Allostatic load in bipolar disorder: Implications for pathophysiology and treatment

被引:364
作者
Kapczinski, Flavio [1 ,2 ]
Vieta, Eduard [3 ,4 ]
Andreazza, Ana Cristina [6 ]
Frey, Benicio N. [5 ]
Gomes, Fabiano A. [1 ,2 ]
Traniontina, Juliana [1 ,2 ]
Kauer-Sant'Anna, Marcia [6 ]
Grassi-Oliveira, Rodrigo [7 ]
Post, Robert M. [8 ]
机构
[1] Hosp Clin Porto Alegre, Lab Psiquiatria Mol, Ctr Pesquisas, BR-90035000 Porto Alegre, RS, Brazil
[2] Hosp Clin Porto Alegre, Bipolar Disorders Program, Ctr Pesquisas, BR-90035000 Porto Alegre, RS, Brazil
[3] Univ Barcelona, Hosp Clin, Bipolar Disorders Program, E-08036 Barcelona, Spain
[4] Harvard Univ, McLean Hosp, Cambridge, MA 02138 USA
[5] McGill Univ, McConnell Brain Imaging Ctr, Montreal Neurol Inst, Montreal, PQ H3A 2B4, Canada
[6] Univ British Columbia, Dept Psychiat, Mood Disorders Ctr, Vancouver, BC V6T 2A1, Canada
[7] Pontificia Univ Catolica Rio Grande do Sul, Inst Psychol, BR-90610000 Porto Alegre, RS, Brazil
[8] Penn State Coll Med, Chevy Chase, MD 20815 USA
基金
加拿大健康研究院;
关键词
allostatic load; bipolar disorder; clinical morbidity; cognitive impairment; comorbidity; sensitization; kindling; stress;
D O I
10.1016/j.neubiorev.2007.10.005
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Current literature on the effects of chronic stress in general health converges to the concept of allostatic load (AL). AL is the bodily 'wear and tear' that emerges with sustained allostatic states. In the field of bipolar disorder (131)), AL offers an important clue as to why patients who undergo recurrent mood episodes are clinically perceived as less resilient. In addition, AL helps explaining the cumulative disruptive health effects of intermittent episodes and stressors. Stress- and episode-induced changes in brain regions involved in the emotional circuitry may lead to dysfunctional processing of information, which would render BD patients more vulnerable to subsequent environmental stressors, episodes, and drugs of abuse. Mood stabilizing agents exert opposite effects than chronic stress in neurons, increasing neuroprotective factors what may help to quench the cycle of affective episode recurrence and neural and bodily deterioration. Therefore, AL provides an explanatory link to apparently unrelated findings such as cognitive impairment and higher rates of physical comorbidity and mortality that are observed in the course of 1313 and further highlight the importance of effective long-term prophylaxis. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:675 / 692
页数:18
相关论文
共 211 条
[1]   Changes in gray matter volume in patients with bipolar disorder [J].
Adler, CM ;
Levine, AD ;
DelBello, MP ;
Strakowski, SM .
BIOLOGICAL PSYCHIATRY, 2005, 58 (02) :151-157
[2]   An MRI study of temporal lobe structures in men with bipolar disorder or schizophrenia [J].
Altshuler, LL ;
Bartzokis, G ;
Grieder, T ;
Curran, J ;
Jimenez, T ;
Leight, K ;
Wilkins, J ;
Gerner, R ;
Mintz, J .
BIOLOGICAL PSYCHIATRY, 2000, 48 (02) :147-162
[3]  
ANDREAZZA AC, 2007, PSYCHIAT RES 0619
[4]   Serum S100B and antioxidant enzymes in bipolar patients [J].
Andreazza, Ana Cristina ;
Cassini, Carina ;
Rosa, Adriane Ribeiro ;
Leite, Marina Conch ;
de Almeida, Lucia M. V. ;
Nardin, Patricia ;
Cunha, Angelo B. N. ;
Cereser, Keila Maria ;
Santin, Aida ;
Gottfried, Carmem ;
Salvador, Mirian ;
Kapczinski, Flavio ;
Goncalves, Carlos Alberto .
JOURNAL OF PSYCHIATRIC RESEARCH, 2007, 41 (06) :523-529
[5]   Mortality of patients with mood disorders: follow-up over 34-38 years [J].
Angst, F ;
Stassen, HH ;
Clayton, PJ ;
Angst, J .
JOURNAL OF AFFECTIVE DISORDERS, 2002, 68 (2-3) :167-181
[6]  
Arnow BA, 2004, J CLIN PSYCHIAT, V65, P10
[7]   Glutathione transferases catalyse the detoxication of oxidized metabolites (o-quinones) of catecholamines and may serve as an antioxidant system preventing degenerative cellular processes [J].
Baez, S ;
SeguraAguilar, J ;
Widersten, M ;
Johansson, AS ;
Mannervik, B .
BIOCHEMICAL JOURNAL, 1997, 324 :25-28
[8]   Medical progress: Bipolar disorder [J].
Belmaker, RH .
NEW ENGLAND JOURNAL OF MEDICINE, 2004, 351 (05) :476-486
[9]   The expression of proapoptosis genes is increased in bipolar disorder, but not in schizophrenia [J].
Benes, FM ;
Matzilevich, D ;
Burke, RE ;
Walsh, J .
MOLECULAR PSYCHIATRY, 2006, 11 (03) :241-251
[10]  
Berk M, 2007, BIPOLAR DISORD, V9, P21