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)

Directly measured food intake in 31 overweight female smokers to test whether (a) calorie and carbohydrate intakes increase after smoking cessation and (b) double-blind d-fenfluramine (30 mg), a serotonin-releasing drug, suppresses weight gain, overeating, and dysphoric mood associated with stopping smoking. Placebo-treated patients grew dysphoric after smoking withdrawal and ate 300 kcal/day more from 2 to 28 days after, showing a 3.5-lb weight gain. Fat and protein intakes did not change, but carbohydrate intake increased (30% to 40%). D-fenfluramine prevented postcessation dysphoria. Although drug-treated patients ate more carbohydrate snacks just after quitting, they returned to baseline by 4 weeks, showing a 1.8-lb weight loss. Agents that enhance brain serotonin-mediated neurotransmission may help prevent weight gain, overeating, and dysphoric mood after smoking withdrawal.
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PMID:Weight gain and withdrawal symptoms after smoking cessation: a preventive intervention using d-fenfluramine. 187 94

The utility of bipolar type II affective disorder subgrouping is discussed. There is low diagnostic agreement among clinicians for this putative condition. However, the clustering of cases in families and the poor response to standard treatments suggest that it is a distinct subgroup. The clinical features of the depressive phase of this condition including chronicity, intermittency, hyperphagia, hypersomnia, and reactivity relate it to the constructs of "hysteroid dysphoria," atypical depression, and seasonal affective disorder. Its association to several abnormal motivated behaviors such as alcoholism and eating disorders allows the speculation that a distinct morbid mechanism involving serotonin may underlie it and that new serotonin reuptake blocking drugs may be useful in treating it. Finally, the genetic identity of this subgroup in all likelihood will be established or rejected by genetic linkage studies utilizing the restriction fragment length polymorphism map of the genome.
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PMID:Therapeutic and genetic prospects of an atypical affective disorder. 332 66

A general theory of heritable personality traits and their neurobiological basis is described. Three independent dimensions of personality are defined and related to heritable variation in patterns of response to specific types of environmental stimuli: 'novelty seeking' is due to a heritable tendency toward frequent exploratory activity and intense excitement in response to novel stimuli; 'harm avoidance' is due to a heritable tendency to respond intensely to aversive stimuli and to learn to avoid punishment, novelty, and non-reward passively; and 'reward dependence' is due to a heritable tendency to respond intensely to reward and succorance and to learn to maintain rewarded behavior. Evidence suggests that variation in each dimension is strongly correlated with activity in a specific central monoaminergic pathway: novelty seeking with low basal dopaminergic activity, harm avoidance with high serotonergic activity, and reward dependence with low basal noradrenergic activity. These neurobiological dimensions interact to give rise to integrated patterns of differential responses to punishment, reward, and novelty. The combination of high novelty seeking, high reward dependence, and low harm avoidance (histrionic personality) or the combination of high harm avoidance, low reward dependence, and low novelty seeking (obsessional personality) are each associated with information-processing patterns that lead to unreliable discrimination of safe and dangerous situations and hence to chronic anxiety. In individuals with high novelty seeking, chronic anxiety is characterized by global uneasiness or alarm without specific premonitory cues, frequent bodily pains due to low pain and sensation thresholds, low sedation threshold, and slow fatigability. In contrast, in individuals with high harm avoidance, chronic anxiety is characterized by frequent anticipatory worries based on specific cues, high pain and sedation thresholds, and easy fatigability. In response to frustrative non-reward, individuals with high reward dependence are susceptible to compensatory noradrenergic hyperactivity and hence acute or recurrent states of agitated dysphoria associated with reward-seeking behaviors such as overeating and increased sexual activity. Specific predictions are made about normal personality development as well as the development and familial aggregation of anxiety, somatoform, depressive and personality disorders. These predictions are compared with available information, and recommendations are made for future research.
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PMID:A unified biosocial theory of personality and its role in the development of anxiety states. 380 56

Thirty-two patients who complained of episodes of ravenous overeating which they felt unable to control (bulimia) were asked to describe their behaviour and symptoms. There was considerable variation both between and within individuals, but a number of factors were defined which appeared to be common to all with the complaint. It is difficult to set up strict criteria for the recognition of bulimia, and those that have recently been proposed are criticized in the light of our present findings. Bulimia is usually associated with an excessive concern about body weight. It occurs in patients with anorexia nervosa, in whom it is often a relatively early feature of the illness, but it is also found in subjects of normal weight or obese subjects who have never been emaciated. Episodes of bulimia are usually preceded by dysphoric mood states. The gorging may alleviate the dysphoria temporarily, but many patients later experience negative feelings such as depression and self-depreciation. The ability to induce vomiting after a bulimic episode is a major influence determining the clinical presentation.
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PMID:How patients describe bulimia or binge eating. 695 5

There is significant evidence that altered dopamine activity plays a role in seasonal affective disorder (SAD). The current study examined three separate genetic hypotheses for SAD related to the 7-repeat allele (7R) of the dopamine-4 receptor gene (DRD4), a variant associated with decreased affinity for dopamine. We examined the possible contribution of 7R to the overall expression of SAD, attention deficit disorder (ADD) comorbidity, and body weight regulation. As part of an ongoing genetic study of increased eating behavior and mood in female subjects, 108 women with winter SAD and carbohydrate craving/weight gain were administered the Wender-Utah Rating Scale to measure childhood ADD symptomatology, and a questionnaire to assess maximal lifetime body mass index (BMI). To test for an association between 7R and the categorical diagnosis of SAD, the transmission disequilibrium test (TDT) was used in a subsample of probands providing familial DNA. Standard parametric tests were used to compare childhood ADD symptoms and maximal lifetime BMI across the two genotypic groups defined by the presence or absence of 7R. The TDT found no initial evidence for an association between 7R and the categorical diagnosis of SAD. However, 7R carriers reported significantly greater inattention and dysphoria in childhood (p=0.01 and 0.001, respectively) and a higher maximal lifetime BMI (p=0.007) than did probands without this allele. Furthermore, excluding probands with extreme obesity (maximal BMI >40), a strong correlation was found linking childhood inattentive symptoms and maximal lifetime BMI (r=0.35, p=0.001). In overeating women with SAD, the 7R allele of DRD4 may be associated with a unique developmental trajectory characterized by attentional deficits and dysphoria in childhood and mild to moderate obesity in adulthood. This developmental course may reflect different manifestations of the same underlying vulnerability related to central dopamine dysfunction. Given the possibility of population stratification when studying genotype/phenotype relationships, future use of genomic controls and replication of our findings in other overeating and/or ADD populations are needed to confirm these initial results.
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PMID:Childhood inattention and dysphoria and adult obesity associated with the dopamine D4 receptor gene in overeating women with seasonal affective disorder. 1456 Mar 22

Sensory, physiological and psychological mechanisms are reviewed that underlie emotional influences on food choice. Both moods and emotions are considered. Eating a meal will reliably alter mood and emotional predisposition, typically reducing arousal and irritability, and increasing calmness and positive affect. However, this depends on the meal size and composition being close to the eater's habit, expectations and needs. Unusual meals--e.g. too small, unhealthy--may negatively affect mood. Sweetness, and sensory cues to high energy density, such as fatty texture, can improve mood and mitigate effects of stress via brain opioidergic and dopaminergic neurotransmission. However, adaptation in these pathways, perhaps enhanced by inherited sensitivity, with chronic exposure to such sensory qualities, could lead to overeating of energy-dense foods and consequent obesity. Sweet, fatty foods low in protein may also provide alleviation from stress in vulnerable people via enhanced function of the serotonergic system. Moreover, in rats, such foods seem to act as part of a feedback loop, via release of glucocorticoid hormones and insulin, to restrain activity of the hypothalamic pituitary adrenal axis during stress. However, this effect is also associated with abdominal obesity. In humans, a number of psychological characteristics predict the tendency to choose such foods when stressed, such as restrained or emotional eating, neuroticism, depression and premenstrual dysphoria, all of which could indicate neurophysiological sensitivity to reinforcing effects of such foods. Greater understanding of such predictive traits and the underlying mechanisms could lead to tailoring of diet to meet personal emotional needs.
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PMID:Emotional influences on food choice: sensory, physiological and psychological pathways. 1654 3

Withdrawal from psychostimulants, including methamphetamine, induces a depressive state associated with lethargy, dysphoria, hyperphagia and psychomotor retardation. Previous work with repeated administration of amphetamine in rats has shown that amphetamine withdrawal produces decreased motivation to work for a non-drug reward, and this withdrawal is reversed by administration of a dopamine partial agonist. The purpose of the present study was to examine decreased motivation to work for a non-drug reward during methamphetamine withdrawal and explore the effects of a dopamine agonist, dopamine partial agonist, and indirect monoamine agonist on methamphetamine withdrawal. During withdrawal from repeated methamphetamine administration, rats showed reduced responding for a sweet solution in a progressive-ratio schedule of reinforcement, and this effect was significantly more pronounced than previously observed with amphetamine. Repeated systemic treatment with the dopamine partial agonist terguride (0.2 and 0.4 mg/kg, i.p., twice daily), the full dopamine agonist ropinirole (1 mg/kg, i.p., twice daily), and acetyl-L-carnitine (60 and 100 mg/kg, i.p.), a compound with a potential antidepressant effect, during methamphetamine withdrawal restored responding for the sweet solution, suggesting that these drugs may represent potential therapeutic strategies for the treatment of methamphetamine addiction during the withdrawal phase.
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PMID:Effects of terguride, ropinirole, and acetyl-L-carnitine on methamphetamine withdrawal in the rat. 1664 7

This report describes and compares four current concepts and definitions of atypical depression. Since its emergence, atypical depression has been considered a depressive state that can be relieved by MAO inhibitors. Davidson classified the symptomatic features of atypical depression into type A, which is predominated by anxiety symptoms, and type V, which is represented by atypical vegetative symptoms, such as hyperphagia, weight gain, oversleeping, and increased sexual drive. Features that are shared by both subtypes include: early onset, female predominance, outpatient predominance, mildness, few suicide attempts, nonbipolarity, nonendogeneity, and few psychomotor changes. Based on these features, bipolar depression can also be defined as atypical depression type V. Herein, we examine and classify four concepts of atypical depression according to the endogenous-nonendogenous (melancholic-nonmelancholic) and unipolar-bipolar dichotomies. The Columbia University group (see Quitkin, Stewart, McGrath, Klein et al.) and the New South Wales University group (see Parker) consider atypical depression to be chronic, mild, nonendogenous (nonmelancholic), unipolar depression. The former group postulates that mood reactivity is necessary, while the latter asserts the structural priority of anxiety symptoms over mood symptoms and the significance of interpersonal rejection sensitivity. For the Columbia group, the significance of mood reactivity reflects the theory that mood nonreactivity is the essential symptom of "endogenomorphic depression", which was proposed by Klein as typical depression. Thus, mood reactivity is not related to overreactivity or hyperactivity, which are often observed in atypical depressives. However, Parker postulates that psychomotor symptoms are the essential features of melancholia, which he recognizes as typical depression; therefore, the New South Wales group does not recognize the significance of mood reactivity. The New South Wales group accepts the relationship between anxiety symptoms and interpersonal rejection sensitivity, while the Columbia group does not recognize the importance of anxiety symptoms because they could not identify a relationship between such symptoms and the efficacy of MAO inhibitors. The concept of atypical depression proposed by the New South Wales group overlaps considerably with that of hysteroid dysphoria, which was proposed by Klein et al., and was the progenitor of Columbia group's concept of atypical depression. The Pittsburgh University group (see Himmelhoch, Kupfer, Thase et al.) and the soft bipolar spectrum group (see Akiskal, Perugi, Benazzi et al.) regard atypical depression as a depressive state that can be observed in bipolar disorder. The former groups takes into account reversed vegetative symptoms and lethargy as signs of bipolar disorder, while the latter recognizes that atypical depression shares features with bipolar II disorder or soft bipolar spectrum disorder. The soft bipolar spectrum group maintains their unique concept of bipolar disorder, which regards some unipolar depressions as bipolar disorder, while the Pittsburg group continues to share the conventional concept of a unipolar-bipolar dichotomy with other groups. The fundamental pattern of atypical depression is represented by chronic mild depressions, which are characterized by a younger age at onset, female predominance, interpersonal rejection sensitivity, and mood lability, which are difficult to distinguish from a characterological pathology. Patients who present with such patterns are frequently diagnosed with borderline, histrionic, or avoidant personality disorders; therefore, we must recognize the significance of atypical depression as a concept that can suggest the utility of medication for these patients. For such patients, however, various groups have proposed different kinds of definition and therapeutic guidelines that are difficult to synthesize and utilize in clinical settings. Moreover, some features of atypical depression outlined in the Columbia University criteria, such as a younger age at onset, chronicity, mildness, and female predominance, were excluded from DSM-IV. Consequently, the concept of atypical depression has become overextended and gradually lost its construct validity. Therefore, the diagnostic criteria for atypical depression should be reconsidered in reference to various definitions and concepts and refined through accumulated clinical research.
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PMID:[The modern concept of atypical depression: four definitions]. 2018 36

Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.
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PMID:Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms. 2520 50