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Schizophrenia as an Evolutionary Advantage
Theories positing the evolutionary advantages of schizophrenia usually focus on 1 of 3 vehicles of selection: individual, kin, or group. Evolutionary adaptation primarily functions at the level of the individual. In other words, individuals compete with each other, with those being most “fit” surviving and populating the next generation with their progeny. Although typically less prominent than individual adaptation, evolutionary competition can also occur among families or groups. In humans, group competition presumably occurred between hunting and gathering tribes (33). In some circumstances, even a trait disadvantageous to the individual, such as altruism, can exist if kin or group derives benefit. Thus, evolutionarily advantageous traits could be bestowed specifically upon an individual, family, or tribe.
Individual Advantages. In 1964, Huxley, Mayr, Osmond, and Hoffer published the first model that unequivocally connected evolutionary concepts to schizophrenia (34). They identified 2 characteristics related to schizophrenia that were ostensibly incompatible unless subjected to evolutionary explanations. They reasoned that schizophrenia’s relatively high prevalence of about 1% could not be easily reconciled with its low fecundity rate. Simply, if persons with schizophrenia were having fewer progeny owing to their illness, how was the disease being maintained in the gene pool? Huxley and others postulated that schizophrenia represented a genetic polymorphism accompanied by advantageous and disadvantageous characteristics. The net result would be no positive or negative selection pressure upon the genotype. The authors speculated that reduced fecundity in schizophrenia was compensated by higher resistance to shock, allergies, and infection—an idea that has never been substantiated.
The discrepancy between high prevalence and reduced fecundity is now known as the “schizophrenia paradox,” but how axiomatic are its 2 primary assumptions? The incidence and prevalence of schizophrenia have been carefully studied in many distinct cultures throughout the world, and its prevalence is invariably about 1% (15,35,36). From an evolutionary perspective, this is considered to be a high-prevalence condition, because 1% exceeds common mutation rates. The conclusion is that some presumed force—perhaps an unknown advantageous phenotypic quality—is maintaining the genotype.
A recent review of fertility and fecundity in schizophrenia confirmed the presence of reproductive deficits, particularly in men (37). Still, it cannot be assumed that schizophrenia always conferred reproductive disadvantage throughout humankind’s existence. Almost every study that demonstrates reproductive deficits in schizophrenia was devised within the last 50 years, and no accurate fecundity rates exist from traditional societies. In fact, some evidence implies that schizophrenia’s incidence may be declining in Western cultures (38–40). Nonetheless, most evolutionary-based hypotheses that are related to schizophrenia accept the assumptions of the schizophrenia paradox.
There is another model that has ascribed possible phenotypic advantages to individuals with schizophrenia. Kellet suggested that characteristics associated with schizophrenia may have helped early man’s territorial instincts, whereas affective disorders could have assisted in negotiating hierarchical tensions (41). Schizophrenia traits, such as inventiveness and the ability to tolerate low levels of stimulation while remaining alert, could have been advantageous to territorial animals. Kellett, however, addresses only a small component of schizophrenia, providing no evolutionary explanation for psychotic symptoms. Further, the social structure of Homo sapiens lineages is better characterized as hierarchical rather than territorial (42).
Advantages to Kin. Several ideas that explain the persistence of schizophrenia amidst reduced fecundity have pointed toward enhanced physiological or psychological adaptation among relatives. Among the first, Kuttner, Lorincz, and Swan proposed that the beneficial features of schizophrenia could be found in the domain of social behaviour (43). They invoked the genetic mechanism of balanced polymorphism to explain the persistence of schizophrenia. Exemplified by the classic sickle cell anemia model, genes associated with deleterious phenotypes can survive if the heterozygote demonstrates some advantage over its associated homozygotes. They speculated schizophrenia to be a homozygotic condition and proposed that the asymptomatic “schizophrenic heterozygote may enjoy a selective advantage over normal citizens in frequent retirement from a traumatic environment into a mental sanctuary.” Persons with active schizophrenia withdraw from anxiety-inducing environments excessively and thus behave in a nonadaptive manner. The authors acknowledged that they had little evidence supporting the notion that relatives of individuals with schizophrenia demonstrated superior social adaptation. Further, the balanced polymorphism argument may not be suitable to explain the appearance of social behavioural traits. There are few proven cases of balanced polymorphisms in nature, presumably because it is not an ideal mechanism for adaptation (44). The typical examples of balanced polymorphism, such as sickle cell anemia, Tay-Sachs disease, and cystic fibrosis, appear to be imperfect stop-gap measures to contend with the sudden presence of specific infectious agents (45–47).
Erlenmeyer-Kimling, in a thoughtful paper, considered a possible physiologic advantage associated with schizophrenia that explains an unexpected result in a retrospective study of schizophrenia mortality (48). In a sample from New York state hospitals, female children of parents with schizophrenia enjoyed increased survival. Male children did not demonstrate any advantage or disadvantage. The author noted that these findings were inconsistent with 3 previous similar studies, demonstrating no survival advantage in children of parents with schizophrenia.
Carter and Watts also conducted a retrospective study that supported the notion of a possible physiologic advantage related to schizophrenia (49). They found a significantly diminished incidence of virus infections among relatives of patients with schizophrenia. Patient sample sizes were small and were derived from only 2 English medical practices. Omission of a Bonferroni corrected analysis is the most probable reason for this seemingly spurious finding that has never been replicated or otherwise supported.
The potential relation between exceptional ability and mental illness has been used to explain the persistence of schizophrenia genes. In Western culture, associating creativity with mental illness dates back to Aristotle (50). A study by Karlsson found superior academic success among relatives of schizophrenia patients (51). Accessing records from Iceland’s stable population and using diverse methods to measure creative intelligence strengthened the confidence in the results. Karlsson relied on the balanced polymorphism paradigm to explain his results, suggesting that creative relatives of schizophrenia patients were super-adaptive heterozygotes. He also provided compelling anecdotal evidence, demonstrating that genius and mental illness were often in genetic proximity: Sir Isaac Newton became psychotic at age 51 years, and Albert Einstein’s son was diagnosed with schizophrenia (52). Other examples include Nobel laureate John Nash, who developed schizophrenia in his 30s and Bertrand Russell, who apparently had several relatives with schizophrenia (20). Indeed, it is a controversial topic, and evidence for a connection appears stronger for affective disorders than for schizophrenia (53). A recent review of the related literature suggested that little evidence exists to link creativity and mental illness (50). However, historical references to mental illness have likely been underreported, while achievements are widely recognized. Likewise, if psychiatric conditions were responsible for only a fraction of all demonstrations of creativity, proving an association could be difficult.
Allen and Sarich postulated that the “schizophrenia advantage is in the somewhat touchy relationship between an individual and his culture and society” (54). Using the balanced polymorphism argument, overt schizophrenia, or having no genetic loading for schizophrenia, would be nonadaptive. Asymtomatic heterozygotes, perhaps 5% with some genetic loading for schizophrenia, would possess survival advantages by being able to resist the “shared biases and misconceptions of the group.” In other words, conforming would not always be advantageous to the individual. The integrity of the group could sustain some betrayal if there were few nonconformists. Allen and Sarich emphasize that their hypothesis explains why schizophrenia appears to demonstrate greater prevalence in industrial societies: complex societies can tolerate, sustain, and even flourish when some persons possess a greater sense of individuality.
Horrobin has developed an interesting argument that relates neuronal membrane phospholipid metabolism to the evolutionary cerebral changes that created man (55,56). Over the last 2 million years, the seemingly greater availability of some essential fatty acids (arachidonic acid and docosahexaenoic acid), combined with phospholipase mutations, could have resulted in enhanced neuronal microconnectivity. Amplifying neural connections would generate superior creativity manifested in various ways, including schizophrenia, dyslexia, and manic-depressive illness. Growing evidence of cerebral phospholipid dysregulation in schizophrenia supports the pathophysiological aspect of this concept (57). Horrobin emphasizes the possible connection between bipolar disorder and schizophrenia, which suggests psychosis possesses attributes that could have been helpful to early man. For example, mania induces dynamic energy, while paranoia results in prudence. Citing Karlsson’s work, close relatives of individuals with psychosis may have accrued evolutionary advantages through enhanced creativity—a trait that has now permeated all people. Horrobin concludes that these neuropsychiatric conditions could reflect the foundations of man’s creativity.
Group Advantages. Stevens and Price have put forward a “group-splitting hypothesis of schizophrenia” (58). They presume that proliferating tribal communities must eventually split to maintain optimum numbers. Schizotypal traits in certain prominent individuals may be necessary to ensure survival of the offshoot group. Stevens and Price argue that schizotypal traits are frequently found in charismatic leaders; namely, Adolph Hitler, Joan of Arc, and Charles Manson. These shaman-like individuals use paranoia, delusions, religious themes, and even neologisms, to fraction disaffected groups and to seed new cultures. They propose that this type of leadership is essentially altruistic and thus maintained by group selection.
Polimeni and Reiss have proposed a group selection hypothesis for schizophrenia with a different emphasis: schizophrenia could have enhanced a shaman’s ability to conduct religious-based rituals (59). Because religious rituals are universally observed in all cultures, this activity is likely both genetically rooted and critical to humankind’s survival. With the exception of the last few thousand years, humans have always lived in hunting and gathering societies that all demonstrate some form of shamanism. Therefore, a genetic foundation to shamanism must also be considered. Psychosis would be advantageous to shamans spearheading religious rituals. The substantial prevalence of religious-based delusions in schizophrenia supports this position (60,61). Although shamans are sometimes typified as community leaders, evidence exists to the contrary—especially in less technologically advanced cultures (62). Polimeni and Reiss provide a plausible evolutionary mechanism that explains reduced fecundity in schizophrenia by making clear parallels to the group-selection dynamics of honeybee colonies. Similar to sterile worker bees that continue to proliferate because they must somehow be crucial to the colony’s survival, schizophrenia symptoms in certain individuals may reflect an ancient form of behavioural specialization for hunting and gathering tribes.
Conclusion
Darwin was prescient with respect to the possible importance of evolutionary theory to mental conditions: “In the distant future I see open fields for far more important researches. Psychology will be based on a new foundation, that of the necessary acquirement of each mental power and capacity by gradation. Light will be thrown on origin of man and his history” (Origin of the Species, 1859).
Evolutionary principles could be relevant to schizophrenia, owing to its presumed genetic basis and supposed long history. Although neglected prior to the 1960s, several evolutionary-based theories have since emerged that speculate on the possible origins of schizophrenia. These evolutionary perspectives tend to fall into 1 of 2 general categories: 1) theories that assume schizophrenia to be a disadvantageous byproduct of human brain evolution and 2) theories that propound evolutionary advantages that are associated with the condition. Considering an evolutionary perspective can only enhance our understanding of schizophrenia.
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