Recent media coverage of a report examining nicotine’s effects on the heart and blood vessels has renewed debate about cardiovascular risk and nicotine regulation. In response, experts contributing to the UK Science Media Centre (SMC) have provided important clarification that adds nuance often missing from public discussion. Their commentary reinforces a central principle in tobacco control: nicotine has physiological effects, but the scale of cardiovascular harm depends critically on how nicotine is delivered.
This distinction has direct implications for regulation, clinical guidance, and public communication.
What the report suggests
The report under discussion highlights evidence that nicotine can influence cardiovascular function through mechanisms such as increased heart rate, elevated blood pressure, and activation of the sympathetic nervous system. These effects are well documented and biologically plausible. The concern raised is that nicotine exposure, regardless of delivery method, could contribute to cardiovascular risk.
However, the broad framing of these findings has prompted expert responses cautioning against interpreting them as evidence that all nicotine products pose equivalent cardiovascular danger.
What Science Media Centre experts are clarifying
In their expert reactions published by the Science Media Centre, several leading researchers emphasise that nicotine’s acute cardiovascular effects are not equivalent to the long-term damage caused by smoking.
Professor Peter Hajek of Queen Mary University of London notes that while nicotine can affect heart rate and blood pressure, cigarettes expose users to a complex mixture of toxic substances that dramatically increase the risk of cardiovascular disease. Professor Lion Shahab, also of Queen Mary University of London, highlights that epidemiological evidence consistently shows much lower cardiovascular risks among users of nicotine replacement therapy compared with smokers. Professor Martin McKee of the London School of Hygiene & Tropical Medicine stresses the importance of distinguishing between nicotine itself and the broader harms caused by combustion-related toxicants.
Together, these expert perspectives underline that combustion products, such as carbon monoxide, fine particulates, and oxidants, are the dominant drivers of smoking-related cardiovascular harm, not nicotine alone.
Evidence from clinical and population studies
Long-term observational studies of people using licensed nicotine replacement therapies have not shown the elevated risks of heart attack or stroke observed in smokers. Clinical trials and switching studies further indicate that individuals who move from smoking to non-combustible nicotine products often experience improvements in blood pressure, endothelial function, and other cardiovascular markers within relatively short periods.
These findings do not suggest that nicotine is harmless. Rather, they demonstrate that removing combustion substantially alters cardiovascular risk, a point repeatedly emphasised by experts responding through the Science Media Centre.
Why communication matters
Several SMC contributors caution that public messaging which collapses all nicotine products into a single risk category can have unintended consequences. If smokers are led to believe that smoke-free alternatives carry cardiovascular risks comparable to cigarettes, they may be less inclined to switch away from smoking. From a public-health perspective, this risks prolonging exposure to the most harmful form of nicotine delivery.
Accurate communication of relative risk is therefore essential, not optional. Public-health credibility depends on describing both risk and risk reduction clearly, particularly for populations with high smoking prevalence.
Implications for regulation
The expert reactions reinforce the need for risk-proportionate regulatory frameworks. Combustible tobacco products warrant the strongest controls given their unparalleled contribution to cardiovascular disease and premature death. Non-combustible nicotine products, while not risk-free, require differentiated regulation that reflects substantially lower toxicant exposure, alongside robust safeguards such as age restrictions, product standards, and post-market surveillance.
Treating all nicotine products as equivalent may simplify policy design, but it does not align with the scientific evidence or with the goal of reducing cardiovascular harm at population level.
Conclusion
The Science Media Centre expert responses reaffirm a consistent scientific message: nicotine is addictive and has measurable physiological effects, but combustion is the primary driver of smoking-related cardiovascular disease. Public-health policy is strongest when it reflects this distinction with clarity and proportionality.
For regulators, clinicians, and communicators, the challenge is not to minimise risk, but to describe it accurately. Recognising differences in delivery, exposure, and harm is essential to reducing the burden of heart disease caused by smoking.
Expert reactions referenced via the UK Science Media Centre:https://www.sciencemediacentre.org/expert-reaction-to-report-on-nicotine-and-heart-blood-vessels/
