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Biomedical subjects

D T George

Publications and source records attributed to D T George.

At least 73 records · Page 4Linked to original sources
PubMed1988

Bingeing behavior and plasma amino acids: a possible involvement of brain serotonin in bulimia nervosa.

It has been suggested that bingeing and vomiting behavior may be an attempt to suppress hunger or reduce dysphoria. Theoretically, such relationships could involve a mechanism whereby bingeing and vomiting change plasma amino acids which, in turn, enhance brain serotonin-mediated satiety and/or improvement in mood. This hypothesis is based on data showing that the intake of dietary carbohydrates increases the uptake of tryptophan (TRP), the precursor of serotonin, into the brain by increasing the plasma TRP ratio (the ratio of the plasma TRP concentration to the summed concentrations of other amino acids that compete with TRP for brain uptake). Plasma prolactin (PRL) release might reflect the activation of this system. We found that an increase in the TRP ratio during bingeing and vomiting was associated with satiety (i.e., cessation of bingeing and vomiting), but not change in mood. In other words, bulimic subjects who developed an increased plasma TRP ratio during bingeing and vomiting had fewer cycles of bingeing and vomiting and a greater increase in plasma PRL than did subjects who did not develop an increase in the plasma TRP ratio. This study raises the possibility that an increase in the TRP ratio may be associated with the termination of bingeing and vomiting, perhaps due to its effects on brain serotonin metabolism.

Amino Acids↗
PubMed1988

CSF somatostatin in anorexia nervosa and bulimia: relationship to the hypothalamic pituitary-adrenal cortical axis.

The eating disorders, anorexia nervosa and normal weight bulimia, are associated with disturbances of hypothalamic-pituitary-adrenal cortical (HPA) and growth hormone function. Because somatostatin (SRIF) is one of the neuropeptides known to modulate feeding behavior and neuroendocrine systems, we measured cerebrospinal fluid (CSF) concentrations of this peptide in patients with eating disorders. CSF SRIF concentrations in patients with anorexia nervosa, both at low weight and after weight recovery, were similar to those in controls. When normal weight bulimic women stopped binging, they had a modest but significant increase in CSF SRIF. CSF SRIF was not related to plasma growth hormone concentrations but did show relationships to HPA axis hormones. Healthy volunteer women had a significant positive relationship between CSF SRIF and CSF corticotropin releasing hormone (CRH). In underweight anorectics, CSF SRIF was negatively related to both 24-hr urinary free cortisol and plasma cortisol concentrations after dexamethasone, but it was not significantly related to CSF CRH. These relationships more closely resembled those of healthy controls after weight correction. In bulimics, CSF SRIF was positively related to CSF CRH and negatively related to plasma cortisol. Our findings support a previously described relationship between CSF SRIF and HPA axis activity. The differences in SRIF-HPA relationships in anorectics and bulimics may constitute or reflect pathophysiological distinctions between these disorders.

Adult↗
PubMed1988

Relative importance of calorie intake needed to gain weight and level of physical activity in anorexia nervosa.

We assessed whether level of physical activity of anorexia nervosa patients could influence caloric consumption needed to gain weight during hospitalization. Seventy-three percent of patients with anorexia nervosa had higher levels of motor activity than did healthy female volunteers. Anorectics required 8301 +/- 2272 kcal (mean +/- SD) to gain 1 kg body wt. Activity levels and caloric consumption needed to gain 1 kg were significantly correlated; the most active patients needed to consume more calories to gain weight. A median split of anorectic patients by level of activity showed that the group with lower activity levels gained 1 kg every 5.1 +/- 1.2 d, whereas the group with higher activity levels gained 1 kg every 7.2 +/- 1.9 d. These data suggest that the rate of weight gain can be accelerated, and the cost of hospitalization decreased, by restricting exercise in anorectics during refeeding.

Adult↗
PubMed1987

Reduced cerebrospinal fluid levels of immunoreactive pro-opiomelanocortin related peptides (including beta-endorphin) in anorexia nervosa.

The discovery that the endogenous opioid peptides contribute to the modulation of appetitive behavior and neuroendocrine function has raised questions as to whether disturbances of opioids contributes to the pathophysiology of eating disorders. To assess central nervous system (CNS) beta-endorphin in patients with anorexia nervosa we measured cerebrospinal fluid (CSF) beta-endorphin concentrations before, and at intervals after weight correction. In addition, we measured three sister peptides (beta-lipotropin, adrenocorticotropic hormone (ACTH), and the N-terminal fragment) derived from the same precursor molecule, pro-opiomelanocortin (POMC) to determine whether possible disturbances might extend to sister peptides. Underweight anorectics (58 +/- 5% of average body weight (ABW), n = 10) had significantly lower CSF concentrations of all 4 peptides compared to healthy controls (102 +/- 10% ABW, n = 11). CSF concentrations of all 4 POMC-related peptides were found to be significantly increased when the same anorectics were restudied 4 to 6 weeks after weight gain (83 +/- 4% ABW). After weight gain, levels of CSF beta-endorphin, beta-lipotropin, and ACTH were similar to controls, whereas levels of CSF N-POMC remained significantly less than controls. Another group of women, previously underweight with anorexia nervosa, but weight-restored (93 +/- 11% ABW, n = 12) for greater than 1 year had CSF concentrations of all 4 POMC-related peptides that were similar to controls. We conclude that underweight anorectics have state-associated disturbances of CNS beta-endorphin as well as other POMC-related peptides. These abnormalities are part of the neurobiological syndrome of anorexia nervosa and may contribute to the characteristic alterations in behavior and neuroendocrine function.

Adrenocorticotropic Hormone↗
PubMed1987

Comparison of lactate-induced anxiety in bulimic patients and healthy controls.

Clinical symptomatology and diagnostic interview studies suggest that patients with bulimic disorder have some characteristics in common with patients with generalized anxiety disorder or panic disorder. The purpose of this study was to compare sodium lactate-induced physiological responses and anxiety symptoms in hospitalized normal weight bulimic patients and healthy controls. Bulimic patients had significantly elevated anxiety ratings at baseline, and showed a trend toward greater increases in anxiety ratings after lactate administration. Lactate-induced anxiety did not provoke an urge to binge in the bulimic patients. In keeping with the specificity of lactate-induced panic attacks in panic disorder, none of the bulimic subjects experienced a panic attack during lactate infusion.

Adult↗
PubMed1987

Effect of pregnancy on panic attacks.

Three women with panic disorder showed marked improvement in their panic symptoms during pregnancy. Such effects might be due to pregnancy's blunting of the sympathoadrenal response to simple physiologic stimuli, effects on barbiturate receptors, or improvement in psychological functioning.

Adult↗
PubMed1987

Elevated cerebrospinal fluid levels of immunoreactive corticotropin-releasing hormone in anorexia nervosa: relation to state of nutrition, adrenal function, and intensity of depression.

To study the pathophysiology of hypercortisolism in anorexia nervosa, we measured the cerebrospinal fluid (CSF) levels of corticotropin-releasing hormone (CRH) in patients when they were underweight and at intervals after weight restoration. CSF CRH levels were significantly elevated in hypercortisolemic underweight patients. Both CSF CRH levels and pituitary-adrenal function normalized after weight recovery. A significant positive correlation was found between CSF CRH levels and depression ratings in weight-corrected patients. We conclude that the hypercortisolism of anorexia nervosa reflects a defect at or above the hypothalamus which results in the hypersecretion of endogenous CRH. The positive correlation between CSF CRH and depression in the weight-restored patients is compatible with previous data indicating increased CRH secretion in the depressed phase of primary affective disorder and supports the notion of a relationship between CRH and depressive symptomatology. Moreover, these data are compatible with observations that depression is part of the anorexia nervosa syndrome.

Adrenal Glands↗
PubMed1986

Relationship of mood alterations to bingeing behaviour in bulimia.

Twelve women with bulimia participated in a study in which they binged and vomited on the day after hospital admission. Caloric intake, time spent bingeing and vomiting, and self-reported mood ratings demonstrated much variation from subject to subject. Both subjective and objective ratings of mood indicated that anxiety decreased more frequently and to a greater extent than depression, both during and after bingeing and vomiting. The present data, obtained in a controlled setting, tend to confirm previous information on binge episodes obtained by self-report from bulimic patients. Bingeing and vomiting episodes may provide bulimic patients with a physiological mechanism for temporarily relieving a dysphoric mood state.

Adult↗
PubMed1985

Adrenocorticotropin-stimulated adrenal androgen secretion in anorexia nervosa: impaired secretion at low weight with normalization after long-term weight recovery.

Adrenal androgen secretion is decreased in patients with anorexia nervosa. To assess the reversibility of the decreased secretion with recovery of body weight, we measured ACTH-stimulated adrenal androgen levels at different stages of recovery. Basal plasma GH and somatomedin-C levels also were measured, because both have been proposed as potential stimuli for adrenal androgen secretion. When studied at low body weight [58 +/- 3% (+/- SEM) ideal BW], women with anorexia nervosa had decreased ACTH-stimulated levels of dehydroepiandrosterone (DHA), DHA sulfate (DHAS), and androstenedione and decreased DHA to cortisol, DHAS to cortisol, and androstenedione to cortisol ratios compared to normal women. Women who had recently completed a refeeding program (within 2-4 weeks, 81 +/- 2% ideal BW) had an increased somatomedin-C level compared to low weight patients, but similar ACTH-stimulated adrenal androgen levels. Long term weight-recovered women (86 +/- 4% ideal BW, recovery for more than 6 months, with resumption of menses), however, had significant increases in ACTH-stimulated DHA and DHAS levels and DHA to cortisol and DHAS to cortisol ratios, and their hormone levels and ratios were not different from those in normal women. GH levels fell during weight recovery, although the values in the three patient groups did not differ significantly. We conclude that the recovery of adrenal androgen secretion while GH levels were falling provides evidence against a direct effect of GH as a stimulus for adrenal androgen secretion. The recovery of somatomedin-C before the recovery of adrenal androgens, however, and the positive correlation between plasma somatomedin-C and the integrated level of plasma DHAS (r = 0.50; P less than 0.02) are consistent with the hypothesis that somatomedin-C is a stimulus for adrenal androgen secretion.

Adrenal Glands↗
PubMed1984

Symptom perception by nonpsychiatric physicians in evaluating for depression.

A questionnaire was constructed and used to assess the perception of symptoms of a depressive disorder by nonpsychiatric physicians in patient evaluations. Results showed that respondents consistently perceived depression as resulting from psychological rather than biological factors. It is suggested that such perception on the part of physicians may hinder consolidation of a patient's symptom complex with the degree of certainty necessary for a diagnostic consideration of depressive disorder.

Attitude of Health Personnel↗
PubMed1983

Recognition and treatment of depression in a family medicine practice.

To test the hypothesis that depression is significantly underdiagnosed in general medical settings, the Zung Self-Rating Depression Scale was administered to 1,086 family medicine outpatients seen during a 12-month period before their initial medical examination. The effects of such screening on clinical recognition and treatment of depression were examined. Of the 1,086 patients, 143 (13.2%) were symptomatically depressed. These patients were randomized into two groups: 102 were identified as clinically depressed to their physician, and the remaining 41 were not (control group). Physicians diagnosed depression in 15% of the control group and in 68% of the identified group. At 4-week follow-up, 64% of the identified patients who were treated with maprotiline (16 of 25) showed improvement; only 28% of the identified patients who were electively not treated improved. Improvement occurred in only 18% of the control group. It appears that the diagnosis of depression is not ordinarily made in family medicine outpatient settings and that self-rating depression scales are useful diagnostic aids, whose regular use is indicated by the high prevalence of depression in general medical populations.

Adult↗
PubMed1981

The metabolic response to yellow fever immunization: protein-sparing modified fast.

The metabolic response to yellow fever immunization was investigated in five obese patients who were consuming a protein-sparing modified fast for 3 wk. Fasting 1/2, 1, and 2 h postprandial values for insulin, glucagon, glucose, lactate, beta hydroxybutyrate, acetoacetate, and free fatty acids were assessed before and the 1st, 3rd, and 5th day after immunization. The hormone and substrate responses to meat ingestion in patients well adapted to a protein-sparing modified fast and prior to infection was a rise in glucagon, no change in insulin, lactate, or ketone bodies and slight increase in serum free fatty acid and glucose levels. Over the entire period a significant (p less than 0.01) postprandial rise in glucagon was noted. Significant increases in insulin (p less than 0.01) and lactate (p less than 0.01) and falls in beta hydroxybutyrate (p less than 0.01) and acetoacetate (p less than 0.01) were noted in the postinfection period. There was also a significant interaction of diet and infection to increase insulin levels (p less than 0.05). The clinically mild infection produced by yellow fever immunization elicits a metabolic response which thus may be useful to investigate intermediary metabolism in the hospital setting.

Adult↗
PubMed1981

Effect of diet on the metabolic response to infection: protein-sparing modified fast plus 100 grams glucose and yellow fever immunization.

The metabolic response to yellow fever immunization was investigated in four obese subjects who were consuming a protein-sparing modified fast plus 100 g glucose (PSMF + 100 g) for 3 wk. Fasting, 1/2, 1, and 2 h postprandial values for insulin, glucagon, glucose, lactate, beta hydroxybutyrate, acetoacetate, and free fatty acids were assessed before and the 1st, 3rd, and 5th day postimmunization. The hormone and substrate response to dietary protein plus glucose was a substantial rise in insulin (p less than 0.005), glucose (p less than 0.005), and fall in free fatty acid and ketone levels (p less than 0.005). These results are distinctly different from the response to dietary protein ingestion only (PSMF) determined in a previous study which was a slight rise in insulin and glucose and slight fall in ketone bodies, but a substantial rise in glucagon. The only significant (p less than 0.05) change following immunization in the PSMF + 100 g was a rise in serum glucagon on day 1. During the PSMF significant elevations in insulin and lactate and falls in serum ketones were noted postimmunization. The metabolic response to mild infection is dependent on the diet consumed. These differences may have a clinical impact when the infection is severe, but this possibly requires study in an experimental infection of greater severity.

Adolescent↗
PubMed1980

A probable endocrine basis for the depression of ketone bodies during infectious or inflammatory state in rats.

The effects of infection with Streptococcus pneumoniae, Francisella tularensis, and Venezuelan equine encephalitis virus as well as inflammatory stress induced by the administration of turpentine and endotoxin on plasma ketone bodies and insulin were studied in white rats. All of the infectious/inflammatory stresses caused a significant decrease in the ketonemia of fasting and an elevation of plasma insulin. When a pneumococcal infection was initiated in a diabetic rat, inhibition of fasting ketonemia did not occur. Similarly, pneumococcal infection in the hypophysectomized rat did not result in a noticeable depression of either fasting ketonemia or plasma FFA. The increase in circulating insulin appears to be closely correlated with the inhibition of fasting ketonemia noted in the infectious/inflammatory stress.

Animals↗