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| Pharmaceutical Company Johnson & Johnson |
These decisions aren’t the win for consumers that they might seem to be. Instead, they represent a search for a scapegoat that distorts the science of cancer as well as society’s conception of the disease.
I study the molecular mechanisms of cancer, and occasionally my job comes up in casual conversation. More often than not, what follows is a question or comment along these lines: “Is it true that deodorant gives you cancer?” “Eating organic can prevent cancer, right?” “My husband stopped eating sugar, and I know it cured his cancer.”
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| A close up of a farmer harvesting some organic carrots from a small, independant urban crop. |
This line of thinking makes a certain sense, as many cancers are undoubtedly linked to lifestyle choices and environmental exposure. Yet it is fundamentally flawed because it overestimates the magnitude of these effects—assuming they are real, which many probably aren’t—and because it confuses measures of probability with direct causation.
Exposure to carcinogens influences the risk of developing cancer, which is a function of many factors, including the dose and duration of the exposure. Other factors, such as inherited genetic mutations, also create risk. To say something is a carcinogen encompasses a wide spectrum of risk. A properly conducted, well-controlled epidemiological study may reveal a statistically significant increase in risk related to a certain lifestyle choice or exposure, but it is critical to consider the magnitude of the risk when applying this to any individual case of cancer.
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| Genetic engineeering concept with 3d rendering dna helix and a part of dna |
Certain risk factors, like inheriting a mutant BRCA1 gene (which causes breast and ovarian cancer), more or less ensure tumor development. Some, like tobacco exposure, are clearly causal, even if most individuals exposed are spared (80% to 90% of smokers do not develop cancer, but lung-cancer rates are far higher than among nonsmokers). Yet many substances labeled “carcinogens” have relatively weak effects and must be judged alongside the myriad other factors that increase or decrease cancer risk. With a few exceptions, carcinogens work on the margins, acting as one of many factors tipping the scale toward cancer.
For glyphosate, the scientific evidence is decidedly mixed. A direct link to cancer is still debatable, but even if one accepts the high end of the reported risks the effects are, at best, modest. The upper estimate (relative risk of 1.3 to 1.4) is an order of magnitude lower than the risk associated with heavy smoking (relative risk 15 to 30). To put it another way, the risk associated with glyphosate falls somewhere between the small hazard that comes from eating a considerable amount of bacon (for colorectal cancer) and consuming very hot tea (for esophageal cancer).
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| Patients women saline drilling |
Either directly or indirectly, many carcinogens lead to DNA damage, which is the underlying cause of cancer. Assuming glyphosate could have inflicted some genetic damage, it would still be difficult to say with any certainty that it actually caused a cancer because an untold number of additional steps stand between an exposure to carcinogenic agents and the diagnosed disease—a long and tortuous road that stretches from the initially damaged cell to a resulting cancer.
Our bodies have many processes to repair cell damage or eliminate cells in which repair has been unsuccessful. Even when damaged cells persist, they have to circumvent additional biological barriers before a cell becomes cancerous. The immune system is also adept at seeking out mutated cells and eliminating them long before they develop into cancer. All this helps explain why most cancers take decades to develop.
It isn’t necessary to map every step of this journey to establish a connection between a carcinogenic exposure and cancer. But the smaller the risk associated with a carcinogen, the more important it is to account for the unknown. Were additional carcinogens involved? How do lifestyle choices interact with the initial exposures? What was the status of the immune system? Did other pre-existing genetic differences play a role?
The truth is that we have no idea why some people develop cancer while many others do not. Risk factors alter the odds but are hardly determinative. For any individual case there is a sizable variable of uncertainty, representing factors that are either poorly understood or truly random.
My principal concern isn’t the liability of the companies involved. The most important ramification of these lawsuits is their impact on the public psyche, suggesting that there is a definitive explanation for every case of cancer.
Cancer is horrible, and the desire to find a clear and definable cause, including factors that could have prevented it, is understandable. But these cause-and-effect judicial decisions imply that it’s possible to trace a straight line from some specific event in the past leading straight to a cancer. That we can break open a tumor, rewind it to the beginning, and see exactly when and where things went wrong. In most cases this simply isn’t possible.
And so we are left to deal with the uncomfortable reality that although we have come far in our understanding of cancer, there is still so much that remains a mystery.
Mr. Lambert is a postdoctoral researcher at the Whitehead Institute for Biomedical Research.
