Saturday, November 2, 2019

Evolutionary Psychology and Suicidology

Evolutionary Psychology and Suicidology. John F. Gunn III, Pablo Malo, and C. A. Soper. SAGE Handbook of Evolutionary Psychology, Vol 3, Part 7, Chapter 69.

ABSTRACT: Suicide – deliberate, intentional self-killing – is a major cause of human mortality and a global public health concern. Suicidology emerged as an interdisciplinary field focused on the prediction and prevention of suicide. Progress has been disappointing: suicide rates resist efforts to reduce them, and there is no theoretical consensus on suicide’s causation. At least since the writing of Sigmund Freud, the search for a scientific understanding of suicide has included theories with evolutionary links. Apparently a human universal behavior, suicide presents a longstanding evolutionary puzzle: the fitness cost of suicide, of being dead, is predictably injurious for the individual’s reproductive future. Some adaptationist theories have been advanced from the neo-Darwinian idea of inclusive fitness: selection may produce behaviors that, while self-injurious for the individual, favor the reproductive prospects of individual’s genetic kin, but there are multiple theoretical and empirical problems with such proposals. Others suggest “by-product” explanations, that suicide is not in itself adaptive, but may be a noxious side-effect of evolved adaptations that are fitness enhancing overall. Most of these proposals coalesce around the central idea that pain, particularly social pain, a vital protective signal which demands the organism take action to end or escape it, may incidentally provoke suicide as a means to achieve that escape. A minimal level of cognitive functioning appears to operate as a second, incidentally suicidogenic, adaptation among adult humans. Together these twin “pain-and- brain” conditions appear to be both necessary and sufficient for suicide, a formulation that implicitly reframes self-killing as an adaptive problem in the evolution of the human species. The explanatory focus shifts, on this basis, from attempting to identify causes of suicide, to identifying adaptive solutions that operate to prevent suicide. A general framework recently proposed by Soper envisages multiple lines of “pain-type” and “brain-type” antisuicide defenses, transmitted culturally and genetically across generations. One class of evolved psychological mechanisms, “keepers”, is reviewed in detail. Soper posits keepers to mobilize as emergency interventions among people at imminent risk of taking their own lives. Challengingly, the hypothesized features of keepers appear to match symptoms of several common mental disorders, including depression, addictions, non-suicidal self-harm, and psychoses. The model would help to explain why it has not proved possible to predict suicide at the individual level: any and all usefully predictive clues would probably already have been exploited and exhausted by evolved antisuicide defenses. The framework may also account for, among other things, the close association of diverse, and often comorbid, psychopathologies with suicidal ideation, but the only weak association of psychopathologies with the progression from ideation to suicidal action. Major implications of, and problems with, Soper’s conceptual approach are discussed. In conclusion, it is suggested that evolutionary psychology offers fresh perspectives for suicidology, and potentially a means to achieve a long overdue, and much needed, integration and unification of suicide theory.

“Natural selection will never produce in a being anything injurious to itself, for natural selection acts solely by and for the good of each” (Darwin, 1859, p. 201).

Suicide, “the act of deliberately killing oneself” (W.H.O., 2014, p. 12) accounts for some million deaths around the world each year and ends about 1.4% of human lives: more people die by intentional self-killing than from wars, accidents, homicide and all other forms of violent death put together (W.H.O., 2013). Many millions of the living are affected, left to deal with the aftermath of others’ suicides (Cerel et al., 2019). A cross-cultural killer, suicide is viewed as a global public health challenge – a major, and preventable, cause of mortality and misery (Satcher, 1999; W.H.O., 2012, 2014). A new multi-disciplinary field of research emerged in the second half of the 20th century, suicidology, focused on trying to understand and tackle the problem (American Association of Suicidology, 2019; Shneidman, 2001).

But frustratingly, by most accounts, decades of concerted effort have made little impression. While other forms of violent mortality have markedly reduced (Pinker, 2011) the global suicide rate is probably much the same now as it was 50 or 100 years ago (Linehan, 2011; Nock et al., 2012; Nock, Ramirez, & Rankin, 2019). Indeed, self-killings in the USA are reportedly on the increase (Hedegaard, Curtin, & Warner, 2018). Progress in building a theoretical base has been equally disappointing, the causation of suicide remaining a scientific mystery (Lester, 2019; Soper, 2019b). As a report published by the World Health Organization admits, “we continue to lack a firm understanding of why, when, and among whom suicidal behavior will occur” (Nock, Borges, & Ono, 2012a, p. 222). Diverse ideas have accumulated over more than a hundred years of theorizing – reviews of prominent offers can be found in the general suicidology literature (Gunn, 2019; Gunn & Lester, 2014; O’Connor & Portzky, 2018; Paniagua, Black, Gallaway, & Coombs, 2010; Selby, Joiner, & Ribeiro, 2014). But perhaps reflecting widespread acceptance that the proximal causes of suicide are complex and multifactorial, no model has won a consensus of support (Hjelmeland, Jaworski, Knizek, & Marsh, 2019; Lester, 2019). Suicidology is fragmented to the extent that a recent meta-review describes the field as “still in a preparadigmatic phase” (Franklin et al., 2017, p. 188) – that is, still in its infancy.

A subset of theories with evolutionary links shows a long-held, if often implicit, acceptance that a coherent understanding of suicide needs to take its place, alongside other fields of modern life sciences, within an evolutionary paradigm. A hundred years ago, Freud (1920/1991) proposed a potentially suicidogenic “death drive” in the context of his broader theory of libido, a framework which, in keeping with the evolutionist spirit of the age, sought to build on the Darwinian premise that selection is predicated on sexual success (Gilbert, 1989; Litman, 1967; Tolaas, 2005).

Psychoanalysis failed to find a satisfactory explanation for suicide, as its practitioners acknowledged at the time (Zilboorg, 1936a), although comparable ideas continue to circulate in suicidology (Selby et al., 2014). Many alternative approaches have been advanced in the intervening century, as we will discuss, but suicide is still widely viewed as an evolutionary puzzle (Aubin, Berlin, & Kornreich, 2013; Blasco-Fontecilla, Lopez-Castroman, Gomez-Carrillo, & Baca-Garcia, 2009; Confer et al., 2010). The conundrum follows from our opening quotation: how is it that, seemingly contradicting Darwin’s (1859) prediction, selection permits so self-destructive a behavior? 

In search of answers, we review and critique prominent ways in which evolutionary ideas have informed suicide research, and outline a new general approach, the modelling of suicide as an evolutionary by-product which, we believe, offers scope for long overdue convergence in suicide theory and, it is hoped, prospects for saving lives (Gunn, 2017; Humphrey, 2018; Soper, 2016, 2017, 2018).

7 Concluding comments

At one level this chapter carries an encouraging message. The evolutionary approach would seem, in principle, capable of bringing much needed and long overdue unity and coherence to suicidology’s current morass of unconnected theory. A “pain-and-brain” framework in particular could offer a rallying point for numerous, superficially disparate, theoretical positions, including IPTS (Van Orden et al., 2010), IMV (O’Connor et al., 2016), SPM (Gunn, 2017) and others, which essentially characterize suicide as a way to escape intolerable emotional states. None would appear incompatible with the view that pain, as a biological imperative, demands action to end or escape it, while regular adult human cognition offers intentional self-killing as an effective, but genetically destructive, means to answer that demand.

But the corollary, that humans are protected from suicide by evolved psychological mechanisms, may be harder to digest. Blind to our own instinctual motivations (Cosmides & Tooby, 1994), we may be oblivious to their functioning. The idea of antisuicide defenses is not new (e. g., Himmelhoch, 1988; Hundert, 1992; Miller, 2008), but it is only now gaining momentum in the research agenda (Humphrey, 2011, 2018; Soper, 2016, 2017, 2018, 2019a, 2019b; Soper & Shackelford, 2018). Their implications may run wide and deep, and call some long-held preconceptions into question: as Lester (2019) finds, accepting the ramifications requires close reading of the arguments.

Progress is not helped by what Soper (2018) believes to be a two-way blockage in communication between suicidology and evolutionary psychology that may go beyond the kind of institutional fragmentation seen elsewhere in psychological sciences (Staats, 2004). Soper posits that suicide and evolution, each for its own reasons, are concepts that many people, researchers included, find intuitively uncomfortable to think or talk about. It may be for this reason that, in one direction, evolutionary psychology has largely ignored suicide, as has psychology generally (J. R. Rogers, 2001): in view of the gravity and ubiquity of suicide as a human phenomenon, and the conspicuous evolutionary puzzle it presents, remarkably little has been written on the subject from an evolutionary psychology perspective, at least until recent years. It is a reticence traceable to Darwin himself: as Tolaas (2005) points out, it is remarkable that a thinker as fearless as Darwin did not confront suicide as a potential problem for his theory. In the other direction, suicidology has largely ignored evolutionary psychology. Illustratively, a review article promisingly titled “Evolutionary processes in suicide” (Chiurliza, Rogers, Schneider, Chu, & Joiner, 2017) attempts to appraise its research group’s ideas (and their ideas alone) without reference to evolutionary psychology’s corpus of texts and tenets – a surprising omission given that evolutionary psychology, “the study of behavior from an evolutionary perspective” (Cornwell, Palmer, Guinther, & Davis, 2005, p. 369), is centrally relevant.

This chapter proposes a pragmatic consilience between the two fields. An evolutionary stance would not seem in itself to entail a radical departure for suicidology: it would, rather, follow the lead set by Freud (1920/1991), Shneidman (1985), Joiner (2005), and other prominent researchers who have drawn on evolutionary ideas across more than a century. Evolutionary psychology could coalesce, not replace, suicidology’s existing theoretical content. There may be little to lose in such an incremental move. The upsides, on the other hand, may be great. Evolutionary psychology offers fresh perspectives and ready tools that could be decisive in a battle currently at stalemate. Evolutionary psychology and suicidology deserve each other’s attention.

Association between childhood adoption & bad mental health: Not fully to be attributed to stressful environments; it is partly explained by differences in genetic risk between adoptees & those not-adopted

Childhood adoption and mental health in adulthood: The role of gene-environment correlations and interactions in the UK Biobank. Kelli Lehto et al. Biological Psychiatry, October 31 2019.

Background Being adopted early in life, an indicator of exposure to early life adversity, has been consistently associated with poor mental health outcomes in adulthood. Such associations have largely been attributed to stressful environments, e.g. exposure to trauma, abuse or neglect. However, mental health is substantially heritable, and genetic influences may contribute to the exposure to childhood adversity, resulting in potential genetic confounding of such associations.
Methods Here we explored associations between childhood adoption and mental health-related outcomes in mid-life in 243 797 UK Biobank participants (n adopted=3151). We used linkage disequilibrium score regression and polygenic risk scores for depressive symptoms, schizophrenia, neuroticism and subjective wellbeing to address potential genetic confounding (gene-environment correlations) and gene-environment interactions. As outcomes we explored depressive symptoms, bipolar disorder, neuroticism, loneliness, and mental health-related socioeconomic and psychosocial measures in adoptees compared to non-adopted participants.
Results Adoptees were slightly worse off on almost all mental, socioeconomic and psychosocial measures. Each standard deviation increase in polygenic risk for depressive symptoms, schizophrenia, and neuroticism was associated with 6%, 5%, and 6% increase in the odds of being adopted, respectively. Significant genetic correlations between adoption status and depressive symptoms, major depression, and schizophrenia were observed. No evidence for gene-environment interaction between genetic risk and adoption on mental health was found.
Conclusions The association between childhood adoption and mental health cannot fully be attributed to stressful environments, but is partly explained by differences in genetic risk between adoptees and those not-adopted (i.e. gene-environment correlation).

Keywords: gene-environment interplaydepressive symptomsschizophrenianeuroticismchildhood adversitypolygenic risk scores

Happiness is not best understood as an affective state, but better understood within its behavioral context, as an emergent property of activity

Imaging Happiness: Meta Analysis and Review. Joshua Ray Tanzer, Lisa Weyandt. Journal of Happiness Studies, October 31 2019.

Abstract: A challenge in studying happiness is its conceptual nature. Is the happiness of hedonistic indulgence the same as the happiness of selfless volunteering? To understand some of these questions, a narrative review of 64 neuroimaging studies between 1995 and 2018 was conducted. Studies were grouped based on how they conceptualized happiness based on Seligman’s (Authentic happiness: using the new positive psychology to realize your potential for lasting fulfillment, Simon and Schuster, New York, 2002) authentic happiness theory. A qualitative narrative review was performed as well as an ALE meta analysis of activation regions. Happiness was identified in 33 separate brain regions across the telencephalon, diencephalon, and metencephalon. Stratifying results by definition of happiness, regions of activity were generally relevant to the tasks performed during the experiment and the kinds of tasks enjoyed by the phenomenon of happiness examined. The ALE analysis identified the claustrum, insula, basal ganglia, and thalamus as showing meaningful activation clusters across studies. Happiness as pleasure and engagement demonstrated close relevance of neural activity to literal activities being performed. Tasks for happiness as meaning, on the other hand, were generally more abstract. Likewise, there was less direct relationship between behavior and phenomenon of happiness, the insula most likely to activate for happiness as meaning. It was concluded that happiness is not best understood as an affective state, but better understood within its behavioral context, as an emergent property of activity. For pleasure and engagement, this meant a literal relationship between behavioral and neurological activity. For meaning, this meant the ongoing assessment of the moral implications of events. Limitations included cross sectional design and hemodynamic focus. Future research should consider concordance of happiness and brain activity across the lifespan. Additionally, future studies should consider the dynamics of neuropeptides.

Keywords: Authentic happiness Neuroimaging Review

Fear‐containing dreams serve an emotion regulation function; the stronger the recruitment of fear‐responsive regions during dreaming, the weaker their response to actual fear‐eliciting stimuli during wakefulness

Fear in dreams and in wakefulness: Evidence for day/night affective homeostasis. Virginie Sterpenich et al. Human Brain Mapping, October 30 2019.

Abstract: Recent neuroscientific theories have proposed that emotions experienced in dreams contribute to the resolution of emotional distress and preparation for future affective reactions. We addressed one emerging prediction, namely that experiencing fear in dreams is associated with more adapted responses to threatening signals during wakefulness. Using a stepwise approach across two studies, we identified brain regions activated when experiencing fear in dreams and showed that frightening dreams modulated the response of these same regions to threatening stimuli during wakefulness. Specifically, in Study 1, we performed serial awakenings in 18 participants recorded throughout the night with high‐density electroencephalography (EEG) and asked them whether they experienced any fear in their dreams. Insula and midcingulate cortex activity increased for dreams containing fear. In Study 2, we tested 89 participants and found that those reporting higher incidence of fear in their dreams showed reduced emotional arousal and fMRI response to fear‐eliciting stimuli in the insula, amygdala and midcingulate cortex, while awake. Consistent with better emotion regulation processes, the same participants displayed increased medial prefrontal cortex activity. These findings support that emotions in dreams and wakefulness engage similar neural substrates, and substantiate a link between emotional processes occurring during sleep and emotional brain functions during wakefulness.


Converging evidence from human and animal research suggests functional links between sleep and emotional processes (Boyce, Glasgow, Williams, & Adamantidis, 2016; Perogamvros & Schwartz, 2012; Wagner, Hallschmid, Rasch, & Born, 2006; Walker & van der Helm, 2009). Chronic sleep disruption can lead to increased aggressiveness (Kamphuis, Meerlo, Koolhaas, & Lancel, 2012) and negative mood states (Zohar, Tzischinsky, Epstein, & Lavie, 2005), whereas affective disorders such as depression and post‐traumatic stress disorder (PTSD) are frequently associated with sleep abnormalities (e.g., insomnia and nightmares). Experimental evidence indicates that acute sleep deprivation impairs the prefrontal control over limbic regions during wakefulness, hence, exacerbating emotional responses to negative stimuli (Yoo, Gujar, Hu, Jolesz, & Walker, 2007). Neuroimaging and intracranial data further established that, during human sleep, emotional limbic networks are activated (e.g., Braun et al., 1997; Corsi‐Cabrera et al., 2016; Maquet et al., 1996; Nofzinger, Mintun, Wiseman, Kupfer, & Moore, 1997; Schabus et al., 2007). Together these findings indicate that sleep physiology may offer a permissive condition for affective information to be reprocessed and reorganized. Yet, it remains unsettled whether such emotion regulation processes also happen at the subjective, experiential level during sleep, and may be expressed in dreams. Several influential theoretical models formalized this idea. For example, the threat simulation theory postulated that dreaming may fulfill a neurobiological function by allowing an offline simulation of threatening events and rehearsal of threat‐avoidance skills, through the activation of a fear‐related amygdalocortical network (Revonsuo, 2000; Valli et al., 2005). Such mechanism would promote adapted behavioral responses in real life situations (Valli & Revonsuo, 2009). By contrast, other models suggested that dreaming would facilitate the resolution of current emotional conflict (Cartwright, Agargun, Kirkby, & Friedman, 2006; Cartwright, Luten, Young, Mercer, & Bears, 1998), the reduction of next‐day negative mood (Schredl, 2010) and extinction learning (Nielsen & Levin, 2007). Although these two main theoretical lines differ, because one focuses on the optimization of waking affective reactions (Perogamvros & Schwartz, 2012; Revonsuo, 2000) and the other on the resolution of current emotional distress (e.g., fear extinction; Nielsen & Levin, 2007), both converge to suggest that experiencing fear in dreams leads to more adapted responses to threatening signals during wakefulness (Scarpelli, Bartolacci, D'Atri, Gorgoni, & De Gennaro, 2019). The proposed mechanism is that memories from a person's affective history are replayed in the virtual and safe environment of the dream so that they can be reorganized (Nielsen & Levin, 2007; Perogamvros & Schwartz, 2012). From a neuroscience perspective, one key premise of these theoretical models is that experiencing emotions in dreams implicates the same brain circuits as in wakefulness (Hobson & Pace‐Schott, 2002; Schwartz, 2003). Preliminary evidence from two anatomical investigations showed that impaired structural integrity of the left amygdala was associated with reduced emotional intensity in dreams (Blake, Terburg, Balchin, van Honk, & Solms, 2019; De Gennaro et al., 2011).

Like during wakefulness, people experience a large variety of emotions in their dreams, with rapid eye movement (REM) dreaming being usually more emotionally loaded than non‐rapid eye movement (NREM) dreams (Carr & Nielsen, 2015; Smith et al., 2004). While some studies found a relative predominance of negative emotions, such as fear and anxiety, in dreams (Merritt, Stickgold, Pace‐Schott, Williams, & Hobson, 1994; Roussy et al., 2000), others reported a balance of positive and negative emotions (Schredl & Doll, 1998), or found that joy and emotions related to approach behaviors may prevail (Fosse, Stickgold, & Hobson, 2001; Malcolm‐Smith, Koopowitz, Pantelis, & Solms, 2012). When performing a lexicostatistical analysis of large data sets of dream reports, a clear dissociation between dreams containing basic, mostly fear‐related, emotions and those with other more social emotions (e.g., embarrassment, excitement, frustration) was found, highlighting distinct affective modes operating during dreaming, with fear in dreams representing a prevalent and biologically‐relevant emotional category (Revonsuo, 2000; Schwartz, 2004). Thus, if fear‐containing dreams serve an emotion regulation function, as hypothesized by the theoretical models, the stronger the recruitment of fear‐responsive brain regions (e.g., amygdala, cingulate cortex, and insula; see Phan, Wager, Taylor, & Liberzon, 2002) during dreaming, the weaker the response of these same regions to actual fear‐eliciting stimuli during wakefulness should be. This compensatory or homeostatic mechanism may also be accompanied by an enhanced recruitment of emotion regulation brain regions (such as the medial prefrontal cortex, mPFC, which is implicated in fear extinction) during wakefulness (Dunsmoor et al., 2019; Phelps, Delgado, Nearing, & LeDoux, 2004; Quirk, Likhtik, Pelletier, & Pare, 2003; Yoo et al., 2007).

Here, we collected dream reports and functional brain measures using high‐density EEG (hdEEG) and functional MRI (fMRI) across two studies to address the following questions: (a) do emotions in dreams (here fear‐related emotions) engage the same neural circuits as during wakefulness and (b) is there a link between emotions experienced in dreams and brain responses to emotional stimuli during wakefulness. By addressing these fundamental and complementary topics, we aim at clarifying the grounding conditions for the study of dreaming as pertaining to day/night affective homeostasis.