The etiology of the increase in lung cancer over the course of the 20th century has been a large area of debate. Was it smoking that caused cancer? Or was some other, unknown, factor the cause? Causation is multifactorial and multi-level—that is, causes of anything are numerous and these causes all interact with each other. But when it comes to smoking, it was erroneously argued that genotypic differences between individuals were the cause of both smoking and cancer. We know now that smoking is directly related to the incidence of lung cancer, but in the 20th century, there were researchers who were influenced and bribed to bring about favorable conclusions for the tobacco companies.
Psychologist Hans Eysenck (1916-1997) was a controversial psychologist researching many things, perhaps most controversially, racial differences in intelligence. It came out recently, though, that he published fraudulent papers with bad data (Smith, 2019). He, among other weird things, believed that smoking was not causal in regard to cancer. Now, why might Eysenck think that? Well, he was funded by many tobacco companies (Rose, 2010; Smith, 2019). He accepted money from tobacco companies to attempt to disprove the strong correlation between smoking and cancer. Between the 1977-1989, Eysenck accepted about 800,000 pounds from tobacco companies. He is not alone in holding erroneous beliefs such as this, however.
Biostatistician Ronald Fisher (1890-1962) (a pipe smoker himself), the inventor of many statistical techniques still used today, also held the erroneous belief that smoking was not causal in regard to cancer (Parascandola, 2004). Fisher (1957) argued in a letter to the British Medical Journal that while there was a correlation between smoking and the acquisition of lung cancer, “both [are] influenced by a common cause, in this case the individual genotype.” He went on to add that “Differentiation of genotype is not in itself an unreasonable possibility“, since it has been shown that genotypic differences in mice precede differences “in the frequency, age-incidence and type of the various kinds of cancer.”
So, if we look at the chain it goes like this: people smoke; people smoking is related to incidences in cancer; but it does not follow that since people smoke that the smoking is the cause of cancer, since an unknown third factor could cause both the smoking and cancer. So now we have four hypotheses: (1) Smoking causes lung cancer; (2) Lung cancer causes smoking; (3) Both smoking and lung cancer are caused by an unknown third factor. In the case of (3), this “unknown third factor” would be the individual genotype; and (4) the relationship is spurious . Fisher was of the belief that “although lung cancer occurred in cigarette smokers it did not necessarily follow that the cancer was caused by cigarettes because there might have been something in the genetic make up of people destined to have lung cancer that made them addicted to cigarettes” (Cowen, 1999). Arguments of this type were popular in the 19th and 20th century—what I would term ‘genetic determinists’ arguments, in that genes dispose people to certain behaviors. In this case, genes disposed people to lung cancer which made them addicted to cigarettes.
Now, the argument is as follows: Smoking, while correlated to cancer is not causal in regard to cancer. Those who choose to smoke would have acquired cancer anyway, as they were predisposed to both smoke and acquire cancer at X age. We now know, of course, that such claims are ridiculous—no matter which “scientific authorities” they come from. Fisher’s idea was that differences in genotype caused differences in cancer acquisition and so along with it, caused people to either acquire the behavior of smoking or not. While at the time such an argument could have been seen as plausible, the mounting evidence against the argument did nothing to sway Fisher’s belief that smoking did not outright cause lung cancer.
The fact that smoking caused lung cancer was initially resisted by the mainstream press in America (Cowen, 1999). Cowen (1999) notes that Eysenck stated that, just because smoking and lung cancer were statistically associated, it did not follow that smoking caused lung cancer. Of course, when thinking about what causes, for example, an observed disease, we must look at similar habits they have. And if they have similar habits and it is likely that those with similar habits have the hypothesized outcome (smokers having a higher incidence of lung cancer, in this case), then it would not be erroneous to conclude that the habit in question was a driving factor behind the hypothesized disease.
It just so happens that we now have good sociological research on the foundations of smoking. Cockerham (2013: 13) cites Hughes’ (2003) Learning to Smoke: Tobacco Use in the West where he describes the five stages that smokers go through: “(1) becoming a smoker, (2) continued smoking, (3) regular smoking, (4) addicted smoking, and, for some, (5) stopping smoking.” Most people report their first few times smoking cigarettes as unpleasant, but power through it to become a part of the group. Smoking becomes somewhat of a social ritual for kids in high-school—with kids being taught how to light a cigarette and how to inhale properly. For many, starting smoking is a social thing that they do with their friends—it can be said to be similar to being social drinkers, they were social smokers. There is good evidence that, for many, their journey as smokers starts and is fully dependent on their social environment than actual physical addiction (Johnson et al, 2003; Haines, et al, 2009).
One individual interviewed in Johnson et al (2003: 1484) stated that “the social setting
of it all [smoking] is something that is somewhat addictive itself.” So, not only is the nicotine the addictive substance on the mind of the youth, so too is the social situation for the youth in which the smoking occurs. The need to fit in with their peers is one important driver for the beginning—and continuance—of the behavior of smoking. So we now have a causal chain in regard to smoking, the social, and disease: youths are influenced/pressured to smoke by their social group which then leads to addiction and then, eventually, health problems such as lung cancer.
The fact that the etiology of smoking is social leads us to a necessary conclusion: change the social network, change the behavior. Just as people begin smoking in social groups, so too, do people quit smoking in social groups (Christakis and Fowler, 2008). We can then state that, on the basis of the cited research, that the social is ultimately causal in the etiology of lung cancer—the vehicle of cancer-causation being the cigarettes pushed bu the social group.
Eysenck and Fisher, two pioneers of statistics and different methods in psychology, were blinded by self-interest. It is very clear with both Eysenck and Fisher, that their beliefs were driven by Big Tobacco and the money they acquired from them. Philosopher Donald Davidson famously stated that reasons are causes for actions (Davidson, 1963). Eysenck’s and Fisher’s “pro-belief” (in this case, the non-causation of smoking to lung cancer) would be their “pro-attitude” and their beliefs lead to their actions (taking money from Big Tobacco in an attempt to show that cigarettes do not cause cancer).
The etiology of lung cancer as brought on by smoking is multifactorial, multilevel, and complex. We do have ample research showing that the beginnings of smoking for a large majority of smokers are social in nature. They begin smoking in social groups, and their identity as a smoker is then refined by others in their social group who see them as “a smoker.” Since individuals both begin smoking in groups and quitting in groups, it then follows that the acquisition of lung cancer can be looked at as a social phenomenon as well, since most people start smoking in a peer group.
The lung cancer-smoking debate is one of the best examples of the dictum post hoc, ergo propter hoc—or, correlation does not equal causation (indeed, this is where the dictum first originated). While Fisher and Eysenck did hold to that view in regard to the etiology of lung cancer (they did not believe that since smokers were more likely to acquire lung cancer that smoking caused lung cancer), it does speak to the biases the two men had in their personal and professional lives. These beliefs were disproven by showing a dose-dependent relationship in regard to smoking and lung cancer: heavier smokers had more serious cancer incidences, which tapered down the less an individual smoked. Fisher’s belief, though, that differences in genotype caused both behavior that led to smoking and the lung cancer itself, while plausible at the time, was nothing more than a usual genetic determinist argument. We now know that genes are not causes on their own; they do not cause traits irrespective of their uses for the physiological system (Noble, 2012).
Everyone is biased—everyone. Now, this does not mean that objective science cannot be done. But what it does show is that “… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends” (Hilliard, 2012: 85). This, and many more examples, speak to the biases of scientists. For reasons like this, though, is why science is about the reproduction of evidence. And, for that, the ideas of Eysenck and Fisher will be left in the dustbin of history.