Over the ensuing weeks, my new evolutionary biology colleagues helped me to recognize that everything in the natural world needs two kinds of explanations. The usual approach describes the body’s mechanisms and how they work; biologists call these proximate explanations. The other kind of explanation describes how those mechanisms came to be the way they are; biologists call these evolutionary or ultimate explanations.13,14,15,16 My medical education had been entirely about the proximate half of biology, which describes mechanisms, none about the half that explains how bodies got to be the way they are.
Failure to recognize that evolutionary explanations are essential complements to proximate explanations causes enormous confusion. If you ask for an explanation of eyebrows, one person is likely to say they are explained by genes that induce synthesis of certain proteins in certain locations. Another might point out that you also need to describe the process by which eyebrows develop. Another will likely say you need to know about eyebrows in other primates. Someone will likely note that eyebrows keep sweat out of the eyes. And someone will likely raise an eyebrow to demonstrate its utility as a signaling device. The first two explanations describe proximate mechanisms; the others are about evolution.
The Nobel Prize–winning ethologist Niko Tinbergen expanded the distinction in a 1963 article that described what have come to be known as “Tinbergen’s Four Questions”: What is the mechanism? How does the mechanism develop in an individual? What is its adaptive significance? And what is its evolutionary history?17 After relying on them for years, I finally saw that two are proximate and two are evolutionary and that two are about a slice in time, while two are about change across time. They fit nicely into a neat two-by-two table. When I added a slide showing the table in my lectures, the audience was more interested in the table than in my talk. When I put a PDF of the table on my website, it spread fast.
TINBERGEN’S FOUR QUESTIONS, ORGANIZED18
PROXIMATE
EVOLUTIONARY
SLICE IN TIME
What is the mechanism?
What is its adaptive significance?
SEQUENCE ACROSS TIME
How does it develop in an individual?
What is its evolutionary history?
Tinbergen’s questions made me recognize that some late-night debates with medical school classmates arose from mistakenly thinking the questions are alternatives. They aren’t. Answers to all four are necessary for a full explanation. The questions also made me realize that many things I had thought of as abnormal were actually useful. My medical education taught the details of the mechanisms in stomach cells that secrete acid and their role in causing ulcers but nothing about how stomach acid kills bacteria and digests food and why too little acid is as big a problem as too much. We learned all about the causes of diarrhea but little about its role in clearing toxins and infections from the GI tract. Coughing clears foreign matter from the respiratory tract. Fever is a carefully controlled response that fights infection. Even pain needs to be understood in terms of its function as well as its mechanisms; people born without the ability to experience pain usually die in early adulthood.19 I started to think about the utility of anxiety and low mood.
While many things that seem useless turn out to have a function, others are abysmal designs. The eye would be better without a blind spot. The birth canal is too narrow. Cancer protection mechanisms are insufficient, as are those that protect against infection. Ability to regulate eating is weak. Anxiety and pain are often excessive. I started wondering full-time about why selection left the body riddled with such imperfections.
When George Williams visited for a conference, he was easy to recognize; he looked remarkably like Abraham Lincoln. I knew his 1957 paper was admired, but no one had told me that he was one of the leading biologists of the twentieth century, certainly not Williams himself. He didn’t talk much, but when he did, everyone paid attention. Over beer, he explained how he had come up with his idea that selection can preserve the genes that cause aging. I saw a way to test his theory. It predicts that mortality rates should increase with age for some animals in the wild. The alternative theory, that genes for aging are outside the reach of selection, predicts that mortality rates should stay the same across the adult life span.
A few months of library work would be needed to find data on mortality rates for animals in the wild. I told my psychiatry department chair, John Greden, about my idea. He was new in the job and eager to encourage creativity, so he said I could devote half time to the project for the summer. By fall, I had found the data and a way to calculate how strongly selection was acting on aging in wild animals: very strongly indeed.20 George’s theory was right: genes that speed aging are not all unfortunate mutations whose effects come too late in life to be eliminated by natural selection; some give advantages that increase reproduction earlier in life. The idea has been confirmed in many studies that bred beetles and fruit flies for longer or shorter life spans.21,22 Selecting for earlier reproduction results in a shorter life span. Selecting for longer life span results in fewer offspring, especially in the wild. Aging has an evolutionary explanation.23
By the next time George visited, I knew enough about evolutionary biology to have a coherent conversation, and my research on aging had been published. I told George I thought that evolution could offer a new kind of explanation not just for aging but for diseases. He had been thinking the same thing. We decided to write a paper about how evolution could be useful for medicine.
During the first several months of our work, we made a fundamental mistake: we tried to find evolutionary explanations for diseases. Why, we asked, did natural selection shape coronary artery disease? Why did it shape breast cancer? Why did it shape schizophrenia? Finally we recognized our mistake. We were Viewing Diseases As Adaptations (VDAA). VDAA is a serious error that remains common in evolutionary medicine. But diseases are not adaptations. They do not have evolutionary explanations. They were not shaped by natural selection. However, aspects of the body that make us vulnerable to diseases do have evolutionary explanations. Shifting the focus from diseases to traits that make bodies vulnerable to diseases was the crucial insight that became a cornerstone for evolutionary medicine.
We spent days discussing the appendix, wisdom teeth, inflammation in the coronary arteries, cancer, and, of course, the human back. George saw the implications more clearly than I did and insisted on giving our article the grand title “The Dawn of Darwinian Medicine.” Our book, Why We Get Sick: The New Science of Darwinian Medicine, reached a wider audience and encouraged the growth of what is now called evolutionary medicine. There are now a dozen books on the topic, a scientific society, a journal, international conferences, and classes in most major universities.
Evolutionary medicine is not a method of practice or in any way an alternative to standard medicine. It just uses the principles of evolutionary biology to solve health problems the same way we use genetics and physiology. Evolutionary psychiatry is the part of evolutionary medicine that asks why natural selection left us vulnerable to mental disorders.
The New Question
The usual questions in medicine are those of a mechanic: How does the body work? What is broken? Why did it break? How can we fix it? These are proximate questions about how bodily mechanisms work and how they differ in people with a disease: What immune system mechanisms cause multiple sclerosis? What brain abnormalities explain why some people have schizophrenia? Answers to these questions advance the most important goal: finding causes and ways to fix problems. Asking such questions and finding their answers has vastly improved human health. If medicine is to use only one-half of biology, this is the half with the big practical payoffs.
The other, evolutionary half of biology poses questi
ons that take an engineer’s point of view: How did the body get to be the way it is? What selection forces shaped this trait? How do variations influence reproductive success? What trade-offs limit its reliability? In its general form, the new question asks, Why did natural selection leave our bodies with traits that make us vulnerable to disease?
The question is new, but it is close to one of the oldest questions. Why is life so full of suffering? Debated in religious and philosophical contexts for millennia as “the problem of evil,” answers have proved elusive.24,25,26 The Greek philosopher Epicurus recognized the conundrum 2,400 years ago; a slight adaptation of David Hume’s terse summary is widely quoted: “Is God willing to prevent evil, but not able? Then He is not omnipotent. Is He able, but not willing? Then He is malevolent. Is He both able and willing? Then whence cometh evil? Is He neither able nor willing? Then why call Him God?”27
Ever since, philosophers and theologians, especially those in the Abrahamic tradition, have struggled to explain evil and suffering. Possible explanations have a special name, “theodicies.” There are many of them, because none is fully satisfying.28 The problem is also central to Buddhism, whose first noble truth is “Life is suffering.”29,30 Its second noble truth is that suffering is caused by desire, more specifically the inability of ever fully satisfying desire. The third is that relief from suffering requires recognizing that desire is an illusion. An evolutionary view explains why we have desires, why we can’t satisfy them, and why it is so hard to set them aside: our brains were shaped to benefit our genes, not us.31,32,33
Reconciling the ways of God to man is far beyond the scope of this book. Explaining the prevalence of evil and suffering in general is also out of reach. However, most suffering is emotional suffering. Anxiety and low mood exist for the same reason as pain and nausea: because they are useful in certain situations. They are often excessive for good evolutionary reasons. There are also good reasons why we are vulnerable to addiction, schizophrenia, and all the other mental maladies. Reasons plural, because several are relevant in different combinations depending on the disorder.
Trying to explain why mental life is so often painful, and why thinking and behavior so often go awry, reveals another equally profound question. How can mindless selection that maximizes only reproductive success have shaped brains that make committed loving relationships and meaningful happy lives possible? Most people’s lives are nothing like the selfish competition for money and sex imagined by naive Darwinians. People meditate, pray, cooperate, love, and care for others, even strangers. Our species is remarkably endowed, not only intellectually but also socially, morally, and emotionally. Understanding the origins of love and morality is a crucial foundation for understanding social anxiety and grief and the deep relationships they make possible.
Jonas Salk, the inventor of the polio vaccine, said, “What people think of as the moment of discovery is really the discovery of the question.” We have a new question.
CHAPTER 2
ARE MENTAL DISORDERS DISEASES?*
There is little reason to believe that these diagnostic categories are valid.1
—A comment about the DSM diagnostic categories on the first page of the leading psychiatry textbook
There is no point in trying to explain mental disorders without first describing and defining them. That seems simple enough. The current edition of Diagnostic and Statistical Manual of Mental Disorders describes more than three hundred different ones. Problem solved? Hardly. The diagnostic system generates interminable debate—and intense controversy.
Definitions of diagnostic categories make mental disorders seem like diseases. Many are, but they are a bit different from most other diseases. They don’t have specific causes we have been able to identify, such as the bacteria that cause pneumonia. They can’t be diagnosed with blood tests the ways diabetes can. They don’t have definitive tissue abnormalities, such as the dying neurons in multiple sclerosis. Instead, mental disorders are defined by clusters of symptoms. People who say that food tastes like cardboard are often depressed and suicidal. Paranoid people often hear voices. Dangerously thin people who think they are fat are often high-achieving young women. Each disorder is defined by a list of symptoms. If a person has enough symptoms on the list for long enough, the diagnosis applies.
This checklist approach has vastly increased agreement about who has what, but at a high price. It encourages the assumption that the diagnosis contains all information needed and a corresponding neglect of the life situations that set off many disorders. Combined with an age of computer-accessible records, it discourages recording relevant but potentially embarrassing details. So clinical records now tend to provide a few sterile paragraphs that describe the symptoms and justify the diagnosis. For instance, here is a summary of Ms. B’s psychiatric evaluation.
Ms. B is a 37-year-old white, married mother of three, who is referred by her general physician for depression. She was well until four months ago, when she experienced the sudden onset of early-morning awakening, decreased appetite, low motivation, and feelings of guilt and hopelessness. She lost ten pounds in the past two months. Sometimes she wishes she were dead, but she has no plans to commit suicide. Symptoms are present every day, but they are much worse on some days than others, and they vary diurnally, worse in the morning. She reports chronic anxiety for several months, characterized by worry, sweating, and gastrointestinal symptoms. She also has periods of more intense anxiety lasting for hours, with trembling, shortness of breath, and a bad feeling in the pit of her stomach, but no panic attacks and no agoraphobia. She says that she has developed an intense discomfort in social situations, which she now avoids. She drinks one or two glasses of wine nightly, but she has no history of substance abuse. She attributes the onset of symptoms to marital conflicts. There is no previous history of psychiatric disorder. She is physically healthy, takes no medications, and has no allergies. There is a history of alcoholism in the father and anxiety in the mother. Her sister takes antidepressants. She grew up in a stable home. She denies abuse and traumatic events in childhood. She has three children ages 3, 5, and 9, who are doing well. Her husband is a manager at a local manufacturing plant. They live in a suburban neighborhood. She previously taught elementary school full-time, but she now works part-time as a teacher’s aide. Diagnosis: Major depression. Treatment Plan: Initiate antidepressant treatment and cognitive behavioral therapy, return in two weeks for follow-up.
The case report summarizes the facts that justify the diagnosis, but it gives no inkling of what brought on her symptoms. That came flooding out when she described seeing her former lover in a grocery store.
I was trying to buy groceries, but it was like I was walking in a swamp. I could hardly put one foot in front of the other. I had a list, but it didn’t help. Nothing seemed to matter. But the boys needed food, so I went. Halfway through, I saw Jack wheeling his cart around the far end of the aisle. For months, I thought I saw him all the time, like a ghost. But this time I was almost sure it was him. My heart started pounding and I froze and had a flashback to six months ago sitting in Starbucks.
We were going to meet at seven the way we always did, then move our stuff into the apartment where we had been meeting. We promised each other that at midnight on November second I would tell Sam and he would tell Sally. We wanted to do it November first, but we postponed it because of the kids and Halloween. I will always remember the sparkling flakes of snow as I opened the door to our Starbucks; they seemed like symbols of our new life together.
I told Sam I was leaving at midnight. He blew up, but I knew he would. He yelled so loud a car slowed down outside. That made it easier to go through with it. We were done a long time ago. Enough of living a lie. All I wanted was to be with Jack. I brought him a bouquet of freesias. But he didn’t come. I texted him at 7:30, thinking that maybe Sally had tried to jump out a window or something. Nothing. I called him. No answer. I couldn’t believe
it. I just went numb and sat there staring at the table so long the flowers got all wrinkled and limp, like fossils in the marble tabletop. That was pretty much the end of my life, right then.
I finally snapped out of my flashback and got up my nerve to follow where Jack had gone. Nothing. I went to check out. He wasn’t in line. So I tried to track him. There was a cart by the pork ribs with all his usual things in it, organic Mr. Coffee Filters, those little sugar cubes, Sominex, unwaxed dental floss. I am sure it was his. He must have seen me and snuck out. I don’t know what I would have said to him anyhow.
Ms. B’s story provided more insight into her problem than the entire case report and vastly more than her diagnosis. Nonetheless, diagnosis is essential. It provides a shorthand description of symptom patterns. Recognizing common patterns can make even ordinary clinicians seem like mind readers. Asking a patient who reports lacking hope, energy, and interest, “Does your food taste like cardboard, and do you awaken at four a.m.?” is likely to elicit “Yes, both! How did you know?” Patients who report excessive hand washing are astounded when you guess correctly, “Do you ever drive around the block to see if you might have hit someone?” If a student has weight loss and a fear of obesity, she will likely be astonished when asked, “You get all A’s, right?” Clinicians recognize these clusters of symptoms as syndromes: major depression, obsessive-compulsive disorder, and anorexia nervosa. After seeing thousands of patients, expert clinicians recognize different syndromes as readily as botanists recognize different species of plants. If only different illnesses were as distinct as different kinds of plants!
Good Reasons for Bad Feelings Page 3
