion rate is different for different animals. Humans have a F-F rate of around 60 refreshes or flickers per second. I’m betting the superstar ball catcher may actually have a higher flicker-fusion rate, but now I’m wandering again. Dogs have a F-F rate of about 70-80 refreshes or pictures in a second. That doesn’t mean they will see more detail, but they will see movement faster. Hence, frisbee champions.  Apparently, the canine eye also refreshes fast enough to see the individual frames in the TV video instead of a smooth flow and this might explain their disinterest in watching Lassie. If your dog loves Rin-Tin-Tin then you might wonder if Poochie has a slower F-F rate than its litter-mates.

But you’re interested in horses. Well, so am I. And the flicker-fusion rate made me wonder about horses. What is their refresh rate and how does it affect what we do in their environment and what they see?

Turns out, I checked with a nationally known equine ophthalmologist, the horse’s flicker-fusion rate hasn’t been studied. It is assumed it’s probably similar to a dogs. I’m betting it’s even higher because they are prey and susceptible to minute movements.

Doesn’t it make you pause to think about the florescent light flicker? We seem to be aware of it on a subconscious level because it is almost identical to the human flicker-fusion rate. Those office headaches are often attributed to the florescent light flicker. The horse probably sees the light as a real ANNOYING flicker. If we have a stressed animal in a barn, do we ever think about the flicker effect of the lights? How about those fans? Bet fans are like a strobe light to horses. Some adapt, but that one guy who stays in the corner, turns away, etc, could it be to get away from the fan?

How many times do we wonder why the horse acts the way it does and we can’t see any reason. Maybe the reason we can’t see is because we have a slower F-F rate and we don’t see the movement the horse does. Is the trickle of water that looks like a stream to us a series of individual dots to the horse?

a stream or droplets- depends on the flicker-fusion rate

a stream or droplets- depends on the flicker-fusion rate

I’ll certainly be looking at my horse through a new set of eyes in the future. I wonder if his eyes dilate when he becomes afraid, and would I ever be able to see that?

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