“Okay,” I said brightly, “who wants to pick one up?”
The students eyed me with suspicion, and then turned their gaze to the aquarium at the front of the classroom. I was the teaching assistant for animal behavior, and the lab of the day was on dominance and territoriality in crayfish. The creatures are easy to obtain from laboratory supply companies, they subsist quite well in aquaria outfitted with some rocks and a few inches of water, and they exhibit stereotyped aggressive and submissive displays that have been documented by biologists for many decades. As a way to demonstrate how to take data on behavior and analyze the results, they are perfect subjects.
Except that their lobster-like appearance extends to a pair of pincer-like claws at the front end, and the students didn’t want to get pinched. I demonstrated, showing them how to grab the crayfish high on their midsection, right behind the claws so that the animals couldn’t get a purchase on their skin. After a bit of practice and only a few mishaps, the students caught on, with each pair of lab partners taking a couple of crayfish to a separate tank, marking them with different colors of nail polish so they could tell the individuals apart, and painstakingly writing down movements like “approach,” “claws up,” and “tailflip” to determine which member could be considered dominant. It was all a pretty standard exercise, and the students ended up enthusiastically naming their crayfish and carefully selecting the right color of nail polish to suit.
What we didn’t do was consider how this all went down with the crayfish. Recent work by researchers in France1 has explored the behavior and chemicals circulating inside crayfish after they have undergone stressful events, and it suggests that the crustaceans are experiencing anxiety, physiologically akin if not identical to what we term anxiety in humans, and that it is controlled by serotonin, the same chemical used in many drugs for combating psychological ills in humans.
I will explain more about the crayfish, and just what led the researchers to call them anxious, later on in the chapter. But for now they serve to introduce the idea that if our normal behavior is deeply entwined with our biology, then we should be able to say the same about the times when our psychological state malfunctions. After all, our ideas about the source of mental dysfunction should follow from our ideas about the source of other kinds of dysfunction. What is the difference between physical illness and mental illness? And why should humans and animals share one but not the other? In this chapter I look at mental disorders in animals as illustrations of the way physical characteristics are entwined with behavioral ones, whether in sickness or in health.
We accept that our physical being has evolved, and our brain and nervous system, the source of our mental state, presumably did as well. Despite the oft-repeated “chemical imbalance” explanation for mental disorders, what do we really know about the link between the brain and our state of being? In many cases, the answer is not enough. But this question has bearing on whether we favor medicating mood, and why we think it’s okay to put a Band-Aid on any wound that bleeds but think we should tough out bouts of depression as if they were the psychological equivalent of a paper cut.
An Obsession with Obsessions
Interest in whether and how mental disorders can be inherited has a long and rich history. Many early scientists, like the seventeenth-century French alienists, as those who studied the mind and its illnesses were called, were convinced that mental diseases could be passed from parents to their children. Charles Darwin became caught up in the idea; as Carl Zimmer says in She Has Her Mother’s Laugh, “Darwin turned to humans for clues to heredity as well, but he mainly studied how they went mad.”2 A similar concern with “feeblemindedness” and its potential for being passed from one generation to another led in part to various social policies in many parts of the world, including unconscionable acts such as forced sterilization.
Darwin was intent not only on studying humans for their own sake, but also on demonstrating the unbroken links between humans and other species of animals, and thus he was fascinated by the potential for insanity in animals as well. If chimpanzees, for example, could feel emotions that were similar to jealousy or anger, why wouldn’t they have defects in those responses? Without much justification, he speculated that insanity in animals, while present, would be less common than in humans. Other intellectuals at the time went further, and saw connections between criminals, animals behaving “savagely,” and people who had gone mad. We certainly still talk about “mad dogs,” since rabies can produce what looks like mental illness in animals. Extending this idea, it would seem odd that no other mental disorders would appear in nonhuman animals.
Current thinking about animals and mental disorders takes three forms. First is the idea that while animals can serve as models for human mental diseases, they do not suffer from such disorders themselves; they are simply convenient vessels of brain components and neurochemicals. Joshua Gordon, the director of the National Institute of Mental Health bluntly stated, “Mice do not have schizophrenia. Or any other mental illness.”3 Some researchers even suggest that the ability to suffer from mental illness is a hallmark of being human, though this view is contested. In her book Animal Madness, science writer Laurel Braitman says, “Every animal with a mind has the capacity to lose hold of it from time to time.”4 Of course, this merely kicks the can down the road—which animals do we think have minds to begin with, and which do not? Pavlov, who pioneered animal psychology by studying dogs salivating at the sound of a bell, was the first scientist to suggest that animals would be useful models to study psychiatric problems in humans. Since that time, a variety of laboratory animals have been used to understand how behavior goes awry, and perhaps how it can be fixed. As you might imagine, I think it would be odd if, of all things, mental illness were the source of human exceptionalism.
The second notion acknowledges behavioral dysfunction in animals, but largely attributes it to mistreatment by people. As one interview with a Norwegian researcher of animal welfare put it, “Blame it on humans when animals become mentally ill.”5 The website Online Psychology Degree Guide (onlinepsychologydegree.info) admittedly not the most intellectually rigorous of sources, claims that “veterinarians and animal psychologists also agree that animals wouldn’t suffer from mental disorders if we’d only treat them right.”6 The number of veterinarians specializing in behavior, and treating problem behavior in pets, has skyrocketed over the last couple of decades, and books about how to fix Fido’s phobias have been reliable bestsellers. Although I agree that people can induce bad behavior in their pets, we can’t lay the blame entirely on human error.
A third approach suggests that wild animals can indeed suffer from mental disorders, though evidence is scant for things like psychotic zebras or sloths with agoraphobia. One magazine article did include “hoarding” in hamsters as a potential disorder, despite the fact that the behavior of cramming food into the rodents’ furlined cheek pouches is a completely functional activity that enables them to survive the winter. A 2015 BBC Earth story suggests, somewhat more broadly than Braitman, that “all animals with brains have the capacity to experience some form of mental illness.”7 The story also suggests that complex mental illness is a manifestation of higher-level cognition, or even greater intelligence, an idea that I will revisit later in the chapter in the context of schizophrenia. Certainly the idea that mental suffering is tied to artistry has been a recurrent one.
I am not so willing to see mental disorders, representing real suffering as they do, as a price anyone pays for heightened insight, much less for being human. My own opinion is that while we shouldn’t expect to see the same disorders in animals that we do in humans, our connections with other species make the third approach the most plausible. After all, we think that other animals get physical ailments similar to those of humans—why wouldn’t mental ailments be found in them as well? As I noted previously, it would seem beyond bizarre if mental illness—not tools, not language, not a capacity for empathy—were what separated us from all other animals. Following I will consider each of these approaches, but before getting to animals it makes sense to think about how we view the evolution of mental illness in humans.
The Evolution of Our Discontent
Although we no longer see mental illness as a single entity that can be passed from parent to child, like eye or hair color, we have long recognized that genes contribute to a tendency for many disorders. But two puzzles about this connection immediately present themselves. First, despite decades of concerted research, progress toward finding a single gene, or even a suite of genes, responsible for most of the major mental disorders in humans has been dismal. The same is true for our ability to isolate a particular part of the brain as responsible for a disorder, with a few exceptions such as Huntington’s disease and, to an extent, Alzheimer’s disease. When putatively relevant genes are identified, and hundreds if not thousands have been, each one increases the risk of developing a given disorder, such as bipolar disorder, by perhaps 1 percent or even less.
This should not be surprising. We are never going to find a single gene or group of genes responsible for mental illnesses, for the same reason we can’t isolate a solely genetic cause for any trait, behavioral or physical. Genes simply don’t “cause” behaviors, despite behaviors, whether healthy or not, having a genetic basis, as I explain in chapter 3. Finding a “genetic marker” for a psychiatric disorder is not synonymous with finding its genetic cause, and such a marker has almost no predictive value for identifying individuals who will develop the disorder. This does not preclude using genetic information to develop tailored treatments for psychiatric ailments, and we have made enormous strides in understanding the way that genetics underlie behavioral disorders just as they do physical diseases, but it does mean that we need to temper our expectations.
The second puzzle is an evolutionary one. If we assume that humans as well as animals evolved through natural selection, and we know that natural selection means that those individuals best suited to their environments leave more offspring, why do so many apparently defective behaviors exist? Surely it can’t be any more helpful to a dog to be afraid of thunderstorms than it is for a human to fear heights. This is a form of a larger concern, namely, as psychiatrist and evolutionary medicine proponent Randy Nesse puts it, “Why did natural selection leave our bodies with traits that make us vulnerable to disease?”8 In other words, why hasn’t evolution taken care of our defects and left us perfectly adapted to our circumstances?
An early version of this question and a proposed answer appeared in the estimable medical journal The Lancet in 1967, when John Price from the Institute of Psychiatry in London plaintively asks, “Why then are we as a species lumbered with these most disagreeable tendencies—why are we all not paragons of calm, energetic happiness?”9 Price suggests that we can ascribe our difficulties to a problem in our dominance relationships, inherited from our primate ancestors, and has a rather Mad Men approach that does not wear well with the ensuing decades since his paper. He claims that “in our evolution we passed through a stage in which small social groups were regulated by strict dominance hierarchy, much as now exists in societies of baboons and macaques.” Well, except that as it happens, baboons and macaques are a diverse group of primates, with a wide variety of social systems, not all of which exhibit a dominance hierarchy at all. Further, little evidence exists that we humans had such a hierarchy in our evolutionary history; the family life of early humans is still hotly contested.
Undaunted, Price thinks our troubles are all rooted in problems with our place in the hierarchy, suggesting that “in depressed patients the irritability is manifested to ‘inferiors,’ such as the wife and children (or husband).”10 Here the idea seems to be that lower-ranking individuals can keep from sinking even lower if they are irritable in their responses to others. Again, no evidence exists that irritability keeps a baboon from being dominated, even if said baboon is actually in such a hierarchy. Finally, Price says, “Depression may be commoner in females, and this accords with the fact that in animal groups the status of a female depends not only on the status of her males, but also on her status within her male’s harem.” This statement briskly ignores that human social systems show no evidence of having been harem based. He also suggests that psychiatrists are like the “overlords” in baboon society, which is not a term I have ever heard used by primatologists and which does not, mercifully, seem to have gotten any traction among people who treat mental disorders.
Although Price suggests a test of his theory, using two groups of patients with psychiatric disorders, treating one in the usual way and the other by reducing hierarchy, I am unaware of any efforts ever made along those lines, which is probably all to the good. His ideas seem at best antiquated, but I detail them because they illustrate how easy it is to construct plausible (at least to some) stories about the evolution of behavior without considering alternative explanations or even making sure they are based in fact. And to his credit, Price was one of the few psychologists willing to entertain the idea that animals themselves might show a form of a human disorder, even if it is a baboon sulking because it has descended from alpha to beta.
Other theories about the evolution of human mental illness have often focused on depression, perhaps because it is so pervasive, with the World Health Organization declaring it to be the leading cause of disability worldwide.11 Those theories all posit a potential benefit to depression, or at least one that might have applied during our evolutionary history. For example, maybe depressed people can better conserve their resources in times of scarcity for use at a more propitious time, or (linked to Price’s idea) perhaps being depressed means you are more likely to retreat from a fight with a more powerful opponent. Another suggestion is that depression is a kind of cry for help, so that if a bond is threatened, depression serves to keep sufferers from being socially excluded. In a related hypothesis, depressed people are less likely to take risks in social situations, something that may be useful if those situations are challenging to their welfare.
Nesse takes a different approach, one that does not suggest an advantage to the ailments themselves. He points out that saying disorders exist for a reason is vastly different than saying they exist for a purpose.12 Illnesses and dysfunction abound, both mental and physical, and we know—or at least we should know—that natural selection doesn’t produce the absolute best solution to a problem, for many reasons. A thorough discussion of these reasons is beyond the scope of this book, but a few are obvious. For one thing, bodies and minds evolve with many attributes at once. It would be ideal, for instance, to have lower backs that did not ache with age or exertion, but our spines are structured the way they are because of our bipedal stance. Such trade-offs may constrain the evolution of many things. We also get sick because many of the microorganisms that make us ill evolve more quickly than we do, and sometimes they get the upper hand.
It’s also often been suggested that mental illness is one of the so-called diseases of civilization, emerging from the stresses of modern life. The notion that agriculture, or the Industrial Revolution, or the advent of other forms of technology made us worse off than our forebearers has a long history. Such notions are often accompanied by romanticizing the practices of hunter-gatherers and assuming that life closer to nature, whatever that means, is preferable. It is true that some ailments, like hypertension and diabetes, are much more common than they used to be, and that our diets of calorie-rich and nutrient-poor foods, combined with a lack of exercise, are not conducive to health, mental or physical. But we still see cancer in preindustrialized peoples, and depression, as well as other mental illnesses, occurs in cultures all around the world, even if they are not given the same term.
Instead, Nesse makes the case that “anxiety and low mood exist for the same reason as pain and nausea: because they are useful in certain situations.”13 Pain can help you yank your hand away from a fire, and nausea rids the body of harmful substances. This doesn’t mean that they are pleasant, just that they have a function. More broadly, he argues, diseases themselves are not adaptive or advantageous. Instead, the things that make us vulnerable to disease, such as the aforementioned trade-offs, are the result of evolution.
Although a psychiatrist himself, Nesse takes a dim view of the way traditional psychiatry characterizes the symptoms of mental disorders. Rather than seeing such symptoms as responses produced by a particular illness, according to Nesse, traditional psychiatry confuses the symptoms with the illness itself. It would be as if we had a disorder called Fever, or Abdominal Pain, rather than recognizing that many different diseases can produce either one. He suggests that, similarly, depression is not a single disease, but a symptom of potentially several disorders. What we call mental disorders may be either extreme versions of symptoms, or system failures—dysfunction of a part of the brain or nervous system—that can manifest in several ways.
This doesn’t mean that treating symptoms is not useful. Quite the opposite. Indeed, treating a symptom like anxiety without knowing the underlying cause can actually be effective. To explain why, Nesse invokes what he calls the Smoke Detector Principle. Smoke detectors are notoriously sensitive; they often sound their alarms when you burn toast. That same sensitivity means that they will be very likely to respond to even the smallest actual fire. Similarly, we have nervous systems that overreact and worry about things that actually are of little threat. This sensitivity ensures we avoid the saber-tooth tiger or dodge the approaching car, but it also allows us to overreact to nonlethal threats and do things such as spend far too much time doomscrolling on the internet. Nesse hastens to point out that even if anxiety is useful under some circumstances, that doesn’t mean we shouldn’t treat it. Likewise, physical pain is valuable, but there are circumstances when it’s best to alleviate it, such as when we anesthetize patients during surgery.
A group of psychologists from Canada offered a slightly different but complementary approach.14 They distinguish between mental disorders that exist despite natural selection, and those that exist because of it. The former group includes autism and some forms of schizophrenia and bipolar disorder; evolution does not produce perfection, and many characteristics in both animals and humans are present because, for instance, the genes associated with producing them are linked to genes that are very favorable. The latter group includes anxiety and depression, as well as potentially some forms of bipolar disorder. Here, the idea is that under some circumstances, exhibiting a version of the disorder can be helpful, a la Nesse’s idea about anxiety and smoke detectors. Either way, these views of mental illness suggest that they would be found in animals as well as people.
A Model Mental Patient: Too Much of a Good Thing
One of the best places to see the continuity of behaviors in humans and animals, along with their dysfunction, is in forms of obsessive-compulsive disorder, OCD. This disorder is characterized in humans by patterns of unwanted thoughts and fears, often of germs or infection or the need to order elements in the environment, that then lead to repetitive behavior like hand washing. The National Institute of Mental Health estimates the lifetime prevalence of OCD among US adults at 2.3 percent, with high costs in both productivity and functioning.15 It is treated with a combination of drugs and behavioral therapy.
People have noticed for many years that some of the characteristics of OCD are also seen in other animals, particularly dogs. Some breeds of dogs are prone to what is called canine compulsive disorder, CCD, which makes dogs exhibit exaggerated and repeated licking, tail chasing, and other behaviors that are normal if they are only performed in limited amounts but pathological if they are performed to extremes. The name is different, because we can’t know what dogs are or aren’t obsessing over, but in both humans and dogs the disorder is characterized by what Elinor Karlsson, the scientist studying dog genetics I mentioned in chapter 4, calls “doing normal things too much.”16 She points out that both OCD and CCD are treated with the same drugs, and with about the same success, which unfortunately isn’t very high. She and her colleagues have been studying CCD as a way to both treat our pets and to understand the genes associated with human OCD.
Karlsson and her team have identified variants of genes that affect a dog’s risk of showing the disorder.17 These genes govern the way nerve cells communicate, in particular within the regions of the brain that have to do with learning and memory. Dobermans are one of the breeds particularly prone to CCD, and so her lab initially zeroed in on testing Dobermans for the presence or absence of the genes in question. As with virtually all characteristics, however, simply knowing a dog’s genetic makeup won’t tell you definitively whether or not he or she will exhibit the disorder. Dogs, like humans, inherit one copy of any particular gene from their mother and one copy from their father, offering the opportunity to have both copies be the same variant or to have one of each. Of the Dobermans with two “normal” copies, 10 percent have CCD; of the ones with one copy of each type, the “normal” and the “abnormal” one, 25 percent have it; and of the dogs with two “abnormal” copies, 60 percent show CCD. Knowing the dog’s genetic profile doesn’t let you know the dog’s behavior. This is why we can’t ever expect to see a genetic diagnostic test for CCD, much less OCD.18
Karlsson emphasized that the connection between the gene copy and CCD is just the start to understanding how the disorder is inherited. After finding the genetic variants associated with CCD in that first group of Dobermans, you then need to get a completely new group of dogs, use their genetic information to predict which ones are likely to have the disorder, and then see whether you are correct. After that, you have to repeat the whole procedure with mixed-breed dogs and dogs from other breeds. Such a daunting set of tasks is virtually never performed with large populations of animals, but Karlsson is determined to take it on, and then some. She is using the Darwin’s Dogs project, which I noted in chapter 4, in part to unravel the connection between genes and disorders such as CCD. When Karlsson is asked how many dogs she wants to enroll in the project, sometimes she says, “All of them!” with a smile. Other times she offers a more modest “Zillions!”
Dogs are not the only creatures used as models for OCD. A group of scientists from South Africa has been examining repetitive behaviors such as jumping and backward somersaulting in deer mice,19 which are native to North America and differ from the common laboratory mouse, which is bred from the European house mouse. The deer mice can be reared in groups like lab mice, and they vary in how much of the stereotyped behaviors they exhibit. Researchers can separate them into groups that show a lot, some, or none of the actions. The mice are useful because they are easier to experiment on than dogs. Their OCD-like activities can be modified with both drugs and by changing their social environment—mice from the high compulsive group can be made to spend more time with each other than they do with a mouse that didn’t show the stereotyped movements.
In people, dogs, and mice, we say that some individuals have a disorder because they do a particular behavior “too much.” So how much—turning, flank chewing, somersaulting—is too much, and what does it mean to see similar dysfunction in such different animals? Nicholas Dodman, a veterinarian who has written extensively on animal behavioral disorders,20 wonders if OCD in humans emerged from hunting and gathering, so that behaviors that were normal in moderate amounts, such as a concern with storing food, became hoarding. Since similar behavioral compulsions occur in other species, it seems unlikely that OCD emerged after the hominin line became distinct. Dodman’s speculation, however, is another good illustration of how easy it is to construct a story about the evolution of a human behavior based on something that is imagined to have occurred in our prehistory. Psychologists studying both animals and humans struggle with definitions of diseases, and OCD and CCD (no one seems to call the mouse equivalent MCD) show us the blurred line not only between animal and human behavior but also between normal and abnormal behavior in both.
Even if animals exhibit symptoms that look like human mental disorders, that doesn’t mean they are the same thing. Instead, the symptoms just may be alike because common evolutionary roots in our brains and bodies can give rise to different structures or behaviors. Animals often show highly stereotyped behaviors; early observers of animals were fascinated by the way that many species repeat the same behavior in exactly the same way, even if the stimulus is removed. For example, a nesting goose retrieves an egg that rolls away from her using a set series of movements with her head and neck. If a curious scientist removes the egg while the goose is midway through her actions, the goose simply carries on as if nothing had happened, carefully angling the invisible egg back into the nest the exact same way she does every other time. She does not have what I suppose we could call GCD, for goose compulsive disorder, but the stereotyped, invariant repetition of a behavior, one that suggests the roots of human OCD lie deep in our evolutionary history.
The Anxious Crayfish
It’s time to return to the crayfish. As I mentioned previously, the only anxiety I observed in my animal behavior lab was in the students, but I may not have been looking hard enough. Pascal Fossat and his colleagues from the Université de Bordeaux in France say that they have demonstrated “anxiety-like behavior”—which the media quickly abbreviated to simply anxiety—in the clawed crustaceans.21 The researchers presented the crayfish with a maze in an aquarium in which some arms were lit and others were left in darkness. Under ordinary circumstances, the animals explore the whole area but prefer the darker branches, presumably an evolved response that enables them to avoid daytime predators like herons. But if the crayfish were stressed by subjecting them to mild electric shocks, they stopped exploring the maze and were less likely to stay even briefly in the lighted arm, a response the scientists interpreted as characteristic of anxiety. That same behavior could be induced by injecting nonstressed crayfish with serotonin, a hormone also associated with human anxiety. A drug that reduces anxiety in people likewise reversed the changes in behavior when it was administered to the stressed crayfish, but the drug had no effect on unstressed crayfish.
Crayfish readily fight with each other, with a recognizable winner and loser, and a later study by this group of scientists found that the loser of staged battles was more likely to avoid the lighted branch of the maze than the winner, a response that again could be modified with an antianxiety drug. And in 2019, the same research group published a paper22 in which they asked, “Do arthropods [the group of animals that includes insects, spiders, and crustaceans] feel anxious during molts?”
Crayfish, along with many other members of their tribe, certainly seek out safe places when they are shedding their outer skeleton; think of it like shedding a pair of extremely tight, stiff pajamas that keep your internal organs contained, revealing a damp and flimsy pair underneath that takes time to harden. During and immediately after that transformation, the animal is extremely vulnerable to being eaten, and Fossat’s group says that “molt events can be considered very stressful, which raises the question of whether arthropods fear molting.”23 They hint that the answer might be yes.
But does it, in fact, raise that question? Certainly we humans would find completely changing our skeleton unsettling, but maybe it’s no different for the crayfish than it is for us changing clothes. Maybe it’s like being able to put on sweat pants after struggling through a day in Spanx.
The scientists are not claiming that crayfish feel exactly what a person with social anxiety feels when walking into a room of strangers, though that is certainly the conclusion drawn in most of the media coverage of the work. The same drug affects both crayfish and humans, but that simply underscores how we arose, all of us, from common ancestors. Serotonin, sometimes called the happiness hormone, also affects feeding in Drosophila; urine production in assassin bugs; sleep in pigeons; social status or cooperation in lizards, reef fish, and octopus; and learning and memory in bees. In worms, it slows down movement when a hungry worm encounters food. It’s all a far cry from targeting anxiety, much less happiness.
That laundry list of effects of serotonin reminds me of the old saying from Nobel laureate Francois Jacob that “evolution is a tinkerer, not an engineer.”24 We don’t start afresh with each new species, reinventing a limb or a nerve cell as if engineering it for the first time. Instead, like a tinkerer making something out of the bits and pieces lying around in the garage, the same scraps of DNA in one animal appear in a different form in a new one. This means that we don’t need to figure out whether the crayfish feel anxiety the way people do. They almost certainly do not, given our different environments, brains, and lifestyles—it would make me extremely anxious to lay a batch of eggs and wander around with them pressed to my abdomen for days until they hatch, but the crayfish seem unperturbed. Our serotonin has simply been used for something different from theirs.
Unhappiness at the Zoo
Having discovered that the same drugs can work in animals and people, veterinarians have often employed them not only in pets but also in other animals that are around people. In the book Animal Madness, author Laurel Braitman describes behavioral dysfunction, often heartbreaking, in captive animals ranging from elephants to dolphins to pet dogs and cats. Noting that many of them are on psychotropic drugs, she says, “Finding out that the gorillas, badgers, giraffes, belugas, or wallabies on the other side of the glass are taking Valium, Prozac, or antipsychotics to deal with their lives as display animals is not exactly heart-warming news for most people who go to zoos, theme parks, and aquariums.”25 It’s hard to disagree. We like to think that animals we watch in enclosures are going about their business, but simply made more visible to us as observers, even though that is almost certainly not true.
At the same time, the statement reveals our ambivalence about the distinction between mental and physical illnesses, as well as between human and animal mental disorders. Presumably, if we learned that the zoo animals were being treated for physical ailments, if they were getting deworming medicine and having their kidney stones removed—which they are—we would wholeheartedly approve. And animals in nature certainly do suffer from a wide variety of parasites and diseases, all of which go untreated by veterinarians in the wild, and we seem fine with that as well, or at least accepting.
Why, then, do we feel so differently about treatment for mental illness, or are so convinced that behavioral dysfunction is caused by something we humans do? The answer, I suppose, is that we see the behavioral disorders as a preventable outcome of mistreatment. Many of the authors writing about mental illness in pets agree. The implication is that animals in nature never get mental diseases, which I freely confess doesn’t sit well with me. For one thing, it brings us back to that separation between humans and other animals: Does it really make sense that people can have disorders like depression, which are seen in many different cultures and environments around the world, but animals never do? When in our evolution did our capacity for such dysfunction emerge? Did Neanderthals have OCD or depression? Since behavior and physical appearance and function are so closely linked, as I have been arguing throughout this book, it seems unnecessarily artificial to be okay with helping animals with broken legs but not with broken hearts. There are differences, to be sure, but they are not as clear-cut as one might think.
Furthermore, if we are going to be so distressed about elephants on Prozac, how do we feel about people who need the medication? Finding out that our colleagues, neighbors, and relatives are using psychotropic drugs “to deal with their lives” on our own side of the glass shouldn’t make us cringe, should it? So why would learning that animals can be helped by such drugs trouble us? Valid concerns exist about the use of drugs to treat mental problems, but why wouldn’t medication be at least part of the treatment? The issue of overmedicating people to treat their psychological conditions is beyond the scope of this book, but we need to come to terms with our double standards, both with regard to human versus animal mental disorders, and with regard to physical versus mental conditions. An important distinction is that the animals cannot choose to be medicated, or made captive for that matter. This is to say the issue of the welfare of zoo animals is separate from how we feel about their mental disorders or lack thereof.
Schizophrenia
If it seems hard to say whether an animal is obsessed with a particular thought or idea, that difficulty is magnified many times over when humans try to decide whether animals suffer from hallucinations or delusions, as they would if they had schizophrenia. Scientists have known for some time that a tendency toward schizophrenia can be inherited. They also agree that many genes contribute to the likelihood of developing the disorder, and that the environment also plays a large role.
Modern genomic techniques, in which large swathes of DNA can be examined from thousands of people, are giving some clues about which genes might be important in schizophrenia, and when they might have evolved. A study led by Barbara Stranger of the University of Chicago identified genetic regions that seemed to protect against schizophrenia and found that selection favored those variants, meaning that they were more common than expected through chance.26 Why, then, does the disease persist? No one knows for certain, but several researchers have suggested that the rapid evolution of the human brain, and particularly the regions associated with speech, may have produced vulnerability to schizophrenia. One section of the genome that evolved rapidly in the ancestors of modern humans is important in transmission of a neurochemical that regulates nerve activity, particularly speech and language, and that same neurochemical malfunctions in people with schizophrenia. Joel Dudley, a scientist involved in the work, speculated that the risk of schizophrenia might have evolved as humans became more intelligent.
All of these scenarios assume that other animals do not suffer from schizophrenia, and indeed, as I noted earlier, some psychologists say exactly that. They still, however, use animals to understand both the brain alterations that occur in people with the disease and the potential effects of antipsychotic medications. For example, a 2018 study27 found that mice deprived of their mothers at a young age showed brain and neurochemical changes similar to those in people with schizophrenia. The mice also behaved differently compared with mice left with their mothers. This does not mean that the absence of a mother—whether you are a person or a mouse—induces psychosis. However, it does reinforce the notion that the environment and genes interact, as they do for all behaviors.
Similarly, scientists found a genetic variant in humans involving about twenty genes that changes the way the nervous system develops.28 About 30 percent of people who show this variant will develop schizophrenia. It is possible to engineer mice with a similar genetic alteration, but the mice do not have schizophrenia themselves, and that is not why the mice were bred. Instead, these mice enable researchers to determine which drugs might be most effective at countering the nervous system changes caused by the genes, and to see how the molecular mechanisms that mice have in common with humans can help us understand the brain.
As with other mental disorders, people have tried to think of ways that schizophrenia could have been advantageous in our evolutionary history, including the idea that people with the disease became shamans or exceptionally creative individuals who fulfilled important societal roles. Even if this were true, for the disease to have been the result of natural selection, people with it would have to have more children to pass along their genes than people without it, and no evidence suggests that this is the case. Other correlations between schizophrenia and various attributes such as where people live have been found now that big genetic datasets can be screened. A genetic tendency to schizophrenia was found more often in parts of Europe that had relatively lower winter temperatures, for instance, but it’s hard to even know where to start inventing an evolutionary rationale for that one. I think it is more likely that, as Nesse points out, there are limits to what natural selection can do, and eliminating schizophrenia may simply not be possible.
Schizophrenia as we characterize it in people may have emerged with the evolution of our gigantic brains, which makes it reasonable to think that other species don’t suffer from it. At the same time, since we can only rely on people’s reports of what they experience when they have the disease, it’s hard to definitively say that animals don’t have some version of similar brain dysfunctions. Part of the problem is the confusion of symptoms with disease: Is schizophrenia equivalent to the delusions and disordered speech we use to diagnose it? Lacking a definitive test that we could administer to either people or animals, we are left without an answer.
Philosophy, Veterinarians, and Alcoholism
The question of mental disorders in animals has not been of interest only to psychologists. Philosophers Krystyna Bielecka and Mira Marcinów29 suggest that animals do indeed have what they refer to as mental misrepresentations, which means they can be just as delusional as human beings. Like other scholars, they note that depression, or behavior that looks like it, arises in animals from what is called learned helplessness. If one places animals under conditions where they cannot escape a painful stimulus that arrives unpredictably, they develop a kind of resignation in which, even after the opportunity to better their situation presents itself, they do not take it. Similarly, in humans one notion is that depression emerges partly from a sense that circumstances are so beyond one’s control that effort is futile.
The philosophers argue that stereotyped behaviors in zoo animals, such as repeated pacing or swimming in circles, may well result from delusions that are hard to distinguish from what we see in humans who are likewise misrepresenting reality. They go so far as to draw an analogy to a frog that flicks its tongue out to catch a fly, expecting a tasty snack, but nabbing a bee instead.30 This suggests to the philosophers that the frog has been delusional. I am not convinced by this, since it seems difficult to posit expectation in an amphibian, but then we may find it hard to declare for certain that another person’s delusion is false as well.
On a more practical level, veterinarian Nicholas Dodman takes a kind of reverse engineering approach to mental illness in animals.31 He has had great success in treating animals with several behavioral problems, including compulsive disorders, post-traumatic stress disorder, and a form of attention deficit disorder, using the same drugs that would treat a similar mental condition in humans. He concludes that if the same solution works in both, the cause of the problem must be the same as well. In books like Pets on the Couch and The Dog Who Loved Too Much, Dodman expounds on the idea that animals’ emotions, and hence their behavioral disorders, are very much like those of humans. Although he acknowledges that “humans have the edge cognitively” (as we will see in chapters 7 and 8, that depends on one’s definition of edge), he mocks scientists who, he claims, dismiss out of hand the idea that their pets or farm animals are experiencing the same emotions as humans: “At times it seems as though some scientists are the ones with conditioned reflexes, not animals. They hold stubbornly to their mistaken beliefs, all evidence to the contrary.”32
But is all evidence really to the contrary? Just because the same drugs that change behavior in humans change analogous behavior in animals doesn’t mean that we all have the exact same disease; it just means that our brains and bodies are similar, something our shared evolutionary history already told us. It seems to me that we can be similar without being exactly the same, and furthermore that we can be similar to different degrees. Not all animals are the same, and indeed a dog is different from a gazelle or a parakeet. I am not sure what Dodman would conclude about those crayfish, for example. He claims that “we possess the mental equivalent of a mainframe computer atop our shoulders, while the animals must make do with the less sophisticated but functionally similar Commodore 64 version.”33
Some of the discussions about mental diseases in animals act as though we only have two choices: either animals are unfeeling robots that share no similarity with humans, or we are all exactly the same, with things such as jealousy in a cat or anxiety in a crayfish being indistinguishable from the same conditions in a person. I don’t think that’s accurate. When it comes to mental disorders in animals, and whether or how they are like the same disorders in humans, I feel about the same way I do about animal emotions, namely that they don’t have to be just like the human version to exist. This is no surprise, since of course emotions are often malfunctioning in mental diseases. It doesn’t make sense that humans and only humans would suffer from mental disorders. We all aren’t alike physically, so why should we be alike behaviorally?
Finally, an interesting way to think about animal- and human-shared mental state comes from a 2020 examination of intoxication in animals.34 Humans have been producing and drinking alcohol for many thousands of years, and the popular media is filled with stories of drunk moose, monkeys, elephants, and even birds and butterflies. It would be easy to conclude that a fondness for alcohol, and the subsequent dangers of its abuse, is deeply ingrained in our biology. Yet not all animals show the same predilections. Indeed, there is difficulty in using rodents as models for research on alcoholism because rats and mice will not drink enough to become intoxicated, even if the alcohol is offered in unlimited quantities.
A group of scientists from the University of Calgary decided to test an idea about how the genes that are important in the metabolism of alcohol would be expected to vary across eighty-five species of mammals depending on the animals’ diet.35 The researchers hypothesized that animals that eat fruit or nectar, which have the potential to ferment, would be more likely to show genes that would be able to break down alcohol than animals that eat other things. This thesis turned out to be only partially correct. Although many species that consume fruit do indeed have genes that help them process alcohol, those genes are also present in animals such as shrews, which live exclusively on insects and wouldn’t touch a rotting fruit if they tripped over it. What this means is that alcohol metabolism, and hence an ability to become intoxicated or seek out the source of intoxication, is not one of those deep-seated characteristics that we inherited from our evolutionary ancestors. The researchers conclude that “human-level efficiencies” in alcohol digestion are unlikely in other mammals, and further caution that “it is a mistake to assume that animals share our metabolic and sensory adaptations or limitations.”36
Such findings do not mean that we cannot compare ourselves to other species, whether in our search for models of alcoholism or OCD, but that we need to do those comparisons judiciously. As with the idea of emotions in nonhumans, our choice is not that animals are either exactly like us or completely different. We also do not need to create a club in which we admit dogs with CCD, pacing polar bears, and anxious crayfish, but exclude everyone else. When it comes to mental illness, animals can be like us in some ways and like themselves in others.