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PubMed1998

Risk for valvular heart disease among users of fenfluramine and dexfenfluramine who underwent echocardiography before use of medication.

BACKGROUND: Because uncontrolled echocardiographic surveys suggested that up to 30% to 38% of users of fenfluramine and dexfenfluramine had valvular disease, these drugs were withdrawn from the market. OBJECTIVE: To determine the risk for new or worsening valvular abnormalities among users of fenfluramine or dexfenfluramine who underwent echocardiography before they began to take these medications. DESIGN: Cohort study. SETTING: Academic primary care practices. PATIENTS: 46 patients who used fenfluramine or dexfenfluramine for 14 days or more and had echocardiograms obtained before therapy. MEASUREMENTS: Follow-up echocardiography. The primary outcome was new or worsening valvulopathy, defined as progression of either aortic or mitral regurgitation by at least one degree of severity and disease that met U.S. Food and Drug Administration criteria (at least mild aortic regurgitation or moderate mitral regurgitation). RESULTS: Two patients (4.3% [95% CI, 0.6% to 14.8%]) receiving fenfluramine-phentermine developed valvular heart disease. One had baseline bicuspid aortic valve and mild aortic regurgitation that progressed to moderate regurgitation. The second patient developed new moderate aortic insufficiency. CONCLUSION: Users of diet medications are at risk for valvular heart disease. However, the incidence may be lower than that reported previously.

Adult↗

PubMed1996

The addition of dexfenfluramine to fluoxetine in the treatment of obesity: a randomized clinical trial.

Current evidence demonstrates that pharmacologic agents, alone or in combination produce short-term weight-loss and may remain effective for extended periods of time in obese patients. We have evaluated the weight loss of a selective inhibitor of serotonin uptake, fluoxetine, alone as compared with combined therapeutic trial with another serotoninergic drug, dexfenfluramine. Thirty-three patients were randomly assigned in a double-blind randomized clinical trial divided to two groups: Group I [Fluoxetine 40 mg and placebo (n = 13)] and Group II [Fluoxetine 40 mg plus dexfenfluramine 15 mg at night (n = 20)]. Both groups had a significant weight loss at the end of 8 months (Group I, mean +/- SEM 6.2 +/- 2.8 kg and Group II 13.4 +/- 6.3 kg, p < 0.05). Group II patients had a significantly greater weight loss as compared with Group I both in terms of mean weight loss in kg and BMI in kg/m2. However significance between Group I and II related to BMI mean values and weight mean values were only achieved after, respectively, 4 and 6 months of treatment. At laboratory level there was an elevation of HDL-cholesterol and lowering of serum lipids values (cholesterol and triglycerides) in both groups. Side effects were relatively minor and no altered clinical vital signs or abnormal laboratory values were observed. We concluded that the combination of fluoxetine (daytime) and dexfenfluramine (at night) may be more effective than fluoxetine alone in weight reduction although the small size of this study does not permit broad generalization.

Adult↗

PubMed1991

Dexfenfluramine neurotoxicity in brains of non-human primates.

Dexfenfluramine, a drug prescribed for appetite suppression, was evaluated in non-human primates for its potential to produce toxic effects on brain serotonin (5-HT) neurons. Squirrel monkeys received dexfenfluramine subcutaneously twice daily for four days at doses of 1.25 or 5.00 mg/kg. Two weeks later, a dose-related depletion of 5-HT and 5-hydroxyindoleacetic acid was found, together with a reduced number of 5-HT uptake sites. Morphological studies showed acute pathological changes in 5-HT axons, followed by a persistent decrease in 5-HT axon density. Our findings indicate that dexfenfluramine damages central 5-HT neurons in monkeys and raise concern about the potential neurotoxicity of this drug in man.

Animals↗

PubMed1989

[Quantified EEG and psychometric effects of 3 doses of dexfenfluramine in the young adult].

In an acute, double-blind placebo-controlled study, three groups of nine healthy subjects were included. Each group received, in randomized and weekly intervals, a single oral dose of dexfenfluramine (15 mg, 30 mg or 60 mg) or placebo. Psychometric and EEG studies were carried out before as well as 1, 2, 3, 4, 5 and 6 h after drug administration. Changes from predrug to postdrug conditions for each time were determined by the ratio of absolute spectral power and compared to the evolution of power spectra under placebo conditions. Statistical evaluation was done with ANOVA. Dexfenfluramine induced a dose-dependent decrease of power spectra for theta and alpha 1 bands and an increase for the beta band. Topographic brain mapping of these significant changes displayed a central and posterior decrease for theta and alpha 1 bands, and a temporal localization for the beta-power. Maps of relative power-enhanced changes were seen in absolute power and provided false displays. Psychometric evaluation of dexfenfluramine effects only showed trends to extraversion and increased mood scores but no statistical significance was found. Arousal and performance tests were unchanged. These results suggest that qEEG variations are more sensitive to serotonergic drug effects than psychometric investigations. It appears that spontaneous EEG power spectra variations with time must be accounted for by drug evaluation. Absolute power variations are more reliable than relative power. Methodological implications are discussed.

Adult↗

PubMed1993

Dexfenfluramine in type II diabetes: effect on weight and diabetes control.

OBJECTIVE: To assess the effect of dexfenfluramine on weight loss, diabetic control and blood lipids in type II diabetics over a three-month period. DESIGN, SETTING AND PATIENTS: Forty overweight patients in the Diabetic Clinic, Fremantle Hospital, were studied in a double-blind, placebo-controlled trial with a run-in period of one month followed by three months on either dexfenfluramine or placebo. MAIN OUTCOME MEASURES: Changes in body weight, and fasting plasma glucose, glycosylated haemoglobin, plasma cholesterol and triglyceride levels. MAIN RESULTS: The median change in weight was -3.8 kg in the treatment group (Df) and +0.3 kg in the placebo group (PI) (P = 0.006). The median changes in fasting plasma glucose levels were -1.0 mmol/L (Df) and +0.6 mmol/L (PI) P = 0.010). The median changes in glycosylated haemoglobin levels were -1.4% (Df) and +0.2% (PI) (P = 0.002). The median changes in triglyceride levels were -0.3 mmol/L (Df) and +0.2 mmol/L (PI) (P = 0.017). Cholesterol level did not change significantly. CONCLUSION: Dexfenfluramine is effective in achieving weight loss and also improved diabetic control in obese type II diabetics over a three-month period.

Adult↗

PubMed1988

Place of dexfenfluramine in the management of obesity.

The treatment of obesity remains a puzzling challenge because long-term maintenance of weight loss--one of the most suitable goals--is rarely achieved with conventional methods. Among the theoretical measures able to maintain a permanent and bearable constraint to obtain the maintenance of weight loss is long-term (life-long?) pharmacotherapy. Dexfenfluramine is a good candidate for such a use; the demonstration of its long-term efficacy, i.e., maintenance of the initial weight loss with no escape with time, is in progress (ISIS study). Although the correct use of dexfenfluramine in obese patients remains to be more precisely defined, its pharmacological profile leads us to consider that it could be useful for those with normo or hyperphagia and stress induced compulsive feeding behavior, and/or for avoiding relapse in restrained patients. The use of dexfenfluramine must not excuse other types of interventions when needed.

Fenfluramine↗

PubMed1988

Dexfenfluramine and feeding reward.

This review describes background experiments and new findings showing that dexfenfluramine inhibits self-stimulation of a lateral hypothalamic (LH) feeding-reward system. Earlier work suggested that self-stimulation excites a pathway to the ventral tegmental area (VTA), where the mesolimbic dopamine system is involved in self-administration of food and drugs. LH stimulation also excites taste neurons in the nucleus tractus solitarius (NTS). This helps explain why stimulation can induce feeding responses and also reward self-stimulation responses. Stimulation-induced feeding and self-stimulation are modulated by physiological signals that control an animal's appetite and body weight. An animal will self-stimulate at a slower rate after it has just eaten, or if it is overweight, or if it is given an anorectic dose of insulin. At the same time, responses to turn off automatic stimulation tend to increase. Paradoxically, racemic fenfluramine decreased both self-stimulation and stimulation-escape, which suggested overall lethargy, but new results show this can be avoided by using just the d isomer. Dexfenfluramine inhibited LH self-stimulation but not stimulation-escape. It also released serotonin in the LH, as shown by microdialysis. These results suggest that dexfenfluramine can release serotonin that has as one of its effects the inhibition of circuitry for feeding-reward.

Animals↗

PubMed1993

Prolonged surveillance of dexfenfluramine in severe obesity.

Forty-two obese patients entered a placebo-controlled, double-blind 1-year study on dexfenfluramine, a serotonergic anorectic drug. Obesity was severe (mean body mass index 38.4 kg/m2), and of early onset and long duration. A mean of 8 attempts to lose weight was undertaken. After randomisation to 1 year of dexfenfluramine (dF) or placebo (non-dF) treatment, weight losses and changes in health risk indicators were investigated. Thereafter, continued follow-up by physician and dietician was encouraged. Seven patients withdrew, 4 (2 dF, 2 non-dF) because of dissatisfaction. Three patients (2dF, 1 non-dF) failed to lose weight. After initially greater weight losses in dF patients, the mean weight loss after 12 months was not significantly different, i.e. 12.8 kg in the dF vs. 8.6 kg in the non-dF group. Health risk indicators ameliorated to the same extent in both groups. Discontinuation of the active drug resulted in more weight gain [3.24 (dF) vs. 0.82 (non-dF) kg] in the following 2 months. After completion of the 1-year trial and the 2-month drug-free observation period, 8 of the 17 dF patients remained in follow-up for half a year, 5 for 1 year and 3 for 2 years. A respective 61%, 48% and 45% of the weight loss was maintained. The 13, 11 and 10 patients of the placebo group maintained 71%, 37% and 30% of the weight losses at half a year, 1 year and 2 years, respectively. Because of the modest weight loss, dexfenfluramine may not be a break-through in 1-year strategies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Effect of dexfenfluramine on body weight, blood pressure, insulin resistance and serum cholesterol in obese individuals.

The effect of the serotonergic agent dexfenfluramine on weight loss, blood pressure, insulin sensitivity and serum lipid levels was determined in a 3-month randomised, double-blind, placebo controlled parallel design study in 50 obese subjects (body mass index 30-44 kg/m2). When compared with placebo treated patients, the dexfenfluramine group lost more weight (3.8 vs 1.1 kg, P < 0.01), had lower diastolic blood pressure (-5 vs -1.5 mmHg, P < 0.05), and lower cholesterol levels (-0.38 vs + 0.06mmol/l, P < 0.05), and showed improved insulin sensitivity (+ 11% vs + 4%, P < 0.03). Significant effects on blood pressure and insulin sensitivity were apparent after 1 week of treatment during which time weight did not change, suggesting a direct effect of the agent independent of weight loss. Dexfenfluramine thus improves a number of cardiovascular risk factors associated with obesity, with benefits additional to those achieved by weight reduction alone.

Adult↗

PubMed1999

Serial echocardiographic and clinical evaluation of valvular regurgitation before, during, and after treatment with fenfluramine or dexfenfluramine and mazindol or phentermine.

OBJECTIVE: The prevalence of cardiac valvular regurgitation demonstrated by echocardiography in patients who took appetite-suppressant medication for weight loss has been assessed at 5%-30%. We studied 86 patients who had echocardiograms before treatment with appetite suppressants to determine the incidence of new cases and to evaluate the clinical implication of the echocardiographic findings. RESEARCH METHODS AND PROCEDURES: We studied 69 men [Mean+/-Standard Deviation (S) age 49+/-8] and 17 women (mean+/-S age 50+/-7) who had 233 echocardiograms before, during, and after a weight-loss program that used predominantly fenfluramine (or dexfenfluramine) with mazindol (or phentermine). Mean drug exposure was 17 months. Blinded echocardiographic readings were performed to identify and grade aortic regurgitation (AR) or mitral regurgitation (MR). RESULTS: Seven of 86 patients (8%) had pre-existing regurgitation with five (6%) meeting our case definition. Thirteen (16.5%) of initially normal patients developed valvular regurgitation and were new cases. Of the new cases, 12 were grade I/IV AR and one was both grade II/III MR and II/IV AR. All 13 patients were asymptomatic, and only two aortic insufficiency murmurs could be auscultated. There was significantly greater risk for developing valvulopathy for those who took medications longer than 6 months (p = 0.03), and no new cases were observed in patients exposed for less than 8 months. No increased risk associated with age, presence of hypertension, or exposure to fenfluramine-phentermine combination was demonstrated. Although there was a higher incidence of new regurgitation in women (31% vs. 13% for men), this was not statistically significant (p = 0.093). DISCUSSION: Some patients who had normal echocardiograms at baseline developed cardiac valvular regurgitation after exposure to fenfluramine or dexfenfluramine with mazindol or phentermine. The development of valvulopathy was significantly correlated with duration of exposure. The clinical implications of echocardiographically demonstrated regurgitation are uncertain, since there were only two audible murmurs and no other clinically relevant signs or symptoms among the patients.

Aortic Valve Insufficiency↗

PubMed1999

Three-month treatment with metformin or dexfenfluramine does not modify the effects of diet on anthropometric and endocrine-metabolic parameters in abdominal obesity.

Abdominal obesity is connoted by hyperinsulinism and insulin insensitivity, a trend toward glucose intolerance, hypoactivity of GH/IGF-I axis and alterations of hypothalamo-pituitary-adrenal (HPA) axis. It has been hypothesized that treatment with metformin (MET) and dexfenfluramine (DEX) could counteract those endocrine-metabolic alterations. Thus, we studied the effects of 3-month treatment with MET or DEX on anthropometric (BMI, WHR, FM and FFM), metabolic (basal and OGTT-induced glucose) and hormonal variables (IGF-I, DHEA-S, androstendione, testosterone, fT3, fT4, TSH, basal and OGTT-induced insulin) as well as on blood pressure in 28 normotensive patients with abdominal obesity (OB, 3 M, 25 F; 47.5+/-1.5 yr [mean+/-SE], BMI 35.4+/-1.1 kg/m2, WHR 0.98+/-0.04 and 0.86+/-0.07, in M and F, respectively). All patients were on balanced hypocaloric diet (1400 Kcal/day). Patients were randomly assigned to treatment with MET (no.=10, 500 mg twice daily po) or DEX (no.=10, 15 mg thrice daily po) or placebo (no.=8). Before treatment all groups had similar anthropometric, metabolic and hormonal values. After 3-month treatment with MET, DEX or placebo, weight, BMI and WHR reductions were similar in all groups (p<0.05 vs baseline in either group). In each group FFM/FM ratio showed non significant trend toward increase. No significant variations in metabolic and endocrine variables were recorded in each group after 1 and 3-month treatment. However, glucose tolerance, OGTT-induced insulin response, glucose/insulin ratio showed a similar trend toward improvement in all groups, while IGF-I, 24 h urinary cortisol, DHEA-S, androstendione, testosterone, thyroid hormone and TSH levels did not show any variation. Significant (p<0.02) and similar reductions of DBP, but not of SBP, levels were found in all groups. In conclusion, our findings demonstrate that, at least after 3-month treatment, metformin and dexfenfluramine do not modify the effects of diet on anthropometric, metabolic and hormonal parameters as well as on blood pressure in patients with abdominal obesity.

Abdomen↗

PubMed2001

Effects of the cannabinoid receptor antagonist SR 141716, alone and in combination with dexfenfluramine or naloxone, on food intake in rats.

RATIONALE: Recent studies in animals have implicated endogenous cannabinoids in the regulation of palatable food intake, but it is not yet clear to what extent pharmacological agents acting on this system may have sustained actions and applicability to different feeding protocols. OBJECTIVES: In the present study, we examine the effects of the cannabinoid CB1 receptor antagonist SR 141716 on food intake of rats, and its behavioral specificity. We examine whether tolerance develops to the anorectic actions of SR 141716, and whether it has either additive or synergistic actions with dexfenfluramine or naloxone. METHODS: Undeprived rats were trained to eat a daily sweet milk dessert and on test days were administered single or combination drugs and intakes were recorded. In other studies, rats were deprived for 24 h of either food or water and intakes recorded after drug administration at the end of this time. In one study, rats were fed ad libitum chow with SR 141716 added. RESULTS: SR 141716 (1-3 mg/kg) suppressed both palatable food intake in undeprived rats and food, but not water, intake after deprivation. Using an isobolographic analysis, SR 141716 had an additive anorectic effect with dexfenfluramine. In contrast, SR 141716 in combination with naloxone had a significantly supra-additive anorectic action. SR 141716 was also effective orally and no tolerance to its anorectic effect developed over 3 days. CONCLUSIONS: These data show that SR 141716 is an effective anorectic agent using both palatable foods and bland chow, and is selective because water intake was unaffected. SR 141716 is also effective orally and has an effect sustained for at least several days. There appears to be a synergistic interaction between opioid and cannabinoid systems in the regulation of feeding, whereas the combination of a serotonin releasing agent and the CB1 antagonist is additive.

Animals↗

PubMed1999

Echocardiographic prevalence of mitral and/or aortic regurgitation in patients exposed to either fenfluramine-phentermine combination or to dexfenfluramine.

We evaluated the prevalence of valvular regurgitation in patients who have taken anorectic medications. Two-dimensional echocardiograms with color flow Doppler were recorded in 200 consecutive patients referred to a major metropolitan hospital for evaluation of cardiac function because of a history of anorectic medication use. Each patient filled out a questionnaire at the time of the visit or through telephone contact. Each echocardiogram was reviewed by 2 observers. The degree of valvular regurgitation was graded by a consensus of both observers. Significant valvular regurgitation was defined as at least moderate mitral regurgitation (MR) or at least mild aortic regurgitation (AR), as recommended by the Food and Drug Administration and Centers for Disease Control and Prevention. For all patients having taken anorectic drugs, there was a 5% prevalence of at least moderate MR, a 12% prevalence of at least mild AR, and a 16% prevalence of significant MR and/or AR. Patients with significant AR and/or MR were older than those without significant valvular regurgitation (49+/-12 vs 44+/-11 years, p = 0.03). Patients with significant MR and/or AR had a longer exposure duration (8 vs 6 months, p = 0.049) to anorectic drugs. There was no difference in weight loss between those with and without significant regurgitation (p = NS). The 2 largest subgroups were patients who took the fenfluramine-phentermine combination (n = 127) and those who took dexfenfluramine alone (n = 42). The prevalence of significant MR and AR was 5% and 9% for the fenfluramine-phentermine group and 0% and 14% for the dexfenfluramine group, respectively. There was also a high subthreshold level of MR and AR in these patients.

Adult↗

PubMed2001

Anorectic effect of dehydroepiandrosterone combined with dexfenfluramine or thionisoxetine.

Free feeding rats given supplementary 1 h access per day to a palatable dessert test meal were tested for the anorectic effect of dehydroepiandrosterone alone or in combination with either the serotonin releasing agent dexfenfluramine or the norepinephrine uptake inhibitor thionisoxetine (LY 368975). Isobolographic analysis showed that the effect of dehydroepiandrosterone combined with either dexfenfluramine or thionisoxetine was within the range predicted for additivity of action.

Animals↗

PubMedDate not supplied

Reversal of delta 9-THC hyperphagia by SR141716 and naloxone but not dexfenfluramine.

Presatiated adult male Lister hooded rats received oral administration of the exogenous cannabinoid Delta-9-tetrahydrocannabinol (Delta(9)-THC; 1.0 mg/kg) in combination with subcutaneous injection of either the cannabinoid CB1 antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (SR141716; 0, 0.05, 0.1, 0.5 or 1.0 mg/kg), the CB2 antagonist N-[(1S)-endo-1,3,3-trimethyl bicyclo[2.2.1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; 0, 0.05, 0.1, 0.5 or 1.0 mg/kg), the general opioid antagonist naloxone (0.1, 0.5, 1.0 or 5.0 mg/kg) or the 5-HT agonist dexfenfluramine (0.05, 0.1, 0.5, 1.0 or 5.0 mg/kg). Food (chow) intake was measured over 2 h from the onset of the dark period. Delta(9)-THC induced significant hyperphagia, which was attenuated by subanorectic doses of SR141716 and naloxone. Neither SR144528 nor dexfenfluramine affected Delta(9)-THC-induced feeding. These data confirm mediation of Delta(9)-THC hyperphagia by central-type CB1 receptors, and support a functional relationship between cannabinoid and opioid systems in relation to appetite regulation. Stimulation of CB1 receptors may promote feeding by actions on food reward rather than by inhibition of serotonergic satiety mechanisms.

Animals↗

PubMed1999

Prevalence of valvular-regurgitation associated with dexfenfluramine three to five months after discontinuation of treatment.

OBJECTIVES: The goal of this study was to determine the prevalence of valvular regurgitation and abnormal valve morphology in patients three to five months after discontinuation of dexfenfluramine (Dexfen) therapy. BACKGROUND: We previously reported the results of a randomized, double-blind, placebo-controlled trial of valvular structure and function in 1,073 patients treated either with Dexfen, with an investigational sustained-release dexfenfluramine (Dexfen SR), or with a placebo, with echocardiograms performed approximately one month from the last dose. Using FDA criteria (aortic regurgitation [AR] > or =mild and/or mitral regurgitation [MR] > or =moderate) we found no statistical difference among the groups, but when all degrees of valvular regurgitation were considered and when the two Dexfen groups were combined, there was a higher prevalence of any degree of AR, any degree of MR, and restricted posterior mitral leaflet mobility. However, it was unknown whether these differences in prevalence persisted. METHODS: The double blind was maintained, and all patients were invited to return for a follow-up echocardiogram. Echocardiograms were acquired using a standardized protocol and assessed blindly to determine the degree of valvular regurgitation and valve leaflet thickness and mobility. We had an 80% power to detect a statistically significant change in paired proportions using the McNemar test (alpha = 0.05). RESULTS: Echocardiograms were obtained on 941 patients with a median of 137 days after drug discontinuation. Aortic regurgitation (of any degree) was present in 13.8% of Dexfen (p = 0.41 compared to placebo), 10.7% of Dexfen SR (p = 0.64 compared to placebo), and 11.9% of placebo patients. The minor differences between patients treated with active drug versus placebo, which were found in the previous study, were no longer significant even when the groups were combined (p = 0.83 compared to placebo). Mitral regurgitation (of any degree) was present in 71.5% (p = 0.15 compared to placebo), 69.8% (p = 0.30 compared to placebo), and 70.5%, respectively. This was also not significantly different from placebo when both Dexfen groups were combined (p = 0.16). There was no difference in the prevalence of restricted posterior mitral leaflet mobility among the three groups (p = 0.19). CONCLUSIONS: The small increase in prevalence of minor degrees of AR and MR in patients treated with two to three months of Dexfen previously reported is no longer present three to five months after discontinuation of medication. These data suggest that the degree of regurgitation observed in patients who used Dexfen for a relatively short duration does not progress over time.

Adolescent↗

PubMed2002

Flavor avoidance induced by LiCl and dexfenfluramine in rats and mice using nondeprivation protocols.

Using dexfenfluramine as unconditional stimulus (US), the authors confirmed that sham-operated and area postrema (AP)-lesioned rats form comparable conditioned flavor avoidances. When lithium chloride (LiCI) was used as the US, AP-lesioned rats did not learn to avoid a drug-paired flavor conditional stimulus (CS+). Sham-operated, but not AP-lesioned, rats had low intakes of the placebo-paired flavor (CS-), which suggests that the lesions disrupted generalization of avoidance. Generalized avoidance in intact rats was similar when either sweetened milk or Polycose was used as the caloric vehicle for the CSs. When flavored gels of Polycose were used as CSs, C57BL/6J mice developed flavor avoidance with either LiCl or dexfenfluramine as US. Compared with rats, mice required higher doses of these agents, avoidance was not complete after many pairings, and there was no generalization to the CS-.

Animals↗

PubMed2000

Efficacy of fenfluramine and dexfenfluramine in the treatment of obesity: a meta-analysis.

A meta-analysis was conducted to estimate the difference of weight loss among patients treated with placebo and with fenfluramine or dexfenfluramine after 1, 2, 3, 6, and 12 months of treatment. Placebo-controlled, double-blind, randomized clinical trials, whose results were presented as weight loss by the placebo group and the drug-treated patient group, were selected for the analysis. For the pooled estimations, the method of the weighted means by the inverse of the variance was used. The association between the difference of means and several predictive variables was studied by means of weighted linear regression. Patients treated with fenfluramine or dexfenfluramine achieved a higher weight loss than those receiving placebo in all the periods studied. The greatest efficacy was observed after 3 months of treatment. Beyond this time, there is a decline in the effectiveness. Based on the efficacy data, treatments longer than 3 months would not be justified.

Appetite Depressants↗