16.3: Other Diseases

CARDIOVASCULAR DISEASE

Cardiovascular disease (CVD)—which includes coronary heart disease, hypertension (high blood pressure), and stroke—is the leading cause of death globally, and heart disease remains the number one cause of death in the United States (American Heart Association 2018). Risk factors for cardiovascular disease include diet, obesity/overweight, diabetes, and physical inactivity, as well as smoking and alcohol consumption. The connections between these factors and heart disease may not seem obvious and will be addressed here beginning with diet. Diets high in saturated fat and cholesterol can lead to atherosclerosis, a condition in which fat and cholesterol form plaque inside the arteries, eventually building up and hardening to the point that blood flow is blocked. Too much salt in the diet leads to fluid retention, which increases blood volume and thereby blood pressure, taxing the heart. Obesity/overweight contribute to cardiovascular disease directly through increases in total blood volume, cardiac output, and cardiac workload. In other words, the heart has to work much harder if one is overweight (Akil and Ahmad 2011).

Definition: cardiovascular disease (CVD)

A disease of the heart and blood vessels, often related to atherosclerosis, CVD is a condition in which a substance called plaque builds up in the walls of the arteries, blood vessels that carry blood away from the heart, compromising the flow of blood to the heart or brain.

Obesity also relates to CVD indirectly through elevation of blood pressure (hypertension) and diabetes. High levels of blood glucose from diabetes can damage blood vessels and the nerves that control the heart and blood vessels. Physical activity also alters the likelihood of having heart disease, both directly and indirectly. Regular exercise of moderate to vigorous intensity strengthens the heart muscle and allows capillaries, tiny blood vessels in your body, to widen, improving blood flow. Regular exercise can also lower blood pressure and cholesterol levels and manage blood sugar levels, all of which reduce the risk of CVD. Alcohol consumption can raise blood pressure and triglyceride levels, a type of fat found in the blood. Alcohol also adds extra calories, which may cause weight gain, especially around the abdomen, which is directly associated with risk of a heart attack (Akil and Ahmad 2011). Cigarette smoking also increases the risk of coronary heart disease. Nicotine increases blood pressure; in addition, cigarette smoke causes fatty buildup in the main artery in the neck and thickens blood, making it more likely to clot. It also decreases levels of HDL (“good”) cholesterol (American Heart Association 2014). Even secondhand smoke can have an adverse effect if exposure occurs on a regular basis. Chronic psychological stress also elevates the risk of heart disease (Dimsdale 2008). The repeated release of stress hormones like adrenaline elevates blood pressure and may eventually damage artery walls. The human stress response and its connections to health and disease are discussed in more detail below.

Definition: stress response

A predictable response to any significant threat to homeostasis. The human stress response involves the central nervous system and the endocrine system acting together. Sudden and severe stress incites the “flight or flight” response from the autonomic nervous system in conjunction with hormones secreted by the adrenal and pituitary glands, increasing our heart rate and breathing and releasing glucose from the liver for quick energy.

OSTEOARTHRITIS

The appearance of osteoarthritis in skeletal remains from the Neolithic has been attributed to the repetitive loading of articular joints due to the manual labor associated with early agricultural production (Larsen 2014). In modern populations, overweight and obesity are major contributing factors to arthritis, due not only to the overloading of joints that comes with excess weight (Guilak 2011) but also to the action of fat cells that generate low-level inflammation in response to high levels of glucose in the blood (Issa and Griffin 2012). Meaning, diabetes is a risk factor for osteoarthritis (Berenbaum 2011). A high percentage of obese individuals with knee osteoarthritis are sedentary, suggesting lack of physical activity may increase susceptibility to inflammation (Issa and Griffin 2012). Again, excess body weight and lack of physical activity are a mismatch for Stone Age bodies making their way in the space age (Eaton et al. 1988).

Definition: osteoarthritis

Refers to the degeneration of joint cartilage and underlying bone, causing pain and stiffness. In the absence of previous injury, it is most common in modern populations from middle age onward.

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).

Definition: cancer

A collection of related diseases in which some of the body’s cells begin to divide without stopping and spread into surrounding tissues.

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. https://news.nationalgeographic.com/2016/07/oldest-human-cancer-disease-origins-tumor-fossil-science/

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).

Definition: incidence

The rate at which new cases of a disease occur in a population over a given period of time.

Definition: menarche

The first occurrence of menstruation.

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).

Special Topic: The Paleo Diet

Given the impact of diet on every health condition discussed so far in this chapter, you may be considering changing what you eat. But what diet to follow? Given your interest in human evolution, have you ever wondered about the Paleo diet? Popularized by the 2002 book, The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat, by professor of nutrition and exercise physiology Loren Cordain, the Paleo diet is an eating plan based on the idea that eating like our ancestors is protective against weight gain, metabolic disorders, and other maladies of modern life. Its publication spawned an entire industry of diets, exercise plans, cookbooks, and other products based on the “Paleolithic prescription.”

Recommendations of the Paleo diet include eating high amounts of protein, fewer carbohydrates, more fiber, certain fats, and foods rich in plant phytochemicals, vitamins, minerals, and antioxidants. Sounds good so far, but let’s dive a little deeper. Protein in the Paleo diet consists of lean meats (including organ meats), fish, and seafood. And not industrially produced versions of these. The meat should be grass- not grain-fed, and the fish should be wild-caught, not farmed. All fruits are included in the diet, but only non-starchy vegetables make the cut, meaning no tubers like potatoes. The recommended carbohydrates have a low Glycemic Index, meaning they are more slowly digested and metabolised causing a lower, slower rise in blood glucose and insulin levels. There are also no cereals, no legumes (beans), no dairy products, no processed foods, no refined sugars (including honey), and no added salt. The primary fats in the diet are monounsaturated, polyunsaturated, and omega-3 fats, rather than the trans fats and saturated fats most often found in contemporary diets (Cordain 2002).

Particular attention is given to counteracting what many people think of as high-protein foods. Hamburger, eggs, and cheese, which are 24%, 34%, and 28% protein, respectively, are off the list, as opposed to skinless turkey breast (94% protein) and shrimp (90%). There is also the idea that current Western diets are more acidic than alkaline, reducing calcium levels in the body by promoting excretion of calcium in the urine. Cereals, dairy products, legumes, meat, fish, eggs, and salty processed foods elevate acid loads in the body, while fruits and non-starchy vegetables produce net alkaline loads. The diet advises eating 35% of your daily calories as fruits and veggies to balance out the high recommended protein intake. These recommendations are based on the premise that this represents a typical diet of hunter-gatherers in our ancient past before the transition to agriculture. Given what you have learned about human evolution from this text, what might be some problems with this assumption? How about with the diet itself?

To begin, there is no such thing as the Paleo diet. Hominins occupied a variety of ecological niches, with corresponding variety in what they ate (Lucock et al. 2014), including wide variation in their consumption of meat (Wrangham 2009). There is also archaeological evidence and dietary analysis of teeth demonstrating that hominin foragers ate cooked grains as far back as two million years ago (Zuk 2013). Although modern foragers are not an analogue for the past, they vary widely in their dietary intake. Meat forms 99% of the traditional Inuit diet (McElroy and Townsend 2009), while the diet of the !Kung of sub-Saharan Africa is mostly vegetarian (Lee 2013). In the case of the Inuit, they have genetic mutations related to the processing of omega-3 fatty acids that allow them to live on such a high-protein, high-fat diet without the cardiovascular disease and metabolic issues found in other populations (Fumagalli et al. 2015). Similarly, some pastoral populations became lactase persistent over time, allowing their members to digest milk as adults (Crow and Kimura 1970), and there are genotypes favored among peoples with high-starch diets that improve the digestion of starches (Marciniak and Perry 2017) and promote resistance to infectious disease (Lucock et al. 2014). Clearly, not all humans ate the same things, and natural selection favored genotypes that allowed populations to survive as they encountered new food sources and their diets changed. The modern Paleo diet also does not take into account the difficulty of procuring the lean protein that it recommends in the absence of hunting it yourself. Furthermore, it leaves out fermented foods, like pickled vegetables, yogurt, and cheeses, that contribute to a healthy microbiome (Graber 2014), something researchers are coming to find is essential to health (Shreiner et al. 2015).

What, then, to eat? As with Paleo diets, what humans eat today varies by geography, economics, and cultural preferences, among other factors. The burgeoning science of nutrigenomics hopes to one day be able to provide each individual with a customized diet based on analysis of your own DNA, lifestyle, and disease risk (Neeha and Kinth 2013). Until that time, World Health Organization dietary recommendations for the prevention of chronic diseases like cardiovascular disease, diabetes, and cancer emphasize diets that are low in saturated fat, salt, and sugar, high in fiber, and feature lean proteins (including nuts and fish) and carbohydrates from whole grains, legumes (beans), fresh fruits, and vegetables (WHO 2018c). Fiber, in particular, has been shown to be protective. Epidemiological and clinical studies demonstrate that intake of dietary fiber from plants and whole grains is inversely related to obesity, Type 2 diabetes, colon cancer, and cardiovascular disease (Lattimer and Haub 2010). Newer research suggests diets high in fiber also boost immune function, mood, and cognition (Kaczmarczyk et al. 2012).

Can these recommendations be met with a vegetarian or vegan diet? Research suggests this is the case, if one is conscientious and knowledgeable about the combination and timing of foods to obtain essential nutrients (McEvoy et al. 2012; Woo et al. 2014). Research introduced earlier in this chapter regarding the negative health effects of cooked meats suggests that eating meat four times per month or less, eating it rare, and avoiding processed meats altogether, is less likely to result in cancer, diabetes, and hypertension (Abid et al. 2014; Liu 2018; Liu et al. 2018; Trafialek and Kolanowski 2014). Additionally, according to the EAT-Lancet Commission on healthy diets from sustainable food systems, global consumption of foods such as red meat and sugar will have to decrease by half to make sure the Earth will be able to feed a growing population of 10 billion people by 2050. At the same time, people will need to double the amount of plant-based foods they eat, including nuts, fruits, vegetables, and legumes (Willett et al. 2019).

STRESS

Have you ever been “stressed out” in class? Say you’re in a large lecture hall with a hundred other people, or even in a small class where you don’t know anyone. You’re not sure about something the professor just said and you would really like to ask about it, so you start to raise your hand. Does your heart begin to pound and your mouth get dry? Do you sometimes get so nervous you choose to catch up with a classmate after lecture instead? If so, you are not alone. Fear of speaking in public is one of the most common social phobias (APA 2013). It has been estimated that 75% of all people experience some degree of anxiety or nervousness when it comes to public speaking (Hamilton 2011), and surveys have shown that most people fear public speaking more than they fear death (Croston 2012).

We have evolution to thank for this.

Humans, like other primates, are social animals. Being part of a group helped us to survive predation, get enough to eat, and successfully raise our young. When faced with standing up in front of a group, or even speaking up in class, we break into a sweat because we are afraid of rejection. Psychologist Glenn Croston (2012) writes, “The fear is so great because we are not merely afraid of being embarrassed or judged. We are afraid of being rejected from the social group, ostracized and left to defend ourselves all on our own. We fear ostracism still so much today it seems, fearing it more than death, because not so long ago getting kicked out of the group probably really was a death sentence.” Hence, it is no surprise that public speaking triggers a stress response among much of humankind.

The human nervous system evolved in a context where quick responses to perceived threats presented an evolutionary advantage. The “fight or flight” response with which we are all familiar was honed during millions of years when threats more often took the form of an approaching lion than an approaching deadline. Our body’s response, however, is triggered by a wide variety of stressors that produce the same general pattern of hormonal and physiological adjustments (Martini et al. 2013). In today’s world, the system is often stuck in the “on” position due to the constant pressures of modern life, and this is a significant influence on health and disease.

The human stress response involves the Central Nervous System acting in concert with the endocrine and circulatory systems. It includes three phases: alarm, resistance, and exhaustion (Martini et al. 2013). The alarm phase is the automatic, short-term response to a crisis, the “fight or flight” response you might have experienced when thinking about raising your hand in class. Epinephrine is the dominant hormone of this phase. Its secretion stimulates activation of the sympathetic nervous system, including sudden increases in heart rate, respiration, mental alertness, sweat gland excretion, and energy use. If the stress-inducing situation lasts more than a few hours, the body shifts to the resistance phase. Glucocorticoids are the dominant hormones of this phase, which involves mobilizing the body’s metabolic reserves to maintain the energy levels necessary for the brain to function during continued stress. A side effect of glucocorticoids is suppression of inflammation and the immune response, and cardiovascular damage can occur from elevations in blood pressure and blood volume from the action of ADH (antidiuretic hormone) and aldosterone (a hormone that regulates salt and water in the body). The resistance phase can be maintained for weeks or months, but eventually homeostatic regulation breaks down and leads to the exhaustion phase. If corrective actions are not taken, organs begin to fail, and death follows (Martini et al. 2013).

Definition: Central Nervous System

The complex of nerve tissues stemming from the brain and spinal cord that controls the activities of the body

Definition: circulatory system

The biological system that circulates blood around the body via the heart, arteries, and veins, delivering oxygen and nutrients to organs and cells and carrying waste products away.

The negative effects of sustained, elevated cortisol levels on health are well documented. These include higher levels of infectious disease and slowed growth in childhood (Flinn and England 2003) and increased incidence of heart disease, obesity, and diabetes in adults (Worthman and Kuzara 2005). As opposed to what might have been the case in our evolutionary past, many causes of sustained stress in contemporary societies are psychosocial rather than physical threats. These can include an unhappy marriage or frustrations at work (Dimsdale 2008). Stressors can also be more subtle. For example, a recent review of research into the effects of stress on health indicated internalized racism was a significant stressor that was positively associated with alcohol consumption, psychological distress, overweight, abdominal obesity, and higher fasting-glucose levels among minority groups (Williams and Mohammed 2013). Chronic everyday discrimination is also positively associated with coronary artery calcification, elevated blood pressure, giving birth to lower-birth-weight infants, cognitive impairment, poor sleep, visceral fat, and mortality. These effects have been shown to increase morbidity and mortality among members of affected groups.

Epigenetics can also be a factor in how a person is able to deal with stressful situations. Maternal experiences of stress during pregnancy have the potential to permanently alter the physiology of mothers’ offspring, especially the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis regulates metabolism, blood pressure, and the immune response, and these alterations can predispose prenatally stressed individuals to suffer metabolic, cardiovascular, and mental disorders in adulthood (Palma-Gudiel et al. 2015). These experiences carry across generations, with children of Holocaust survivors who experienced PTSD demonstrating similar changes in neurochemistry in the absence of a sustained, traumatic event, as did infant offspring of mothers who developed PTSD during pregnancy after witnessing the traumatic events of 9/11 (Yehuda and LeDoux 2007). Clearly, stress has a profound impact on human health and is one more example of a biological system that is maladaptive in many modern contexts.

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