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Appetite during consumption of enteral formula as a sole source of nutrition: the effect of supplementing pea-fibre and fructo-oligosaccharides.

Liquid enteral formulas are commonly used as a sole source of nutritional support of patients in hospital and community settings. Their effect on appetite has important consequences for dietary management of such patients and is likely to be affected by the formula composition. The aim of the present study was to compare appetite within healthy subjects consuming both a standard formula and one supplemented with pea-fibre (10 g/l) and fructo-oligosaccharide (FOS; 5 g/l) as a sole source of nutrition. Eleven healthy subjects consumed a standard formula or a pea-fibre/FOS formula as a sole source of nutrition for 14 d in a double-blind, cross-over trial. Appetite was recorded using standard 100 mm lines anchored at each end by a phrase denoting the most extreme appetite sensation. Consumption of the pea-fibre/FOS formula resulted in higher mean fullness (46 v. 37 mm, P=0.035), minimum fullness (13 v. 9 mm, P=0.024) and minimum satiety (12 v. 8 mm, P=0.012) compared to the standard formula. As there were no differences in macronutrient intake between formulas, these differences are likely to be due to supplementation with pea-fibre and FOS. The effect on appetite of the composition of an enteral formula, both with respect to nutrient content and functional components such as pea-fibre and FOS, may be an important aspect to consider in the dietary management of patients consuming enteral formula as a sole source of nutrition.

Adult↗

Impact of weight loss, appetite, and the inflammatory response on quality of life in gastrointestinal cancer patients.

The relationship between weight loss, appetite, the inflammatory response, and quality of life in patients with advanced gastrointestinal cancer was examined. Height, weight, and skinfold anthropometry were measured in 119 patients. Blood was taken for analysis of C-reactive protein and albumin. Appetite, performance status, and quality of life were assessed using EuroQol EQ-5D and EORTC QLQ-C30 questionnaires. Weight loss was > 5% (median 17.1%) of their preillness weight in 97 patients; the remaining 22 patients were weight stable. Anthropometric measurements and circulating albumin concentrations were significantly lower (p < 0.01) and circulating concentrations of C-reactive protein were significantly higher in the weight-losing than in the weight-stable group (p < 0.001). Appetite scores, performance status, and EuroQol EQ-5D and EORTC QLQ-C30 scores were also lower in the weight-losing group (p < 0.01). When the weight-losing cancer patients were divided on the basis of whether they had a marked inflammatory response, albumin concentrations, appetite, and Karnofsky performance status were significantly lower (p < 0.05) in the group with a marked inflammatory response. The results of the present study are consistent with weight loss, reduction of appetite, and an elevated inflammatory response being important related factors in lowering the quality of life of gastrointestinal cancer patients.

Aged↗

Increasing preload volume with water reduces rated appetite but not food intake in healthy men even with minimum delay between preload and test meal.

The role of gastric volume in the short-term control of eating in humans remains unclear, with some studies reporting that food volume alone can reduce appetite but others finding no such effect. A recent study in our laboratory, found effects of preload volume on subjective appetite (hunger, fullness) but not intake, and found effects of preload energy on intake but not appetite. That study used an interval of 30 min between serving preloads and the test meal, and the present study attempted to maximise the effects of the volume manipulation by removing the delay between the preload and test meal. We administered four soup-based preloads varying in volume (150 and 450 ml) using water, and energy density (1.4 and 4.2 kJ/ml) using maltodextrin, producing three energy levels (209, 629, 629 and 1886 kJ; repeated measures). These were followed immediately by an unlimited hot pasta lunch, during which food weight was monitored continuously by computer. Increasing soup volume at constant energy (629 kJ) reduced appetite ratings, but not intake. In contrast, increasing soup energy at constant volume (450 ml) reduced intake, without affecting appetite. The discrepancies between our results and other reported studies suggest that volume is more influential when intakes are large, or that there may be a threshold concentration for nutrients in the GI tract before volume alone is tangibly expressed in subsequent eating.

Adult↗

Effects of weekly administration of pegylated recombinant human OB protein on appetite profile and energy metabolism in obese men.

BACKGROUND: Results of leptin administration in mice, rats, and humans provide a rationale for therapeutic augmentation of circulating leptin (OB protein) concentrations in obese humans; this may reduce food intake, increase metabolic rate, and lower body mass. OBJECTIVE: We assessed the effects of weekly subcutaneous pegylated polyethylene glycol (PEG)-OB protein administration on appetite and energy metabolism in obese men. DESIGN: We performed a randomized, double-blind, placebo-controlled trial in 30 obese men [body mass index (in kg/m(2)): 34.2 +/- 3.6; age: 44.7 +/- 7 y]. Subjects received 20 mg PEG-OB protein/wk for 12 wk while limiting their energy intake to 2.1 MJ/d. RESULTS: During treatment, appetite and hunger before breakfast decreased and remained lower in the PEG-OB-protein group, whereas they increased and remained higher in the placebo group (P < 0.0001). During treatment, hunger decreased in the PEG-OB-protein group (P < 0.05) and cognitive restraint increased in the placebo group (P < 0.0001). Neither appetite nor food intake changed significantly during the ad libitum evening meal. Under energy balance conditions in the respiration chamber, appetite at the end of treatment was not significantly different from baseline despite similar, significant reductions in 24-h energy intake, energy expenditure, sleeping metabolic rate, body mass, fat mass, and fat-free mass (P < 0.01 for all) in both groups. CONCLUSION: Treatment with PEG-OB protein modified subjective appetite at a dosage that produced no changes in body composition, energy expenditure, or body mass loss relative to placebo treatment, suggesting that PEG-OB protein has central rather than peripheral biological activity in obese men.

Adult↗

Effect of 3 modified fats and a conventional fat on appetite, energy intake, energy expenditure, and substrate oxidation in healthy men.

BACKGROUND: Different dietary fats are metabolized differently in humans and may influence energy expenditure, substrate oxidation, appetite regulation, and body weight regulation. OBJECTIVE: We examined the short-term effects of 4 triacylglycerols (test fats) on subjective appetite, ad libitum energy intake, meal-induced thermogenesis, and postprandial substrate oxidation. DESIGN: Eleven healthy, normal-weight men (mean age: 25.1 +/- 0.5 y) consumed 4 different test fats [conventional fat (rapeseed oil) and 3 modified fats (lipase-structured fat, chemically structured fat, and physically mixed fat)] in a randomized, double-blind, crossover design. RESULTS: No significant differences in appetite sensations or ad libitum energy intakes were observed between the 4 test fats. Overall, the 4 fats exerted different effects on energy expenditure (meal effect: P < 0.01) and substrate oxidation (interaction between meal and time: P < 0.05). In post hoc tests, the 3 modified fats resulted in significantly higher postprandial energy expenditure and fat oxidation than did the conventional fat (P < 0.008, Bonferroni adjusted); no significant differences were observed between the 3 modified fats. CONCLUSIONS: Structured fats do not change short-term postprandial appetite sensations or ad libitum energy intakes but do result in higher postprandial energy expenditure and fat oxidation than do conventional fats and hence promote negative energy and fat balance. In humans, a physically mixed fat (trioctanoate + rapeseed oil) is metabolized as quickly as are structured fats. The position of medium-chain fatty acids on the glycerol backbone of triacylglycerols does not seem to affect energy expenditure or appetite.

Adult↗

Short-term continuous enteral tube feeding schedules did not suppress appetite and food intake in healthy men in a placebo-controlled trial.

Tube feeding (TF) provides a model with which to study appetite when nutrient delivery bypasses the upper gastrointestinal (GI) tract and associated cephalic phase response. Nocturnal, diurnal and 24-h TF schedules are used clinically, but their effects on satiety have not been distinguished. This study tested two hypotheses: 1) bypassing the upper GI tract with TF has little satiating effect, and 2) diurnal TF suppresses appetite and food intake more than nocturnal or 24-h schedules. Six healthy men, residing in a metabolic suite, each received three continuous TF schedules (diurnal 12-h, nocturnal 12-h and 24-h; 6.86 +/- 0.51 MJ/d) in random order for 3 d over separate 10-d periods. Two days before and after TF, a placebo feed (<0.4 MJ/d) was given. Weighed measurements of ad libitum food consumption, hourly tracking of appetite and metabolic and hormonal measurements were undertaken. Compared with placebo feeding, there was a nonsignificant reduction in oral intake (1.01-2.49 MJ reduction), little change in appetite sensations with TF and an increase in total energy intake from 14.88 to 20.42 +/- 3.25 MJ. The schedules did not differ although diurnal TF was the most satiating. Changes in a variety of mediators (including leptin, insulin, cholecystokinin, metabolites and respiratory quotient) did not relate to immediate assessments of appetite and food intake. This trial suggests that continuous TF has little effect on satiety in healthy men over a period of 3 d, irrespective of the timing of the schedule. This could not be explained by changes in a variety of metabolic and hormonal signals within the time frame studied.

Appetite↗

A novel technique to demonstrate disturbed appetite profiles in haemodialysis patients.

BACKGROUND: Malnutrition is common among dialysis patients and is associated with an adverse outcome. One cause of this is a persistent reduction in nutrient intake, suggesting an abnormality of appetite regulation. METHODS: We used a novel technique to describe the appetite profile in 46 haemodialysis (HD) patients and 40 healthy controls. The Electronic Appetite Rating System (EARS) employs a palmtop computer to collect hourly ratings of motivation to eat and mood. We collected data on hunger, desire to eat, fullness, and tiredness. HD subjects were monitored on the dialysis day and the interdialytic day. Controls were monitored for 1 or 2 days. RESULTS: Temporal profiles of motivation to eat for the controls were similar on both days. Temporal profiles of motivation to eat for the HD group were lower on the dialysis day. Mean HD scores were not significantly different from controls. Dietary records indicated that dialysis patients consumed less food than controls. CONCLUSIONS: Our data indicate that the EARS can be used to monitor subjective appetite states continuously in a group of HD patients. A HD session reduces hunger and desire to eat. Patients feel more tired after dialysis. This does not correlate with their hunger score, but does correlate with their fullness rating. Nutrient intake is reduced, suggesting a resetting of appetite control for the HD group. The EARS may be useful for intervention studies.

Adult↗

Increased maternal nutrition alters development of the appetite-regulating network in the brain.

Individuals exposed to an increased nutrient supply before birth have a high risk of becoming obese children and adults. It has been proposed that exposure of the fetus to high maternal nutrient intake results in permanent changes within the central appetite regulatory network. No studies, however, have investigated the impact of increased maternal nutrition on the appetite regulatory network in species in which this network develops before birth, as in the human. In the present study, pregnant ewes were fed a diet which provided 100% (control, n = 8) or approximately 160% (well-fed, n = 8) of metabolizable energy requirements. Ewes were allowed to lamb spontaneously, and lambs were sacrificed at 30 days of postnatal age. All fat depots were dissected and weighed, and expression of the appetite-regulating neuropeptides and the leptin receptor (OBRb) were determined by in situ hybridization. Lambs of well-fed ewes had higher glucose (Glc) concentrations during early postnatal life (F = 5.93, P<0.01) and a higher relative subcutaneous (s.c.) fat mass at 30 days of age (34.9+/-4.7 g/kg vs. 22.8+/-3.3 g/kg; P<0.05). The hypothalamic expression of pro-opiomelanocortin was higher in lambs of well-fed ewes (0.48+/-0.09 vs. 0.28+/-0.04, P<0.05). In lambs of overnourished mothers, but not in controls, the expression of OBRb was inversely related to total relative fat mass (r2 = 0.50, P = 0.05, n = 8), and the direct relationship between the expression of the central appetite inhibitor CART and fat mass was lost. The expression of neuropeptide Y and AGRP was inversely related to total relative fat mass (NPY, r2 = 0.28, P<0.05; agouti-related peptide, r2 = 0.39, P<0.01). These findings suggest that exposure to increased nutrition before birth alters the responses of the central appetite regulatory system to signals of increased adiposity after birth.

Adipose Tissue↗

Ethanol- and sucrose-reinforced appetitive and consummatory responding in HAD1, HAD2, and P rats.

INTRODUCTION: Ethanol-preferring (P) rats and high-alcohol-drinking (HAD1 and HAD2) rats have been selectively bred to consume greater amounts of ethanol than nonselected rat strains. These three rat lines also show increased levels of responding for ethanol in operant paradigms that assess a combined appetitive/consummatory response. METHODS: The present experiment used a model of reinforced responding that procedurally separates the appetitive, or seeking, response requirement from consummatory responding to compare seeking and intake responding in P and HAD rats. Subjects (n = 7 or 8 per group) were trained to make 25 lever-press responses, which were followed by 20 min of access to a sipper tube spout containing either 10% ethanol (10E) or (in separate groups of subjects) 3% sucrose (3S). After training, a single nonreinforced session was conducted to assess the limit to appetitive responding under extinction conditions. After this single nonreinforced session, three successive across-session breakpoint determinations were made for 10E and 3S by increasing the response requirement over days until subjects failed to complete the requirement. A final extinction session was then conducted. RESULTS: Appetitive responding during both the nonreinforced and breakpoint sessions indicated that P rats made significantly more responses overall than HAD rats in both the ethanol and sucrose groups. P rats also consumed more sucrose than HAD rats, with no differences in ethanol consumption between the lines (1.0-1.5 g/kg/20 min). Appetitive responding in the HAD rats in the ethanol groups was comparable to that reported previously for nonselected Long-Evans rats. CONCLUSIONS: These findings indicate that appetitive and consummatory processes are distinct and that P rats have an increased tendency to both seek and drink ethanol and sucrose solutions, making this selected line useful when modeling both "craving" and "loss of control" related behaviors involved in excessive alcohol consumption.

Alcohol Drinking↗

Salt appetite in the pigeon in response to pharmacological treatments.

1. In response to furosemide-induced sodium depletion pigeons showed a robust salt appetite. Following the 1st depletion they started to ingest 3% NaCl after a latency of 373 +/- 69 s and in 24 h they took 21.16 +/- 3.07 ml of this solution (vs. a daily mean intake of 1-2 ml prior to the depletion). 2. The appetite was selective as shown by the fact that when, after depletion, 0.34 M-CaCl2 was offered (which is equiosmotic to 3% NaCl) pigeons took just a trivial amount of it. 3. Analysis of sodium losses following the natriuretic treatment revealed that pigeons respond to sodium depletion with an excessive overconsumption of NaCl solution. In the 2 h after access to salt they took about 3 times the amount of sodium lost. 4. Repeated sodium depletions sharply reduced the latency to the ingestion of salt and produced larger intakes. However, the overall amount of salt taken in 24 h after the later depletions was very similar and statistically indistinguishable from that taken following the 1st depletion. 5. Subchronic deoxycorticosterone acetate treatment (2 mg pigeon-1 day-1 I.M.) increased daily 3% NaCl intake, but large variability was observed in the response. 4 mg pigeon-1 day-1 evoked a reliable 3% NaCl intake which was particularly marked from the 5th day of the treatment. 6. Pulse intracerebroventricular (I.C.V.) injection of purified hog renin evoked water intake within about 1 min of injection, followed (about 6 h later) by increased salt intake. In the 24 h after renin injection pigeons took 16.58 +/- 2.89 ml of 3% NaCl. On the 2nd day following injection salt intake was still higher than in controls. 7. In conclusion, our results show that pigeons respond to sodium depletion with a robust salt appetite. Moreover, salt appetite can be evoked by deoxycorticosterone acetate as well as by renin. These findings suggest that in the pigeon salt appetite may be an endocrine-induced behaviour controlled by mineralocorticoids and by the renin-angiotensin system.

Animals↗

Appetite suppressants and primary pulmonary hypertension in the United Kingdom.

OBJECTIVE: Amphetamine-like appetite suppressants, particularly fenfluramines, have been implicated in the aetiology of primary pulmonary hypertension. At one specialist centre in France 20% of patients with primary pulmonary hypertension had been exposed to fenfluramine. The prevalence of primary pulmonary hypertension associated with fenfluramines and other appetite suppressants in the United Kingdom is unknown. This study was performed to measure prior exposure to appetite suppressants in patients with primary pulmonary hypertension. SETTING: Heart lung transplantation centres in England. PATIENTS: United Kingdom residents with proven primary pulmonary hypertension referred for consideration of heart lung transplantation. METHODS: Case surveillance study, obtaining data from the hospital and general practitioner's notes and directly from the patients or their relatives. RESULTS: 55 patients were identified. Drug histories were available from hospital records in all patients, from the general practitioner's notes in 51, and from the patients or relatives in 44. Of these, 3 female patients had been exposed to appetite suppressants (2 fenfluramine, 1 diethylpropion): 2 have since died. In each case exposure was brief and apparently predated the development of symptoms by several years. CONCLUSIONS: Exposure of patients with severe primary pulmonary hypertension to fenfluramine and other appetite suppressants is uncommon in the United Kingdom unlike in France, where most of the cases associating primary pulmonary hypertension with fenfluramine use have originated. This may reflect more conservative prescribing of these agents in the United Kingdom.

Adult↗

Evaluation of interactions between CCK and GLP-1 in their effects on appetite, energy intake, and antropyloroduodenal motility in healthy men.

There is evidence that CCK and glucagon-like peptide-1 (GLP-1) mediate the effects of nutrients on appetite and gastrointestinal function and that their interaction may be synergistic. We hypothesized that intravenous CCK-8 and GLP-1 would have synergistic effects on appetite, energy intake, and antropyloroduodenal (APD) motility. Nine healthy males (age 22 +/- 1 yr) were studied on four separate days in a double-blind, randomized fashion. Appetite and APD pressures were measured during 150-min intravenous infusions of 1) isotonic saline (control), 2) CCK-8 (1.8 pmol.kg(-1).min(-1)), 3) GLP-1 (0.9 pmol.kg(-1).min(-1)), or 4) both CCK-8 (1.8 pmol.kg(-1).min(-1)) and GLP-1 (0.9 pmol.kg(-1).min(-1)). At 120 min, energy intake at a buffet meal was quantified. CCK-8, but not GLP-1, increased fullness, decreased desire to eat and subsequent energy intake, and increased the number and amplitude of isolated pyloric pressure waves and basal pyloric pressure (P < 0.05). Both CCK-8 and GLP-1 decreased the number of antral and duodenal pressure waves (PWs) (P < 0.05), and CCK-8+GLP-1 decreased the number of duodenal PWs more than either CCK-8 or GLP-1 alone (P < 0.02). This was not the case for appetite or isolated pyloric PWs. In conclusion, at the doses evaluated, exogenously administered CCK-8 and GLP-1 had discrepant effects on appetite, energy intake, and APD pressures, and the effects of CCK-8+GLP-1, in combination, did not exceed the sum of the effects of CCK-8 and GLP-1, providing no evidence of synergism.

Adolescent↗

Sodium appetite during captopril blockade of endogenous angiotensin II formation.

Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. In addition, they may act synergistically to arouse a sodium appetite. If so, then blockade of endogenous angiotensin should decrease the appetite. In experiments reported here, captopril (SQ 14,225) was given peripherally to rats to block conversion of angiotensin I to angiotensin II. It both enhanced and suppressed sodium depletion-induced sodium appetite. The appetite was suppressed when captopril was given in high doses, which block conversion centrally as well as peripherally. The same doses of captopril had no effect on urinary sodium excretion or on sodium appetite aroused by mineralocorticoid treatment. Low doses, which block conversion only in the periphery, enhanced salt intake elicited by depletion, and the enhancement was abolished by captopril given directly into the brain. Therefore the enhancement was probably due to a captopril-induced increase of peripheral angiotensin I, which gained access to the brain and was converted there to angiotensin II.

Administration, Oral↗

Interference with central actions of angiotensin II suppresses sodium appetite.

We have proposed that sodium appetite is aroused by a synergy in the brain of angiotensin II and aldosterone. This hypothesis was tested with 1) chronic intracerebroventricular infusion of captopril, which blocks the conversion of angiotensin I to angiotensin II, or 2) intracerebroventricular injection of eight-substituted analogues of angiotensin II, which block its receptors. Both treatments resulted in a suppression of the sodium appetite induced by sodium deficiency. The suppression was specific for the deficiency-induced appetite, because spontaneous ingestive behaviors were not changed nor was sodium excretion. In addition, the rats continued to express a sodium appetite aroused by pharmacological doses of deoxycorticosterone acetate when they received the highest dose of chronic intracerebroventricular captopril. These results offer compelling evidence for the idea that angiotensin II action in the brain is necessary for expression of sodium appetite.

Angiotensin II↗

Peripheral angiotensin causes salt appetite in rats.

The prevailing theory of sodium depletion-induced salt appetite states that angiotensin (ANG) of cerebral origin, not of renal origin, causes the behavior. This assertion depends partly on an experiment that suppressed salt appetite using an intravenous infusion of a dose of angiotensin-converting enzyme (ACE) inhibitor (captopril, 2.5 mg/h) that supposedly blocked both central and peripheral enzyme (17). The present experiments used the same dose of captopril to suppress salt appetite both in 24-h and in 3-h models of sodium depletion-induced behavior. The captopril-infused rats 1) increased water intake normally after central injections of ANG I given immediately after each salt appetite test, 2) had no arterial pressor response after intravenously injected ANG I, and 3) had normal arterial pressor responses after either intravenously injected ANG II or centrally injected ANG I. Thus, although the peripheral ACE was completely blocked in captopril-infused rats, the central ACE was not, because the central thirst and arterial pressor responses to ANG I were indistinguishable from controls. This demonstrates that ANG of renal origin is necessary for the expression of sodium depletion-induced salt appetite.

Angiotensin II↗

Changes in Fos expression in various brain regions during deoxycorticosterone acetate treatment: relation to salt appetite, vasopressin mRNA and the mineralocorticoid receptor.

Salt appetite, a conditioning factor for hypertension and cardiovascular diseases, is produced when high doses of mineralocorticoids are given to experimental animals. A commonly used procedure to identify neuronal activation is to determine the number of Fos-immunoreactive cells. In rats with established salt appetite after 8 days of deoxycorticosterone acetate (DOCA) treatment, Fos-positive cells were studied in seven brain areas. Significant increases in Fos activity were recorded in the paraventricular (PVN) and supraoptic (SON) nuclei, median preoptic nucleus (MnPO), organum vasculosum of the lamina terminalis (OVLT), preoptic area (POA), bed nucleus of the stria terminalis (BNST) and amygdala (AMYG). In most of these areas, increased Fos expression was also observed early (2 h) after a single DOCA injection, well before salt appetite develops. Using a mineralocorticoid receptor (MR) antibody, we studied whether Fos-active regions also expressed MR. MR-positive cells were found in the OVLT, MnPO, AMYG and BNST, but not in the POA, PVN and SON. In the PVN and SON, nevertheless, prolonged or single DOCA treatment increased expression of mRNA for arginine vasopressin (AVP). The present demonstration of Fos activation, in conjunction with differential expression of MR and stimulation of AVP mRNA, suggests that a neuroanatomical pathway comprising the AMYG, osmosensitive brain regions and magnocellular nuclei becomes activated during DOCA effects on salt appetite. It is recognized, however, that DOCA effects may also depend on mechanisms and brain structures other than those considered in the present investigation. Since some Fos-positive regions were devoid of MR, a comprehensive view of DOCA-induced salt appetite should consider nongenomic pathways of steroid action, including the role of reduced DOC metabolites binding to GABAergic membrane receptors.

Animals↗

Salt appetite and the renin-angiotensin system: effect of oxytocin deficiency.

To explore the role of oxytocin in the regulation of salt appetite and blood pressure, we conducted studies in oxytocin gene-knockout mice and determined (1) blood pressure and heart rate during day and night periods, (2) salt appetite after iso-osmotic volume depletion, and (3) salt appetite and blood pressure after central injection of angiotensin II. Long-term arterial catheters were inserted, and blood pressure and heart rate were recorded for 24 hours. There was a modest decrease in blood pressure and heart rate in knockout mice. Salt appetite was measured with a 2- bottle choice (water and 2% NaCl), with measurement of licking activity. Mice were injected subcutaneously with 30% polyethylene glycol (0.5 mL), and voluntary intakes were measured for 24 hours. Knockout mice consumed 3 times the amount of NaCl than did controls, 276+/-77 vs 90+/-38 licks/24 h (P<0.05). Water consumption was similar between groups. Angiotensin II (5, 50, and 200 ng/3 microL) injected intracerebroventricularly produced dose-related increases in intake, with no differences between the groups. The 50-ng dose of angiotensin II elicited salt and water intakes of 151+/-43 vs 160+/-33 licks and 250+/-53 vs and 200+/-51 licks, respectively (control vs knockout). The pressor response to angiotensin II was not different between the groups. Results suggest that oxytocin plays a role in the regulation of blood pressure and salt appetite, specifically as mediated by volume receptors, and that the renin-angiotensin system is not involved in these changes.

Administration, Oral↗

Changes occurring in appetite and weight during short-term antidepressant treatment.

Changes in appetite and weight were recorded in mild to moderately depressed out-patients during the course of clinical trials of various antidepressant drugs. After six weeks, differences due to treatment regimes were minimal. Patients who on becoming depressed experienced severe changes in appetite and weight in either direction, tended to return to normal. The significant associations of appetite and weight change during treatment were with weight, appetite, and carbohydrate preference at presentation, and also with the 'appetite history' and 'weight history'. The associations with the degree of depression were relatively minor.

Antidepressive Agents↗