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February 4, 2002 - Midnight raids of refigerators more than appetite; Night Eating Syndrome may be related to the performance of the body -- not the mind
A study results published in the February 2002 edition of the American Journal of Physiology -- Endocrinology and Metabolism indicate that the midnight raid on the refrigerator may not be just appetite.
According to new research findings by Norwegian physiologists, the midnight raid on the refrigerator may not be the product of an insatiable appetite. Instead, the night eater may be suffering from a failure of the body to respond appropriately to stress. In addition to irregular eating habits, this condition can lead to a number of harmful psychological and physical disorders. Night eating syndrome will soon join the ranks of conditions related to the performance of the body, and not state of mind.
The anatomical and functional relationships between the nervous system and the endocrine apparatus of the night eating syndrome has previously been described as changes in the circadian rhythm (biologic variations or rhythms with a cycle of about 24 hours) by a nocturnal rise of plasma concentrations of melatonin and leptin and an increased circadian secretion of the steroid hormone, cortisol.
Cortisol, melatonin, and leptin are regulatory hormones with typical circadian rhythms that regulate various physiological and metabolic functions. Another main regulator is the hypothalamic-pituitaryadrenal (HPA) axis, which coordinates several biological functions. The circadian rhythms represent the biological endocrine clock, whereas the HPA represents the stress-induced biological response. However, the interplay between these two main regulators of biological functions is not well understood. Therefore, observations of irregular secretions of circadian neuroendocrine secretions inclusive of cortisol are of special interest, as the night eating syndrome most likely represents changes in the HPA axis.
The aim of this study was to test the hypothesis that night eaters have an overexpressed hypothalamic-pituitary-adrenal axis with a diminished response to stress.
The authors of "Hypothalamic-Pituitary-Adrenal Axis in the Night Eating Syndrome" are Grethe S. Birketvedt, Johan Sundsfjord, and Jon R. Florholmen, all from the University of Tromsų, Tromsų, Norway. Their findings are published in the February 2002 edition of the American Journal of Physiology -- Endocrinology and Metabolism.
This study investigated the neuroendocrine patterns of subjects with night- ating syndrome. Five female night eaters and corresponding age and weight-matched healthy controls were recruited, with the night-eaters diagnosed with the consumption of >50 percent of the daily food intake after 8:00 PM and with one or more nighttime awakenings associated with food intake.
Night-eating episodes were recorded for seven consecutive days. Subjects were then admitted to the Clinical Research Center at 8:00 AM after an overnight fast. Shortly after admission, blood samples were drawn from an indwelling catheter during the next 150 min. After an observation period of 30 min of rest in bed, 100g of corticotropin-releasing hormone (CRH; corticorelin human trifluoroacetat) were injected intravenously, and the response parameters of ACTH (adrenocorticotropic hormone) and cortisol levels in plasma were measured.
The subjects stayed in bed during the observation period. Blood was collected in precooled glass tubes containing 20 mmol EDTA and 1,000 KIU aprotinin) per milliliter blood and were kept on ice until centrifugation at 4°C and storage at -27°C. Cortisol and ACTH were then measured using commercial immunoassay.
The significance of differences between the two groups in the plasma concentrations at time point 0 was evaluated by a Wilcoxon's rank sum test. The significance of differences between the two groups in the changes in plasma concentrations (after subtracting the levels at baseline, 0 min) during the CRH test was evaluated by repeated-measures multivariate analysis of variance. P >0.05 was considered statistically significant.
The incidence of night-eating episodes during the seven 7-day observation period was 3.2 + 0.5 among the night eaters, whereas among the healthy controls no night eating episodes took place.
The results showed that, in night eaters compared with controls, the CRH-induced ACTH and cortisol response was significantly decreased to 47 percent and 71 percent, respectively. Disturbances in the hypothalamic-pituitary-adrenal axis with a diminished ACTH and cortisol response to CRH were found in subjects with night eating syndrome.
The study found that:
The results indicate that the night eating syndrome is associated with a reduced pituitary-adrenal response to CRH.
The elevated plasma levels of cortisol reflect increased activity of CRH, as expressed by an attenuated ACTH and cortisol response that may well explain the disrupted sleep and appetite pattern observed in night eaters. Several other disorders, such as obesity, fatigue syndrome, anorexia nervosa, bulimia nervosa , insomnia, and depression, have been linked to disturbances in the HPA axis. All of these disorders share some phenotypes with the night eaters, such as mood disruptions, eating disorders, and sleeping disorders. Whether these clinical features are the result of common pathophysiological mechanisms in the HPA axis remains to be clarified and awaits further studies.
The authors also concluded that subjects suffering from night eating episodes have signs of disturbances in the HPA axis with an attenuated ACTH and cortisol response to CRH. The mechanisms behind the increased CRH stimulation may involve alterations in the neurotransmitter systems, causing increased nocturnal appetite and disruption in the sleep pattern. This may, to some extent, explain the disturbances in the circadian secretions of melatonin and leptin and the behavioral characteristics of the night eating syndrome.