Many of us have known a dog on Prozac. Additionally, we have seen the eye rolls that accompany canine psychiatry Doting pet owners, like myself, attribute all kinds of dubious psychological disorders to our four-legged friends. However, science does indicate that a variety of non-human species experience psychiatric symptoms. Birds have obsessions, horses occasionally experience pathological compulsive behavior, and dolphins and whales, particularly those kept in captivity, self-mutilate. And when your dog sadly gazes out the window as you pull out of the driveway, that may be DSM-diagnosed separation anxiety. Every creature with a mind has the ability to occasionally lose control of it, according to science historian and author Dr. Laurel Braitman in “Animal Madness. “.
But while many mental illnesses affect humans, at least one appears to have spared all other animals: schizophrenia. Although psychotic animals may exist, psychosis has never been seen outside of our own species, in contrast to the many non-human species that have been reported to exhibit depression, OCD, and anxiety traits. When it would seem that genes predisposing to psychosis would have been strongly selected against, it begs the question of why such a potentially devastating, frequently fatal disease—which we now know is heavily genetic, thanks to some genomically homogenous Icelanders and plenty of other recent research—is still around. A recent study offers hints as to how schizophrenia might have developed in the human brain and suggests potential treatment targets as a result. It appears that psychosis may be an unfavorable side effect of our large brains and higher-order cognitive abilities.
The study, led by Mount Sinai researcher Dr. Joel Dudley suggested that since schizophrenia affects over 1% of adults despite being extremely harmful, it may have a complicated evolutionary history that would explain its persistence and uniqueness to humans. They were particularly interested in our genome’s human accelerated regions, or HARs. Short DNA segments known as HARs, which are conserved in other species but rapidly evolved in humans after our separation from chimpanzees, are likely responsible for some benefit unique to our species. HARs frequently assist in regulating nearby genes rather than encoding for proteins themselves. The researchers questioned whether there might be a connection between schizophrenia and HARs since both conditions appear to be primarily human-specific.
Dudley and colleagues used information from the Psychiatric Genomics Consortium, a large study that identified genetic variants linked to schizophrenia, to find out. They first determined whether genes linked to schizophrenia are located near HARs along the human genome—closer than would be anticipated by chance. It turns out that they do, indicating that HARs participate in the control of genes linked to schizophrenia. Additionally, it was discovered that HAR-associated schizophrenia genes were under more evolutionary selective pressure than other schizophrenia genes, suggesting that human variants of these genes are useful to us despite carrying schizophrenia risk.
Dudley’s group then turned to gene expression profiles to clarify what these advantages might be. Gene expression profiling reveals the locations and times in the body where specific genes are actually active, as opposed to gene sequencing, which provides the genome sequence of an organism. The prefrontal cortex, a part of the brain located just behind the forehead involved in higher order thinking, is a region that Dudley’s team discovered to contain HAR-associated schizophrenia genes. Its dysfunction is thought to be a factor in psychosis.
Additionally, they discovered that these offending genes play a role in a number of crucial human neurological processes, including the synaptic transmission of the GABA neurotransmitter, in the PFC. By suppressing dopamine in specific regions of the brain, GABA acts as an inhibitor or regulator of neuronal activity. Its impaired transmission is thought to play a role in schizophrenia. If GABA isn’t working properly, dopamine overflows and contributes to the psychotic symptoms of hallucinations, delusions, and disorganized thinking. In other words, the schizophrenic brain lacks restraint.
The study’s ultimate objective, according to Dudley, was to determine whether evolution could offer new insights into the genetic makeup of schizophrenia that would help us better comprehend and identify the condition. Finding out which genes are most associated with schizophrenia and how they express themselves could result in more efficient treatments, such as those that affect GABA function.
But the research also provides a potential explanation for how schizophrenia first developed in humans and why it doesn’t appear to affect other animals. According to some theories, the development of human speech and language has a connection to the genetics of both autism and schizophrenia, says Dudley. In fact, GABA is essential for speech, language, and many other aspects of higher-order cognition, and language dysfunction is a characteristic of schizophrenia. Our evolutionary analysis’ convergence on GABA function in the prefrontal cortex appears to provide evidence that schizophrenia risk and intelligence have evolved together over time. ”.
Or, to put it another way, perhaps there’s just more that can go wrong with complex, highly social human thought—and the complex genetics at the foundation of higher cognition: complex function begets complex malfunction.
Dudley takes care not to overstate the implications of his research for evolution. He notes that although the goal of the study was not to evaluate an “evolutionary trade-off,” the results “support the hypothesis that the evolution of our advanced cognitive abilities may have come at a cost—a propensity for schizophrenia.” He also acknowledges the profound complexity of schizophrenia genetics and the lack of “smoking gun genes” found in the new research. However, he believes that evolutionary genetic analysis can assist in identifying the most pertinent genes and pathologic mechanisms involved in schizophrenia, as well as perhaps other mental illnesses that predominately affect humans, particularly autism and ADHD, which are neurodevelopmental disorders linked to higher-cognition and GABA activity.
In fact, a recent study in Molecular Psychiatry reports a connection between genes linked to autism spectrum disorder and improved cognitive function in people without the condition. The findings may explain why people with autism occasionally display exceptional talent in certain cognitive abilities. They also support Dudley’s hypothesis that enhanced cognition may have had a cost. Our genomes, and HARs in particular, hastily evolved as we split off from our primate cousins, giving us an increasing number of traits that other species do not possess. They may have done so by leaving our brains susceptible to complex dysfunction on occasion, but they may also have made them capable of biomedical research aimed at hopefully one day curing the ailing brain. At least our pugs, poodles, and pot-bellied pigs appear to be free of psychosis as Dudley and others unravel the genetic underpinnings of schizophrenia and other mental illnesses in search of improved diagnosis and treatment.
Bret Stetka is a freelance health, science, and food writer and the editorial director at Medscape, a division of WebMD. He received his MD from the University of Virginia in 2005, and he has written about brains, genomics, and occasionally both, for WIRED, Slate, and Popular Mechanics. Follow Bret on Twitter @BretStetka.
Please send suggestions to Mind Matters editor Gareth Cook, a Pulitzer Prize-winning journalist at the Boston Globe. If you are a scientist with expertise in neuroscience, cognitive science, or psychology, and have read a recent peer-reviewed paper that you would like to write about, please send suggestions. He can be reached at garethideas AT gmail. com or Twitter @garethideas.
In addition to serving as editorial director of Medscape Neurology, a division of WebMD, Bret Stetka is a writer based in New York City. His work has appeared in Wired, NPR and the Atlantic. He received his medical degree from the University of Virginia in 2005. Follow Bret Stetka on Twitter Credit: Nick Higgins.
An evolutionary approach to the genetics of schizophrenia
Why is schizophrenia uniquely human? Researchers at Mount Sinai Medical School came up with a brilliant evolutionary approach to the question.
Schizophrenia is relatively prevalent in humans despite being detrimental. The condition affects over 1% of adults. Therefore, it must be linked to something that offers a competitive advantage. And that “something” must be uniquely human.
Indeed, there are segments of our genome that are called human accelerated regions, or HARs. HARs are short stretches of DNA that while conserved in other species, underwent rapid evolution in humans following our split with chimpanzees. This is presumably because they provided some benefits specific to our species.
On the other hand, neurosis is a mental condition in which the patient is experiencing emotional stress while still being able to react to stimuli. A neurotic dog is aware of what is going on but may not react in a manner that would be considered “normal.” Genetic, environmental, or a combination of the two factors may contribute to neuroses. For instance, the neurotic behavior of a dog will only worsen if her guardian punishes her for being excessively hypervigilant toward other dogs or introduces her to a highly social environment too soon. Even though they can be controlled, obsessive-compulsive dogs—such as those who chew when stressed out, experience separation anxiety, or pace constantly—are still propelled to engage in the behavior by a confluence of genetic and environmental factors.
Four-year-old Briggs, Judy’s Labradoodle, never did well around strangers. He’d bitten several and couldn’t be trusted around most people. But Briggs could be sweet and gentle one second, then turn into a fire-breathing dragon the next, unlike the majority of aggressive dogs whose actions are motivated by fear and predictable. The local trainer had helped Judy make some progress, but Briggs’ “Jekyll-and-Hyde” behavior had everyone baffled.
Sometimes abnormal behaviors in dogs are caused by hormonal, rather than environmental, factors, such as hypothyroidism or hyperthyroidism. One typical illustration is when a dog’s thyroid gland either produces too many (hyper) or too few (hypo) hormones that control metabolism for a variety of medical reasons. Lethargy, weight gain, hair and skin problems, and other metabolic symptoms are frequently caused by hypothyroidism, whereas hyperthyroidism, a less frequent condition, results in weight loss, overeating, hyperventilating, and excessive thirst. Oddly, both conditions may make your pet angrier and less reliable. Only a veterinarian’s diagnosis and treatment of these conditions can heal them; behavior changes cannot. The need to rely on your veterinarian and a qualified behaviorist to diagnose and resolve the problem arises.
In an effort to eliminate the conditioned responses he created to deal with years of undiagnosed brain dysfunction, Briggs continues to work with trainers and takes his medication. Judy still struggles on a daily basis, but her devotion to her dog continues to be the best treatment for a condition that might lead other people to consider euthanasia. Dogs like Briggs can be managed and given a second chance with the assistance of a good behaviorist and the tender care of an excellent veterinarian.
There are numerous canine behavioral disorders that can be treated with medication that alters behavior, according to Dr. Susan Mailheau, a Seattle, Washington-based veterinarian. “These include Clomipramine, Fluoxetine, Benzodiazepine, and Phenobarbital. ”.
But while many mental illnesses affect humans, at least one appears to have spared all other animals: schizophrenia. Although psychotic animals may exist, psychosis has never been seen outside of our own species, in contrast to the many non-human species that have been reported to exhibit depression, OCD, and anxiety traits. When it would seem that genes predisposing to psychosis would have been strongly selected against, it begs the question of why such a potentially devastating, frequently fatal disease—which we now know is heavily genetic, thanks to some genomically homogenous Icelanders and plenty of other recent research—is still around. A recent study offers hints as to how schizophrenia might have developed in the human brain and suggests potential treatment targets as a result. It appears that psychosis may be an unfavorable side effect of our large brains and higher-order cognitive abilities.
In fact, a new study published in Molecular Psychiatry reports a link between gene variants associated with autism spectrum disorder and better cognitive function in people without the disorder. The findings may help explain why those with autism sometimes exhibit extraordinary skill at certain cognitive abilities. They also support Dudley’s speculation that higher cognition might have come at a price. As we broke away from our primate cousins our genomes—HARs especially—hastily evolved, granting us an increasing cache of abilities that other species lack. In doing so, they may have left our brains prone to occasional complex dysfunction—but also capable of biomedical research aimed at one day, hopefully, curing the ailing brain. As Dudley and others untangle the genetic underpinnings of schizophrenia and other mental illnesses in search of improved diagnosis and treatment, at least our pugs, poodles and pot-bellied pigs seem to be psychosis free.
Many of us have known a dog on Prozac. Weve also witnessed the eye rolls that come with canine psychiatry. Doting pet owners—myself included—ascribe all sorts of questionable psychological ills to our pawed companions. But the science does suggest that numerous non-human species suffer from psychiatric symptoms. Birds obsess; horses on occasion get pathologically compulsive; dolphins and whales—especially those in captivity—self-mutilate. And that thing when your dog woefully watches you pull out of the driveway from the window—that might be DSM-certified separation anxiety. “Every animal with a mind has the capacity to lose hold of it from time to time” wrote science historian and author Dr. Laurel Braitman in “Animal Madness.”
The study, led by Mount Sinai researcher Dr. Joel Dudley, proposed that since schizophrenia is relatively prevalent in humans despite being so detrimental—the condition affects over 1% of adults—that it perhaps has a complex evolutionary backstory that would explain its persistence and exclusivity to humans. Specifically they were curious about segments of our genome called human accelerated regions, or HARs. HARs are short stretches of DNA that while conserved in other species, underwent rapid evolution in humans following our split with chimpanzees, presumably since they provided some benefit specific to our species. Rather than encoding for proteins themselves, HARs often help regulate neighboring genes. Since both schizophrenia and HARs appear to be for the most part human-specific, the researchers wondered if there might be a connection between the two.
Additionally, they discovered that these offending genes play a role in a number of crucial human neurological processes, including the synaptic transmission of the GABA neurotransmitter, in the PFC. By suppressing dopamine in specific regions of the brain, GABA acts as an inhibitor or regulator of neuronal activity. Its impaired transmission is thought to play a role in schizophrenia. If GABA isn’t working properly, dopamine overflows and contributes to the psychotic symptoms of hallucinations, delusions, and disorganized thinking. In other words, the schizophrenic brain lacks restraint.
FAQ
Can your dog have schizophrenia?
Science suggests that numerous non-human species suffer from psychiatric symptoms. But while many mental illnesses affect humans, at least one appears to have spared all other animals: schizophrenia. Although there may be psychotic animals, psychosis has only ever been seen in members of our own species.
How can you tell if your dog is mentally ill?
…
Compulsive Behaviors
- Barking.
- Chewing.
- Excessive licking.
- Pacing.
- Snapping at the air.
- Spinning.
- Sucking on toys.
- Tail chasing.
What mental disabilities can dogs have?
- Separation Anxiety. One of the most prevalent canine mental illnesses is this one.
- Social Anxiety. …
- Noise Anxiety. …
- Depression. …
- CCD (OCD) …
- Post-Traumatic Stress Disorder (PTSD) …
- Exercise. …
- Mental stimulation.
Why is my dog acting delusional?
Dogs can behave strangely in a variety of ways, but they can all elicit the same unsettling emotions in us. Your dog may be acting strangely for a variety of reasons, such as illness, injury, boredom, anxiety, issues with their diet, or changes to their environment.