Number of words: 875

Cancer starts with the origin of a single cheat: this solitary cell has a dangerous mutation and multiplies to form a small lesion. Now a few thousand cells have this mutation. Nothing might happen for years. Or nothing might ever happen at all. If another mutation allows this ensemble of cheats to grow, it could give rise to what is called an adenoma. Adenomas can become large and contain perhaps 100 billion cells. But they are still constrained and encapsulated by surrounding tissue.

All the while the cheats can accumulate several more mutations. Many are deleterious and make the cheats worse off. Even more are neutral and do not alter the cell’s behavior. But a small fraction of these changes enable the cells to grow with more vigor. Eventually there might be a mutation that allows them to become “locally invasive.” This is the transition from adenoma to carcinoma. The carcinoma grows and invades the surrounding tissue, but the tumor still remains confined to one part of the body for some time. It could be removed by surgery. Eventually, if the tumor has not been successfully eradicated, cells will arise that have the ability to travel elsewhere in the body. This is the most deadly aspect of cancer, called metastasis.

In metastasis cells set up homes in distant sites around the body. For example, colon cancer tends to generate liver metastasis. A surgeon can no longer remove all of the secondary tumors. The remaining hope is to use chemotherapy. Traditional forms of this treatment rely on the fact that, because they tend to divide faster than ordinary cells, cancer cells are more likely to succumb to poison. But because chemotherapy is not very specific, bluntly attacking fastdividing cells whether cancerous or not, there is always collateral damage: side effects, such as nausea, baldness, and deafness.

We do have natural anticancer mechanisms. But they are far from perfect. Evolution works hardest to keep us alive to reproduce. In fact, reproduction is the major game in town. Once a person has successfully passed his or her genes on to the next generation, those genes “care” less if that creature lives on. In this way, genes are favored that shift the balance toward investing scarce resources in mechanisms that promote reproductive fitness and the maintenance of egg and sperm cells—the germ line—rather than the body, or soma. This echoes an ancient idea: Epictetus the Stoic philosopher once wrote that if we were useful alive, “should we not be still more useful to mankind by dying when we ought, as we ought?”

There is strong selection pressure to ensure that cancer does not occur too early, rather than to build us to last forever. Natural selection is relatively indifferent to the fate of the old, since their relevance to evolution is waning fast (unless, for example, elders use their wisdom to help their families to cooperate and to survive). Natural selection is honed by the death of the young, who have not passed on their genes, and by those who survive to bestow their genes on their children.

 The opportunity to sire the next generation was particularly narrow for our ancestors. For most of human evolutionary history, people did not live as long as they do now. Genetic variants that could help to keep us cancer free in our eighties made no difference to the lives of our ancestors, who were likely to perish relatively young from starvation, infectious disease, an attack by a wild animal, or a sharp blow from the flint axe of a rival.

 That is one reason why, in today’s greying society, cancer is a growing problem. There are various possible mechanisms by which cancer becomes more prevalent with age. Imagine a gene that prevents cancer in children but increases the risk of cancer in the elderly. Even more likely: imagine a gene that enhances the ability to have more children at the cost of a higher risk of cancer later in life. Nature tunes female anatomy to increase her capacity for conceiving or nourishing children and, in return, cuts the probability of living an extremely long life.

Cancer is also linked with lifestyle, and that has changed radically over human evolution. One example is exposure to pollutants and carcinogens. Thanks to the efforts of the Oxford statistician Sir Richard Doll, along with many others, smoking is the best-known risk factor, being linked with lung and other cancers. Some chemicals in tobacco smoke can directly damage part of our DNA, including key genes that protect us against cancer. Others interfere with our bodies’ defense systems and prevent them from repairing damaged DNA, making it more likely that damaged cells will eventually turn cancerous.

After smoking, obesity is the lifestyle factor that presents the highest preventable cancer risk. Our bodies are not adapted to deal with a constant oversupply of energy. Yet thanks to the rise of industrial farming we can eat whenever we want, and to excess as well. Activity levels have also declined. There is now an epidemic of obesity in the West. So there is a deep link between the way our bodies have evolved and the rise of cancer.

Excerpted from page 143-145 of ‘Super co-operators ’ by Martin Nowak