A tale of two smoking studies led by Sir Richard Peto - Foundation for a Smoke-Free World

A tale of two smoking studies led by Sir Richard Peto

In 1951, Sirs Richard Doll and Austin Bradford Hill began surveying thousands of doctors to determine the cause of rising lung cancer rates in the United Kingdom. Initial results clearly identified smoking as the culprit; and follow-up studies revealed additional causes of death attributable to the habit. This research galvanized doctors to take concrete actions: stop smoking, advise patients to stop smoking, and become public advocates for tobacco control.

In the 1970s, Sir Richard Peto joined the “British Doctors” research team, bringing with him a statistical expertise that proved invaluable to subsequent follow-up analyses. Half a century later, Peto and his colleagues continue to enhance our understanding of the long-term effects of smoking. Two recently published studies offer epidemiological insights that, like those early surveys, should inspire action.

The first, a study of 120,000 Cubans followed for almost 20 years, extends the knowledge gained from British Doctors cohort. The researchers found that smokers who started before 15 years of age (a third of all smokers) had twice the relative risk of dying prematurely, as compared to never-smokers. Further, they showed that smokers who quit before age 40 avoided almost all the excess risks of smoking. Helpfully, this study also includes a large portion of women (54 percent), whose smoking prevalence is rising at alarming rates in many regions. In Cuba, the frequency of deaths from lung, tracheal, or bronchus cancer now far outpaces deaths due to breast cancer (respectively: 37.7 and 29.9 per 100,000 persons).

Findings from the Cuban population study underscore the fact that children should never start smoking; and, fortunately, there exist many policies addressing the need to limit youth uptake of tobacco. Yet, the study’s second finding—that smokers can reap the benefits of cessation well into adulthood—is often neglected by policymakers. This study highlights the value of quitting before 40; and our work shows that substantial benefits can be achieved when cessation occurs as late as the 60s. These outcomes should emphasize that no population is a “lost cause,” and that we must devote public health resources to helping smokers of all ages quit.  

In a second study, Peto and his colleagues again follow up with the British Doctors cohort to investigate the the relationship between smoking, quitting, and Parkinson’s Disease (PD). Smokers, they found, have a 30 percent reduced risk of PD over time. The authors also noted an inverse relationship between the amount of tobacco smoked and the probability of developing PD—leading them to suspect that “smoking is causally protective [against PD].”

Numerous studies have reported reduced PD risk among smokers. More recently, similar findings have been reported for people who use snus, with one survey showing that never-smoking snus users have a 60 percent lower risk of developing PD. As with Peto et al.’s study, this outcome was both dose- and duration-of-use-dependent. Relatedly, a recent analysis of genetic variants within the Zoroastrian-Parsi community revealed no genetic indicators of lung cancer, but notable indicators of PD—perhaps due to centuries of abstaining from smoking.

In cases where smoking seems to reduce the risk of PD, it is reasonable to believe that nicotine is the “protective” ingredient. Broadcasting this information, of course, holds its challenges. Any protection conferred by smoking, certainly, does not outweigh its massive ill effects; and any public messaging on this topic must convey as much. Yet, optics should not impede research into the beneficial effects of nicotine. Indeed, this is a critical area of research, which has become newly relevant in the context of COVID-19. Currently, researchers are examining whether nicotine might reduce severity of the disease.

While epidemiological studies can highlight important trends, they cannot, alone, identify causal mechanisms. For this reason, we are only just beginning to suss out which cigarette constituents actually cause excess deaths and which may reduce the risks for certain diseases. This area of research may profoundly expand the scientific understanding of nicotine, with the potential to inspire related policy change.

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