Tobacco smoking alone isn’t enough: More than smoking important in lung cancer death

Christopher Russell and Adi Jaffe

The tobacco epidemic already kills 5.4 million people a year from lung cancer, heart disease and other illnesses. By 2030, the death toll will exceed eight million a year. Unless urgent action is taken tobacco could kill one billion people during this century. (The World Health Organization Report on the Global Tobacco Epidemic, 2008)

These are some scary numbers, right? Cigarette smoking, according to the WHO, is the single most preventable cause of death in the world today, and in conveying these deadly statistics to the general public, cigarettes have come to be alternatively referred to by smokers and non-smokers as “cancer sticks”, “nicotine bullets”, and “coffin nails”.

But does smoking really ‘kill’ anybody in the literal sense with which we use this word?  To an epidemiologist, tobacco smoking (nor many other drugs of abuse for that matter) does not “kill” a person or “cause” illness or death in the way the words “kill” and “cause” are typically understood by the media and general public. For example, if I shoot someone in the head, stab another in the heart, and strangle a third till he stops breathing, it is reasonable to say that my actions were the direct, sole, and sufficient causes of death – I would have killed them. Smoking, however, is often neither a sole nor sufficient ‘cause’ of lung cancer, coronary heart disease, or myocardial infarction because non-smokers die from these diseases, and for example, because only 1 in 10 heavy smokers die from lung cancer when one looks at the overall numbers.

This does not mean that smoking is harmless, but rather that other risk factors must be causing or interacting with smoking to cause the other 9 out of 10 deaths from lung cancer. Rather than “kill” anyone, it is more empirically accurate to talk of smoking as a risk factor for diseases that interacts in complex ways with other risk factors such as genetic heritability, diet, stress, and personality factors. Most importantly however, in the absence of these other risk factors, the odds of a smoker dying from lung cancer are roughly the same as those of a non-smoker dying from lung cancer!

Relative risks of smoking, genetic heredity, and stress for lung cancer

In 1973, Grossarth-Matticek administered a questionnaire about smoking, parental deaths from lung cancer and level of stress to 16,200 men and 3,620 women. On the basis of their responses, respondents were split into four groups:

(1)   Smoking, low stress, and low biological heredity

(2)   Smoking , high stress, low biological heredity

(3)   Smoking, low stress, and high biological heredity

(4)   Smoking, high stress, high biological heredity

— A sub-sample of respondents was followed up in 1994 (21 years later) to establish the rate of deaths from lung cancer. Grossarth-Matticek found that when smoking was the only risk factor, the odds of dying from lung cancer was 0.76%, or less than 1 in 100! The rate of death from lung cancer in those who were non-smokers was slightly lower at 0.57%. This basically indicates that smokers who had low biological heredity for lung cancer and had low levels of stress were highly unlikely to have died from lung cancer 21 years later, and were only very slightly more likely to have died from lung cancer than non-smokers with low biological heredity and low stress.

— Among smokers who had low heredity but high stress, the lung cancer death rate was slightly higher at 3.03%, meaning that 3 in every 100 smokers with low heredity and high levels of stress died from lung cancer. At this point, high stress began to interact with smoking to more than triple the lung cancer deaths solely attributable to smoking.

— Among smokers who had high heredity and low stress, the risk of lung cancer death more than doubled  to 6.38%, meaning 1 in 20 smokers with high heredity and low levels of stress died from lung cancer. Here the absolute risk and relative risks were starting to increase significantly, pointing to an important genetic risk factor for lung cancer, something that’s been found to be true for most cancers.

— Not surprisingly, the risk of lung cancer death was highest among smokers who had high heredity and high levels of stress (20.00%), meaning that 1 in 5 smokers with high stress and high heredity died from lung cancer. Among non-smokers with high heredity and high stress, the risk of lung cancer death was a lowly 2%. This means that smoking became a significant risk factor for lung cancer only when the smoker also had high stress and a hight biological heredity for lung cancer.

Implications for dealing with disease risk, smoking, and more

The results of this study suggest that among those who are at low risk for lung cancer (low stress and low heredity), smokers were almost as likely to die from lung cancer as were non-smokers. However, smoking interacted with high heredity and high stress to increase the risk of death from lung cancer to 1 in 5.

The obvious implication of this is that smokers and non-smokers are almost equally highly unlikely to die from lung cancer if they do not have a family history of lung cancer and do not have high levels of stress (which itself is the product of intracting biological, cognitive, and environmental processes). Smoking may be thought of as the match which lights the existing risk-bomb; the match and the bomb when kept apart are relatively harmless, but combine to become far more destructive than the sum of the parts.

We can therefore approach the problem of tobacco-related deaths in two ways: 1) Continue to vilify smoking and seek to reduce the global smoking prevalence (i.e. to stub out the lit match) or 2) Emphasise that tobacco-related deaths are also, and sometimes more so, stress-related deaths, personality-related deaths, and disease vulnerability-related deaths and attempt to treat these risk factors (i.e. move the bomb away from the match), or we can do both.

It is our opinion that reducing tobacco-related deaths will depend on a shift away from the public conceptualisation of smoking as the ‘lone gunman’ to a view emphasising the independent and interactive contributions of person-related risk factors with smoking. By identifying and educating those smokers at the greatest risk of disease, we can advise and assist with making changes to their smoking, if they no longer wish to smoke, and to the risk factors on which smoking relies to pose a significant mortal threat. Indeed, for deaths from cancer and cardiovascular disease, several studies have shown that psychological risk factors (e.g. neuroticism, emotional dependence, autonomy) are largely independent from physical risk factors, and can be adapted through cognitive-behavioural therapy (CBT), therefore reducing mortality.

In conclusion, we should never try to calculate or convey the calculated mortality risk of smoking when we don’t have data for or do not include data on other important risk factors in the analyses. Leaving psychological risk factors out of statistical analyses can give a spectacularly misleading impression of the mortality risk posed by cigarette smoking alone. When we read headlines about the number of people killed by smoking, it is important to remember that cigarette smoking is the accomplice to a death, not the lone gunman.  If we only seek to persecute cigarettes and smokers, we let the other suspects off the hook.

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