The Dog That Did Not Bark

LAURA@STOCK.ADOBE.COM

The genome consortium studies have established, with a high degree of confidence, that certain loci genes are associated with schizophrenia and bipolar disorder.¹ The tempting assumption from this finding is that somehow this group of genes is directly involved in the development of these disorders. Not so. The aforementioned genes are directly involved in the expression of premorbid personality/traits, since the presence of these traits invariably antedates the disorders. This temperamental configuration, ie, personality, is made up of traits from evolutionary pressures on the individual-albeit of an exaggerated form-such as aloofness, inner directness, autonomy, and an aversion to social interaction. Comprising, according to E.O. Wilson, one part of our human nature from birth, the other from being social creatures.²

Similar to the dog that did not bark is the dearth of the traits (whose presence normally ensures sociality) that creates the vulnerability for schizophrenia. They emanate from evolutionary pressures on social experiences, such as cooperation, empathy, mutuality, friendly competitiveness, and a tendency for social give and take. As E. O. Wilson³ concluded, these traits together, but not amalgamated, with the “selfish” traits, complete our conflictual human nature.

Yet the presence of a group of gene loci associated with the expression of our sociality is not even being considered in current studies. It is important to note that although the lopsided temperament varies somewhat between sufferers, the cardinal symptoms are felt as alienation and a disconnectedness by all of them.

The premorbid personality made of “lopsided asocial” traits creates a pool of vulnerable individuals in whom schizophrenia and bipolar disorder may develop by a periodic phase-shift of the overall coordinating faculty of brain function that ensures synchrony.⁴ This synchrony is an emergent property of complexity. This probabilistic shift heralds the expression of the disorders and results in the development of characteristic symptoms for both schizophrenia and bipolar disorder. In addition to the presence of psychoses, symptoms are made up of antithetical substitutes with an “either/or” nature in their expression.⁵ The concomitant manifestations of psychosis differ only in the “narcissistic” nature of the delusions to that of other psychoses, which are usually present in all major disturbances of brain function, such as high fever, brain trauma, and toxicity.

It is important to note that as an advantageous evolutionary trade off, some individuals in this vulnerable pool, because of their “lopsided” temperamental traits, are able to think in alternatives and discern novel scientific, mathematical, musical, and artistic patterns. Because of their “premorbid personality” unencumbered by social algorithms, they can be more creative in all areas of human endeavors at a much greater rate than the occurrence of the disorder itself. Not all will go on to have schizophrenia or bipolar disorder.^6,7 Significantly, this advantageous evolutionary trade-off explains the persistence of the 4% prevalence for both disorders world-wide in spite of its evolutionary unfitness ( ie, early onset, early death, low fertility).^8-10

The quickly advancing developments in molecular genetics, evolutionary biology, and gene editing (CRISPR) and the fusion of these disciplines with electronic technology are presenting mind-boggling opportunities for prevention as well treatment of major mental disorders. It also presents us with ethical and existential dilemmas that will tax our wisdom and have a bearing on our very survival as a species as we deal with conundrums such as what constitutes treatment and what constitutes cure. Moreover, we must consider the ramifications of attempting to modify elements of the genome that pertain to human nature (eg, what kind, for whom, by whom, for what purpose) as well as what might the consequences be for the future of humanity.

Disclosures:

Dr Pediaditakis retired recently after 63 years of clinical practice. He is a graduate of the Aristotelian School of Medicine in Thessaloniki, Greece. After completing his internship in Cleveland, OH, he obtained a fellowship/residency in psychiatry at the University of Colorado, School of Medicine. After completing his residency, he spent more than 20 years as Director of a major mental health center in the metropolitan area of Wake County in NC as well as private practice and consultation. He is an Affiliate Professor at East Carolina University, Brody School of Medicine in Greenville, NC. He now writes essays and raises black angus as a hobby. He just published the book Chroniclers of the Soul, which comprises essays relevant to us all. Dr Pediaditakis reports no conflicts of interest concerning the subject matter of this article.

References:

1. Lee SH, Ripke S, Neale BM, et al. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet. 2013;381:1371-1379.

2. Wilson EO. The Social Conquest of Earth. New York: Liveright Pub Corp; 2012.

3. Wilson EO. On Human Nature. Boston: Harvard College; 1978.

4. Arieti S. American Handbook of Psychiatry, 1st ed. New York, NY: Basic Books; 1959.

5. Pediaditakis N. Origins and mechanisms in the development of major mental disorders: a clinical approach. J Behav Brain Sci. 2012;2:269-275.

6. Andreasen NC. Creativity and mental illness prevalence rates in whites and their first-degree relatives. Am J Psychiatry. 1987;144:1288-1292.

7. Goodwin FK, Jamison KR. Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression. New York: Oxford University Press; 2007.

8. Leboyer M, Henry C, Paillere-Martinot ML, Bellivier F. Age at onset in bipolar affective disorders: a review. Bipolar Disor. 2005;7:111-118.

9. Collingwood J. Premature Death Rates Rising in Schizophrenia, Bipolar Patients; 2018. https://psychcentral.com/lib/premature-death-rates-rising-in-schizophrenia-bipolar-patients/. Accessed November 2, 2018.

10. Giudice MD. Reduced fertility in patients’ families is consistent with the sexual selection model of schizophrenia and schizotypy. PLoS 1. 2010;5:e16040.