Depression and Evolution

As humans, we often hold ourselves above most other animals in the world, as if we are somehow inherently more special or more important, but the fact is that we are victims to evolution just as much as anything else. The human genus, homo, developed from the Australopithecus genus, and over a few million years came to encompass nine currently known different human species, like the Homo neanderthalensis, Homo erectus, and of course Homo sapiens.

Everyone currently alive is of the human species sapien, and for a myriad of reasons all other human species have gone extinct, usually due to Homo sapiens out hunting them or encroaching on their habitats.

“The Neanderthals were displaced very soon after modern humans encroached on their habitat,” says Jean-Jacques Hublin of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.

Homo sapiens were the human best suited to long-term survival as their evolution was more focused on developing the brain it was more and more essential to develop tightly knit social bonds and communities as well as develop complex and innovative tools. Homo sapiens couldn’t physically overpower prey anymore, they had to be smarter.

Human evolution like this has had a long winding path, as the first humans or human-like creatures appeared between 5 and 7 million years ago when a type of ape-like creature started walking upright. Fast forward to today and I’m writing a piece that could theoretically be shared with thousands of people in completely different timezones, people that I’ve never met and probably never will meet. We began life as humble creatures and have since conquered the world, and are beginning to look outward toward the universe.

The primary founder of the theory of evolution, Charles Darwin, is commonly believed to have suffered from depression, among other ailments, and one of his few escapes from those ongoing issues was his work.

“Work is the only thing which makes life endurable to me,” Darwin wrote and later remarked that it was his “sole enjoyment in life.”

Ironically, depression is one of the things that, at the surface, is at odds with Darwin’s theory of evolution.

On the surface level, depression appears to be paradoxically linked to the theory of evolution. Depression is characterized by apathy, loss of interest in pleasurable activities, slowness in action, fatigue, potentially thoughts of suicide, among many other things. This appears to stand at odds with evolution, as the primary purpose of evolution is to pass on the genes best suited to survival and reproduction. More people die every year from suicide than from murder and war combined, and a leading cause of that is ongoing and chronic depression.

Many people have theorized that depression is a result of our rapid societal and technological expansions, in ways that our brains were not equipped to handle. Similar to the ongoing obesity epidemic our bodies may have just not been adapted to our modern conditions.

Though this answer doesn’t cover all the bases either, as depression has been observed in animals, and in basically every human society that has ever been closely observed, including small scale societies like the Ache of Paraguay, that lived similarly to our evolutionary ancestors.

So then, why would humans and other animals evolve depression?

One prevalent theory coming to light is that depression shouldn’t be considered a disorder at all, and instead, in most cases, it is an adaptation to extenuating factors. One reason to think that is the presence of the molecule known as the 5HT1A receptor.

The 5HT1A receptor binds to serotonin, a molecule known for its connection to depression, and most anti-depressants target serotonin. In a study of rodents, those without the 5HT1A receptor showed less depressive symptoms in response to stress when compared to those that did have it, and the rodent 5HT1A receptor is 99 percent similar to that of a human’s. The molecule shows that there is most likely an evolutionary connection to depression.

But what then is the use of depression?

The Problem Solving Hypothesis

Some hypothesize that depression allows room for rumination, or deep thoughts about negative stimuli, either past or present. This deep thought is often highly analytical and allows people to break their problems into smaller pieces to make whatever is ailing them easier to accomplish. Rumination appears in areas like mathematics tests, in which difficult or complex problems are broken up into smaller pieces and as such can be more easily solved.

An example of this is David Foster Wallace’s short story, “The Depressed Person,” which highlights this cycle of deep, ruminative thinking.

Another aspect of depressive rumination is that the analytical thinking must go on uninterrupted, and as such symptoms like hyper-isolation developed to push away distractions, as well as the inability to pull pleasure from generally pleasurable things to again, stave off any distraction.

Studies by Paul W. Andrews, J. Anderson Thomson Jr. have shown that diving deep into the thoughts elicited by this rumination, either through expressive therapy, or writing generally helps alleviate depressive symptoms faster than normal as well. Laboratory studies also show that people with depressive symptoms are more able to solve complex social dilemmas as well.

A counter to this hypothesis, however, is the evolutionary penalties that come with depression, including a decreased libido, and the prevalence of suicide among those afflicted with the disorder.

It’s estimated that at least 60 percent of the people that commit suicide have a major depressive disorder, and that stands firmly against the idea of depression as just a mental tool, though it still may be.

Many scientists believe that the rumination theory is just another solution for an incredibly complex problem, similar to the “plea for help” hypothesis that signals a need to loved ones, or the “depressive realism” hypothesis that suggests that those with depression are more able to accurately portray reality and to predict future events.

“To say that depression can be useful doesn’t mean it’s always going to be useful,” Thomson says in a New York Times Magazine article. “Sometimes, the symptoms can spiral out of control. The problem, though, is that as a society, we’ve come to see depression as something that must always be avoided or medicated away. We’ve been so eager to remove the stigma from depression that we’ve ended up stigmatizing sadness.”

Thomson still believes that his theory at least aids in his psychological practice, and he adds that he now uses fewer anti-depressants in depression treatment as he believes it stunts actual recovery.

“I remember one patient who came in and said she needed to reduce her dosage,” he says in the same article. “I asked her if the antidepressants were working, and she said something I’ll never forget. ‘Yes, they’re working great,’ she told me. ‘I feel so much better. But I’m still married to the same alcoholic son of a bitch. It’s just now he’s tolerable.’ ”

There is support for Thomson’s aversion to anti-depressants, as a 2005 paper by a Vanderbilt psychologist, Steven Hollon, found that those that stopped anti-depressants found a 76 percent higher relapse rate within a year than those that had a form of cognitive talk therapy, which had a relapse rate of about 31 percent.

The information is still kind of grey, as much of the evidence is complex and open to interpretation. Joe Forgas, a social psychologist at the University of New South Wales in Australia, has repeatedly demonstrated in experiments that negative moods lead to better decisions in complex situations. So there may be some credence to the hypothesis.

The Immune Response Hypothesis

Another evolutionary theory for the existence of depression is pathogen and immune response in the body. In a 2012 study Dr. Andrew Miller and Dr. Charles Raison, physicians at Emory University and the University of Arizona, respectively, proposed that some of the alleles (forms of genes) that increase one’s risk for depression also enhance immune responses to infections.

Commenting on their hypothesis, Dr. Miller noted, “Most of the genetic variations that have been linked to depression turn out to affect the function of the immune system.” Dr. Charles Raison of the University of Arizona added, “The basic idea is that depression and the genes that promote it were very adaptive for helping people — especially young children — not die of infection in the ancestral environment.”

Before 1900 some of the top causes of infant mortality were infections and between revolutions in science and medicine infant mortality has dropped from about 16 percent in 1900 to under 7 percent in the 2000s, but one such thing that has remained consistent is a gene called “NPY.” Mutated versions of NPY are associated with increased inflammation which helps fight off infection, something probably very helpful for our ancestors. Today, however, people observed with the mutated NPY gene show a higher correlation for major depressive disorder, as researched by the University of Michigan’s Molecular and Behavioral Neuroscience Institute.

Per a 2013 article in The Atlantic, “Drs. Miller and Raison believe that acute (or severe but short-term) stress can not only lead to depression but also jump-start the immune system.”

It’s believed that high-stress environments for our ancestors usually resulted in wounds or injuries, and unlike today those wounds or injuries usually spelled infection and/or death, highlighting the need for an immune response which in turn is connected to depression, and as those with the mutated NPY gene were more likely to have that response and survive, they were in turn more likely to pass that gene on to their offspring.

Also in the same study, the researchers hypothesize that the body leverages the symptoms of depression to strengthen the immune response, as lethargy allows the body to focus more energy on immunity, and social isolation lowers the risk of more infectious agents from entering the body.

As a response to these correlations, researchers tried to treat those with hard to treat depression with the anti-inflammatory drug infliximab. The study as a whole did not see perfect results, but those with higher inflammation and major depressive symptoms did see a reduction in their symptoms.

The conclusion in this study was that while chronic stress overall lowers the body’s immune response, we may have, evolutionarily, found a way to alleviate some of that immune deficiency.

Another aspect of this immune response to depression is the existence of seasonal affective disorder, colloquially known as SAD. A 2004 study proposed that SAD was evolutionarily beneficial, as it lowered women’s libido during times of the year, primarily the winter, when a child born is much less likely to survive.

The Creativity Hypothesis

Another hypothesis for depression is closely related to Thomson’s rumination theory of depression though it is slightly different. Proposed in a survey led by the neuroscientist Nancy Andreasen 30 different writers from the Iowa Writer’s Workshop were questioned about their mental history, and a clear correlation between them and depression was apparent as eighty percent of the writers met the criteria for some form of depression. To further corroborate that, a deep dive into biographical studies of British creatives by Kay Redfield Jamison, a professor of psychiatry at Johns Hopkins, found that those in question were eight times more likely to suffer from a form of depression.

Andreasen argued that a certain cognitive style brought about by depression is conducive to creativity and as such cultivates creative ability, though in the same study she admitted the obvious costs of such a state of mind.

“Unfortunately, this type of thinking is often inseparable from the suffering,” she says. “If you’re at the cutting edge, then you’re going to bleed.”

The link between creativity and depression has been seen across many studies and among many creatives.

“Men have called me mad,” wrote Edgar Allan Poe, “but the question is not yet settled, whether madness is or is not the loftiest intelligence — whether much that is glorious — whether all that is profound — does not spring from disease of thought — from moods of mind exalted at the expense of the general intellect.”

Mood disorders like depression may be a benefit to creativity just hidden under a plethora of other debilitating symptoms that often don’t appear in these studies.

Though there is much debate about the said link, as Jamison writes, “Most manic-depressives do not possess extraordinary imagination, and most accomplished artists do not suffer from recurring mood swings. To assume, then, that such diseases usually promote artistic talent wrongly reinforces simplistic notions of the ‘mad genius.’”

An alternative explanation for the link between depression and creativity in people may instead focus on the lives that creatives live. Living as a creative is often punishing, with many suffering for enough money to eat or shelter themselves, and at least in historical ages, many creatives were looked down upon, or outright cast out of society.

In Conclusion

Much of the research on mental illness is in its relative infancy. The often stigmatized depictions of those suffering from mental illness make research less available, and those that suffer are often less likely to self-report. The research is still mostly theoretical, but as more work is done the picture becomes slightly clearer. This is what’s interesting about evolution, even our pain can be useful.