Cerebral atrophy and plasma cortisol levels in alcoholics after short or a long period of abstinence

Hypothalamic Function in Response to 2‐Deoxy‐d‐Glucose in Long‐Term Abstinent Alcoholics

“…The HPA functional abnormalities noted by George et al (1994) in alcoholics abstinent 3 weeks are therefore most likely related to the effects of recent alcohol consumption and withdrawal. These findings parallel the findings of other research that shows that HPA axis function normalizes with extended abstinence (Adinoff et al, 1990;Ehrenreich et al, 1997;Marchesi et al, 1994). Future investigations into the metabolic function of alcoholics, particularly investigations involving the HPA system, should consider the possibility that normalization is still occurring up to 6 months after withdrawal from alcohol.…”

“…Plasma cortisol increases have been observed concurrently with alcohol consumption (Rivier et al, 1984;Wright, 1978) and also during the early alcohol withdrawal period (Adinoff et al, 1991). In abstinent alcoholics, baseline plasma cortisol generally returns to normal (Marchesi et al, 1994).…”

Hypothalamic Function in Response to 2‐Deoxy‐d‐Glucose in Long‐Term Abstinent Alcoholics

“…The HPA functional abnormalities noted by George et al (1994) in alcoholics abstinent 3 weeks are therefore most likely related to the effects of recent alcohol consumption and withdrawal. These findings parallel the findings of other research that shows that HPA axis function normalizes with extended abstinence (Adinoff et al, 1990;Ehrenreich et al, 1997;Marchesi et al, 1994). Future investigations into the metabolic function of alcoholics, particularly investigations involving the HPA system, should consider the possibility that normalization is still occurring up to 6 months after withdrawal from alcohol.…”

“…Plasma cortisol increases have been observed concurrently with alcohol consumption (Rivier et al, 1984;Wright, 1978) and also during the early alcohol withdrawal period (Adinoff et al, 1991). In abstinent alcoholics, baseline plasma cortisol generally returns to normal (Marchesi et al, 1994).…”

The contribution of hypercortisolaemia to the cognitive decline of geriatric depression

“…A causative role for steroids is supported by the illustration that normalization of glucocorticoid levels is followed by correction of the anatomical abnormalities in Cushing's disease (Heinz et al, 1977) and exogenous steroid states (Lagenstein et al, 1979). In addition, the morphological changes in anorexia and chronic alcoholism reverse in parallel with the levels of cortisol following disease remission (Marchesi et al, 1994), but this has yet to be shown in depressive disorder. Overall, much work supports the role of glucocorticoids in the production of neuroanatomical abnormalities, but what evidence suggests that these changes may also be the mechanism for cognitive decline?…”

Hypothalamic Function in Response to 2‐Deoxy‐d‐Glucose in Long‐Term Abstinent Alcoholics

“…The HPA functional abnormalities noted by George et al (1994) in alcoholics abstinent 3 weeks are therefore most likely related to the effects of recent alcohol consumption and withdrawal. These findings parallel the findings of other research that shows that HPA axis function normalizes with extended abstinence (Adinoff et al, 1990;Ehrenreich et al, 1997;Marchesi et al, 1994). Future investigations into the metabolic function of alcoholics, particularly investigations involving the HPA system, should consider the possibility that normalization is still occurring up to 6 months after withdrawal from alcohol.…”

“…Plasma cortisol increases have been observed concurrently with alcohol consumption (Rivier et al, 1984;Wright, 1978) and also during the early alcohol withdrawal period (Adinoff et al, 1991). In abstinent alcoholics, baseline plasma cortisol generally returns to normal (Marchesi et al, 1994).…”

The contribution of hypercortisolaemia to the cognitive decline of geriatric depression

“…A causative role for steroids is supported by the illustration that normalization of glucocorticoid levels is followed by correction of the anatomical abnormalities in Cushing's disease (Heinz et al, 1977) and exogenous steroid states (Lagenstein et al, 1979). In addition, the morphological changes in anorexia and chronic alcoholism reverse in parallel with the levels of cortisol following disease remission (Marchesi et al, 1994), but this has yet to be shown in depressive disorder. Overall, much work supports the role of glucocorticoids in the production of neuroanatomical abnormalities, but what evidence suggests that these changes may also be the mechanism for cognitive decline?…”

Hypothalamic Function in Response to 2‐Deoxy‐d‐Glucose in Long‐Term Abstinent Alcoholics

“…The HPA functional abnormalities noted by George et al (1994) in alcoholics abstinent 3 weeks are therefore most likely related to the effects of recent alcohol consumption and withdrawal. These findings parallel the findings of other research that shows that HPA axis function normalizes with extended abstinence (Adinoff et al, 1990;Ehrenreich et al, 1997;Marchesi et al, 1994). Future investigations into the metabolic function of alcoholics, particularly investigations involving the HPA system, should consider the possibility that normalization is still occurring up to 6 months after withdrawal from alcohol.…”

“…Plasma cortisol increases have been observed concurrently with alcohol consumption (Rivier et al, 1984;Wright, 1978) and also during the early alcohol withdrawal period (Adinoff et al, 1991). In abstinent alcoholics, baseline plasma cortisol generally returns to normal (Marchesi et al, 1994).…”

The contribution of hypercortisolaemia to the cognitive decline of geriatric depression

“…A causative role for steroids is supported by the illustration that normalization of glucocorticoid levels is followed by correction of the anatomical abnormalities in Cushing's disease (Heinz et al, 1977) and exogenous steroid states (Lagenstein et al, 1979). In addition, the morphological changes in anorexia and chronic alcoholism reverse in parallel with the levels of cortisol following disease remission (Marchesi et al, 1994), but this has yet to be shown in depressive disorder. Overall, much work supports the role of glucocorticoids in the production of neuroanatomical abnormalities, but what evidence suggests that these changes may also be the mechanism for cognitive decline?…”