Steiger H, Gauvin L, Israël M, Koerner N, Ng Ying Kin N M, Paris J, Young S N
Eating Disorders Program, Douglas Hospital, 6875 LaSalle Blvd, Verdun, Quebec H4H 1R3, Canada.
Arch Gen Psychiatry. 2001 Sep;58(9):837-43. doi: 10.1001/archpsyc.58.9.837.
Bulimia nervosa (BN) is reported to co-occur with childhood abuse and alterations in central serotonin (5-hydroxytryptamine [5-HT]) and cortisol mechanisms. However, findings also link childhood abuse to anomalous 5-HT and cortisol function, and this motivated us to explore relationships between childhood abuse and neurobiological variations in BN.
Thirty-five bulimic and 25 nonbulimic women were assessed for childhood physical and sexual abuse, eating symptoms, and comorbid psychopathological tendencies. These women provided blood samples for measurement of platelet hydrogen-3-paroxetine binding and serial prolactin and cortisol responses following oral administration of the partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP).
Bulimic women showed markedly lower mean +/- SD density (B(max)) of paroxetine-binding sites (631.12 +/- 341.58) than did normal eaters (1213.00 +/- 628.74) (t(54) = -4.47; P =.001). Paroxetine binding did not vary with childhood abuse. In contrast, measures of peak change on prolactin levels after m-CPP administration (Delta-peak prolactin) indicated blunted response in abused bulimic women (7.26 +/- 7.06), nonabused bulimic women (5.62 +/- 3.95), and abused women who were normal eaters (5.73 +/- 5.19) compared with nonabused women who were normal eaters (13.57 +/- 9.94) (F(3,51) = 3.04, P =.04). Furthermore, individuals reporting childhood abuse showed decreased plasma cortisol levels relative to nonabused women who were normal eaters.
Findings imply that BN and childhood abuse are both generally associated with reduced 5-HT tone but that childhood abuse may be somewhat more specifically linked to reduced cortisol levels (ie, hypothalamic-pituitary-adrenal axis) activity.
据报道,神经性贪食症(BN)与童年期受虐以及中枢5-羟色胺(5-羟色胺[5-HT])和皮质醇机制的改变同时出现。然而,研究结果也将童年期受虐与异常的5-HT和皮质醇功能联系起来,这促使我们探索童年期受虐与神经性贪食症神经生物学变异之间的关系。
对35名贪食症女性和25名非贪食症女性进行童年期身体虐待和性虐待、饮食症状以及共病心理病理倾向的评估。这些女性提供血样,用于测量血小板对氢-3-帕罗西汀的结合以及口服5-HT部分激动剂间氯苯哌嗪(m-CPP)后催乳素和皮质醇的系列反应。
贪食症女性的帕罗西汀结合位点平均密度(Bmax)(631.12±341.58)明显低于正常饮食者(1213.00±628.74)(t(54)=-4.47;P=0.001)。帕罗西汀结合情况与童年期受虐无关。相比之下,服用m-CPP后催乳素水平的峰值变化测量值(Δ峰值催乳素)表明,受虐的贪食症女性(7.26±7.06)、未受虐的贪食症女性(5.62±3.95)以及受虐的正常饮食女性(5.73±5.19)的反应迟钝,而未受虐的正常饮食女性的反应为(13.57±9.94)(F(3,51)=3.04,P=0.04)。此外,报告童年期受虐的个体相对于未受虐的正常饮食女性,血浆皮质醇水平降低。
研究结果表明,神经性贪食症和童年期受虐通常都与5-HT张力降低有关,但童年期受虐可能更具体地与皮质醇水平降低(即下丘脑-垂体-肾上腺轴)活动有关。