Semaglutide and Walking Capacity: What the STRIDE Trial Means for People with PAD and Type 2 Diabetes

In recent years, medications like Wegovy (Semaglutide) and Mounjaro (Tirzepatide) have taken the world by storm, revolutionising the management of Type 2 diabetes and obesity. Their profound impact on blood sugar control and weight loss has generated headlines and offered new hope to millions. But what if this was just the beginning? What if the next generation of metabolic medicine could deliver even more powerful results?

Enter Retatrutide, an investigational medicine that is rapidly becoming one of the most talked-about drugs in development.

Nicknamed the "Triple G" drug, Retatrutide is currently undergoing extensive Phase 3 clinical trials and is not yet available to the public.

Its unique power lies in its ability to target not one, not two, but three key metabolic hormone receptors, a triple-action mechanism that promises to push the boundaries of what's possible in diabetes and weight management.

This article will delve into the ground-breaking science to discover how Retatrutide could revolutionise diabetes and weight loss management with its triple-agonist action.

How Retatrutide Works: The 'Triple G' Advantage

The excitement surrounding Retatrutide stems from its sophisticated and unprecedented mechanism of action. While older drugs target a single hormone pathway, Retatrutide is a triple receptor agonist, engaging with three distinct hormones that play a crucial role in regulating our metabolism, appetite, and blood sugar. This multi-pronged attack is what sets it apart and gives it a potential clinical edge. 

To understand its power, we need to break down each component of its "Triple G" action:

• GLP-1 (Glucagon-like peptide-1) Receptor Agonism: This is the same mechanism used by drugs like Ozempic and Wegovy. Activating the GLP-1 receptor tells the brain you are full, significantly reducing appetite. It also slows down the rate at which your stomach empties, prolonging the feeling of satiety after a meal. For individuals with Type 2 diabetes, it stimulates the pancreas to release insulin in response to high blood sugar levels.
• GIP (Glucose-dependent insulinotropic polypeptide) Receptor Agonism: This is the second target, which Retatrutide shares with the dual-agonist drug Mounjaro. GIP also enhances the body's insulin release in response to glucose, working synergistically with GLP-1 to improve blood sugar control. Furthermore, research suggests GIP may play a role in how the body processes and stores fat.
• Glucagon Receptor Agonism: This is Retatrutide's unique and game-changing feature. While it might seem counterintuitive to activate the receptor for glucagon, a hormone that raises blood sugar, the effect in this context is profoundly different. Activating the glucagon receptor in combination with GLP-1 and GIP appears to increase energy expenditure. In simple terms, it helps the body burn more calories and fat, even at rest. This action specifically targets the liver, reducing fat accumulation and improving overall metabolic health.

This triple-action mechanism results in a powerful synergy. The GLP-1 and GIP components work together to control blood sugar and suppress appetite, while the glucagon component accelerates fat burning and energy use. For a person with Type 2 diabetes, this combination is revolutionary. It not only addresses high blood sugar (hyperglycaemia) but also tackles one of the primary drivers of the condition: excess body weight, particularly visceral fat. The strong link between weight loss and improved diabetes outcomes is well-established, with bodies like the American Diabetes Association (ADA) highlighting that significant weight reduction can even lead to remission in some cases.

Clinical Breakthroughs in Diabetes Treatment

The theoretical promise of Retatrutide's triple-action mechanism has been powerfully validated by its clinical trial results. The data from the Phase 2 trial, published in The Lancet, has sent waves of excitement through the medical community. The study evaluated the drug's effects on individuals with Type 2 diabetes over 36 weeks, revealing unprecedented efficacy in both blood sugar control and weight loss.

Focus on HbA1c (Glycosylated Haemoglobin) and Glucose Control

A key measure for diabetes management is HbA1c, which reflects average blood glucose levels over the preceding two to three months. According to NICE guidelines in the UK, a target HbA1c for adults with Type 2 diabetes is typically 48 mmol/mol (6.5%) or lower.

In the Phase 2 trial, participants receiving the highest doses of Retatrutide saw their HbA1c levels fall by a staggering average of 2.02% (22.1 mmol/mol). This reduction is significantly greater than that seen with many existing diabetes medications. To put this into perspective, a large number of participants achieved levels that are considered non-diabetic:

• 92% of participants on the 8mg dose achieved an HbA1c of 6.5% or less.
• An incredible 78% of participants on the 12mg dose reached an HbA1c below 5.7%, which is the threshold for normal glucose levels in individuals without diabetes.

These results suggest that Retatrutide has the potential not just to manage Type 2 diabetes, but to normalise blood sugar

The Weight Loss Factor

While glucose control was impressive, the weight-loss results were truly groundbreaking.

Obesity is a major risk factor and complicating factor for Type 2 diabetes, and achieving substantial weight loss is critical for improving insulin sensitivity and overall health.

The trial participants on the highest dose of Retatrutide lost an average of 16.9% of their body weight (around 17.5 kg or 38.6 lbs) in just 36 weeks. A separate Phase 2 trial focusing on obesity, published in The New England Journal of Medicine, showed even more profound results over a longer period, with participants losing up to 24.2% of their body weight at 48 weeks.

This level of weight loss, achieved without intensive surgical intervention, was previously unimaginable for a pharmaceutical drug. Crucially, a substudy using advanced imaging techniques revealed that this weight loss was primarily due to a reduction in fat mass, not muscle. 

Participants lost up to 26.1% of their total fat mass while largely preserving lean muscle tissue, which is vital for maintaining metabolic health and physical strength. This targeted fat reduction directly contributes to improved insulin sensitivity and can significantly ease the metabolic burden of Type 2 diabetes.

Retatrutide vs. Mounjaro (Tirzepatide) and Ozempic (Semaglutide)

The Edge: Why Triple Action Matters

The research data strongly suggest that adding glucagon receptor agonism provides a significant clinical advantage. While Mounjaro's dual action demonstrated the benefit of targeting more than one pathway, Retatrutide's third mechanism appears to unlock a new level of efficacy. The glucagon action's ability to increase energy expenditure and burn fat on top of the appetite suppression and insulin regulation from GLP-1 and GIP creates a comprehensive metabolic treatment that tackles the problem from three different angles. This is why experts believe Retatrutide could offer superior and more durable results for both diabetes control and weight reduction.

Crucial Warning: Availability and Safety

While the clinical trial results for Retatrutide are incredibly promising, it is absolutely vital for the public to understand its current status. 

Current Investigational Status

Retatrutide is an investigational drug and is NOT approved for public use anywhere in the world yet ( 12 December 2025), including the United Kingdom.

If you see advertisements for Retatrutide or its compounded form on social media like TikTok or Instagram, you should not purchase it, as this substance is currently an investigational drug, has not been approved by the MHRA or other regulatory bodies for prescription or sale, and is only legally available to participants in clinical trials, which are not expected to conclude until 2026 at the earliest; consequently, any website or seller offering it is doing so illegally, and buying unregulated, non-pharmacy grade compounds carries serious health risks, including potential contamination, incorrect dosages, and severe adverse effects.

The Dangers of the Unregulated Trade

The extraordinary public appetite for these groundbreaking new metabolic drugs has, regrettably, given rise to a perilous unregulated trade for unapproved substances. Unscrupulous sellers are frequently peddling these products online, often marketing them dishonestly as "research peptides" in an attempt to sidestep crucial regulations. It is absolutely vital that the public understands the serious risks associated with buying these illicit products:

• Uncertain Dosage and Purity: Products from the unregulated supply chain are subject to no quality control whatsoever. The active substance you receive could be underdosed, overdosed, or, indeed, contain an entirely different active ingredient to what was advertised.
• Absence of Sterility: Injectable medicines must be manufactured in strictly sterile environments. Illicit products are routinely concocted under unsanitary conditions, presenting a significant risk of bacterial contamination and subsequent serious infection.
• Dangerous Contaminants: Vials sourced through these illegal channels may be contaminated with heavy metals, unidentified chemical by-products, or other deeply harmful substances.
• Risk of Severe Side Effects: Taking such a potent, unapproved drug without proper medical supervision could trigger life-threatening adverse reactions, including severe hypoglycaemia (dangerously low blood sugar), pancreatitis, heart complications, and acute allergic reactions.

Regulatory bodies are actively cracking down on this illegal trade. The MHRA recently announced a raid on an illegal manufacturing facility, seizing thousands of doses of unapproved products. This highlights the very real and present danger of the unregulated market.

Conclusion

Retatrutide represents a potential paradigm shift in the treatment of Type 2 diabetes and obesity. Its unique triple-action mechanism has delivered unprecedented results in clinical trials, offering the possibility of not just managing these chronic conditions, but of normalising key metabolic markers to a degree previously thought impossible with medication alone.

The significant reductions in HbA1c and body weight point to a future where medicine moves beyond simple glucose control and towards a more comprehensive and holistic approach to metabolic health. However, excitement must be tempered with patience and caution.

The global medical community now awaits the results of the large-scale Phase 3 trials to confirm these promising findings and, most importantly, to establish a long-term safety profile. Retatrutide is a beacon of hope and a testament to the incredible pace of medical innovation. While it is not a solution for today, it provides a tantalising glimpse into the future of metabolic medicine, a future that looks brighter and more hopeful than ever before.

Don't Wait for Tomorrow

You do not have to wait for Retatrutide to be approved.

You can start transforming your life and health today with currently approved, effective treatments like Wegovy or Mounjaro (where clinically appropriate).

Looking for effective and weight management solutions? Discover our evidence-based weight loss programme at SheMed, designed for lasting results and delivered with clinical excellence.

Key Takeaways from SheMed

1. It's a "Triple Threat" Drug: Retatrutide uniquely targets three metabolic hormone receptors (GLP-1, GIP, and glucagon), making it potentially more powerful for blood sugar and weight loss than current single or dual-action drugs.
2. Promising But Preliminary: Clinical trial results show unprecedented efficacy (e.g., ~24% weight loss), but it remains an investigational drug. It is NOT approved for use by any regulatory authority worldwide.
3. Zero Legal Availability: It will not be available for prescription until at least 2026-2027. Any product being sold now is illegal, counterfeit, and dangerous.
4. Severe Safety Warning: Obtaining it outside of clinical trials poses extreme risks, including contamination, incorrect dosing, infection, and severe side effects. Only use MHRA/TGA/FDA-approved medications prescribed by your doctor.

Frequently Asked Questions (FAQs)

1. What is Retatrutide?
   A "Triple G" investigational drug that targets three hormone receptors for potentially superior blood sugar and weight control. It is not approved anywhere yet.
2. How does Retatrutide compare to Wegovy or Mounjaro?
   It is a triple-hormone agonist (GLP-1, GIP, glucagon), while Wegovy is single and Mounjaro is dual, which may lead to stronger effects. However, it is not yet approved, unlike the others.

References

1. Jastreboff, A. M., et al. (2023). Triple–Hormone-Receptor Agonist Retatrutide for Obesity — A Phase 2 Trial. The New England Journal of Medicine, 389(6), 514-526. DOI: 10.1056/NEJMoa2301972.
2. Rosenstock, J., et al. (2023). Efficacy and safety of a novel triple hormone receptor agonist retatrutide in people with type 2 diabetes: A randomised, double-blind, placebo and active-controlled, parallel-group, phase 2 trial in the USA. The Lancet. DOI: 10.1016/S0140-6736(23)01727-4.
3. American Diabetes Association (2022). Weight Loss is Key to Remission of Type 2 Diabetes. Press Release. Available at: https://diabetes.org/newsroom/press-releases/2022/weight-loss-key-remission-type-2-diabetes.
4. National Institute for Health and Care Excellence (NICE). (2022). Type 2 diabetes in adults: management. NG28. Available at: https://www.nice.org.uk/guidance/ng28.
5. Medicines and Healthcare products Regulatory Agency (MHRA). (2023). MHRA and partners shut down illegal manufacturing of weight loss products. Press Release. Available at: https://www.gov.uk/government/news/mhra-and-partners-shut-down-illegal-manufacturing-of-weight-loss-products.

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Semaglutide (Wegovy) has rapidly evolved from a metabolic therapy to a major force reshaping cardiovascular medicine. Originally developed for glycaemic control in type 2 diabetes, the drug soon gained prominence for its unmatched ability to drive substantial, sustained weight loss. But as its use expanded and large-scale outcome trials matured, a more profound insight emerged: semaglutide may protect the heart through mechanisms that extend far beyond its influence on body weight.

This revelation is significant because cardiometabolic medicine has long relied on a simple framework: excess adiposity increases cardiovascular risk, and weight reduction decreases that risk. Weight-loss medications were therefore expected to improve cardiovascular outcomes mainly by reducing fat mass. Yet, data from the trials challenged this linear view. Individuals across a wide spectrum of BMI, waist circumference, and other adiposity markers showed similar reductions in major adverse cardiovascular events (MACE), regardless of how high their adiposity was at baseline. Even more compelling was the finding that these benefits persisted after adjusting for the amount of weight they actually lost.

What We Previously Believed About Semaglutide and Heart Health

Excess adiposity has long been recognised as a potent driver of cardiovascular disease. This understanding created a straightforward narrative: reduce weight, reduce cardiovascular risk. Semaglutide’s early success in producing substantial and sustained weight loss reinforced this assumption, and its cardiovascular benefits were widely interpreted as a downstream effect of losing fat mass.

The dominant belief was that improvements in blood pressure, inflammation, lipids, and glycaemic control that accompany weight reduction were the primary reasons patients experienced fewer cardiovascular events while using semaglutide.

However, this weight-centric model left an important question unanswered: was semaglutide improving cardiovascular outcomes simply because patients were losing weight, or was the drug exerting protective effects through additional biological pathways? Distinguishing between these possibilities matters greatly. If the benefit were driven solely by weight loss, then the degree of cardiovascular protection would depend directly on how much weight a patient managed to lose.

But if other intrinsic mechanisms were involved, semaglutide could be reframing how we treat cardiovascular risk in people with excess body weight, even in those who may not lose substantial amounts of it. This question set the stage for deeper analyses aimed at disentangling weight-related effects from the drug’s broader cardiometabolic actions.

A New Understanding Emerges: Cardiovascular Protection Beyond Fat Loss

The latest scientific insights have now expanded this narrative in a transformative way. When researchers examined semaglutide’s cardiovascular effects across a broad range of adiposity measures such as BMI, waist circumference, and abdominal fat distribution, the results were remarkably consistent.

Individuals with moderate overweight, marked obesity, or substantial central adiposity all experienced similar reductions in major cardiovascular events. This uniformity challenges the assumption that people with higher fat mass stand to gain the most from treatment. Instead, the benefit appears to extend broadly across the entire spectrum of body sizes represented in the study population.

What the Weight-Adjusted Analyses Showed

To further clarify whether weight loss itself was the primary mechanism behind the cardiovascular improvement, investigators evaluated how early weight change influenced long-term cardiovascular risk. Traditionally, early weight reduction is seen as a reliable predictor of later cardiometabolic outcomes, especially in weight-loss trials. But in this case, early weight loss did not predict future cardiovascular events among those taking semaglutide. Even individuals who lost less weight enjoyed a similar degree of cardiovascular protection.

The mediation analysis offered an even deeper layer of understanding. When reductions in waist circumference, a more precise marker of visceral fat, were examined, they accounted for only about one-third of the overall cardiovascular benefit. This means that even improvements in abdominal fat, arguably the most harmful type of adiposity, explained only a fraction of the drug’s total effect.

Why This Changes the Way We Understand Semaglutide

The most important takeaway from this analysis is that roughly 67% of the cardiovascular protection cannot be explained by weight loss or fat reduction alone. In other words, semaglutide is doing much more than altering body composition. It appears to be influencing biological pathways that directly improve cardiovascular health, such as reducing systemic inflammation, enhancing endothelial function, improving metabolic signalling, and possibly altering myocardial energetics.

How Semaglutide May Protects the Heart Beyond Weight Loss

Systemic and Vascular Pathways: Semaglutide’s Multi-Layered Influence on Cardiovascular Health

One of the first pathways to be recognised involves systemic inflammation, a central driver of atherosclerosis. Individuals with overweight or obesity often have persistently elevated inflammatory markers that accelerate plaque formation and destabilisation. GLP-1 receptor activation appears to dampen this inflammatory environment by reducing pro-inflammatory cytokines, improving immune cell function, and decreasing oxidative stress within blood vessels. These effects can occur even before substantial weight loss is achieved, offering an early layer of cardiovascular protection.

Another key mechanism relates to endothelial function, which determines how well blood vessels dilate, respond to stress, and maintain vascular integrity. In metabolic disease, endothelial dysfunction contributes significantly to hypertension, plaque buildup, and vascular stiffness.

Semaglutide has been shown to enhance endothelial nitric oxide availability and improve vascular responsiveness. This leads to better blood pressure regulation, improved arterial elasticity, and overall healthier vascular physiology. Importantly, these improvements have been observed in experimental models independent of weight change, supporting the idea that GLP-1 receptor activation exerts direct vascular benefits.

Metabolic and Cardiac Effects: Beyond Adiposity Into Cellular and Hormonal Regulation

Semaglutide also influences a range of metabolic pathways that collectively promote cardiovascular stability. These include improvements in lipid handling, reductions in triglyceride-rich lipoproteins, enhanced metabolic flexibility, and improved glucose-insulin dynamics even in individuals without diabetes.

Although some of these changes correlate with weight loss, others occur as a direct consequence of GLP-1 signalling, suggesting a broader cardiometabolic role independent of adiposity reduction. By improving metabolic homeostasis, semaglutide reduces the burden of atherogenic lipids and mitigates the metabolic stress that contributes to cardiovascular disease progression.

Emerging research also points toward effects within the myocardium itself. Preclinical studies suggest that GLP-1 receptor activation can modify cardiac energy utilisation, improve mitochondrial efficiency, and reduce cardiomyocyte inflammation.

These changes may make the heart more resilient to ischemia, reduce left ventricular stress, and potentially slow pathological remodelling. Although still an active area of investigation, these findings imply that semaglutide may influence the heart at the cellular level, not merely through improvements in systemic risk factors.

Clinical Implications: Shifting From a Weight-Centric to a Biology-Centric Model of Cardiovascular Risk

The recognition that semaglutide protects the heart through mechanisms that extend far beyond weight loss represents a fundamental shift in how clinicians conceptualise cardiovascular risk in individuals with overweight or obesity. For decades, weight reduction was positioned as the primary conduit through which cardiovascular risk could be modified. This view was grounded in the undeniable fact that excess fat mass disrupts metabolic and inflammatory pathways that accelerate atherosclerosis.

But as the mechanisms become clearer, the relationship between adiposity and cardiovascular disease is not linear. This understanding moves clinical practice away from a weight-centric paradigm and toward a more biology-centric view of cardiometabolic health.

A Broader Therapeutic Role for Semaglutide in Cardiovascular Prevention

These insights may also expand the therapeutic relevance of semaglutide. For patients with high cardiovascular risk, especially those with established vascular disease, semaglutide may now be considered not only a weight-loss agent but a cardiovascular risk-reducing therapy. This matters especially for individuals who, despite appropriate medical therapy with statins, antiplatelet agents, blood pressure control, and lifestyle measures, continue to carry significant residual risk.

Importantly, this shift benefits patients whose weight-loss response is modest. Traditionally, poor weight responders were assumed to derive limited cardiovascular benefit from weight-loss medications. But the emerging evidence suggests that even those with smaller reductions in scale weight can still gain meaningful cardiovascular protection. This redefines treatment expectations and offers reassurance to patients who may struggle with large, sustained weight loss but still need aggressive cardiometabolic risk modification.

Improved Adherence and Shared Decision-Making

Understanding that semaglutide’s cardiovascular benefits are only partially dependent on fat reduction can significantly influence how patients perceive and adhere to therapy. Many individuals discontinue treatment when weight loss plateaus, assuming that the medication is no longer providing value. But the recognition that semaglutide improves vascular, inflammatory, and metabolic health even when weight loss stabilises allows clinicians to reinforce the broader rationale for continuation.

This enhanced communication supports more effective shared decision-making. Patients are more likely to stay engaged when they understand that the therapy is acting on deeper biological pathways, even during periods when their weight is not changing dramatically. This perspective also helps clinicians move the conversation beyond weight alone, bringing focus to markers like blood pressure, inflammation, quality of life, and long-term cardiovascular protection.

Conclusion

The evolving understanding of semaglutide’s cardiovascular effects marks one of the most significant shifts in modern cardiometabolic medicine.

What began as an obesity and diabetes medication has emerged as a therapy capable of modifying cardiovascular biology through pathways that extend far beyond fat mass reduction. While improvements in adiposity, especially abdominal or visceral fat, contribute meaningfully to reduced cardiovascular risk, they represent only a portion of the whole story.

The majority of semaglutide’s protective effect arises from bigger physiological changes, including reductions in systemic inflammation, improvements in endothelial function, enhanced metabolic efficiency, and potentially even myocardial-level benefits.

This new evidence reframes how clinicians approach cardiovascular risk in people with excess weight. Instead of relying solely on the number on the scale, the narrative now includes a broader and more biologically grounded understanding of cardiometabolic health.

As ongoing research clarifies additional mechanisms and potential therapeutic uses, semaglutide is poised to redefine not only obesity care but also cardiovascular prevention strategies for years to come.

Frequently Asked Questions

1. Does semaglutide reduce cardiovascular risk even if I do not lose much weight?

Recent analyses show that semaglutide’s cardiovascular benefits are not solely dependent on weight loss. While reductions in visceral fat contribute, they explain only about one-third of the total cardiovascular risk reduction. Approximately 67% of the benefit comes from mechanisms unrelated to fat loss, such as improved endothelial function, reduced inflammation, and enhanced metabolic signalling. This means patients with modest weight loss still experience meaningful cardiovascular protection.

2. If waist circumference explains some of the benefits, does that mean visceral fat is still important?

Waist circumference shows visceral and abdominal fat, which is strongly linked to atherosclerosis and cardiometabolic dysfunction. In the latest mediation analysis, reductions in waist circumference accounted for a significant but partial portion of semaglutide’s effect, around one-third. This reinforces that visceral fat reduction matters, but it is not the full explanation. The majority of cardioprotective benefits arise from additional biological effects.

3. Are semaglutide’s cardiovascular benefits seen only in people with severe obesity?

The cardioprotective effect was consistent across all baseline BMI categories, including people with moderate overweight and those with higher levels of obesity. This suggests the benefit is broad and not restricted to individuals with very high adiposity. Semaglutide exerts protective effects across a wide spectrum of body sizes, reinforcing that its mechanisms extend beyond pure fat reduction.

4. How soon do cardiovascular benefits begin after starting semaglutide?

Although exact timelines are still being studied, early indicators suggest that vascular and inflammatory improvements may begin before substantial weight change. This is supported by the finding that early weight loss (at 20 weeks) did not predict cardiovascular outcomes. This implies that some protective mechanisms activate early, potentially within the first few months of treatment.

5. Can these findings be generalised to people without overweight or obesity?

Current evidence comes from populations with BMI ≥27 kg/m² and established cardiovascular disease. Trials in normal-BMI populations are lacking. While the mechanistic pathways are promising, more data are needed before extending the findings to people at lower body weights or in primary prevention settings.

References

1. Gerstein, H. C., Colhoun, H. M., Dagenais, G. R., Diaz, R., Lakshmanan, M., Pais, P., ... & Mann, J. F. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. New England Journal of Medicine, 389(24), 2247–2257. https://doi.org/10.1056/NEJMoa2307563
2. Deanfield, J., Lincoff, A. M., Kahn, S. E., Emerson, S. S., Lingvay, I., Scirica, B. M., ... Ryan, D. H. (2025). Semaglutide and cardiovascular outcomes by baseline and changes in adiposity measurements: A prespecified analysis of the SELECT trial. The Lancet. Advance online publication. https://doi.org/10.1016/S0140-6736(25)01375-3
3. Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., ... & Stroke Statistics Subcommittee. (2016). Heart disease and stroke statistics—2016 update: A report from the American Heart Association. Circulation, 133(4), e38–e360. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11522117/
4. Khera, R., Valero-Elizondo, J., Nasir, K., Virani, S. S., Blankstein, R., & De Lemos, J. A. (2023). Cardiovascular risk factors in the United States: Trends and disparities. Journal of the American College of Cardiology, 81(7), 595–606. https://doi.org/10.1016/j.jacc.2023.01.068
5. Lee, C. M., Gallagher, D., & Park, J. (2025). Adiposity and cardiometabolic risk factors: New insights from recent trials. Current Opinion in Clinical Nutrition and Metabolic Care, 28, 213–219. https://doi.org/10.1016/j.cmet.2025.04.003
6. Yusuf, S., Hawken, S., Ôunpuu, S., Dans, T., Avezum, A., Lanas, F., ... & INTERHEART Study Investigators. (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. The Lancet, 364(9438), 937–952. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413075/