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Leo Sher

Publications and source records attributed to Leo Sher.

At least 55 records · Page 3Linked to original sources
PubMed2004

The number of previous depressive episodes is positively associated with cortisol response to fenfluramine administration.

Multiple reports document hypothalamic-pituitary-axis (HPA) hyperactivity in depressed patients. Measurement of cortisol levels after ingestion of fenfluramine, a specific serotonin releaser/uptake inhibitor agent, provides an index of HPA activity. To our knowledge, this is the first study of the effect of a number of previous depressive episodes on cortisol responses to fenfluramine administration. Thirty-one unipolar depressed patients and 23 healthy volunteers entered the study. Demographic and clinical parameters were assessed and recorded. Response to fenfluramine administration was measured by the difference between maximum hourly plasma cortisol measurements after fenfluramine administration and baseline levels measured before fenfluramine administration. The number of previous major depressive episodes was a predictor of cortisol response to fenfluramine administration in depressed subjects. Higher cortisol responses were associated with more prior episodes of major depression. The relationship of cortisol to the number of previous depressive episodes remained significant after controlling for age. Our finding highlights the importance of possible cumulative effects of repeated episodes of major depression. Prevention and early recognition of depressive episodes may prevent these cumulative adverse effects.

Adult↗
PubMed2003

Lower CSF homovanillic acid levels in depressed patients with a history of alcoholism.

Major depression and alcoholism are often comorbid, resulting in more impairment and more suicidal behavior compared with either diagnosis alone. This study compared clinical features and cerebrospinal fluid (CSF) monoamine metabolites in depressed subjects with and without a history of alcoholism and healthy volunteers. We hypothesized that depressed subjects with a history of alcoholism would be more aggressive, impulsive, and suicidal than depressed subjects without a history of alcoholism, and would have lower CSF monoamine metabolite levels. We compared 63 subjects with a current major depressive episode (MDE) and a history of alcoholism, 72 subjects with a current MDE but without a history of alcoholism, and 22 healthy volunteers. Participants with a history of alcoholism were in remission for at least 6 months. All subjects were free from prescribed medications known to affect brain serotonin, dopamine, or norepinephrine systems for a minimum of 14 days. Depressive symptoms, lifetime aggression, impulsivity, Axis II disorders, and suicidal behavior were assessed. CSF was sampled and homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were assayed by high-performance lipid chromatography with electrochemical detection. Depressed subjects with a history of alcoholism did not differ from depressed subjects without a history of alcoholism in current severity of depressive symptoms, or in past suicidal behavior. Depressed subjects with a history of alcoholism had lower CSF HVA levels, and higher lifetime aggression and current suicide ideation scale scores and were more likely to be tobacco smokers compared with depressed subjects without a history of alcoholism. Low HVA was present after adjustment for sex, aggression and depression scores, cigarette smoking, antisocial and borderline personality disorders, psychomotor retardation, and delusions. Controls had CSF HVA levels intermediate between the two depressed groups. We found no group difference in CSF 5-HIAA and MHPG levels. In individuals with current MDE, those with a history of comorbid alcoholism had lower CSF HVA levels compared with those without a history of alcoholism. Low CSF HVA suggests that impaired dopaminergic activity is associated with a history of alcoholism in persons with current MDE.

Adult↗
PubMed2003

Prolactin response to fenfluramine administration in patients with unipolar and bipolar depression and healthy controls.

The hormonal response to the serotonin releasing agent/uptake inhibitor fenfluramine has been used as an indicator of central serotonin system function. The serotonergic system plays an important role in the etiology and pathogenesis of mood disorders. We compared the prolactin response to fenfluramine administration in unipolar depressed patients (major depressive disorder), depressed patients with bipolar disorder, and healthy controls. We found a trend towards a blunted prolactin response in depressed patients compared to healthy controls, after controlling for sex, family history, family history-by-gender interaction, and baseline levels. There was no significant difference between unipolar and bipolar patients in the baseline prolactin levels or the response to the fenfluramine administration. We also found a negative correlation between aggression and impulsivity scores and prolactin responses in subgroup with unipolar but not bipolar depression. Female patients with unipolar depression who had first-degree relatives with unipolar depression and normal controls had significantly higher prolactin responses than female patients with unipolar depression who did not have first-degree relatives with unipolar depression. The lack of difference in the response to fenfluramine administration between unipolar and bipolar depressed patients may indicate that overall serotonergic function in unipolar and bipolar depressed patients is similarly impaired.

Adult↗
PubMed2003

Effects of heavy alcohol consumption on the cardiovascular system may be mediated in part by the influence of alcohol-induced depression on the immune system.

The harmful effects of heavy alcohol use are well-documented and wide-ranging. Heavy drinking may cause or exacerbate cardiovascular disorders. The author suggests that effects of heavy alcohol consumption on the cardiovascular system may be mediated in part by the influence of alcohol-induced depression on the immune system. This hypothesis is based on the following data: (1) alcohol misuse may cause or exacerbate depression; (2) depressive disorders are associated with increased incidence, morbidity, and mortality of cardiovascular disorders; (3) the immune system may mediate effects of depressive disorders on the cardiovascular system. Further studies are needed to clarify the etiopathogenesis of alcohol-related disorders and develop new treatment modalities.

Alcohol Drinking↗
PubMed2003

A longer biological night in long sleepers than in short sleepers.

Habitual sleep duration varies greatly among individuals. The physiological basis of this variation is unknown. We sought to determine whether individual differences in sleep duration are associated with systematic differences in the duration of the biological night that is programmed by the circadian pacemaker and reflected in the nocturnal interval of circadian rhythms in neuroendocrine function, body temperature, and arousal. Ten young, healthy long sleepers (sleep duration >9 h) and 14 short sleepers (<6 h) were studied under constant environmental conditions and in the absence of sleep. The nocturnal intervals of high plasma melatonin levels, increasing cortisol levels, low body temperature, and increasing sleepiness were longer in long sleepers than in short sleepers. The maxima in cortisol and sleepiness exhibited a close relationship to habitual wake-up time, which occurred approximately 2.5 h later in long sleepers than in short sleepers. It is concluded that the circadian pacemaker programs a longer biological night in long sleepers than in short sleepers. We propose that individual differences in the circadian pacemaker's program may contribute to the variability of sleep duration in the general population. The persistence or inertia of an individual's circadian program, as was evident in constant conditions, may underlie the commonly experienced difficulty of changing habitual sleep duration willfully.

Adult↗