Gender Differences in Depression
←
→
Page content transcription
If your browser does not render page correctly, please read the page content below
Coll. Antropol. 26 (2002) 1: 149–157 UDC 616.895.4-055.1/.2 Original scientific paper Gender Differences in Depression M. [agud, Lj. Hotujac, A. Mihaljevi}-Pele{ and M. Jakovljevi} Department of Psychiatry, University Hospital Center »Zagreb«, Zagreb, Croatia ABSTRACT Depression is twice as common in women as in men, although some concern has been raised in terms of misdiagnosing depression in men. The incidence of depression in wo- men varies during the life span. The peak incidence during childbearing years appears to be associated with cyclic hormonal changes. Women also present with reproductive -specific mood disorders: pre-menstrual dysphoric disorder (PMDD), depression in preg- nancy, postpartal mood disorder (PDD) and perimenopausal depressive disorder. Gen- der differences were repeatedly observed in response to antidepressant medication. Premenopausal women appear to respond poorly and to show low tolerability to TCAs, but they tend to show greater responsiveness to the SSRIs. In contrast, men and post- menopausal women can respond equally to the TCAs and SSRIs. These differences are contributed to gender differences in pharmacokinetics of antidepressants and to the influence of menstrual cycle. These findings suggest the need for a gender-specific approach to the evaluation and management of depression. Introduction The interest in gender differences in the differences in response to various depression is relatively new. This is largely treatments. In 1993 FDA encouraged the the result of the exclusion of women from inclusion of both women and men in clini- clinical trials in the past and the lack of cal trials and the analysis of drug data data analysis by gender in the studies separately for men and women (Federal that did include women1. Registry, July 1993). Thus, information Exclusion of women from clinical tri- regarding sex differences in psychophar- als was due to thalidomide tragedy. How- macology will increase in the coming years. ever, the assumption of similarity be- Here we present what is known about tween men and women was wrong. The sex differences in epidemiology, hormonal findings of the past studies suggested dif- influences, differences in pharmacokine- ferences not only in prevalence and clini- tics of antidepressants and in treatment cal presentation of depression but also response. The aim of our paper was to es- Received for publication April 7, 2002 149
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 tablish gender-specific approach to the symptom presentation in women may dif- evaluation and treatment of depression. fer from that in men. In general, the symptoms are similar in men and women, but women are more Gender Differences in likely to present with atypical symptoms, Epidemiology of Depression such as increased appetite and weight gain and tend to report more anxiety and Women have a significantly higher somatic symptoms. Men typically exhibit risk for developing depressive disorders classic symptoms of depression, such as than men. At first, several epidemiologi- insomnia and weight loss13,14. cal studies showed approximately a 2:1 However, there is yet unresolved puz- ratio of women to men for major depres- zle regarding the relationship between sive disorder2,3. This ratio has been found depression and suicide. Depression is the consistently across ethnic groups and in main precursor of suicide, and depression cross-national studies. is twice as common in women. However, Rates of dystimia are also twice as suicide is three times more common in common in women4. Moreover, nearly 80% men15–18. Men also tend to use more vio- of individuals with seasonal affective dis- lent methods of suicide, such as guns and order are women5. Bipolar affective disor- hanging, which along with less help-seek- der is an exception. Men and women have ing behavior may explain their higher an equal lifetime risk for bipolar affective suicide completion rate15. The depression disorder of approximately 1%2. in males may manifest itself in ways un- The second important issue is that recognized by current diagnostic system. this difference in prevalence of depres- The male pattern is characterized by irri- sion varies during the life-span. Boys and tability, aggressiveness, an acting-out be- girls have the same incidence of depres- havior, a lowered stress tolerance, and al- sion6, and in elderly the rate is also simi- cohol abuse. In general, it is yet to be lar between the men and women. The diffe- determined whether an overrepresenta- rence begins in adolescence6 and persists tion of depression in women is simply an until midlife2,7, corresponding roughly to artifact because alcoholism and antiso- the childbearing years in women. Major cial behavior mask depression in men18. depression is an essential disorder of In terms of comorbidity, women ap- childbearing age. The peak incidence is pear to have higher rates of comorbid dis- between the age 20 and 40. orders, the most common being anxiety Although reasons for these differences and eating disorders3,18. In contrast, de- are not fully understood, hormonal and pressed men have higher rates of comor- psychosocial influences have direct or in- bid alcohol and substance abuse and de- direct effect on mood. The new identities pendence14. formation in adolescence8, an unhappy Course of illness has also been evalu- marriage9, the presence of young children ated. Some studies have found a younger at home10, increased likelihood of experi- age of onset of depression in women14. encing victimization or abuse11, and more Women also tend to have a longer dura- frequent help-seeking behavior12 were all tion of episodes19, as well as a greater risk found to make women more vulnerable to for chronicity and recurrence20. While men depression compared to men. and women have similar incidence of bi- Not only women are at greater risk for polar disorder2, they differ in its course. depression, but also once depressed, the Namely, women are more likely to de- 150
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 velop the rapid cycling form of the illness jor depression35 appear to be at highest and may also suffer from more episodes of risk for postpartum mood disturbance. depression21. There are some groups of women for whom there is an increased risk for de- pression in perimenopause2,36. Middle-aged The Influence of Reproductive women presenting with affective liability Cycle to Depression in Women should be evaluated for perimenopause When evaluating a female patient, it -related depression. Perimenopause-rela- is always important to consider the influ- ted depression is a hormonally mediated, ence of the menstrual cycle to her de- phase-specific mood disorder, likely to re- pression22. Periods of increased vulnera- spond to estrogen replacement alone37. It bility in women are premenstrual period, should be differentiated from the major pregnancy, postpartal period, and peri- depression in perimenopause, that re- menopausal years23. All those periods can quires treatment with antidepressants. trigger a new depressive episode in wo- Women in menopause, on the other hand, men with a history of depression, or gen- were not found to be in an increased risk erate a period of vulnerability for devel- of depression. Characteristics of repro- oping a first episode of depression22. Worse- ductive-associated mood disorders are ning of depression in the premenstrual presented in Table 1. phase of the cycle is a rule rather than an The marked sex differences in rates of exception. Even 80% of depressed women depression that begin with reproductive reported worsening of their depression age suggest hormonal factors to play a prior to menses. On the other hand, 2–8% role in this difference. The onset of pu- of women does have the criteria for pre- berty, rather than chronological age, is menstrual dysphoric disorder (PMDD)24. linked to the increase in rates of depres- Pregnancy is usually considered to be sion in women41. In puberty, female brain the time of emotional well being. How- is exposed to estrogen, and hormone lev- ever, the risk of depression in pregnancy els in women fluctuate cyclically over a is estimated to be around 10%25,26. Not much larger range than in men42. At fe- only women are not protected from de- male menopause, ovarian secretion shuts pression during pregnancy, but also the down. In men of the same age, however, infant is not protected from maternal de- testes continue to produce testosterone, pression. Depression in pregnancy car- which is partially converted to estradiol ries the risk of preterm delivery27. Fur- in the brain42. Men, on the other hand, thermore, infants of depressed mothers seem to be spared from rapid hormone have, in terms of behavioral28,29 and EEG fluctuations. finding30,31, have brains, as they are de- Increased incidence of depression in pressed themselves. It is unknown whe- women in reproductive age is not caused ther those striking findings will extend to by specific hormone abnormalities, and childhood. measuring serum FSH and estrogen lev- The incidence of postpartum depres- els has very limited diagnostic value 20,43. sion between 5% and 10% is the same as However, an abnormal response to nor- in non-puerperal, age-matched women32. mal cyclic hormone fluctuations, at the This period is characterized by rapid synapse level and at the receptor le- shifts in hormone concentration. Particu- vel38,44,45 is supposed to be involved in the larly women with bipolar disorder who etiology of depression in vulnerable wo- discontinue lithium treatment33 or have a men, through the neuromodulatory role history of postpartal depression34 or ma- of estrogen on the serotonergic system38, 151
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 TABLE 1 REPRODUCTIVE-ASSOCIATED MOOD DISORDERS38–40 Disorder Endocrine environment Special issues PMDD • Cyclic changes in gonadal • Serotonergic antidepressants hormone concentrations work better than noradrenergic • Also occurs in anovulatory • Response to SSRIs is very fast, cycles and in the absence of within the hours lutheal phase Depression in • Very gradual rise in estrogen • Risk of preterm delivery pregnancy levels • Infants may have depressed patterns Postpartum depressive • Sudden and dramatic decline • Thyroid status should be disorder (PDD) in estrogen concentrations checked, while thyroid • Supersensitive dopamine disfunction is an associated receptors after sharp factor reduction of antidopaminergic • In women with a previous effect of estrogen episode of PDD antidepres- sants within the first 24 hours may prevent recurrence Perimenopause-related • Variable decline in estrogen • Estrogen replacement therapy depression concentrations, estrogen is the first line of treatment unopposed by progesterone due to anovulatoy cycles which is supposed to play a key role in the personal or family psychiatric history. etiology of depression. Animal studies de- The authors presumed early serotoniner- monstrated that ovariectomy causes de- gic events in serotonin synthesis in the creases in 5-HT1 binding, 5-HT2A bind- brain organization, or effects of circulat- ing and expression and 5-HT transporter ing gonadal hormones. This is one of the binding and expression44, the points in largest differences observed to date be- serotonin transmission that are all re- tween the brains of the healthy men and ported to be altered in depression46. In women, which is not related to hormone- humans, women were found to have de- -binding sites49. Regarding peripheral se- creased 5-HT2 receptor binding capacity rotonergic markers, healthy women were when compared to men47. The augmenta- consistently found to have lower platelet tion of serotonergic activity in postmeno- serotonin levels than healthy men50–52. pausal women with estrogen replacement Depressed drug-free women were also therapy48 supports the evidence of the re- found to have decreased platelet seroto- lation between estrogen and serotonergic nin concentration when compared to de- system in humans. Gender-related differ- pressed men50. These data suggest that ences were also found in the rate of sero- women in their childbearing years, either tonin synthesis, which has been found to healthy or depressed, may have decreased be as much as 52% greater in males than serotonergic function, associated with in females49. The reason for this remark- physiological fluctuations in gonadal hor- able difference is not clear. All subjects mone concentrations. Tryptophan, a sero- were in age from 18 to 35 years, without tonin precursor, is converted to serotonin 152
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 in the brain, or, alternatively, to kynu- likely than men to be prescribed antide- renine in liver. Estrogen enhances the pressants. When compared to men, kynurenine pathway in the liver. There- women were found to have slower gastric fore, the availability of tryptophan may emptying time, lower gastric acid secre- be lower, and may eventually decrease se- tion, lower body weight, lower blood vol- rotonin content in the brain 53. Given that ume, higher percentage of body fat, lower stress plays a major role in the onset of plasma protein binding, higher cerebral depression, gender differences in the re- blood flow, lower hepatic biotransforma- sponse to stress could increase women’s tion and lower renal clearance57. vulnerability to depression54. Interesting The possible application of these find- finding is that decreased cortisol suppres- ings is that women tend to have higher sion to dexamethasone was found during plasma levels of antidepressants and high- luteal phase when compared to the folli- er incidence of adverse events thereafter. cular phase in the same healthy women55. However, the menstrual cycle may affect This change is believed to be related to ei- pharmacokinetics in a different manner. ther increased estradiol or progesterone, Specifically, the late luteal or premen- or their interaction, during the luteal strual phase has been associated with phase. The worsening of depression in possible sodium retention and increased premenstrual phase could be attributed total body water, possible increase in he- to increased resistance to glucocorticoids patic metabolism and possible increase in induced by these hormonal changes. Sim- creatinin clearance57. The consequence of ilarly, oral contraceptives, particularly these changes is the decrease in antide- with a high progestin content, may in- pressant blood concentrations. These find- duce depression53. ings seem not to be applied to fluoxetine, In contrast to changing hormonal mi- due to its long half-life1. lieu during reproductive age, postmeno- pausal women have low estrogen and pro- gesterone levels. The decline in rate of Gender Differences in Treatment depression in this age group2 suggests Response that estrogen deficiency is not a risk fac- Gender differences were also observed tor for depression. This finding reinforces in terms of treatment response to antide- the hypothesis that it is the change in es- pressant drugs. Imipramine was the first trogen that may be the critical hormonal antidepressant widely used and has long risk factor in reproductive-endocrine-as- been the gold standard against which sociated depression38. newer agents have been compared. It may not be equally effective in men and women, however. That women may be Gender Differences in less responsive than men to imipramine Pharmacokinetics of was notified as long as several decades Antidepressants ago. The first study to demonstrate this The differences in pharmacokinetics difference was the Raskin study58, when have been demonstrated in all of the ar- women and men were stratified by gen- eas of absorption, distribution, metabo- der and age (younger than 40 years, and lism and elimination56. However, data 40 years or older). In men, imipramine re- are limited until recently, due to previ- sponse rates for both groups did not differ ously mentioned exclusions of women and were significantly better than pla- from clinical trials. This is unfortunate, cebo. Response rate in women, however, because women are significantly more differed by age group. While women in 153
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 the age of 40 years or older showed a re- that taking sertraline. Premenopausal sponsiveness to imipramine similar to women were more than 3 times as likely that of men, younger women were no to drop out of imipramine treatment than more responsive to imipramine than to postmenopausal women61. placebo58. These findings are consistent When comparing imipramine and pa- with the study carried out 25 years later. roxetine in outpatients62, women respon- In meta-analysis of 35 studies by Ha- ded significantly better to paroxetine than milton, response rates to imipramine we- to imipramine, but women responded bet- re reported separately by gender59. Over- ter to both active treatments compared all response rates to imipramine differed with placebo. It is noteworthy that in by 11% between men and women. Women men, however, because of high placebo re- showed lower response to imipramine sponse rates, there were no significant than men, despite higher plasma concen- differences among the three treatment trations. regimens. Women had lower placebo re- The old age interest group60 in Britain sponse than men in this study. has found that women taking dothiepine In contrast to previous two studies were more likely to experience a recurrence that demonstrated better response to of depression, than men were. Further- SSRIs paroxetine and sertraline than to more, women taking placebo were also sig- imipramine in women, this difference nificantly more likely to suffer recurrence was not found for fluoxetine62. Women re- of depression compared with men taking sponded equally to both fluoxetine and placebo. These findings suggest that wo- imipramine. Unfortunately, there were no men have a worse prognosis in terms of a comparison data given for placebo or for risk of recurrence of depression. men. In this study fluoxetine was better Really interesting and important find- tolerated than imipramine63. A recent ings were found in comparison between study, however, demonstrated that de- imipramine and sertraline61. Men res- pressed women younger than 44 years re- ponded significantly better to imipra- sponded significantly better to fluoxetine mine. Women in general responded to than to noradrenergic agent, maprotili- sertraline better than to imipramine. ne64. The men had similar response across However, when data were analyzed sepa- different age groups. While women are rately due to menopausal status, it was reported to tolerate better imipramine found that premenopausal women re- than sertraline61, the whole SSRI group sponded better to sertraline, whereas re- seems to be tolerated similar in males sponse rates of postmenopausal women and females65. were similar in both drugs! There was also a meta-analysis of 8 The authors suggested that female placebo-controlled studies of citalopram ovarian hormones may enhance response in women and men with depression66. to SSRIs, or inhibit the response to TCAs. Women treated with either citalopram or The reason for this difference may be also placebo showed a significantly greater re- related to sex differences in depressive sponse to treatment than men, although subtypes, i.e. more atypical depression in drug-placebo difference was the same in women1. The difference disappears in both men and women66. Why do premeno- menopause. In this study gender differ- pausal women respond better to SSRIs ence in drug-tolerability was also noted. than to other classes of antidepressants? Women taking imipramine were more We hypothesize that SSRI treatment could likely to drop out from the study than reverse lower serotonergic function50–53, 154
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 associated with cyclic changes in gonadal No specific relationship between lower hormone levels. testosterone levels and depression in men has been established75. Recent data, how- Gender differences were also observed ever, suggest the possibility that testos- in augmentation studies. As long as sev- terone deficiency leads to late life mild eral decades ago, a trend for greater effi- depression76. Unlike in women, it is not cacy in women using T3 augmentation of clear whether aging men experience »an- antidepressant treatment67,68 was noted. dropause«, whether there is the testoster- More specifically, addition of T3 to imi- one »threshold« associated with CNS ef- pramine regimen was found to accelerate fects and/or whether are some men the recovery of the women but not the particularly vulnerable to testosterone- men, beginning as early as the third day -mediated depression76. Anecdotal re- of treatment68. However, clinical impro- ports and uncontrolled data suggest that vement may be attributed rather to the in some men with hypogonadism comor- correction of mild thyroid dysfunction69, bid major depression remits with testos- since women have ten times the incidence terone replacement76. of thyroid disease as men53. On the other In terms of electroconvulsive treat- hand, a trend for greater efficacy of either ment (ECT), the data suggest that wo- T3 or T4 antidepressant augmentation men have a lower seizure threshold77, a was reported, in women with no differ- more favorable response rate and less se- ence in baseline serum T3, free T4 and vere side effects men78. However, data re- TSH levels in responders and non-res- garding efficacy by gender are inconsis- ponders70. tent1. The inability to provide treatment in double-blind fashion is a consistent While the efficacy of lithium augmen- confounding factor in interpreting the im- tation of antidepressant response has portance of those findings1. been documented since the early 1980s, the data were reported by gender in only 2 studies71,72, when lithium was added to Conclusion different classes of antidepressants. In Although research on gender effects in both studies, significantly better response depression has been limited, existing lit- rate was achieved in women. However, erature shows clear evidence of sex-re- the recent literature analysis indicated lated differences 79. In general, younger similar response rates for lithium in bipo- premenopausal women appear to respond lar and related affective disorders73. poorly and show low tolerability to TCAs, Estrogen was suggested to play a per- but tend to show greater responsiveness missive role in imipramine-induced chan- to the SSRIs. In contrast, men and post- ges in serotonergic receptor binding, with menopausal women can respond equally possible clinical significance for patients well or better to the TCAs. with ovarian hormone deficiency. Prelim- Because of pharmacokinetic differen- inary studies suggest that estrogen re- ces and increased sensitivity to side ef- placement therapy (ERT) given in con- fects, women may require a lower dosage ventional doses (high-0.05 and low-0.025 of some medications. mg) to antidepressant treatment may en- Because of a possible risk of recur- hance mood in postmenopausal women48,74. rence of depression among women, a long However, the lack of double-blind studies -term treatment may be required. Meno- limits any conclusion from currently ava- pausal status may be an important con- ilable data. sideration not only in choosing an antide- 155
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 pressant agent, but also in deterring aug- The preliminary nature of these con- mentation strategies. Similarly, the men- clusions suggests need for future research. strual cycle may affect pharmacokinetics Clearly, more data are needed to under- of antidepressant agents of women. In- stand the feature. creasing the dosage of SSRIs premen- strual can result in a very rapid response. REFERENCES 1. KORNSTEIN, S. G., B. A. WOJCIK, Psychiat- STEIN, S. PERRY, D. BENDELL, S. SHANBERG, E. ric Clinics North America: Annual of Drug Therapy, 7 A. ZIMMERMAN, C. KUHN, Child Develop, 59 (1998) (2000) 23. — 2. KESSLER, R. C., K. A. McGONA- 1561. — 30. JONES, N. A., T. FIELD, N. A. FOX, B. GLE, M. SWARTZ, D. G. BLAZER, C. B. NELSON, J. LUNDY, M. DAVALOS, Development & Psychopath., Affect. Disord., 29 (1993) 77. — 3. REGIER, D. A., J. 9 (1997) 491. — 31. DAWSON, G., K. FREY, H. PA- D. BURKE, K. C. BURKE, In: MASER J. D., C. R. NAGIOTIDES, H., J. J. OSTERLINE, J. Child Psy- CLONIGER (Eds.): Comorbidity of mood and anxiety chol. & Psychiatry & Allied. Discipl., 38 (1997) 179. — disorders. (American Psychiatric Press, Washington 32. O’HARA, M. W., J. A. SCHLECHTE, D. A. LE- DC, 1990) — 4. MARKOWITZ, J. C., M. E. MORAN, WIS, M. V. VARNER, J. Abnorm Psychol., 100 (1991) J. H. KOLSIS, A. J. FRANCES, J. Affect. Disord., 42 63. — 33. VIGUERA, A. C., R. NONACS, L. S. CO- (1992) 63. — 5. LEIBENLUFT, E, T. A. HARDIN, N. HEN, L. TONDO, A. MURRAY, R. BALDESSARINI, E. ROSENTHAL, Depression, 3 (1995) 13. — 6. Am. J. Psychiat., 157 (2000) 179. — 34. COOPER, P. NOLEN-HOEKESEMA, S., J. S. GIRGUS, Psychol. J., Y. L. MURRAY, Br. J. Psychiatry 166 (1995) 191. Bull., 115 (1994) 424. — 7. BUCHANAN, C. M., J. B. — 35. KUMAR, R., K. M. ROBSON, Br. J. Psychiatry, BECKER, S. ECCLE, Psychol. Bull., 111 (1992) 62. — 144 (1984) 35. — 36. AVIS, N. E., D. BAMBILLA, S. 8. CICHETTI, D., S. L. TOTH, Am. Psychol., 53 (1998) M. McKINLAY, K. A. VASS, Ann. Epidemiol., 4 (1994) 221. — 9. WISNER, K. L., J. M. PEREL, S. M. 214. — 37. SCHMIDT, P. J., P. R. GINDOFF, D. A. WHEELER, Am. J. Psychiat., 150 (1993) 1541. — 10. BARON, D. R. RUBINOW, Am. J. Obstet. Gynecol., ROSS, C. E., J. MIROWSKY, Health Soc Behav., 29 183 (2000) 414. — 38. JOFFE, H., L. S. COHEN, Biol. (1988) 127. — 11. CARMEN, E. H., P. P. RIEKER, T. Psychiatry, 44 (1998) 798. — 39. PRITCHARD, D. B., MILIS, Am. J. Psychiat., 141 (1984) 378. — 12. ALM- B. HARRIS, Br. J. Psychiatry, 169 (1996) 555. — 40. QVIST, F., Acta Psychiatr. Scand., 73 (1986) 295. — WIECK, A., R. KUMAR, A. D. HIRST, M. N. MARKS, 13. FRANK, E., L. L. CARPENTER, D. J. KUPFER, I. C. CAMPBELL, S. A. CHECKLEY, Br. Med. J., 303 Am. J. Psychiat., 145 (1988) 41. — 14. KORNSTEIN, (1991) 613. — 41. ANGOLD, A., E. F. COSTELLO, C. S. G., A. F. SCHATZBER, K. A. YONKERS, Psycho- M. WORTHMAN, Psychol. Med., 28 (1998) 51. — 42. pharmacol. Bull., 31 (1995) 711. — 15. ISOMETSA, SEEMAN, M. V., Am. J. Psychiat., 154 (1997) 1641. E. T., M. M. HENRIKSSON, H. M. ARO, M. E. HEI- — 43. BRAMBILLA, F., M. MAGGIONI, E. FERRA- KKINEN, K. I. KUOPPASALMI, T. LONNQUIS, Am. RI, S. SCARONE, M. CATALONO, Psychiatry Res., J. Psychiat., 151 (1994) 530. — 16. BROCKINGTON, 32 (1990) 229. — 44. SCHMIDT, P. J., L. K. NEIMAN, I., Int. Clin. Psychopharmacol., 16 Suppl. 2 (2001) 7. M. A. DANAEAU, L. F. ADAMS, D. R. RUBINOW, N. — 17. HOTUJAC, LJ., M. VELDI], J. GRUBI[IN, Engl. J. Med., 338 (1998) 209. — 45. RUBINOW, D. Soc. Psihijatr., 28 (2000) 32. — 18. WALINDER, J., W. R., P. J. SCHMIDT, C. A. ROCA, Biol. Psychiatry 44 RUTZ, Int. J. Clin. Psychopharmacology, 16 Suppl. (1998) 839. — 46. LUCKI, I., Biol. Psychiatry, 44 (2001) 21. — 19. SARGEANT, J. K., M. L. BRUCE, L. (1998) 151. — 47. BIVER, F., F. LOTSTRA, M. MON- P. FLORIO, M. M. WEISSMAN, Arch. Gen. Psychia- CLUS, D. WIKLER, P. DAMHAUT, J. MENDLE- try, 47 (1990) 519. — 20. WINOKUR, G., W. CORY- WITZ, S. GOLDMAN, Neurosci. Lett., 204 (1996) 25. ELL, M. KELLER, J. ENDICOTT, H. A. AKISKAI, — 48. HALBREICH, U., N. ROJANSKY, Y. BAKHAI, Arch. Gen. Psychiatry, 50 (1993) 457. — 21. LEIBEN- H. TWOREK, P. HISSIN, K. WANE, Biol. Psychiatry, LUFT E., J. Clin. Psychiatry, 58 Suppl. 15 (1997) 5. — 37 (1995) 434. — 49. NISHIZAWA, S., C. BENKE- 22. ENDICOTT, J., J. Affect. Disord., 29 (1993) 193. FALT, S. N. YOUNG, M. LEYTON, S. MZENGEZA, — 23. KORNSTEIN, S. G., J. Clin. Psychiatry, 58 C. DE MONTIGNY, P. BLIER, Proc. Natl. Acad. Sci., Suppl. 15 (1997) 12. — 24. YONKERS, K. A., J. Clin. USA 94 (1997) 5308. — 50. MÜCK-[ELER, D., M. Psychiatry, 58 Suppl. 14 (1997) 4. — 25. O’HARA, M. JAKOVLJEVI], N. PIVAC, J. Affect. Disord., 39 W., Arch. Gen. Psychiatry, 43 (1986) 569. — 26. ORR, (1996) 73. — 51. MÜCK-[ELER, D., N. PIVAC, M. S. T., C. A. MILLER, Epidemiol. Rev., 17 (1995) 165. JAKOVLJEVI], J. Neural Transm., 106 (1999) 337. — 27. ABRAMS, S. M., T. FIELD, I. SCAFID, M. — 52. PIVAC, N., D. MÜCK – [ELER, I. BARI[I], PRODROMIDIS, M., Infant Mental Health J., 16 M. JAKOVLJEVI], Z. PURETI], Life Sci., 68 (2001) (1995) 233. — 28. HART, S., N. A. JONES, T. FIELD, 2423. — 53. PARRY, B. L., P. HAYNES, J. Gend. Spe- B. LUNDY, Child Psychiatry & Human Develop, 30 cif. Med., 3 (2000) 53. — 54. YOUNG, E., J. Gend. (1999) 11. — 29. FIELD, T., B. HEALY, S. GOLD- Specif. Med., 1 (1998) 21. — 55. ALTEMUS, M., L. 156
M. [agud et al.: Gender Differences in Depression, Coll. Antropol. 26 (2002) 1: 149–157 REDWINE, L. YUNG – MEI, T. YOSHIKAWA, R. (2001) 258. — 66. MACKLE, M., M. GUITERREZ, In: JEHUDA, S. PETERA-WADLEIGH, D. L. MURPHY, Proceedings (152th Annual Meeting of the American Neuropsychopharmacology, 17 (1997) 100. — 56. Psychiatric Association, Washington, DC, 1999). — YONKERS, K. A., J. C. KANDO, J. O. COLE, S. BLU- 67. PRANGE, A. F., I. C. WILSON, A. M. RABON, M. MENTHAL, Am. J. Psychiat., 149 (1992) 587. — 57. A. LIPTON, Am. J. Psychiat., 126 (1969) 457. — 68. HAMILTON, J. A., K. A. YONKERS, A., In: JENS- WHYBROW, P., R. NOGUERA, R. MAGGS, A. J. Jr. VOLD, M. F., U. HALBREICH, J. A. HAMILTON PRANGE, Arch. Gen. Psychiatry, 26 (1972) 234. — (Eds.): Psychopharmacology and women: sex, gender, 69. GERWIRTZ, G. R., D. MALASPINA, J. A. HAT- and hormones. (American Psychiatric Press, Wash- TERER, S. FEVREDEN, D. KLEIN, J. M. GORMAN, ington DC, 1996). — 58. RASKIN, A., J. Nerv. Ment. Am. J. Psychiat., 145 (1988) 1012. — 70. FRYE, M. A., Dis., 159 (1974) 120. — 59. HAMILTON, J. A., M. K. D. DENICOFF, D. A. LUCKENBAUGH, In: Pro- GRANT, M. F. JENSVOLD, In: JENSVOLD, M. F., U. ceedings (150th Annual Meeting of the American Psy- HALBREICH, J. A. HAMILTON (Eds.): Psychophar- chiatric Association, San Diego, CA, 1997). — 71. macology and women: sex, gender, and hormones. DALLAL, A., R. FONTAINE, A. ONTIVEROS, R. (American Psychiatric Press, Washington DC, 1996). ELIE, Can. J. Psychiat.-Rev. Can. Psychiat., 35 — 60. OLD AGE DEPRESSION INTEREST GROUP, (1990) 608. — 72. FLINT, A. J., S. L. RIFAT, J. Clin. Br. J. Psychiatry, 162 (1993) 175. — 61. KORN- Psychopharmacology, 14 (1994) 353. — 73. VIGU- STEIN, S. G., A. F. SCHATZBERG, M. E. THASE, K. ERA, A. C., L. TONDO, R. J. BALDESSARINI, Am. A. YONKERS, J. P. McCULLOUGH, G. I. KEITNER, J. Psychiat., 157 (2000) 1509. — 74. SCHNEIDER, L. A. J. GELENBERG, S. M. DAVIS, W. M. HARRISON, S., G. W. SMALL, S. HAMILTON, A. BYSTRITSKY, M. B. KELLER, Am. J. Psychiat., 157 (9) (2000) 1445. C. B. NEMEROFF, B. S. MEYERS, Am. J. Geriatr. — 62. STEINER, M., D. E. WHEADON, M. S. KREI- Psychiatr., 5 (1997) 97. — 75. SEIDMAN, S. N., B. T. DER, In: Proceedings (146th Annual Meeting of the WALSH, Am. J. Geriatr. Psychiatr., 7 (1999) 18. — American Psychiatric Association, San Francisco, CA, 76. SEIDMAN, S. N., J. Gend. Specif. Med., 4 (2001) 1993). — 63. LEVIS-HALL, F. C., M. G. WILSON, R. 44. — 77. COLENDA, C. C., W. V. McCALL, Convul- G. TEPNER, S. C. KOKE, J. Women’s Health, 6 (1997) sive Therapy, 12 (1996) 3. — 78. COFFEY, C. E., J. 337. — 64. MARTENYI, F., M. DOSSENBACH, K. LUCKE, R. D. WEINER, A. D. KRYSTAL, M. AQUE, MRAZ, S. METCALFE, S., Eur. Neuropsychophar- Biol. Psychiatry, 141 (1995) 713. — 79. GODFROID, macol., 11 (2001) 227. — 65. DALFEN, A. K., D. E. I. O., Can. J. Psychiat. – Rev. Can. Psychiat., 44 (1999) STEWART, Can. J. Psychiat.-Rev. Can. Psychiat., 46 362. M. [agud Department of Psychiatry, University Hospital Center »Zagreb«, Ki{pati}eva 12, 10000 Zagreb, Croatia RAZLI^ITOST DEPRESIJE U @ENA I MU[KARACA SA@ETAK Depresija se javlja dvostruko ~e{}e u `ena, premda postoji podatak da se ona ~esto kod mu{karaca previdi i rje|e dijagnosticira. Incidencija depresije u `ena razlikuje se obzirom na dob. S najve}om u~estalo{}u javlja se tijekom fertilne dobi, {to se tuma~i cikli~kim djelovanjem hormona. Razlikujemo ~etiri poreme}aja specifi~na za repro- duktivno razdoblje: premenstrualni disfori~ni poreme}aj, depresija u trudno}i, post- partalna depresija, te depresivni poreme}aj u perimenopauzi. Razlike obzirom na spol opa`ene su tako|er u odgovoru na antidepresivnu terapiju. Dok je u `ena u fertilnoj dobi imipramin slabije u~inkovit i podno{ljiv, za razliku od selektivnih inhibitora po- novne pohrane serotonina (SSRI), u `ena u menopauzi i mu{karaca ta se razlika ne nalazi. Razlika se nastoji protuma~iti razlikama u farmakokinetici antidepresiva te utjecaju hormona. Sukladno spomenutim navodima, smatramo da je prilikom dijagno- sticiranja i lije~enja depresije va`no uzeti u obzir i spol bolesnika. 157
You can also read