ethicaldilemmasantidepressants

.pdf

School

Pensacola Christian College *

*We aren’t endorsed by this school

Course

NU 214

Subject

Medicine

Date

Oct 30, 2023

Type

pdf

Pages

Uploaded by ChiefUniverse5971

See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/11658377 Ethical Dilemmas in Prescribing Antidepressants Article in Archives of General Psychiatry · December 2001 DOI: 10.1001/archpsyc.58.11.1085 · Source: PubMed CITATIONS 2 READS 268 2 authors: Robert J Gregory State University of New York Upstate Medical University 60 PUBLICATIONS 1,085 CITATIONS SEE PROFILE Ripu Jindal University of Alabama at Birmingham 56 PUBLICATIONS 1,503 CITATIONS SEE PROFILE All content following this page was uploaded by Robert J Gregory on 20 September 2019. The user has requested enhancement of the downloaded file.

Depression Is an Adaptation D r Nesse, in raising the question, “Is Depression an Adaptation?” 1 has contributed greatly to un- derstanding this poorly understood, unpredict- able condition. He offers many possible functions for low mood and depression, but he stops short of firmly con- cluding that depression has adaptive significance. A strong case for the phylogenetically adaptive sig- nificance of depressive symptoms can be made, how- ever. Depression has a genetic component: parents of persons with major depressive disorder (MDD) are 2 to 3 times more likely to have had the disease themselves than parents of persons without depression. 2 Depres- sion is also common. Lifetime prevalence of MDD is 15.8%. 2 The rate of spontaneous mutation in humans is 1 per 10000 to 1 per 1000. 3 Taking the conservative values of 1 in 10 for MDD and a mutation rate of 1 per 1000, depression is observed at more than 100 times the mutation rate. Depression must have had a definite se- lective advantage in the ancestors of modern humans; otherwise, it would be rare. Not all modern depression is necessarily adaptive, of course. Depression consequent to hypothyroidism, for example, is clearly pathological. Also, even if some de- pression is strongly disadvantageous in modern condi- tions, the effect of negative selection on prevalence will not be apparent for many generations. Knowing that depression was adaptive to our an- cestors and may often still be adaptive as Nesse has shown, encourages a new view of this old disease. This evolu- tionary view implies that triggers of depression are likely to bear a recognizable relationship to situations in which depression would have improved fitness in ancestral con- ditions. Seasonal affective disorder, triggered by low light conditions 4 and enforcing reduced energy consumption at times when our ancestors would have suffered sea- sonal scarcity, may be an example of this. The typical relapsing, noncontinuous course of depression may have increased fitness by enabling be- haviors adapted to circumstances. Nesse, noting that re- peated episodes of endogenous depression often seem unrelated to life events, argues that these depressive episodes are not defenses. If previous depressive epi- sodes increase sensitivity to subsequent triggers, how- ever, heightened reactions to triggers we do not yet rec- ognize may explain the apparent absence of life events triggering recurrent endogenous depression. In any case, we can say with confidence that de- pression is an adaptation—the result of eons of positive selection. As the origins, physiology, and adaptive sig- nificance of depressive symptoms become better under- stood, it may become possible to predict and prevent de- pression in its more deleterious forms. Alison J. Longley, PhD Pacific Sciences Institute Box 85813 Seattle, WA 98145 (e-mail: longley@u.washington.edu) 1. Nesse RM. Is depression an adaptation? Arch Gen Psychiatry. 2000;57:14-20. 2. Kessler RC, Zhao SY, Blazer DG, Swartz M. Prevalence, correlates, and course of minor depression and major depression in the national comorbidity sur- vey. J Affect Disord . 1997;45:19-30. 3. EdwardsJH.Themutationrateinman.In:SteinbergAG,BearnAG,eds. Progress in Medical Genetics. Vol 10. New York, NY: Grune & Stratton; 1974:1-16. 4. Rosenthal NE, Sack DA, Gillin JC, Lewy A J, Goodwin FK, Davenport Y, Muel- ler PS, Newsome DA, Wehr TA. Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy. Arch Gen Psychia- try. 1984;41:72-80. Sex Hormones, Darwinism, and Depression T wo recent articles published in the same issue of the A RCHIVES 1,2 pose interesting questions re- garding the evolutionary roots of depression and depression in women. We would like to propose a point of view that connects the two, and examine its practical implications. Depression in Women vs Men. Women have an in- creased incidence of depression compared with men, by a ratio of 2:1. 2 Moreover, not only clinical depression, but also more subtle dysthymic traits have had a higher preva- lence in women after the onset of puberty. 3 In evolution- ary terms, if depression is viewed as conducive to staying out of danger in a sheltered place, 1 it may have made sense historically for women to manifest more of that trait than men. Women have traditionally been involved in child- bearing and child rearing, whereas men have tradition- ally been the providers of food, material resources, and protection. Dysthymic traits would have kept a woman shelteredfromdangertobearandcareforchildren;whereas a dysthymic man would have been impaired in perform- inghismainroleasaproviderandprotector.Assuch,traits predisposing to dysthymia may have been selected for in women, and selected against in men over time. Sex hormones may be important mediators of these evolutionarily selected behavioral differences. It is inter- esting to note the antidepressant, novelty-seeking, and ag- gression-promoting effects of testosterone. 4 It is also in- teresting to note in a woman’s life cycle, the increased incidence of first-trimester and postpartum depression. 5,6 Both are critical periods for the offspring, and a lower level of activity of the mother, keeping out of danger, may have been reproductively advantageous in times past. LETTERS TO THE EDITOR (REPRINTED) ARCH GEN PSYCHIATRY/VOL 58, NOV 2001 WWW.ARCHGENPSYCHIATRY.COM 1083 ©2001 American Medical Association. All rights reserved. Downloaded From: http://jamanetwork.com/pdfaccess.ashx?url=/data/journals/psych/11822/ by a Upstate Medical University User on 01/16/2017

Agoraphobia, 7 a condition related to depression and anxiety, has also been described in the postpartum pe- riod, as have sex differences in social anxiety disorder. 8 Depression and anxiety often coexist 9 clinically and ge- netically. It may well be that the dimensions of restraint and concern shared by both depression and anxiety 10 were evolutionarily advantageous to women in terms of child- bearing and child rearing. Depression and the Menstrual Cycle. On a smaller time scale, the menstrual cycle has a phase leading to ovula- tion and a dysphoric phase following that. The initial eu- thymic phase leading to ovulation is conducive to mating and makes evolutionary sense. Following potential im- pregnation, a lower-energy dysthymic phase would make the women stay out of danger and provide more safety for thepotentialproductofconception.Progesterone,thehor- mone that promotes pregnancy, as its name suggests, has been implicated in inducing dysthymia and overt depres- sion in susceptible individuals. 11 It seems to be the driv- ing force of premenstrual dysphoric disorder, 12 and it has been implicated in postpartum depression. 13 Practical Implications. Natural selection has selected for different traits in men and women in terms of propen- sity to mood disorders, specifically dysthymia and de- pression. The propensity varies during the menstrual cycle and life cycle of a woman, and sex hormones seem to be powerful regulators. Understanding dysthymia and de- pression in women, not as an aberration, but as some- thing that has a biological rationale, will have 2 practi- cal implications. It will remove some of the ignorance andstigmasurrounding “ moodiness ” inwomen,andmore importantly, since the evolutionary reasons that led to this biological difference are not valid anymore in mod- ern times, nature can and should be be gently corrected. Using lifestyle changes, somatic therapies, 14,15 psycho- therapy, and pharmacotherapy more proactively and in a prophylactic 16,17 fashion 13,15,18,19 at selective junctures in a woman ’ s life cycle may significantly improve their quality of life and minimize discomfort and morbidity. Alexander B. Niculescu, MD, PhD La Jolla, Calif Hagop S. Akiskal, MD Department of Psychiatry University of California San Diego School of Medicine La Jolla, CA 92093-0603 1. Nesse RM. Is depression an adaptation? Arch Gen Psychiatry. 2000;57:14-20. 2. Cyranowski JM, Frank E, Young E, Shear MK. Adolescent onset of the gender difference in rates of major depression. Arch Gen Psychiatry . 2000;57:21-28. 3. Placidi GF, Signoretta S, Liguori A, Gervasi R, Maremanni I, Akiskal HS. The semi-structured affective temperament interview (TEMPS-I): reliability prop- erties in 1010 14-26-year students. J Affect Disord. 1998;47:1-10. 4. Pope HG Jr, Kouri EM, Hudson JI. Effects of supraphysiologic doses of tes- tosterone on mood and aggression in normal men. Arch Gen Psychiatry . 2000; 57:133-140. 5. ParryBL.Reproductivefactorsaffectingthecourseofaffectiveillnessinwomen. Psychiatr Clin North Am . 1989;12:207-220. 6. Downey JI. Recognizing the range of mood disorders in women. Medscape Womens Health [serial online]. 1996;1:4E. 7. Roth M. The phobic anxiety-depersonalization syndrome. Proc R Soc Med . 1959;52:587-595. 8. Weinstock LS. Gender differences in the presentation and management of social anxiety disorder. J Clin Psychiatry . 1999;60(suppl 9):9-13. 9. Kendler KS, Neale MC, Kessler RC, Heath AC, Eaves LJ. Major depression and generalized anxiety disorder: same genes, (partly) different environ- ments? Arch Gen Psychiatry. 1992;49:716-722. 10. Akiskal HS. Toward a definition of generalized anxiety disorder as an anx- ious temperament type. Acta Psychiatr Scand. 1998;393:66-73. 11. Epperson CN, Wisner KL, Yamamoto B. Gonadal steroids in the treatment of mood disorders. Psychosom Med. 1999;61:676-697. 12. Gold JH, Endicott J, Parry BI, Severino SK, Stotland N, Frank E. Late luteal phase dysphoric disorder. In: Widiger TA, ed. DSM-IV Sourcebook . Vol 2. Washington, DC: American Psychiatric Association; 1996:317-394. 13. Abou-Saleh MT, Ghubash R, Karim L, Krymski M, Bhai I. Hormonal aspects of postpartum depression. Psychoneuroendocrinology. 1998;23:465-475. 14. ParryBL,UdellC,ElliotJA,etal.Bluntedphase-shiftresponsetomorningbright light in premenstrual dysphoric disorder. J Biol Rhythms . 1997;12:443-456. 15. Parry BL, Mostofi N, LeVeau B, et al. Sleep EEG studies during early and late partial sleep deprivation in premenstrual dysphoric disorder and nor- mal control subjects. Psychiatry Res. 1999;85:127-143. 16. Niculescu AB. Prophylactic antidepressant treatment before patients are ad- mitted. Lancet. 2000;355:406-407. 17. Wisner KL, Wheeler SB. Prevention of recurrent postpartum major depres- sion. Hosp Com Psychiatry. 1994;45:1191-1196. 18. Steiner M, Steinberg S, Stewart D, et al. Fluoxetine in the treatment of pre- menstrual dysphoria. N Engl J Med. 1995;332:1529-1534. 19. Griffin LD, Mellon SM. Selective serotonin reuptake inhibitors directly af- ter activity of neurosteroidogenic enzymes. Proc Natl Acad Sci U S A . 1999; 96:13512-13517. Clinical Depression Is a Disease State, Not an Adaptation I n his recent A RCHIVES article, Nesse 1 discusses de- pression as a possible evolutionary adaptation. Dr Nesse presents some interesting arguments that in certain stressful situations, the symptoms of depression can help increase the likelihood of an individual ’ s sur- vival. One cardinal symptom of depression that Dr Nesse fails to discuss, however, is suicidal behavior. In Darwinian analyses, natural selection will tend to favor behavioral traits that will maximize an individu- al ’ s reproductive capacity. 2 It is hard to imagine a behav- ior that is less likely to maximize an individual ’ s contri- bution to his or her gene pool than suicide. There is no way that suicidal thoughts or behaviors can lead to a per- son ’ s surviving any situation. Even if suicidal behavior in an individual somehow conveyed an advantage to the species as a whole, genetically determined suicidal be- havior would rapidly be selected against as individuals who displayed it killed themselves before being able to increase the frequency of these “ suicidal ” genes in the population by reproducing. Suicide (and hence severe depression) can thus only be seen as a disease state that conveys no benefits to an individual. Fleeting suicidal thoughts (as opposed to ac- tual suicide) are common even in mildly depressed in- dividuals. Thus, the clinical depression that psychia- trists most often see and treat must be seen as primarily a disease state and not adaptation. The depression that Dr Nesse describes is part of an individual ’ s normal be- havioral repertoire. Robert Feder, MD Behavioral Health Network 1 Pillsbury St, Suite 300 Concord, NH 03301 1. Nesse RM. Is depression an adaptation? Arch Gen Psychiatry . 2000;57:14-20. 2. Dawkins R. The Selfish Gene . New York, NY: Oxford University Press; 1990. (REPRINTED) ARCH GEN PSYCHIATRY/VOL 58, NOV 2001 WWW.ARCHGENPSYCHIATRY.COM 1084 ©2001 American Medical Association. All rights reserved. Downloaded From: http://jamanetwork.com/pdfaccess.ashx?url=/data/journals/psych/11822/ by a Upstate Medical University User on 01/16/2017

Your preview ends here

Eager to read complete document? Join bartleby learn and gain access to the full version