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<block/copy/paste version>Timely Top Med Cardiovasc Dis 2005 Oct 28; Vol. 9: E31
Original Papers
Drug-Induced Weight Gain [October 28, 2005]
Rosane Ness-Abramof1 and Caroline M. Apovian2
1Endocrine Unit, Sapir Medical Center, Tel Aviv University, Israel; 2Division of Endocrinology, Diabetes, Nutrition and Metabolism, Boston Medical Center, Boston University, Boston, Massachusetts, USA
SummaryIntroduction
Diabetes Therapy and Weight Gain
Psychiatric Therapy and Weight Gain
Neurologic Therapy and Drug-Induced Weight Gain
Therapy for Hypertension and Drug-Induced Weight Gain
Steroid Hormone Therapy and Weight Gain
Conclusions
References
Summary
Drug-induced weight gain is a serious side effect of many commonly used drugs leading to noncompliance with therapy and to exacerbation of comorbid conditions related to obesity.Improved glycemic control achieved by insulin, insulin secretagogues or thiazolidinedione therapy is generally accompanied by weight gain. It is a problematic side effect of therapy due to the known deleterious effect of weight gain on glucose control, increased blood pressure and worsening lipid profile. Weight gain may be lessened or prevented by adherence to diet and exercise or combination therapy with metformin.
Weight gain is also common in psychotropic therapy. The atypical antipsychotic drugs (clozapine, olanzepine, risperidone and quetiapine) are known to cause marked weight gain. Antidepressants such as amitriptyline, mirtazapine and some serotonin reuptake inhibitors (SSRIs) also may promote appreciable weight gain that cannot be explained solely by improvement in depressive symptoms. The same phenomenon is observed with mood stabilizers such as lithium, valproic acid and carbamazepine.
Antiepileptic drugs (AEDs) that promote weight gain include valproate, carbamazepine and gabapentin. Lamotrigine is an AED that is weight-neutral, while topiramate and zonisamide may induce weight loss.
Introduction
Obesity is now viewed as a global epidemic that carries severe health implications (1). In the United States more than 60% of the population is overweight, as defined as a body mass index (BMI) ≥25 kg/m2, and 30.5% are obese (BMI ≥30 kg/m2) (2). The etiology of obesity is multifactorial including decreased physical activity and increased caloric intake in genetically susceptible individuals.Overweight and obesity carry increased morbidity and mortality (3-5). Obesity is known to exacerbate many comorbid conditions such as type 2 diabetes, hypertension, dyslipidemia, coronary heart disease, certain cancers, obstructive sleep apnea and osteoarthritis, among others. Modest weight loss of 5-10% of initial body weight was shown to clinically improve many of the comorbidities associated with obesity (6). In view of the hazards of overweight and obesity and the benefits derived of modest weight loss, it is clear that drug-induced weight gain is an undesirable side effect. Patients should be informed concerning the potential of weight gain, and medical care providers need to follow closely patients treated with such medications and intervene even with modest weight gain (Table I) (7).
Diabetes Therapy and Weight Gain
Type 2 diabetes is strongly associated with obesity: approximately 80% of patients with type 2 diabetes are overweight or obese. There is a strong correlation between BMI and the risk for developing type 2 diabetes in men and women (8, 9). In the Nurses' Health Study, women with a BMI >35 kg/m2 had a risk that was 93 times higher than in women with a BMI <22 kg/m2. In this cohort, women who lost 5 kg (11 lb) reduced their risk of developing type 2 diabetes by 50% (9). The pattern of fat distribution also has clinical importance with visceral adiposity increasing the risk for insulin resistance and diabetes (10).Recently, prospective studies have shown that lifestyle changes (weight reduction, increase in fiber, diet and increased physical activity) were effective in preventing type 2 diabetes in patients with impaired glucose tolerance (11, 12). Most of the current medications for the treatment of diabetes cause weight gain of varying degrees, leading to the worsening of insulin resistance, increase in hypertension and lipid levels among other deleterious effects (13).
Insulin therapy
Insulin is the only available therapy for patients with type 1 diabetes. It is used alone or in combination with oral therapy in patients with type 2 diabetes not adequately controlled by diet and oral therapy alone.
In the Diabetes Control and Complication Trial (DCCT), 1,330 patients with type 1 diabetes were assigned to intensive insulin therapy consisting of three or more daily insulin injections, continuous subcutaneous insulin infusion (CSII) or to conventional insulin therapy consisting of one or two injections of insulin per day (14). This study was the first one to establish that maintaining near-normal glycemia was associated with a reduction in microvascular complications; however, intensive insulin therapy was associated with a greater weight gain in the intensive care group of 4.6 kg more than the patients treated with conventional insulin therapy.
In the UK Prospective Diabetes Study (UKPDS) (15), 4,209 patients newly diagnosed with type 2 diabetes were assigned to conventional therapy (diet) or intensive therapy (sulfonylurea [cholorpropamide or glibenclamide] or insulin) and followed for 10 years. The conventional therapy aimed to achieve a fasting blood glucose of less than 270 mg/dl with diet, while the goal of the intensive therapy was to achieve a fasting blood glucose of less than 108 mg/dl. Once again in this study, tight glycemic control was related to a reduction in microvascular complications. Patients assigned to insulin therapy gained 4 kg (8.8 lb) more than patients assigned to diet alone, and the insulin-treated group had a higher rate of weight gain compared to patients treated with oral medications.
The benefits of tight glycemic control are well documented, but intensive insulin therapy comes at the price of weight gain. The weight gain in insulin-treated patients may be attributed to the anabolic effect of insulin, increase in appetite, reduction of glycosuria due to improved glycemic control, and some fluid retention (16). Combination therapy of insulin and metformin has been shown to decrease the daily insulin requirements and promote less weight gain compared to insulin therapy alone (17). In patients in whom oral therapy fails, adding a long-acting insulin to the present oral therapy may offer better glycemic control without promoting weight gain and may be preferred to exclusively switching to insulin therapy (18, 19).
Insulin glargine is a new peakless long-acting insulin analog that is used as a basal insulin. Most, but not all, clinical studies report less weight gain with insulin glargine compared to treatment with NPH insulin (20). In a 28-week trial in 58 patients with type 2 diabetes assigned to insulin glargine or NPH insulin, the glargine group gained 0.4 kg, while patients treated with NPH gained 1.4 kg (p <0.001) (21). A newer basal insulin, insulin detemir, was approved for therapy in patients with type 1 and type 2 diabetes. In clinical studies, patients treated with insulin detemir gained less weight compared to patients treated with NPH while achieving similar glucose control (22).
Sulfonylureas
Sulfonylureas (SUs) bind to the SU receptor on pancreatic beta cell, leading to closure of voltage-dependent potassium adenosine triphosphate (KATP) channels, which leads to cell depolarization, calcium entry and insulin secretion. Second-generation sulfonylureas (glyburide, glipizide and glimepiride) have replaced the first generation (chlorpropamide, tolbutamide, acetohexamide and tolazamide) due to increased potency and safety. As insulin secretagogues, sulfonylureas cause weight gain between 2-5 kg (23). In the UKPDS, patients treated with sulfonylurea gained 2 kg more than those on diet alone, while patients on metformin did not experience more weight gain compared to diet-treated patients.
Non-sulfonylurea secretagogues
The non-SU secretagogues are a relatively new class of drugs for the treatment of type 2 diabetes. The mechanism of action is similar to SU through interaction with the KATP channels. Due to their short half-lives, there is a brief stimulation of insulin secretion mostly appropriate for the treatment of postprandial glucose excursions. Presently, repaglinide (a benzoic acid derivative) and nateglinide (a phenylalanine derivative) are the only drugs of this class clinically available. Weight gain has been reported in patients treated with these drugs, although seemingly less than with SUs (23, 24).
Thiazolidinediones
The thiazolidinediones (TZDs) are pharmacologic ligands to the peroxisome proliferator-activated receptor-gamma (PPAR-γ). Their main effect is an improvement in insulin resistance in peripheral tissues. The first glitazone introduced was troglitazone, which was later removed from the market due to idiosyncratic hepatotoxicity. Presently two drugs, rosiglitasone and pioglitazone, are available, but other compounds are under different stages of evaluation in clinical trials (23).
One of the main side effects of TZD therapy is weight gain that is possibly related to increased adipogenesis and fluid retention. It is puzzling that a drug that improves insulin sensitivity promotes weight gain. One of the possible explanations is a favorable shift in fat distribution from visceral depots to subcutaneous depots, with subsequent improvement in hepatic and peripheral insulin sensitivity (25, 26). A comparison of glyburide and rosiglitazone therapy for 52 weeks showed that patients treated with rosiglitazone 4 mg and an SU had a similar mean weight gain of 1.9 kg, while patients treated with a higher dose of rosiglitazone (8 mg) gained 2.9 kg. Pioglitazone therapy used alone also promoted weight gain (0.9, 1 and 2.6 kg with 15, 30 and 45 mg, respectively) and when combined with insulin therapy mean weight gain was higher (2.3 and 3.6 kg at 15 and 30 mg) (27).
The weight gain with TZDs is particularly pronounced when given in combination with insulin therapy (28). The main culprits for the weight gain when TZDs and insulin are combined are the anabolic effect of insulin, the adipogenic effect of TZDs and fluid retention, which may be caused by either drug.
Metformin
Metformin is a weight-neutral medication for the treatment of type 2 diabetes. In the UKPDS, overweight patients treated with metformin did not experience weight gain in spite of improved glycemic control, while the SU- and insulin-treated patients gained weight. Combination of metformin with TZDs attenuates the weight gain promoted with TZDs (29); the same was observed with the combination of metformin with insulin therapy as previously stated (17). In the Diabetes Prevention Program, metformin therapy was associated with a 31% decreased risk for developing diabetes in patients with impaired glucose tolerance compared to placebo therapy, but it was not as effective as lifestyle changes, which reduced the incidence of diabetes by 58% (12).
α-Glucosidase inhibitors
Acarbose and miglitol are the two agents of this class in clinical practice. The mechanism of action of these drugs is delayed absorption of carbohydrates in the small intestine, therefore decreasing post-prandial glucose levels. Therapy with either medication has not been associated with weight gain.
Psychiatric Therapy and Weight Gain
Weight gain is a common side effect of many drugs used to treat patients with psychiatric disorders, leading to patient noncompliance and health risks related to obesity (30).Tricyclic antidepressants
Weight gain during therapy with tricyclic antedepressants (TCAs) is a well-known side effect. Weight gain varies with different agents of this class, with amitriptlyline and imipramine therapy associated with higher weight gain, while desipramine and nortriptiline have less effect on weight gain. The dose and duration of therapy are also positively correlated with weight gain. Overall, reports of weight change from -0.4 kg to 4.12 kg per month have been reported during TCA therapy (31). The mechanism of weight gain is increased appetite and carbohydrate craving.
Monoamino oxidase inhibitors
Monoamino oxidase inhibitors (MAO-Is) are also known to cause weight gain, although the weight gain is less than that observed with TCAs. Weight gain varies within different agents of this class, with some agents such as moclobemide showing a weight-neutral effect (32). Phenelzine caused the most prominent weight gain within this class, comparable to that of imipramine (33).
Selective serotonin reuptake inhibitors
The selective serotonin reuptake inhibitors (SSRIs) are the most prescribed drugs for the treatment of depression and anxiety. Members of this class are citalopram, fluoxetine, fluvoxamine, paroxetine and sertraline. According to their mechanism of action, they were thought to promote weight loss rather than weight gain; unfortunately, in clinical practice marked weight gain is a common side effect of paroxetine therapy and to a lesser extent of fluoxetine and sertraline (32). One placebo, controlled trial where patients were treated with fluoxetine reports a mean initial weight loss of 0.4 kg during the first 12 weeks of therapy, but after 38 weeks the weight gain was comparable to that of the placebo group (3 kg above baseline) (34). The pattern of initial weight loss followed by an increase in weight is characteristic of SSRI therapy (35). Fava et al. (36) reported differences in weight gain in 284 patients with major depressive disorder randomized to fluoxetine, sertraline or paroxetine and treated for 26-32 weeks. Weight gain was most pronounced in paroxetine-treated patients (3.6%), followed by those treated with sertraline (1%). Although the difference was not statistically significant, patients treated with fluoxetine lost 0.2% of their basal weight. Futhermore, a weight gain of >7% was more common in paroxetine-treated patients (25.5%) compared to fluoxetine- (6.8%) and sertraline-treated (4.2%) patients. It is not clear if the weight gain is due to improvement of depressive symptoms, a direct pharmacologic effect or a combination of both.
Mirtazapine
Mirtazapine is a tetracyclic antidepressant that was introduced over the last few years. Its use has been reported to cause considerable weight gain due to increased appetite (32). Interestingly, weight gain is observed during the first weeks of therapy with no further weight increase despite ongoing treatment (37).
Other antidepressants
Venlafaxine and nefazodone are antidepressants with a weight-neutral effect, while bupropion-treated patients more often report weight loss than weight gain (38, 39). Patients with major depression treated with sustained-release bupropion experienced a small weight loss that was sustained over the long term. Weight loss was proportionately higher in patients with higher BMIs than in patients with lower BMIs (30, 40). Bupropion is presently being evaluated as a weight loss medication (41). It should be considered as first-line therapy for overweight and obese patients with major depressive disorders.
Mood stabilizers: Anticonvulsants and lithium
During the last few years anticonvulsants have been combined in psychiatric therapy as mood stabilizers. Carbamazepine and valproic acid are the two main drugs used for this indication. They both may cause appreciable weight gain (most of the data collected on their use is from epileptic patients) (32). Data concerning weight gain in patients with bipolar disorder treated with these medications is still scarce, but their effect on weight gain appears to be similar. Topiramate is a novel antiepileptic drug also used as a mood stabilizer. It promotes weight loss rather than weight gain, an effect that was seen when topiramate was given alone or in combination (42). Lithium therapy is related to appreciable weight gain in up to 65% of patients. A mean weight gain of 10 kg has been reported in patients treated with lithium for several years (43). In a double-blind, placebo-controlled study assessing weight gain, 62% of lithium-treated patients gained more than 4.5 kg within the first year of therapy compared to 8% in the placebo group (44). The weight gain seems to be more pronounced in women, stabilizes after 2 years despite continuous therapy, and is independent of treatment outcome (32).
Atypical antipsychotic drugs
The atypical antipsychotic drugs include clozapine, olanzepine, risperidone, quetiapine, ziprasidone and amisulpride. They offer the advantage of fewer extrapyramidal symptoms compared to conventional agents, but they may cause appreciable weight gain and interference with glucose metabolism. The United States Food and Drug Administration issued a class warning that these drugs may promote weight gain and may cause or worsen diabetes (45). The effect on weight gain is not similar among the different members of this class. Clozapine causes the highest weight gain, ranging from 3-16.2 kg (32, 46). Olanzepine and risperidone promote weight gain ranging from 1.4-6.8 kg. Both drugs caused a greater weight gain compared to haloperidol-treated patients (32). Quetiapine therapy was associated with a 5.6 kg increase in weight after 1 year of therapy, and 25% of patients gained >7% of their initial body weight (30).
Amisulpiride and ziprasidone caused less weight gain compared with the other members of this class. Amisulpiride was associated with a weight gain of 1.4 kg during 6 months of therapy (47). Simpson et al. (48) randomized patients with schizophrenia and schizoaffective disorder to ziprasidone or olanzepine therapy for 6 weeks. In this short-term study, patients treated with olanzepine had a mean weight increase of 3.6 kg, while ziprasidone therapy had a neutral effect on weight. Previous studies have also shown a lower incidence of weight gain in patients treated with ziprasidone compared to the other atypical agents (49). Table II summarizes the metabolic abnormalities associated with atypical antipsychotic therapy (50).
Neurologic Therapy and Drug-Induced Weight Gain
Antiepileptic drugsAntiepileptic drugs comprise a heterogenous group of drugs used for the treatment of convulsive disorder. Valproic acid is widely used as an anticonvulsant since it is well tolerated with relatively few side effects. One of the most disturbing side effects related to valproic therapy is weight gain, reported to range from 5 kg to 49 kg. Its effect on weight is not related to pre-morbid weight, sex or age. The weight gain in valproic acid-treated women is related to endocrine abnormalities such as menstrual abnormalities, hyperandrogenism and the emergence of polycystic ovary syndrome (51). Carbamazepine also may promote weight gain (52) but to a lesser extent than that observed in valproic acid-treated patients (53). Gabapentin is an antiepileptic drug that is structurally related to GABA. Its use has also been related to weight gain when given alone or in combination (54, 55). Topiramate is a new antiepileptic drug that is mostly associated with weight loss. A pooled data analysis of 743 patients treated with topiramate as add-on therapy experienced a weight loss of 2-7%. The weight loss was dose dependent and patients with higher basal weight lost proportionally more weight (56). Zonisamide is another antiepileptic drug that produced weight loss rather than weight gain in short-term clinical trials. Both topiramate and zonisamide are now being evaluated as weight loss medications in obese non-epileptic individuals (57, 58).
Lamotrigine is an antiepileptic drug also used as therapy for bipolar disorder. Its use is not associated with weight gain or an increase in androgen levels (59, 60).
Migraine prophylaxis and weight gain
Drugs from different classes are presently used as migraine headache prophylaxis including anticonvulsants, antidepressants and antihypertensive agents. Anticonvulsants prescribed for migraine prophylaxis include valproic acid, gabapentin and topiramate. While the first two drugs are associated with weight gain, topiramate has been consistently related to weight loss ranging from 2.3 kg to 54.5 kg (61, 62).
Beta-blockers are also widely used for migraine prophylaxis. A mean weight gain of 1.2 kg, possibly due to a decrease in metabolic rate, has been reported in patients treated chronically with beta- blockers (63). Weight gain was not properly evaluated in patients with migraine headaches treated with beta-blockers.
Calcium channel blockers are weight neutral with the exception of flunarizine, which is associated with weight gain possibly due to increased appetite due to blockade of dopamine receptor. Flunarizine is used in migraine prophylaxis and was shown to promote weight gain. Therapy with flunarizine 10 mg for 60 days was associated with a mean weight gain of 4 kg (64).
Drugs that block serotonin and histamine receptors used for migraine prophylaxis include pizotifen and cyproheptadine. Chronic use of both drugs are associated with weight gain (65).
Therapy for Hypertension and Drug-Induced Weight Gain
Medical therapy with beta-blockers is associated with a mean weight gain of 1.2 kg (63). The weight gain is possibly related to decreased basal metabolic rate, mediated by beta adrenoreceptor blockade. Weight gain is observed during the first few months of therapy and no further weight increase is seen with long-term therapy (66). Clonidine, a centrally acting α2-adrenoreceptor agonist, also decreases metabolic rate by decreasing sympathetic activity and may cause weight gain (67).Steroid Hormone Therapy and Weight Gain
Chronic corticosteroid therapy causes weight gain, the magnitude of which depends on the dose and duration of therapy. The weight gain is due to increased truncal adipose tissue (68). Weight gain has also been documented with combination oral contraceptive use (estrogen plus progestin) and may cause discontinuation of oral contraception. A review of 42 randomized controlled trials included in a systematic review recently published concluded that the available data is not sufficient to determine the effect of combination contraceptives on weight, but there is no evidence of a marked effect (69). Contraception with depot medroxyprogesterone acetate induces a moderate weight gain. Women treated for 5 years with medroxyprogesterone acetate gained 2.5 kg more than women treated with a copper intrauterine device (70). Progestin-releasing uterine systems have caused systemic effects such as mood changes and acne, but not weight gain (71).Conclusions
Drug-induced weight gain is a common side effect of many widely used medications. Weight gain is a serious side effect that may be prevented or lessened by diet and exercise or selection of an effective therapy that promotes less weight gain. Weight gain may jeopardize effective medical therapy, leading to noncompliance or discontinuation of therapy. Furthermore, it may cause and exacerbate comorbid conditions associated with obesity. Patients should be informed of this potential side effect and health care providers should be aware and carefully monitor weight changes. In many circumstances, weight gain is not inevitable and may be prevented.References
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This article originally appeared in Drugs of Today Vol. 41, No. 8, 2005, pp. 547-555. © 2005 Prous Science.
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