Serum electrolytes as markers of vomiting in bulimia nervosa.

OBJECTIVE: Patients with bulimia nervosa often have serum electrolyte abnormalities that result from vomiting and/or laxative or diuretic use. Thus, serum electrolytes could serve as an objective marker of such behaviors. METHOD: This study is a retrospective examination of serum electrolyte levels and vomiting behavior in 138 bulimic women, and of serum electrolyte levels in 70 control women. RESULTS: Logistic regression analyses demonstrated that only potassium values distinguished bulimic subjects from controls. Potassium levels below the lower limit of normal (3.7 mg/l) occurred only in the bulimic group. DISCUSSION: Abnormally low values for potassium are a specific, but not sensitive, predictor of recent vomiting episodes.

Refeeding, metabolic rate, and weight gain in anorexia nervosa: a review.

Patients with anorexia nervosa require refeeding to restore normal body weight. A variety of studies have examined the role of metabolic rate in the refeeding of anorectic patients. Several measurement techniques have been used to divide metabolic rate into its components: basal metabolic rate, resting energy expenditure, activity-induced thermogenesis, and dietary-induced thermogenesis. In anorexia nervosa patients several consistent findings are present. First, the number of kilocalories required for weight gain or weight maintenance increases as weight increases. Second, over 50% of the body mass gained in anorectic individuals represents fat tissue. Finally, both a history of bulimic symptoms and a higher premorbid body weight may lead to lower calorie requirements. These findings suggest the need for gradual increase in calories provided throughout treatment; resting energy expenditures may aid the determination of caloric requirements

Preference for NaCl solutions in sham drinking Sprague-Dawley rats: water deprivation, sodium depletion, and angiotensin II.

Male Sprague-Dawley rats were fitted with closable gastric fistulas and were then tested under closed fistula (real intake) and open fistula (sham intake--fluids drain from the stomach without appreciable absorption) conditions in one of three states: fluid deprivation, sodium depletion, and infusion of angiotensin (Ang) II. Water and various concentrations of NaCl were offered to drink in 1-h one- or two-bottle intake tests. In Experiment 1, water-deprived rats with closed fistulas drank more 0.15 M NaCl than either water or 0.3 M NaCl, offered in one-bottle tests. In sham drinking tests, the intake decreased monotonically as NaCl concentration increased. In two-bottle tests, water was greatly preferred over NaCl solutions. In Experiment 2, sodium-depleted rats preferred NaCl over water, again demonstrating a peak intake at 0.15 M in closed fistula conditions. However, with the fistula open the intakes of 0.05 and 0.15 M were similar, and 0.45 M considerably lower. In Experiment 3, Ang II-infused rats consumed both water and NaCl in two-bottle tests in both open and closed fistula trials. The quantity ingested on sham trials was only modestly elevated over real intake trials with Ang II compared with sham tests in Experiments 1 and 2.

Bone mineral density and anorexia nervosa in women.

OBJECTIVE: A review of reports of reduced bone mineral density in women with anorexia nervosa was undertaken in order to profile specific risk factors, which could then be used as the basis for suggestions for future research and treatment. METHOD: Thirteen research studies and four case studies of reduced bone mineral density and fractures in women with anorexia nervosa were reviewed. The relationships between bone mineral density and amenorrhea, estrogen, calcium intake, physical activity, parathyroid hormone, alkaline phosphatase, 1,25-dihydroxyvitamin D, cortisol, and growth hormone were examined in the reports of these studies and other reports of altered physiology during anorexia nervosa. RESULTS: The average spinal, radial, and femoral bone mineral density in anorexic women was significantly lower than it was in normal control subjects. Concurrent with the low intake of nutrients by individuals with anorexia nervosa, low body weight, early onset and long duration of amenorrhea, low calcium intake, reduced physical activity, and hypercortisolism appeared more likely to contribute to decreased bone mineral density than did other abnormal aspects of the disorder. CONCLUSIONS: Future research needs to address how such factors as amenorrhea and hypercortisolism affect bone mineral density in anorexia nervosa. Since no controlled trials of estrogen replacement or calcium supplementation in anorexia nervosa have been reported, the proper treatment for decreased bone mineral density is not known. However, the most obviously important intervention is to encourage medical stabilization and weight gain.

Sham drinking in rats: osmotic and volumetric manipulations.

Male rats, fitted with indwelling gastric fistulas, were tested with either a closed fistula (normal drinking) or an open fistula (sham drinking) following either intracellular dehydration (with NaCl), extracellular dehydration (with PEG), or the combination of the two stimuli. In normal drinking tests, the combined stimulus induced an intake of water that was the sum of the individual effects. In sham-drinking tests, both NaCl- and PEG-treated rats drank up to twice that of their normal drinking counterparts, but those given NaCl + PEG showed no such increase. Various body fluid measurements confirmed the persistence of the respective dehydration states at the end of sham-drinking sessions. The relatively poor or absent sham drinks after these stimuli are contrasted with vigorous sham drinking following fluid deprivation. In a second experiment, sham drinking following NaCl injections did not improve with repeated testing, but intake after intravenous infusion of NaCl did show some increase but was still modest and slow compared with that after fluid deprivation.

Postingestional modulation of drinking induced in rats by angiotensin II: intragastric infusion and sham drinking studies.

The dipsogenic potency of angiotensin II (ANGII, 200 micrograms/kg, SC) was examined after the removal of various postingestional factors. In the first experiment, rats with intragastric catheters were injected SC with ANGII and allowed water to drink. During the induced drinking, either NaCl (1.5 M) or water was injected into the stomach via the catheter at a rate of 0.1 ml for each ml water ingested orally. The water intake was identical in the two conditions. In a second experiment, rats, fitted with gastric fistulas, were administered ANGII and subsequent water intake with fistulas open was compared to that occurring with the fistulas closed. Rats drank more water during the first trial with fistulas open than with fistulas closed. Water intake during subsequent trials with an open fistula rose above that observed on the first trial. In a third experiment, rats with gastric fistulas were offered 0.15 M NaCl to drink. Intake was greater when the fistula was open than when it was closed. Intake of 0.15 M NaCl increased during the second trial with fistula open. Rats drank more 0.15 M NaCl during the first trial with an open fistula in Experiment 3 than those rats given water to drink on their first trial with fistula open in Experiment 2. These data suggest both oropharyngeal and postingestional factors interact in the control of ANGII-induced fluid intake.

Role of anorexia and behavioral activation in amphetamine-induced suppression of feeding: implications for understanding tolerance.

In order to gain further insight into the mechanism of contingent tolerance to amphetamine anorexia (Carlton & Wolgin, 1971), an attempt was made to determine the role of anorexia and behavioral activation (increased locomotion and/or stereotypy) in the initial suppression of feeding produced by the drug. Rats administered chronic injections of either saline or amphetamine (2 or 4 mg/kg) were given milk either directly into the mouth through an intraoral cannula or in a standard drinking tube. It was reasoned that although drug-induced anorexia would affect intake with both methods of feeding to the same degree, the disruptive effect of behavioral activation would be greater in bottle-fed rats. The results revealed that bottle-fed rats given amphetamine showed substantially greater suppression of intake than cannula-fed rats. Saline-treated rats showed almost identical milk intake with the two methods. Recovery of intake occurred in all drugged rats except those given 4 mg/kg and fed by bottle. In the tolerant groups, rats fed by bottle and given 2 mg/kg recovered at a faster rate than cannula-fed rats at either dose. These results demonstrate that in the normal drinking condition, the initial suppression of intake is caused by a combination of anorexia and behavioral interference and that tolerance occurs to both of these effects.

Amphetamine tolerance and body weight set point: a dose-response analysis.

The theory that amphetamine anorexia and tolerance reflect the lowering of a set point for body weight regulation was evaluated. In the first experiment, rats given either 2 or 4 mg/kg d-amphetamine and access to milk ultimately achieved comparable levels of tolerance and maintained their weight at 94%-96% of control levels. Thus, the level of maintained body weight was not dose-dependent. In the second experiment, increasing the doses resulted in renewed anorexia and weight loss, and the appearance of behavioral stereotypies. Whereas mean intake then recovered, body weight remained at 79%-82% of control levels. However, milk intake for individual rats was extremely variable. Such variability is inconsistent with the notion that body weight was actively regulated by caloric intake. Drug withdrawal had little further effect on intake, and it led to weight "rebound" in only one group. When subsequently retested with the original doses, both groups were again anorexic and showed more intense stereotypy. This finding suggests that drug withdrawal caused a general increase in sensitivity to amphetamine, rather than a set-point-related change in feeding. Taken together, the data do not support the set point theory of amphetamine tolerance.