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A questionnaire that assessed a broad range of eating-related characteristics for unselected, normal subjects was factor analyzed in a two-step process proposed by Comrey (1984). Twelve "factored homogeneous item dimensions" were identified first and yielded three primary-level factors in a second factor analysis: Predisposition to Obesity (including Dieting and Preoccupation with, and Fear Of, Gaining Weight), Uncontrollable Urges to Eat (including Eating Momentum Beyond Control, Food a Panacea and Constant Temptation, and Secret Binging), and Predisposition to Anorexia (including Insufficient Eating Obvious to Others, Food Phobia, Inability to Eat, and Vomiting After Meals). The three primary-level factors were positively intercorrelated and exhibited significant positive, though weak, correlations with a measure of trait arousability. Also, weak results tentatively indicated that individuals with more pleasant and/or more arousable temperaments were less likely to be overweight. Subjects reported sharply higher levels of food consumption when feeling "depressed" (i.e., bored, lonely, sad) than when feeling "distressed" (i.e., uncomfortable, anxious, in pain). Uncontrollable Urges to Eat correlated positively and significantly with self-reports of food consumption while depressed, showing that those lacking control over eating ate especially more while feeling bored, lonely, or sad. Predisposition to Obesity correlated negatively and significantly with self-reports of food consumption while distressed, showing that those tending more toward obesity ate less while upset or anxious.
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PMID:Measures of eating-related characteristics for the general population: relationships with temperament. 1636 30

Cognitive attitudes and beliefs towards food and body shape are repeatedly reported as a maintaining factor of obesity. In order to assess evolution of those cognitions following a dietary treatment 18 overweight and obese females undergoing a dietary treatment were assessed using the Mizes Anorectic Cognitions questionnaire (revised form) before and after a 3-month moderate calorie restricted diet. Binge eating status was also assessed in pre-treatment. The main finding of the present study is persistence of anorectic cognitions following a moderate calorie restricted diet treatment, and furthermore a more pejorative evolution of those cognitions in patients with binge symptomatology.
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PMID:Persistence of anorectic cognitions following a moderate calorie restricted diet. 1680 36

Obesity is a major global epidemic, with over 300 million obese people worldwide, and nearly 1 billion overweight adults. Being overweight carries significant health risks, reduced quality of life, and impaired socioeconomic success, with profound consequences for health expenditure. The most successful treatment for obesity is gastric bypass surgery, which acts in part by reducing appetite through alterations in gut hormones. Circulating gut hormones, secreted or suppressed after eating food, act in the brain, particularly the hypothalamus, to alter hunger and fullness. Stomach-derived ghrelin increases food intake even in those with anorexia from chronic illness, while pancreatic polypeptide (PP), intestinal peptide YY 3-36 (PYY), oxyntomodulin, and other hormones reduce food intake and appetite. While obese subjects have appropriate reductions in orexigenic ghrelin, other gut-hormone disturbances may contribute to obesity such as reduced anorexigenic PYY and PP. Prader-Willi syndrome (PWS) arises from the loss of paternally inherited genes on chromosome 15q11-13, leading to life-threatening insatiable hunger and obesity from early childhood, through developmental brain, particularly hypothalamic defects. The study of genetically homogenous causes of abnormal-feeding behavior helps our understanding of appetite regulation. PWS subjects have inappropriately elevated plasma ghrelin for their obesity, at least partly explained by preserved insulin sensitivity. It remains unproven if their hyperghrelinemia or other gut-hormone abnormalities contribute to the hyperphagia in PWS, in addition to brain defects. Postmortem human hypothalamic studies and generation of animal models of PWS can also provide insight into the pathophysiology of abnormal-feeding behavior. Changes in orexigenic NPY and AGRP hypothalamic neurons, or anorexigenic oxytocin neurons have been found in illness and PWS. Functional neuroimaging studies, using PET and fMRI, will also allow us to tease apart the hormonal and brain pathways responsible for controlling human appetite, and their defects in obesity.
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PMID:The hypothalamus, hormones, and hunger: alterations in human obesity and illness. 1687 68

With one billion people overweight worldwide, the need to identify risk factors and treatments for obesity is urgent. The present study determined whether rats genetically prone to diet-induced obesity (DIO) show preexisting differences in meal microstructure and are sensitive to central anorectic effects of corticotropin-releasing factor type 2 (CRF(2)) receptor stimulation. Male, selectively bred DIO rats and their diet resistant (DR) counterparts (n = 9/genotype) were weaned onto low-fat chow and compared as young adults for spontaneous or intracerebroventricular urocortin 2 administration-induced (0, 0.3, 1, 3 microg) differences in ingestion. DIO rats were hyperphagic selectively at the dark cycle onset, showing shorter latencies to initiate feeding, faster returns to eating following meal completion, and a lower satiety ratio than DR rats. At other times, DIO rats had briefer postmeal intervals, but ate smaller and briefer meals, resulting in normal intake. DIO rats also ate faster than DR rats. Urocortin 2 was less potent in DIO rats, ineffective at the 0.3 microg dose, but produced CRF(2) antagonist-reversible anorexia at higher doses. Though heavier, chow-maintained DIO rats were proportionately as or more lean than DR rats. Thus, DIO rats showed signs of a preexisting, heritable deficit in the maintenance of postmeal satiety and a reduced sensitivity to anorectic CRF(2) agonist stimulation. The meal patterns of DIO rats temporally resemble human 'snacking' behaviour, which predicts adult obesity. Because central CRF(2) stimulation retains full anorectic efficacy at higher doses in the DIO model, manipulating this neuropeptidergic system might yield new therapeutic approaches for diet-induced obesity.
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PMID:Feeding microstructure in diet-induced obesity susceptible versus resistant rats: central effects of urocortin 2. 1762 84

In the first description of the night eating syndrome (NES) 1955 by Stunkard et al. the criteria included (1) consumption of at least 25% of the total calories for the day after the evening meal, (2) sleeplessness, at least until midnight more than one half of the time and (3) morning anorexia with negligible food intake at breakfast. Further studies altered these criteria step by step, without ever relating to the changes already made by other authors. So today our knowledge about NES and its related features is based on an amazing variety of constructs merely referred to by the same term. However, there seems to be an agreement about a higher prevalence of the NES in overweight and obese treatment seeking samples. The relationship between NES, body weight and a possible influence of NES on overweight and obesity remains unclear and needs to be further examined. In addition to the research activities regarding NES as a possible eating disorder, sleep disorder specialists showed a growing interest in patients with sleeplessness and nocturnal eating episodes. New definitions were developed: the "night eating/drinking syndrome" (synonymous: NES), a disorder occurring mainly in infancy and early childhood but also seen in adults. Today the less restrictive concept "sleep related eating disorder" (SRED) eliminated the NES-concept, but also states a sleep disorder that is not clearly distinguishable from NES described by several authors as a possible eating disorder. In psychosomatic research the criteria of nocturnal eating (recurrent awakenings & getting up to eat) was included in the NES by a growing number of authors in the last 15 years. Based on this diversity of diagnostic criteria in two different fields of expertise a lot of research was done do investigate the prevalence of NES and further describe patients with NES. Today a meaningful summary of these findings is not possible and despite a growing number of research in NES and obesity the clinical relevance of the concept NES remains unclear. In this article diagnostic criteria so far will be summarized and a rough differentiation of NES to related constructs and disorders will be given.
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PMID:[Night eating syndrome and nocturnal eating--what is it all about?]. 1840 50

The protein fragment nesfatin-1 was recently implicated in the control of food intake. Central administration of this fragment results in anorexia and reduced body weight gain, whereas antisense or immunological nesfatin-1 antagonism causes increased food intake and overweight. Nesfatin-1 is derived from the precursor nucleobindin-2 (NUCB2). To identify the neurocircuitry underpinning the catabolic effects of NUCB2/nesfatin-1, we have used in situ hybridization and immunohistochemistry to map the distribution of this protein and its mRNA in the rat CNS and performed double-labeling experiments to localize its expression to functionally defined neuronal populations. These experiments confirm previous observations but also present several novel NUCB2 cell populations. Both NUCB2 mRNA and nesfatin-like immunoreactivity was most concentrated in the hypothalamus, in the supraoptic, paraventricular, periventricular and arcuate nuclei and the lateral hypothalamic area/perifornical region. Additionally, outside of the hypothalamus, labeling was observed in the thalamic parafascicular nucleus, the Edinger-Westphal nucleus, locus coeruleus, ventral raphe system, nucleus of solitary tract and in the preganglionic sympathetic intermediolateral cell column of the spinal cord, and the pituitary anterior and intermediate lobes. In neurons, immunoreactivity was almost exclusively confined to perikarya and primary dendrites with virtually no labeling of axonal terminals. Double-labeling immunohistochemistry revealed colocalization of nesfatin with vasopressin and oxytocin in magnocellular neuroendocrine neurons, thyrotropin-releasing hormone, corticotropin-releasing hormone, somatostatin, neurotensin, and growth-hormone-releasing hormone in parvocellular neuroendocrine neurons, pro-opiomelanocortin (but not neuropeptide Y) in the arcuate nucleus and melanin-concentrating hormone (but not hypocretin) in the lateral hypothalamus. Furthermore, nesfatin was extensively colocalized with cocaine- and amphetamine-regulated transcript in almost all NUCB2-expressing brain regions. These data reveal a wider distribution of NUCB2/nesfatin-1 than previously known, suggesting that the metabolic actions of this protein may involve not only feeding behavior but also endocrine and autonomic effects on energy expenditure. In addition, the subcellular distribution of nesfatin-like immunoreactivity indicates that this protein may not be processed like a conventional secreted neuromodulator.
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PMID:Distribution and neuropeptide coexistence of nucleobindin-2 mRNA/nesfatin-like immunoreactivity in the rat CNS. 1876 Oct 59

The melanocortins (alpha, beta and gamma-melanocyte-stimulating hormones: MSHs; adrenocorticotrophic hormone: ACTH), a family of pro-opiomelanocortin (POMC)-derived peptides having in common the tetrapeptide sequence His-Phe-Arg-Trp, have progressively revealed an incredibly wide range of extra-hormonal effects, so to become one of the most promising source of innovative drugs for many, important and widespread pathological conditions. The discovery of their effects on some brain functions, independently made by William Ferrari and David De Wied about half a century ago, led to the formulation of the term "neuropeptide" at a time when no demonstration of the actual production of peptide molecules by neurons, in the brain, was still available, and there were no receptors characterized for these molecules. In the course of the subsequent decades it came out that melanocortins, besides inducing one of the most complex and bizarre behavioural syndromes (excessive grooming, crises of stretchings and yawnings, repeated episodes of spontaneous penile erection and ejaculation, increased sexual receptivity), play a key role in functions of fundamental physiological importance as well as impressive therapeutic effects in different pathological conditions. If serendipity had been an important determinant in the discovery of the above-mentioned first-noticed extra-hormonal effects of melanocortins, many of the subsequent discoveries in the pharmacology of these peptides (feeding inhibition, shock reversal, role in opiate tolerance/withdrawal, etc.) have been the result of a planned research, aimed at testing the "pro-nociceptive/anti-nociceptive homeostatic system" hypothesis. The discovery of melanocortin receptors, and the ensuing synthesis of selective ligands with agonist or antagonist activity, is generating completely innovative drugs for the treatment of a potentially very long list of important and widespread pathological conditions: sexual impotence, frigidity, overweight/obesity, anorexia, cachexia, haemorrhagic shock, other forms of shock, myocardial infarction, ischemia/reperfusion-induced brain damage, neuropathic pain, rheumathoid arthritis, inflammatory bowel disease, nerve injury, toxic neuropathies, diabetic neuropathy, etc. This review recalls the history of these researches and outlines the pharmacology of the extra-hormonal effects of melanocortins which are produced by an action at the brain level (or mainly at the brain level). In our opinion the picture is still incomplete, in spite of being already so incredibly vast and complex. So, for example, several of their effects and preliminary animal data suggest that melanocortins might be of concrete effectiveness in one of the areas of most increasing concern, i.e., that of neurodegenerative diseases.
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PMID:Brain effects of melanocortins. 1899 99

White coat hypertension (WCH) is most likely a disorder associated with metabolic syndrome. The study was performed at the Internal Medicine Polyclinic of Dumlupinar University on routine check-up patients. WCH cases who were overweight or obese and desiring weight loss were divided into two subgroups according to whether they preferred to achieve weight loss by medication or diet therapy. The study included 324 cases (204 females) with WCH, 45 of whom were in normal weight range. Therefore, 86.1% (279) of cases with WCH were either overweight or obese, and 41.3% (134) of all WCH cases had dyslipidemia. Twenty-five cases (14.7%) stopped metformin therapy due to excessive anorexia. At the end of a 6-month period, there were highly significant differences between the two groups with respect to the prevalences of resolved WCH, hyperbetalipoproteinemia, hypertriglyceridemia, dyslipidemia, overweight and obesity, and decreased fasting plasma glucose below 110 mg/dL (P < 0.001 for all). Due to gradually increased prevalences of impaired glucose tolerance, type 2 diabetes mellitus, dyslipidemia, excess body weight, and obesity-like disorders from sustained normotension towards WCH and hypertension (HT) cases, and very high prevalences of excess weight and dyslipidemia in the WCH group, WCH may be an associated disorder of metabolic syndrome rather than just being a predisposing factor of atherosclerosis or HT alone. Thus, the management of WCH should not focus solely on the regulation of blood pressure with antihypertensive medications, but rather on the prevention of future excess weight and various associated disorders, and metformin alone is an effective therapeutic option, most likely due to its powerful inhibitory effect on appetite.
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PMID:Treatment of white coat hypertension with metformin. 1907 83

Migraine is a common episodic headache disorder characterized by attacks that consist of various combinations of headache and neurologic, gastrointestinal and autonomic symptoms. Migraine with aura may be due to neuronal hyperexcitability, perhaps from cortical disinhibition. It is likely that headache results from the activation of meningeal and blood vessel nociceptors combined with a change in central pain modulation. Antiepileptic drugs are increasingly being recommended for migraine prevention since placebo-controlled, double-blind trials prove them to be effective. Topiramate is a structurally unique antiepileptic drug that was discovered by serendipity. It is a derivative of the naturally occurring monosaccharide D-fructose and contains sulfamate functionality. Topiramate may bind to membrane channel complexes at phosphorylation sites in the inner loop and, thereby, allosterically modulate ionic conductance through the channels. The topiramate MIGR-001, MIGR-002 and MIGR-003 trials represent the largest controlled trials of a migraine preventive agent ever performed. Treatment with 100 or 200 mg/day of topiramate was associated with significant reductions in migraine frequency, migraine days and the number of migraine attacks per month. Topiramate was also associated with a reduced use of acute medications. The most common adverse events were difficulty with concentration and attention, difficulty with memory, mood problems, anorexia and weight loss, paresthesias, hypoesthesia and language problems. Topiramate is a first-line migraine preventive drug and should be considered preferentially for all patients in whom weight gain is a concern, who are currently overweight or who have coexistent epilepsy or bipolar disease.
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PMID:Topiramate in migraine prevention. 1981 Aug 79

A two-step interview study of eating disorders (EDs) and sub-clinical EDs in 15-year-old adolescents was carried out in western Finland. The sample consisted of all ninth graders in a well-defined catchment area (n=606, 98.2% of eligible students). In the first step, a self-report questionnaire was administered at schools regarding mental health problems and life circumstances. The questions concerning anorectic and bulimic eating pathology were formulated according to the DSM-IV diagnostic criteria of EDs. The second step consisted of a semi-structured interview Rating of Anorexia and Bulimia-Teenager version (RAB-T) to which 128 subjects were invited, on the basis of their answers to questions about eating pathology in the questionnaire. The participation rate in the interview was 88.3%. The lifetime prevalence rate for anorexia nervosa (AN) in 15-year-old girls was 1.8% and the point prevalence rate 0.7%. No cases of AN were found among the boys. All criteria fulfilling cases of bulimia nervosa (BN) were not found in our sample. High rates of AN not otherwise specified (AN-NOS; 4.9%) and sub-clinical EDs (4.9%) were found among the girls; 6.7% of girls and 0.6% of boys were regarded as being "at risk" of developing EDs. Data on height and weight are based on current measurements taken at school healthcare; 22% of boys were overweight or obese compared with 16% of girls.
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PMID:Obesity and eating disturbances are common in 15-year-old adolescents. A two-step interview study. 1988 93


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