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Biomedical subjects

T A Wehr

Publications and source records attributed to T A Wehr.

At least 19 recordsLinked to original sources
PubMed1995

Bimodal patterns of human melatonin secretion consistent with a two-oscillator model of regulation.

In many animals, changes in duration of nocturnal melatonin secretion chemically mediate effects of seasonal changes in nightlength on behavior and physiology. According to one model, the changes in duration of secretion result from adjustments in the timing of two circadian oscillators, one entrained to dusk, controlling onset, and another entrained to dawn, controlling offset. Consistent with this model, in six women, we found separate and reproducible evening and morning peaks of melatonin secretion that might represent the separate expressions of rhythms of two oscillators.

Adult↗
PubMed1995

Suppression of men's responses to seasonal changes in day length by modern artificial lighting.

We recently reported that humans have conserved mechanisms, like those that exist in other animals, which detect changes in day length and make corresponding adjustments in the duration of nocturnal periods of secretion of melatonin and of other functions. We detected these responses in individuals who were exposed to artificial "days" of different durations. The purpose of the present study was to determine whether men who are exposed to natural and artificial light in an urban environment at 39 degrees N are still able to detect and respond to seasonal changes in duration of the natural photoperiod. We measured profiles of circadian rhythms during 24-h periods of constant darkness (< 1 lx) and found no summer-winter differences in durations of nocturnal periods of active secretion of melatonin, rising levels of cortisol, high levels of thyrotropin, and low levels of rectal temperature. The results of this and our previous study suggest that modern men's use of artificial light suppresses responses to seasonal changes in the natural photoperiod that might otherwise occur at this latitude.

Adaptation, Physiological↗
PubMed1994

Extended sleep in humans in 14 hour nights (LD 10:14): relationship between REM density and spontaneous awakening.

The sleep patterns of 8 normal subjects living in a winter-type photoperiod (10 h light and 14 h darkness; LD 10:14) for 4 weeks were characterized by the presence of periods of spontaneous wakefulness alternating with periods of spontaneous sleep. Transitions from sleep to wakefulness occurred much more frequently out of REM sleep than out of NREM sleep (P < 0.002). REM periods that terminated in wakefulness showed shorter REM durations (P < 0.0005) and higher REM densities (P < 0.0005) than REM periods that did not terminate in wakefulness. The authors discuss these results in terms of a possible relationship between REM density and arousal level. The higher REM density preceding wakefulness and the increased number of REM periods terminating in spontaneous awakenings could reflect an enhanced level of a brain arousing process, resulting from reduced sleep pressure in the extended nights.

Adult↗
PubMed1992

Fluoxetine decreases brain temperature and REM sleep in Syrian hamsters.

The antidepressant drug, fluoxetine (FLX), a selective serotonin reuptake inhibitor, was administered to Syrian hamsters, and its acute and chronic effects on EEG sleep and hypothalamic temperature were recorded. Acute fluoxetine treatment at doses of 5, 10, 20 and 40 mg/kg decreased REM sleep and hypothalamic temperature in a dose-dependent manner. It increased NREM sleep, and, at doses of 20 and 40 mg/kg, it increased wakefulness. At 40 mg/kg, it decreased motor activity. During chronic treatment, tolerance developed to FLX's REM sleep-inhibiting effects, but tolerance did not develop to FLX's hypothalamic temperature-decreasing effects. Chronic FLX treatment produced circadian phase-dependent decreases in temperature beyond those that were observed during acute treatment. The apparent dissociation during chronic treatment between FLX's temperature-lowering effects and its REM-decreasing effects might be related to long-term changes in 5HT receptor function or FLX pharmacokinetics.

Animals↗
PubMed1992

Diurnal variation: reliability of measurement and relationship to typical and atypical symptoms of depression.

We used three rating scales to study diurnal variation of mood in 37 patients with major depressive disorder (17 drug-free patients and 20 treatment refractory patients on stable regimens of antidepressant medication). The three rating scales included global self-ratings administered twice a day; an itemized, prospective, observer-rated scale administered twice a day; and the retrospective item on the Hamilton Depression Rating Scale. Z scores and Intraclass Correlation Coefficients demonstrated a poor level of agreement between the itemized, prospective scale and the self-ratings. In addition, stepwise multiple regression analysis and point bi-serial correlation showed no systematic relationship between atypical diurnal variation (i.e., mood worsening in the evening) and atypical depressive symptoms (weight gain, hypersomnia, etc.), or between typical diurnal variation (i.e., mood worsening in the morning) and typical depressive symptoms (weight loss, insomnia, etc.). This lack of relationship was observed in both drug-free and medicated patients using each of the three rating scales. We discuss possible explanations for these negative findings.

Adult↗
PubMed1992

A brain-warming function for REM sleep.

During REM sleep, arterial blood flow, neuronal firing rates, metabolism, and temperature increase in many parts of the CNS. Eye muscle tone also increases, and the eyes exhibit bursts of rapid movements. If one of the functions of sleep is to conserve energy, then it is curious that energy is so conspicuously expended in the vicinity of the CNS during REM sleep. The author hypothesizes that homeotherms use REM sleep to produce heat in order to maintain a high, stable temperature in a restricted CNS core during sleep. The fact that several of the active features of REM sleep heat the CNS, and the fact that REM sleep propensity increases when core temperature physiologically decreases, seem consistent with the hypothesis that REM sleep is a regulated mechanism for warming the CNS.

Animals↗
PubMed1992

Is sleep deprivation useful in the treatment of depression?

OBJECTIVE: The authors critically reviewed the literature on clinical applications of sleep deprivation in the treatment of depression. DATA COLLECTION: They included all studies using sleep deprivation for clinical purposes, with the exception of treatment studies that did not provide follow-up beyond a night of recovery sleep. They focused on six uses of sleep deprivation: 1) to potentiate response to antidepressant medication (13 studies), 2) to hasten the onset of action of antidepressant medication or lithium (five studies), 3) to prevent recurrent mood cycles (four studies), 4) as an alternative to antidepressant medication (five studies), 5) as a diagnostic probe (two studies), and 6) to predict response to antidepressant medication (nine studies). FINDINGS: Although the literature appears to demonstrate the efficacy of sleep deprivation as a potentiation strategy, these treatment studies have substantial methodological shortcomings. Well-designed pilot studies indicate that sleep deprivation may hasten the onset of action of thymoleptic medications. Sleep deprivation may prevent premenstrual mood swings, and response to sleep deprivation may differentiate depressive pseudodementia from primary degenerative dementia with depression. Studies attempting to use sleep deprivation to predict response to antidepressant medication have yielded inconsistent results. CONCLUSIONS: Given the noninvasive nature of sleep deprivation, it would be useful to determine if even a small subset of refractory patients respond to it. The authors suggest future research directions to determine the usefulness of this potential treatment.

Depressive Disorder↗
PubMed1992

Seasonal vulnerability to depression. Implications for etiology and treatment.

The risk for depression increases at two opposite times of the year--late spring/early summer and late fall/early winter. In 15% of patients with recurrent major depression, depressive episodes regularly recur on an annual basis in one of the two seasonal risk periods. Thus, there are primarily two forms of seasonal affective disorder: recurrent fall-winter depression and recurrent spring-summer depression. The opposite seasonal types of depression tend to have opposite vegetative symptoms. Sleep, appetite and weight increase in winter depression and decrease in summer depression. An important implication of the seasonality of depression is that some type of depression may be caused by changes in the physical environment and that manipulations of the physical environment may be used as treatments. There is now extensive evidence that exposure to bright artificial light is an effective treatment of recurrent winter depression. A corollary is that seasonal deficiency of natural light probably induces winter depression. There have been considerable efforts to elucidate the biological mechanisms of winter depression and its response to phototherapy. Although no single system has been shown to be responsible for the syndrome, there is evidence that the indole hormone melatonin, the indole neurotransmitter serotonin, and the peptide neurohormone corticotropin releasing hormone (CRH) play roles in the pathophysiology and phototherapy of winter depression.

Corticotropin-Releasing Hormone↗
PubMed1992

Cerebral glucose metabolism in patients with summer seasonal affective disorder.

Positron emission tomography scans of nine patients diagnosed with summer seasonal affective disorder (SSAD) were compared with scans of 45 normal control subjects to investigate differences in brain glucose metabolism. All subjects performed an auditory discrimination task beginning several minutes before injection of F-18-deoxyglucose and continuing for 30 minutes after injection. Regional glucose metabolic rates were extracted from 60 rectangular regions of interest measured in five planes selected as atlas matches from 28 total slices. Statistically significant differences between patients with SSAD and normal control subjects were found in cerebral glucose metabolic rate and also in normalized regional glucose metabolic rates in the orbital frontal cortex and in the left inferior parietal lobule.

Adult↗
PubMed1992

The role of sleep and wakefulness in the genesis of depression and mania.

Disturbances of the sleep-wake cycle are frequently seen in affective illness and are exhibited in other psychiatric illness as well. In addition to being a useful research probe, manipulations of the sleep-wake cycle such as sleep deprivation (SD) and phase advance can cause depression to remit and thus can be used as alternative or as adjunctive to pharmacologic treatment. The antidepressant response to SD occurs whether antidepressant drugs are administered or not. However, there is some evidence that the concomitant use of antidepressants may prevent the relapses that occur after recovery sleep. Data from clinical investigations also indicate that disrupted sleep can trigger and intensify mania. Rapid cycling bipolar patients may be especially vulnerable to mania/hypomania after disrupted sleep or SD. Characteristic changes in body temperature have been recorded in sleep deprivation as well as in other antidepressant treatment modalities. Thermoregulatory physiology may therefore provide a framework for understanding the effects of sleep-wake manipulations in affective illness.

Bipolar Disorder↗
PubMed1991

Evaluation of seasonality in six clinical populations and two normal populations.

The Seasonal Pattern Assessment Questionnaire (SPAQ) was used to evaluate retrospectively self-reported seasonal changes in mood and behavior (seasonality) of two normal and six clinical populations: patients with winter-seasonal affective disorder (SAD), summer-SAD, eating disorders, bipolar affective disorder, major depressive disorder and subsyndromal winter-SAD. The SPAQ successfully discriminated between groups expected to have high seasonality scores, such as winter-SAD, summer-SAD and subsyndromal winter-SAD, and normal controls. Bipolars and major depressives had normal seasonality scores. Patients with eating disorders had unexpectedly high scores. There was a general tendency for all groups to eat and sleep more and to gain weight in the winter. The implications of these findings are discussed.

Adult↗
PubMed1991

Contrasts between symptoms of summer depression and winter depression.

Epidemiological studies and studies of clinical populations suggest that there are primarily two opposite patterns of seasonally recurring depressions: summer depression and winter depression. In addition, there is preliminary evidence that the two seasonal types of depression may have opposite types of vegetative symptoms. In the present study, we prospectively monitored symptoms of depression in 30 patients with recurrent summer depression and 30 sex-matched patients with recurrent winter depression and compared the symptom profiles of the two groups. Consistent with predictions based on the earlier reports, we found that winter depressives were more likely to have atypical vegetative symptoms, with increased appetite, carbohydrate craving, weight gain and hypersomnia, and that summer depressives were more likely to have endogenous vegetative symptoms, with decreased appetite and insomnia. A cluster analysis performed on the patients' symptom profiles without reference to season of occurrence of their episodes separated 78% of the summer depressives and winter depressives from each other on the basis of their symptoms (chi 2 = 19.29, P less than 0.001).

Adult↗
PubMed1991

Atenolol in premenstrual syndrome: a test of the melatonin hypothesis.

Eleven patients with prospectively documented premenstrual depression were given 100 mg atenolol or placebo daily to suppress melatonin secretion during the symptomatic premenstrual phase of the menstrual cycle. There was no significant improvement in mood following treatment with atenolol vs. placebo. These findings suggest that bright light may exert antidepressant effects in patients with premenstrual syndrome through mechanisms other than melatonin suppression and that atenolol does not appear to be a viable treatment modality for the majority of patients with premenstrual depression.

Affect↗
PubMed1991

Sleep-loss as a possible mediator of diverse causes of mania.

When sleep duration and mood were monitored longitudinally in a 59-year-old woman with bipolar illness, sleep loss appeared to mediate the triggering of mania by psychosocial and pharmacological precipitating factors. This interpretation was supported by observations that mania could repeatedly be induced experimentally by depriving her of sleep for one night. The patient's data illustrate how sleep-loss might be a preventable cause of mania in a variety of situations.

Bipolar Disorder↗
PubMed1991

Abnormal pituitary-adrenal responses to corticotropin-releasing hormone in patients with seasonal affective disorder: clinical and pathophysiological implications.

CRH has been shown to produce increased locomotion, arousal, and anorexia in experimental animals. A deficiency of CRH in patients with seasonal affective disorder could contribute to the characteristic lethargy, hypersomnia, and hyperphagia characteristic of this illness. To test this hypothesis, we studied basal plasma ACTH and cortisol levels and their responses to ovine CRH in controls and depressed patients with seasonal affective disorder before and after light treatment. Untreated seasonal affective disorder patients showed normal basal plasma cortisol and ACTH levels, but their responses to CRH tended to be delayed and were significantly reduced. When patients were studied after 9 days of light treatment, a significant increase in plasma ACTH and cortisol responses to CRH was observed. Our findings in untreated patients with seasonal affective disorder are similar to those in patients with Cushing's disease 2 weeks after transsphenoidal hypophysectomy, who uniformly show sustained suppression of their CRH neuron because of long-standing hypercortisolism. This findings suggest that the CRH neuron of patients with seasonal affective disorder is hypofunctional. We postulate that the clinical symptomatology in patients with seasonal affective disorder could reflect deficient activity of this important arousal-producing system.

Adrenocorticotropic Hormone↗
PubMed1991

The durations of human melatonin secretion and sleep respond to changes in daylength (photoperiod).

Seasonal changes in daylength (photoperiod) modify the duration of nocturnal melatonin (MT) secretion in many vertebrates. In some cases the changes in MT act as chemical signals that trigger photoperiodic induction of breeding and other seasonal phenomena. It is unclear whether, and to what extent changes in daylength modify the duration of human MT secretion. To address this question, I investigated whether the duration of human MT secretion could be altered by artificial photoperiods. I exposed eight healthy volunteers to a conventional "summer" photoperiod of 16 h light and 8 h darkness for 1 week and to a "winter" photoperiod of 10 h light and 14 h darkness for 4 weeks. As occurs in animals, the duration of nocturnal MT secretion in human beings was longer after exposure to the short photoperiod (12.5 +/- 1.8 vs. 10.3 +/- 0.8 h, t = 3.778, P less than 0.01). The duration of the sleep-phase (recorded by electroencephalogram) was also longer (11.0 +/- 0.8 vs. 7.7 +/- 0.2 h, t = 11.754, P less than 0.001). Whether such changes would lead to significant seasonal changes in human physiology and behavior under natural lighting conditions may be worthy of further investigation.

Adult↗