Evolutionary Mismatch as a Causal Factor in Adolescent Dysfunction and Mental Illness
“In the 1990s, about 40 young elephants were taken a few hundred miles closer to Johannesburg . . .
The male elephants that had been transferred became unusually violent. They were attacking each other much more frequently, sometimes attacking people, pushing cars off the road (which, in a tourist center, is more than a little concerning), but most of all, rebuffed by older females, they were going after female white rhinos, the largest available pachyderm in the neighborhood, and raping them. Then killing them.
The New York Times reported that in one month in Pilanesberg Park, officials “shot three young male elephants who were responsible for the killings of 63 rhinos, as well as attacks on people in safari vehicles.” . . .
When young male elephants approach sexual maturity, they go through a phase called “musth,” where testosterone floods in at up to 60 times the usual levels, making them highly aggressive, irritable and dangerous. This usually lasts a short time — but not for the Pilanesberg Park males: They entered musth earlier and stayed in it longer, much, much longer. Instead of weeks, their frenzies lasted months — in one case for “as many as five months,” reports J.B. MacKinnon. Why were these episodes happening for so long? Why weren’t they un-happening?
That’s when elephant scientists had a suggestion. In ordinary herds — where there are lots of big, older, respected male bull elephants around — when a teenager goes through his wild phase, he will get slapped down by a larger, older male. The younger male will attack, and when he’s beaten … something chemical happens …
Says J.B.MacKinnon: “After standing down to a dominant bull, the rush of hormones in the younger male stops, in some cases in a matter of minutes.” The cue to turn off the testosterone comes from getting bonked. So biologists suggested reintroducing a group of elders into Pilanesberg.
Six older elephants arrived, did what oldsters do to rambunctious youngsters, and not long thereafter, says MacKinnon, “the killing of rhinoceroses stopped.” The verdict: The young elephants went wild mostly because there were no older elephants around to keep them in check.” (NPR)
Clearly elephants evolved in multi-age tribal groups. When a group of young elephants were isolated, extremely violent behaviors took place. When this particular “evolutionary mismatch” condition was eliminated by bringing in older male elephants, the extreme behaviors stopped. In this particular case, we have a biochemical explanation connecting the return to an environment close to that of evolutionary adaption to a return to more normal behavior — standing down to a dominant bull reduces the hormonal rush in younger males.
Brain Behavior Interactions in Human Puberty
A recent paper by Jiska Peper and Ronald Dahl summarizes the rapidly growing domain of brain-behavior interaction in human puberty:
“As reviewed recently in (Crone & Dahl, 2012) amidst the myriad of social, emotional, cognitive and biological changes during adolescence, there is growing evidence in both humans and animals that pubertal hormones may influence (bias) some neural and neurobehavioral tendencies of social and affective processing. . . .
Changes in these brain areas and circuits appear to sensitize youth to their social world. A tendency to direct increased attention and motivation to social domains may have adaptive advantages in this developmental window. The fundamental task of adolescence — to achieve adult levels of social competence — requires a great deal of learning about the complexities of human social interactions. Puberty appears to create a neurobehavioral nudge toward exploring and engaging these social complexities. These tendencies to explore and engage can promote adaptive social and affective learning across adolescence; however these same tendencies appear to create some vulnerabilities toward negative developmental trajectories. . . .
Recently, it has been proposed that pubertal maturation impacts social and affective processing in ways that contribute to an adolescent flexibility in cognitive engagement, depending on the social and motivational salience of the context (Crone and Dahl, 2012). The model suggests that interactions between social–affective processing systems in the brain and cognitive control systems can lead to healthy adaptation to the complex and rapidly changing social contexts of adolescence. However, these can also lead to negative trajectories such as substance abuse or depression. These negative trajectories may begin as small changes, but over time can lead to patterns of behavior that have cascading effects: brain-behavior interactions with spiraling impact across adolescence.” (bold emphasis added)
None of this should be surprising. But so far the interactions between an adolescent’s social world and potentially “negative trajectories” has not been adequately explored. Nor have we explicitly considered the relationship between these potentially negative trajectories and the social environments in which adolescents often find themselves.
For instance, the CDC cites “school connectedness” and “family connectedness” as the two strongest protective factors for a wide range of teen dysfunctions. With respect to school connectedness,
“School connectedness was found to be the strongest protective factor for both boys and girls to decrease substance use, school absenteeism, early sexual initiation, violence, and risk of unintentional injury (e.g., drinking and driving, not wearing seat belts). In this same study, school connectedness was second in importance, after family connectedness, as a protective factor against emotional distress, disordered eating, and suicidal ideation and attempts.”
From an evolutionary mismatch perspective, this is not the least bit surprising. If we evolved in small tribal groups in which we would have been tightly connected with our peers, parents, and community more generally, then the experience of disconnection for extended periods of time would be quite unnatural.
Separately, Stanford psychologist William Damon has found that a sense of purpose correlates highly with various measures of adolescent well-being (“PIL” below being one such measure).
“The most common work on purpose is a variety of studies that utilize Crumbaugh and Maholick’s(1967) PIL. In the original study conducted by the authors, results revealed that the PIL distinguishes significantly between psychiatric patient and nonpatient populations. . . . This was the beginning of a trend that looked at the relation between purpose and a number of maladaptive behaviors and outcomes. For example, studies suggest a relation between lower scores on the PIL and drug involvement, young peoples’ participation in risky and antisocial behaviors, and alcoholism. On the more positive side, the PIL has been related to young people’s commitment to social action and is a mediating factor between religiosity and happiness .Thus a sense of purpose is connected to health and productive behaviors in all their manifestations — psychologically, socially, and physically.This finding tends to be confirmed.”
Damon also cites evidence that most teens lack a sense of purpose,
“In a study that followed 7,000 American teenagers from eighth grade through high school, Barbara Schneider and David Stevenson came to a surprising conclusion: contrary to popular images of hedonistic, fun-crazed youth, most of today’s young do have ambitions they would like to achieve. Yet few have any real prospect of realizing them. “Most high school students . . . have high ambitions but no clear life plans for reaching them,” the authors write. They are, in the authors’ phrase, “motivated but directionless.” As a consequence, they become increasingly frustrated, depressed, and alienated. The authors also point out that “many parents do not see it as their responsibility to actively help their adolescents form plans for their futures.””
Again, from an evolutionary perspective, teens would have had a strong sense of purpose based on the norms of their community. At least insofar as we know of the practices of indigenous tribes today, they would have been raised within a coherent meaning system with myths and behavioral expectations to which they were universally expected to adhere (at least there is no evidence to contradict this generalization for as far back in evolutionary time for which we have any inkling of the contents of human mind).
Adolescence in the Environment of Evolutionary Adaptation
Human beings evolved over many millions of years in diverse physical environments. But with respect to social structure, until the dawn of agriculture and empire, almost all adolescents:
1. Lived in a small tribal community of a few dozen to a few hundred with few interactions with other tribal groups.
2. These tribes would have shared one language, one belief system, one set of norms, one morality, and more generally a social and cultural homogeneity that is unimaginable for us today.
3. They would have been immersed in a community with a full range of ages present, from child to elder.
4. From childhood they would have been engaged in the work of the community, typically hunting and gathering, with full adult responsibilities typically being associated with puberty.
5. Their mating and status competitions would have mostly been within their tribe or occasionally with nearby groups, most of which would have been highly similar to themselves.
Contemporary adolescents in developed nations, by contrast:
1. Are often exposed to hundreds or thousands of age peers directly in addition to thousands of adults and thousands of electronic representations of diverse human beings (both social media and entertainment media).
2. Are exposed to many languages, belief systems, norms, moralities, and social and cultural diversity.
3. Are largely isolated with a very narrow range of age peers through schooling.
4. Have little or no opportunities for meaningful work in their community and no adult responsibilities until 18 or even into their 20s.
5. They are competing for mates and status with hundreds or thousands directly and with many thousands via electronic representations (both social media and entertainment media).
We do not know for certain exactly which of these differences between our environment of evolutionary adaptation and contemporary adolescence in developed nations result in which manifestations of mental illnesses and to what extent. But it would be surprising if these rather dramatic changes in the social and cultural environment did not have some impact.
Considering Evolutionary Mismatch as a Causal Factor in Adolescent Mental Illness
Around the world as nations become more prosperous, traditional public health concerns such as infant mortality and contagious diseases become less prevalent. At the same time, new public health concerns such as obesity, heart disease, and type 2 diabetes become more prevalent. Daniel E. Lieberman, a professor of human evolutionary biology at Harvard, explains the role of evolutionary mismatches as a causal factor in the increasing prevalence of such diseases,
“Broadly speaking, most mismatch diseases occur when a common stimulus either increases or decreases beyond levels for which the body is adapted, or the stimulus is entirely novel and the body is not adapted at all. Put simply, mismatches are caused by stimuli that are too much, too little, or too new. For example, as cultural evolution transforms people’s diets, some mismatches occur from people eating too much fat, others from eating too little fat, and yet others from people eating new kinds of fat that the body cannot digest (such as partially hydrogenated fats).” 169
Lieberman’s book The Story of the Human Body: Evolution, Health, and Disease, is the definitive treatment of such mismatch diseases.
While the book largely focuses on physical diseases, Lieberman recognizes that the same mismatch principle is likely to be responsible for some mental illnesses,
“There is good reason to believe that modern environments contribute to a sizable percentage of mental illnesses, such as anxiety and depressive disorders.” 159
In addition to anxiety and depression, he also adds ADHD, eating disorders, chronic insomnia, and OCD as mental illnesses whose modern prevalence is likely due in part to an evolutionary mismatch.
Evolutionary Mismatch Does Not Exclude a Genetic Causal Component
Type 2 Diabetes is a reasonable analogue to the situation of many mental illnesses. It unambiguously has a heritable component:
“T2D clusters in families and it is well established that the risk of developing T2D depends on both genetic and environmental factors. However, heritability estimates have varied between 25%–80% in different studies; the highest estimates are seen in those studies with the longest follow-up periods. The lifetime risk of developing T2D is 40% for individuals who have one parent with T2D and almost 70% if both parents are affected . Furthermore, the concordance rate of T2D in monozygotic twins is about 70%, while the concordance in dizygotic twins is only 20%–30%. The proband-wise concordance rates (number of affected twins having a diabetic co-twin) for monozygotic twins vary between 34% and 100% [42,43,44,45].” (see here)
And yet the more we learn about the genetics of diabetes, the more we realize how complex the situation is,
“The technical revolution in the field of genetics has allowed identification of numerous genetic variants that associate with T2D. The genetic landscape of T2D susceptibility is as yet incomplete, thus far only explaining a small proportion of the total heritability of diabetes. Many possibilities to dissect the architecture of T2D etiology have emerged in the form of large-scale genetic studies, meta-analyses and sequencing in families. It has already greatly contributed to our understanding of disease mechanisms by identifying pathways that could not be linked to diabetes by existing hypothetical models, even though many genetic findings are very recent and have yet to make their contribution to our knowledge about diabetes pathogenesis. However, one must bear in mind that diabetes is probably a much more diverse disease than the current subdivision into T1D and T2D implies and more precise subdivision into subgroups may both facilitate the investigation of T2D genetics and pave the way for more individualized treatment. A holistic systems biology approach will also be required to obtain a complete picture of how genetic variation leads to diabetes.” (see here)
Few would claim that diet and lifestyle are irrelevant to type 2 diabetes. Daniel Lieberman, cited above, uses type 2 diabetes as one of the most compelling examples of an evolutionary mismatch disease — yes, there is a genetic component, but in the environment of evolutionary adaptation far fewer people developed type 2 diabetes.
Analogously, a recent paper that found definitive proof that there was no “depression gene” first acknowledges significant heritability,
“Major depressive disorder (hereafter referred to as“depression”) is moderately heritable (twin-based heritability,∼37%”
But then goes on to conclude that there genetics of depression are complex,
“The genetic underpinnings of common complex traits such as depression appear to be far more complicated than originally hoped (60, 61), and large collaborative efforts have not supported the existence of common genetic variants with large effects on depression liability (18). In the context of our understanding of psychiatric genetics in the 1990s and early 2000s, the most studied candidate genes and the polymorphisms within them were defensible targets for association studies. However, our results demonstrate that historical depression candidate gene polymorphisms do not have detectable effects on depression phenotypes. Furthermore, the candidate genes themselves (with the possible exception ofDRD2) were no more associated with depression phenotypes than genes chosen at random.”
“However, an evolutionary geneticist points out that there are evolutionary reasons why we should not expect to find common genes with significant negative effects:‘Geographically dispersed or common risk alleles are older and more likely to be repeatedly detected . . . But, their widespread dispersion indicates that those alleles are benign (at least in regard to fitness history), so if they are associated with disease the causal finger actually points to recent environmental change rather than primarily to genetic etiology’.8This changes the model from a search for defective genes to recognition that many genes causing highly heritable common disorders are normal variations that cause disease only when they interact with aspects of the environment that are novel in the past few hundred generations.” (bold emphasis added)
Thus the examination of evolutionary mismatches that may trigger mental illness is a complement to the recognition that some subsets of a population may be more genetically sensitive to the evolutionary mismatch. As always, many outcomes represent a genetic-environmental interaction.
Is Adolescent Mental Illness Due in Part to an Evolutionary Mismatch?
The journalist Johann Hari argues in Lost Connections that depression is caused by the absence of:
1. Disconnection from meaningful work
2. Disconnection other people
3. Disconnection meaningful values
4. Disconnection childhood trauma
5. Disconnection status and respect
6. Disconnection the natural world
7. Disconnection a hopeful and secure future
While some of these disconnections are more robustly supported than others as causal factors in depression, all but the fourth and seventh one may be regarded as evolutionary mismatches (it is not clear that we can make meaningful generalizations about childhood trauma in a world in which death was common, and there is no reason to believe that humans experienced a “hopeful and secure future” in the environment of evolutionary adaptation). But certainly “meaningful” work was the norm, connectedness to other people was the norm, a profoundly coherent system of meaningful values was the norm, most people would have experienced largely stable status and respect hierarchies, and of course they lived in the natural world.
With respect to the chapter on disconnection from other people, Hari cites the work of John Cacioppo, one of the founders of “social neuroscience,” whose work provides extensive physiological documentation of evolutionary biologist E.O. Wilson’s simple statement, “People must belong to a tribe.” Cacioppo is explicit in connecting social neuroscience to mental health,
“Social neuroscience is a new, interdisciplinary field devoted to understanding how biological systems implement social processes and behavior. . . . Our goals in this article are to review the development of this field, examine some currently promising approaches, identify obstacles and opportunities for future advances and integration, and consider how this research can inform work on the diagnosis and treatment of mental disorders.”
In addition to summarizing a significant amount of information on the physiological correlates of mental illness, the article explicitly analyzes the role of social behavior, “Social behavior can be classified into broadly defined subcategories including (a) self-perception, (b) self-regulation, ©interpersonal perception, and (d) group processes.”
The article concludes that the social factors and deficits are both causes and consequences of psychopathology,
“Understanding the human brain and mind, when healthy and in plight, requires the merging of multiple, distinct disciplines with translation across scientific perspectives and levels of analysis. The emerging field of social neuroscience constitutes such an approach. As understanding of the social brain advances, this knowledge can support understanding of mechanisms by which social factors and social deficits operate as causes and consequences of psychopathology. This perspective assumes mutual influences among biological and social factors in determining behavior. Accordingly, accounts of human function will be limited to the extent that any level of analysis is neglected.” (bold emphasis added)
From the perspective of evolutionary psychiatry, the fact that social factors and deficits are sometimes the causes of psychopathology should not be the least bit surprising. We are now living in a social environment that is dramatically different from the environment of evolutionary adaptation.
To explore yet an additional direction, Liah Greenfeld is a Durkheimian sociologist who specifically attributes the modern epidemic of depression, bipolar, and schizophrenia to the burden of creating an autonomous identity in the modern world. She argues that in the past few centuries modernity has gradually shifted away from traditional identities that were largely stable over generations to the modern notion of personal identity in which we each are expected to have the freedom and opportunity to create our own identity and pursue our own individual destiny. While this major sociological transition has been incredibly liberating, it has also been an immense and growing burden for which many young people are unprepared.
Again, whether or not the details of Greenfeld’s account hold up, it is certainly the case that in paleo-lithic cultures human beings did not have the range, opportunity of choice, or responsibility to create their own identities that they have today.
Of course, there are those who question the evidence regarding a modern epidemic of depression, bipolar, and schizophrenia. Those who hold to a strictly genetic cause for these mental illnesses believe that because the genetic makeup of humans has not changed significantly in recent centuries there is therefor no reason to suspect a change in the incidence of these conditions.
On the other hand, to avoid the issue of differences in the extent to which these conditions have been recognized and diagnosed over the centuries, we can look at changes in suicide rates. Certainly teen suicide rates have increased dramatically in the 20th century,
“From 1950 to 1980, rates among white males aged 15 to 19 increased by 305%; among white males aged 20 to 24, by 196%. . . . In 1950,5.8% of all suicide deaths in the nation were youth suicides (ages 15 to 24). By 1980, almost one in five suicide deaths (19.5%) were youth suicides, and the rate had increased from 4.5 deaths per 100,000 population to 12.3.”
They have since fluctuated but remained about 3x relative to 1950,
“The suicide rate for males aged 15–19 years increased from 12.0 to 18.1 per 100,000 population from 1975 to 1990, declined to 10.8 by 2007, and then increased 31% to 14.2 by 2015. The rate in 2015 for males was still lower than the peak rates in the mid- 1980s to mid-1990s. Rates for females aged 15–19 were lower than for males aged 15–19 but followed a similar pattern during 1975–2007 (increasing from 2.9 to 3.7 from 1975 to 1990, followed by a decline from 1990 to 2007). The rates for females then doubled from 2007 to 2015 (from 2.4 to 5.1). The rate in 2015 was the highest for females for the 1975–2015 period.”
Might the growth in teen suicides from 1950 to 1980 be a result of an increased evolutionary mismatch during that period?
High School as Evolutionary Mismatch
We don’t know why, exactly, teen suicide increased 3x during that period. That said, the correlation with schooling is intriguing. For instance, white students completing high school increased from about 30% to about 70% from 1950 to 1980. “Black and other” students increased from about 10% completing high school in 1950 to about 60% in 1980.
If we look at suicide rates age 15–19, white males increase from 3.7 per 100,000 in 1950 to 15.0 per 100,000 in 1980, more than 4x. Black and other males increase from 2.2 per 100,000 in 1950 to 7.5 per 100,000 in 1980, more than 3.4x. Female rates did not increase at the same rate: White females age 15–19 went from 1.9 per 100,000 in 1950 to 3.3 in 1980, 1.7x. Black and other females increased from 1.5 per 100,000 in 1950 to a peace of 3.0 in 1970 before coming back down to 1.8 per 100,000 in 1980, 2x at the peak, 1.2x by 1980.
For males, at least, the growth in high school enrollment tracks the growth in teen suicides. Is there some proportion of adolescent males who are not thriving in the high school environment? Might these males have been less stressed in a work environment, the most common environment for adolescent males prior to the rise of universal high school as an ideal?
We really don’t know which factors in contemporary adolescence might be responsible for the evolutionary mismatch. As specified above, there are many ways in which the environment in which adolescents today find themselves today differs dramatically from the environment(s) of evolutionary adaptation. It might be:
1. The lack of multi-age groupings (Bull elephants needed?)
2. Small changes leading to cascades of dysfunction (Peper and Dahl)
3. The lack of a sense of purpose through work and survival needs (Damonian possibilities)
4. The lack of human connection (Hari/Cacioppo possibilities)
5. The lack of a shared culture and belief system leading to anomie through a malfunctioning process of identity formation (Greenfeld/Durkheimian possibilities)
These are not mutually exclusive possibilities. Without providing any particular conclusive evidence connecting a particular phenomenon with a particular evolutionary mismatch, for now I simply want to open up the direction of evolutionary mismatch for adolescent dysfunction and mental illness for continued exploration and investigation.
I became interested in this possibility after decades of creating small, personalized schools at which many teens were manifestly better off. I’ve seen dozens of teens move from clinical anxiety and depression, suicidal thoughts, and school refusal to happy flourishing teens, often leaving behind psychiatric medications in the process. Many of them have explicitly acknowledged that the change in social environments was key to their recovery. I’ve been on the front lines of teens escaping a dysfunctional environment that was not aligned with the social and cultural needs of our environment of evolutionary adaptation.
For years this phenomenon has been obvious to me. But I’ve found that simplistic understandings concerning the notion that mental illness was primarily a genetic phenomenon has led many people to be skeptical of the hypothesis that a dramatically different social environment could have a significant impact on clinical mental illness.
The present paradigm of adolescent mental health takes the existing schooling system as a given. Given that system, mental health advocates seek to increase access to mental health resources. For instance, descriptions of the scale of the problem are often used to support increased treatment opportunities,
“One in five children in the United States has a diagnosable mental health condition. Unfortunately, access to care for these children is poor: At least 85 percent of those in need of treatment do not get it.1 More than half of mental illness emerges before age 14, so getting children the help they need, in addition to ameliorating their immediate suffering, can also prevent future pain. The result of not getting help can be dire, as suicide is now the second leading cause of death for those between ages 10 and 34.2
Mental illness exacts a staggering cost on society. It leads most measures of economic burden for noncommunicable diseases. The World Economic Forum issued a report that mental illness has a greater impact on economic output than cancer, heart disease, or diabetes.3 The report’s authors estimate the worldwide cost of mental illness to be $16 trillion between 2011 and 2030. Other recent research has indicated that untreated anxiety and depression costs society $1.15 trillion annually.4”
But remember the Hippocratic Oath: First, do no harm.
While the need for greater access to mental health resources is certainly urgent, I want readers to take another possibility seriously: Perhaps a re-examination of the institution of schooling is even more urgent. If our existing schooling system is unnecessarily exacerbating mental health issues, then parents, teens, educators, and policy-makers should re-evaluate the premises of our existing schooling system. If schooling-as-we-know-it is excessively different from our environment of evolutionary adaptation, then how should we rethink schooling in order to create healthier adolescent populations in the future?