Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss

Thomas P. Beresford, David B. Arciniegas, Julie Alfers, Lori Clapp, Brandon Martin, Henry F. Beresford, Yiping Du, Dengfeng Liu, Dinggang Shen, Christos Davatzikos, Mark L. Laudenslager

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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] μg/dl, p = .012; at waking + 30 minutes: 0.57 [0.37] vs 0.28 [0.11] μg/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.

Original languageEnglish
Pages (from-to)861-867
Number of pages7
JournalJournal of Studies on Alcohol
Volume67
Issue number6
Publication statusPublished - 2006 Nov 1
Externally publishedYes

Fingerprint

Cushing Syndrome
Alcoholism
Hydrocortisone
alcohol
Alcohols
Hippocampus
Drinking
Group
test subject
Sampling
Control Groups
brain
ethnicity
Magnetic resonance
Alcohol Drinking
lack
Brain
gender
Magnetic Resonance Imaging
Imaging techniques

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Psychology(all)

Cite this

Beresford, T. P., Arciniegas, D. B., Alfers, J., Clapp, L., Martin, B., Beresford, H. F., ... Laudenslager, M. L. (2006). Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss. Journal of Studies on Alcohol, 67(6), 861-867.

Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss. / Beresford, Thomas P.; Arciniegas, David B.; Alfers, Julie; Clapp, Lori; Martin, Brandon; Beresford, Henry F.; Du, Yiping; Liu, Dengfeng; Shen, Dinggang; Davatzikos, Christos; Laudenslager, Mark L.

In: Journal of Studies on Alcohol, Vol. 67, No. 6, 01.11.2006, p. 861-867.

Research output: Contribution to journalArticle

Beresford, TP, Arciniegas, DB, Alfers, J, Clapp, L, Martin, B, Beresford, HF, Du, Y, Liu, D, Shen, D, Davatzikos, C & Laudenslager, ML 2006, 'Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss', Journal of Studies on Alcohol, vol. 67, no. 6, pp. 861-867.
Beresford TP, Arciniegas DB, Alfers J, Clapp L, Martin B, Beresford HF et al. Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss. Journal of Studies on Alcohol. 2006 Nov 1;67(6):861-867.
Beresford, Thomas P. ; Arciniegas, David B. ; Alfers, Julie ; Clapp, Lori ; Martin, Brandon ; Beresford, Henry F. ; Du, Yiping ; Liu, Dengfeng ; Shen, Dinggang ; Davatzikos, Christos ; Laudenslager, Mark L. / Hypercortisolism in alcohol dependence and its relation to hippocampal volume loss. In: Journal of Studies on Alcohol. 2006 ; Vol. 67, No. 6. pp. 861-867.
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AU - Martin, Brandon

AU - Beresford, Henry F.

AU - Du, Yiping

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N2 - 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] μg/dl, p = .012; at waking + 30 minutes: 0.57 [0.37] vs 0.28 [0.11] μg/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.

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