• Juan-Fernando Duque-Osorio

Darwinian Evolution of the Bipolar Affective Gradient Conditions

Updated: Feb 9

Key words: Bipolar Affective Disorder or Disorder (BPAD), Evolutionary Psychology, Darwinian Medicine, Seasonal Affective Disorder, Psychotherapy, Psychoeducation, Seasonality, Pleistocene.

Leer este artículo en español

Read this article in PDF format

Summary: Bipolar affective disorder (BPAD) is a condition that, depending on its severity, leads the patient from the extreme euphoria (or mania in clinical cases) to dysphoria (or clinical depression) affects approximately approximately 4% of the population On the BPAD there is considerable information on its next causes and little information on its last (evolutionary) causes. Within these there are a few authors who begin to point out that the BPAD could have, among its evolutionary causes, a climatic component, within which it should be noted that the BPAD has a very related entity called seasonal affective disorder. With all this in mind, attention is drawn to the fact that more research is needed on the evolutionary (latest) causes of BPAD that give cohesion to the fragmentary information about the nearby causes of BPAD, especially as regards Seasonality effect is concerned. In addition to being interesting from the scientific point of view, the fact that physicians, especially psychologists know more about BPAD will help to treat patients better.

All human beings have mood fluctuations, usually related to positive or negative events that happen in our lives. But when these mood changes exceed the healthy, socially acceptable limits, persist in a disorderly manner over relatively long periods of time, and make it impossible for the person to function and enjoy life, one can start talking about a bipolar case (Fink & Kraynak, 2011). In general terms, bipolar disorder is a mental condition in which the patient suffers from neurochemical imbalances that affect his mood, emotional stability and circadian rhythm, which leads to sleep problems as well. Depending on the intensity of the condition, the patient can cycle from euphoria to sadness with periods of relative balance. It affects up to 4% of the planet's population (Wormer, 2004). The frequency of crises and their intensity depend on the severity of the condition. That is why we speak of the gradient or bipolar or manic-depressive spectrum (Angst, 2007; Ghaemi & Baldessarini, 2007; Goodwin & Jamison, 2007). Concisely, the entities of the bipolar gradient can be hierarchized as follows in ascending severity in: cyclothymia (the mildest form), bipolarity as such, manic-depressive illness and affective psychosis. This is a hierarchy in which no one wishes to advance. Fortunately, with current pharmaceutical technology, a properly treated bipolar can never really get sick. While the person is treated at home and through outpatient consultations, he or she is not sick and is subclinical or even sub-syndromal (Jamison, 1994). With proper care a patient can lead an acceptably happy and productive life. But if the person must be admitted to a mental institution, we are faced with a sick person, who at least for the period of time that he is hospitalized will not be able to function properly society. To explain the symptoms and help in the diagnosis of mental conditions, the “Diagnostic and Statistical Manual of Mental Disorders” has been developed, which is currently in its fifth version [DSM-V (APA, 2013)]. In summary, the main forms of bipolar disorders can be summarized in Figure 1:

Figure 1. Cyclothymia is the mildest form of the bipolar gradient or manic-depressive spectrum (Ghaemi & Baldessarini, 2007; Goodwin & Jamison, 2007). It is characterized by mood changes that can last a few days, ranging from euphoria to dysphoria but do not become as severe as those of a bipolar as such. Bipolarity is more marked: it is characterized by mood swings that range from hypomania to depression. A manic-depressive has even more frequent and extended mood changes, which can range from mania to clinical depression (Müller-Oerlinghausen et al., 2002). One of the main difference between the subclinical forms of the bipolar gradient and the clinical forms (manic depressive illness in this graph) is that manias and depressions can, among other symptoms, include auditory hallucinations in which the patient can hear a voice that he tells him that he will be the president of the world (during mania), or on the contrary, in a clinical depression, he can hear a voice that tells him that he is the cause of all the evils of the world and that he must commit suicide, among other manifestations. Graphic taken from Black (2013).

BPAD is the mental condition with the best prognosis when properly treated (Fink & Kraynak, 2011). But if the treatment does not start in a timely and correct manner, increasingly extreme mood phases begin to appear and the stability phases begin to get shortened (Wormer, 2004). One in three untreated cyclothymics develop depressions and clinical manias (Jamison, 1994, 2000). This last author is a bipolar psychologist and writer who has become one of the bipolar authorities in North America. It makes an exhaustive review of the psycho-biographical record (Jamison, 1994, 2008) and shows us how artists, especially famous writers, who lived before today existing pharmaceutical technology, left great artistic works, motivated mainly by their mood swings, but by not having adequate treatments typically ended up abusing drugs (which are different from medicines) and committing suicide. Even today, with many and better treatment options, 10 to 20% of bipolar patients take their lives (Müller-Oerlinghausen et al., 2002). However, in our days, these new treatments, applied on time and correctly, allow to reduce the symptoms, without the patient losing the great and creative potential that usually accompanies the BPADs (Jamison, 1994). The treatment consists of three pillars: pharmacotherapy led by a psychiatrist, psychotherapy (Jones, 2004; Lam et al., 2010) and psychoeducation [this is about the fact that the patient and family must learn the more the can about their condition (Colom & Vieta, 2006)], complemented with other therapies such as support groups (Wormer, 2004) that in Colombia are led by the Colombian Bipolar Association (ACB, 2014). In all this type of therapies that complement the pharmacological one (carried out by the psychiatrist), the protagonist is the psychologist. In fact, good psychological therapy may cause the patient to need fewer medicines (Jamison, 1994).

About the proximate [physiological (Nesse, 2007; Nesse & Williams, 2012)] causes of a condition such as bipolar, there is considerable information (Fink & Kraynak, 2011; Goodwin & Jamison, 2007; Jamison, 1994, 2000, 2008; Wormer, 2004). Basically, it is a neurochemical imbalance, caused by several genes (Baum et al., 2007) that is triggered by some change in the environment. Many patients have their bipolar condition discovered by a change of life, such as moving out of town, changing jobs, retiring or a traumatic event. So, like any characteristic of a living being, it is the result of the interaction of genetics with the environment (Wilson, 2000). Taking into account aforementioned, it should be noticed that psychology is increasingly moving to biological approaches (Cacioppo et al., 2000; Jamison, 1994) and among this is Evolutionary Psychology (Cosmides & Tooby, 2012; Dunbar et al., 2011; Evans & Zarate, 2010; Pinker, 2009; Workman & Reader, 2008). Evolutionary psychology is the union of two great paradigms: cognitive psychology and Darwinian evolution theory. In addition, between the humanities and a hard science like biology, there is a gray territory that promises many discoveries (Wilson, 1975, 2004). What percentage of X or Y behavior has a biological cause and cultural one? Regarding the causes and symptoms of BPAD, what percentage is biological and which is environmental? In addition to the proximate (neurophysiological) explanations, can the ultimate (evolutionary) explanations give us light on this and other related mental problems? Could these evolutionary explanations help to develop more effective treatments with fewer side effects? A branch of knowledge closely related to Evolutionary Psychology is Darwinian Medicine (Nesse, 2007; Nesse & Williams, 2012), especially in the behavioral part of the latter [Evolutionary Psychopathology = Darwinian Medicine (Workman & Reader, 2008)]. It is obvious that an evolutionary approach to seeing the BPAD will provide lights to improve treatments such as the manipulation of hours of exposure to light (Leibenluft et al., 1994; Sit et al., 2007; Wehr et al., 1998), among other. All this without abandoning pharmacotherapy, because giving out with the latter in disorders such as bipolar is considered a bad medical practice (Jamison, 1994). A focus will be made on therapies that involve light manipulation because, and although the information is fragmentary, it is suspected that within the ultimate (evolutionary) causes there is a relationship between BPAD and seasonality (Sherman, 2006, 2012), as among other things, an entity such as seasonal affective disorder (Davis & Levitan, 2005; Eagles, 2004; Sher, 2000) that is practically part of the bipolar gradient should not be overlooked. And here is the crux of this article. It seems that the conditions of the affective-bipolar gradient evolved as over adaptations to the hard seasonal regime of the Pleistocene (it began 2.5 million years ago and ended 10 thousand years ago) where, thanks to the glaciations, there were very long and severe winters with very short summers. Faced with this scenario, the most adaptive is to be depressed in the hardest part of winter so as not to waste energy in an environment that only offers ice and snow. In summer, however, hypomania helps to efficientlyu use time on hunting (mammoths, for example, that we took them to extinction), making strategic alliances with other individuals (suddenly the verbiage) and time must also be used to procreate. Suddenly from there comes the hyper-sexuality that occurs in the hypomanic and manic phases. In any case, it was necessary to take advantage of the short summers to do everything that cannot be done during the winter, within which the most important thing was the accumulation of food by those communities of hunters and gatherers. Hence the typical hyperactivity of manias and hypomanias. But being over-adapted to the seasons is the same as being poorly adapted as there is a philosophical principle that says the extremes come together. In other words, bipolars are extremely sensitive to changes in photoperiods and temperature. Even here in the tropics it has been observed that manic episodes tend to occur in the “summer” (Volpe et al., 2010).

The mere fact of proposing a model that largely explains the evolutionary aspects of BPAD is already a sufficient scientific justification to continue investigating this issue, as it is something very interesting. But in an area that is already more practical, more applied, the best knowledge of BPAD has obvious implications in the ability of physicians to treat it and of patients to better understand themselves and their disorder. As already said, the three pillars of the treatment of any mental condition, but especially bipolar disorder are: pharmacotherapy, psychotherapy and psychoeducation. Given the health system that currently shelters us, it is clear that the psychiatrist hardly has time to make the relevant pharmacological adjustments in each session. But he will not have the time to have a long conversation with the patient, listen to him, help him in his relief and he will not have time to explain key things about his condition that could help him manage it better. This is how psychotherapy and psychoeducation should be tasks carried out by the psychologist so that the more the physicians know about this condition, a more comprehensive and efficient treatment of the patient can be made. Knowing how and what key environmental conditions, such as weather changes, may affect the patient, will allow preventive corrective action, thus reducing the likelihood of relapse.

Thank you very much for reading this article.

Literature Cited:

ACB. 2014. Asociación Colombiana de Bipolares. Consultado el 11-Dic-2014 en http://www.bipolarescolombia.com/ .

Angst J. 2007. The bipolar spectrum. The British Journal of Psychiatry 190(3): 189-191.

APA. 2013. The Diagnostic and Statistical Manual of Mental Disorders: DSM 5. bookpointUS.

Baum AE, Akula N, Cabanero M, Cardona I, Corona W, Klemens B, Schulze TG, Cichon S, Rietschel M, Nothen MM, Georgi A, Schumacher J, Schwarz M, Abou Jamra R, Hofels S, Propping P, Satagopan J, Detera-Wadleigh SD, Hardy J & McMahon FJ. 2007. A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder. Mol Psychiatry 13(2): 197-207. http://dx.doi.org/10.1038/sj.mp.4002012 .

Black S. 2013. Cyclothymia. Consultado el 11-Dic-2014 en http://sachablack.wordpress.com/2013/04/10/cyclothymia/ .

Cacioppo JT, Berntson GG, Sheridan JF & McClintock MK. 2000. Multilevel integrative analyses of human behavior: social neuroscience and the complementing nature of social and biological approaches. Psychological bulletin 126(6): 829.

Colom F & Vieta E. 2006. Psychoeducation manual for bipolar disorder. Cambridge University Press.

Cosmides L & Tooby J. 2012. Center for Evolutionary Psychology. University of California at Santa Barbara. Consultado el 17-Dic-2013 en http://www.psych.ucsb.edu/research/cep/ .

Davis C & Levitan RD. 2005. Seasonality and seasonal affective disorder (SAD): An evolutionary viewpoint tied to energy conservation and reproductive cycles. Journal of Affective Disorders 87(1): 3-10.

Dunbar R, Barrett L & Lycett J. 2011. Evolutionary Psychology: A Beginner's Guide: Human Behaviour, Evolution and the Mind. Oneworld - Oxford. 228 pp.

Eagles JM. 2004. Seasonal affective disorder: a vestigial evolutionary advantage? Medical hypotheses 63(5): 767-772.

Evans D & Zarate O. 2010. Introducing Evolutionary Psychology: A Graphic Guide. Totem Books. 176 pp.

Fink C & Kraynak J. 2011. Bipolar Disorder For Dummies. Wiley. 340 pp.

Ghaemi SN & Baldessarini RJ. 2007. The manic-depressive spectrum and mood stabilization: Kraepelin’s ghost. Psychotherapy and psychosomatics 76(2): 65-69.

Goodwin FK & Jamison KR. 2007. Manic-depressive illness: bipolar disorders and recurrent depression. Oxford University Press.

Jamison KR. 1994. Touched with Fire: Manic-Depressive Illness and the Artistic Temperament. Free Press Paperbacks. 370 pp.

Jamison KR. 2000. Suicide and Bipolar Disorder. The Journal of Clinical Psychiatry 61 Suppl 9: 47-51.

Jamison KR. 2008. Manic Depressive Illness and Creativity. Pp 52-64 en: Scientific American: What Makes a Genius. The Rosen Publishing Group, Inc, New York. 111 pp.

Jones S. 2004. Psychotherapy of bipolar disorder: a review. Journal of Affective Disorders 80(2): 101-114.

Lam DH, Jones SH & Hayward P. 2010. Cognitive Therapy for Bipolar Disorder: A Therapist's Guide to Concepts, Methods and Practice. John Wiley & Sons. 344 pp.

Leibenluft E, Turner E, Feldman-Naim S, Schwartz PJ, Wehr TA & Rosenthal NE. 1994. Light therapy in patients with rapid cycling bipolar disorder: preliminary results. Psychopharmacology bulletin 31(4): 705-710.

Müller-Oerlinghausen B, Berghöfer A & Bauer M. 2002. Bipolar disorder. The Lancet 359(9302): 241-247.

Nesse RM. 2007. Evolutionary Explanations Mood Disorders. Pp 159-175 en: The American Psychiatric Publishing Textbook of Mood Disorders (eds: Stein DJ, Kupfer DJ & Schatzberg AF). American Psychiatric Publishing. Obtenido el 08-Dic-2014 en http://bit.ly/1scCvQ7 .

Nesse RM & Williams GC. 2012. Why We Get Sick: The New Science of Darwinian Medicine. Knopf Doubleday Publishing Group. 304 pp.

Pinker S. 2009. How the Mind Works. W. W. Norton. 661 pp.

Sher L. 2000. The role of genetic factors in the etiology of seasonality and seasonal affective disorder: an evolutionary approach. Medical hypotheses 54(5): 704-707.

Sherman JA. 2006. Bipolar disorder evolved as an adaptation to severe climate. Behavioral and Brain Sciences 29(04): 421-422.

Sherman JA. 2012. Evolutionary origin of bipolar disorder-revised: EOBD-R. Medical hypotheses 78(1): 113-122.

Sit D, Wisner KL, Hanusa BH, Stull S & Terman M. 2007. Light therapy for bipolar disorder: a case series in women. Bipolar disorders 9(8): 918-927.

Volpe FM, da Silva EM, dos Santos TN & de Freitas DEG. 2010. Further evidence of seasonality of mania in the tropics. Journal of Affective Disorders 124(1): 178-182.

Wehr TA, Turner EH, Shimada JM, Lowe CH, Barker C & Leibenluft E. 1998. Treatment of a Rapidly Cycling Bipolar Patient by Using Extended Bed Rest and Darkness to Stabilize the Timing and Duration of Sleep. Biological Psychiatry 43(11): 822-828.

Wilson EO. 1975. Sociobiology: The New Synthesis. (1 ed). Harvard University Press. Cambridge (MA)-USA. 697 pp.

Wilson EO. 2000. Sociobiology: The New Synthesis. Belknap Press of Harvard University Press. 697 pp.

Wilson EO. 2004. On Human Nature: With a New Preface. Harvard University Press. 260 pp.

Workman L & Reader W. 2008. Evolutionary Psychology: An Introduction. Cambridge University Press. 486 pp.

Wormer EJ. 2004. Bipolar: Depresión y Manía: Vivir con Emociones Extremas. Ediciones Robinbook. Barcelona. 287 pp.

USA, Canada & Puerto Rico


Cellular & WhatsApp:


  • Facebook JFDO
  • Twitter JFDO
  • LinkedIn JFDO
  • Canal YouTube JFDO
  • ResearchGate JFDO
  • Academia.edu JFDO
  • Google Académico JFDO
  • GoodReads JFDO
  • ClassGap JFDO
  • Autor de Amazon JFDO

You're visitor number:

© 2020 by Juan-Fernando Duque-Osorio. MSc. Ibagué-Colombia