How Inequality Shortens Lifespans

It’s late October, and I am kneeling in Old Chapel Hill Cemetery, brushing the fallen leaves from a small, flat stone sunken into the earth. Percy R. Baker, June 23, 1913–May 11, 1966. A few more weeks and he would have turned 53. Several feet away I am startled by a marker the size of a lunch box that is half covered by a shrub. Thomas W. Battle, Jr., Mar. 15, 1918–May 10, 1918.

On the other side of the cemetery stands an imposing stone monument the size of an upright piano. In letters large enough to read from yards away, it reads: William F. Strowd, 1832–1911. The memorial documents that he was a devout man, a member of the North Carolina Constitutional Convention, and a member of the United States Congress. Strowd lived to the age of 79, impressive in an era when the life expectancy was 51. Nearby is an extravagant obelisk taller than a man, bearing a coat of arms in gold against black granite, marking the grave sites of Eugene Simpson, who lived 79 years, and Margaret Simpson, who lived to 85.

I did not know the descendants of the Bakers or the Battles or the Simpsons, but I had just read about a research finding so curious that I had to test it for myself. You could predict the life span recorded on a tombstone, the study claimed, by the size of the monument. The explanation for this, of course, is money: The wealthier you are, the longer you live, and the bigger the tombstone your family can afford. This link between longevity and tombstone size was documented by George Davey Smith, an epidemiologist in Scotland. His team roamed the graveyards of Glasgow, recording the height of the gravestones and the birth and death dates inscribed on them. He found that each meter of height was associated with a little more than two additional years of life. I brought my class of undergraduates out to the campus graveyard equipped with tape measures to test whether we would find the same relationship at another time and place. Sure enough, we found the same phenomenon in Chapel Hill: Longer lives were recorded on larger stones.

There are a lot of reasons, of course, why poverty could be bad for one’s health. The poor may do without basic medical care, safe living conditions, and good sanitation. If conditions are truly desperate, they might die of hunger. More commonly, malnourished children fail to develop healthy immune systems and can die from common infections, like measles. Those two sources of death together make up the statistics we occasionally hear that a child dies of hunger every eight seconds (or ten seconds, or fifteen; as global poverty has been reduced over the last decade, that grim statistic is dropping).

When we examine the data within individual countries, we also see a very clear link between money and health. The more money you have, the better your health and the longer you are likely to live. Take, for example, the difference in death rates across the richest and poorest zip codes in America. In the richest zip codes, the annual death rate is about 50 deaths per 10,000 people. In the poorest zip codes, that number nearly doubles to 90 deaths per 10,000. Each step up in wealth translates into extra years in life.

We can see this pattern even more clearly in data from a massive study of more than ten thousand British Civil Service employees that has been in progress since the 1960s. Her Majesty’s Civil Service has an exquisitely detailed hierarchy, with dozens of clearly defined job grades from cabinet secretaries who report directly to the prime minister all the way down to entry-level clerical jobs. Physician Michael Marmot has found that each rung down the ladder is associated with a shorter life span. The pattern is strikingly linear, so that even the difference between the highest-status government officials and those just one rung below was linked to increased mortality.

The Scottish gravestone research also included a telling detail that sheds further light on the nature of the link between money and health. Smith notes that the graves they studied belonged mostly to middle and upper-class people. (The poor were often buried with no gravestone, or with a wooden marker that did not survive the elements.) That particular fact may not sound very significant, but it offers a clue to a much bigger truth about how wealth shapes health.

In the story “Silver Blaze,” Sherlock Holmes investigates the murder of a horse trainer and the disappearance of his famous racehorse the night before a contest. A Scotland Yard detective asks Holmes, “Is there any other point to which you would wish to draw my attention?” Holmes answers, “To the curious incident of the dog in the night-time.” “The dog did nothing in the nighttime,” says the detective. To which Holmes replies, “That was the curious incident.” The dog that didn’t bark tells Holmes that the horse thief must have been an insider, familiar to the dog. It takes Holmes’s extraordinary wit to notice the absence of evidence as evidence. For their part, it took scientists a while to realize that there was something missing from the graph relating money to life span within developed countries.

But within a rich country, there is no bend; the relationship between money and longevity remains linear. If the relationship was driven by high mortality rates among the very poor, you would expect to see a bend. That is, you would expect dramatically shorter lives among the very poor, and then, once above the poverty line, additional income would have little effect. This curious absence of the bend in the line suggests that the link between money and health is not actually a reflection of poverty per se, at least not among economically developed countries. If it was extreme poverty driving the effect, then there would be a big spike in mortality among the very poorest and little difference between the middle- and highest-status groups.

The linear pattern in the British Civil Service study is also striking, because the subjects in this study all have decent government jobs and the salaries, health insurance, pensions, and other benefits that are associated with them. If you thought that elevated mortality rates were only a function of the desperately poor being unable to meet their basic needs, this study would disprove that, because it did not include any desperately poor subjects and still found elevated mortality among those with lower status.

Psychologist Nancy Adler and colleagues have found that where people place themselves on the Status Ladder is a better predictor of health than their actual income or education. In fact, in collaboration with Marmot, Adler’s team revisited the study of British civil servants and asked the research subjects to rate themselves on the ladder. Their subjective assessments of where they stood compared with others proved to be a better predictor of their health than their occupational status. Adler’s analyses suggest that occupational status shapes subjective status, and this subjective feeling of one’s standing, in turn, affects health.

If health and longevity in developed countries are more closely linked to relative comparisons than to income, then you would expect that societies with greater inequality would have poorer health. And, in fact, they do. Across the developed nations surveyed by Wilkinson and Pickett, those with greater income equality had longer life expectancies. Likewise, in the United States, people who lived in states with greater income equality lived longer. Both of these relationships remain once we statistically control for average income, which means that inequality in incomes, not just income itself, is responsible.

But how can something as abstract as inequality or social comparisons cause something as physical as health? Our emergency rooms are not filled with people dropping dead from acute cases of inequality. No, the pathways linking inequality to health can be traced through specific maladies, especially heart disease, cancer, diabetes, and health problems stemming from obesity. Abstract ideas that start as macroeconomic policies and social relationships somehow get expressed in the functioning of our cells.

To understand how that expression happens, we have to first realize that people from different walks of life die different kinds of deaths, in part because they live different kinds of lives. People in more unequal states and countries have poor outcomes on many health measures, including violence, infant mortality, obesity and diabetes, mental illness, and more. Inequality leads people to take greater risks, and uncertain futures lead people to take an impulsive, live fast, die young approach to life. There are clear connections between the temptation to enjoy immediate pleasures versus denying oneself for the benefit of long-term health. Inequality is linked to risky behaviors. In places with extreme inequality, people are more likely to abuse drugs and alcohol, more likely to have unsafe sex, and so on. Other research suggests that living in a high-inequality state increases people’s likelihood of smoking, eating too much, and exercising too little.

Taken together, this evidence implies that inequality leads to illness and shorter lives in part because it gives rise to unhealthy behaviors. That conclusion has been very controversial, especially on the political left. Some argue that it blames the victim because it implies that the poor and those who live in high-inequality areas are partly responsible for their fates by making bad choices. But I don’t think it’s assigning blame to point out the obvious fact that health is affected by smoking, drinking too much, poor diet and exercise, and so on. It becomes a matter of blaming the victim only if you assume that these behaviors are exclusively the result of the weak characters of the less fortunate. On the contrary, we have seen plenty of evidence that poverty and inequality have effects on the thinking and decision making of people living in those conditions. If you or I were thrust into such situations, we might well start behaving in more unhealthy ways, too.

The link between inequality and unhealthy behaviors helps shed light on a surprising trend discovered in a 2015 paper by economists Anne Case and Angus Deaton. Death rates have been steadily declining in the United States and throughout the economically developed world for decades, but these authors noticed a glaring exception: Since the 1990s, the death rate for middle-aged white Americans has been rising. The increase is concentrated among men and whites without a college degree. The death rate for black Americans of the same age remains higher, but is trending slowly downward, like that of all other minority groups.

The wounds in this group seem to be largely self-inflicted. They are not dying from higher rates of heart disease or cancer. They are dying of cirrhosis of the liver, suicide, and a cycle of chronic pain and overdoses of opiates and painkillers.

The trend itself is striking because it speaks to the power of subjective social comparisons. This demographic group is dying of violated expectations. Although high school–educated whites make more money on average than similarly educated blacks, the whites expect more because of their history of privilege. Widening income inequality and stagnant social mobility, Case and Deaton suggest, mean that this generation is likely to be the first in American history that is not more affluent than its parents.

Unhealthy behaviors among those who feel left behind can explain part of the link between inequality and health, but only part. The best estimates have found that such behavior accounts for about one third of the association between inequality and health. Much of the rest is a function of how the body itself responds to crises. Just as our decisions and actions prioritize short-term gains over longer-term interests when in a crisis, the body has a sophisticated mechanism that adopts the same strategy. This crisis management system is specifically designed to save you now, even if it has to shorten your life to do so.

The system is called the stress response. Stress is the body’s original payday loan. For such a remarkable system, stress was discovered rather late, operating in plain sight for eons before anyone realized the effect it was having. János Hugo Bruno “Hans” Selye was a young Hungarian endocrinologist at McGill University in the 1930s. His research at the time involved injecting rats with chemicals extracted from rat ovaries to measure their effects on the animals’ bodies, and ideally to identify a new hormone.

At first the experiment looked like a huge success. The rats treated with the ovarian extract showed enlargements of certain glands, while other glands shrank, and the subjects developed stomach ulcers. Something was happening, and it looked very much like a new hormonal effect. Selye then examined his control group of rats, which had been injected with a different kind of hormonal extract. The puzzling thing was that they showed the same symptoms. So he tried another kind of extract, and then another. In trial after trial, whatever he injected into the rats seemed to have the same physical results.

Rather than discovering the unique effects of some unknown hormone, Selye had stumbled on a response to . . . what exactly? Having material injected into one’s body? Being poked with needles? Selye did more studies to determine precisely what kinds of traumas it took to generate the symptoms. The studies involved the kind of grim procedures that would probably never be allowed by research ethics boards today. He injected other chemicals, like morphine and formaldehyde. He cut some rats’ skin and broke the bones of others. He placed some in freezing cold, and others were starved for days.

Following each experiment, Selye dissected the rats and carefully noted the bodily consequences of each particular type of treatment. He ultimately discovered that the rats showed virtually the same pattern of biological responses to every kind of distress.

His results reminded him of something that he had noticed years earlier as a medical student. His professor had presented students with five patients to observe, each suffering from a different ailment. The point of the exercise was to get the students to notice the unique symptoms that marked each disease, like the little red spots that differentiated the measles from the flu. But what Selye had found most striking was that all of the patients shared many symptoms, like fever, loss of appetite, aches and pains, and swollen tonsils. When Selye suggested that there seemed to be a “syndrome of just being sick,” his professor was not impressed, and his idea went nowhere. Until, that is, Selye noticed the same generality in rats’ symptoms regardless of the treatments to which they were exposed.

Selye first called this “general adaptation syndrome” and later renamed it simply “stress.” The idea was unpopular among physiologists, who were primarily interested in mapping the links between particular chemicals and particular bodily effects. They thought of the body as something like a Swiss army knife, with a special tool for every job, or a collection of delicate keys to open each intricate lock. But Selye was saying that things were much messier than that. Disturb the system in any way, and you get this same generalized response. His supervising professor called it the “pharmacology of dirt.”

Selye had many of the details wrong. He thought, for example, that long-term stress was harmful because the body ran out of stress hormones and couldn’t replenish them quickly enough, leaving the body unguarded once the hormones ran out. And his motivations were called into question when evidence later emerged that he had been funded heavily by tobacco companies, which used his research to argue that it wasn’t cigarettes, but stress, that was dangerous: People simply smoked to relieve stress.

The concept of stress as a general bodily reaction to any kind of crisis has, however, withstood the test of time. Today we understand the stress response as the way the body prepares to expend a great deal of energy to respond to a threat or an opportunity.

To understand how stress works, imagine that you are a hunter-gatherer type searching for food on the grasslands. Suddenly, you hear a shuffling behind the tall grass. It could be a lion, or a warrior from an enemy tribe. In either case, you are in danger and will have to either fight or run. Or it could be a rabbit, in which case you will have to act quickly to secure tonight’s dinner. Or it might be a wild boar, which is also potentially dinner, but might also be a threat if you are not quick and careful with his tusks. You don’t have much time to determine whether the noise represents a crisis, an opportunity, or both, and within a fraction of a second your entire body has reoriented itself to prepare you for whatever the surprise might actually be.

Your brain directs various glands to release a complex chain reaction of hormones into your bloodstream that cause changes in your cells. Two of the most important stress hormones are adrenaline (also called epinephrine) and cortisol. These and other hormones unlock glucose, proteins, and fat stored in cells from food you’ve eaten and flush them into the bloodstream, where they can be used as energy by the muscles. They also interfere with insulin, whose job it is to remove glucose from the bloodstream and store it in your cells for later use.

Now that you have a massive energy supply flooding your bloodstream, you need to kick-start the circulatory system so that everything gets quickly transported where it needs to go. Stress hormones speed up the heart and lungs to supply more oxygen to the bloodstream and also cause the blood vessels to contract, which makes every heartbeat pump blood with greater force. Like water through a partially crimped hose, it turns from a stream to a spray as your blood pressure rises. Heart attacks are more likely to occur during these moments of stress, as it is then that the heart is working its hardest.

Another vital resource for your body in a potential crisis is water. Stress hormones tell your kidneys to stop taking water out of the bloodstream to make urine, while throughout the body water is diverted from tissues to the bloodstream, where it is available for use as needed. This explains why your mouth gets dry when you are about to make a wedding toast, just when you’d like to have a tongue that did not stick to the roof of your mouth.

Finally, your stress system triggers an immune response called inflammation. We ordinarily experience inflammation as a painful red swelling around a cut or insect bite. Or you feel it as the sore, scratchy feeling in your throat when you realize you’re not just tired, you’re coming down with a cold. The body is flooding the potentially infected tissues with immune cells, ready to kill invading organisms. The painful feeling that we experience as the infection is actually the body’s reaction against it. It is the body’s own cocktail of antibiotics and antivirals.

One of the leading roles in this assault is played by a kind of cell called a macrophage (which translates to “big eater”). Unlike other parts of the immune system that remember specific invaders and target them directly for destruction, inflammation’s tactic is equivalent to a carpet bombing. These cells ask only one question: Is it me or not-me? If the answer is not-me (that is to say, if the molecular markers of one’s own body are not detected), then the big eaters gobble it up.

We normally think of the immune system as reactive, in that once a bacterium or virus has infiltrated the body, it mounts a counterattack. That’s true, but the stress response does not wait until the body’s perimeter has actually been breached. As soon as the grass starts rustling, the body scrambles to prepare a preemptive response. Inflammatory cells are secreted into the bloodstream to be ready as a precaution.

This impressive crisis response system raises an important question: If our body has the power to boost our energy, deploy a preemptive immune shield, and make us faster to respond to a challenge, then why do we wait for a stressful situation to put these impressive abilities to use? Why don’t we exploit them all the time?

The first reason is that in evolution, as in other areas of life, there is no such thing as a free lunch. Stress does not create new energy; it only redirects it: When the stress response gives a boost in one area, it has to take something away somewhere else. In the face of the potential emergency stirring in the grass, your body shuts down all unnecessary functions. The glucose and proteins that flood your bloodstream are now being taken away from longterm projects like cell division, maintenance, and repair and redirected to the muscles.

Digestion, for example, grinds to a halt because that is a longterm project that will be irrelevant if you don’t survive the next few minutes. Growth processes also get shut down, which accounts for a condition known as “stress dwarfism.” Children who experience prolonged periods of intense stress, like abuse or neglect, may have stunted growth even if their nutrition is adequate.

The second reason we can’t enjoy stress’s benefits all the time is that it causes terrible side effects. We are accustomed to thinking of the body’s responses as natural and, therefore, not harmful to us. But the hormones released during stress are essentially powerful drugs made in-house. Doctors use adrenaline and cortisol (in its synthetic form, cortisone) and other stress hormones as medications for a variety of problems, but do so sparingly, however, because they have serious consequences. As with other drugs, our naturally produced stress hormones are safe if used only occasionally and for short periods. But that isn’t the way we typically employ them.

Robert Sapolsky, a Stanford biologist and expert on stress, has argued that if we utilized our stress response the way other animals do, we would reap its benefits and avoid many of its costs. But it is the very qualities that make stress a brilliant power booster throughout the animal kingdom that also make it a cause of misery and disease for humans. As we have seen, the brilliance of stress is that it does not wait until there is actual tissue damage: It kicks in when faced with a potential threat. Humans, however, can sense a threat that is not actually physically present. Just spend a minute thinking about something that terrifies you or makes you anxious. Soon you will notice your heart beating faster. Your temperature may rise and you might start to sweat a bit. You are triggering your stress response merely with your thoughts. Unlike other animals, we humans have the ability to lie awake at night worrying about tomorrow’s PowerPoint presentation, next month’s mortgage payment, or a weird-looking mole on your back.

Also unlike other animals, humans can turn the stress response on for weeks, months, or years at a time. Think of the ramifications: We are exploiting a system that is designed to ignore long-term costs in order to redirect every resource to escaping an immediate emergency, but using it over the long term.

When stress hormones stop insulin from storing glucose for extended periods of time, we are at greater risk for diabetes and obesity. When they make the heart pump harder and the blood vessels constrict for months on end, we become prone to cardiovascular disease. And when inflammation goes unchecked, the immune system can become overactive—so eager to attack that it ceases to differentiate between cells that are “me” and “not-me.” When the immune system starts to mount an offensive against our own body’s cells, it causes autoimmune diseases.

Another way it can become overstimulated is by failing to differentiate between harmful invaders (bacteria and viruses) and harmless substances (like pollen, dust mites, or certain ingredients in foods). When that happens, an allergy develops. Long-term inflammation is also a risk factor for heart disease, depression, and other serious disorders.

None of this seems very adaptive, does it? Our craving for status, like our appetites for food and sex, can get us in trouble because what worked well for millennia is not always suited to our modern environment. The same mismatch is true of stress. Recall that our ancestors were hunter-gatherers for much, much longer than we have lived as we do today. Archaeologists estimate that 15 percent of the population in prehistoric times died a violent death. That is five times higher than the comparable rate in the 20th century, including all the deaths from both world wars, the Holocaust, and other genocides. Before modern sanitation and antibiotics, simple infections caused astronomical mortality rates. Life expectancy among the ancient Greeks, for example, was about 35 years. In the presence of so much violence and disease, with none of modern medicine’s cures, the self-medication of stress provided the best shot at beating these acute threats of infection and injury. Today, the massive arsenal of our threat response system is the same, but the nature of the threats has changed.

Our ancestors could lie awake in their caves worrying about tomorrow just as we do. But for them, the downsides of stress were massively outweighed by its benefits. Unlike our ancestors, we are now fortunate to live long enough to succumb more often to the diseases of old age, rather than to predators in the grass. The downside of that trade is that the side effects of stress can be more harmful in the contemporary environment than the threats it evolved to protect us from. Today in economically developed countries, some of the most common causes of death are heart disease, stroke, and diabetes, all of which can be caused or worsened by stress. Now that fewer organisms are able to kill us, we are left with a cure that may be worse than the disease.

Because stress is the body’s way of focusing on an immediate crisis at the expense of long-term costs, it’s not surprising that economic hardship and low social status can lead to bodily stress reactions. Many different kinds of studies have confirmed the link between status and stress. Consider, for example, Robert Sapolsky’s work with baboons living wild in a national park in Kenya. Sapolsky spent his summers observing the animals for years, getting to know individual members of their troops, and what rank each animal held in the hierarchy. To measure their stress, he would anaesthetize a baboon with a medicated dart and then take a blood sample. He found that the lower the baboon’s rank in the pecking order, the higher its stress hormone levels and the more likely it was to suffer from stress-related illnesses such as ulcers. But high-ranking males, who could mate with any females they chose and take out aggression on any lower-ranking male, had much lower levels of stress.

One summer Sapolsky noticed that the baboons had taken to foraging in a garbage pit next to a tourist lodge. From the monkeys’ point of view, it was an easy buffet. Of course, not all the baboons were allowed to enjoy the feast, as dominant males mainly kept the spoils for themselves, getting fat as they ate the junk food. Ironically, the baboons eating from the garbage pile contracted bovine tuberculosis, a disease they never would have been exposed to in their natural foraging grounds. Within three years, the more dominant males died off, leaving the troop with a hierarchy, but the most aggressive males were no longer at the head of it. When Sapolsky analyzed blood samples from the subordinate males in this newly flattened social order, he found lower levels of stress hormones.

Studies in laboratory monkeys have shown a correlation between having higher rank in the troop and having less bodily stress. But that correlation doesn’t tell us whether it is low rank itself that causes increased stress or whether increased stress causes low rank. It might be that the anxious monkeys are the ones who are dominated by less stress-prone members of the troop. So researchers at Wake Forest University experimentally altered the hierarchy of monkeys living in laboratory-based troops to better understand cause and effect. First, they confirmed that, in a primate hierarchy, the lower down the social ladder an animal is, the higher its stress hormones will tend to be. They then did the lower-ranking monkeys a big favor by permanently removing the dominant ones from the troop.

The researchers found that if you remove the most dominant animals, the stress hormones of the “middle management” animals decrease, as they find themselves suddenly “promoted” by the absence of the boss. The laboratory experiments confirmed what Sapolsky suspected from his field research: Rank in the hierarchy is responsible for differences in levels of stress hormones, rather than the other way around.

Heightened stress responses in low-ranking primates makes biological sense, because it is the low-ranking animals who are most likely to be beaten, bitten, and deprived of their dinner. They need to mobilize their bodies’ resources to deal with emergencies a lot more often than the alpha males do. Is this also true of humans? We don’t exactly have dominance hierarchies, but we do have plenty of hierarchical structures just the same. We measure them not with food and mating rights, but with money, power, social class, and social comparison. Based on the animal research, we should expect that individuals of lower status should be more stressed than others.

Indeed, studies have shown that people with lower incomes tend to have higher levels of stress hormones, like cortisol and adrenaline, in their bloodstreams. They tend to have hyperreactive immune systems and higher levels of inflammation in particular. Some studies have measured stress hormones and inflammation as people go about their daily business, and found that those who are poorer or who feel lower in status have slightly higher levels. But the differences really ramp up if you expose individuals to stress and see how their bodies react.

One study by Andrew Steptoe at University College London recruited volunteers from high- and low-status occupations within the British Civil Service and gave them stressful tasks to do. In one experiment, subjects had to use a pen to trace a moving star on a computer screen. That sounds easy, but the subjects could only see their hand through a mirror, so right appeared as left and vice versa. The experiment was designed so that the star moved quickly enough that the subjects would make mistakes, and the computer beeped loudly whenever the pen veered off the path. To guarantee the task would be stressful, the experimenters told the subjects that “the average person” could trace the star accurately, implying that the inevitable errors would leave them feeling less than average.

During and after the star-tracing task, the experimenters measured subjects’ heart rate and markers of inflammation in their blood. Both high- and low-status groups rated the task as equally stressful. But their bodies reacted differently. The low-status group showed more inflammation markers in their bloodstream. And although both groups had higher heart rates during the test, those of the high-status group soon returned to normal. The low-status group was still showing elevated rates two hours later.

A continent away in Los Angeles, psychologist Keely Muscatell and colleagues obtained similar results using a completely different method, and added a fascinating new wrinkle. This study began by interviewing volunteers while video-recording them. Imagine what it’s like to be a subject in this study: You go to a lab at UCLA, where you fill out a questionnaire, including information about your income and your position on the Status Ladder. You are then interviewed by a pleasant, professional college student, who asks personal questions like: What are you most proud of in your life? What would you most like to change about yourself?

The following day you go to a laboratory where a nurse places a needle in your arm to sample your blood, and then lie down in an fMRI machine to have your brain scanned. The device looks like a hospital bed, except that you place your head in the center of a white donut-like structure. It is made of smooth plastic, like the overhead baggage compartments in an airplane, and is the size of a Volkswagen. As you take your position, you look up at a little computer screen inside the donut hole and learn that another experimental subject is going to watch the interview you just recorded and rate what she thinks of you. And you get to watch her ratings. On a little computer screen appears a grid of squares, and within each square is a personality description. As the other subject watches your video, she moves a cursor around the screen, effectively complimenting or insulting you with her clicks. One minute she thinks you’re—click—intelligent. The next, she decides you are—click—annoying. How rude! A moment later, she sees the real you again—click—caring. The process goes on for a while, but what you didn’t know is that the “subject” in the other room was a sham, and it was the experimenters who were systematically praising and insulting you with those mouse clicks while scanning your brain and monitoring your blood throughout the emotional roller-coaster ride.

The researchers found that when volunteers were being evaluated by the person in the other room, markers of inflammation in their blood rose significantly. This effect was especially powerful for those who rated themselves as low on the Status Ladder: Their inflammation spiked.

There are several striking things about these findings. First, we have experimental evidence that the social evaluation actually caused the changes in inflammation, not simply that the two are correlated. Second, the whole process took place over the course of about ninety minutes, and inflammatory changes were detected in less than an hour. The human social hierarchy was playing out and expressing itself throughout nearly every cell in the body on a scale of minutes.

The study made one more startling discovery. The pathway from subjective ratings of status to inflammation in the bloodstream was controlled by brain activity in a particular network of regions in the frontal cortex. These regions are activated, among other things, when people think about the thoughts, feelings, and perspectives of others. Although more research is needed to confirm this initial finding and its interpretation, the authors suggest that the brain may be actively computing where we fall along the Status Ladder using the same neural machinery we ordinarily use to assess what other people are thinking of us. Like Sapolsky’s baboons, humans in this study were reacting to a low rank in the hierarchy as if it were a physical threat. Their bodies mobilized an immune response as if social slights were literal attacks.

For public relations firms or emergency medical responders or biological organisms, there is only one way to manage a crisis: to prioritize immediate necessities and deal with the future later. There may, of course, have been organisms that took a different approach. But the ones who ignored the most pressing demands in a critical situation are no longer with us to share their wisdom. Tending to immediate needs at the expense of the future is what your brain is doing when it dumps cortisol and adrenaline into the bloodstream. It is unleashing the energy and inflammation that ready you for battle, and if it risks diabetes and heart disease one day, then so be it. That is what your brain is doing when it tunes attention to the rustling in the bushes and ignores everything in the background. When you feel that you have nothing, even the cells in your body start demanding to take what they need now and worry about the future later. Inequality accelerates this process by making everyone feel less secure. It does not matter whether we measure the effects in dry mortality statistics or in the faded granite of a tombstone. Eventually we pay the price for this crisis management, as the future becomes now and our later becomes sooner.

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From The Broken Ladder: How Inequality Affects the Way We Think, Live, and Die. Used with permission of Viking. Copyright © 2017 by Keith Payne.