4.6: CANCER

Cancer is the second-leading cause of death globally, causing one in every six deaths and killing nearly nine million people in 2015 (WHO 2018b). Lifetime cancer risk in developed Western populations is now one in two, or 50% (Greaves 2015). Approximately one-third of deaths from cancer are due to behavioral and dietary factors, including high Body Mass Index (BMI), low fruit and vegetable intake, lack of physical activity, and the use of tobacco and alcohol. Depending on the type of cancer and one’s own genetic inheritance, these factors can increase cancer risk from 2- to 100-fold (Greaves 2015). Cancer is the result of interactions between a person’s genes and three categories of external agents: physical carcinogens (e.g., ultraviolet radiation), chemical carcinogens (e.g., tobacco smoke, asbestos), and biological carcinogens, such as infections from certain viruses, bacteria, or parasites (WHO 2018b). Obesity is also a risk factor for cancer, including of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik and Stains 2012).

Cancer has been regarded as a relatively recent affliction for humans that became a problem after we encountered exposure to modern carcinogens and lived long enough to express the disease (David and Zimmerman 2010). Given the long history that humans share with many oncogenic (cancer-causing) parasites and viruses (Ewald 2018), and the recent discovery of cancer in the metatarsal bone of a 1.8-million-year-old hominin (Odes et al. 2016), this view is being challenged (See Special Topics). The difficulties of identifying cancer in archaeological populations are many. Most cancer occurs in soft tissue, which rarely preserves, and fast-growing cancers would likely kill victims before leaving evidence in bone. It is also difficult to distinguish cancer from benign growths and inflammatory disease in ancient fossils, and there is often post-mortem damage to fossil evidence from scavenging and erosion. In light of these challenges, Paul Ewald (2018) suggests using other lines of evidence to discern the prevalence of cancer in ancient humans, including examining the history of cancer-causing parasites and viruses. His complete analysis is beyond the scope of this chapter, but one example of a virus you may be familiar with will serve to illustrate the concept.

SPECIAL TOPIC

Earliest evidence of cancer in hominins: Using 3-D images, South African researchers diagnosed a type of cancer called osteosarcoma in a toe bone belonging to a human relative who died in Swartkrans Cave between 1.6 and 1.8 million years ago.

Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States, and 79 million Americans, most in their late teens and early twenties, are infected with HPV (CDC 2017). HPVs are transmitted through sexual activity and can cause cancers of the cervix, vulva, vagina, penis, or anus. It can also cause cancer in the back of the throat, including at the base of the tongue and tonsils. The Centers for Disease Control recommends all 11–12 year olds, both girls and boys, get two doses of the HPV vaccine to protect against diseases, including cancers, caused by HPV. One such disease is cervical cancer, the fourth-leading cause of death for women in the world, and the second most common cause of death by cancer (surpassed only by breast cancer) for women ages 15–44 (Bruni et al. 2017). There are over 100 different strains of HPV, but Types 16 and 18 cause 70% of all cervical cancers (Bruni et al. 2017). Type 16 is the most oncogenic of the HPVs, and it has been present in the genus Homo for half a million years, suggesting cervical cancer and other cancers caused by HPV may have been too (Ewald 2018).

Behavioral or “lifestyle” choices have an impact on cancer risk. Breast cancer is one example. It is the most common cancer in women worldwide, but incidence of new cases varies from 19.3 per 100,000 women in Eastern Africa to 89.7 per 100,000 women in Western Europe (WHO 2018b). These differences are attributable to cultural changes among women in Western, industrialized countries that are a mismatch for our evolved reproductive biology. Age at menarche, the onset of menstrual periods, has dropped over the course of the last century from 16 to 12 years of age in the U.S. and Europe, with some girls getting their periods at nine or ten years old and developing breasts as young as eight years old (Greenspan and Deardorff 2014). A World Health Organization study involving data from 34 countries in Europe and North America suggests the primary reason for the increase in earlier puberty is obesity, with differences in Body Mass Index (BMI) accounting for 40% of individual- and country-level variance (Currie et al. 2012). Exposure to hormone-disrupting chemicals in utero and childhood may also be a factor (Greenspan and Deardorff 2014). As with other aspects of health discussed in this chapter, social and economic factors also influence earlier puberty, with girls who grow up in homes without their biological father twice as likely to experience early puberty, as is the case for girls who experience childhood trauma and/or grow up in a home with a depressed mother (Greenspan and Deardorff 2014). There is also ethnic variation in early puberty, with African American and Latina girls much more likely to experience puberty at younger ages. These factors combine in that African American and Latina girls are more likely to be overweight or obese and to grow up in low-income neighborhoods, where they are more likely to be exposed to environmental pollutants. Early puberty in girls has been associated with increased risk of breast cancer, ovarian cancer, obesity, diabetes, and raised triglycerides in later life (Pierce and Hardy 2012). In addition, there are negative social consequences, with girls who develop early more likely to experience anxiety, depression, poor body image, and eating disorders (Greenspan and Deardorff 2014).

At the same time, age at puberty is dropping for girls in Western nations and age at birth of the first child is later, on average at 26 years old (Mathews and Hamilton 2016). Women are also having fewer children, two on average (Gao 2015), with 15% of women choosing to remain childless (Livingston 2015). Rates of breastfeeding have risen in recent decades but drop to only 27% of infants once babies reach 12 months of age (CDC 2014). Nearly one-third of women also take oral contraceptives or use another hormonal method of birth control (Jones and Dreweke 2011). In contrast, data from modern foraging populations (Eaton et al. 1994) indicate age at menarche is around 16 years old, age at birth of the first child is 19, breastfeeding on-demand continues for three years for each child, and the number of live births to women who survive to age 60 averages six. These differences relate to elevated risk for reproductive cancers among women in developed countries.

Other than an established genetic risk (e.g., BRCA gene), the primary risk factor for breast cancer is exposure to estrogen. For women living in modern, industrialized economies, this exposure now often comes from women’s own ovaries rather than from external environmental sources (Stearns et al. 2008). There is nothing biologically normal about regular monthly periods. Women in cultures without contraception are pregnant or lactating (breastfeeding) for much of their reproductive lives, resulting in 100 or so menstrual cycles per lifetime. In contrast, Western women typically experience 400 or more (Strassmann 1997). This is partly due to younger ages at menarche. From menarche to the birth of a woman’s first child can be 14 years or longer in modern, Western populations, after which breastfeeding, if undertaken at all, lasts for a few weeks or months and is not on-demand, negating the natural birth control provided by frequent lactation. Women may also choose to use oral contraceptives or other hormonal methods to control reproduction. In their current form, these drugs induce a monthly period. Age at menopause (the cessation of menstrual cycles) is constant at 50–55 years old across human populations. For Western women, this translates into forty years of nearly continuous menstrual cycling between menarche and menopause. Each month the body prepares for a pregnancy that never occurs, increasing cell divisions that put women at risk for cancers of the breast, endometrium, ovaries, and uterus (Strassmann 1999). Obesity adds to this risk, as obese women have greater proportions of bioavailable estrogen (Eaton et al. 1994). In obese and overweight postmenopausal women, adipose (fat) tissues are the main source of estrogen biosynthesis. Thus, weight gain during the postmenopausal stage means higher exposure to estrogen and greater risk of cancer (Ali 2014). Factors associated with reduced risk of reproductive cancers are late menarche, early first birth, high numbers of pregnancies, early menopause, and breastfeeding.

Again, humans cannot return to our evolutionary past, and there are important social and economic reasons for delaying pregnancy and having fewer children. These include achieving educational and career goals, leading to greater earning power and a reduction in the gender pay gap, as well as more enduring marriages and a decrease in the number of women needing public assistance (Sonfield et al. 2013). There are also cultural means by which we might reduce the risk of reproductive cancers that do not involve increases in family size. These include reformulating hormonal contraceptives with enough estrogen to maintain bone density and stave off osteoporosis, but reducing the number of menstrual periods over the reproductive lifespan (Stearns et al. 2008). Reducing fat intake may also lower serum estrogen concentrations, while high-fat diets have been shown to contribute to breast tumor development. High-fiber diets are also beneficial in decreasing intestinal resorption of estrogenic hormones. Exercise also appears protective, with studies of former college athletes demonstrating risks of breast, uterine, and ovarian cancers later in life two to five times lower than those of non-athletes (Eaton et al. 1994).