A New Perspective on Rumination
How Group Selection Theory Explains Species Survival
In the early 1900s, Emil Kraepelin, the father of modern psychiatry, stated that it was nearly impossible to establish a fundamental difference between normal and pathological mental states. Over the past century, little has changed in this regard. Doctors and scientists still debate how accurately current diagnostic criteria distinguish between normal and pathological conditions. We know that not all unpleasant reactions or experiences are necessarily diseases or disorders. For example, fever and diarrhea are unpleasant, but they are not diseases in themselves—they help the body rid itself of dangerous pathogens.
Similarly, some non-psychotic mental “disorders” accompanied by strong emotions (especially depression and anxiety) emerged as adaptations to serve specific functions in our evolutionary past. In this sense, they are not “diseases” or “disorders” but rather common responses to external threats that increase the chances of passing on genes to offspring. While unpleasant and potentially disruptive to life, these adaptations were selected for by evolutionary pressures because they increased reproductive fitness.
Evolutionary biology recognizes the theory of inclusive fitness, systematized by British biologist William Hamilton. According to this theory, organisms pass on their genes not only through direct descendants but also by helping their relatives. From the gene’s perspective, evolutionary success is achieved by leaving as many copies of itself in the population as possible. Previously, it was believed that genes achieved this only through direct offspring, but this view was revised in the 1960s.
Today, biology distinguishes two main indicators of evolutionary success: 1) direct fitness—the number of offspring an individual produces, and 2) indirect fitness—the number of offspring an individual helps raise or support through its behavior. This theory allows us to interpret altruistic social behavior in animals in terms of kin (group) selection.
According to this logic, evolution selects for the survival of the most fit genetic lines, not just the most fit individual. Thus, inclusive fitness is the sum of an individual’s reproductive fitness (direct fitness) and that of their biological relatives (indirect fitness). Sometimes, actions that reduce an individual’s chances of reproduction can increase the reproductive success of their genetic line.
How Evolutionary Psychology Helps Explain the Adaptive Role of Depression
Clinical psychologists often label behavior as “maladaptive” if it does not directly benefit the individual. However, they may overlook that some traits, which contributed to gene survival, could have been selected for during evolution and persist today—even if they are unfavorable for the individual. This affects how terms like “maladaptive” are used. From an evolutionary perspective, “maladaptive” means a trait reduces inclusive fitness, while clinically it means the trait is not useful for the person. The key point is that evolution may have selected certain traits that are adaptive for gene propagation, but not for the individual.
Evolutionary adaptations are traits that exist now because they formed under selective pressures in the past. However, the modern environment can differ greatly from that of our ancestors, so what was adaptive then may not be adaptive now. For example, most people have a preference for sweet tastes. This was adaptive in our evolutionary history, when fruits rich in vitamins were the main source of simple carbohydrates, but today it leads to problems like obesity and tooth decay.
Retrospective studies estimate that 16% of all people experience a major depressive episode at some point in their lives. Cohort studies, which follow people from birth, show this number is three times higher. Most of these additional cases occur in response to major life stressors that are unlikely to recur. In other words, depression can happen to anyone, but it does not always become a chronic pathology.
In some cases, depression may play an evolutionarily useful role, paradoxically increasing an individual’s biological adaptation, survival chances, and ability to pass on genes. Psychology uses the concept of rumination—painful fixation on negative thoughts and experiences, often accompanying depression. According to the analytical rumination hypothesis (ARH), depression arises as an evolutionary response to complex life problems and simultaneously helps address them. When facing difficulties, a person experiences a negative state, and their cognitive resources are directed toward analytical thinking—reflecting on the causes of the problem and possible solutions. By helping people solve complex problems, rumination may theoretically contribute to depression remission. Thus, ARH can be seen as a working model for the evolutionary explanation of depression, while CBT (Cognitive Behavioral Therapy) is a treatment that can facilitate the functions depression once served by managing rumination. The main principle of evolutionary medicine is that any intervention supporting the functions for which negative affect evolved is more likely to be successful long-term than one that simply numbs or removes symptoms. To understand this better, several questions need to be addressed.
What Evidence Supports Depression as an Adaptation?
Many evolutionary theories suggest that unpleasant feelings are caused by painful situations and motivate us to avoid them. For example, anger helps avoid social pressure, anxiety helps avoid external threats, and pain helps avoid bodily harm. Emotions trigger coordinated bodily responses to successfully handle such situations.
Cognitive psychology recognizes two types of thinking—fast (type 1) and slow (type 2). This theory applies here. Depression is an emotional reaction to maladaptive mistakes, promoting a learning style aimed at avoiding similar situations in the future. In this sense, it aligns with slow thinking, which is better suited for solving complex social problems where analysis, not speed, is key. This idea is related to psychologist Daniel Kahneman’s work on fast and slow thinking.
Sadness—a key symptom of depression—is known for its influence on type 2 information processing. Other depression symptoms are organized around the time and attention needed for this kind of thinking. For example, anhedonia (lack of interest in pleasure) may help focus on analytical information processing.
There are three syndromes associated with depressed mood and anhedonia. First, during infection, the body’s activity is directed toward the immune system, not cognitive functions. Second, during hunger, activity is redirected to maintain vital organs, especially the brain. Finally, during depression, activity shifts from the immune system to the cerebral cortex. These processes are coordinated by serotonin—a primitive neurotransmitter that has existed for over 600 million years.
Serotonin is synthesized in the raphe nuclei, a structure in the medulla oblongata. When the raphe nuclei are activated, they engage the amygdala to focus on stress, the hippocampus to activate working memory, and the prefrontal cortex to concentrate attention. This redistribution of brain activity promotes rumination, which triggers avoidance learning and mirrors depression symptoms—a result of natural selection for environmental adaptation.
British neuropsychologist Jeffrey Gray described two interconnected neurobiological systems: 1) the behavioral inhibition system (BIS), based on norepinephrine, which warns of threats, and 2) the behavioral activation system (BAS), based on dopamine, which drives pleasure-seeking. In depression, the second system is suppressed. Serotonin, the main target of almost all antidepressants, regulates the balance between inhibition (BIS) and activation (BAS), coordinating these two types of activity and their related affective syndromes.
How does this work? Norepinephrine and dopamine are two other neurotransmitters linked to depression. Serotonin receptors modulate their release. Norepinephrine is heavily involved in regulating the stress response (BIS), while dopamine is involved in reward-seeking (BAS). In other words, the first mediator is activated to avoid danger, the second to motivate goal achievement. If serotonin levels drop, the body’s activity aimed at avoiding threats and seeking pleasure also drops, leading to a depressive state with rumination.
What Is the Purpose and Function of Rumination?
Clinical psychologists associate rumination with depression and often see it as having no useful function—either as a symptom or a causal factor of depression. However, the brain seems predisposed to rumination after loss or failure. Most depressive episodes resolve on their own without treatment (so-called “spontaneous remission”), which is not typical for most other disorders. For example, fear of heights persists for life unless actively addressed, while depression can fade away. This raises the question: why does depression resolve? There must be a mechanism in our ancestors’ past that explains what appears to be “spontaneous remission.”
Depressive thinking (rumination) involves self-criticism, feelings of worthlessness, and guilt. These thoughts may seem useless, but the authors argue that reflecting on loss or failure is not in vain if it helps solve the current problem or avoid similar events in the future. Emotions evolved to motivate adaptive responses to specific situations. Positive emotions encourage seeking opportunities that increase fitness (BAS), while aversive emotions encourage avoiding harm that decreases fitness (BIS). Normal emotions subside when the opportunity or problem that triggered them is resolved. This largely explains why rumination can contribute to remission by helping solve problems caused by failure or loss.
Analyzing the chain of events leading to loss or failure, and focusing on points in the causal chain where preventive measures could have been taken, is called root cause analysis (RCA). This type of problem-solving uses type 2 thinking. We have to reconstruct the sequence of events that led to failure, considering different possible actions. As a result, we often arrive at counterfactual thoughts—”If I had done X, Y wouldn’t have happened.” These thoughts help us understand what caused the problem and what could have been done to avoid it.
Thus, type 2 thinking, which helps us learn from mistakes, is not coincidentally linked to complex states like sadness, guilt, and low self-esteem. All these experiences are meant to help us avoid future mistakes and likely serve a social function in conflict resolution. Low self-esteem and pessimism, often accompanying depression, may also play a role by prompting deeper analysis and problem-solving. According to sociometer theory, self-esteem “tracks” how valuable we are to significant others and motivates us to behave in ways that improve our social standing (beliefs about oneself without social context are unlikely to be selected for by evolution, since natural selection shapes how organisms interact with their environment).
In other words, according to the analytical rumination hypothesis, depressive episodes resolve through a sequential two-step rumination process: problems trigger depression, which then stimulates causal analysis, leading to problem-solving and, as the problem is resolved, a reduction in depressive symptoms and spontaneous remission—which is not truly “spontaneous,” but the result of a specific process. In engineering terms, depression is part of a “closed system” that responds to disruptions and then returns the system to equilibrium. Spontaneous remission can be seen as “problem resolution without outside help,” where depression does its job (motivating steps toward a solution) and then fades, much like a fever subsides.
As for relapses, the authors identify several causes. These include individual differences (people with higher risk for depression, whether genetic or acquired), the inherent “normality” of depressive states in response to stressors (as with any recurring experience in life), and different coping strategies. Avoidance (distraction, thought suppression, self-medication, or other tactics to avoid painful feelings) is associated with worse depression outcomes and higher relapse risk. Essentially, if a person does not learn from experience (even painful experience), they are likely to repeat the same mistakes. Another reason relates to the complexity of the problem faced—some solutions require slow, thorough analysis of dominant mental models, formulating and systematically testing different hypotheses, which may involve alternating phases of intense depressive thinking and periods of respite. Ultimately, people prone to depression are not unique in their inflexibility when it comes to changing beliefs—this is a common human trait. New information that contradicts existing beliefs is met with more skepticism than information that confirms what we already believe.
If “insanity” is doing the same thing over and over and expecting different results, then most of humanity is functionally “insane,” since most of us act this way. It’s not that new ideas never win out (if they better reflect reality), but a critical mass of anomalies must accumulate before the existing paradigm begins to shift. Usually, a paradigm shift requires an alternative that better accounts for the anomalies.