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Robert M. SapolskyA modern alternative to SparkNotes and CliffsNotes, SuperSummary offers high-quality Study Guides with detailed chapter summaries and analysis of major themes, characters, and more.
People who eat more when stressed are called hyperphagic, while those who eat less are hypophagic. The CRH released by the brain suppresses appetite, but glucocorticoids stimulate appetite and cravings for fatty, sugary, starchy foods. Frequent stress that occurs intermittently leads to higher levels of glucocorticoids and, thus, to overeating.
The type of stressor and individual differences in stress-responses or mindsets also impact appetite, with restrained eaters, or those who actively mitigate their food intake, being more likely to become hyperphagic. Apple-shaped is the term applied to individuals who collect more abdominal or visceral fat, while pear-shaped individuals collect gluteal fat on their hips and legs. High glucocorticoid levels are correlated with apple-shaped body types, and apple-shaped individuals have higher rates of cardiovascular and metabolic diseases. Researcher Mary Dallman found that junk food decreases the stress-response, meaning that hyperphagia and visceral fat collection may serve to mitigate stress-responses.
Digestion is an energy-intensive process, using between 10% and 20% of a mammal’s daily energy expenditure. The stress-response shuts down digestion—“Your stomach grinds to a halt, contractions stop, enzymes and digestive acids are no longer secreted, your small intestines stop peristalsis, nothing is absorbed” (79). During extreme stress, contractions in the large intestine increase, and the bowels are voided, often resulting in diarrhea.
Gastrointestinal (GI) disorders are classified as organic—meaning their cause is identifiable—or functional disorders, or those without identifiable causes. Functional disorders, like irritable bowel syndrome (IBS), are often exacerbated by stress. In IBS, contractions and intestinal pain increase with stress. However, many scientists are skeptical of the influence stress has on IBS, as early connections were based on Freudian psychoanalysis and some modern studies have not shown a correlation between stress and IBS, likely due to the fluctuating natures of both IBS and stress, the retrospective study methods, and the unknown underlying causes of IBS.
Peptic ulcers are holes that develop in and around the stomach—gastric ulcers occur in the stomach, and esophageal and duodenal ulcers appear at the entrance and exit to the stomach, respectively. Some ulcers appear rapidly after crises, such as massive physical trauma, but they can also develop slowly. A bacteria called Heliobacter pylori can withstand the acidic environment of the stomach, and it causes peptic ulcers. Before the discovery of Heliobacter pylori, scientists thought ulcers were caused by diet and stress; after the discovery, research on examining the connection between ulcers and stress declined. This was an issue because some individuals with duodenal ulcers—around 15%—do not have Heliobacter pylori in their systems.
Stress increases the risk of duodenal ulcers, and Sapolsky poses a few explanations for the correlation. Stress can lower stomach acid production and subsequently lowers production of the protective mucous lining; when acid levels rise, it leaves the stomach tissue vulnerable to the digestive acids. Reduced blood flow to the GI system, suppression of the immune system, lower prostaglandins—chemicals involved in repairing tissue—and reduced stomach contractions resulting from the stress-response may also contribute to peptic ulcer formation.
Growth, which takes a significant amount of energy, is managed via hormones, including growth and reproductive hormones, insulin, and somatomedins, which promote cell division. Sapolsky warns that the content of the chapter may increase parental anxiety. Assessments of the world made during childhood, including the prenatal environment, are lasting. If a child perceives the world as a stressful place, they are more likely to experience stress, anxiety, and depression in adulthood, and if a fetus is exposed to famine, they are more likely to be overweight as an adult. Low birth weight also predicts the later development of metabolic syndrome.
Fetal impacts on adult health are termed Fetal Origins of Adult Disease, or FOAD. Prenatal stress can have long-term adverse health impacts. If rat fetuses are exposed to high levels of maternal stress, they have increased levels of stress hormones as adults; the same appears to be true in humans, as demonstrated through studies that compare low birth weights to adult levels of glucocorticoids. Higher glucocorticoid rates result in higher rates of metabolic syndrome. Prenatal stress may also impact sexual function, anxiety, and memory, and FOAD issues can be passed down through multiple generations.
Postnatal stress can also have lasting health implications. Animal studies show that infants separated from their mothers or raised by inattentive mothers have higher levels of stress hormones in adulthood. Human studies have shown a correlation between childhood stress and adult depression, suggesting that childhood stress can cause health issues later in life, though more studies are needed on the subject.
Stress dwarfism provides some insight. The condition is rare, occurring only under extreme stress. When children with stress dwarfism are moved into a healthy environment, the condition reverses, resulting in more typical growth rates. Sapolsky provides four real-world examples. King Frederick II ordered an experiment to completely seclude children so they could determine humans’ “natural language,” and all the children died. In the second example, the growth rates of the children in two German orphanages were linked to the personality of their respective headmistresses. The author of Peter Pan, J. M. Barrie, developed stress dwarfism from severe parental neglect after his older brother died. Peter Pan was inspired by his own experiences and his desires to stay young and earn his mother’s love. In the final example, a young boy was hospitalized for stress dwarfism, and his growth rates and hormone levels fluctuated in response to his favorite nurse’s work schedule, though his food intake remained consistent.
The stress-response inhibits the release of growth hormones and makes the body less responsive to circulating growth hormones. Stress dwarfism also impedes the absorption of nutrients. Studies on rats have shown that a lack of active, meaningful touch leads to stress dwarfism. Similar findings have been demonstrated in humans through studying orphan mortality rates and studying the impact of touch on hospitalized premature infants. Stressors initially activate growth hormones to help break down stored fat and turn it into usable energy; however, somatomedin growth hormones are suppressed, preventing cell-division. In a study conducted in the 1960s, researchers Landauer and Whiting found that in tribal cultures, males’ heights were correlated to the stressfulness of the cultural rites of passage they endured.
While high prenatal exposure to glucocorticoids is correlated with smaller head circumference, delayed development, and behavioral and emotional problems, there is not enough research to declare the effects permanent. Studies comparing birth-weight, adult glucocorticoid levels, and the risk of metabolic syndrome demonstrate that even typical pre- and postnatal stress can have lasting impacts.
The impacts of stress are, in some cases, reversible, as seen in the improvement of children with stress dwarfism once their environment was changed. Sapolsky cites Meredith Small who, in her book Our Babies, Ourselves, suggests that every parenting style has lasting effects, that there is no perfect method, and that methods are tailored to the cultural environment, resulting in children who are adapted for their social settings.
In adults, growth hormones serve to maintain and repair the body. Bones, for instance, undergo consistent change and require significant amounts of calcium, but stress and glucocorticoids impede calcium transport, leading to more bone disintegration than growth. Chronic stress may increase the risk of developing osteoporosis, or the weakening of the skeletal system.
Love, Sapolsky posits, plays a significant role in growth, but researchers have been slow to acknowledge the significance of love. In the 1950s, experts disregarded human connection, deeming it irrelevant to infant development. Love was proven as critical to development through an experiment in which isolated monkey infants opted for an artificial mother with a soft towel over one with a bottle of milk. Harry Harlow conducted the experiments, which are considered controversial because they were exceedingly cruel to the animal subjects.
Sapolsky first addresses the male reproductive system because he claims it is “easier.” Luteinizing hormone releasing hormone (LHRH) released by the brain triggers the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH triggers testosterone release from the testes, while FSH encourages the production of sperm (120). Stressors inhibit LHRH, resulting in subsequent declines in LH, FSH, and testosterone. Testosterone release is inhibited by endorphins, prolactin, and glucocorticoids. Erections are activated by the parasympathetic nervous system, and ejaculations are instigated by the sympathetic nervous system.
Male sexual function can be impeded in multiple ways. Impotency can be the result of vascular disease due to chronic stress or to the activation of the sympathetic nervous system, which can inhibit erections or result in premature ejaculation. Whether erectile dysfunction is physiological or psychological can be determined by tracking whether a male gets an erection while sleeping—if an erection takes place, the issue is psychological. While many stressors can inhibit sexual function, some, including male-to-male competition, boost the function of sex hormones. Hyenas have a unique sexual response to stress, in that stress triggers erections in both males and subordinate females. These erections are a sign of submission.
The hormone release sequence in females is similar to that in males but is impacted by the menstrual cycle. Estrogen is the primary sex hormone in the weeks leading up to ovulation, and progesterone is the primary hormone in the weeks following ovulation. Stress inhibits estrogen and allows for the accumulation of androgens released by the adrenal glands, which further inhibit the reproductive system. As in males, stress and intense exercise alter the release of sex hormones; menstruation can become irregular, ovulation can cease—a disorder called anovulatory amenorrhea—and the uterine lining can fail to properly develop. Lower estrogen comes with higher risks of osteoporosis and cardiovascular disease.
Stress can also raise prolactin, which prevents pregnancy; prolactin released during breastfeeding can also prevent pregnancy, but breastfeeding must take place frequently. Hunter-gatherers have a child approximately every four years; during the pregnancy and the three years of breastfeeding, they don’t menstruate. This demonstrates that female humans likely evolved to have around 24 periods in their lifetimes, rather than the hundreds that most Western females experience. Stress can lower a female’s libido, which, Sapolsky suggests, is due to lower estrogen levels. Paradoxically, the stress caused by artificial fertilization techniques can, Sapolsky posits, prevent procreation, although more research is needed to verify the connection.
Stress is linked to higher rates of miscarriage in multiple species. In social species where only the dominant male reproduces, when a new male takes over, he kills the infants and may harass pregnant female until they miscarry. In some species, including rodents, the presence or smell of a new male is enough to stimulate a miscarriage. However, in humans, miscarriages are rarely caused by stress, and generally only extreme stress increases the likelihood of a miscarriage.
Sapolsky clarifies that, while stress can inhibit a female’s reproduction system in multiple ways, the effects are minimal. This is demonstrated by examining females who live stressful lives but still have multiple children, such as farmers in Kenya who experience seasonal malnutrition and high rates of disease but have an average of eight children. Studies in concentration camps also showed that 54% of females ceased menstruating, meaning almost half maintained reproductive function under the extreme stress. Stress has a more significant impact on libido than on fertility.
Psychoneuroimmunology is the study of the interconnected nature of the brain—psychology and neurology—and the immune system. The link can be demonstrated through conditioned immunosuppression: If an animal is given an immune suppressor and another stimulus at the same time, their body will learn to associate the substances, so if they are presented with only the stimulus, their immune system will respond the same as if they had been given the drug. The immune system protects the body against pathogens and parasites.
The immune system contains white blood cells, lymphocytes—further divided into T and B cells—and monocytes, like macrophages. Macrophages work with T cells to attack invading material, and B cells form antibodies, which are proteins that bind to and neutralize specific invading bodies. Chemicals called cytokines help white blood cells distinguish between friendly and unfriendly cells. Sapolsky describes these processes as acquired immunity; the body also has innate immunity, which involves generalized processes, such as secreting mucous to trap pathogens or promoting inflammation at wound sites.
The immune system can misfunction in two ways—it can ignore invading bodies, or it can attack benign cells, as happens in allergic reactions, or body cells, resulting in autoimmune disorders. Glucocorticoids suppress the production, shorten the circulating time, and disrupt the communication of lymphocytes and can cause them to self-destruct. Stress inhibits the innate immune system, preventing antibody formation. Stress-caused immune suppression not only pauses the immune system, but also actively disassembles the system, which takes energy.
Immediately following a stressor, immunity is boosted, but, if the stressor lasts for a significant length of time, the immune system response declines and can be suppressed up to 70% below its typical baseline. Some of the declines are advantageous, such as the elimination of aged lymphocytes. The immune response can be divided into three phases—Phase A, or a boost in immunity, Phase B, the return to baseline, and Phase C, a drop in immunity. Frequent stress, causing fluctuations between Phases A and B, is correlated with autoimmune diseases, while prolonged stress triggers Phase C and results in decreased immunity.
Sapolsky divides the link between stress and immune issues into four steps—stress events, stress-responses, level and length of stress, and health consequences—to demonstrate the complexity of studying the correlation. Measuring Step 1 is complex because stress perception varies among individuals and because self-reporting is often inaccurate. The middle steps are unreliable because stress-responses and stressors are highly variable and because retrospective studies are unreliable. Regarding Step 4, researchers are not yet sure to what extent stress-related fluctuations impact immunity. To study the full series of steps in a lab setting would be both time-consuming and costly. Scientists can speed up the process by introducing diseases, but that would interfere with the validity of the experiment.
Although it is difficult to study the correlation, the stress-disease link is seen in various circumstances. People who experience social isolation and a lack of social support have shorter life expectancies and more severe responses to infectious diseases, and the loss of a loved one appears to be linked with stress-related disease. Studies have shown that stress makes people more susceptible to the common cold, and some evidence points to a similar phenomenon in the development of acquired immunodeficiency syndrome (AIDS).
Latent viruses, like herpes, go dormant for a time before flaring again. Herpes can monitor glucocorticoid levels, and, when it becomes active, it can trigger further release of glucocorticoids. In rodent studies, high glucocorticoid levels correlate to faster tumor growth; glucocorticoids prune natural killer cells, promote capillary growth in tumors, and mobilize glucose, which feeds tumors. However, these results are largely irrelevant because they deal with induced tumors. Human studies linking cancer and stress are unreliable and limited and cannot be used to claim that stress-induced immunosuppression causes cancer or cancer relapse.
Some studies have found stress management practices like psychotherapy can improve cancer survival rates, but it is likely that lifestyle changes account for the results. Sapolsky criticizes the idea that a positive mindset can prevent or cure cancer, and he targets Bernie S. Siegel, who supported such ideas in his book Love, Medicine and Miracles. Siegel suggests that childhood cancer is caused by “parental conflict or disapproval” (180), and he claims that diseases are caused by straying from God. Seigel’s perspective is damaging because it places undue blame on the cancer patient, and Sapolsky focuses on Seigel because his message has had widespread consequences, as demonstrated through a study in which women revealed self-blame for their development of breast cancer. The connections between stress and disease should not be exaggerated—diseases can neither be prevented nor cured through positive thinking.
Sapolsky notes the newness of psychoneuroimmunology and reflects on sudden infant death syndrome (SIDS). Before scientists understood the cause of SIDS—believed to be linked to oxygen crises during the third trimester—they conducted autopsies on deceased children and noted larger thymus glands in children who died from SIDS. They concluded that SID was caused by abnormally large thymus glands. However, most non-SIDS autopsies were conducted on children from poor families. Their smaller thymus glands were the result of stress, and the SIDS infants from wealthier family had normal-sized thymus glands. Sapolsky extracts multiple lessons from these events, warning against declaring traits as “normal” because it eliminates objectivity.
The Biology and Effects of Stress continues as the predominant theme in these chapters as Sapolsky explores biological systems and phenomena that are impacted by chronic stress. Sapolsky begins each chapter with relevant background information on the systems or processes, he then discusses how stress impacts the events from a biological perspective, such as the digestive system pausing most functions. After examining the biological effects of stress, he explains how such events impact health.
A recurring pattern emerges, which Sapolsky draws attention to: Short-term stress-responses appear beneficial—for example, they boost growth—but long-term stress or frequent exposure to stress causes adverse effects, like inhibiting growth. These findings support Sapolsky’s claim that the stress-response evolved to mitigate short-lived physical stress rather than the extended bouts of psychological and social stress experienced by modern humans, particularly in industrialized nations, thereby invoking the theme of The Implications of Modern Chronic Stress.
While the focus of the text is on the adverse health impacts of chronic modern stress, Sapolsky repeatedly expresses the limits of health implications of stress. He writes, “Obviously a theme of this book is how many things can go wrong in the body because of stress and how important it is for everyone to recognize this. However, it would be utterly negligent to exaggerate the implications of this idea” (181). His point is demonstrated through the discussion on Siegel and the faulty message that cancer is caused and cured by certain mindsets. Siegel’s viewpoint is an example of sensationalized scientific information, where findings of studies have been taken out of context to elicit high levels of attention from society.
Sapolsky actively avoids this approach, instead providing detailed descriptions and acknowledging limitations and biases in the available research and in the implications of stress. He uses literary devices to make the straightforward information more accessible for lay-readers. For instance, he uses hypophora in the discussion on stress dwarfism:
Suppose one of your parents had a job necessitating frequent moves, and every year or two throughout childhood you were uprooted, forced to leave your friends, moved off to a strange school. Is this the sort of situation associated with psychogenic dwarfism? Definitely not (102).
Sapolsky also enhances his explanations by continuing to use metaphorical analogies. He compares the body’s self-maintenance in adulthood to building maintenance—“shoring up the sagging foundation, plastering the cracks that appear here and there” (114)—and he relates the immune system to military defenses—“Metaphorically, why not have your military that defends you always on maximal alert?” (156). As with many of the metaphorical analogies and other literary device uses, these serve to make the scientific material more digestible to the intended lay-reader, showing that creative devices are a critical tool for promoting science literacy.
Although Sapolsky addresses biases and experimental flaws in the studies he cites, his language choices suggest that he, too, is susceptible to implicit bias. Sapolsky draws attention to sex-limited studies, such as in his remark, “Reflecting the anthropological tunnel vision of the time, Landauer and Whiting only studied males” (111). This statement implies that Sapolsky is aware and critical of the sexism that has long existed in science, particularly in medical and biological science. However, in Chapter 7, he refers to androgens in females as a “male sex hormone” (130). This is an unintended oxymoron, as if the hormone naturally occurs in females, then it is not exclusively a “male” hormone. The sex-based designation “male” is, thus, inaccurate and reflects the commonly-held misbelief that only males have androgen hormones like testosterone.
A similar sex bias is suggested through Sapolsky’s choice to discuss male sexual function first and to refer to male sexual function as “easier”; however, he later remarks on the complexity of male sexual function: “Getting an erection to work properly is so incredibly complicated physiologically that if men ever actually had to understand it, none of us would be here” (123, emphasis added). This remark conflicts with his earlier presentation of male sexuality as simple, and it suggests that the distinction between which sex is “easier” to understand comes down to the fact that significantly more research has been conducted on males, and to the historical presentation of male humans as the human default while relegating female humans as “other.”
By Robert M. Sapolsky