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Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 55 records · Page 3Linked to original sources
PubMed1997

Depressive symptoms in California adolescents: family structure and parental support.

PURPOSE: To examine the relationship between family structure, parental social support, and depressive symptoms among California adolescents. METHODS: The depressive symptom instrument consisted of a previously validated self-report scale. The sample was the 1993 California Youth Tobacco Survey respondents (N = 5,531). The analysis classified adolescents in the highest 15% on the depressive symptom scale as having notable depressive symptoms and related the prevalence of depression to family structure (two-parent, single-mother, single-father, and neither parent present) and to parental support (adolescents naming parents as someone they could talk to about problems). RESULTS: Girls reported significantly higher rates of depressive symptoms than boys. Although adolescents in single-parent households tended to show slightly higher rates of depressive symptoms, these rates did not differ significantly across the four types of family structures for either sex. Significantly higher rates of depressive symptoms were found among both boys and girls who resided with parent(s) not named as supportive than those who lived with supportive parent(s). Girls appeared particularly vulnerable if they lived in a nonsupportive, single-father household. CONCLUSION: Lack of perceived parental social support is highly related to depressive symptoms in California adolescents. Helping parents establish and maintain supportive relationships with the children in their household may decrease the likelihood of depressive symptoms among adolescents.

Adolescent↗
PubMed1997

Positive correlations between cerebral protein synthesis rates and deep sleep in Macaca mulatta.

Local rates of cerebral protein synthesis (ICPSleu) were determined with the autoradiographic L-[1-14C]leucine method in seven awake and seven asleep, adult rhesus monkeys conditioned to sleep in a restraining chair in a darkened, ventilated chamber while EEG, EOG, and EMG were monitored. Prior to the period of measurement all animals slept for 1-4 h. Controls were awakened after at least one period of rapid-eye-movement (REM) sleep. Experimental animals were allowed to remain asleep, and they exhibited non-REM sleep for 71-99% of the experimental period. Statistically significant differences in ICPSleu between control and experimental animals were found in four of the 57 regions of brain examined, but these effects may have occurred by chance. In the sleeping animals, however, correlations between ICPSleu and percent time in deep sleep were positive in all regions and were statistically significant (P < or = 0.05) in 35 of the regions. When time in deep sleep was weighted for the integrated specific activity of leucine in grey matter, positive correlations were statistically significant (P < or = 0.05) in 18 regions in the experimental animals. These results suggest that rates of protein synthesis are increased in many regions of the brain during deep sleep compared with light sleep.

Animals↗
PubMed1997

REM sleep eye movement counts correlate with visual imagery in dreaming: a pilot study.

Based on the findings of our previously published positron emission tomography study, we proposed that recorded eye movements during REM sleep are visually targeted saccades. In the present study, we examined the correlation between the number of eye movements in REM sleep (EM) and visual imagery in dreaming (V) and provided further support for our proposal. All the observations (N = 11) were made with one individual to eliminate interindividual variation and were made during the second REM sleep period to control for a time-of-night effect. V, with or without dream report length partialled out, was strongly associated with EM only in the 1-min interval immediately preceding awakening. The time course of the association suggests that the strong EM-V association reflects a phasic, localized activation of the eye-movement-control system in association with REM sleep eye movements.

Adult↗
PubMed1997

Assessment of the quality of life of patients with major depression.

OBJECTIVE: This study examined the relationship between a measure of quality of life and measures of depressive symptoms among patients with major depression. METHODS: One hundred patients with primary major depression and 61 control subjects from the San Diego Veterans Affairs Medical Center and surrounding area were compared using a variety of measures, including the Quality of Well-Being (QWB) scale, the Hamilton Rating Scale for Depression, and the Beck Depression Inventory. RESULTS: After analyses controlled for age, gender, family history of mental illness, and comorbid axis III diagnosis, subjects' scores on the QWB were significantly correlated with their scores on the Hamilton scale and Beck inventory. The severity of depressive symptoms was inversely related to quality of life as measured by the QWB, independent of the variables that were controlled for. CONCLUSIONS: The QWB is sensitive to symptoms of depression among patients diagnosed with major depression. The reduction in quality of life associated with psychiatric symptoms of depression is comparable to that observed among physically ill patients.

Adult↗
PubMed1997

Temperature circadian rhythms during the menstrual cycle and sleep deprivation in premenstrual dysphoric disorder and normal comparison subjects.

The aim of this study was to test the hypothesis that the circadian rhythm of core body temperature is altered in premenstrual dysphoric disorder (PMDD) subjects compared to that in normal comparison (NC) subjects and that it is normalized in PMDD subjects after treatment with early night partial sleep deprivation (ESD) or late night partial sleep deprivation (LSD). A total of 23 subjects meeting DSM-IV criteria for PMDD and 18 NC subjects had 24-h core body temperature recordings taken during the following conditions: (1) baseline midfollicular (preovulatory) and (2) late luteal (postovulatory) menstrual cycle phases and after a randomized crossover trial in subsequent luteal phases of (3) ESD, in which subjects slept from 03:00 to 07:00 h, followed by (4) a night of recovery sleep (ESD-R: sleep 22:30 to 06:30 h), and (5) LSD, in which subjects slept from 21:00 to 01:00 h, also followed by (6) a night of recovery sleep (LSD-R: sleep 22:30 to 06:30 h). Temperature amplitudes were significantly decreased in the luteal phase compared to those in the follicular menstrual cycle phase and increased after nights of recovery sleep. Compared to the baseline late luteal phase, during LSD, temperature amplitude increased in PMDD subjects but decreased in NC subjects. During ESD, the temperature acrophase was delayed in PMDD subjects but was advanced in NC subjects; during LSD, the temperature acrophase was advanced in PMDD subjects but was delayed in NC subjects compared to the late luteal baseline. Nocturnal temperature and temperature maxima and mesors tended to be higher in PMDD subjects than in NC subjects; when not reduced during sleep deprivation interventions, these were not associated with therapeutic effects. Alterations in both phase and amplitude of temperature circadian rhythms characterize PMDD subjects as contrasted with NC subjects in response to sleep deprivation. The changes in phase reflected more shifts in temperature acrophase in response to shifts in sleep in PMDD subjects. This realignment of the timing of sleep and temperature in addition to the enhancement of blunted amplitude rhythms during recovery nights of sleep may provide corrective mechanisms that contribute to the therapeutic effects of sleep deprivation.

Adult↗
PubMed1997

Blunted phase-shift responses to morning bright light in premenstrual dysphoric disorder.

Patients with premenstrual dysphoric disorder (PMDD) respond therapeutically to sleep deprivation and light therapy. They have blunted circadian rhythms of melatonin. The authors sought to test the hypothesis that these disturbances are a reflection of a disturbance in the underlying circadian pacemaker or, alternatively, that they reflect a disturbance in the input pathways to the clock. To test these hypotheses, after a 2-month diagnostic evaluation, 8 patients who met DSM-IV criteria for PMDD and 5 normal control (NC) subjects underwent two studies to determine whether PMDD subjects showed (1) altered melatonin sensitivity to light suppression (Study 1) and (2) altered phase-shift responses to morning light as a measure of the functional capacity of the underlying pacemaker (Study 2). In both studies, measurements were made during asymptomatic follicular and symptomatic luteal menstrual cycle phases in PMDD patients. The results of Study 1 showed no significant effect of group or menstrual cycle phase on the amount or percentage of suppression of melatonin by light. The results of Study 2 showed that with respect to the variable of offset time, PMDD subjects, when symptomatic, showed a reduced and directionally altered melatonin phase-shift response to a morning bright light stimulus; in 4 of 5 NC subjects, melatonin offset was advanced by bright morning light, whereas in PMDD subjects, it was delayed (3 subjects) or not shifted (5 subjects) (group effect, p = .045). Study 2 also revealed that area under the curve also changed differentially in PMDD versus NC subjects. In summary, the primary findings from this pilot study suggest that in PMDD there is a maladaptive (directionally altered and blunted) response to light in the symptomatic luteal phase. Because the suppressive effects of light were similar in PMDD and NC subjects, the previously observed low melatonin levels in this disorder do not likely represent a disturbance in pineal reactivity to suprachiasmatic nucleus efferents. Instead, the findings support a possible disturbance in PMDD in the clock itself or its coupling mechanisms.

Adult↗
PubMed1997

A comparison of nefazodone and fluoxetine on mood and on objective, subjective, and clinician-rated measures of sleep in depressed patients: a double-blind, 8-week clinical trial.

BACKGROUND: Previous small trials have suggested that nefazodone does not suppress rapid-eye-movement (REM) sleep or increase REM latency in depressed patients, in contrast to fluoxetine. The effects of nefazodone and fluoxetine on sleep architecture and on clinician- and patient-rated sleep measures were directly compared in this 8-week, multicenter, double-blind, randomized, parallel-group study. METHOD: Forty-four outpatients with moderate to severe, nonpsychotic major depressive disorder (DSM-III-R) and insomnia were randomly assigned to receive nefazodone (Days 1-7, 200 mg/day; Days 8-56, 400 mg/day) or fluoxetine (Days 1-56, 20 mg/day). Sleep measures were obtained at baseline, while patients were unmedicated, and at Weeks 2, 4, and 8 of treatment. RESULTS: In 43 evaluable patients (23 nefazodone, 20 fluoxetine), nefazodone and fluoxetine demonstrated similar antidepressant efficacy. All significant values were p < .05. Fluoxetine significantly decreased sleep efficiency and REM sleep and increased number of awakenings, Stage 1 sleep, and REM latency compared with baseline. In contrast, nefazodone significantly decreased percentage of awake and movement time and did not alter sleep efficiency or number of awakenings, Stage 1 or REM sleep, or REM latency compared with baseline. Nefazodone was associated with significantly less change from baseline for sleep efficiency, number of awakenings, percentage of awake and movement time, percentage of REM and Stage 1 sleep, and REM latency compared with fluoxetine. Both fluoxetine- and nefazodone-treated patients also showed significant improvement in some clinician- and patient-rated sleep disturbance scores, but nefazodone-treated patients improved to a significantly greater extent than fluoxetine-treated patients in most measures. CONCLUSION: While nefazodone and fluoxetine showed equivalent antidepressant efficacy, more objective, subjective, and clinician-rated measures of sleep disturbance were improved during treatment with nefazodone than with fluoxetine. These results suggest that antidepressant effects of medications can occur independently of drug-induced changes in objective, subjective, and clinician-rated measures of sleep. Further studies, including parallel placebo-controlled comparisons with nefazodone, are needed to further test this hypothesis.

Adult↗
PubMed1997

Preliminary longitudinal assessment of quality of life in patients with major depression.

This study examines the longitudinal relationships between a health-related quality of life measure and depressive symptoms in patients with major depression. One hundred eighteen patients with primary major depression and 81 controls were evaluated. The patients were divided into three groups based on Diagnostic Interview Schedule criteria for a major depressive episode at baseline (T1) and 6 months later (T2). Results indicate that the Quality of Well-Being (QWB) measure is sensitive to different levels of depressive symptoms over a 6-month period. The QWB is a health-related quality of life and cost/utility measure that may be useful for pharmacoeconomic analysis. The reduction in quality of life associated with symptoms of depression is comparable to that observed with chronically physically ill patients. As a generic symptom/function measure, the QWB may be very useful in evaluating public health policy.

Depressive Disorder↗
PubMed1996

Circadian rhythms of prolactin and thyroid-stimulating hormone during the menstrual cycle and early versus late sleep deprivation in premenstrual dysphoric disorder.

The present study extended previous work by examining whether disturbances in the circadian rhythms of prolactin (PRL) and thyroid-stimulating hormone (TSH) distinguish patients with premenstrual dysphoric disorder (PMDD) from normal volunteers. In addition, the effects of therapeutic interventions with early and late partial sleep deprivation were explored. Both PRL and TSH levels were measured every 30 min from 18:00 h to 09:00 h during midfollicular and late luteal menstrual cycle phases in 23 PMDD patients and 18 normal volunteers. Hormone levels were measured again after a randomized crossover trial of early (sleep 03:00-07:00 h) versus late (sleep 21:00-01:00 h) partial sleep deprivation administered in two separate luteal phases. Compared with normal volunteers, PMDD patients had higher PRL concentrations, consistent with previous findings. TSH rhythms occurred earlier in PMDD than in normal subjects. PRL levels decreased and TSH levels increased with sleep deprivation compared with baseline conditions. The timing of PRL secretion shifted earlier with late sleep deprivation and later with early sleep deprivation. Although circadian disturbances of PRL and TSH were found in PMDD patients compared with normal volunteers, the therapeutic effects of early and late sleep deprivation do not appear to be mediated by correcting these disturbances.

Affect↗
PubMed1996

The 5-HT1A agonist ipsapirone enhances EEG slow wave activity in human sleep and produces a power spectrum similar to 5-HT2 blockade.

The REM sleep-suppressing effect of postsynaptic 5-HT1A stimulation has been well established. Here we investigate the effects of the 5-HT1A agonist ipsapirone (10 and 20 mg) on sleep EEG power spectra during non-REM sleep in nine healthy humans. At the lower dose, slow wave activity (SWA; EEG power in the delta (1-4.5 Hz) range) was significantly enhanced. At the higher dose, where side-effects occurred, the enhancement in SWA was not significant. The spectral profile was characterized by a bimodal increase of power in the lower delta and in the theta (5-8 Hz) frequencies, and by troughs at 4 Hz and at 11 Hz, a pattern compellingly similar to that reported for a 5-HT2 antagonist (seganserin). We propose that the spectral data following the lower ipsapirone dose reflect a net decrease of neuronal activity at 5-HT2 receptors, mediated through stimulation of somatodendritic autoreceptors in the raphe nuclei (presynaptic) and/or through stimulation of postsynaptic 5-HT1A receptors colocalized with 5-HT2 receptors. The spectral non-REM sleep EEG profile might be used to investigate central 5-HT function in humans.

Adult↗
PubMed1996

Sleep and dreams in Vietnam PTSD and depression.

The present study compares the sleep and dreams of three groups of subjects: 1) Vietnam veterans with posttraumatic stress disorder (PTSD) and major depression, 2) veterans with depression alone, and 3) veterans with neither PTSD nor depression (i.e., normal controls). Sleep recordings indicate only one significant difference between the PTSD/depressed and depressed alone groups: sleep latency was prolonged in the depressed alone patients compared with the other two groups. The two patient groups differed from controls in the manner already reported for depressed patients (decreased REM latency, increased REM density, reduced total sleep time, reduced sleep efficiency), with some of the differences significant only at the trend level. Dreams were obtained from REM awakenings. Dream recall rate and report length did not differ between groups. Mean anxiety level in dreams was less than 1 (mild) for all three groups, with major depression patients scoring significantly higher than controls. Dreams of PTSD/depressed patients were significantly less likely to be set in the present than dreams of the other two groups.

Adult↗
PubMed1996

Brain glucose metabolism during non-rapid eye movement sleep in major depression. A positron emission tomography study.

BACKGROUND: Depression is characterized by several sleep-related abnormalities shortly before and after sleep onset, such as prolonged sleep latency, loss of stage 3-4 sleep, reduced rapid eye movement (REM) latency, increased nocturnal core body temperature, and abnormal hormone secretion patterns. Sleep deprivation is associated with a temporary improvement in depression. We hypothesized that depressed patients may be "overaroused" and that absolute cerebral glucose metabolism would be elevated during the first nocturnal non-REM sleep period in depressed patients compared with normal controls. In addition, since hypofrontality (greater metabolic activity in occipital compared with frontal cortical activity) has been reported in waking positron emission tomographic studies of depressed patients compared with controls, we predicted significant hypofrontality in depressed patients during the first non-REM period. METHODS: Positron emission tomography with fludeoxy-glucose F 18 was used to compare 10 unmedicated men with unipolar depression with 12 normal men during the first non-REM sleep period at normal bedtime. RESULTS: Whole-brain absolute metabolic rate during non-REM sleep was significantly elevated (+47%) in patients compared with controls. Mean absolute cerebral glucose metabolic rate was also higher in every area of the brain in patients compared with normal controls. The greatest significant mean increases were in the posterior cingulate and amygdala (+44%), hippocampus (+37% to +43%), occipital and temporal cortex (+33% to +34%), and pons (+33%). Relative metabolic rates in specific neroanatomical areas, however, varied considerably both within the patient group and between patients and controls. Patients showed significant hypofrontality, particularly in the medio-orbital frontal cortex, compared with controls. Patients also showed significant reductions of relative metabolic rate in the anterior cingulate, caudate, and medial thalamus compared with controls. CONCLUSIONS: These findings provide further support for the hyperarousal hypothesis of some types of major depressive disorder. Abnormal patterns of cerebral metabolism during non-REM sleep in depressed patients confirmed earlier waking findings of decreased relative frontal and abnormal limbic metabolic activity and striatal metabolism in association with posterior cortical increases.

Adult↗
PubMed1996

Ipsapirone, a 5-HT1A agonist, suppresses REM sleep equally in unmedicated depressed patients and normal controls.

To determine whether ipsapirone, a 5-HT1A agonist, differentially suppresses REM sleep in depressed patients compared with normal controls, we administered placebo, ipsapirone 10 mg, or ipsapirone 20 mg in a double-blind, random order before bedtime in 18 unmedicated patients with depression and 16 age-matched, gender-matched normal controls. Compared to placebo, ipsapirone affected REM sleep measures equally in depressed patients and controls as follows: (1) increased REM latency; (2) reduced total REM percent, REM time, and REM density; and (3) delayed the onset of REM sleep. In addition, ipsapirone had similar effects in patients and controls in other sleep measures: (1) reduced total sleep time; (2) delayed sleep onset time; and (3) increased sleep latency, stage 1%, stage 2%, the amount of stage 3 & 4 sleep in the first non-REM period, and wake time after sleep onset. The study does not support the hypothesis that downregulated 5-HT1A receptors mediate the pathophysiology or sleep disturbances of depression, although further studies are needed as these patients did not differ from controls in baseline sleep measures.

Adult↗
PubMed1996

Effects of zolpidem on local cerebral glucose metabolism during non-REM sleep in normal volunteers: a positron emission tomography study.

Using positron emission tomography with fluorodeoxyglucose (18FDG or FDG), we compared the effects of zolpidem (10 mg), an imidazopyridine hypnotic, which is relatively selective for the BZ1 or omega receptor and placebo on cerebral glucose metabolism during the first non-REM sleep period of 12 young normal volunteers. Plasma zolpidem pharmacokinetics varied considerably among subjects, and plasma concentrations were lower than usually reported. In general, the effects of zolpidem on local cerebral glucose metabolism varied directly with plasma concentrations of zolpidem. Zolpidem induced changes in local cerebral glucose metabolism were unevenly distributed throughout the brain and were greater in subcortical areas than lateral cortical areas. Significant negative correlations were found between change in local absolute glucose metabolic rate (calculated by subtracting individual data on placebo nights from that on zolpidem nights) and plasma concentration of zolpidem for the following areas: medial frontal cortex, cingulate gyrus, putamen, thalamus, and hippocampus. The effects of zolpidem on local cerebral glucose metabolism were partially but not closely related to the reported density of BZ1 receptors.

Adult↗
PubMed1996

Language in dreaming and regional EEG alpha power.

In an intensive single-subject design, electroencephalographic (EEG) alpha power and receptive and expressive language in dreaming were studied in 12 dreams during rapid eye movement (REM) sleep on 12 separate nights. Bilateral EEG was recorded continuously from 21 sites and digitized. We used the Fast Fourier transformation (FFT) for power spectral analysis to measure EEG power in the alpha frequency range (8-12 Hz) at each of the EEG sites. The subject was awakened after about 14 minutes into the second REM period, and dream reports were collected. We scored the dream reports for expressive and receptive language. The lower the alpha power on the left sides of those homologous pairs that roughly correspond to Broca's (C3) or Wernicke's area (P3), the more expressive or receptive language in dream reports. The largest difference between the correlation of the left and that of the right homologous pair of regions was found in the central (C3, C4) area for expressive language and in the parietal (P3, P4) area for receptive language. Our finding suggests lateralized and localized cortical activation in relation to language in dreaming.

Adult↗
PubMed1996

Partial night sleep deprivation reduces natural killer and cellular immune responses in humans.

Prolonged and severe sleep deprivation is associated with alterations of natural and cellular immune function. To determine whether alterations of immune function also occur after even a modest loss of sleep, the effects of early-night partial sleep deprivation on circulating numbers of white blood cells, natural killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleukin-2 (IL-2) production were studied in 42 medically and psychiatrically healthy male volunteers. After a night of sleep deprivation between 10 P.M. and 3 A.M., a reduction of natural immune responses as measured by NK cell activity, NK activity per number of NK cells, LAK activity, and LAK activity per number of LAK precursors (CD16,56, CD25) was found. In addition, concanavalin A-stimulated IL-2 production was suppressed after sleep deprivation due to changes in both adherent and nonadherent cell populations. After a night of recovery sleep, NK activity returned to baseline levels and IL-2 production remained suppressed. These data implicate sleep in the modulation of immunity and demonstrate that even a modest disturbance of sleep produces a reduction of natural immune responses and T cell cytokine production.

Cell Adhesion↗
PubMed1995

Polygraphic sleep measures differentiate alcoholics and stimulant abusers during short-term abstinence.

We hypothesized that stimulant abusers would sleep more and have more rapid eye movement (REM) sleep than primary alcoholics during acute withdrawal (first 10 days drug free) but would have opposite patterns during subacute withdrawal (days 11-14 drug free). We compared polygraphic sleep patterns during acute withdrawal (days 3-10) for 7 stimulant abusers and 8 alcoholics and during subacute withdrawal (days 11-14) for 7 different stimulant abusers and 8 different alcoholics. For comparison purposes, a group of normal controls from our preexisting database were matched for age and gender. Two statistically significant interactions were found: consistent with our hypothesis, stimulant abusers showed greater total sleep (TST) and REM sleep during acute withdrawal than subacute withdrawal, compared with alcoholics. In contrast, alcoholics showed less TST and REM sleep during acute withdrawal than during subacute withdrawal. Our polygraphic sleep data support the hypothesis that physiological withdrawal differs in alcoholics compared with stimulant abusers. Different mechanisms may underlie withdrawal in these two substances.

Acute Disease↗