In part 1 of Mental illness exists for a reason, we discussed the evidence behind genetic control of temperament in two different primate species, Chimpanzees and Bonobos.
In part 2, we discussed how having a variation of behaviours within a species makes that species adaptable to a broad range of environments. Voles were a great case study on how polymorphic genes lead to a variety of behaviours within a species, allowing voles to thrive in a wide range of habitats on the planet.
In part 3, we will be discussing the role of the gene we have been examining, vasopressin 1a receptor, in human behaviour, and extrapolating from that why mental illness may exist.
Humans are not voles. Before we get started, I want to reiterate that there are thousands of genes which interact to have an effect on human behaviour. No one gene is responsible for the beauty that is the human mind. When we examine human behaviours in studies, like the one I will be discussing today, we are observing trends in behaviour, and not absolute rules. Remember, personality is thought to be at most 50% genetic, and each one of those thousand genes are in direct interaction with each other, and our ever changing environment, at any given moment, to produce the “climate” of traits that becomes our personality.
So what’s the deal with vasopressin 1a receptor? What is it anyway?
In the human body, brain function is dependent on something called neurotransmission. In a nut shell, neurotransmission is when two different nerve cells, called neurons, communicate with each other. Neurons are constantly communicating with each other at any given time to produce consciousness, vision, hearing, touch, and just about any neurological function you can imagine.
How does neurotransmission occur? Through chemicals called neurotransmitters. In a neuron “discussion,” the first neuron sends a neurotransmitter to the second neuron. There is a receptor on the second/receiving neuron that picks up the message. Vasopressin 1a is this kind of receptor. Depending on the shape or form of the receptor, different things will happen to the second/receiving neuron. This is how variation in the receptor produces variation in effects!
Why is this important? Vasopressin 1a receptor has been implicated in pair bonding behaviours, across a wide range of species, including humans, chimpanzees, bonobos, and voles. Consistently, a “longer” form of the gene has been associated with increased pair bonding and less aggressive behaviours. Think the lazy, horny Bonobo and the monogamous Prarie Vole’s. And some humans.
A group at John Hopkins set out in the mid-2000’s to investigate the role of vasopressin 1a receptor in humans. You can read their study here. To summarize, the group found that a number of variations of the vasopressin 1a receptor exist in humans. That makes this a polymorpic gene. As expected, certain forms of the gene correlated with certain behaviours in humans. Longer forms of the gene were associated with increased pair bonding, as determined by a questionnaire. Amazingly, not only did carriers of the longer gene tend to report happier marriages, their partners did as well. Carriers of the shorter gene were unhappier in their marriages on average and were considerably more likely to have had a threatened divorce within the last year.
So why can’t we all be married, well fed, and happy?
Like the Prarie Vole, humans live in a wide variety of environments. This is different than Chimpanzee’s and Bonobo’s, who are really good at living in the kinds of places they live, but not great at living elsewhere. Humans live in mountains, on swamps, the plains, the coasts. There’s hardly a terrestrial environment on this planet that we haven’t conquered. The point? Humans have had to be extremely adaptable to achieve this level of success across the wide range of environments we inhabit. This doesn’t only apply to geography. The massive differences between an urban metropolis and a rural village cannot be understated. The variation in cultures across the West and East is difficult to appreciate. These differences in the societies in which we lives requires a broad range of behaviours to be within our species to succeed. We need people who thrive in a big city, among thousands of their peers, in cramped, noisy, stimulating environments. Without them, the economic engines of our nations would collapse. We need people that can’t stand the city, who need wide, open expanses, and tranquility to survive. Without them we wouldn’t be able to feed the masses. The point is that variation in our personalities allows some of us to succeed, and to excel, so that society and the species may go on.
But that doesn’t mean we are all meant to succeed. Or rather, that we are all meant to succeed in every environment.
Variation means exactly that – variety. For every person that thrives in a city there’s another who suffers. Sometimes, there is a fundamental mismatch between our personality, and our environment. Try as you may, a monogamous Vole ain’t gonna do well at a polygamous Vole frat party. A Bonobo chimp would be dead meat caught in a Chimpanzee civil war.
These mismatches occur in humans as well; sometimes, we may call that mismatch, a mental illness.
Join me in part 4 for a discussion of how we can use our understanding of why mental illnesses may exist to help guide treatment and recovery!
Editor’s note: I do not want to diminish the role of, “nurture,” in the nature vs nurture argument. By no means in personality 100% genetic (most studies show it’s around 50%)! This blog simply looks at the genetic side of things.
I would like to credit Dr. Albert Wong at the Centre for Addiction and Mental Health for inspiring most of the content of this blog post.
Dr. Travis Barron is a resident physician in Toronto, Canada.