Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is the first comprehensive description of winter depression (WD), as part of seasonal affective disorder (SAD), from Norway, and one of the very few from so far north. A total of 128 media-recruited people had first been screened with the Seasonal Pattern Assessment Questionnaire and were thereafter personally interviewed. The criteria for DSM-III-R mood disorder, seasonal pattern, were satisfied by 85%, whereas 73% satisfied the criteria of Rosenthal et al. for SAD. Seven percent were diagnosed as subsyndromal SAD. The main characteristics of our patient group were in reasonable accordance with other clinical SAD materials: there were 81% women; the mean age was 44 years (range: 20 to 76); the mean age for SAD debut was 24 years (range: 4 to 71); and the duration of WD was most often from October to March or April. Only 12% had ever been manic or hypomanic in summer. During their WD, most patients suffered at least one of the symptoms hypersomnia, hyperphagia or carbohydrate craving; 16% also had a craving for fatty food in winter, but this may be considered "normal" at this northerly latitude.
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PMID:Characteristics of winter depression in the Oslo area (60 degrees N). 821 3

The consumption of excess calories as carbohydrates (CHO)-rich, protein-poor snacks characterizes the overeating of obese CHO cravers, premenstrual women, patients with Seasonal Affective Disorder, and former smokers. This specific appetite for CHOs may involve brain serotonin, as the synthesis and release of this neurotransmitter can increase following consumption of CHO-rich foods. To examine whether weight loss produced by serotoninergic drugs involves a selective reduction in CHO intake, obese females who consumed at least 30% of their daily calories from CHO-rich snacks were treated with dexfenfluramine ([DF] 15 mg b.i.d.); fluoxetine ([FL] 20 mg t.i.d.); or placebo (PL) for 12 weeks. Weekly weight loss for 25 of 29 PL completers was 0.22 kg +/- 0.06 (mean +/- SEM); for 21 of 28 DF completers, 0.56 +/- 0.08 kg; and for 18 of 30 FL completers, 0.58 +/- 0.09 kg (PL < DF = FL; p = .039). Seven FL subjects, 2 PL subjects, and 1 DF subject withdrew from the study due to side effects; other withdrawals were due to intercurrent illness or personal problems. Prior to treatment, subjects consumed over 40% of their daily CHO intake from snacks. Both of the drugs selectively decreased CHO snack intake (p < 0.05); DF, but not FL, also decreased meal CHO intake (p < .025). These results suggest that weight loss following treatment with serotoninergic drugs may relate to a selective decrease in CHO appetite.
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PMID:Dexfenfluramine, fluoxetine, and weight loss among female carbohydrate cravers. 828 Mar 44

Thirty-four patients with seasonal affective disorder, winter depression type (WD) were randomly distributed to receive the selective monoamine oxidase-A inhibitor moclobemide (400 mg daily) or placebo in a double-blind, parallel group study lasting for up to 14 weeks. Severity measures were the Montgomery-Asberg Depression Rating Scale (MADRS) extended with characteristic symptoms of WD; summed score of the "atypical" symptoms hypersomnia, hyperphagia and carbohydrate craving; and Clinical Global Impressions (CGI). After 3 weeks, patients with unsatisfactory response were switched to open moclobemide. Three patients on placebo dropped out before 3 weeks. Extended MADRS and CGI showed no significant difference between the groups at 3 weeks, whereas the atypical score was reduced significantly more on moclobemide than on placebo already after one week. Nonresponders after 3 weeks (9 of 16 on moclobemide and 7 of 15 on placebo) improved rapidly after being given open moclobemide. Predictor analysis showed a remarkably high negative correlation between improvement at 3 weeks (extended MADRS) and age in the placebo group and a strong, nonsignificant trend in the same direction in the moclobemide group. Dichotomizing the patients according to the median age (45 years) resulted in a somewhat better effect of moclobemide than placebo in the older age group. There were no significant differences in side effects between moclobemide and placebo.
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PMID:Treatment of winter depression in Norway. II. A comparison of the selective monoamine oxidase A inhibitor moclobemide and placebo. 829 82

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression. Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression. In a series of studies, commencing in patients with Cushing's disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide. In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.
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PMID:Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. 859 44

The aim of the present study was to examine whether high or low levels of platelet monoamine oxidase (MAO) activity were associated with an increased risk of winter seasonal affective disorder (SAD) or of developing characteristic vegetative symptoms during episodes of the disorder. We also investigated the relationship between MAO activity and the Global Seasonality Scale (GSS), a measure of seasonal variation in sleep length, social activity, mood, weight, appetite, and energy level. Patients with SAD (n = 49), patients with subsyndromal SAD (n = 11), and normal volunteers (n = 25) participated in the study. We found significantly higher levels of platelet MAO activity in females but did not observe significant differences across age groups or between groups of patients tested in different seasons or mood states. MAO activity (whether high or low) was not associated with a significant increase in risk of SAD or of developing hypersomnia, hyperphagia, or carbohydrate craving during episodes of winter depression. We found no significant relationship between GSS and MAO activity. Patients who had made suicide attempts during an episode of SAD had significantly lower mean levels of platelet MAO activity than other patients.
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PMID:Platelet monoamine oxidase activity in patients with winter seasonal affective disorder. 880 38

The authors examined the rates of atypical depression and prevalence of specific atypical symptoms in patients with seasonal versus non-seasonal depression. Fifty-three patients with seasonal affective disorder (SAD) were compared to 54 patients with non-seasonal major depressive disorder (MDD) using the atypical depression diagnostic scale (ADDS). SAD patients scored significantly higher than non-seasonal MDD patients in hyperphagia and hypersomnia, and significantly lower in interpersonal sensitivity and other rejection avoidance. There was no difference in the rate of ADDS diagnosis of atypical depression. Differences between atypical depression and SAD suggest that they are separate subtypes of depression with an overlapping symptom picture.
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PMID:Atypical depressive symptoms in seasonal and non-seasonal mood disorders. 918 1

This study was designed to evaluate the antidepressant effect of negative ions in the ambient air as a potential treatment modality for seasonal affective disorder. Twenty-five subjects with winter depression underwent a double-blind controlled trial of negative ions at two exposure densities, 1 x 10(4) ions/cm3 or 2.7 x 10(6) ions/cm3, using an electronic negative ion generator with wire corona emitters. Home treatments were taken in the early morning for 30 min over 20 days, followed by withdrawals. The severity of depressive symptoms (prominently including the reverse neurovegetative symptoms of hypersomnia, hyperphagia, and fatigability) decreased selectively for the group receiving high-density treatment. Standard depression rating scale assessments were corroborated by clinical impressions. When a remission criterion of 50% or greater reduction in symptom frequency/severity was used, 58% of subjects responded to high-density treatment while 15% responded to low-density treatment (chi 2 = 5.00, df = 1, p = 0.025). There were no side effects attributable to the treatment, and all subjects who responded showed subsequent relapse during withdrawal. Treatment with a high-density negative ionizer appears to act as a specific antidepressant for patients with seasonal affective disorder. The method may be useful as an alternative or supplement to light therapy and medications.
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PMID:Treatment of seasonal affective disorder with a high-output negative ionizer. 939 4

Seasonal affective disorder (SAD) is a condition characterized by annually occurring major depressive episodes which was described by Rosenthal et al. in 1984. It occurs most commonly in women and the onset usually being in early adulthood. These episodes are regularly occurring in fall and winter with full remission during the following spring and summer. The patient's mood is a combination of depression and mild anxiety accompanied by fatigue, loss of libido, and a profound reduction of socialisation. During winter depression, most of these patients complain of atypical vegetative symptoms accompanied by hypersomnia, hyperphagia, carbohydrate craving, and weight gain. Hypotheses on the underlying mechanisms of these behavioral and neurovegetative disorders indicate that environmental variables, e.g., climate, latitude, light, and changes in neurotransmitter fraction that naturally occur with the seasons may be important. Phototherapy is being increasingly used for the treatment of seasonal affective disorder. The antidepressant effect of light therapy in the treatment of SAD has been widely shown. The response in patients with SAD is contingent on the exposure of the patients' eyes to light. Further important factors are the duration of daily treatment and light intensity. However, the role of timing of phototherapy remains controversial. The biological basis of the diverse psychological and biological changes in SAD and the underlying mechanisms of action of phototherapy are still unclear and require further study.
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PMID:[Seasonal depression]. 945 88

Winter depression (seasonal affective disorder, SAD) is characterised by a seasonal major depressive episode in the last 2 years. Hypersomnia, carbohydrate-craving and weight-gain are specific traits. These patients preferentially seek help from their General Practitioner. Current research on the aetiology of SAD covers fields such as retinal deficiency, phase-disturbance of the internal circadian rhythms given by internal oscillators and neuro-endocrinologically expressed disorders, assuming that melatonin is the main mediator of human circadian systems in the CNS. Disorders of neurotransmitters (serotonin) are another cue. Recent longitudinal studies show a prevalence of seasonal depressive symptoms in up to 10% of the general population. Among patients treated for depression, the prevalence of SAD is even higher. The SAD sex-ratio of women to men of 3 to 1 is found repeatedly. SAD becomes rare above the age of 50. Effectiveness of phototherapy is showed in nearly all controlled studies. Bright light appears to be most effective for patients with mild SAD. Hypersomnia and hyperphagia seem to be predictors of response to bright light therapy. To enable evaluation of unspecific therapeutic factors in phototherapy a true placebo for bright light-studies is still to be found. Possible new indications for photo therapy are currently being explored. Bright light for non- seasonal depression has been tested with encouraging results; panic disorders seem to have features in common with SAD; effectiveness in bulimia has been suggested and recently sleep disorders in elderly patients have been successfully and substantially diminished.
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PMID:[Winter depression and phototherapy. The state of the art]. 952 84

This study aimed to determine symptom patterns in patients with chronic fatigue syndrome (CFS), in summer and winter. Comparison data for patients with seasonal affective disorder (SAD) were used to evaluate seasonal variation in mood and behavior, atypical neurovegetative symptoms characteristic of SAD, and somatic symptoms characteristic of CFS. Rating scale questionnaires were mailed to patients previously diagnosed with CFS. Instruments included the Personal Inventory for Depression and SAD (PIDS) and the Systematic Assessment for Treatment Emergent Effects (SAFTEE), which catalogs the current severity of a wide range of somatic, behavioral, and affective symptoms. Data sets from 110 CFS patients matched across seasons were entered into the analysis. Symptoms that conform with the Centers for Disease Control and Prevention (CDC) case definition of CFS were rated as moderate to very severe during the winter months by varying proportions of patients (from 43% for lymph node pain or enlargement, to 79% for muscle, joint, or bone pain). Fatigue was reported by 92%. Prominent affective symptoms included irritability (55%), depressed mood (52%), and anxiety (51%). Retrospective monthly ratings of mood, social activity, energy, sleep duration, amount eaten, and weight change showed a coherent pattern of winter worsening. Of patients with consistent summer and winter ratings (n = 73), 37% showed high global seasonality scores (GSS) > or = 10. About half this group reported symptoms indicative of major depressive disorder, which was strongly associated with high seasonality. Hierarchical cluster analysis of wintertime symptoms revealed 2 distinct clinical profiles among CFS patients: (a) those with high seasonality, for whom depressed mood clustered with atypical neurovegetative symptoms of hypersomnia and hyperphagia, as is seen in SAD; and (b) those with low seasonality, who showed a primary clustering of classic CFS symptoms (fatigue, aches, cognitive disturbance), with depressed mood most closely associated with irritability, insomnia, and anxiety. It appears that a subgroup of patients with CFS shows seasonal variation in symptoms resembling those of SAD, with winter exacerbation. Light therapy may provide patients with CFS an effective treatment alternative or adjunct to antidepressant drugs.
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PMID:Chronic fatigue syndrome and seasonal affective disorder: comorbidity, diagnostic overlap, and implications for treatment. 979 Apr 93


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