Nutritional status in anorexia nervosa: clinical chemistry, vitamins, iron and zinc

Routine clinical chemical variables and parameters of the vitamin, iron and zinc status were measured in 20 female patients with anorexia nervosa (AN) and in 10 lean and 10 normal weight, healthy, female control subjects. Patients with AN had higher activities of L-gamma-glutamyl transferase (gamma-GT) and glutamate pyruvate transaminase (SGPT) and a higher concentration of prealbumin in serum and lower leucocyte and lymphocyte counts in blood. For the other routine clinical chemical parameters no significant differences between the groups were observed. AN patients had higher serum vitamin B12 and retinol levels. No significant differences were found for the status parameters of thiamin, vitamin B6, vitamin C, folate, vitamin E and vitamin D. Contradictory results were obtained for the riboflavin status: AN patients had a lower level of flavin adenine dinucleotide (FAD) in blood and a lower stimulation ratio of the glutathione reductase activity in erythrocytes (alpha-EGR). Patients with AN had higher serum ferritin concentration and lower total iron binding capacity (TIBC). However, haemoglobin (Hb), haematocrit (Ht) and iron saturation were not significantly different. No significant difference was found in the concentration of zinc in plasma. In spite of the poor intake of nutrients and energy, the results obtained did not indicate an inadequate status of vitamins, iron and zinc in patients with AN.     

β-Endorphin and adrenocortical function in obesity

OBJECTIVE: To test the hypothesis that the hyperendorphinaemia in obesity originates from outside the pituitary. DESIGN: Intravenous administration of corticotrophin-releasing hormone (CRH) after overnight suppression with 2 mg of dexamethasone in normal-weight controls and in obese subjects before and after weight reduction. PATIENTS: Eleven obese females, age (mean +/- SEM) 30 +/- 2.1 years, body mass index (BMI) 41.2 +/- 1.9 kg/m2. Eight normal-weight females served as controls, age 26 +/- 2.1 years, BMI 21.4 +/- 0.5 kg/m2. Five obese subjects were also studied after weight loss of 18.4 +/- 1.0% of original weight. MEASUREMENTS: Plasma beta-endorphin, ACTH and cortisol. Cortisol production rate in 24-hour urine. Basal (without dexamethasone suppression) plasma beta-endorphin levels. RESULTS: Basal (without dexamethasone suppression) beta-endorphin levels were 7.7 +/- 0.8 pmol/l in the obese and 3.8 +/- 0.5 pmol/l in the control subjects (P less than 0.005). The degree of suppression of beta-endorphin after dexamethasone was similar in the obese (23.2 +/- 3.7%) and in the control subjects (28.2 +/- 0.12%). Administration of CRH following dexamethasone suppression resulted in a small but significant increase of plasma beta-endorphin in both obese (from 1.55 +/- 0.12 to 2.32 +/- 0.28 pmol/l) and control subjects (from 0.98 +/- 0.24 to 1.69 +/- 0.33 pmol/l). The groups did not differ regarding this response, nor regarding the release of ACTH and cortisol after CRH. Cortisol production rate was higher (P less than 0.001) in the obese (68.7 +/- 3.3 mumol/24 h) than in the controls (40.0 +/- 3.0 mumol/24 h). No correlation between cortisol production rate and basal beta-endorphin levels was found. Weight loss appeared to have no influence on cortisol production rate, basal beta-endorphin levels, or on the responses to dexamethasone or CRH. CONCLUSIONS: Plasma beta-endorphin in obese subjects can be affected by manipulations of the hypothalamic-pituitary-adrenocortical axis; the hypothesis that the hyperendorphinaemia of obesity originates from outside the pituitary cannot be confirmed.     

Effect of serotonin re-uptake inhibition by fluoxetine on body weight and spontaneous food choice in obesity.

The effect of fluoxetine on body weight and spontaneous food choice was studied in twenty-three healthy, non-depressed, obese females on an outpatient basis. After a one week placebo run-in period, subjects were randomized to receive either fluoxetine (FXT) 60 mg daily (n = 11) or placebo (P) (n = 12) for 6 weeks in a double blind study design. BMI (35.2 +/- 0.8 vs 36.4 +/- 1.3 kg/m2, mean +/- s.e.m.) and age (38.1 +/- 239 vs 37.3 +/- 2.7 years) were not different in either group. No specific diet was prescribed. On four separate days per 14 days food records were collected. Data were analysed with the use of food composition tables. Statistical analysis was performed using Student's t test for independent samples for data on body weight and calorie intake. Macro-nutrient composition of the diet was analysed using multivariate analysis of variance and post hoc Student's t test for independent samples. All subjects lost weight during fluoxetine treatment. Mean (+/- s.e.m.) weight loss in the fluoxetine treated group was 3.6 +/- 0.5 kg, compared to a mean weight gain of 0.3 +/- 0.5 kg in the placebo treated group (P less than 0.001). In all patients food intake was reduced during fluoxetine treatment and this reduction could fully account for the observed weight loss. The mean total caloric intake per day was significantly lower during fluoxetine treatment compared with placebo (FXT 1123 +/- 118 kcal vs P 1845 +/- 87 kcal, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynamic exercise discloses different time-related responses in stress hormones

OBJECTIVE: Responses to stressful events are generally regarded as reactions of the organism to accommodate to or compensate for stress. This reaction is classically described as an activation of the sympathoadrenal system and the hypothalamic-pituitary-adrenocortical (HPA) axis. Activation of the release of growth hormone and prolactin in blood also occurs during various types of stress. Assuming that the stress response is a neuroendocrine mechanism that occurs in anticipation of physical exercise, we investigated whether an incremental exercise protocol can be used as a model stressor to disclose a distinct pattern of activation in these hormonal systems, which would support the notion that these systems have different roles in preparing the organism for physical activity and recovery. Moreover, such a model may help improve our understanding of the endocrine expressions of psychological stress. METHODS: After an overnight fast, 8 healthy men (age, 19-26 years) cycled at 40, 60, 80, and 100% of the power output at VO2max in successive time blocks of 10 minutes each up to exhaustion. Venous blood was sampled immediately before exercise, at the end of each block, and during the recovery phase 5 and 30 minutes after exercise. Plasma adrenalin and noradrenalin were measured by high-performance liquid chromatography; plasma adrenocorticotropic hormone, beta-endorphin, cortisol, growth hormone, and prolactin were measured by specific immunoassays. Heart rate and levels of blood lactate and adrenalin were measured as markers of workload-related responses. RESULTS: Results showed that increases in heart rate, lactate, adrenalin, noradrenalin, and growth hormone reflected the relative workload, in contrast to increases in adrenocorticotropic hormone, beta endorphin, and prolactin, which were observed only after exercise reached an intensity of 80% VO2max. Increases in cortisol were found just after exhaustion. The delayed response of cortisol may be initiated by a drop in blood glucose levels but may also be considered preparatory to vigorous muscular effort and protective against tissue damage. CONCLUSIONS: Measurement of the cumulative response to exercise shows that activation of stress hormones occurs at different time points, supporting the notion that these hormones have different roles in preparing the organism for physical activity and recovery: ie, workload- and effort-related adaptation on one hand and protection against disturbed homeostasis on the other. The delayed response of the HPA axis during incremental exercise contrasts with the nondelayed HPA axis response observed during psychological stress and points to involvement of different neurobiological and cognitive emotional mechanisms.     

Analysis of seasonal training volume and working capacity in elite female rowers.

Preceding the 1988 Olympic Games 6 elite female rowers were regularly subjected to an exercise test on a rowing ergometer (REM-test) with a time interval of about 5 weeks. Daily training volume was analysed in terms of rowed kilometres (RKM) and training time (TOTMIN, rowing and land training). The purpose of this study was to investigate the training volume during a season and to study possible changes in the working capacity of elite female rowers. The REM-test consisted of 3 consecutive blocks: 3 min warming up, 5 min standard load at anaerobic threshold and 2 min "all-out". Blood lactic acid concentration (LA) was determined for the construction of a LA-power curve. The power at 4.0 mmol/l (P4) was estimated as a measure of the aerobic capacity. The "all-out" score was used for calculating the maximal power (PM). Results show that both RKM and TOTMIN increase (range resp. 40-400% and 20-25%) when compared with the initial value. P4 also increases, in parallel with changes in both RKM and TOTMIN, with 8-10% of the initial value. PM increases continuously during the season up to 10% of its initial value. However, based on maximal heart rate and lactate values, it is concluded that PM was maximal in only 15% of the tests. Our data suggests that evaluation of training volume in elite female rowers is better done with P4 than with PM. The behaviour of P4 shows a parallel with the seasonal changes in the training load.(ABSTRACT TRUNCATED AT 250 WORDS)