There’s a valuable book out there on cancer prevention written by Richard Beliveau, a biochemist who specializes in cancer prevention and by Denis Gingras, an oncology researcher, both of whom work at UQAM. They start with the following tantalizing question:
Why do many spontaneously formed cancerous lesions remain latent in one person and yet develop into cancer in another? Factors beyond our control, like aging and heredity are often cited as the main agents determining cancer risk, but their influence is in fact much weaker than might be thought.
To back this thesis they cite evidence that in every age group, including in people over 75, esophageal cancer rates have jumped 3 to 12 times between the 1975-79 period and between 2000-2004.
But there are a couple of things that irk me about the book.
(1) If there isn’t strong evidence that age plays a major role in cancer development, why aren’t the authors criticizing organizations like the American Cancer Society and Center for Disease Control for consistently presenting age-adjusted cancer data to the public?
Given that heredity and age are not the most fundamental variables in cancer formation, why then will the number of new cases possibly rise by about 70% over the next 2 decades according to the World Health Organization? The authors focus on individual lifestyle choices, and in their defense, tobacco smoke is indeed one of the main causes of cancer, accounting for 30% of worldwide cases. In the same manner that production of goods has shifted overseas where standards are lower and therefore inexpensive, tobacco companies have found new nicotine users in a global market. Consequently, tobacco consumption is still increasing worldwide even though the number of smokers has gone down in several Western countries. Of the 4000 compounds and elements in tobacco smoke that include radioactive polonium 210, 70 are known carcinogens, and those in group I include benzene, benzopyrene, NNK, arsenic, chromium and four others. As a result of this, smoking increases the risk of lung cancer by a factor of 25 and also plays a role in other cancers.
Also central to the authors’ thesis is that along with tobacco smoke, other lifestyle-roles including exposure to UV, poor diet, obesity, alcohol and physical activity supposedly account for 75% of cancers.
(2) This brings us to a second flaw in the book: “Chance” accounts for the rest of the causes, where “pollution” is clumped with inflammatory diseases, infections, defective genes, cell division and spontaneous DNA damage, factors that are beyond the individual’s control. Beliveau and Gingras make no mention of the 2010 President’s Cancer Panel report which stated that :
- There’s a growing body of evidence linking environmental exposures to cancer.
- There’s much work ahead to identify the many existing but unrecognized environmental carcinogens and eliminate those that are known from our workplaces, schools, and homes.
- The true burden of environmentally induced cancer has been grossly underestimated. With nearly 80,000 chemicals on the market in the United States, many of which are used by millions of Americans in their daily lives and are understudied and largely unregulated, exposure to potential environmental carcinogens is widespread.
- The public remains unaware of many common environmental carcinogens such as naturally occurring radon and manufacturing and combustion by-products such as formaldehyde and benzene.
In fact benzene, the group I carcinogen in tobacco smoke, is not only a combustion byproduct, but we expose ourselves to benzene each time we gas up at the fuel pump. At best, 0.62% of the volume of gasoline is benzene.
What I do like about the UQAM researchers’work is that they not only present epidemiological statistics, but they provide the chemical basis of cancer-preventative strategies. For instance:
- Depending on the amount of consumption, red meat and processed meat increase the colon cancer rate by 10 to 50 % due to PhIp, a heterocyclic amine formed during cooking and due to nitrosamines formed from the addition of nitrites, respectively.
Although other variables are involved, India’s cancer rate is only about 1/4 of that of Europe and the U.S. partly because of their six to 12 times rate of spice consumption. Turmeric has over 200 polyphenolic compounds, including curcumin, which inhibits cancer cell growth and blocks angiogenesis. Angiogenesis, the process where new blood vessels form from old ones, is used by some cancer growths. Curcumin also has anti inflammatory properties and it induces apoptosis, in this context, the death of cancer cells in a tumor. Although curcumin on its own is poorly absorbed in the intestine due to conversion by the enzyme UDP glucorryl transferase, the latter is inhibited by a component of another common spice used by Indians, piperidine in pepper.
In a nutshell then, many cancers can be prevented but not only from making lifestyle changes but by pressuring our governments to further limit our exposure to industrial carcinogens.