Metformin and Ageing: The TAME Trial Explained

Medically reviewed by Dr Zeeshan Afzal (MBBS), Medical Officer at Welzo. Last updated: July 2026.

Metformin is one of the oldest, cheapest and most widely prescribed medicines in the world — and for the past decade it has also been the single most talked-about candidate in metformin longevity research. The reason is a trial that has never actually started: TAME, or Targeting Aging with Metformin. TAME was designed to be the first study in history to treat ageing itself as a medical target rather than treating one disease at a time.

This guide explains what the TAME trial is, why metformin was chosen over every other compound, exactly what the evidence does and does not show, where the trial stands in 2026, and what all of this means for a UK reader who is thinking about their own healthspan. It is written for people without a medical background, but it does not simplify away the parts that matter.

Metformin is prescription-only, so for readers looking at what is actually available without one, our pillar guide to longevity supplements sets out the non-prescription options and how strong the evidence is for each, alongside the anti-ageing and longevity range. Our NMN benefits, side effects and dosage guide and NMN supplements collection cover the most widely studied of them.

Key takeaways

• TAME is a proposed six-year, 14-site trial of roughly 3,000 adults aged 65–79, coordinated by Wake Forest University School of Medicine and championed by the American Federation for Aging Research (AFAR).
• As of July 2026, AFAR still lists TAME as awaiting funding. No efficacy results have been published, and any article claiming TAME has "proven" metformin slows ageing is inaccurate.
• The strongest evidence for metformin as a geroprotector comes from cell, worm, mouse and — since 2024 — monkey studies. The human evidence is observational and heavily disputed.
• The most rigorous human data available, a 21-year follow-up of the Diabetes Prevention Program published in JAMA in June 2026, found that intensive lifestyle change reduced multimorbidity risk while metformin did not.
• Metformin is a prescription-only medicine (POM) in the UK. It is not licensed for ageing, longevity or healthspan, and it cannot legally be sold over the counter.

Table of contents

• What is the TAME trial?
• Why metformin? The case for an 80-year-old drug
• How metformin works at a cellular level
• The evidence for metformin and longevity
• Where TAME actually stands in 2026
• The exercise trade-off nobody talks about
• Safety, side effects and monitoring
• Can you get metformin for longevity in the UK?
• What the evidence supports while TAME waits
• Who might reasonably discuss metformin with a doctor
• Frequently asked questions
• References

What is the TAME trial?

TAME stands for Targeting Aging with Metformin. It was designed by Dr Nir Barzilai and colleagues at the Albert Einstein College of Medicine, and it is managed as an initiative by the American Federation for Aging Research.

The concept is deceptively simple. Conventional medicine treats heart disease, cancer and dementia as separate problems with separate specialists and separate drugs. Geroscience argues that these conditions share a common upstream driver — biological ageing — and that slowing that driver should delay all of them at once. TAME was built to test that argument in humans for the first time.

Trial design at a glance

Why the composite endpoint is the real innovation

Most trials measure one thing. A statin trial measures cardiovascular events. An oncology trial measures tumour progression. TAME does something different: it counts whichever age-related disease appears first, then stops the clock.

That design choice is what makes TAME historically significant. If a drug delays the first appearance of several unrelated diseases simultaneously, the most parsimonious explanation is that it has slowed the shared biology underneath them. That is the geroscience hypothesis stated as a testable endpoint — and it is why regulators, not just researchers, have paid attention. To understand which shared processes are being targeted, it helps to read our explainer on the hallmarks of ageing.

What "an indication for ageing" would actually mean

AFAR's stated goal is for regulators to recognise ageing as an indication — a condition a drug can legitimately be prescribed for. Today, no medicine anywhere in the world is licensed to treat ageing. That has a knock-on effect far beyond metformin: without a regulatory pathway, pharmaceutical companies have little incentive to develop geroprotective drugs, because there is no approvable endpoint to aim at.

In other words, TAME was never really about metformin. Metformin was chosen as the cheapest, safest available vehicle for establishing a precedent that every subsequent longevity drug could follow.

Why metformin? The case for an 80-year-old drug

Goat's rue (Galega officinalis), the plant behind metformin's guanidine chemistry. Image: H. Zell, CC BY-SA 3.0, via Wikimedia Commons.

From goat's rue to the NHS

Metformin descends from guanidine, a compound found in Galega officinalis — goat's rue, or French lilac — a plant used in European folk medicine for centuries to relieve excessive thirst and urination, which we now recognise as diabetes symptoms. The biguanide chemistry was refined in the 1920s, metformin entered clinical use in France in the 1950s, and it reached the United States in 1994.

Today it is the NHS first-line treatment for type 2 diabetes, on the WHO Model List of Essential Medicines, and taken by hundreds of millions of people. That accumulated exposure is precisely why the NIH-funded Geroscience Network recommended it for TAME: no novel compound could offer a comparable safety record, and its off-patent price makes a six-year trial in 3,000 people financially conceivable.

The paradox that made everyone pay attention

Large observational datasets of people with type 2 diabetes repeatedly showed that metformin users had lower rates of certain cancers and cardiovascular events than diabetics on other drugs. Then came the finding that genuinely startled the field: a 2014 UK study reported that diabetics on metformin monotherapy appeared to outlive matched non-diabetic controls.

That result is the origin of almost every "metformin longevity" headline you have read since. We will look closely at whether it survives scrutiny below — because it largely does not.

How metformin works at a cellular level

The metformin molecule: a biguanide with a deceptively simple structure. Image via Wikimedia Commons.

AMPK activation

Metformin indirectly activates AMP-activated protein kinase (AMPK), the cell's low-fuel sensor. When AMPK switches on, the cell shifts away from growth and storage and towards energy production, mitochondrial biogenesis and autophagy. This is the same broad signalling direction produced by fasting and by sustained exercise, which is why metformin is often described as a partial calorie-restriction mimetic. If that mechanism interests you, our guide to autophagy explained covers the cellular recycling side in more detail.

Mild inhibition of mitochondrial complex I

Metformin mildly and reversibly inhibits complex I of the mitochondrial electron transport chain. Reducing hepatic energy availability suppresses gluconeogenesis — the liver's glucose production — which is the primary way metformin lowers blood sugar. This same action is thought to trigger a mild hormetic stress response, and it is also the mechanism most implicated in metformin's interference with exercise adaptation.

Reduced insulin and IGF-1 signalling

By improving insulin sensitivity, metformin lowers circulating insulin. Chronically elevated insulin and IGF-1 signalling is one of the most conserved pro-ageing pathways across species, from nematodes to humans. Damping it is a plausible route to slower biological ageing.

Gut microbiome and inflammation

A substantial share of metformin's metabolic effect occurs in the gut, where it alters bile acid handling, increases GLP-1 secretion and shifts microbial composition. It also appears to reduce markers of chronic low-grade inflammation, sometimes called "inflammaging". Related gut-axis work is covered in our pages on Akkermansia and butyrate supplements.

The evidence for metformin and longevity

This is where careful reading matters most. The evidence base is a pyramid, and the layers are not equally strong.

Invertebrates and mice

Mouse lifespan studies form the backbone of geroprotector testing. Image: Rama, CC BY-SA 2.0 FR, via Wikimedia Commons.

Martin-Montalvo and colleagues reported in Nature Communications in 2013 that metformin started in middle age extended healthspan and lifespan in male mice, with lifespan gains of roughly 4–6% at an appropriate dose. Crucially, a tenfold higher dose was toxic and increased mortality. Healthspan measures such as rotarod performance, treadmill distance, cataract index and glucose tolerance improved by up to around 30%.

Not every model agreed. In fruit flies, metformin robustly activated AMPK and reduced lipid stores but did not extend lifespan. In rats given very high doses, no lifespan benefit appeared.

The Interventions Testing Program: the toughest test

The National Institute on Aging's Interventions Testing Program (ITP) is the gold standard for geroprotector claims. It runs identical protocols across three independent sites using genetically heterogeneous mice, specifically to weed out results that only appear in one lab.

Metformin alone did not extend lifespan in the ITP. Metformin combined with rapamycin did produce robust lifespan extension — but rapamycin alone extends lifespan too, and subsequent ITP analyses could not establish that the combination beat rapamycin by itself. This is one of the most important and least-reported facts in the metformin longevity conversation. For context on the other half of that pairing, see our overview of rapamycin and longevity in the UK.

The 2024 monkey study

Cynomolgus monkeys (Macaca fascicularis) were used in the first long-term primate trial of metformin's geroprotective effects. Image: Charles J. Sharp, CC BY-SA 4.0, via Wikimedia Commons.

In September 2024, researchers at the Chinese Academy of Sciences published a 40-month study in Cell in which male cynomolgus monkeys aged 13–16 years (roughly equivalent to humans in their forties) received 20 mg/kg metformin daily. Using multi-omic "ageing clocks" built from transcriptomic, methylomic, proteomic and metabolomic data, the team reported that metformin decelerated ageing indicators across multiple tissues, with plasma protein age reduced by an average of about 6.4 years and brain ageing regressed by roughly six years. Senescent-cell markers fell in heart, kidney, skin, lung, liver and stomach tissue, and treated animals performed better on memory tasks.

This is the strongest mechanistic evidence to date — and it still comes with caveats. The sample was small, male-only, and the endpoints were biological ageing clocks rather than lifespan or disease incidence. Ageing clocks are proxies, and a proxy improving is not the same as a life being longer. If you want to understand what these measures do and do not capture, read our guide to biological age.

The human observational data — and why it is contested

The 2014 Bannister study analysed around 78,000 UK patients on metformin monotherapy, roughly 12,000 on sulphonylurea monotherapy, and around 200,000 matched non-diabetic controls drawn from the Clinical Practice Research Datalink. Metformin initiators showed lower all-cause mortality than both comparison groups.

Three serious objections have since been raised:

• Immortal time bias. To be prescribed metformin, a patient must survive long enough after diagnosis to receive it. That guaranteed survival window is silently credited to the drug. Suissa and Azoulay demonstrated that this and related time-related biases inflated metformin's apparent benefits across a large body of observational cancer research.
• Selection bias in both directions. Patients kept on metformin monotherapy are, by definition, the diabetics whose disease is mildest and best controlled. Meanwhile "non-diabetic" control groups in large UK datasets inevitably contain undiagnosed diabetics and people with less contact with primary care.
• Failed replication. A Danish national-registry study by Keys and colleagues attempted to reproduce the finding using four separate designs, including discordant twin pairs to control for genetic and familial factors. It found no survival advantage and no survival equalisation for metformin initiators; mortality was consistently higher than in non-diabetic controls.

A Mendelian randomisation analysis published in The Lancet Healthy Longevity in 2023, which uses genetic variants to approximate lifelong drug-target modulation and is far less vulnerable to these biases, also did not support a general effect of metformin targets on phenotypic age or mortality.

The 2026 DPP/DPPOS result: the most decision-relevant data we have

In June 2026, the Diabetes Prevention Program research group published a 21-year follow-up in JAMA. This matters more than most metformin studies because participants were randomised in the late 1990s to intensive lifestyle intervention, metformin 850 mg twice daily, or placebo — eliminating the selection biases that plague observational work.

Among 1,173 participants with linked Medicare data through 2021, the lifestyle group had a 21% lower risk of developing two or more chronic conditions and a 25% lower risk of three or more, compared with placebo. For the costliest disease combinations, the reduction reached 43%. Metformin did not differ significantly from placebo on any of these measures. The lifestyle advantage persisted even when diabetes itself was removed from the definition of multimorbidity.

This is not proof that metformin does nothing for ageing — the trial was not designed as a geroscience study, the population was prediabetic, and multimorbidity is a coarse endpoint. But it is currently the closest thing we have to a randomised, long-term test of "does metformin reduce the accumulation of age-related disease in people without diabetes?" And the answer it gave was no, while lifestyle gave a clear yes.

Evidence summary

Where TAME actually stands in 2026

AFAR's official TAME resource, as of July 2026, still describes the trial in prospective terms: the study design is prepared, and what is needed is funding, participants, and a regulatory indication for ageing. It has been in this state since the FDA agreed to the composite endpoint framework around 2015.

Why an $80 million trial cannot find $80 million

The obstacle is structural, not scientific. Metformin is off-patent and costs pennies per tablet. No pharmaceutical company can recoup a nine-figure trial cost on a generic drug, and public research funders have historically been reluctant to fund trials of ageing as an endpoint precisely because ageing is not a recognised indication — the exact circularity TAME was designed to break.

Be sceptical of any source claiming TAME has reported results. Several AI-generated health sites have published detailed "findings" from TAME, including specific effect sizes. These are fabrications. When TAME does report, it will appear in a major journal and on AFAR's own site first.

What would count as a genuine update

• A trial registration with a unique identifier, named sponsor and recruiting status
• A published protocol with the primary endpoint stated explicitly
• An announcement from AFAR or Albert Einstein College of Medicine
• Peer-reviewed publication of results, not a press summary

Smaller biomarker studies — including MILES (Metformin In Longevity Study), which examined gene expression in older non-diabetic adults over six weeks — are useful but are not TAME, and should not be reported as such.

The exercise trade-off nobody talks about

Regular aerobic and resistance training remain the best-evidenced healthspan interventions available. Image: Seattle Municipal Archives, CC BY 2.0, via Wikimedia Commons.

This is the finding that most changes the practical calculus. In a double-blind randomised trial published in Aging Cell in 2019, Konopka and colleagues assigned 53 adults averaging 62 years old to metformin or placebo during 12 weeks of aerobic exercise training. Both groups improved body composition and glycaemic measures. But the metformin group showed attenuated improvement in whole-body insulin sensitivity and VO2max, and metformin abolished the exercise-driven increase in skeletal muscle mitochondrial respiration.

Subsequent work has produced mixed results, and not all studies find the same blunting. But the mechanistic story is coherent: if exercise adaptation depends on a mitochondrial stress signal, and metformin dampens mitochondrial respiration, the two interventions may partially cancel.

The implication is uncomfortable for the biohacking framing. Exercise has vastly stronger evidence for healthspan than metformin does. Taking a drug with weak longevity evidence that may blunt the benefits of an intervention with strong longevity evidence is a poor trade for a healthy, active person. Our pages on zone 2 training and longevity and creatine for longevity cover the alternative side of that equation.

Safety, side effects and monitoring

Metformin 500 mg tablets as dispensed on NHS prescription. Image via Wikimedia Commons.

Common side effects

According to the NHS, the most common side effects — affecting more than one in 100 people — are nausea, vomiting, diarrhoea, stomach pain and loss of appetite. These are usually worst in the first weeks and improve with gradual dose escalation, taking tablets with food, or switching to a modified-release formulation.

Vitamin B12 depletion

This is the most clinically important long-term issue. In the DPPOS analysis published in the Journal of Clinical Endocrinology & Metabolism in 2016, combined low and borderline-low B12 was more common in the metformin group at both 5 years (19.1% vs 9.5%) and 13 years (20.3% vs 15.6%). Each additional year of metformin use was associated with a 13% increase in the odds of B12 deficiency. Neuropathy prevalence was higher in metformin users with low B12.

The NHS lists B12 deficiency as a common side effect at higher doses or with long-term use. Anyone taking metformin chronically should have B12 status checked periodically. This is not optional monitoring — untreated B12 deficiency can cause irreversible neurological damage. If methylation status is relevant to your wider supplement plan, see our comparison of TMG versus methylfolate.

Lactic acidosis and contraindications

Lactic acidosis is rare but serious. Risk rises substantially with significant kidney impairment, severe liver disease, unstable heart failure, dehydration, acute illness and heavy alcohol use. These are also the standard exclusion criteria in metformin research. Renal function must be assessed before starting and monitored during treatment.

Interactions

Metformin does not usually cause hypoglycaemia on its own, but it can when combined with insulin or sulphonylureas such as gliclazide. Concurrent use of proton pump inhibitors or H2 antagonists has been associated with an increased risk of B12 deficiency. Always tell a prescriber about every supplement you take — our guide on whether you can take supplements together is a useful starting point, but it does not replace a pharmacist's review.

Can you get metformin for longevity in the UK?

Metformin is classified as a prescription-only medicine (POM) in the UK. It cannot legally be sold over the counter, and no UK pharmacy can supply it without a valid prescription.

It is licensed for type 2 diabetes, gestational diabetes and prevention of type 2 diabetes in high-risk individuals. It is also prescribed off-label for polycystic ovary syndrome. It is not licensed anywhere in the world for ageing, longevity or healthspan. A UK GP is very unlikely to prescribe it to a metabolically healthy person for anti-ageing purposes, and that reluctance reflects the evidence rather than conservatism.

Buying metformin from overseas websites without a prescription carries real risks: no clinical assessment of kidney function, no baseline bloods, no B12 monitoring, no interaction check, and no guarantee of product identity or purity. If you are evaluating supply chains for anything you take, our guides to third-party tested supplements and reading a certificate of analysis apply the same scrutiny to the supplement market.

What the evidence supports while TAME waits

If your goal is compressing morbidity rather than chasing a specific molecule, the current evidence hierarchy is fairly clear.

Among supplemental approaches, NAD+ precursors are the most researched. NAD+ declines with age and is required for sirtuin activity, DNA repair and mitochondrial function — overlapping mechanistically with several pathways metformin touches, but without the prescription barrier or the exercise-blunting concern. Our complete guide to NMN benefits, side effects and dosage sets out what the human trials actually show, and our NAD supplement guide compares the precursor forms.

If you want to explore that route, Welzo's NMN supplement range is third-party tested and UK-dispatched, with NMN Pro 1000 being the most commonly chosen daily dose among readers building a first stack. For a broader view of how these pieces fit together, see our longevity supplements guide and how to start longevity supplements.

Equally important is knowing what to skip. Our honest assessments of longevity supplements that don't work and whether resveratrol works apply the same evidence standard used above.

Who might reasonably discuss metformin with a doctor

Nothing here is a recommendation, and metformin should only ever be started under medical supervision. But the profile of someone for whom a conversation is reasonable looks quite different from the biohacker stereotype:

• People with diagnosed type 2 diabetes, for whom metformin is standard first-line care
• People with prediabetes or established insulin resistance, where NICE-recognised indications may apply
• Women with PCOS, where off-label use is well established in UK practice
• Older adults with existing metabolic dysfunction, where the metabolic benefit is real regardless of any ageing effect

Conversely, the group with the weakest case is the one most likely to want it: metabolically healthy, physically active adults in their thirties and forties. For that group the evidence suggests little to gain and a plausible mechanism for loss. If that describes you, our guides to longevity supplements in your 30s, longevity supplements for men over 50 and longevity supplements for women over 40 are more relevant starting points.

Frequently asked questions

Has the TAME trial finished?

No. As of July 2026, AFAR still describes TAME as prepared but awaiting funding and participants. No efficacy results have been published. Any article reporting specific TAME outcomes is not describing real published data.

Does metformin actually extend lifespan in humans?

There is no randomised trial evidence that it does. Observational studies suggesting a mortality advantage have failed replication and are affected by immortal time bias and selection bias. The best randomised long-term data available, the 2026 DPP follow-up, found no significant reduction in multimorbidity versus placebo.

What dose of metformin is used in longevity research?

TAME's design uses 1,500 mg daily, and the DPP used 850 mg twice daily. However, there is no validated dose for longevity in healthy adults, because no trial has established that any dose produces a longevity benefit in people without diabetes.

Can I buy metformin over the counter in the UK?

No. Metformin is a prescription-only medicine in the UK and cannot be sold without a prescription. It has no licensed indication for ageing or longevity.

Does metformin interfere with building muscle or fitness?

Possibly. A randomised trial in older adults found metformin attenuated gains in VO2max and insulin sensitivity from 12 weeks of aerobic training, and blocked the increase in muscle mitochondrial respiration. Findings across studies are mixed, but the signal is strong enough that anyone training seriously should weigh it.

Should I take vitamin B12 with metformin?

Long-term metformin use is associated with reduced B12 status, and the NHS lists B12 deficiency as a common side effect at higher doses or with prolonged use. Rather than self-supplementing blindly, ask your GP to check your B12 level and follow their advice on whether supplementation is needed.

Is metformin better than NMN for longevity?

They are not directly comparable: metformin is a prescription medicine with weak longevity evidence in healthy people, while NMN is a supplement targeting NAD+ decline with early-stage human data. Neither has demonstrated lifespan extension in humans. Our is NMN a scam? article applies the same scepticism used in this guide.

What did the 2024 monkey study actually prove?

It showed that 40 months of metformin slowed multi-omic ageing clocks across tissues in male cynomolgus monkeys, including roughly a six-year regression in brain age, alongside better memory performance and fewer senescent-cell markers. It did not measure lifespan or disease incidence, and it did not involve humans.

Is berberine a natural alternative to metformin?

Berberine has some overlapping metabolic effects and is sometimes marketed that way, but it is not equivalent in potency, regulation or evidence base, and it carries its own interaction profile. We compare them in detail in berberine vs metformin.

If TAME never runs, does that mean metformin doesn't work?

No — it means the question stays open. TAME's stall is a funding and regulatory problem, not a scientific verdict. But in the absence of that trial, the honest position is that metformin's longevity benefit in people without diabetes is unproven, and the interventions with proven healthspan benefits are the ones worth prioritising now.

References

1. American Federation for Aging Research. TAME — Targeting Aging with Metformin. https://www.afar.org/tame-trial
2. Barzilai N, Crandall JP, Kritchevsky SB, Espeland MA. Metformin as a Tool to Target Aging. Cell Metabolism. 2016;23(6):1060–1065. https://pubmed.ncbi.nlm.nih.gov/27304507/
3. Yang Y, Lu X, Liu N, et al. Metformin decelerates aging clock in male monkeys. Cell. 2024;187(22):6358–6378. https://www.cell.com/cell/fulltext/S0092-8674(24)00914-0
4. Abou Zaki R, El-Osta A. Metformin: decelerates biomarkers of aging clocks. Signal Transduction and Targeted Therapy. 2024;9:319. https://www.nature.com/articles/s41392-024-02046-1
5. Strong R, Miller RA, Antebi A, et al. Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an α-glucosidase inhibitor or a Nrf2-inducer. Aging Cell. 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5013015/
6. Bannister CA, Holden SE, Jenkins-Jones S, et al. Can people with type 2 diabetes live longer than those without? Diabetes, Obesity and Metabolism. 2014;16(11):1165–1173. https://pubmed.ncbi.nlm.nih.gov/25041462/
7. Suissa S, Azoulay L. Metformin and the risk of cancer: time-related biases in observational studies. Diabetes Care. 2012. https://pubmed.ncbi.nlm.nih.gov/23173135/
8. Emerging uncertainty on the anti-aging potential of metformin (review of failed replications including Keys et al., 2022). Ageing Research Reviews. 2025. https://www.sciencedirect.com/science/article/pii/S1568163725001631
9. Luo S, et al. Effects of putative metformin targets on phenotypic age and mortality: a Mendelian randomisation study. The Lancet Healthy Longevity. 2023;4(6):e335–e344. https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(23)00085-5/fulltext
10. National Institutes of Health. For adults with prediabetes, lifestyle intervention lowered risk of developing multiple chronic conditions. June 2026. https://www.nih.gov/news-events/news-releases/adults-prediabetes-lifestyle-intervention-lowered-risk-developing-multiple-chronic-conditions
11. Konopka AR, Laurin JL, Schoenberg HM, et al. Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults. Aging Cell. 2019;18(1):e12880. https://pubmed.ncbi.nlm.nih.gov/30548390/
12. Aroda VR, Edelstein SL, Goldberg RB, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study. J Clin Endocrinol Metab. 2016;101(4):1754–1761. https://academic.oup.com/jcem/article/101/4/1754/2804585
13. NHS. About metformin. https://www.nhs.uk/medicines/metformin/about-metformin/
14. NHS. Side effects of metformin. https://www.nhs.uk/medicines/metformin/side-effects-of-metformin/
15. Diabetes UK. Metformin — uses, how it works and side effects. https://www.diabetes.org.uk/about-diabetes/looking-after-diabetes/treatments/tablets-and-medication/metformin
16. Weiss R, Fernandez E, Liu Y, Strong R, Salmon AB. Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice. Aging. 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5892694/

Medical disclaimer

This article is for general information and education only. It is not medical advice and does not replace consultation with a qualified healthcare professional. Metformin is a prescription-only medicine in the UK and should only be taken under the supervision of a prescriber who has assessed your kidney function, medication list and overall health. Never start, stop or change a prescribed medicine on the basis of an online article. If you have questions about your own health, speak to your GP, pharmacist or another registered clinician.

Reviewed by Dr Zeeshan Afzal (MBBS), Medical Officer at Welzo.