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)

Seasonal Affective Disorder (SAD) has received formal research attention only within the last eight years. Diagnostic criteria for SAD include many characteristics typical of depression: sadness, low self-esteem, lack of energy, social withdrawal, and suicide ideation, and features of atypical depression: carbohydrate craving, overeating, weight gain, and hypersomnia. Differential diagnosis of the disorder depends on an onset in fall/winter and remission in spring/summer. It was hypothesized that spinal cord injury (SCI) patients would have a higher incidence of the disorder in the northern latitudes because of decreased outdoor activities in winter and because of such light-depriving winter survival tactics as installing opaque plastic for storm windows. SCI patient responded to a postal survey which included Rosenthal's Seasonal Pattern Assessment Questionnaire (SPAQ) and the Beck Depression Inventory (BDI). Results showed a substantially higher rate of SAD among SCI patients than in the normative sample.
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PMID:Seasonal affective disorder in a spinal cord injury population. 158 5

Data for 401 depressed outpatients with mood reactivity who participated in a randomized trial comparing placebo, imipramine, and phenelzine were analyzed for predictors of differential response by stepwise multiple regression techniques. Features of the Columbia criteria for atypical depression including oversleeping, overeating, severe anergy, and pathologic rejection sensitivity were each predictive of a poorer response to imipramine than to phenelzine only when compared to those patients with none of the features. These features were not additive in their contribution to differential outcome. Lack of endogenous features was not predictive of a differential drug treatment response. Compared with patients who have no symptoms of atypical depression, patients with any of the four features had an inferior imipramine response rather than a superior phenelzine response. These analyses indicate that the clear differential responsivity to medication treatment in atypical depression is not simply related to any one defining symptom and that further correlates of this apparent biological heterogeneity need to be explored.
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PMID:Predictive value of symptoms of atypical depression for differential drug treatment outcome. 162 87

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.
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PMID:Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression. 181 84

Psychogenic influences on the immune system become evident via the nervous system, particularly in its paraspecific part and the parameters there of. On the one hand the sifting and systematization of the investigations carried out so far forces criticism and evaluation of methods, shows on the other hand however a number of important findings and conclusions, which can be deduced from this knowledge. (1) Immunosuppressive effects have to a great extent their roots in psycho-social influences, leading to an overtaxing of the human capacity to adapt; occupational stress, depression, helplessness, loneliness, hopelessness, lack of social support, suppression of emotional disturbance and aggression, psychological vulnerability, etc. (2) A psychogenic stimulation of the immune system is founded in certain personality traits (self-confidence, openness, etc.) and a life-style, which is characterized by security and support in the social sphere, by the ability to handle one's illness positively, by recognizing effective forms of coping with stress, as well as trust and faith in realizing the unlikely and a will to survive based on self-discipline. (3) Forms of hyperalimentation, malnutrition and wrong eating habits result in immunosuppressive effects and, in highly developed industrial countries, have their roots in stress situations, which cannot be coped with (e.g. stress due to separation from partner, stress connected with divorce, occupational stress, loneliness, helplessness, lack of social support, suppression of emotional disturbance and aggression, sleep deprivation, immobilization, etc.) and are therefore founded in variables of life-style and biography.
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PMID:[Psychogenic stimulation of the immune system by nutrition]. 205 87

Lead (Pb) depresses growth in infants and young children. Our earlier studies using a weanling rat model of Pb exposure suggest that this Pb effect is due to depression of appetite. In the present study we examined whether this depression of appetite is consistent with a down-regulation of the appetite "set point" as described using dietary manipulations following either lesions of certain hypothalamic regions or 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Two types of dietary manipulations were employed: (a) consumatory response to hyperalimentation (force-feeding), and (b) consumatory and growth response during the catch-up period following food restriction. In the hyperalimentation experiments, food intake was determined (a) with and without force-feeding, and (b) without Pb and with Pb administered either orally or systemically. Pb exposure reduced food consumption compared to controls. Force-feeding of a liquid diet further reduced food consumption, but only to the level that maintained total caloric intake at, or close to, the level of Pb animals not force-fed. In the food-restriction experiments, weanling rats had their food intake restricted for 4 days and then were provided free access to food, at which time one subgroup of these animals was exposed to Pb. Catch-up of previously food-restricted animals, in terms of food consumption and growth, was the same in the first 2 days, regardless of whether Pb was administered. During the next 10 days, the food intake and growth of the non-Pb-exposed, food-restricted animals gradually converged on the previously free-fed, non-Pb-exposed animals, whereas the food-restricted. Pb-exposed animals converged on the growth-depressed, previously free-fed Pb-exposed animals. All these responses to dietary manipulations are consistent with a reduced set point for appetite rather than with a nonspecific effect of Pb, e.g., aversion to food or general malaise.
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PMID:Lead exposure lowers the set point for food consumption and growth in weanling rats. 212 80

Similar symptomatology has been described for both seasonal affective disorder (SAD) and atypical depression. For example, hyperphagia, hypersomnia, and intense lethargy are common to both, suggesting that they might be subtypes of the same disorder. If SAD and atypical depression are different manifestations of the same underlying pathophysiology, treatment effective for one might also benefit the other. Bright artificial lights (2500 lux, 6-8 a.m. and p.m.) were significantly less effective in treating eight patients diagnosed as having atypical depression without a seasonal pattern than 25 SAD patients. Differential treatment outcome suggests that SAD and atypical depression are separate disorders.
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PMID:Is seasonal affective disorder a variant of atypical depression? Differential response to light therapy. 224 88

An investigation has been made with regard to the clinical picture of 87 terminally ill patients with lung cancer. It has yielded the following points. 1) Seven patients had been informed of their diagnosis. 2) Intravenous hyperalimentation was administered in 78 cases (90%), oxygen therapy in 68 cases (78%), and morphine in 35 cases (40%). 3) The most frequent cause of death in these patients was respiratory failure, due to progress of cancer, then infection, pleural, or pericardial effusion, or interstitial pneumonitis. 4) Psychic disturbances involved anxiety over breathing, depression, and delirium. In only 12% of the patients did the mental condition seem normal until death. 5) To deal with the dying patient's needs, it is necessary to establish proper treatment for the control of sensory dyspnea and for psychosocial support by a psychiatrist and other professionals for members of the family.
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PMID:[The clinical picture of terminally ill patients with lung cancer]. 250 34

Six self-rated items of interpersonal sensitivity (IPS) were examined in 174 depressed outpatients. These items were "feeling critical of others," "your feelings being easily hurt," "feeling others do not understand you or are unsympathetic," "feeling others are unfriendly," "feeling inferior to others," "feeling shy or uneasy with the opposite sex." The population was grouped into tertiles based on their pretreatment IPS score. High levels of IPS were associated with earlier onset and greater chronicity of depression, higher Hamilton Rating Scale for Depression (HRSD) score, more severe depressed mood, guilt, suicidality, impaired work and interest, retardation, depersonalization, paranoia, and cognitive symptoms of depression. More frequent atypical features were found, e.g., overeating/weight gain, self-pity, phobic avoidance, and panic attacks. Response to a monoamine oxidase (MAO) inhibitor drug increased at higher levels of IPS, while the response to a placebo decreased.
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PMID:Symptoms of interpersonal sensitivity in depression. 267 37

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

Increased O2 consumption was found in rats after bilateral lesions of the lateral hypothalamus (LH) or during voluntary overeating. This phenomenon appears to be mediated by the sympathetic nervous system (SNS) in both conditions, since it is blocked by the beta-blocker propranolol administration. In the first experiment we showed that the brain cortex is involved in the thermogenesis induced by LH lesion and this effect is mediated by SNS, since bilateral functional decortication induced by cortical-spreading depression (CSD) impaired the increase of O2 consumption to the same extent as administration of propranolol. In the second experiment the role played by the cerebral cortex on thermogenesis in rats during voluntary overeating of "cafeteria" diet and in control rats was investigated. Cafeteria rats showed a significantly higher colonic temperature, brown adipose tissue temperature (Tbat), and rate of O2 consumption than control animals. CSD led to a significant decrease of Tbat and O2 consumption in cafeteria rats but not in controls. On the basis of the results obtained in the two experiments, the possibility that the cerebral cortex could be involved in the metabolic responses for reduction of body weight to the "set-point" is hypothesized.
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PMID:Cortical control of thermogenesis induced by lateral hypothalamic lesion and overeating. 288 75


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