Other Medications for Weight and Metabolic Health

Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Information is based on current medical literature and clinical guidelines but may not apply to your specific situation. Individual responses vary based on personal medical history and concurrent conditions. Always consult qualified healthcare providers for medical decisions. Never delay seeking medical care based on content you’ve read. If experiencing a medical emergency, seek immediate medical attention.

These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not replace medical care.

In Brief

The incretin-based medications in Article 5 are the most effective medications currently approved for chronic weight management, but they are not the only ones, and they are not right for everyone. This article covers the rest of the landscape and, more importantly, the reasoning behind it — not just what each drug does, but why someone might still choose it, what evidence question it answers, and when continuing a poorly effective treatment stops making sense. The older anti-obesity medications — orlistat, phentermine, phentermine/topiramate, and naltrexone/bupropion — generally produce less weight loss than the incretins but remain useful for reasons of cost, access, oral dosing, tolerability, or individual circumstance. A second group — metformin and the SGLT2 inhibitors — is prescribed mainly for another reason entirely: diabetes, heart failure, or kidney disease, with weight change a secondary effect. Two practical points complete the picture: many commonly prescribed medications quietly cause weight gain, and the history of weight drugs withdrawn for harm carries a lesson more precise than “be careful” — that improving a number on a chart is not the same as improving health, and clinical outcome and long-term safety evidence are needed to know whether a treatment’s overall effects are beneficial.

Beyond the Incretins

Article 5 covered the GLP-1 and incretin medications in depth because they have changed what obesity treatment can achieve. But focusing only on them would give a distorted picture of the choices people actually face. Some cannot take the incretins, cannot afford them, cannot tolerate the gastrointestinal effects, or do not have access to them; others are already taking medications — for diabetes, blood pressure, mood, or seizures — that interact with weight in ways worth understanding.

It helps to sort these medications by the role they play rather than by rigid drug class, because modern practice increasingly organizes treatment around the specific problem being treated — the complication, the comorbidity, the individual’s risk profile — rather than the historical box a drug was first placed in.¹,¹² Four roles matter here: medications used primarily to treat obesity (the incretins of Article 5, and the older agents covered below); medications prescribed for another cardiometabolic condition that also happen to affect weight (metformin and the SGLT2 inhibitors); medications that unintentionally promote weight gain; and, finally, the withdrawn drugs whose history teaches why weight change alone is never enough to judge a medication. These categories overlap — semaglutide is simultaneously an obesity drug and, in a defined group, a cardiovascular one — and that overlap is the point: the useful question is not which box a drug sits in, but what it is being used to achieve.

This is the second of three treatment articles. Article 5 covered the incretins; Article 7 turns to bariatric and metabolic surgery.

The Other Anti-Obesity Medications

Four medications approved for weight management predate the incretin era or work by different mechanisms. None matches the average weight loss of semaglutide or tirzepatide, but each has a place, and understanding both what they do and their cardiovascular cautions matters.

Orlistat works entirely in the gut. It blocks the enzymes (lipases) that digest dietary fat, so that the prescription dose reduces absorption of roughly 30% of the fat in a meal.⁴ Because it does not act on the brain or appetite, its effect on weight is modest — about 3% of body weight beyond placebo over a year.³ Its side effects follow directly from its mechanism: unabsorbed fat produces oily or loose stools, urgency, and flatulence, and these symptoms are worse the more dietary fat a person eats — which both limits high-fat eating and makes the drug difficult for many people to stay on.³,⁴ Because it reduces absorption of fat-soluble vitamins, a separate multivitamin taken hours apart is advised.³ It carries little cardiovascular risk, has the longest safety record of the group, and comes in prescription and lower-dose over-the-counter forms.³

Phentermine is a sympathomimetic — a stimulant-like appetite suppressant. Its mechanism is also its main caution: it can raise heart rate and blood pressure, so it is not appropriate for people with uncontrolled hypertension or established cardiovascular disease such as coronary artery disease, arrhythmia, or heart failure, and it is a controlled substance.³,¹⁷ One complication matters: phentermine is FDA-approved only for short-term use (generally up to 12 weeks), yet longer-term off-label use is common in real-world obesity practice.³ That gap does not erase its cardiovascular cautions or substitute for the randomized cardiovascular-outcomes evidence it has never had.

Phentermine combined with extended-release topiramate is the most effective of the non-incretin oral options, producing average weight loss of roughly 8–10% over a year in trials — more than the other agents here, though still below the incretins.²,⁵ It also carries the most safety architecture, worth laying out in full rather than reducing to a single warning. From the phentermine component, heart rate can rise. From topiramate come tingling in the hands and feet, altered taste, difficulty with word-finding and concentration, mood changes, and — less commonly but importantly — metabolic acidosis, kidney stones, and acute angle-closure glaucoma.⁵,⁶ Topiramate can also cause birth defects (cleft lip and palate), so reliable contraception is required and it is inappropriate in pregnancy.⁵,⁶ Finally, it must be stopped by gradual tapering rather than abruptly, because sudden withdrawal of topiramate can precipitate seizures.⁶

Naltrexone combined with bupropion acts on the brain’s appetite and reward pathways — bupropion is an antidepressant and smoking-cessation drug, naltrexone an opioid-receptor blocker. Average weight loss is roughly 4–5% beyond placebo over a year.³,⁷ Its cautions include a possible rise in blood pressure and heart rate, and a seizure risk from the bupropion component, which also carries a warning about mood and suicidal thoughts.⁸ The opioid caution needs explaining: because naltrexone blocks opioid receptors, it can block the effect of opioid pain medications and can precipitate acute withdrawal in someone who is dependent on opioids — which is why it should not be used by people taking or dependent on them.⁸ Its dedicated cardiovascular-outcomes trial, LIGHT, ended prematurely without answering the safety question it was built to answer — a story told in full below, because it is one of the more instructive episodes in this field.⁹

A fifth medication, setmelanotide, is different in kind. It activates the MC4 receptor, a specific switch in the brain’s appetite pathway, and is approved only for rare, single-gene forms of obesity — such as POMC, PCSK1, or leptin-receptor deficiency, and Bardet-Biedl syndrome — confirmed by genetic testing.¹⁰ It is not a general obesity treatment, but it is a notable example of a drug matched precisely to an identified biological cause.

The table summarizes the group. The weight figures are approximate, placebo-subtracted averages from different trials, not a head-to-head comparison.

The Non-Incretin Anti-Obesity Medications

Who Might Actually Choose One of These

Knowing what a drug does is only half the question. The more useful one — why a reasonable person and clinician might choose it in 2026, when more effective incretins exist — turns on fit, not just efficacy.

Orlistat suits someone who wants a non-systemic oral option that acts only in the gut, and who understands and accepts the gastrointestinal trade-off that comes with it. Phentermine has a limited role in appropriately selected people without relevant cardiovascular contraindications; its FDA approval is for short-term treatment, although longer off-label use occurs in practice. Phentermine/topiramate is the strongest oral non-incretin choice for someone who needs more than the others offer, provided pregnancy can be reliably prevented and the cognitive, mood, and heart-rate considerations are acceptable. Naltrexone/bupropion can be a reasonable fit for selected people — sometimes where its effects on eating-related reward or its bupropion component align with other goals — as long as opioid use, seizure risk, blood pressure, and psychiatric history are accounted for, and the unfinished cardiovascular-outcome picture is understood. And setmelanotide is chosen in the rare case where genetic testing has identified exactly the pathway it targets. Underlying several of these choices is a practical reality the incretin era has not erased: cost, insurance coverage, and access frequently determine what is actually usable, a point developed below.

Knowing When to Stop

A medication taken indefinitely despite minimal benefit and ongoing side effects is not rational treatment, and this is a place where these drugs come with useful built-in logic. Treatment should be reassessed on a schedule — for effectiveness, tolerability, safety, adherence, and whether the original goal is being met — rather than simply continued by default.¹,¹²

Several of these medications have label-defined response checkpoints. For phentermine/topiramate ER, response is assessed after 12 weeks at the recommended dose; insufficient early response leads to dose escalation, and failure to lose at least 5% of baseline body weight after a further 12 weeks at the maximum dose is a reason to discontinue treatment, with gradual tapering of the highest dose.⁶ For naltrexone/bupropion, response is assessed after 12 weeks at the maintenance dose, and treatment should be discontinued if at least 5% of baseline body weight has not been lost.⁸ The larger principle matters more than the timelines: treatment should be reassessed rather than continued automatically when meaningful benefit is absent.¹ The same logic runs in the other direction — as someone reaches their goal, contemporary guidance favors actively reassessing and, where appropriate, de-escalating treatment to avoid the harms of overtreatment and unnecessary polypharmacy.¹

Prescribed for Another Reason: Metformin and SGLT2 Inhibitors

Two other medications come up constantly, and they belong to a different conversation. Metformin and the SGLT2 inhibitors are not obesity drugs; they are prescribed mainly for diabetes, heart failure, or kidney disease, and they affect weight only modestly. Their relevance here is precisely that: they show why “affects weight” and “matters for cardiometabolic health” are not the same question.

Metformin has long been a foundational treatment for type 2 diabetes, and it remains widely used because it is effective, inexpensive, familiar, and generally well tolerated. Modern diabetes care, however, is increasingly individualized rather than a fixed metformin-first staircase: for people with established cardiovascular disease, heart failure, chronic kidney disease, or substantial weight-management needs, other agents — including the incretins and SGLT2 inhibitors — may be prioritized or started alongside it.¹² Its effect on weight is small — roughly weight-neutral to mildly reducing — so it is not an obesity treatment. Its relevance to this series is instead preventive: in the Diabetes Prevention Program described in Article 1, metformin reduced the development of type 2 diabetes by 31% in people with prediabetes, less than intensive lifestyle change (58%) but a real effect from an accessible, well-understood medication.¹¹ The Diabetes series covers its use in full.

SGLT2 inhibitors (such as empagliflozin, dapagliflozin, and canagliflozin) cause the kidneys to excrete glucose in the urine, which lowers blood sugar and produces modest weight loss — on the order of 2–3 kg — along with a small drop in blood pressure.¹² What makes this class important is not the weight but its effect on hard outcomes, and here precision matters, because the evidence is not one uniform block. Across large outcome trials, these drugs have consistently reduced hospitalization for heart failure and slowed the progression of chronic kidney disease — and, for both, the benefit extends even to people without diabetes.¹³,¹⁴,¹⁵ Their effect on broader cardiovascular events such as heart attack and stroke is real but more variable, established most clearly for particular agents in particular populations — notably people with type 2 diabetes and established cardiovascular disease.¹³ The exact evidence depends on the drug and the group studied. What is striking is that these benefits are far too large, and appear far too quickly, to be explained by the modest weight loss alone; the weight change is a minor part of the story, not the mechanism.¹²

This is the reverse of the anti-obesity drugs: a class whose principal proven benefits are cardiovascular, heart-failure, and kidney outcomes rather than substantial weight reduction. The Diabetes and Heart Failure series cover these medications in the depth they deserve. One practical note bridges the two worlds: in real-world care, a person may be on more than one of these medications at once — an SGLT2 inhibitor for the heart or kidneys and an incretin for weight, for instance — and while sequential and, in selected cases, combination use occurs, the evidence and approved labeling differ across combinations, so these are decisions for a clinician rather than defaults.¹²

The Medications That Can Cause Weight Gain

A practical part of this topic is easy to overlook: a number of commonly prescribed medications promote weight gain, and recognizing them can matter as much as adding a weight-loss drug. Two clues help. The first is timing — weight gain that began after a medication was started or its dose increased points toward the medication. The second is that the effect is not uniform: it varies widely both between drugs and between people, so the question is always about degree and individual response, not a blanket label.¹⁶

The clearest examples come from psychiatry, where the risk falls along a gradient rather than affecting a class evenly. Among antipsychotics, clozapine and olanzapine carry the highest risk of weight gain; quetiapine and risperidone are intermediate; and several agents — such as aripiprazole, ziprasidone, and lurasidone — tend to be more weight-neutral.¹⁶ Among antidepressants, paroxetine and mirtazapine are associated with gain, while bupropion is generally weight-neutral or weight-reducing.¹⁶ Some antiseizure medications (such as valproate), some diabetes medications (insulin, sulfonylureas), and corticosteroids can also add weight.¹⁶,¹⁷

Three principles make this useful rather than alarming. First, never stop these medications abruptly — particularly psychiatric drugs, antiseizure drugs, corticosteroids, and some cardiovascular medications such as beta-blockers — because abrupt discontinuation can be dangerous; the conversation is with a prescriber, not a solo decision. Second, alternatives are indication-specific: within several of these categories a more weight-neutral option exists and is worth discussing, but sometimes the weight-promoting drug is clearly the right drug, and staying on it is correct.¹,¹⁶ Third, weight gain caused by a necessary medication can sometimes reasonably be treated by adding a weight medication — metformin and GLP-1 agents are used this way — but in other cases the more rational step is to reconsider the original regimen with the prescriber rather than layer a second drug onto the first.¹⁶

The Lesson of the Withdrawn Drugs

The history of weight-loss medications is, in large part, a history of drugs that lowered weight and were later removed because they harmed people. This record is not a reason for fear of today’s treatments; it is the reason the field now demands proof of cardiovascular safety, and it directly explains why Article 5 placed such weight on the outcome trials.

The examples are instructive. Fenfluramine, half of the “fen-phen” combination widely used in the 1990s, was withdrawn in 1997 after it was found to damage heart valves and cause pulmonary hypertension.¹⁸ Sibutramine, an appetite suppressant approved in 1997, was withdrawn in 2010 after a dedicated cardiovascular trial (SCOUT) found it increased the risk of heart attack and stroke in people with pre-existing cardiovascular disease.¹⁹ Rimonabant, which acted on the endocannabinoid system, was withdrawn (and never approved in the United States) because of serious psychiatric effects including depression and suicidality.²⁰ Lorcaserin, approved in 2012, was withdrawn in 2020 when a long-term trial revealed a higher rate of cancer.²¹

The obvious lesson — weight loss does not prove safety — is true but shallow. The deeper one is more useful: an improvement in a surrogate marker does not guarantee a net clinical benefit. A medication can lower weight, blood sugar, blood pressure, or cholesterol and still cause harm through an entirely separate pathway — a heart valve, the brain, a cancer. That is why a change in weight or a risk-factor number cannot stand in for evidence about the outcomes that actually matter: heart attack, stroke, heart failure, cancer, and death.

The unfinished LIGHT trial sharpens a related distinction. LIGHT was designed to determine the cardiovascular safety of naltrexone/bupropion, but premature public disclosure of favorable interim results compromised the trial and contributed to its early termination.⁹ When additional events accumulated, the favorable early signal was not confirmed, and the trial ended without answering the question it was designed to settle.⁹ The result was not reassurance and not alarm, but uncertainty — the safety question was left open, and a new trial was required.⁹

That points to a distinction worth carrying forward. There are at least three different evidence states, and they are not interchangeable: a drug with proven cardiovascular benefit; a drug with no demonstrated harm within the limits of the available evidence; and a drug whose cardiovascular effect remains genuinely uncertain because the necessary evidence is incomplete or missing. Failure to prove harm is not proof of benefit, and an unfinished trial leaves an open question rather than a clean bill of health. Among the older anti-obesity medications discussed here, most sit in the second or third state rather than the first — and being honest about which is which is the whole point.

Cost and Access

Affordability is not a footnote to this topic; it is often the deciding factor. Several of the older anti-obesity medications are available as low-cost generics, which is a large part of why they remain in use when incretins are unaffordable or uncovered. Insurance coverage for weight management is uneven and frequently absent, and even among these agents a branded fixed-dose combination can remain expensive despite being built from long-generic components. Cost pressure may also lead people toward compounded products, or toward using separate components in ways that are not equivalent to an approved fixed-dose product; these approaches raise different questions of formulation, evidence, quality, and oversight, and should not automatically be assumed interchangeable with the approved product studied in clinical trials. Contemporary guidance is explicit that coverage, availability, and affordability often dictate which agent is realistically chosen — which is why cost belongs in the medical conversation, not outside it.¹

Questions Worth Asking

Because these medications serve such different purposes, a few plain questions cut through most of the complexity before starting or continuing any of them:

• What is this medication treating — weight, diabetes, heart failure, kidney disease, or weight gain caused by another drug?
• What benefit has actually been proven for someone in my situation?
• Which risks matter most for me — blood pressure, heart rate, pregnancy, mood, seizures, opioid use, kidneys, or cost?
• How will we know if it is working?
• When should we reassess or stop?

Clinical Bottom Line

The most effective drug for weight loss is not automatically the best drug for every person. Some older anti-obesity medications remain useful because of cost, access, oral administration, tolerability, or individual circumstances, but their efficacy and safety profiles differ substantially — and, apart from orlistat, the stimulant-based agents carry real cardiovascular cautions.³,¹⁷ Metformin and SGLT2 inhibitors belong in a different conversation: they are prescribed mainly for metabolic, cardiovascular, heart-failure, or kidney indications, with weight change playing a secondary role, and the SGLT2 class in particular has proven outcome benefits that its modest weight effect cannot explain.¹¹,¹³,¹⁴,¹⁵ Before adding another medication, it is also worth asking whether an existing one is contributing to weight gain, and whether a poorly effective treatment should be reassessed rather than continued.¹,¹⁶ The central task is not choosing the drug that produces the largest number on a weight-loss chart; it is matching a treatment to the condition being treated, the evidence that applies to that particular person, and the risks that matter.

What Comes Next

This article and Article 5 covered the medications for weight and metabolic health. Article 7 turns to the most effective and most durable intervention for severe obesity — bariatric and metabolic surgery — including what the long-term evidence shows about weight, diabetes, and cardiovascular outcomes, and the risks and trade-offs that come with it.

Key Terms

Anti-obesity medication: A drug whose primary purpose is to reduce body weight (for example, orlistat, phentermine/topiramate, naltrexone/bupropion, and the incretins).

Sympathomimetic: A drug that mimics the body’s “fight-or-flight” signals; as an appetite suppressant (phentermine), it can raise heart rate and blood pressure, which is the source of its main cardiovascular cautions.

Lipase inhibitor: A medication (orlistat) that blocks the gut enzymes digesting dietary fat, reducing fat absorption.

Metformin: A foundational, inexpensive medication for type 2 diabetes; roughly weight-neutral, and shown to reduce progression from prediabetes to diabetes.

SGLT2 inhibitor: A medication that makes the kidneys excrete glucose; it produces modest weight loss but has proven benefits for heart failure and kidney disease (and, in some populations, broader cardiovascular events) that are not explained by weight.

MC4-receptor agonist: A medication (setmelanotide) that activates a specific appetite-control receptor in the brain; used only for rare single-gene forms of obesity.

Surrogate marker: A measurable stand-in — such as weight, blood pressure, glucose, or cholesterol — that may or may not track with the outcomes that ultimately matter (heart attack, stroke, heart failure, cancer, death).

Cardiovascular-outcomes trial: A study designed to measure whether a medication changes actual events rather than only surrogate markers.

References

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