Upcoming classes: Dogs! Brains! Hormones!

I have two new courses being offered online with the APDT that I’m really looking forward to teaching:

• Canine Hormones: from molecules to behavior, February 3 - March 11, 2015 (12 CEUs).  Hormones — those chemicals that float around the body to pass messages between different organs — have a lot to do with behavior. What exactly is a hormone? How do hormones pass messages around? What is the stress response, how does it work, and what does it tell us about a dog's stress levels? What about reproductive hormones like estrogen and testosterone — how do they affect behavior?

• The Canine Brain: from neurons to behavior, March 4 - 24, 2015 (12 CEUs). The brain is an incredibly complicated organ, but it’s also incredibly interesting. What do we know about the parts of the brain and which ones affect the kinds of behaviors we care about in dogs (like fear and aggression)? What kind of cells make up the brain and how do they work? When a dog is learning, what is actually changing in the brain?

Both of these classes are intended to have something to offer both for students with very little science background and those with more extensive background — all the way from “what's a hormone?” and “what's a neuron?” to “I know oxytocin is the ’cuddle hormone’ but I hear there’s more to it than that.” If you are wondering if one of these classes is right for you, comment here or email me directly and I’ll help you figure it out, but I am working hard to make sure there is something for everyone.

Most of my audience is usually dog trainers who are looking for continuing education credits, but I love getting interested dog lovers in these classes as well, and there’s a lower cost audit option for you guys.

These classes tend to be quite discussion-heavy — the best part for me is getting to talk directly with you guys and answer the questions you have about this stuff that I hadn’t thought of talking about. It is your chance to have a dog behavior researcher at your beck and call, answering your questions!

For those who just want to read stuff on this blog, note that I’ll be writing and posting most of the course materials here over the next few weeks, so keep an eye out for that.

Hope to see you there!

Dog brains!

The history of dog breeds: Victorians, genetics, and the importance of diversity

Note: there is an interview with me at the Huffington Post about this story.

Dog breeds are amazing creations. I can own a series of Golden Retrievers and predict with fair accuracy how each of them will look and act. (Look more than act, but the incredible variety of dog personalities is a story for another day.) Unfortunately, I can also predict with fair accuracy what diseases each of those dogs will have, because with the Golden looks and personality come the Golden genetic disorders. As a new dog owner years ago, I thought of these genetic problems as part of the package I was handed when I got a purebred dog: you choose the looks and personality, and you choose the diseases at the same time. But there’s a lot more to the story of how dog breeds came to be saddled with particular genetic disorders than just happenstance: we made choices when we created breeds and we continue to make choices about their health today.

Figure from: Genome-wide SNP and haplotype analyses reveal a rich history underlying dog domestication Nature, Vol. 464, No. 7290. (17 March 2010), pp. 898-902, doi:10.1038/nature08837 by Bridgett M. vonHoldt, John P. Pollinger, Kirk E. Lohmueller, et al.

The beginning of dog breeds
Humans have been breeding dogs for thousands of years, but for most of our history with them, function was more important than appearance. Dogs were bred to work, and beauty was a side effect: long coats were for keeping warm, small size was for chasing tunneling vermin, long legs were for speed.

During the Victorian era, things changed, with the spectacular growth of dog fancy. Suddenly people were breeding and showing dogs for how they looked, not how they worked. Breeds were no longer loose groups of dogs who looked kind of similar and did a particular job; now for the first time purebred dogs had carefully maintained pedigrees. This was the era when the breed books closed, meaning that breeds were suddenly defined as the set of dogs whose ancestors belonged to a select list. If you wanted to make more Golden Retrievers, you could only breed dogs descended from that original list. If you bred in dogs with unknown ancestry, their offspring were considered mutts and could not be competitively shown, even if they looked just like purebreds.

What happens when you take a relatively small set of dogs and use them to breed a much larger number of dogs? It’s like this small set of dogs is marooned on a desert island with no way to bring in new genetic diversity, and their pedigrees are what marooned them. Their descendants will look like them and act like them – and have their genetic diseases. The genetics from those few founders are all that's available to the descendants. When this reduced genetic diversity is severe, it can be a big problem.

Basenjis and Fanconi syndrome
Reduced genetic diversity is severe in the Basenji breed. This breed originated in Africa, but only the Basenjis descended from a small number of dogs imported to Europe in the 1930s are considered purebred. The diversity in this breed was so low in Basenjis in the Western world that in 1990, one in ten Basenjis suffered from exactly the same genetic disorder, a kidney disease called Fanconi syndrome. One or a few of the founding dogs must have had this disease, and it was passed on to their descendants until a large percentage of Basenjis suffered from it.

The solution: bring in new Basenjis from Africa, breed them to the Western Basenjis, and declare that their offspring may be considered purebred, despite a lack of pedigree.  This was done in 1990 and again in 2013, and the effects are still spreading through the Western Basenji population over several generations. (You can read about the trip to the Congo to acquire African Basenjis.)

Dalmatians and urinary tract stones
But what if there isn't an ancestral population waiting to be harvested? Dalmatians also suffer from a genetic kidney disease, in their case stones in their urinary tract caused by high levels of uric acid. It's a painful disease and there was no way to breed out of it: at one point, every single Dalmatian in existence had uric acid levels above normal canine values.

The solution? The Dalmatian Backcross Project, which began in 1973 with the breeding of a Dalmatian to a Pointer. The project husbanded along a line of Low Uric Acid (LUA) Dalmatians, also known as Normal Uric Acid Dalmatians, because what's low in a Dalmatian is normal in any other breed. Puppies from this original Dalmatian/Pointer cross were tested for uric acid levels, and those with normal levels were bred to purebred Dalmatians. This continued generation after generation until a line of Dalmatians had been bred which looked like Dalmatians, not Pointers, but had normal uric acid levels. As of 2011, LUA Dalmatians have been registered with the American Kennel Club and are now considered purebred Dalmatians. It remains to be seen how long the problem of high uric acid levels will remain common in this breed, but at least now there’s a solution in sight.

What we're doing about genetic health in dog breeds
With these success stories, you’d think the problem would be solved. But these are the only two breeds so far to open their breed books to bring in new genetic diversity. [ETA: readers note that a few other breeds have opened their books, including Border collies, Chinooks, Salukis, and Azawakh in the US, and several breeds in Europe. Fantastic!] Both the Dalmatian and the Basenji had easy to diagnose, easy to understand health problems that were also easy to identify with genetic testing: problems controlled by a single gene. Such diseases are relatively unusual. Take the case of the Golden Retriever, who is prone to developing cancer at greatly accelerated rates compared to most other breeds. Cancer is controlled by a lot of genes and is very hard to genetically test for – and therefore hard to breed away from.

While introducing new genetics into Golden Retrievers is very likely to improve the health of the breed, it’s hard to convince breeders to take the leap. As was the case with the Dalmatian Backcross Project, such an undertaking would mean producing dogs that didn't look like Goldens for a few generations. They could still make great pets, but they couldn’t be shown and they probably couldn't be sold for as much money as a purebred. And there’s no guarantee that their descendants could ever be registered as purebreds – the fight to get LUA Dalmatians accepted was long and hard. I use Goldens as an example because I live with one, but many of the breeds we love suffer from low genetic diversity and associated genetic health concerns.

I believe we need as a society to get past our obsession with historical breeds. We can breed for appearance, but that has to take a back seat to breeding for health. We have a model with the Dalmatian Backcross Project. All we need is the will to improve the genetic health of more breeds.

Jack the Pumpkin King, my 14 year old Golden Retriever. He has so far only developed a small tumor, which was easily removed. However, he suffers from skin allergies and epilepsy, both genetic disorders.

Testing behavioral assessment

My Bark article, Testing the Tests, is now available on the web for free. I did a lot of background reading for this story and I learned a lot of interesting stuff about shelter behavioral assessments: how they're designed, how to evaluate whether they work, and new work that's going into improving them. Check it out!

How antidepressants work: the good parts version

[Author’s note: Please consider my last post, How do antidepressants work (in dogs and the rest of us)?, to be the director’s cut of this topic: fairly long and juicy, with some bits in which I indulge my inner geek and perhaps go into more detail than is truly necessary. This, then, is the good parts version: the same material, but presented as an overview from a higher altitude, with fewer details and assuming less scientific knowledge. These posts are both intended as material for my upcoming online class with APDT, and I want to make sure students of all levels of science background are covered. Also, it’s good for me to take a step back from time to time and remember that not everyone wants to know every gory detail about this brain stuff.]

We don’t fully understand what causes depression in humans, and we don’t fully understand how the medications we use to treat depression work. We do know that those medications work well in dogs just as they do in us. In dogs, however, they are more often used to treat fearfulness or aggression. We know that antidepressants generally take effect only after several weeks of constant use, and that they work much better if they are paired with behavior modification training in dogs or therapy in humans. And we actually do know enough about how they work to take a guess at why that's true.

You can buy your very own Prozac bone sticker!

Depression in humans and fearfulness and aggression in dogs are related to stress: something in our lives that we can't control and can’t quite adjust to. In humans, that might be extended unemployment or long term caretaking for a sick family member. In dogs, it can be the inability to control who comes to visit your house (that terrifying mailman) or perhaps a lack of understanding of the big scary world (for undersocialized dogs).

Sometimes training or therapy aren’t enough to help us deal with these problems; some problems are too hard for our brains to cope with on their own. Antidepressants seem to help our brains adapt, however. A part of the brain deeply involved in learning and memory, the hippocampus, tends to be smaller in people who are depressed and tends to get larger again when they take antidepressants. This change may be associated with an improved ability to make new mental connections.

So that’s why antidepressants take weeks to take effect: that part of the brain is growing and changing, which doesn’t happen after just one pill. And that may also be why antidepressants work so much better in the context of training or therapy. It’s nice for your brain to be more able to learn new ways of coping with a difficult world, but the ability to learn is not the same as actual learning. To learn, you have to get out there and do: talk through your problems and find the way to feel differently about them and take new approaches to solutions if you’re a human, or get to practice new ways of interacting with the mailman if you’re a dog.

The take home message for dog owners? Don’t expect your dog to respond to antidepressants immediately; it will take a few weeks. And don’t expect your dog to respond without behavior modification. Antidepressants aren’t magic bullets and they won’t fix the problem on their own. But they will make it easier for all the training you do to take effect.

How do antidepressants work (in dogs and the rest of us)?

There are plenty of humans and dogs on antidepressants, and we believe that the mechanisms of these medications are much the same in both human and dog brains. But despite the fact that these are widely used medications, we aren’t completely clear how they work. Yes, this is going to be another post in which I ask a question and then don’t really tell you the answer. But I’ll tell you what we do know.

You can buy your very own Prozac bone sticker!

What is depression?

There are probably many different kinds of depression, so that the disease is slightly different in many (or all) people and dogs. As a result, getting a handle on the mechanisms of depression and its treatments is difficult. So studies about depression and antidepressants have to speak in generalities, such as “this is true for 50% of people with depression.”

In general, then, depression is triggered by chronic stress, which results in increased levels of stress hormones. The major stress hormone in humans and dogs is cortisol, so that’s the term I’ll use in this post. The major stress hormone in mice and rats is the closely-related corticosterone, so if you delve into more of the research in this area, you may find that hormone mentioned as well. It’s basically the same as cortisol. Note that while I’ll talk about depression in this post, in dogs we more commonly perceive stress-related problems as behavior problems, such as shyness or aggression. These problems, in certain cases, can be very successfully treated with antidepressants in combination with training.

Depression and the hippocampus

The area of the brain which is the most sensitive to increased levels of cortisol is the hippocampus, a part of the limbic system which is involved in learning, memory, and emotion. The cells of the hippocampus are armed with little widgets called glucocorticoid receptors, or GR, which grab cortisol molecules as they float by. Once a GR has attached itself to some cortisol, it becomes active, and takes itself over to the cell’s DNA. Here it tells the cell to activate some genes and deactivate other genes. This is how cortisol effects stress-related changes in our body: by telling the massive recipe-book inside our cells which genes to cook up and which ones to leave idle.

Image courtesy of Wikipedia

So the first generality about depression is that it results in more cortisol than normal. The second generality is that it also results in a smaller hippocampus than normal. We can guess, though we’re not sure, that this is somehow related to all that GR activation. We know that in depression, fewer new neurons are born in the hippocampus, so that is probably part of the answer. However, it’s not the whole answer, because even in healthy people, new neurons are created at a very low rate, not fast enough to explain this decrease in size of the hippocampus. Another possibility is that the shape of individual neurons changes. Neurons branch out like trees to touch lots of other neurons, and the neurons of depressed people have fewer branches. So the problem could be caused by fewer neurons, or by neurons that have fewer branches and therefore less communication with other neurons. We’re not sure which, but either way, the changes are significant.

Antidepressants and the GR

Antidepressants affect many substances in the brain (most famously, the class of antidepressants of which Prozac is a member affect serotonin levels). We have trouble picking out cause and effect here. We assume that antidepressants aren’t affecting all of these substances directly; we assume that some of these affects are indirect, in other words, side effects. We’d like to know which substances antidepressants directly affect in the brain, in other words, what their mechanisms are, but we’re still not sure.

We do know that they affect the GR, though we don’t know if they do so directly or indirectly. So far, we haven’t found any direct effects on the GR. One theory is that antidepressants affect another widget, one which pumps cortisol out of cells so that the GR can’t grab it and become active. The decrease in number of active GR, then, causes the changes in the brain which result in mood improvement.

We do know that depressed people on antidepressants start to have increased birth of new neurons in their hippocampus, which itself increases in size. Why does this affect mood? We don’t know, but we can hypothesize that improved ability to make new mental connections and learn is at the heart of the change. This helps us understand why antidepressants typically take several weeks to work: our brains are changing, growing, and that takes time.

Antidepressants and dogs
 
As usual, all the research on how this stuff works was done in rats, mice, and humans. But we do think that the mechanisms are similar in dogs, and indeed in most or all mammals. Many dogs are on antidepressants with positive effects, including my shy dog Jenny, who receives both buspirone and lots of counter-conditioning. As research continues to get us more answers about how these medications actually work in the brain, we will do better and better at understanding which kinds of antidepressants are better for which individuals, when to start them, and when to stop them.



Anacker C., Livia A. Carvalho & Carmine M. Pariante (2011). The glucocorticoid receptor: Pivot of depression and of antidepressant treatment?, Psychoneuroendocrinology, 36 (3) 415-425. DOI: http://dx.doi.org/10.1016/j.psyneuen.2010.03.007

For further reading, check out related posts by Scicurious:

• If low serotonin levels aren't responsible for depression, what is?
• Stress and antidepressants: by their powers combined

Can prenatal stress be reversed?

I was scanning the titles of new journal articles a while back, and came across one that made me think, hey, that may be about rats, but it is totally relevant to dogs. And then I thought, why don’t I teach a class on it? Read and interpret this really interesting journal article with a group of dog trainers and dog lovers?

I will be teaching the class Prenatal Stress and Anti-Depressants for APDT the week of November 18 (and you are invited to take it). This post will be used as reading material for it. In the class, we will talk about this article and what conclusions we can draw from it and apply to dogs. So I may not draw as many the conclusions for you in this post as I usually do; the plan is for the students to do that together in class. But it was a fascinating paper and there’s lots of good material in it, so read on if you want a conclusion-free summary of it!

Pereira-Figueiredo I., Juan Carro, Orlando Castellano & Dolores E. Lopez (2014). The effects of sertraline administration from adolescence to adulthood on physiological and emotional development in prenatally stressed rats of both sexes, Frontiers in Behavioral Neuroscience, 8 DOI: http://dx.doi.org/10.3389/fnbeh.2014.00260


Why prenatal stress?
So what’s prenatal stress and why is it important to dogs? The authors of the article don’t provide much background on this phenomenon, but it’s an interesting one: when a mammal undergoes unusually high stress during her pregnancy, the personality of her offspring can be affected. We believe that the stress hormones rising in her bloodstream can pass through her placenta to the fetus or fetuses, and can change how their brains develop at this very early stage of life. That’s prenatal stress: stress experienced before birth.

Part of what this paper investigates is exactly how prenatal stress affects the developing personality, because we don’t yet fully understand how this stuff works. In general, though, we expect prenatally stressed animals to be more anxious and less confident than animals who were not prenatally stressed.

Does prenatal stress affect dogs? We don’t know for sure, but we think it is something that can affect most or all mammals. Would it happen commonly? Hard to say, but I imagine a pregnant dog who is stray or in a shelter and highly stressed, and I wonder what effects this might have on her puppies.

What can you do about it?
If you have a puppy that you believe was prenatally stressed and whose personality you thought was adversely affected, what are your options? Careful socialization and good enrichment are always an excellent choice, but in some cases you might consider medication. This study looks at whether a particular anti-depressant, sertraline, might help change the individual’s personality long-term if given in adolescence. Sertraline is an SSRI, in the same class of medications as Prozac. These are widely used medications believed to be fairly safe, but one of the questions these researchers ask is whether it is safe when given throughout an animal’s entire adolescence.

SSRIs such as sertraline affect the levels of serotonin in your brain. Serotonin is a chemical which affects mood; depressed people tend to have less of it, as do aggressive people. As a result, it is the target of a fair number of anti-depressants, which work to increase its levels. Prenatal stress is known to disrupt the serotonin system in the brain, so a medication which affects serotonin is a reasonable choice for prenatally stressed individuals.

So the idea is: give these prenatally stressed animals a medication which increases their serotonin levels while they are adolescents and their brains are still developing. The hope is that they will develop into more normal adults than they would have without the medication. So, exactly how do you investigate such a question?

Methods: how the study worked
First, the researchers stressed some pregnant rats by putting them in clear tubes to restrain them, and shining bright light on them. This was repeated for forty-five minutes at a time, three times a day. They also kept control rats, who were not stressed during their pregnancy. The pups born to these two sets of rats were then in two categories: prenatally stressed pups and non-stressed pups.

The rat pups began their anti-depressant treatment with sertraline when they were one month old. Now there were four groups of rat pups:

prenatal stress anti-depressants	prenatal stress no anti-depressants
no prenatal stress anti-depressants	no prenatal stress no anti-depressants

Having these four groups allowed the researchers to pick apart the two different effects, the effect of prenatal stress and the effect of anti-depressants during adolescence.

The pups were tested at two months of age, the beginning of rat adolescence, to see if the prenatal stress had affected their personalities. They were assessed for how they dealt with startling noises and being exposed to open space (scary for a rat!). Their blood was also tested to see how their immune systems were developing, because immune systems develop differently in animals who have been subjected to high stress. All these tests were run again one month later, at the end of rat adolescence, to see how the anti-depressant given throughout adolescence had affected treated rats compared to the control groups.

Results: what they found

• Although we may think of prenatal stress as mostly affecting an animal’s behavior, it’s been shown to also affect metabolism, so this study looked at birth weight. Interestingly, prenatal stress only reduced the birth weight of the female rat pups, not the males. The weights of these females had equalized compared to non-stressed pups by weaning age. After weaning, though, the prenatally stressed females continued to gain weight and ended up heavier as adults than the non-stressed females. When prenatally stressed females were given the anti-depressant sertraline, however, this weight difference was reduced.
• The pups were also tested for their startle response when they heard a sudden sound. Prenatally stressed rat pups did seem to have a larger startle amplitude (size) compared to controls, but this wasn’t statistically significant, and was not reversed by sertraline treatment.
• Prenatally stressed females did not habituate to the startling sound after several exposures as well as rats from other groups did; treatment with sertraline reversed this effect.
• The pups’ behavior in an open space was tested. No difference was seen between prenatally stressed and non-stressed pups, except in males on their first time being tested (not on later tests).
• In the open space test, only non-stressed females explored more (became more confident) on repeated testing; males and prenatally stressed females did not become more confident with repeated exposure to the open space.
• The pre-natally stressed rats showed a significant decrease in their number of white blood cells. This change was reversed when they were treated with sertraline.

Discussion: what does it all mean?
The study’s main conclusions are that effects of prenatal stress can be seen in rats, and that giving sertraline during adolescence did not harm them.

The rapid weight gain in the pre-natally stressed females is an effect that’s been seen before, and seen in humans. Children born with low birth weights often grow to have issues with their weight and can suffer from diseases related to a poorly regulated metabolism. This loss of control of energy balance has been associated with dysregulation of serotonin in humans, adding additional support to the choice of sertraline, an anti-depressant which interacts with the serotonin system.

It is interesting that no anxiety-like behavioral changes were seen in the prenatally stressed rats. Prenatal stress is known to cause anxious personalities in many cases. However, these rats were as confident (or as anxious!) in the open space test as rats who had not been prenatally stressed. The researchers comment that this particular test has been done on prenatally stressed rats in other studies, and that those rats didn’t show anxiety in the open space test either, so this does seem to be a real result, rather than a statistical error.

They did see some differences, though. Male rats who had been prenatally stressed did show some additional reluctance to explore (i.e. anxiety) on their first day only in the open space test. After that they explored equal amounts compared to other groups.

The researchers also note that while most of the rats that they tested were equally anxious on all days that they were tested in the open space, females who had not been prenatally stressed appeared to begin to explore more on repeated tests, as if they were learning to be less anxious as their surroundings became more familiar. This was not the case in male rats or in rats who had been pre-natally stressed.

Remember also that female rats who were prenatally stressed did not habituate to startling sounds as well as rats from other groups. Is it possible that with this particular model of prenatal stress, the personality effects of prenatal stress appear not as classical anxiety, but as difficulty habituating to new situations or stressors such as loud noises?

Finally, the researchers looked at effects of pre-natal stress on the immune system, and found significant effects (decreased numbers of white blood cells) which were reversed by treatment with the anti-depressant sertraline. Why did they care about the immune system? Because the immune system and the stress system are closely intertwined. Stressed animals show changes in the numbers of their white blood cells just as the prenatally stressed rats did. The researchers were using the changes in the immune system as markers for changes in the stress system.

There are two possibilities for why these prenatally rats showed stress-associated changes in their immune systems: either because they themselves had high stress levels, or because their immune systems were developing prenatally (in utero) in a high stress environment due to their mother’s stress levels. Either way, it is interesting that treatment with sertraline reversed these effects, suggesting that it may have either changed current stress levels in these adolescent rats (even though the only serious stressors they had undergone were before their birth!), or had counteracted other effects from that prenatal stressor.


Conclusions
It can be hard to know exactly what conclusions to draw from a scientific paper. What do you think? What are the most important findings in this paper (maybe just two or three of them)? Do you think those findings are real phenomena, or maybe just statistical mistakes? If they’re real, do you think they can be extrapolated from rats to humans or dogs?

Domestication and human evolution, streaming!

Domesticated humans, domesticated canids, domesticated finches! The Center for Academic Training & Research in Anthropogeny held a conference on domestication and human evolution, and live streamed it. I watched live, refusing to speak to my husband or dogs during it, which didn’t go over well. You, however, can watch the archive on YouTube.

The conference was a series of short talks from researchers. These included:

Robert Wayne, “The transformation of wolf to dog: history, traits, and genetics”

Wayne’s lab published a recent genetics paper on exactly where the dog was domesticated, and in this talk he stepped us through their findings. Previous work (and there has been plenty of it) on the location of dog domestication has begun with the assumption that dogs evolved from a population of wolves which still exists basically unchanged, inhabiting the same range now as it did then. Previous work has suggested that this occurred in Asia or the Middle East. Wayne’s group argues that the population of wolves which gave rise to dogs no longer exists, but lived in Europe about 20,000 years ago. It’s a different perspective on a question which is very difficult to answer, because dogs continue to interbreed with wolves so freely that these genetic studies are awfully hard to interpret.

Anna Kukekova, “Fox domestication and the genetics of complex behaviors”

This talk came out of the lab where I work and I got to see my own name on the list of contributors at the end of the talk. Kukekova gave an overview of the history of the fox domestication project, in which lines of foxes were selectively bred for tame temperament or aggressive temperament, and recent research. Our lab digs in to the question of what it is in the genetics of the tame foxes that makes their personalities so different from those of conventional farm foxes. Since this conference was about domestication, and the tame foxes are the best known and longest running domestication study, speakers returned to the foxes throughout their talks. They are a tough nut to crack. Behavior is exceedingly complex mechanistically and we (by which I mean all behavioral geneticists, not just our lab) are still trying to figure out how to get a handle on the genetics that affect it.

Robert Franciscus, “Craniofacial feminization in canine and human evolution”

Craniofacial feminization means that your face is flat, basically. Look at the reconstruction of a Neanderthal face: the chin juts out. Look at a modern human face: flat. Look at a chimpanzee face: jutting chin. Look at a baby chimpanzee: flat. Do humans look like baby chimps? We kind of do. Is there a significance to this? Franciscus argued convincingly that there is, and discussed differences in dog versus wolf muzzle length (and got quite technical about how his group investigated them). We don’t know why this feminization or neotenization (childlike changes) happens in domestication, but it seems to be a recurrent theme. This was the first talk that really grappled with the idea that humans are domesticated, with changes compared to our recent ancestors that parallel changes between dogs and wolves, or between tame and conventional foxes.

Terrence W. Deacon, “The domesticated brain”

Do domesticated animals have smaller brains than their wild counterparts? This is certainly the case in dogs and wolves. Is it the case in humans and our ancestors? Deacon’s group has studied Neanderthal brain size based on their skulls, and they conclude that modern humans do not have clearly smaller brains. He noted that the tame foxes also do not appear to have smaller brains than their conventional counterparts. Why does the difference in brain size show up in only some, but not all, examples of domestication? Is it perhaps not a necessary part of the domestication process?

Phillipp Kaltovich, “Neotenous gene expression in the developing human brain”

It is pretty difficult to study gene expression in human brains, because you have to cut up brains to get your data. Kaltovich did get his data from somewhere, though, and it was really interesting to see his comparisons of gene expression in young versus older brains. The question was whether gene expression changes with age, which helps get at the bigger question, are there gene expression differences in domesticated species compared to their wild counterparts, and are these expression differences similar to the differences in young versus mature animals? In other words, are domesticated species basically enternally young (neotenized)? He did find differences, but his group will have a long way to go to put them together into findings that really illuminate the domestication question. I have a lot of sympathy for how hard this particular approach is, as my research is currently also focused on brain gene expression.

Tecumseh Fitch, “The domestication syndrome and neural crest cells: a unifying hypothesis”

In a recent paper, Fitch’s group put forth the concept of a domestication syndrome, a set of changes associated with domestication: flatter face, behavioral changes, white markings, etc. Subsets of these changes are seen in all domesticated species. Fitch’s group hypothesizes that a particular kind of cell involved in early development is involved in all of these changes. This cell, the neural crest cell, migrates through the growing embryo and develops into many different structures and cell types, including coloration cells (explaining white markings), teeth (explaining dentition changes), and the adrenal medulla (source of adrenaline, explaining behavioral changes). It’s an interesting hypothesis and I’ll be curious to see where this group goes with validating it.

Kazuo Okanoya, “Domestication and vocal behavior in finches”

Okanoya’s group studies a species of domesticated finch and its very closely related wild ancestor. The wild finch has a simple song, while the domesticated species has a quite complicated one. Okanoya’s group investigates the difference in these songs, as a model for the development of complex language in domesticated humans. He played both songs, wild and domesticated, and the difference was dramatic. He linked the changes in the song between species to sexual selection.

Richard Wrangham, “Did Homo sapiens self domesticate?”

The question of self domestication was one of the recurring themes of the conference, and for me this was the most transfixing session. Wrangham studies chimpanzees and bonobos, two closely related species with very different aggression levels, as models of the difference between humans and our more aggressive, non-domesticated ancestors. He defines domestication as the reduction of reactive aggression. Reactive aggression is different from proactive aggression: humans are quite good at controlling our reactive aggression, as we are able to tolerate strangers and live in large groups very well. But we do still show significant proactive aggression, which he described as aggression performed in cold blood, such as armed robbery. Wrangham suggests that a reduction in aggression is the trait evolutionarily selected for in self-domestication, and the other parts of the package (flatter faces, white markings) come along for the ride as associated traits. Self-domestication is often seen in island species, and he gave the example of the red colobus with a neotonous (childlike) island version compared to the mainland population.

The whole conference was really fascinating. It’s available on YouTube now, so go, check it out!

State of the Zombieverse

I haven’t been blogging much lately, and it’s mostly because I’ve been writing so much for more mainstream media outlets:

• “Neutering without a Scalpel” in the summer issue of the Whole Dog Journal. This story was about Zeuterin, a new product for performing chemical castration on a dog — in other words, non-surgical neutering. I tried to cover all the possible pros and cons of using Zeuterin versus the traditional surgical approach. I don’t think either solution is going to be right for every dog or every situation, and it’s nice to see new options coming out.
• “Testing the Tests“ in the fall issue of The Bark. I read so many journal articles about canine behavioral assessments (also known as temperament tests) for this piece. You know, the tests that are often used in shelters to try to identify behavior problems in dogs before they’re put up for adoption. It was fascinating reading and ended up telling an interesting story about researchers’ attempts to figure out whether behavioral assessments are good at predicting canine behavior. The answer: not really, but some new research approaches have appeared recently which have shed a lot of light on how to interpret these tests and how to approach building better tests.
• I’ve also been writing for DVM360 (I have two pieces going through the pipeline there right now, one about shelters and one about stress), I have another piece pending for the Whole Dog Journal, a guest post for a new dog site, and you already know about my upcoming ultra short, ultra fun online class for APDT, right?

So with all of that, I haven’t been blogging much, but I keep thinking about it and missing it. I figured I should at least report here on where to find me.

Journal articles, stress, and anti-depressants with me and APDT

I’m teaching another online course for APDT: Analyzing Journal Articles: Pre-Natal Stress and Anti-Depressants. I’m trying something new with this one. It's just one week long. Basically, I’m going to be walking through a recent journal article that I thought had interesting implications for dogs. There will be several short lectures at different experience levels. Some will provide background in the area to students who don’t have an extensive science background. Some will be aimed at students who do know a lot of science and want to dig deeper into stuff that isn’t often covered in online courses. And some will be straightforward “what is this article about?”

It's an interesting article, about whether stress before birth can affect an animal’s personality and whether anti-depressant medication change reverse those effects. Hopefully it isn’t hard to see how this could be relevant to dogs with behavior issues.

If we don't get at least ten students signed up, we won’t do it, so go sign up now! You will get CE! If people do sign up and do enjoy it, I’m hoping to do more like this -- providing a way for dog trainers to keep up on recent research and get a better feel for what it’s like to read a scientific paper. So this is my test case. Will people be interested? I really hope so!

[ETA: Although the last time I checked, the APDT web page for this class lists it as "no CEUs," I checked with their education coordinator, and students completing this class will earn 4 CEUs. So yes, you will get CEU credit for it!]

Veterinary super heroes!

V-FORCE from the AVMA

I was tickled to discover that the AVMA published a comic book. V-Force! Veterinarians to the Rescue! Did you know that veterinary superheroes have x-ray vision and use it to diagnose leptospirosis? Did you know that some of them (us? can I say some of us?) even have microscopic vision so that they can see microbes and diagnose infection with West Nile Virus? Why didn't I get these super powers when I graduated?

My favorite scene bar none is the one in which the doctor (that is doctor-of-humans not doctor-of-animals) says "I'm just glad the veterinarian was around to help link the cause of the disease." Words spoken by no doctor ever. More fantastical than teleporting veterinarians?

The point of the comic is to leave it lying around in veterinary waiting rooms for small children to pick up, so that they learn a) some of the alternate careers vets can have besides working as small animal clinicians and b) that veterinary medicine isn't just about helping animals, it's about helping people, too. (OneHealth to the rescue! I want a super hero named OneHealth Man!)

I like this effort by the AVMA to communicate some important information about veterinary careers, but I do wonder if a somewhat heavy-handed comic is the best way to do it. You're not going to get a lot of bang for your buck with it (although on the other hand it probably didn't cost all that many bucks to produce, relatively). Hey, AVMA, are you listening to me? (AVMA reps have commented on my blog posts in the past when I've made enough noise, so consider my voice raised now.) I have an idea.

Did you see the recent SyFy show Helix? Which actually starred a veterinary pathologist, and yet didn't do a great job of portraying what veterinary pathology is really like or why it's an exciting career. I think the AVMA, if they are serious about this goal of getting the public to better understand what veterinarians are capable of, should be trying to get more veterinarian characters on TV shows and in movies, and make sure they are well characterized. I suggest one way to do it is to offer a liaison service to Hollywood: the AVMA would provide a veterinarian consultant appropriate for the particular role, and would pay their salary and expenses for the job. The consultant would help the writers make the role realistic.

I'm completely serious about this: I think Hollywood (or part of it) is starting to realize that a realistic depiction of scientists is something its audience is actually interested in, but it's got to be hard to find someone who can speak to the daily life of a veterinary pathologist. Make it easy for them. Because a favorite character on a TV show is something that makes kids, and even adults, consider their future career options in a different light, not a comic book with a clunky story.

Can a father's stressful experiences affect his offspring's stress system?

I am again indebted to my APDT students, who asked a very interesting question which turned into a blog post. This time it was: “Can a father’s stress be passed on epigenetically to his offspring through sperm?” Warning: epigenetic geekery ahead. If you are not in the mood for some technical terminology, this may not be the post for you.

Source: Wikipedia

I’ve blogged about epigenetics before (on the epigenetics of fear and of stress) and there are summaries of what epigenetics is in those two posts, but basically it’s changes in the DNA that don’t involve the sequence of bases. We’ve been so focused on the importance of DNA sequence as we’ve learned more and more about genetics, but in recent years the importance of other factors has started to become obvious. It’s like saying that the content of a book isn’t the only thing controlling whether the book gets read or not — it also matters whether the cover is appealing, how much it costs, and whether it’s shelved where people can find it.

One of my students tried to answer her own question and found this fascinating article:

Rodgers A.B., S. L. Bronson, S. Revello & T. L. Bale (2013). Paternal Stress Exposure Alters Sperm MicroRNA Content and Reprograms Offspring HPA Stress Axis Regulation, Journal of Neuroscience, 33 (21) 9003-9012. DOI: http://dx.doi.org/10.1523/jneurosci.0914-13.2013

Essentially, Rodgers et al stressed out some male mice and then tested their offspring six ways from Sunday to see if the effects had been passed on. And they had, but in some surprising ways.

The mice

Male mice were chosen because we have evidence that environmental effects can be passed on epigenetically through the sperm. Because sperm are made throughout the male’s lifetime, they can easily serve as messengers to pass information about the environment on from fathers to their offspring. Mothers can’t pass this information on through their eggs (so far as we know), because eggs are made before a female is born, and can’t easily be changed later. Of course, a mother has plenty of other chances to pass on information about the environment to her offspring: while they’re in utero and while they’re dependent on her. But for dad, sometimes he just has that one chance; he may never interact with his offspring in any other way than through the information in his sperm.

(Why do parents want to give their offspring information about the  environment? To let them know, at formative times in their lives, how to develop. If the world is a safe one, you don’t need a highly reactive stress system. But if it’s a dangerous place, you need your store of cortisol ready to go. It’s easiest for these sorts of developmental decisions about how to tune the stress system to be made early in development — in utero or post-natally — so that’s why parents have systems to pass the information on early, early, early.)

Male mice, then, were chosen for this study. In addition to the control group of unstressed mice, there were two groups of stressed mice: mice who were stressed in adolescence, and mice who were stressed as adults. Epidemiological research in humans suggests that adolescence is an important time for epigenetic changes in sperm.

The stressors

The males were subjected to a variety of stressors. In reading the list, I was torn between sympathy for the mice, and bemusement at the entries:

Stressors, selected because they are nonhabituating, do not induce pain, and do not affect food or water intake, included the following: 36 h constant light, 15 min exposure to fox odor, novel object (marbles) overnight, 15 min restraint in a 50 ml conical tube, multiple cage changes, novel 100 dB white noise (Sleep Machine; Brookstone) overnight, and saturated bedding overnight.

Wet beds! Scary white noise! Scary marbles! And yet yes, probably very stressful to a mouse, and I should not make fun.

Breeding
The males were given time to recover from the stress and then bred. They were removed from the cage as soon as they had mated with the female, which took 1-3 days, to minimize their interactions with her, so that their stress levels could not affect her. (However, the smart reviewers at F1000 [warning: not open content] note that a stressed male might have been more aggressive in mating, which could cause the female to alter her care of her offspring.)

Offspring stress response
The offspring of stressed males, it turned out, had a less responsive stress response than the offspring of unstressed males. In other words, when these mice were stressed by being restrained in a conical tube for 15 minutes, the ones whose fathers had undergone the variety of stressors had a smaller cortisol response compared to the ones whose fathers had not been stressed. The result was almost exactly the same whether the fathers had been stressed as adolescents or as adults, which surprised the researchers.

Now, if a mouse receives information from his father (or his father’s sperm, but you know what I mean) that the world he’s going to live in is a stressful place, I would have expected that that mouse would develop a more reactive stress system, not less. Worried that terrifying marbles or a wet bed are going to attack you at any moment? Then you had better have your stress response at the ready, right?

The stress system is, of course, much more complicated than that. We don’t understand yet why some models of stress system dysregulation show less reactive responses and some show more reactive responses. For example, humans with depression or PTSD can both show either more or less reactive stress responses than mentally healthy humans. So what exactly does this mean for these particular mice? The next thing I would do is to look at their behavior. Do they act more stressed?

Offspring behavior
The offspring were subjected to quite a few and quite varied tests to see if their stress behaviors were different. The researchers tested things like how much the offspring startled in response to a loud sound; how fearful they were of being in a brightly lit box versus a dark box (mice feel safer in darkness); how long they struggled when suspended by their tails; and more. Really surprisingly (to me, at least), there were no behavioral differences between the offspring of the stressed fathers and the offspring of unstressed fathers, despite this significant difference in stress system responsiveness. So what does that mean?

The researchers tested a bunch of other stuff that left them empty handed as well, like gene expression differences in the brains and adrenals of the different sets of mice. All nothing. But what did they find that was different? They found an epigenetic difference in the fathers’ sperm.

microRNA changes in sperm
Epigenetics is all about gene expression: determining which genes are used frequently to make their associated proteins, and which are left to lie dormant. The two best understood epigenetic mechanisms, acetylation and methylation, affect how much messenger RNA (mRNA) is transcribed from a particular gene. If there is more messenger RNA for a particular gene, then it’s easier to go the next step and make more of the protein that that gene codes for, and that gene’s expression increases. The mechanism that these researchers looked at is different. Instead of methylation and acetylation, they looked at microRNAs (miRNA) in the sperm of these mice. Where methylation and acetylation affect how much messenger RNA is generated, microRNAs attach to the messenger RNA itself after it has been created, and silence it.

The way it works is this: since RNA is basically half of a double strand of DNA, it’s really sticky. It wants to find something that looks like its complement and stick to it. So microRNAs are little bits of RNA that stick to particular messenger RNAs. Then when the cell takes those messenger RNAs and tries to use them to make a protein — it can’t. Because there’s this microRNA stuck to it, blocking the sequence of the message. So microRNAs reduce the expression of a gene, but they do it one step later on in the gene to protein pathway than methylation or acetylation does.

Back to our book example, it’s like if you have a cookbook (the DNA). You copy out a recipe on a piece of paper for later use (the RNA). Then you use the recipe to make cookies (the protein). Methylation puts big rocks in front of the bookshelf so you can't get to it and get at the cookbook. Acetylation glues the pages of the book together so you can’t read it. But microRNAs are your obnoxious husband who draws in marker all over your copied recipe, so you have to go back and copy it out again. (Disclaimer: while my husband is quite capable of being obnoxious, he has never defaced any of my recipes. He has scribbled notes on the medication list for my dogs in the face of my express requests to the contrary, however. Rosie hasn’t been on ciprofloxacin for six months but it still says “cipro” on her meds list. It’s like he’s incapable of thinking ahead.)

There is a lot we don’t know about microRNAs. The whole epigenetics field is like this: we are getting to the point where we can detect these changes, but we still don’t really know what they mean. So in this study, they found that 9 microRNAs were expressed at different levels in sperm of the stressed mice versus the unstressed mice. We can make some predictions, using computer algorithms, about which messenger RNAs these microRNAs were going to stick to and silence, but we don’t know for sure that that’s what they were actually going to do.

Still, the predicted list is pretty interesting, because it contains the messenger RNA for the enzyme which controls methylation. Methylation! Another epigenetic mechanism! So is there some epigenetic chain going on here? The dad passes on microRNAs which will result in the DNA of the offspring being more or less methylated. It’s so hard to know what that means, because methylation has very different effects depending on which gene is affected, and this change is a more global change. But it’s a really intriguing finding, isn’t it?

Conclusions
This study is exciting, but I still felt a bit of disappointment as I read it. No behavior changes? Really? Is it really significant without the behavior changes? I mean, do we really care about stress system changes if there are no behavior changes? Of course we do, and I wonder if future studies will investigate different behaviors, or behaviors at different points in the mouse’s life, and then we’ll understand this system a little better.

What does it mean for dogs? Of course it is immediately applicable to the question: if a male dog is stressed, will this stress affect his offspring? The answer is a nice solid maybe. In some way that we can’t really predict or define.

But at another level, this is another step in our progress towards understanding how genes and the environment interact. Stressful situations change gene expression in the stressed individual and possibly their offspring. How, why? How can we measure it? How can we use our knowledge to help an animal who has been traumatized, or undersocialized? Watching the field of epigenetics unfold is so much fun: everything is new, we understand so little, but the new technologies are coming so fast that we’re learning more and more.

What percent nature? What percent nurture?

The Nature versus Nurture debate is over: we no longer ask if genetics governs personality or if environment does. They work together, and it’s hard to pick their effects apart. But surely we can pick their effects apart a little? For example, if a dog trainer is trying to impress upon their students the importance of getting a puppy from a good breeder who takes behavior into account — or conversely, the importance of bringing a new puppy to a puppy class: what should she tell them? 50/50? 60/40? Surely there are some numbers we can cite?

It’s a tough question, but one that researchers have tackled. The concept is called heritability: the measurement of how much of a trait is due to genetic influences, and how much is due to environment.

Human researchers have it easier than dog researchers, because humans sometimes produce identical twins, and twin and adoption studies form the basis of human heritability studies. Some twins are identical (100% identical genetics), some are fraternal (around 50% similar genetics); some are raised in the same home, and some are adopted out and raised separately. You can do some complex math to all of these situations and come out with conclusions about particular traits. Identical twins more similar than fraternal twins for a particular trait? Strong genetic component. Raised together twins more similar than raised apart twins? Strong environmental component.

These studies have given us some numbers: IQ (how someone scores on a particular standardized test) is about 40-50% heritable. Environment does the rest.

Dog studies are harder. Dogs don’t have identical twins. Theoretically, the best way to study the heritability of personality traits in dogs would be to breed parents who do or do not show the trait in question and assess the puppies, then rinse, wash, and repeat for several generations. But this is expensive and somewhat ethically fraught to do in a laboratory, so we fall back on finding populations of dogs whose personality traits have been well measured and whose pedigrees are well known.

How often does that happen? Not very. But there is a test, the Swedish Dog Mentality Assessment (DMA), which is given to a large percentage of dogs in Sweden and some other European countries. Those crazy, overly-responsible Europeans measure their dogs’ personalities before breeding them, to make sure they're breeding stable dogs. Researchers have mined this resource repeatedly to learn more about the heritability of a variety of personality traits.

As lucky as we are to have this resource, it’s not an ideal one. The DMA is a suite of behavioral assessments which are given to a dog on a particular day in a strange environment by a judge who doesn’t know the dog well. Ideally, personality is best measured over time, by someone who knows the animal very well — its owner. And, in fact, every study I read that evaluated heritability of personality using the DMA noted that one of the most important factors was not genetics but the identity of the judge who gave the test. Did some judges tend to judge more severely than others? Did dogs respond differently (more or less fearfully, perhaps) to different judges? Hard to say, but we know that the reliability of the test suffered as a result.

Perhaps more alarmingly, we’re not really sure about the validity of the test, either. What are these assessments actually measuring? They’re measuring the response of a dog to a particular stimulus in a particular situation. Can this response be generalized to a personality trait? If the dog reacts fearfully to a person wearing a sheet over his head so he looks like a ghost, does that mean the dog is fearful or just that this was a particularly surprising experience? The DMA asserts that it measures playfulness, chase-proneness, curiosity/fearlessness, and most interestingly, aggressiveness. But does it? Studies of the validity of behavioral assessments in shelter dogs — a similar situation in which a series of small tests are given to a dog by a stranger in a strange situation — have repeatedly shown that the subtleties of personality are really hard to measure in this way.

Ideally, a personality heritability study would be designed using the canine behavioral assessment and research questionnaire (C-BARQ), a questionnaire which relies on the dog's owner to assess the dog’s personality through 101 questions. This test has been found to be valid and reliable. And the University of Pennsylvania has a database of the results of this test when given to thousands of different dogs. Except... they don’t have the pedigree information for many (or perhaps not for any) of these dogs. So this isn’t a practical solution, either.

So it’s hard, and I don’t really trust the studies that are out there as a result. What do these studies find? Most studies out there use the DMA or tests like it, and find roughly 20%-50% heritability for most personality traits studied. These numbers might be artificially low, though, because the tests may not be testing real traits — behavior that is stable over time.

I was able to find one study using the C-BARQ, which had much higher heritabilities, around 70%-100%. It's a dramatic difference, but I would hesitate to assign the responsibility for that difference entirely to the C-BARQ. This study used a non-random set of samples, selecting aggressive golden retrievers and dogs related to them. With no control set of non-aggressive goldens and unrelated animals, it’s hard to know how to interpret the study’s results.

So what are the real numbers? I still want to wriggle away from an answer. I don’t think we really know. I’d love to see a C-BARQ study using a random sample — maybe by finding pedigrees for dogs already in their database, if that’s possible. Until then, I’ll guess that the real answer falls in the 30%-60% range for most traits. But, in the end, does it really matter? Genetics are important and environment is important. The best genetics can fail in the face of a poor environment, and the best environment can fail in the face of poor genetics. We can’t predict everything about our next dog; we can just do our best to make a good decision, and then provide the best possible environment for whoever comes home with us.

I owe the inspiration for this post to my students in APDT's Canine Behavioral Genetics course, who asked about the balance of nature versus nurture and would not be satisfied with vague answers.

References

• Strandberg E. & Peter Saetre (2005). Direct genetic, maternal and litter effects on behaviour in German shepherd dogs in Sweden, Livestock Production Science, 93 (1) 33-42. DOI: http://dx.doi.org/10.1016/j.livprodsci.2004.11.004
• Liinamo A.E., Peter A.J. Leegwater, Matthijs B.H. Schilder, Johan A.M. van Arendonk & Bernard A. van Oost (2007). Genetic variation in aggression-related traits in Golden Retriever dogs, Applied Animal Behaviour Science, 104 (1-2) 95-106. DOI: http://dx.doi.org/10.1016/j.applanim.2006.04.025

Why genetics and dog training?

I won’t lie to you. When I first started thinking about teaching genetics courses for the Association of Professional Dog Trainers, I was mostly excited about the second class, which covers behavioral genetics of dogs. The first class was just something we had to do in order to get everyone up to speed on the basics of genetics, to have the information they needed to understand the second course.

But, of course, basic genetics is relevant to every day life with dogs and is interesting on its own. I don’t blog about genetics much, because I’m shoulders deep in highly technical stuff in my PhD program which is hard to communicate to people who aren’t equally immersed in the field. But when I stop to think, it’s not hard to come up with questions about dogs that you can’t answer without basic genetics.

• In the past decade, new advances in technology have enabled the discoveries of more and more genes in both humans and dogs. These discoveries get reported in the popular press, such as the gene for small size in dogs (discovered in 2007). What exactly is a gene? What does it do? What does it mean to have different “versions” of a gene? It’s hard to understand these news tidbits if you don’t really get some of these basic concepts.
• When you breed a lab and a poodle, you get a labradoodle with very predictable appearance. But if you breed two labradoodles, you can't predict what the puppies will look like. Some will look more like labs, others more like poodles. They're all the same genes, so why is one generation so different from another?
• Why is blue merle color associated with deafness in dogs, so that if you breed two blue merles to each other, you're almost certainly going to have some deaf puppies? 

It’s easy to get caught up in the details of a field and forget that that’s not all there is. I’m trying to remember to get my nose out of the books (or PDFs of articles) once in a while and look around me.

(Genetics is beautiful and fascinating and I’m extremely lucky to have the chance to talk about it, through the lens of a shared love of dogs, in my upcoming classes with the APDT.)

Fish personalities?!

My mobile buzzed: I had a text message from my husband. I’m bored. Call me. He was driving to New England and stuck in traffic.

I called. He asked how my day had been. How was that boring meeting? It was great, I said. I got to talk to a fellow grad student about a project of his during the coffee break. We were talking about a new way of studying fox personalities, using a method he had applied in his study of fish personalities.

Husband: Wait. What personalities?

Me: Fish.

Husband: Did you say fish?

Me (wondering if the connection is bad): Fish.

Husband: The things with scales that swim?

Me: Fish! Yes!

Husband: ...have personalities?

Oh. Right. Sometimes I forget that my world is not other peoples’ world.

Me: Yes! Some are shy and some are bold.

Husband: Oh right. Continue.

I mean, what’s personality, really?  We make it sound like a big deal when we say that fish have them. My boss doesn’t even like me to say that our foxes have them when I am writing grant applications.

When you break it down to these small traits, like shyness and boldness, it makes more sense, though, right? Some fish are shy: when you put food in their tank, they hide a little bit longer before they will come out to eat. Some are bold: not only do they explore more and hide less, they are more likely to attack other fish who try to take their fishy belongings. If you haven’t observed these differences, I assume it's because you haven’t kept fish.


Different personalities are better (“more adaptive,” if we’re speaking Science instead of English) in different environments. An environment with lots of predators? Better to be shy, more cautious, and check out the surroundings before going for some food that's floating out there in the open. An environment with fewer predators, but lots of other fish of the same species as you? You had better go get that food fast before someone else does, rather than waiting to see if the coast is clear.

So it makes sense for a species to have a reservoir of personality types. This way, when an environment changes (there’s a new predator, or increased population density), that variation is there to be drawn upon. Lots more birds around to eat the fish all of a sudden? The fish with shyer personalities will do better, the ones with bolder personalities will do worse, and the population will gradually come to have more shy fish in it, so that the population as a whole can survive the change in environment.

For sure, human personality is a lot more complex than fish personality. But that is exactly why my friend’s lab studies fish: better to try to understand a simple system first before tackling the more complex one. A lesson I don’t seem to have learned, jumping right in with my questions about dog personality. Oh well.

[If you’re a dog trainer or just interested in dog genetics, you can learn about the genetics of dog behavior with me this summer in an online course with the APDT!]

On nature and nurture and their interactions to make a personality

My mom called me yesterday because she had experienced some Science and was excited about it. She was watching a TV episode about aggression and how it appears in nearly every species. She called me to say that she thought my lab should look for the gene for aggression. “It should be easy,” she said, “because it should be the same gene in every animal.”

Aggressive silver fox

Yeah, you’d think that there would be single genes controlling bits of our personalities (human and dog — I think dogs are much more interesting, but in this case it’s much the same problem). Only ten or twenty years ago we thought we were in the endgame to find these genes: once the human genome was sequenced, we expected to be able to do a series of big studies to find these answers. Take a few hundred humans and sort them into “violent“ and “not violent.” Then look at markers in their genomes and use computers to find associations: all the violent people should share one marker, which will tell you where the gene for violence is. Done.

But we did those studies and we found, again and again, that these sorts of personality traits don’t give up their answers this way. In fact, in the case of zero personality traits have we found one (or even two or three) genes that control that trait. Sometimes we find genes that we think control a solid chunk of a trait, only to find that it was a statistical error — if you ask enough questions, you’ll find an interesting set of data just by chance. But if you ask the same question of another set of data (in other words, do another study), you’ll see that the first one was wrong. And this is what we have seen, for trait after trait.

Now, occasionally we’ll find a personality trait for which a little bit of it can be explained by one gene. When I say a little bit, I mean that if there is a normal amount of variety in this trait — say, in how violent a person is, ranging all the way from a pacifist to a psychopath — then the genes we find will explain about 0.1 percent of that variety. The rest is — what? Chance? Environment?

It’s a bunch of things, probably. For one thing, it’s surprisingly hard to define a personality trait. What’s violence? In dogs, we diagnose different kinds of aggression: territorial aggression, owner-directed aggression, dog-dog aggression, fear aggression. Are these all the same thing? Probably not. So instead of looking for one trait, “aggression,” should we look for four traits? Maybe. But do we actually know that those are the right four? Maybe there are six. Maybe there are ten. Maybe there are a hundred. We need to understand the traits we study better, and ask more detailed questions about them.

For another thing, yes, environment is important! Genes are important, but they are nowhere near the whole story. And environment is complicated. Certainly the difference between a pet store puppyhood and early life with a responsible breeder is huge. But can you lump early life experience into two bins, “good” versus “bad”? There are all kinds of variables. In the pet store, what kind of crate was the puppy kept in, how much interaction did it get, how young was it when it arrived? At the breeder’s, were there other adult dogs besides the mother to interact with, were there any small children, were there any bad interactions with other dogs or people? And a hundred, a thousand more questions.

I read recently about a pair of conjoined twins with very different personalities. These two had the same genes, because they came from the same embryo originally. And they had the same environment, because due to being conjoined they had to spend their lives in each other’s company. So how could their personalities differ? The article theorized that they reacted to each other, with one taking a bold, outgoing role and the other becoming shy and retiring in compensation.

And finally, the most interesting idea, in my opinion as a genomics researcher: what if we aren’t going to find the answer by looking at the sequences of DNA that make up genes? What if we are going to find the answer by looking at how the genes are regulated? If it isn’t that my dog is more fearful because some gene is a little broken, but she is more fearful because some gene is getting turned on much more or much less often than it should? It’s hard to investigate gene regulation when you have questions about the brain, because to do it you kind of have to get inside the brain, and it’s hard to do that without killing the person you’re studying. But I think looking at regulation is where things are going to have to go, and researchers are working on finding non-lethal ways of doing it.

So, nature and nurture: both important. Personality: super, super complicated. But also wicked interesting.

[If you’re a dog trainer or just interested in dog genetics, you can learn about the genetics of dog behavior with me this summer in an online course with the APDT!]

I'm not dead

Dear everybody: I'm not dead, I'm just spending all my writing energy writing other things than blog posts. I keep asking my brain for an inspiration for a blog post and it keeps telling me "but you just wrote that long story for that magazine!" Ah well. I will keep asking.

Learn about the genetics of dog behavior with me

As promised, my big announcement: I will be teaching two online courses for the Association of Professional Dog Trainers this summer.

DNA, courtesy of Wikipedia

• Introduction to Canine Genetics
• The Genetics of Canine Behavior

 The courses are open to APDT members and non-members, so anyone can take them. I'm working hard to make them fun, and I would love to see some blog readers or Twitter followers in the class!

The first class is just a basic grounding in genetics, nothing really special about dogs (although I use dogs for many of the examples). So if you have a solid or even just passable genetics background, you don't need to take that. If you're not sure you could explain what a gene is or what a chromosome is, though, you would probably be a bit overwhelmed in the second course without having taken the first one.

The APDT is an organization that I've respected for quite a while, so I'm thrilled to be working with them. If these classes are well-received, they will repeat periodically, so if you can't take one or both this summer, you should get another chance later.

The state of the Zombieverse: spring 2014

No matter how many times I resolve that I will post at least once a week, life always seems to get in the way. So I figured I’d make lemonade from the lemons and tell you guys about what I’ve been up to. I know a lot of you enjoyed the posts about life as a shelter medicine intern, but I’ve been suspicious that life in the lab would be less interesting. (“Today I found the perfect set of pipetters! It was awesome!”) Still, it seems possible that there are people out there who wonder what first year PhD students spend their time doing, so here it is.

Me escaping from lab for Scio!

I went to ScienceOnline Together 2014, which was a great deal of fun. The head of my lab smiled tolerantly and let me go — she doesn’t do much layperson-level science communication herself, but she knows I love that stuff and figures there’s probably a good reason for me to get better at it. I went to a discussion about engaging undergraduates in science (run by two undergraduates), where I learned that Facebook is the Thing right now but Twitter might be catching up; a brainstorming session about providing explanations of various scientific concepts to people at a variety of levels, elementary school through expert; and an intergalactic gala, where I met Malcolm Reynolds, the Doctor, and an inflatable Dalek, and ate carbonated ice cream which was made before my eyes.

Back home but still on the science communication track, I have been kicking around ideas with another science blogger here about improving science communication education at UIUC. Let me tell you a story about how much the world needs help training aspiring scientists about science communication! I was in class with some undergrads, and they were talking about our recent midterm. One said: “I didn’t really understand that question where we were supposed to explain the findings as if to a scientist, and then as if to a non-scientist. What did that mean?” The other replied: “I don’t know, so I just wrote the same thing twice.” Ouch.

So yeah, I had some midterms. The one mentioned above was for an excellent class on genes and behavior. I really dig the structure of this class: every week we read some articles, then discuss them on the message board. We come to class already understanding the articles fairly well, and we discuss them more in person, both in small groups and as a full class with the professor. It’s a great design, though it does suffer around midterm time when the students are too tired to muster the energy to do paper analysis. Still, it is always better to read articles than a text book!

I also had a project for a statistics class. Statistics can be mind-bogglingly boring, but it is really essential to understand it if you want to be able to analyze your data well. In my experience doing my Master’s work, asking a statistician for help will lead to some terrifyingly complicated analyses that you will only understand during the moments that he is explaining them, and will immediately become completely opaque when you are trying to explain them to your advisor the next day. Anyways, this stats class was designed for grad students, not undergrads, and this project was to do some analysis of our own data. I am a first year student, so what do I not have yet? Data. I have a bunch of RNA which had been sitting in the sequencing machine for weeks. My hope was that sequencing would finish up in time for me to analyze that data for the class. Nope. So, with the teacher’s permission, I made up the data. It was kind of fun. Not enough significant results? Let me just change those numbers... This is apparently not something we are supposed to do in real life, unfortunately.

Did you hear me mention RNA in the sequencer? Yes, I am also doing research! Last semester was a lot of time at the bench, doing ridiculously finicky extraction work to get RNA out of tissue samples. RNA, you will remember from high school biology or some such, is a single-stranded copy of DNA. The cell makes these single stranded copies for use in making proteins, so RNA is part of the whole translation mechanism whereby DNA turns into an organism. Because RNA is single stranded, it isn’t as stable as DNA (which is double stranded), so handling RNA is a really annoying process involving gloves and this magic spray bottle which kills the evil RNA-eating demons which apparently live in the air, your hands, on counters, and on the mobile phones that undergraduates like to leave in your work area.

But once you get the RNA extracted into teeeeny little vials, you can send it off to be sequenced. What I will get back (what I got back a few days ago, but which involves a lot of processing before I can extract useful information from it) is information about which genes are expressed at different levels in particular tissues. I am using tissues from foxes selected for tameness versus foxes selected for aggression. (Remember, I work on the tame fox project.) Why is that interesting? Well, it seems likely that a lot of the differences that we see in tame foxes aren’t due to changes in their actual genes, but changes in how those genes are regulated. So maybe tame foxes express more of a particular gene rather than a different form of that gene. If I know which genes are expressed at higher or lower levels in tame foxes, I can start to guess at the functions of those genes, in foxes and, eventually, in dogs and humans.

What else? Helping the head of my lab teach her class in domestic animal behavior. I have been working behind the scenes to find good papers for students to read and writing questions to assess the students’ understanding of those papers. It’s the perfect job for me. I get to read a lot of papers about domestic animal behavior, and I get paid to do it.

Finally, I’ve been working on another project which is days (DAYS, I tell you) away from being ready to be announced here. I think it’s safe to say I find it more exciting than you will, but I still think you should check this blog daily in breathless anticipation!

The spectrum of hoarding

There was almost no furniture in the entire house. This was unusual for hoarder houses, which are usually packed full of stuff or just of trash. But she was a somewhat unusual hoarder, with only 26 cats and one dog. We stood in the living room and talked to her about her animals. We could see into the kitchen, which was swarming with cats, on the counters, poking out of empty cabinets, sleeping in the sink. The woman we were talking to told us how she loved them but how her son had called us in because he was concerned about them and about her.

While we talked, her dog urinated in the middle of the empty floor in front of us. She didn't notice. The room contained a couch and an entertainment center and absolutely nothing else: the entertainment center had a few knicknacks but was mostly empty. On it sat the box of flea preventative that our team had given her months ago. It was unopened.

And everywhere was the smell of urine. I could barely stand to be in the room, but I could do so without a mask, which made it one of the cleaner hoarder homes. All I could think of was getting outside and getting a breath of air that was not thick with ammonia, so thick that my eyes watered and I could not fill my lungs. But this woman lived here. She could no longer smell it. She no longer noticed or cared when her dog urinated in the middle of the floor. And I remembered another time I had smelled this smell: at a cat shelter in another part of the country.

That was in rural New England. The two women running the place called it a shelter, but I knew it was really a hoarding house. They did not know how many cats they had. They would find cats unexpectedly dead, because no one had noticed for days or weeks when they were sick. And everywhere the smell. Not as bad as in the hoarder house in the big city, but bad enough to scare away adopters. Yes, they opened their doors to adopters. They advertised their cats for adoption. But adopters who brought these cats home risked bringing a sick animal into their lives, or contracting ringworm from their new pet, a story I heard unfold at least once from this shelter. The women running the shelter grilled every potential adopter and turned many away for not being good enough for their cats. And they continued taking in more cats — if they turned them away, they said, what would happen to them? But could another fate have been worse than dying trapped in that place, where adopters did not want to come, and were turned away when they did? Was this place a shelter or a hoarding house or some weird combination of the two?

But the combination isn’t weird. It happens all the time. I saw it again at a shelter in the deep South. This shelter proclaimed that they would kill no animals, and they did not, even the dogs who had been there for seven or eight years, that had gone insane and were unadoptable. These dogs were loving with the shelter staff, but when I came within a dozen yards of their enclosures they would erupt in terrifying, violent barking. I had no doubt that if I entered their enclosures I would be badly bitten. One dog was not aggressive, but hardly seemed to see the rest of the world any longer: he spun in circles around his enclosure, up on the roof of his dog house, down on the ground again, paws hitting exactly the same point every time. Over and over and over.

And the dogs who were not yet insane were not moving out fast enough. I could see their fates. This shelter was so overwhelmed with the number of dogs they were managing that they did not have the energy to keep these dogs mentally healthy, or to do the extra legwork it takes to adopt out a large dog in an area like the South which is so overpopulated with them. These dogs needed transfers to different shelters, they needed adoption events, they needed foster care to get a break from the shelter. They got none of those things. And as soon as a cage opened, it was filled with a new dog. This shelter actually transferred dogs in from outside their community. If they had not done so, they told us, what would have happened to those dogs? Where else could they have gone?

When I started to look, I started to see it everywhere. How many shelters provided enough space for their cats? Even the shelters that have big condo-style cages for cats in their adoption areas, with enough space to move around and a separate area for the litter box, even these shelters still have cats in tiny three by three foot cages in the back, in the sick rooms, in the intake and holding rooms: not enough room for a cat to stretch out, not enough room to get away from the litter box to eat. Even these shelters tell me of course they can’t use that antibiotic, because it must be given twice a day, and they don’t have time to visit so many sick animals twice a day, so they must use the one that doesn’t work as well but can be given less often. Even these shelters say, Of course we would love to have dog play groups, but we don’t have enough trained staff to manage them.

So what is sheltering and what is hoarding? A good shelter provides a needed service: a brief place for an animal to stop on its road to a new home, some medical care, some help finding that home. Keeping that stay brief is the hard part. It is, in fact, a very hard part, balancing keeping the animal healthy (it’s hard and potentially unethical to adopt out a sick pet), finding the right adopter (for that pit bull type dog that looks like row upon row of others in your shelter, for that orange cat that doesn’t come to the front of his cage to meet adopters), keeping them mentally healthy while you’re at it (play groups, training, just plain time out of the cage and time with humans).

And keeping large animals like dogs takes space. In fact, keeping a small animal like a cat takes space, much more space than we as a sheltering community realized until recently. Sheltering can so easily start to slip down the spectrum. It is a spectrum! Many shelters, real shelters, shelters that have legal non-profit status with the government, shelters that don’t smell like urine and have lots of volunteers and get grants and have spay-neuter services, yes these shelters too can fail to provide minimally acceptable care for their animals. Simply because they have too many.

What’s the answer? In one sense, it is simple. Call in someone from the outside, who can see your facility with unbiased eyes. Someone who doesn’t have to answer all the calls for pets that need homes. Someone who can look at the pets that you have and tell you how you are keeping them. This person must know how to assess humane capacity, so it can’t be just any animal lover. They should be able to look at your facility, know how much space is appropriate for animals of different sizes, and calculate how much space you have for each animal. Then they must look at your staffing, and calculate how much staff time you have for each animal. Not just to feed and clean them, but to spend time with them. To notice when they are sick: to look at them every day, carefully, and think about what they need and how to get it to them. To not be running ragged putting out fires, but to be able to plan adoption events, and to notice that dog that’s been here for months and needs special work to get out.

When this person tells you how many animals you can care for humanely, not just how many you can fit in your facility, you will be shocked. You will deny it. You will say that’s half what you can handle. You will point to your records: you’ve had many more than that for years! But they will insist: yes, you’ve had more. But you haven’t had them humanely. You have had a toe on the road to the hoarder end of the spectrum.

So in another sense, it is not at all simple. Because embracing humane capacity means accepting that you have not done as well in the past for your animals as you could. It means not beating yourself up over this, not feeling guilty, not indulging in denial. It means moving forward: it means promising yourself and the animals in your care that you will do better in the future.

And even harder, it means saying no. No to the animals that need a place. No to the people who just can’t find a home for their pit bull type dog but have to move, and the new place does not take animals. No to the mom whose dog bit her child but is such a loving dog with adults. No to the stray cat who is so sweet. Surely you can find homes for these animals? If you don’t, who will?

But that is the central point: you can’t do it humanely, but you try anyway, you will add to the problem. Sheltering is where it is because shelters try to do too much, and if a shelter’s doors are open, animals will pass through them. Shelters which have put waiting lists into place have found that many people do manage to find homes for their animals, if they have to keep trying. Some don’t, and they wait until a place opens. Will these people abandon their animals on the street? Will they take them to a quiet spot and shoot them between the eyes? Very, very rarely does this happen: when it does, it is big news. But you know what? Doing that is illegal. And that is where we need to prevent it: with laws, and enforcement of them. Not by saying, Okay, I will take over your responsibility for you.

That is what we as a society must embrace: responsibility. Not taking in animals that we can’t care for appropriately. And not accepting someone else’s responsibility. Being strong, and doing only what we can, and no more. Because by doing more, we actually do less.