Cognitive Behavior Therapy for Depression From an Evolutionary Perspective.

Evolutionary medicine attempts to solve a problem with which traditional medicine has struggled historically; how do we distinguish between diseased states and "healthy" responses to disease states? Fever and diarrhea represent classic examples of evolved adaptations that increase the likelihood of survival in response to the presence of pathogens in the body. Whereas, the severe mental disorders like psychotic mania or the schizophrenias may involve true "disease" states best treated pharmacologically, most non-psychotic "disorders" that revolve around negative affects like depression or anxiety are likely adaptations that evolved to serve a function that increased inclusive fitness in our ancestral past. What this likely means is that the proximal mechanisms underlying the non-psychotic "disorders" are "species typical" and neither diseases nor disorders. Rather, they are coordinated "whole body" responses that prepare the individual to respond in a maximally functional fashion to the variety of different challenges that our ancestors faced. A case can be made that depression evolved to facilitate a deliberate cognitive style (rumination) in response to complex (often social) problems. What this further suggests is that those interventions that best facilitate the functions that those adaptations evolved to serve (such as rumination) are likely to be preferred over those like medications that simply anesthetize the distress. We consider the mechanisms that evolved to generate depression and the processes utilized in cognitive behavior therapy to facilitate those functions from an adaptationist evolutionary perspective.

Disordered doctors or rational rats? Testing adaptationist and disorder hypotheses for melancholic depression and their relevance for clinical psychology.

Most clinicians view depression as a painful disorder in which motivation to pursue adaptive goals is lacking and cognition is impaired. An alternative hypothesis-grounded in a common evolutionary approach-suggests that depression is inherently motivational and evolved to motivate avoidant learning of harmful situations. Testing these hypotheses requires a clear definition of "disorder". Wakefield's harmful dysfunction evolution-based definition proposes that all unambiguous cases of disorder involve a malfunctioning adaptation. These hypotheses-functional adaptation and malfunctioning adaptation-are mutually exclusive and require a common research strategy. One must identify and map out the relevant adaptation-characterized by a high degree of non-random organization and coordination for promoting a function-which will eventually result in a conceptual blueprint of where and how the adaptation can malfunction. Using inescapable shock in rats and physicians' emotional responses to medical errors to provide context, we show how the symptoms of melancholic depression exhibit signs of adaptation for motivating a time-consuming, attentionally-demanding, energetically-expensive avoidant learning style after experiencing a harmful event. We discuss how this adaptationist approach may provide insight into spontaneous remission and the effects of psychotherapies and antidepressant medications.

The Mortality and Myocardial Effects of Antidepressants Are Moderated by Preexisting Cardiovascular Disease: A Meta-Analysis.

BACKGROUND: Antidepressants (ADs) are commonly prescribed medications, but their long-term health effects are debated. ADs disrupt multiple adaptive processes regulated by evolutionarily ancient biochemicals, potentially increasing mortality. However, many ADs also have anticlotting properties that can be efficacious in treating cardiovascular disease. We conducted a meta-analysis assessing the effects of ADs on all-cause mortality and cardiovascular events in general-population and cardiovascular-patient samples. METHODS: Two reviewers independently assessed articles from PubMed, EMBASE, and Google Scholar for AD-related mortality controlling for depression and other comorbidities. From these articles, we extracted information about cardiovascular events, cardiovascular risk status, and AD class. We conducted mixed-effect meta-analyses testing sample type and AD class as moderators of all-cause mortality and new cardiovascular events. RESULTS: Seventeen studies met our search criteria. Sample type consistently moderated health risks. In general-population samples, AD use increased the risks of mortality (HR = 1.33, 95% CI: 1.14-1.55) and new cardiovascular events (HR = 1.14, 95% CI: 1.08-1.21). In cardiovascular patients, AD use did not significantly affect risks. AD class also moderated mortality, but the serotonin reuptake inhibitors were not significantly different from tricyclic ADs (TCAs) (HR = 1.10, 95% CI: 0.93-1.31, p = 0.27). Only "other ADs" were differentiable from TCAs (HR = 1.35, 95% CI: 1.08-1.69). Mortality risk estimates increased when we analyzed the subset of studies controlling for premedication depression, suggesting the absence of confounding by indication. CONCLUSIONS: The results support the hypothesis that ADs are harmful in the general population but less harmful in cardiovascular patients.

Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response.

The role of serotonin in depression and antidepressant treatment remains unresolved despite decades of research. In this paper, we make three major claims. First, serotonin transmission is elevated in multiple depressive phenotypes, including melancholia, a subtype associated with sustained cognition. The primary challenge to this first claim is that the direct pharmacological effect of most symptom-reducing medications, such as the selective serotonin reuptake inhibitors (SSRIs), is to increase synaptic serotonin. The second claim, which is crucial to resolving this paradox, is that the serotonergic system evolved to regulate energy. By increasing extracellular serotonin, SSRIs disrupt energy homeostasis and often worsen symptoms during acute treatment. Our third claim is that symptom reduction is not achieved by the direct pharmacological properties of SSRIs, but by the brain's compensatory responses that attempt to restore energy homeostasis. These responses take several weeks to develop, which explains why SSRIs have a therapeutic delay. We demonstrate the utility of our claims by examining what happens in animal models of melancholia and during acute and chronic SSRI treatment.

Primum non nocere: an evolutionary analysis of whether antidepressants do more harm than good.

Antidepressant medications are the first-line treatment for people meeting current diagnostic criteria for major depressive disorder. Most antidepressants are designed to perturb the mechanisms that regulate the neurotransmitter serotonin - an evolutionarily ancient biochemical found in plants, animals, and fungi. Many adaptive processes evolved to be regulated by serotonin, including emotion, development, neuronal growth and death, platelet activation and the clotting process, attention, electrolyte balance, and reproduction. It is a principle of evolutionary medicine that the disruption of evolved adaptations will degrade biological functioning. Because serotonin regulates many adaptive processes, antidepressants could have many adverse health effects. For instance, while antidepressants are modestly effective in reducing depressive symptoms, they increase the brain's susceptibility to future episodes after they have been discontinued. Contrary to a widely held belief in psychiatry, studies that purport to show that antidepressants promote neurogenesis are flawed because they all use a method that cannot, by itself, distinguish between neurogenesis and neuronal death. In fact, antidepressants cause neuronal damage and mature neurons to revert to an immature state, both of which may explain why antidepressants also cause neurons to undergo apoptosis (programmed death). Antidepressants can also cause developmental problems, they have adverse effects on sexual and romantic life, and they increase the risk of hyponatremia (low sodium in the blood plasma), bleeding, stroke, and death in the elderly. Our review supports the conclusion that antidepressants generally do more harm than good by disrupting a number of adaptive processes regulated by serotonin. However, there may be specific conditions for which their use is warranted (e.g., cancer, recovery from stroke). We conclude that altered informed consent practices and greater caution in the prescription of antidepressants are warranted.

The bright side of being blue: depression as an adaptation for analyzing complex problems.

Depression is the primary emotional condition for which help is sought. Depressed people often report persistent rumination, which involves analysis, and complex social problems in their lives. Analysis is often a useful approach for solving complex problems, but it requires slow, sustained processing, so disruption would interfere with problem solving. The analytical rumination hypothesis proposes that depression is an evolved response to complex problems, whose function is to minimize disruption and sustain analysis of those problems by (a) giving the triggering problem prioritized access to processing resources, (b) reducing the desire to engage in distracting activities (anhedonia), and (c) producing psychomotor changes that reduce exposure to distracting stimuli. As processing resources are limited, sustained analysis of the triggering problem reduces the ability to concentrate on other things. The hypothesis is supported by evidence from many levels-genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition, behavior, and efficacy of treatments. In addition, the hypothesis provides explanations for puzzling findings in the depression literature, challenges the belief that serotonin transmission is low in depression, and has implications for treatment.

Who are we? Where did we come from? How religious identity divides and damns us all.

Charles Darwin's theory of natural selection, now established, is the only workable explanation we have for the remarkable fact of our own existence, the vast diversity of plant and animal life, the compelling illusion of design in nature, and the architecture of the human mind. We are risen apes, not fallen angels. Our different races and ethnicities hide an essential truth: we are all Africans, all siblings, all descendants of a small group of hunter-gatherers who arose in Africa less than 200,000 years ago and conquered the world. There is one universal human nature stemming from our long history as Pleistocene hunter-gatherers. We now know why religion appeared, why particular religious ideas emerged, why they are widespread, why they are recurrent features of human minds and human societies, why they are attractive to human minds, and how and why they are related to survival and deadly violence. What makes us human can also make us religious. Religion is a by-product of cognitive mechanisms that evolved, through natural selection, for other adaptive purposes that were crucial for our survival and reproductive success. Religion's power derives from its ability to utilize these mental mechanisms designed for other tasks: our attachment to parental figures, our wish for help in distress, submission to authority, our sensitivity to hierarchies, our love of kin, and our inclination to see human-like intention as the explanation for any unknown. All individuals are vulnerable to religious beliefs and assuming a religious identity. Religious identity is an accident of geographical birth, is certainly one of the most prevalent identities, and the most at odds with the reality of who we are. It remains one of the most destructive identities we can assume. As long as we tolerate the divisive pretensions of religious beliefs and identities, especially those of the three great Abrahamic faiths, we will all remain in the line of fire.