Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighteen patients with seasonal affective disorder (SAD) participated in a double-blind, placebo-controlled crossover study in 1986-1987. Each received, in random order, d-fenfluramine (15 mg p.o. twice daily)-a serotonin-releasing drug previously shown to suppress carbohydrate craving-or a placebo; these were given for 4 weeks separated by a 2-week washout period. Symptoms were assessed by means of clinical interviews and the Hamilton Rating Scale for Depression (HAM-D) with a special SAD addendum (AAD). Patients were also weighed. Depression scores (mean +/- SE) were identical before treatment with drug (20.9 +/- 1.3, HAM-D; 13.3 +/- 0.8, AAD) or placebo (21.4 +/- 1.2, HAM-D: 13.2 +/- 0.6, AAD). During placebo treatment, mean HAM-D scores declined by 22% (p less than .02) and AAD scores by 9% (p greater than .2). During d-fenfluramine treatment, HAM-D scores fell by 71% (p less than .001) and AAD scores by 73% (p less than .001). Thirteen (72%) of the patients demonstrated complete reversal of their abnormal test scores while taking d-fenfluramine. The group as a whole lost weight (mean = 1.2 kg) while receiving d-fenfluramine (p less than .033) but not when taking placebo. A second study, conducted in 1987-1988 with nine subjects who had previously responded to d-fenfluramine, showed that the drug remains effective for the full 3-month annual period of symptoms. These results indicate that d-fenfluramine may be useful in treating SAD and suggest that serotonin is involved in both SAD's affective and appetitive symptoms.
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PMID:Treatment of seasonal depression with d-fenfluramine. 267 Sep 15

Eleven females and five males with fall/winter seasonal affective disorder were randomly assigned to 7-day treatment regimens from 8 p.m. to 10 p.m. using identical light at 2000 or 300 lux. A modified Hamilton Rating Scale for Depression and a Beck Depression Inventory were administered before treatment, after treatment # 7, and 2 weeks after phototherapy was terminated. Analysis of variance with repeated measures revealed a significant interaction between sex of the patient, intensity of the lights, and day of rating for scores on both the modified Hamilton Rating Scale for Depression and the Beck Depression Inventory. For both measures, the interaction occurred because all groups showed a decrease in depression ratings during the phototherapy exposure period, but only females at the higher intensity continued to have low depression scores 2 weeks after light treatment had stopped. These data indicate that bright light at both high (2000 lux) and low (300 lux) intensities is able to reduce depression in patients with seasonal affective disorder. The data also indicate that both sex of the patient and intensity of the light may interact to determine the latency to relapse.
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PMID:Phototherapy for seasonal major depressive disorder: effectiveness of bright light of high or low intensity. 267 62

Bright artificial light has been found effective in reducing winter depressive symptoms of Seasonal Affective Disorder, although conclusions about the true magnitude of treatment effect and importance of time of day of light exposure have been limited by methodologic problems. Individual subjects' data from 14 research centers studying 332 patients over 5 years were analyzed with a pooled clustering technique. Overall, 2500-lux intensity light exposure for at least 2 hours daily for 1 week resulted in significantly more remissions--Hamilton Depression Rating Scale (HAM-D) score reduction of 50% or more to a level under 8--when administered in the early morning (53%) than in the evening (38%) or at midday (32%). All three times were significantly more effective than dim light controls (11%). Dual daily exposures (morning-plus-evening light) provided no benefit over morning light alone. In morning-evening crossovers, remission rates were 62% under morning light alone, compared with 28% under evening light alone, with a differential morning-evening response present in 59% of morning responders compared with 10% of evening responders (p less than 0.001). Remission rates with morning light were highest given low severity at baseline (HAM-D score of 10-16: 67% remission), as compared with moderate-to-severe cases (HAM-D score above 16: approximately 40% remission) where no morning-evening differences were found. Firmer conclusions await treatment studies with larger sample sizes and full assessment of atypical vegetative symptoms seen in winter depression but underrepresented in the Hamilton scale. Longer treatment course and greater light intensity may help clarify clinical response despite the impossibility of achieving a conventional blind placebo control.
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PMID:Light therapy for seasonal affective disorder. A review of efficacy. 267 25

Numerous endocrine abnormalities are found in depressive illness and, among these, several have been proposed as useful markers in diagnosis, prediction of treatment response, monitoring treatment outcome or in understanding of etiology. This paper reviews five endocrine systems--the hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-thyroid axis, growth hormone regulation, prolactin regulation and pineal function, in which such abnormalities have been reported. The dexamethasone suppression test (DST) results are affected by a variety of other diseases and confounding conditions. Furthermore, variability in dexamethasone availability has recently been shown to be an important factor, influencing post-DST cortisol levels. Refined tests, taking into account all these factors, or alternative tests of hypothalamic-pituitary-adrenal function may lead to improved clinical utility. Pineal function is now the focus of considerable investigation. Low nocturnal output of melatonin is found in unipolar and bipolar affective disorder and is normalized by treatment with antidepressant drugs which block re-uptake of noradrenaline. These findings support the hypothesis of noradrenergic abnormality in depression. In seasonal affective disorder there is evidence for a phase delay in the melatonin rhythm which may be a key factor in the seasonal disorder. Effective light therapy causes a phase advance in the abnormal melatonin rhythm. Whether the normalization of the melatonin rhythm is instrumental in producing the antidepressant effect is yet to be determined. There are wide spread neuroendocrine abnormalities in depressive illness. These abnormalities encompass many different pituitary hormones, as well as the pineal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine probes as biological markers of affective disorders: new directions. 268 81

The satiety-inducing effects of centrally and peripherally administered cholecystokinin (CCK) in experimental animals have been well documented. Recently, studies in humans showed that CCK is released into plasma following food ingestion, a phenomenon postulated to promote meal-related satiety. To explore whether abnormal CCK secretion during feeding may be related to pathophysiological mechanisms in disorders associated with appetite abnormalities, we report here studies of the plasma CCK response to a test meal in patients with bulimia nervosa, as well as seasonal (hyperphagic) and melancholic (anorexic) depression. Compared to controls, bulimic patients had impaired meal-related CCK secretion, correlated with an impaired sense of postprandial satiety. This defect resolved with tricyclic antidepressant-induced amelioration of bulimic behavior, suggesting that deficient CCK secretion may constitute a fundamental pathophysiologic derangement in this disorder. In contrast to patients with bulimia nervosa, hyperphagic patients with seasonal affective disorder failed to show abnormal meal-related CCK secretion. Preliminary evidence shows robust meal-related CCK secretion in melancholic depression with anorexia. We have also begun to explore the dynamics of CCK secretion into cerebrospinal fluid (CSF) utilizing an indwelling lumbar catheter. From studies in humans, we note that this peptide is secreted into the CSF in large (ng/ml) quantities in an episodic fashion that may bear some relationship to food ingestion. Further study of this parameter in volunteers and patients is now underway.
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PMID:Meal-related cholecystokinin secretion in eating and affective disorders. 269 14

We examined the utility of d-fenfluramine, a serotonin-releasing drug previously shown to diminish carbohydrate craving and weight gain in obese people, in treating patients with seasonal affective disorder (SAD), a variant of depression that occurs each fall and winter and is usually associated with hyperphagia and carbohydrate craving. Eighteen patients participated in a double-blind, placebo-controlled study in 1986-1987, each receiving, in random order, d-fenfluramine (15 mg p.o. twice daily) or a placebo for four weeks, separated by a two-week washout period. Symptoms of SAD were assessed before and after each treatment period using clinical interviews by a psychiatrist, and the Hamilton Depression Rating Scale (HDS) with a special SAD addendum (ADD). Subjects were also weighed. Patients' depression scores (mean +/- SEM) were identical before treatment with drug (20.9 +/- 1.3, HDS: 13.3 +/- 0.8 ADD) or placebo (21.4 +/- 1.2, HDS; 13.2 +/- 0.6 ADD). During placebo treatment, HDS scores declined by 22.6% (p less than 0.02) and ADD scores by 9% (p greater than 0.2). During d-fenfluramine treatment, HDS scores fell by 71% (p less than 0.0001) and ADD scores by 73% (p less than 0.0001). Thirteen of the subjects (72%) demonstrated complete reversal of their abnormal test scores on d-fenfluramine. In two others, test scores fell to normal levels with both the drug and its placebo; one subject responded only to placebo; and two failed to show therapeutic responses to either drug or placebo treatment. The group as a whole lost weight (1.2 kg) on d-fenfluramine (p less than 0.033) but not on placebo. A subsequent study on nine of the responders showed that improvements persisted for the full three-month duration of the SAD season. These results indicate that d-fenfluramine, a drug not previously identified as an antidepressant, may be useful in treating SAD. Moreover, since d-fenfluramine acts specifically to enhance serotonin-mediated neurotransmission, the data further suggest that serotonin is involved in both the affective and appetitive symptoms of SAD. Indeed, the carbohydrate craving of these patients may constitute a kind of substance abuse in which the nutrient is eaten precisely for its serotonin-mediated psychotropic effects.
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PMID:Nutrient imbalances in depressive disorders. Possible brain mechanisms. 269 7

It has recently been proposed that alterations in central dopamine (DA) functional activity may, in part, account for certain behavioral changes observed in seasonal affective disorder (SAD) during the winter. To explore this possibility, a preliminary study of thermoregulatory heat loss to an endogenous heat challenge--a strongly DA-dependent process--was undertaken in groups of four SAD woman and four nonpsychiatric control women across three conditions (winter, after successful phototherapy, and summer). Homeostatic heat loss during recovery from heat challenge in SAD, but not in control, subjects was found to be a significant function of light condition and of clinical state. Thermoregulatory heat loss in SAD subjects was significantly blunted in winter during depression, was similar in efficiency to control subjects after a successful antidepressant response to phototherapy, and tended to be more efficient than controls in summer during a euthymic state. Results raise the possibility that a common effect of phototherapy and summer light conditions is a facilitation of central DA activity in SAD.
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PMID:Thermoregulatory response to thermal challenge in seasonal affective disorder: a preliminary report. 276 33

Ten patients with seasonal affective disorder received the following treatments for 5 days each: (a) artificial daylight (2500 lux) from 20.00 to 23.00 and from 07.00 to 10.00 hours; (b) red light (300 lux) from 20.00 to 23.00 and from 07.00 to 10.00 hours; (c) artificial daylight (2500 lux) from 22.00 to 23.00 and from 07.00 to 08.00 hours. The antidepressant effect of treatment (a) was superior to that of treatment (b), suggesting that the effect of light treatment in winter depression is more than that of a placebo. The antidepressant effect of treatment (a) was superior to that of treatment (c), although these two treatments equally suppressed plasma melatonin concentrations. Consequently, in these patients there is a dissociation between the effect of light treatment on melatonin and the reduction of depression ratings.
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PMID:Effects of light treatment upon mood and melatonin in patients with seasonal affective disorder. 279 32

Depression is a common condition in the practice of most physicians. Some depressed patients are prone to suicide, many ambivalent about it. The SAD PERSONS scale may be helpful for the physician in assessing risk. Because of the ambivalence, it is important that an authority figure-physician, friend, family member- not fail to recognize the risk and unthinkingly sanction a destructive act.
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PMID:To be or not to be: the suicidal patient. 279 77

Patients with seasonal affective disorder (SAD) report atypical symptoms of increased appetite, particularly "carbohydrate craving," increased body weight, and sleepiness, during their winter depression. To document feeding behavior in detail, a Food/Drink Frequency Questionnaire (FDFQ) was given to female control subjects and SAD patients at each of the four seasons. SAD patients consumed carbohydrate-rich foods (starch and not sweets) more often than controls (annual mean) and also showed a seasonal rhythm with maximum values in winter and minimum values in summer. In contrast, protein-rich food intake was identical in both groups and did not show seasonal variation. Fiber-rich food intake was also increased in SAD patients. SAD patients ate more meals per day, both at breakfast and in the second half of the day. Again, SAD patients showed seasonal changes of meal number with a minimum in summer. Body weight and body mass index did not undergo significant seasonal changes in the group as a whole, nor did SAD patients differ from controls. These atypical symptoms in SAD can be interpreted as a "medial hypothalamus syndrome" involving alpha 2-noradrenergic and serotonergic mechanisms.
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PMID:The four seasons: food intake frequency in seasonal affective disorder in the course of a year. 318 62


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