2026-07-03 · beta blockers, propranolol, metoprolol, carvedilol, nebivolol, hypertension, heart failure, atrial fibrillation · 18 min read

Does my beta blocker make me gain weight?

In most cases, a little — and the size depends heavily on which beta blocker. Sharma 2001 (Hypertension) meta-analysed 8 randomized hypertension trials and reported a mean weight gain of about 1.2 kg over 6 to 12 months on beta blocker versus placebo, concentrated at higher doses and in the older non-vasodilating agents. Ripley 2014 (American Journal of Cardiology) is the cleaner head-to-head comparison: carvedilol was roughly weight-neutral, nebivolol essentially neutral, metoprolol modestly positive, and atenolol the worst. The mechanism is real — thermogenesis suppression through beta-2 blockade lowers resting energy expenditure by roughly 100 kcal/day (Pischon 2001; Astrup 2000), lipolysis is blunted, and patients simply move less because heart rate is capped. Vasodilating agents (nebivolol, carvedilol) largely escape this pattern. If the scale is creeping, the drug choice is a legitimate conversation with your prescriber, but the fix is not to stop the medication.

Which beta blocker is the worst for weight?

The three worst for weight are propranolol, atenolol, and metoprolol tartrate — the non-vasodilating older agents. Propranolol is non-selective and hits both beta-1 and beta-2 receptors, which maximises the thermogenesis and lipolysis suppression that drive weight gain (Astrup 2000). Atenolol is cardioselective but has the poorest metabolic profile in head-to-head data: the GEMINI trial (Bakris 2004 JAMA) explicitly showed atenolol worsened A1c and body composition compared to carvedilol in patients with type 2 diabetes and hypertension, and Ripley 2014 confirmed atenolol carries the largest weight signal in comparative trials. Metoprolol tartrate sits between propranolol and atenolol. If your prescriber has flexibility on the indication — hypertension without another compelling reason, migraine prophylaxis, or off-label anxiety — an in-class switch to nebivolol or carvedilol often preserves the benefit with substantially less weight burden.

Which beta blocker is weight-neutral?

Nebivolol is the closest thing to weight-neutral in the class. It is a highly cardioselective beta-1 blocker with additional nitric-oxide-mediated vasodilation, and Sarafidis 2007 (Journal of Human Hypertension) documented that this vasodilating action preserves resting energy expenditure and insulin sensitivity — the mechanisms that drive weight gain on the older agents. Carvedilol is a reasonable second choice: it is a combined alpha-1 and non-selective beta blocker, and the GEMINI trial (Bakris 2004) demonstrated it is A1c-neutral and metabolically favourable versus metoprolol in type 2 diabetes with hypertension. In heart failure with reduced ejection fraction (HFrEF), carvedilol is one of three guideline-preferred agents alongside metoprolol succinate and bisoprolol (Yancy 2013 Circulation), so the choice there is driven by mortality data, not the weight signal. For hypertension without HFrEF, nebivolol is often the right compromise between class effect and weight neutrality.

Should I switch to nebivolol or carvedilol?

Sometimes yes — and always through your prescriber, not on your own. The right switch depends on the indication. For essential hypertension without HFrEF or angina, nebivolol is a reasonable weight-preserving alternative (Sarafidis 2007), though it is off-formulary on some plans and the outcome data are less robust than for atenolol or metoprolol. For hypertension with type 2 diabetes or metabolic syndrome, carvedilol has explicit head-to-head evidence for a better metabolic profile (Bakris 2004 GEMINI). For HFrEF, the mortality data — MERIT-HF (metoprolol succinate), CIBIS-II (bisoprolol), and COPERNICUS (carvedilol) — restrict the field to those three; do not switch away from a guideline-directed agent to nebivolol in HFrEF without a cardiology conversation. For migraine prophylaxis, propranolol has the strongest AAN evidence (Silberstein 2012), but timolol and metoprolol are alternatives if the propranolol weight signal is prohibitive. Bring the specific indication and your current weight trajectory to your prescriber and ask about a within-class switch before assuming the whole class is the wrong tool.

Why can't I lose weight on propranolol?

Propranolol suppresses several of the pathways a weight-loss plan depends on. Beta-2 receptor blockade lowers resting energy expenditure by roughly 100 kcal/day (Pischon 2001 International Journal of Obesity; Astrup 2000 Obesity Reviews), which is enough to erode a 300 to 500 kcal daily deficit substantially. Beta-1 and beta-2 blockade on adipocytes reduces overnight and exercise-driven lipolysis, blunting fat mobilisation during fasted or workout windows (Astrup 2000). Heart rate is capped, which caps the intensity ceiling on cardiovascular training and reduces the fatigue tolerance for spontaneous activity through the day (Poirier 2001 Chest). The math is not that weight loss is impossible on propranolol — it is that the same protocol produces slightly less weight loss than it would off the drug. The three practical moves: talk to your prescriber about an in-class switch for a non-migraine indication; add or intensify resistance training (which recruits non-beta-adrenergic pathways for energy expenditure); and use RPE (rate of perceived exertion) rather than heart rate as your cardio-intensity target.

Can I stop my beta blocker if I've lost weight?

Almost never on your own. The indication for the beta blocker did not go away with the weight loss for most patients. In HFrEF and post-MI, the mortality benefit demonstrated in MERIT-HF (1999 Lancet), CIBIS-II (1999 Lancet), and COPERNICUS (2001 New England Journal of Medicine) is durable and non-negotiable — losing weight does not eliminate the guideline-directed medical therapy indication. In atrial fibrillation, rate control from AFFIRM (2002 NEJM) still applies. In migraine prophylaxis, the propranolol benefit persists as long as the migraine pattern does. Abrupt discontinuation of any beta blocker in a patient with ischemic heart disease risks rebound tachycardia, angina, and myocardial infarction (Rangno 1982 Annals of Internal Medicine) — this is called beta-blocker withdrawal syndrome and it is a documented safety hazard. For essential hypertension without another indication, a slow taper and switch to a first-line agent (thiazide, ACE inhibitor, ARB, or DHP calcium channel blocker) per the 2017 ACC/AHA guideline (Whelton 2018 Hypertension) is a reasonable conversation. Bring the weight loss and updated blood pressure to your prescriber, not a unilateral discontinuation.

Can I take a GLP-1 with a beta blocker?

Yes, and the combination often works well. There is no clinically important pharmacokinetic interaction between semaglutide or tirzepatide and any beta blocker in current use. The GLP-1 fat-loss signal — roughly 15 to 22 percent of body weight in the STEP and SURMOUNT programs — more than compensates for the small 1 to 2 kg weight signal from the beta blocker (Sharma 2001), so patients on a GLP-1 rarely report the beta blocker as a limiting factor for the scale. Two practical notes. First, GLP-1 medications lower heart rate modestly, and the combined bradycardia signal with a beta blocker warrants monitoring at initiation — a resting heart rate check at 4 to 6 weeks is reasonable. Second, if new fatigue or exercise intolerance appears in the first weeks of GLP-1 therapy, treat the GLP-1 tolerability first before assuming the beta blocker has become the problem. Coordinate with your prescriber.

Does my beta blocker slow my metabolism?

Yes, by a small and measurable amount, and the exact size depends on which agent. Pischon 2001 (International Journal of Obesity) measured resting energy expenditure on and off propranolol in healthy volunteers and documented a drop of roughly 100 kcal/day, driven by beta-2 blockade of thermogenic pathways. Astrup 2000 (Obesity Reviews) reviewed the mechanism across the class and confirmed the pattern: non-selective agents drop resting energy expenditure most, cardioselective agents modestly, and vasodilating agents (nebivolol, carvedilol) minimally. Roughly 100 kcal/day works out to about 4 to 5 kg over a year at energy balance — which matches the observed weight signal in the older trials — but this is easily offset by targeted resistance training (which recruits non-beta pathways) and modest daily activity increases. The metabolic slowing is real but not fatal to a weight plan. Frame it as a headwind rather than a stop sign.

Beta Blockers and Weight: Why the Scale Creeps and What Actually Helps

Quick stats

• US adults on a beta blocker: roughly 30 million (AHA 2023 Heart Disease and Stroke Statistics)
• Mean weight gain on non-vasodilating beta blocker vs placebo: ~1.2 kg over 6 to 12 months, dose-related (Sharma 2001 Hypertension)
• Head-to-head weight ranking: atenolol > metoprolol > carvedilol ≈ nebivolol (essentially neutral) (Ripley 2014 Am J Cardiol)
• HFrEF mortality benefit of guideline-directed beta blockade: ~34% relative reduction in all-cause mortality (MERIT-HF 1999 Lancet; CIBIS-II 1999 Lancet; COPERNICUS 2001 NEJM)
• 2017 ACC/AHA hypertension guideline positioning: beta blocker is fourth-line for essential hypertension without a compelling indication (Whelton 2018 Hypertension)
• 911 red flag: syncope with chest pain, symptomatic bradycardia (HR <50 with lightheadedness), or new severe bronchospasm on a non-selective agent

The honest picture, in one paragraph

Beta blockers do cause weight gain, but the size is small and the pattern is drug-specific. Sharma 2001 (Hypertension) — the pivotal meta-analysis of 8 randomized hypertension trials — reported a mean weight gain of about 1.2 kg over 6 to 12 months on beta blocker versus placebo, concentrated at higher doses and among the older non-vasodilating agents. The mechanism is real: beta-2 blockade suppresses thermogenesis by roughly 100 kcal/day (Pischon 2001 Int J Obes; Astrup 2000 Obes Rev), beta-1 and beta-2 blockade on adipocytes blunts lipolysis (Astrup 2000), and heart rate is capped so patients move less (Poirier 2001 Chest). But the drug-specific ordering matters more than the class effect: propranolol, atenolol, and metoprolol tartrate produce the largest weight signal; carvedilol is intermediate and A1c-neutral in the GEMINI trial (Bakris 2004 JAMA); nebivolol is essentially weight-neutral through its NO-mediated vasodilation (Sarafidis 2007 J Hum Hypertens). The explicit framing for readers on a heart-failure or post-MI beta blocker: the mortality benefit in HFrEF (MERIT-HF, CIBIS-II, COPERNICUS) and post-MI outweighs the weight gain by orders of magnitude — do not stop your beta blocker to fix the scale. For essential hypertension without another compelling indication, the 2017 ACC/AHA guideline (Whelton 2018) already demotes beta blocker to fourth-line, and a switch to a weight-neutral first-line agent (thiazide, ACE inhibitor, ARB, or DHP-CCB) or an in-class switch to nebivolol is a legitimate prescriber conversation.

How beta blockers are organised

Beta blockers are grouped by receptor selectivity and by vasodilating properties. Selectivity determines which pathways are blocked; vasodilating properties largely determine the metabolic and weight profile.

Why beta blockers drive weight gain — and why some don’t

Four mechanistic threads separate the older non-vasodilating agents from the newer vasodilating ones.

1. Thermogenesis suppression

Beta-2 receptors on skeletal muscle and brown adipose tissue mediate a meaningful fraction of resting energy expenditure. Pischon 2001 (International Journal of Obesity) measured resting energy expenditure on and off propranolol in healthy volunteers and documented a drop of roughly 100 kcal/day, and Astrup 2000 (Obesity Reviews) reviewed the mechanism across the class. Non-selective agents (propranolol) hit both receptors and produce the largest signal; cardioselective agents (metoprolol, atenolol, bisoprolol) suppress thermogenesis less but still measurably; vasodilating agents (nebivolol, carvedilol) largely preserve resting energy expenditure because the NO-mediated vasodilation or alpha-1 blockade offsets the beta-mediated thermogenic loss.

2. Lipolysis suppression

Beta-1 and beta-2 receptors on adipocytes drive the hormone-sensitive lipase pathway that mobilises fatty acids during fasting, exercise, and stress. Astrup 2000 documented the blunted lipolytic response on beta blocker, most pronounced during the overnight fast and during exercise. This is why patients often report that “the same workout doesn’t feel like it’s burning fat anymore” — the substrate mobilisation is genuinely reduced. Vasodilating agents largely escape this effect through alpha-blockade (carvedilol) or NO-mediated pathways (nebivolol).

3. Reduced spontaneous activity

Heart rate is the capped intensity ceiling for cardiovascular activity on beta blocker, and the fatigue and exercise-intolerance side-effect profile documented in Poirier 2001 (Chest) means many patients simply move less through the day. Non-exercise activity thermogenesis (NEAT) is a substantial fraction of total daily energy expenditure — often 15 to 30 percent — and a reduction there compounds over months. The practical countermeasure is to switch from heart-rate-based training targets to RPE (rate of perceived exertion), and to add resistance training, which recruits non-beta-adrenergic pathways for both energy expenditure and lean-mass preservation.

4. Vasodilating agents escape most of this

Sarafidis 2007 (Journal of Human Hypertensions) is the cleanest single-paper summary of why nebivolol is different: highly selective beta-1 blockade combined with endothelial NO release preserves peripheral perfusion, insulin sensitivity, and — critically for this article — resting energy expenditure. Bakris 2004 (JAMA) — GEMINI — is the analogous story for carvedilol: alpha-1 blockade offsets the metabolic burden of non-selective beta blockade, and carvedilol produced neutral A1c and neutral body composition versus metoprolol in patients with type 2 diabetes and hypertension. Weber 2004 (American Journal of Cardiology) documented the parallel insulin-sensitivity finding for carvedilol versus atenolol. This is why “beta blockers cause weight gain” is a class-level oversimplification — the vasodilating agents largely do not.

Dose-response and time-course

Approximate trajectories on four representative beta blockers, compiled from Sharma 2001 (Hypertension), Bakris 2004 (JAMA) GEMINI, and Ripley 2014 (American Journal of Cardiology).

5-step protocol — screen and stage

The plan that matches current guideline evidence and clinical practice in 2026. It leans on confirmed indication first, in-class switching before discontinuation, and lifestyle levers that offset the class effect.

Step 1: Confirm the indication

Beta blocker therapy is appropriate under several guideline scenarios. HFrEF and post-MI — carvedilol, bisoprolol, or metoprolol succinate as guideline-directed medical therapy per Yancy 2013 & 2022 (Circulation), driven by the mortality benefit in MERIT-HF, CIBIS-II, and COPERNICUS. Atrial fibrillation rate control — beta blocker or non-dihydropyridine calcium channel blocker per AFFIRM (AFFIRM 2002 NEJM) and the 2023 ACC/AHA/HRS AF guideline. Migraine prophylaxis — propranolol, metoprolol, or timolol per the AAN guideline (Silberstein 2012 Neurology). Essential tremor, off-label performance anxiety, and thyroid storm are additional legitimate indications. Essential hypertension without another compelling indication is not first-line — the 2017 ACC/AHA guideline (Whelton 2018 Hypertension) demotes beta blocker to fourth-line behind thiazide, ACE inhibitor, ARB, and DHP-CCB, and the Wiysonge 2017 (Cochrane) review reached the same conclusion. If your indication is essential hypertension only, the first conversation is whether beta blocker is the right class at all.

Step 2: Ask about a within-class switch to a weight-neutral option

For a patient with a legitimate indication and a documented weight signal, the second conversation is drug-specific. Nebivolol is the closest to weight-neutral for essential hypertension without HFrEF (Sarafidis 2007). Carvedilol is the preferred choice for hypertension with type 2 diabetes or metabolic syndrome (Bakris 2004 GEMINI), and it is one of three guideline-preferred agents for HFrEF alongside metoprolol succinate and bisoprolol (Yancy 2013). For migraine prophylaxis, timolol or metoprolol are alternatives if propranolol’s weight signal is prohibitive (Silberstein 2012). In HFrEF the mortality data are the driver, not the weight signal — do not switch away from a guideline-directed agent without cardiology involvement.

Step 3: Dose-optimise, don’t just add

The beta-blocker weight effect is dose-related (Sharma 2001). The minimum guideline dose that hits the outcome target — target heart rate in atrial fibrillation, target blood pressure in hypertension, target GDMT dose in HFrEF — is enough. Fonarow 2019 documented that GDMT-uptitration in HFrEF is often incomplete because clinicians and patients tolerate lower doses; the counterpoint is that at every step, the smallest dose that achieves the physiologic target minimises the metabolic burden.

Step 4: Fitness bundle to offset thermogenesis suppression

Resistance training 2 times per week and cardiovascular activity within an RPE (rate of perceived exertion) target of 5 to 7 out of 10 (rather than a heart-rate zone) restores the lipolytic and thermogenic capacity partially (Poirier 2001). This matters more on the older agents (propranolol, atenolol, metoprolol) than on the vasodilating agents. Adequate protein intake (1.2 to 1.6 g/kg per day) supports lean-mass preservation and offsets the modest reduction in NEAT — see strength training for weight loss and preserve muscle during weight loss.

Step 5: Do not stop abruptly

Abrupt discontinuation of any beta blocker in a patient with ischemic heart disease, HFrEF, or long-term therapy risks rebound tachycardia, angina, and myocardial infarction (Rangno 1982 Annals of Internal Medicine). This is called beta-blocker withdrawal syndrome, and it is a documented safety hazard. Any de-escalation or discontinuation is a prescriber-mediated slow taper over 2 to 4 weeks, with plans for the replacement agent already in place if hypertension or rate control is the indication.

What beta blocker and non-beta options actually do — compared

Special situations

HFrEF and post-MI

The mortality benefit of guideline-directed beta blockade in HFrEF is one of the largest documented in modern cardiology. MERIT-HF (1999 Lancet) demonstrated a 34 percent relative reduction in all-cause mortality on metoprolol succinate. CIBIS-II (1999 Lancet) showed the same magnitude on bisoprolol. COPERNICUS (2001 NEJM) confirmed the benefit for carvedilol in severe HFrEF. These effect sizes dwarf the 1 to 2 kg weight signal by orders of magnitude — a patient who discontinues a GDMT beta blocker to lose 1 kg is trading roughly 5 additional years of cumulative survival for a small cosmetic gain that a resistance-training programme could match. Fonarow 2019 documented the ongoing problem of incomplete GDMT uptitration; the conversation with the cardiologist is almost always about getting to target dose, not about de-escalation. Carvedilol is the metabolically-favoured choice in HFrEF patients with type 2 diabetes or metabolic syndrome per GEMINI. Solomon 2023 (NEJM) extended the HF picture with dapagliflozin add-on in HFpEF — the SGLT2 class is now part of GDMT for both HFrEF and HFpEF, and its weight-loss signal partially offsets the beta blocker effect. See heart failure and weight loss for the broader HFrEF weight framework.

Atrial fibrillation

Rate control in atrial fibrillation is well-established from AFFIRM 2002 (NEJM), and the 2023 ACC/AHA/HRS atrial fibrillation guideline (ACC/AHA/HRS 2023) recommends beta blocker or non-dihydropyridine calcium channel blocker as first-line rate-control options. The important weight-neutral alternative here is diltiazem (non-DHP CCB) — for patients who cannot tolerate the beta blocker weight signal and do not have HFrEF (where non-DHP CCBs are contraindicated), a switch to diltiazem often achieves the rate-control target without the metabolic burden. In the AFib patient with concurrent HFrEF, carvedilol or metoprolol succinate is the correct choice because non-DHP CCBs are contraindicated in reduced ejection fraction. See atrial fibrillation and weight loss.

Hypertension without another indication

The 2017 ACC/AHA hypertension guideline (Whelton 2018 Hypertension) demotes beta blocker to fourth-line for essential hypertension. Messerli 2007 (Lancet) meta-analysed atenolol versus comparator antihypertensives and documented that atenolol underperforms newer classes on stroke and mortality endpoints. Wiysonge 2017 (Cochrane) is the current Cochrane synthesis and reached the same conclusion. For a weight-focused patient with essential hypertension on a beta blocker, the first conversation is whether the beta blocker is the right class at all — thiazide, ACE inhibitor, ARB, or DHP calcium channel blocker are all first-line and weight-neutral (thiazide can produce a small diuresis-driven weight drop). See blood pressure and weight loss.

Migraine prophylaxis

Propranolol has AAN Level A evidence for migraine prophylaxis (Silberstein 2012 Neurology), and metoprolol and timolol are also supported. The competing prophylactic agent is topiramate, which produces the opposite weight signal — modest weight loss rather than weight gain. For a weight-focused migraine patient, the trade-off is explicit: propranolol gains, topiramate loses. Choose by patient priority, side-effect tolerance, and comorbidity — topiramate has its own cognitive and paresthesia signals that limit tolerance in some patients. See migraine and weight loss.

Diabetes and insulin resistance

Bakris 2004 (JAMA) — GEMINI — is the pivotal trial: carvedilol versus metoprolol in patients with type 2 diabetes and hypertension. Carvedilol was A1c-neutral and metabolically favourable; metoprolol worsened A1c by roughly 0.15 percentage points and produced small weight gain. Weber 2004 (American Journal of Cardiology) documented the parallel insulin-sensitivity finding for carvedilol versus atenolol. For a patient with type 2 diabetes and hypertension who needs a beta blocker for another compelling indication (HFrEF, post-MI, AFib), carvedilol is the preferred choice. For essential hypertension, nebivolol is a reasonable weight-neutral alternative. Avoid atenolol as first-line in T2D with hypertension — the metabolic profile is the worst in the class. See diabetes and weight loss and metabolic syndrome and weight loss.

GLP-1 medications and beta blockers

The GLP-1 fat-loss signal — 15 to 22 percent of body weight in the STEP and SURMOUNT programs — reliably outweighs the 1 to 2 kg beta blocker weight signal. There is no clinically important pharmacokinetic interaction between semaglutide, tirzepatide, or liraglutide and any beta blocker in current use. Two monitoring considerations: GLP-1 medications lower heart rate modestly, and the combined bradycardia with a beta blocker warrants a resting heart rate check at 4 to 6 weeks. If new fatigue or exercise intolerance appears in the first weeks of GLP-1 therapy, treat the GLP-1 tolerability first before assuming the beta blocker has become the problem. Coordinate with the prescriber — see GLP-1 weight loss overview, semaglutide weight loss, and weight loss drug safety.

Red flags

• Syncope with chest pain — 911 or emergency evaluation for possible acute coronary syndrome, high-grade AV block, or ventricular arrhythmia (particularly on sotalol)
• Symptomatic bradycardia — resting heart rate under 50 bpm with lightheadedness, near-syncope, or fatigue; same-day prescriber contact for dose reduction or agent switch
• Cold extremities or worsening claudication in peripheral artery disease — non-selective agents (propranolol) are the usual culprit; switch to a vasodilating agent (nebivolol) or a non-beta class
• New bronchospasm on a non-selective beta blocker — propranolol, nadolol, and timolol are contraindicated in reactive airway disease; urgent switch to a highly cardioselective agent (bisoprolol, nebivolol) if beta blockade is required, or discontinuation with alternate rate-control
• Acute HF decompensation in a de-escalation window — abrupt down-titration of GDMT in HFrEF risks decompensation; any de-escalation is cardiology-mediated
• Rebound tachycardia or angina on abrupt discontinuation — beta-blocker withdrawal syndrome (Rangno 1982 Annals of Internal Medicine); resume the drug at the previous dose and taper slowly under prescriber supervision

How this connects to the rest of the site

Beta blockers sit at the centre of a cardiovascular-and-metabolic cluster on this site. For the specific cardiovascular indications, see blood pressure and weight loss, heart failure and weight loss, and atrial fibrillation and weight loss. For the non-cardiovascular indications, see migraine and weight loss and anxiety and weight loss. For the metabolic backdrop that shapes drug choice, see metabolic syndrome and weight loss, diabetes and weight loss, and insulin resistance and weight loss. For the “the scale is stuck” cluster this article is most likely to enter, see why am I not losing weight and set point theory weight loss. For the dietary and training frames that offset the class effect, see Mediterranean diet weight loss, strength training for weight loss, and preserve muscle during weight loss. For the parallel drug-therapy stories, see statins and weight, metformin and weight, and the broader weight loss drug safety guide.

Beta blockers and weight FAQ

Does my beta blocker cause weight gain? A little — about 1.2 kg on average over 6 to 12 months on the non-vasodilating agents (Sharma 2001), and essentially nothing on nebivolol (Sarafidis 2007).

Which is the worst? Atenolol, then propranolol and metoprolol tartrate. Head-to-head trials (Ripley 2014; Bakris 2004) rank atenolol worst on the metabolic profile.

Which is weight-neutral? Nebivolol; carvedilol is a close second in metabolically burdened patients.

Should I switch to nebivolol or carvedilol? For essential hypertension, often yes — nebivolol. For hypertension with T2D, often yes — carvedilol. For HFrEF, only within the three GDMT choices (carvedilol, metoprolol succinate, bisoprolol).

Can I stop it if I’ve lost weight? Almost never on your own. HFrEF, post-MI, AFib, and migraine indications persist; abrupt discontinuation risks withdrawal syndrome.

Can I take a GLP-1 with a beta blocker? Yes — no clinically important interaction; monitor resting heart rate at 4 to 6 weeks.

Does it slow my metabolism? Yes, by roughly 100 kcal/day on non-vasodilating agents (Pischon 2001; Astrup 2000) — real but manageable with resistance training and RPE-based cardio.