Assessment of body composition in anorexic patients.
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Biomedical subjects
Publications and source records attributed to C M Shapiro.
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It has been reported that the change in photoperiod induced by the occurrence of daylight saving time has an effect on psychiatric presentation. We therefore investigated the impact of daylight saving time in three conditions: (1) parasuicide presentations; (2) psychiatric outpatient contacts, and inpatient admissions; (3) registered suicides. Results indicate that neither the change in photoperiod nor the effect of a small change in circadian rhythm associated with daylight saving time has an effect on 'cases' in any of the three conditions.
Many established methods of measuring body composition are time consuming and require complex equipment which is not generally available. Bioelectrical impedance analysis is a technique which utilises the difference in conductivity between fat and lean tissues at radiofrequencies. It uses inexpensive equipment which is simple to use and does not involve the use of ionising radiation. We have evaluated this technique in 44 studies on 38 anorexic females with a wide range of body mass index. Fat free mass was obtained from the mean of three established methods. The initial calibration was derived from 21 studies on 19 anorexics. Fat free mass was regressed against impedance and body habitus parameters to establish the prediction equation with the smallest standard error (1.12 kg). Values of fat free mass derived using this prediction equation were then compared with the other methods in a prospective study. The error of the bioelectrical impedance technique compares favourably with the established methods, even in anorexic patients with very low body mass index.
We investigated the effect of a 12-week physical training programme on the sleep of nine unfit women. Data were collected at 0, 4, 8 and 12 weeks of the training programme. Changes in fitness were assessed by changes in maximal oxygen consumption (VO2max) and onset of blood lactate turn point (LTP). Lean body mass (LBM) was calculated from total body potassium measurements. The all-night sleep recordings were made following days during which the subjects carried out their normal daily routines and did no extra exercise. Although cardiorespiratory fitness improved significantly as indicated by an increase in both VO2max and LTP, there was no change in LBM. The improvement in cardiorespiratory fitness did not result in any changes in the sleep parameters measured. Other workers have reported an improvement in sleep quality in eight army recruits during their basic training. The male recruits showed improved cardiorespiratory fitness and an increase in muscle bulk. These results suggest that increased fitness only facilitates sleep when there is an associated increase in LBM. Alternatively it may be that the response of sleep to improved fitness is sex-linked.
The secretion of prolactin and growth hormone (GH), together with subjective ratings of sedation and hunger, were determined in 13 in-patients with anorexia nervosa and 15 controls during the intravenous infusion of L-tryptophan (100 mg/kg). Prolactin responses were not different between groups but GH responses were markedly blunted in patients. In addition sedation responses in patients were attenuated compared with controls. Hunger ratings were reduced by the infusion in controls but were too variable to be interpreted in the patients. Plasma amino acid levels were also determined before and after infusion of L-tryptophan. Tryptophan levels were comparable in the two groups as were the levels of tyrosine, phenyl alanine, valine, leucine and iso-leucine. The results suggest that some aspects of 5-hydroxytryptamine function may be attenuated in anorexia nervosa. However, they undoubtedly contrast with the finding of enhanced hormonal responses in acute dieting and may be relevant to the interpretation of similar experiments in depressive illness.
Airway resistance increases during sleep. We have determined the ventilatory and arousal responses to the addition of inspiratory resistance of 4, 7, or 10 cmH2O/L/s during sleep in 10 normal men who slept wearing valved face masks. Insufficient ventilatory response data were obtained during rapid eye movement (REM) sleep to allow adequate analysis. The immediate responses to loading were decreases in tidal volume (VT), breathing frequency (f), and minute ventilation (VE), with no difference between wakefulness and Stage 2 and Stage 3/4 sleep in the effects of loading on VT and VE, but f fell more during wakefulness than during sleep (p less than 0.05) because of a greater lengthening of inspired time (TI) (p less than 0.05). During the first 10 breaths, occlusion pressure (P0.1) increased similarly in all EEG stages. Averaging responses during the 2-min periods when resistances were applied, the only variable to differ between EEG stages was TI, which increased more in wakefulness than in Stage 2 or Stage 3/4 sleep (p less than 0.01). Arousal within 2 min of application of resistance occurred less frequently from Stage 3/4 sleep than from Stage 2 or REM sleep (p less than 0.02). The study demonstrates that sleep modifies the changes in respiratory timing produced by resistive loading without having a major effect on ventilation or P0.1 responses. The low frequency of arousal from Stage 3/4 sleep with loading may explain why asthmatics rarely awaken from this stage with wheeze.
The role of drug therapy in the treatment of the sleep apnea/hypopnea syndrome is unclear. In a randomised, double-blind, placebo-controlled study, we investigated the value of 14-day therapy with protriptyline (20 mg daily) or acetazolamide (250 mg 4 times per day) on symptoms and on the frequency of apneas, hypopneas, arousals, and 4% desaturations in 10 patients with obstructive sleep apnea/hypopnea syndrome. Overall, protriptyline did not have a significant effect either on symptoms or on any of the above polysomnographic criteria. Acetazolamide reduced the apnea/hypopnea frequency [placebo 50 +/- 26 (SD); acetazolamide 26 +/- 20/h of sleep, p less than 0.03] and tended to decrease the frequency of 4% desaturations (placebo 29 +/- 20; acetazolamide 19 +/- 16/h of sleep, p = 0.06). Despite these physiological improvements, acetazolamide did not significantly improve symptoms and paraesthesiae were common. Contrary to earlier studies, we conclude that protriptyline may have a limited role in the treatment of the sleep apnea syndrome. The reason why acetazolamide produced a physiological, but not a symptomatic, response requires further investigation.
A randomised, double blind, placebo controlled crossover trial of high dose nebulised ipratropium was carried out in 10 asthmatic patients with documented nocturnal bronchoconstriction. Patients received nebulised saline or ipratropium 1 mg at 10 pm and 2 am on two nights. Absolute peak flow (PEF) rates were higher throughout the night after the patients had received ipratropium (at 2 am, for example, mean (SEM) PEF was 353 after ipratropium and 285 l/min after placebo). The fall in PEF overnight, however, was similar with ipratropium and placebo. Patients were given a further 1 mg nebulised ipratropium at 6 am on both nights. There was a significant overnight fall in PEF on the ipratropium night even when comparisons were made between the times that maximal cholinergic blockade would be expected, PEF falling between 11.30 pm and 7.30 am from 429 to 369 l/min. The percentage increase in PEF, though not the absolute values, was greater after ipratropium at 6 am than at 10 pm. These results confirm that ipratropium raises PEF throughout the night in asthmatic patients, but suggest that nocturnal bronchoconstriction is not due solely to an increase in airway cholinergic activity at night.
We have observed patients who clinically have the obstructive sleep apnea syndrome but have no apneas, instead having recurrent nocturnal hypoventilation. There is disagreement about the definition and significance of such sleep-related hypopneas. We have thus analyzed breathing patterns, oxygenation and sleep records of 50 consecutive patients referred with the clinical features of the sleep apnea syndrome and found to have abnormal breathing during sleep to determine: (1) the best definition of hypopnea, and (2) how frequently patients have the clinical features of the sleep apnea syndrome without recurrent apneas. Hypopnea definitions based on decreases in thoracoabdominal movement yielded hypopnea frequencies that were significantly closer to desaturation and arousal frequencies than hypopnea definitions based on flow reduction. The best hypopnea definition was that of a 50% reduction in thoracoabdominal movement lasting for 10 s. This was validated in 33 normal subjects, all of whom had fewer than 11 hypopneas/h, and fewer than 14 apneas plus hypopneas/h of sleep. Thirty-two of the 50 patients had 10 or more apneas/h, the remaining 18 having 9 to 98 hypopneas/h such that all patients had more than 16 apneas plus hypopneas/h. Patients with recurrent hypopneas were clinically indistinguishable from and had a similar frequency of 4% desaturations (zero to 104/h) and arousals (7 to 98/h) to the patients with frequent apneas. This study confirms that hypopneas are clinically important and that the "sleep apnea syndrome" may occur in the absence of recurrent apneas.
Changes in the density of eye movement during rapid eye movement (REM) sleep are associated with changes in ventilation and ventilatory response in animals. Recent data in patients with chronic obstructive pulmonary disease suggest that periods of frequent eye movements may be associated with hypoxemia during REM sleep. We have therefore investigated the association between eye movements and ventilation and ventilatory pattern in 10 normal men. Expired ventilation was measured using a pneumotachograph attached to a valved face mask with a dead space of 50 ml and incorporating a peripheral CO2 leak detector. Ventilation was reduced (p less than 0.02) in all stages of sleep compared with that during wakefulness, with no difference between the level of ventilation in each sleep stage (awake, 7.18 +/- 0.43 SEM; Stage 2, 6.47 +/- 0.43; Stage 3/4, 6.45 +/- 0.52; REM sleep, 6.55 +/- 0.47 L/min). During REM sleep, eye movements (EMs) were associated with rapid shallow breathing. Dividing REM into 20-s epochs with or without EMs, EMs were associated with a raised breathing frequency (no EMs, 14.4 +/- 0.4 breaths/min; EMs, 15.8 +/- 0.5 breaths/min; p = 0.01), reduced tidal volume (0.49 +/- 0.03 L; 0.41 +/- 0.03 L; p less than 0.01), and reduced minute ventilation (6.87 +/- 0.45 L; 6.27 +/- 0.51 L; p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
A survey designed to elicit the subjective effect of specific influences on sleep duration and sleep quality was carried out. The sample consisted of 400 individuals selected in a random manner from the general population and a further 400 individuals representing consecutive attenders at the outpatient department of a large teaching hospital. The response rate for the two groups was 97% and 99% respectively. In a question regarding habits which aid in sleep onset, four-fifths of those exercising with a frequency of at least twice per month spontaneously reported exercise as a factor in promoting sleep.
The sleep patterns of nine male subjects were studied on four consecutive nights comprising two baseline nights, one night on which environmental temperature was elevated from 21 degrees C to 30 degrees C one hour after lights out, and a recovery night. There was a suppression of stage 4 sleep during the initial three hours of sleep on the hot night. A significant increase in stage 4 sleep with a decrease in stage 2 sleep occurred during the first three hours of the recovery sleep. There was a shortening in sleep onset latency and an increase in sleep efficiency on the recovery night. There were no changes in REM latency or REM sleep time. Rectal temperature rose after the increase in ambient temperature on the hot night. These results indicate that elevations in environmental temperature during sleep affect sleep patterns in a manner opposite to elevations of body temperature occurring prior to sleep onset. The curtailing of the usual circadian temperature drop during the first few hours of sleep reduces slow-wave sleep during this period. These findings have implications for those conditions with both altered sleep and altered temperature rhythms, for example, depression.
We studied the sleep patterns of nine young women when sedentary (untrained) and following a 12 week physical fitness training programme. A comparison of baseline sleep patterns and of sleep patterns following one hour of submaximal exercise performed in the evening was carried out at 0 and 12 weeks. The submaximal exercise task was for each subject to cycle for one hour at 70% of her maximal oxygen consumption (VO2 max) as measured when untrained and on completion of the training programme respectively. Changes in fitness were assessed by changes in VO2 max and anaerobic threshold (AT). On the day leading to the all night baseline sleep recordings the subjects carried out their normal daily routines and did no specific exercise. Lean body mass (LBM) was calculated from total body potassium measurements before and after training. A significant improvement in cardiorespiratory fitness did not result in any changes in baseline sleep parameters. The response to the submaximal exercise was an increase in stage 2 NREM sleep and a decrease in slow-wave sleep (SWS, stages 3 & 4) which is possibly indicative of a stress effect. However, in the trained compared to the untrained state, SWS was significantly higher after an exercise load.
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Breathing patterns early and late in the night, at the same sleep stage, were compared in six healthy subjects and 15 adults with nocturnal asthma, to try to identify changes of overnight bronchoconstriction, and breathing patterns at different sleep stages, to see whether there were changes related to sleep stages that were indicative of bronchoconstriction. Despite an average 31% fall in FEV1 overnight in the patients with asthma, neither breathing frequency nor expiratory time, which might be expected to change during bronchoconstriction, was different early in the night from late in the night, nor did they differ between sleep stages. There was no evidence of asynchronous movement of the chest and abdomen in any patient. This study did not identify any abnormality of breathing pattern that would indicate the development of nocturnal asthma without the need to awaken the patient.
Many patients with asthma are troubled by nocturnal wheeze. The cause of this symptom is unknown, but sleep is an important factor. A study was carried out to determine whether nocturnal bronchoconstriction is related to any specific stage of sleep. Eight asthmatics with nocturnal wheeze and eight control subjects performed forced expiratory manoeuvres immediately after being woken from rapid eye movement (REM) or non-REM sleep, wakings being timed to differentiate temporal effects from those related to the stage of sleep. The control subjects showed no significant temporal bronchoconstriction or bronchoconstriction related to the stage of sleep. All patients showed bronchoconstriction overnight, the mean peak expiratory flow rate falling from 410 (SEM 50) 1/min before sleep to 186 (49)1/min after sleep. After the patients had been woken from REM sleep the forced expiratory volume in one second was on average 300 ml lower (p less than 0.02) and peak expiratory flow rate 45 1/min lower (p less than 0.03) than after they had been woken from non-REM sleep. As wakenings from REM sleep were 21(8) minutes later in the night than those from non-REM sleep multivariate analysis was performed to differentiate temporal effects from those related to the stage of sleep. This showed that the overnight decreases in forced expiratory volume in one second and peak expiratory flow rate were significantly related both to time and to REM sleep. This study suggests that asthmatics may suffer bronchoconstriction during REM sleep.