Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss
Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss
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DOI：
10.15288/jsa.2006.67.861
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发表时间：
2006-11-01
期刊：
影响因子：
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通讯作者：
Laudenslager, Mark L.
中科院分区：
文献类型：
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作者：
Beresford, Thomas P.;Arciniegas, David B.;Laudenslager, Mark L.
目的：皮质醇增多症对重度饮酒者海马体积的影响尚未研究。之前的工作表明，酗酒酒精依赖（AD）受试者的下丘脑-垂体-肾上腺活动增加与总海马体积（THV）降低有关。本研究假设如下：（1）慢性重度饮酒受试者的唾液皮质醇浓度将显著高于轻度饮酒对照受试者，（2）整个样本组的数据将呈现皮质醇浓度与THV之间的反比关系。在精心挑选的年龄、性别和种族相匹配的测试和对照受试者组中，我们测量了清醒、清醒+30分钟、中午、下午4点进行脑部磁共振成像。接下来，我们比较了各组之间的平均皮质醇浓度，并评估了皮质醇浓度和海马体积测量之间的统计学关联。结果如下：AD测试受试者（n = 8）和非AD对照受试者（n = 8）的比较发现，在两个早晨采样时间，（清醒时的平均值[SD]：0.49 [0.23] vs 0.24 [0.14] pg/dl，p = 0.012;清醒+30分钟时：0.57 [0.37] vs 0.28 [0.11] 4g/dl，p = 0.043）。控制颅内体积，在总样本组（N = 16）中，清醒皮质醇浓度与THV（p = 0.007）之间存在显著负相关性。然而，当单独分析时，只有对照组保持了强烈的负相关（p = 0.025）。在大量饮酒的受试者之间没有关联。结论：这些小样本的早期数据支持慢性大量饮酒导致高唾液皮质醇浓度的观点。目前尚不清楚的是，皮质醇过多症是否会产生选择性损伤效应，导致观察到的海马体积损失。在更大的群体中使用更频繁的监测采样进行进一步研究必须解决以下问题：（1）这一发现是否可以重复;（2）如果重复，低海马体积和高皮质醇水平之间缺乏关联是否可能表明损伤程度，超过该程度，两者之间的正常关联可能会丢失。
Objective: The effects of hypercortisolism on hippocampal volume have not been studied in heavy drinkers. Prior work suggested increased hypothalamic-pituitary-adrenal activity in relation to lowered total hippocampus volume (THV) in heavy-drinking alcohol-dependent (AD) subjects. The present study hypothesized the following: (1) that chronic heavy-drinking subjects would demonstrate significantly higher salivary cortisol concentrations than light-drinking control subjects and (2) that data from the whole sample group would present an inverse relationship between cortisol concentration and THV Method: In carefully selected test and control subject groups matched for age, gender, and ethnicity, we measured salivary cortisol samples at waking, waking + 30 minutes, noon, and 4 Pm on the day of magnetic resonance imaging of the brain. We next compared mean cortisol concentrations between groups and assessed the statistical association between cortisol concentration and hippocampus volume measures. Results: Comparison of AD test subjects (n = 8) and non-AD control subjects (n = 8) found significantly higher cortisol concentrations at both morning sampling times (mean [SD] at waking: 0.49 [0.23] vs 0.24 [0.14] pg/dl, p = .012; at waking + 30 minutes: 0.57 [0.37] vs 0.28 [0.11] 4g/dl, p = 0.043). Controlling for intracranial volume, there was a significant inverse correlation between waking cortisol concentration and THV (p = .007) in the total sample group (N = 16). However, when analyzed separately, only the control group maintained a strong, inverse association (p = .025). There was no association among the heavy drinking subjects. Conclusions: These early data in a small sample support the view that chronic heavy drinking results in high salivary cortisol concentrations. What remains unclear is whether hypercortisolism exerts a selectively injurious effect that results in observed hippocampus volume loss. Further research in larger groups using more frequent, monitored sampling must address the following: (1) whether this finding can be replicated and (2) if replicated, whether the lack of an association between low hippocampal volumes and high cortisol levels may indicate an extent of injury beyond which a normal association of the two may be lost.