The Patient’s Story
ON MOST SATURDAYS,” Rich says, “my friends and I would hang out in front of Ebbets Field, where the Dodgers played—this was when we were ten or eleven years old—in the hopes that someone would have extra tickets at the last minute and bestow them on us. So we’d stand there and look forlorn, and it worked out for us a surprisingly high percentage of times.
“Well, one day we were there, flipping baseball cards, and up the staircase from the subway came this big black man, and the next thing you know I was blurting out, ‘Hey—you’re Jackie Robinson!’
“I still remember exactly what he was wearing: tan slacks, brown loafers, and a short-sleeve sport shirt with a white and brown stripe. He was a very dark man, very good-looking, and he said, ‘Come here, kid.’ And I went over and lo and behold, he takes my hand in his great big huge black hand and walks across the street with me toward the ballpark.
“I mean it was like I was dreaming. And he said, ‘You play ball, kid?’ and I said, ‘Yeah, yeah—and I do everything you do. I do everything just the way you do it!’ And I stop right in the middle of the street and assume the Jackie Robinson baseball stance, which was the stance that I had—the bat high over my right shoulder, challenging the pitcher, bent over, and slightly pigeon-toed the way he was—and he cracked up.
“Then he grabs my hand and says, ‘Hey—we’re gonna get into an accident.’ So we walk across to the other side, and he smiles at me and taps me on the hand and says, ‘Keep swingin’, kid,’ and goes into the clubhouse. Well, I did not wash my hand for more than a week, and I was in the ozone layer for a month after that—I told all my friends—and I still get into the ozone layer telling the story fifty years later.”
Rich and I are far from Brooklyn, in Palos Verdes, California, on a gorgeous, clear summer day, and while we talk and trade stories, I look out through an open window at the Pacific Ocean, at sailboats drifting gracefully along a horizon speckled in shimmering silvers and golds by a brilliant midday sun. I have swum a mile in the morning, and when we are done taping this part of our conversation, Rich and I will play an hour or two of tennis.
Rich is six feet two inches tall, weighs about 190 pounds, and, in shorts and T-shirt, looks amazingly youthful. He plays tennis several times a week, regularly defeating guys who played varsity tennis in college and are twenty and thirty years younger than he is.
He says that Jackie has always been his great hero, and I tell him Jerry said the same thing when I saw him a few weeks ago. Jackie was my hero too, along with Lou Gehrig (from having read Frank Graham’s biography, Lou Gehrig: A Quiet Hero), and “Pee Wee” Reese (like Reese, I played shortstop). I tell Rich that the main character in one of my novels marks his life by events in Jackie’s life, and we talk for a while about Jackie and the Dodger teams of our youth, and about how and why it is that a bunch of lower-middle-class Jewish kids from Brooklyn so loved, and identified with, this extraordinary black man.
Beyond the fact that we all hoped to play for the Dodgers some day, and the fact that Jackie was the most exciting athlete of his time (in addition to playing baseball for the Dodgers, for the Kansas City Monarchs in the Negro Baseball League, and for his college, UCLA, he was the first four-sport letterman in UCLA history—a baseball player, an All-American in basketball and football, and the NCAA broad jump champion), he was rejected and despised for something—the color of his skin—over which he had no control.
Although, growing up in post-World War II Brooklyn, we did not suffer from anything like the kinds of bigotry, hardship, humiliation, and/or violence most blacks knew—or that our relatives who came from Europe, or did not make it out of Europe, knew—we did know what it felt like to be demeaned for things beyond our control, and what it felt like to have to suck up our rage when injustice prevailed. And we burned with a fierce desire to be accepted—and victorious—in that larger American world that lay beyond our homes and neighborhoods.
Like Jackie, we were determined to do whatever it took to get to the ball, to win a game, to have our moments of glory on the ballfield—and our place in the sun away from the ballfield. We were driven by our parents—to succeed, to excel, to get the best education possible (an education, we were taught, was something nobody could ever take away from us)—and we drove ourselves to get as far away from our parents, and their world, as we could.
We loved playing ball for the sheer joy of playing—the games, the sweat, the camaraderie—and also, I suggest to Rich, because the ballfield and schoolyard were places where life was fair: where you were judged not by the heresy of your birth, but according to your merits and deeds—by how hard and well you played, by how you handled winning or losing, adversity or a lucky break.
“There was no arguing a home run or a clutch basket,” Rich says. “I mean, being in my home, or at school—which for me was another paramilitary indoctrination situation—there was never any joy in learning.* School was strictly a testing ground to see if the home conditioning had succeeded. I knew that early on. After the stultifying environment of my apartment, sports became the great outlet. I lived to play ball, and when I played ball I could let out all the repressed stuff I never expressed at home. Psychologically, sports saved my life.
“I’ll tell you a story,” he says then. “On the Math Regents one year—the statewide exam we all took—I got a ninety-nine, and I raced home to tell my mother. Characteristically, she was sitting in front of the mirror at her vanity table, putting on her make-up, and preoccupied with that. But I came bursting into her bedroom. ‘Mom—guess what?’ I exclaimed, and she said ‘What?’ and I said, ‘I got a ninety-nine on the Math Regents!’
“Then my mother, without looking around, and while continuing to put on her make-up, said, ‘What happened to that other point?’
“Now, at that moment I knew there was no way I was ever going to be able to satisfy her—and right then something changed in me forever. Number one, I knew I would never be good enough—and maybe I wasn’t good enough. And number two, I gave up on the idea of looking or hoping for her approval. After that day, I only went through the motions.”
I quote a character—a psychiatrist—from one of my novels who posits a revision to Freud’s theory about the favorite son of a doting mother going through life with the feeling of being a conqueror. The psychiatrist puts his version this way: that the unloved son of a narcissistic mother goes through life with the feeling that he must become a conqueror.
Rich nods, leans toward me. “Playing ball—being in the schoolyard and the rest of it—that was the only place where I could really be me,” he says.
We reminisce about Erasmus teams, about games of stickball and three-man basketball in the Holy Cross schoolyard, of football and baseball at the Parade Grounds and in Prospect Park, of dodgeball in the third-floor Erasmus gym when Rich and I were in Boy Scout Troop 369 together, and about our synagogue basketball team. Rich was our team’s high scorer, and to his astonishment—I showed it to him when he visited me the previous summer—I still have the scorebook to prove it.
“It was very fortunate I was a good athlete,” Rich says. “This was an enormous boon to my battered self-esteem—to my having any self-esteem. I was unequivocally good at something, and everyone in that world acknowledged it.” Rich worked as hard at being a good tennis player as he later would at becoming a good doctor, and in three years of varsity tennis at Erasmus, he never lost a match.
Several months after my visit to California, when I call and describe a problem I’m having with my (tennis) serve, he immediately diagnoses the problem and gives me a prescription (throw the ball higher, in the same spot each time, and hit it at its peak). When I call back a week or so later to tell him my serve—like my heart?—is working well again, he laughs, and says I called the right guy, because though he doesn’t believe he knows much, really, the two things he does feel somewhat confident about are tennis and cardiology.
At Tufts, Rich did not go out for the tennis team, but played freshman basketball and then, though he had not played organized baseball in high school, went out for and made the varsity baseball team as a third baseman. In his senior year, playing in an exhibition game against a minor league team at Braves Field in Boston, he got his team’s only two hits, including a home run, against a highly touted bonus baby pitcher.
“After the game, this guy came up to me, and said he was a scout for the Philadelphia Phillies, and we talked for a while, and he made me feel really good,” Rich says. “He told me I was a natural and had major league potential, and then he asked what my plans were after graduation, and when I told him I was committed to going to medical school in the fall, he just waved goodbye and walked off.”
Rich learned to play tennis during summers spent in Newport, Rhode Island. His father bought a ladies’ apparel shop in Newport shortly after World War II, and he worked there five days a week all year long.
“The four of us—my mother and father, and me and my sister Lucy—would get to spend summers together in Newport, and it was a wonderful place for us, and for me,” Rich says. “I learned to play tennis there, mostly by sneaking into the country club and watching the older players.”
When he was thirteen, Rich entered the city’s summer tennis tournament, made it to the finals, and, in a three-set match, won the city’s junior championship by defeating Dan Topping, Jr., son of the owner of the New York Yankees.
“He arrived with all his preppie WASP friends—” Rich says, “—the girls in their summer dresses, and the guys in their white bucks, all of them, at least in my memory, very, very blond—and I was behind five-to-two in the third set, but I came back and I beat him, and it felt good, really good.
“I had my first girlfriend that summer,” he adds. “Her name was Irene, and she was older than me, and we played tennis together all the time. She was a terrific player—she beat me regularly—and at dusk, when the club members were gone, we would hop the fence and go out onto the courts—the birthplace of tennis in America—and play there until it was too dark to see the ball.”
Although Rich entered Tufts intending to become a doctor, his decision had not been based on any great desire to pursue a career in medicine.
“My father was a classic Depression product—worrying endlessly about money,” Rich explains. “But we shared a love for baseball, and he was unequivocal in his love for me—he truly thought I was a miracle come to life. He was always gone during the school year, however, and when we were in Newport, I would watch him agonize over his adding machine, trying to make the numbers work, so that the one thing I knew for sure was that I did not want to be a businessman like him. But nothing else appealed to me.
“My mother, though, was a fury of ambition for her son, constantly on my case to make up my mind to do something so I could be somebody. She made me take all these aptitude tests, but they only showed that I could probably do well in everything, and they pointed in no specific direction.
“Then one day I come home from school and she informs me she’s made an appointment for us to see the wisest and most important person in her life, my pediatrician, Doctor Abram Kanof.
“I was embarrassed because I was fifteen or sixteen years old and even though he was a baby doctor, he was still my doctor. I had always loved him when I was a kid—he was a wonderful, sweet man, a very caring man—he made house calls, and he treated me warmly, in a way unlike anything I knew at home—and when he started talking to me about the field of medicine that was his, and that was his wife’s also, and told me that both his daughters were going to be physicians, I listened.”
I tell Rich that I was friends with Dr. Kanof’s younger daughter, Margaret—that we used to play hooky from Hebrew School together after we were let out early from P.S. 246 on Wednesday afternoons for something called “released time for religious instruction,” when the Catholic kids would go to their churches, and we were supposed to go to our synagogue.
“But remember,” Rich says, “this was a time, in the early fifties, when there were virtually no women doctors. Women were nurses. And when Dr. Kanof talked about his life, and about his feeling for medicine as a kind of holy calling—this came through to me.
“Still, though I was moved by what he said about the wonders of being a physician, this had little to do with my decision. What happened instead was that my mother suddenly cut in and asked what I would have to do in order to become a doctor, and he answered that there was a school in Boston called Tufts, which had an excellent pre-medical program—unlike most other elite New England colleges, it also had less stringent quotas on how many Jews it accepted—and that if I went there it would greatly increase my chances of getting into a good medical school.”
Rich says that his mother told Dr. Kanof she had been planning to send him to Brooklyn College, because it was free and because he could live at home, but that if the doctor thought Tufts was the best place for him, she and Rich’s father would do whatever it took to send him there.
“And suddenly,” Rich says, “I hear—‘Tufts…Boston…hundreds of miles away from Brooklyn…!’—and I immediately agree to becoming a doctor.”
I tell Rich about Phil’s nightmare, and what Phil has said about his determination to escape Brooklyn and his apartment. Rich nods and, in words identical to those Phil used, declares that he too would have done anything—anything at all— to get away.
We talk for a while about convergences in our lives—Rich’s grandparents coming to America from places near the villages from which my grandparents came (his mother’s mother from Minsk, his mother’s father from Pinsk); his mother and father having the same names, Anne and Dave, as my parents; his sister being in junior high and Erasmus with my brother Robert (and Phil’s brother Allen); the two of us being trained for our Bar Mitzvahs at Congregation Shaare Torah by Dr. Emanuel H. Baron, and Dr. Baron having trained the two of us (rare event in our synagogue at that time) to chant both the Haftorah (a portion from Prophets) and the Maftir (a portion from the Torah)—and then I ask if, during his years at Tufts, Rich ever doubted his decision to become a doctor.
“I never thought about it,” he replies. “I just knew I had to get certain grades in order to pass muster at home, and to my great joy I found I could get them effortlessly. Two or three days before big exams, I became a demon—I sucked up everything like a sponge, regurgitated it for the exams, got A’s, and promptly forgot it all. At Tufts, I didn’t think about anything except having a good time. I played on teams—school and fraternity—and I partied, and along the way I also discovered a love for literature, words, philosophy, and for music. These were wonderful years for me, but then the chickens came home to roost.
“I hated every minute of my first two years at Bellevue, you see—they were, and to a large extent in my view, still are, a sort of Marine-like boot camp that has virtually nothing to do with being a physician—and at the end of my second year, I went through a real crisis. I was halfway through to becoming a doctor, and I didn’t know anything and I hated all of it. So what was I doing there? I had crammed to pass exams, but it wasn’t working anymore—my grades were slipping below acceptable levels, and I began to realize I was going to have to tell my parents that this had all been a gigantic scam.
“And then I saw a miracle take place, where a life was saved right in front of my eyes. What happened was I was working with these two guys, Dan and Jeff—Dan was an intern and Jeff was the resident, and I was assigned to them as part of a three-man team. They were these swashbuckling young doctors right out of M.A.S.H., and we were called down to see a woman in the emergency room, and she was dying, and for the first time Dan and Jeff had no idea of what was going on or of what to do. None at all.”
I tell Rich what Arthur has said—how, like me, he grew up believing that doctors knew everything—and Rich laughs, says what he has said before about the essence of medicine being fallibility and uncertainty.
“The woman lapsed into a coma, her blood pressure started to drop, froth was coming out of her mouth, and I felt I was in the middle of a nightmare,” he continues. “So they telephoned a man, and he came down—he was this little old Czechoslovakian professor Jerry, Phil, and I talk about all the time—Dr. Joseph V. Brumlik—and he has on these pince-nez glasses, and Jeff is waving frantically, and Dan is telling him what little he could figure out about the woman’s story—but she had been in a coma, so we knew virtually nothing—and without even seeming to hear these two totally panicked guys, Dr. Brumlik just stood at the foot of the bed with his hands on the soles of the woman’s feet, and he studied her, very calmly. Then he looked up, told us the diagnosis—which meant nothing to me—told us what to administer intravenously, and walked out.* Jeff and Dan drew the syringe, injected it into her tubing, and within minutes, right there in front of my eyes, the woman woke up.
“It was like a miracle—it was a miracle—and I asked Dan, ‘Who is that man?’—I mean it was like right out of Butch Cassidy and the Sundance Kid— and then—well, the short of it is that Dr. Joseph Brumlik became my mentor, and my life was changed forever.
“Dr. Brumlik had been a professor of cardiology in Prague when the Nazis took over in 1938. He fled for his life, wound up in Mexico City for a while, where he worked as a cardiologist, and then somehow made his way to Bellevue. And from the moment I met him from that moment in the ER—I became a born-again cardiologist. I mean, when I finished medical school I hardly knew where the liver was, but I had become a sophisticated cardiologist from having sat for two years at Dr. Brumlik’s feet.
“He ran a famous clinic at Bellevue called The Thursday Night Cardiac Clinic, and for some reason he invited me in even though my grades for my first two years were atrocious. Then, in my fourth year, he and about a dozen of the leading cardiologists in New York would gather at Bellevue every Saturday morning and look at the most interesting, involved, and difficult cases. Dr. Brumlik was the acknowledged leader of the group, and he and the other doctors would evaluate the patients, and discuss them, and I would sit there and just suck it all up.”
I mention having read a book by Bernard Lown, the Nobel Prize-winning cardiologist responsible for the invention of the defibrillator and the development of the cardiac care unit—a man under whom Rich worked in the late sixties when Rich was a research fellow at the National Heart Institute and Peter Bent Brigham Hospital in Boston—and I cite Lown’s claim that a doctor who takes a careful history will reach a correct diagnosis 70 percent of the time, and that taking a careful history is far more efficient than relying on all the elaborate tests and technologies currently available.* Lown also reports that in his forty-five years of experience with thousands of patients whose presenting complaint was chest pain, he could, through just an unhurried interview, rule out a diagnosis of angina pectoris 90 percent of the time.
“You could quibble about the percentages, but essentially I do not disagree with him,” Rich says, and then: “I mean, you are the classic example of that, Jay. I made the diagnosis of what was going on in you from three thousand miles away, on the phone, by listening to you give me your history. I didn’t have to examine you, let alone do a fancy test. All the fancy test did—the coronary angiogram—was to confirm what was already clear from talking with you.”
He begins to explain how and why he knew this—he talks about what Osler taught still being true: about the patient giving you the diagnosis if you listen carefully enough—and I tell him about Phil answering his patients’ questions with a shrug and an “I don’t know”—and ask if many doctors would do the same.
“Damned few,” Rich says. “Ninety-nine percent of doctors, in my experience, will just make something up. It’s remarkable that Phil does that, and quite wonderful from my perspective, you see, because all my life I have taught that the very first step is to admit out loud that we do not know things, and that only by acknowledging this can we really find anything out. If you fool yourself with a lot of biomedical jargon, it can obscure the basic fact—what many doctors cannot acknowledge, and what is too scary for them—and that is the vast sea of ignorance in which we all work.”
After we return from playing tennis, we return to our discussion of how it was Rich could diagnose my condition by telephone, and I thank him again, but he only repeats what he said to me a few weeks before: that I should really be thanking my brother Robert and the Redondo Beach Public Library. For if I had not written a book about Robert, and if Rich hadn’t come upon a copy of the book in his library, and if the book hadn’t moved him to write me, we might not be sitting here today and talking.
“You may not remember this now,” Rich says, “but I was pushing you very hard to get the angiogram a.s.a.p. You were sitting on a time bomb, and I knew that one hundred percent.”
“Yet you were the only person, in the two months before surgery, who believed this,” I say, and I remind him that Phil called a few times to suggest I have an x-ray, that he thought what I was describing—the discomfort between my shoulder blades—might be due to a dissection of the aorta (a condition in which the inner lining of the aorta is sheared off, so that the blood stream “dissects” its way through the lining of the blood vessel, forming a double opening that is life-threatening and, characteristically, causes pain between the shoulder blades).
“But Phil trying to diagnose your situation would be like me trying to diagnose a nuance of where in the hippocampus a stroke was taking place,” Rich says. “It’s why I agree with him about the drive toward having more family practitioners and fewer specialists being the reverse of the way things should be.
“But that’s another subject,” he says, and he backtracks to our discussion about what was happening in the weeks preceding surgery, and walks me through the experience again.
“There were two main reasons why I knew your condition was very severe,” he says. “First of all, not only did you have a clear-cut angina, even though it was in a somewhat unusual place—between your shoulder blades—but the symptoms were progressive. They were occurring more frequently, and they were occurring with less physical activity—and I learned this from your telling me about what was happening when you went swimming.
“The second critical factor was that along with the discomfort between your shoulder blades, you were also becoming short of breath, and this told me that when you were experiencing the anginal symptoms, a very large area of your heart was becoming dysfunctional.”
Rich explains: “What happens to the heart when you get angina is this—you are exercising, so your heart needs more oxygen, but because there’s a blockage in an artery in that area of the heart which the artery is supplying, the heart is not receiving the oxygen it needs. So two things occur: One is that the heart says ‘Ouch’—which is what you feel in the symptoms—but what also happens to that area of the heart muscle is that it quite literally stops contracting. And the reason it does this is because it’s making an effort to stay alive—and the way to do that is to minimize the amount of oxygen it’s going to use.
“But when a critical area of the heart muscle stops contracting in order to preserve its oxygen sources as well as it can, the blood backs up into your lungs, and you experience this as shortness of breath.
“Thus, a typical patient with angina will get chest discomfort, pressure, heaviness, or a squeezing—and it can be located in many places: the neck, the jaw, between the shoulder blades—but you will not get shortness of breath along with that unless there is a very large area of the heart involved.”
I ask why he thinks my family doctor diagnosed asthma, and Rich says that for a general doctor to diagnose my condition would be like having a neurologist look at a cardiology problem.
“A family doctor cannot have the depth of perception about the across-the-board panoply of diseases they are called upon to be insightful about,” he says. “So when you told me what your doctor said, I told you with exclamation points that this asthma diagnosis was absolute nonsense.” Rich adds that it was a good thing my doctor eventually realized this (when the inhaler he had prescribed had no effect on my shortness of breath), and that he had ordered a stress test.
But why, I ask, as the weather grew colder, did it get harder and harder for me to walk outdoors?
“Because cold tends to constrict your blood vessels,” Rich answers. “They constrict in order to shut down the blood supply to the skin so that you can maintain body heat. But by doing that, the work that the heart has to do is increased— so the harder the heart has to work, the more oxygen it needs. But a limitation has now developed on how much oxygen you can get through the blocked arteries—those coronary arteries that are the suppliers of oxygen to the heart muscle.”
Rich reminds me that the first time I called, he urged me to go to Boston and see two doctors he knew at Massachusetts General Hospital, and I ask why he was so concerned at the outset, especially since I had few if any risk factors, and virtually no symptoms.
“I’ve always had an intuitive sense of when a patient is in danger—it’s an instinct I’ve learned to trust,” he says. “In your case, even though you lived a healthy lifestyle and the only risk factor you really had was your father’s history—his heart attack, but, then too, he was a chain smoker—all that stuff goes out the window. When tell-tale symptoms develop, factors like family history, cigarette smoking, and cholesterol levels no longer matter. The symptoms themselves are all that count, and they register as being significant and urgent or they don’t.”
I ask what the results of the EKG and the echocardiogram—both of which I had faxed to him—told him.
“Well, the EKG showed an unequivocal abnormality, and an EKG is quite valuable, but only if it’s abnormal. Then it can provide clues. But if it isn’t, it can often be misleading and miss a lot of things. What the echocardiogram did was to confirm my concern about there being a lot of weakness in the way the heart muscle was contracting. This told me that there was a very extensive area of the heart involved in the process, which suggested that several of your coronary arteries had significant blockages. When added to the increasing frequency and severity of your symptoms, the picture that emerged was that you had widespread, severe coronary artery disease, and that the abnormalities had become unstable. One of your major arteries was about to close down and cause a massive, possibly fatal heart attack.”
I remind Rich that when I reported the results of the echocardiogram to him, and reported that the cardiologist had said, “I think it’s viral,” Rich had exploded for the first time, telling me it wasn’t viral—“goddamnit!”— and that he wanted me in the hospital as soon as possible.
“You know, my level of concern had been high from the outset,” Rich says. “Only I did not want you to know because I didn’t want you to panic. What I wanted was to get you into a good hospital where they knew what they were doing, and to get this sorted out and fixed.”
But if what was happening was so obvious, why had two doctors missed it?
“Look,” Rich says. “The EKG and echo simply provided lab evidence that confirmed what your story was telling me loud and clear on the phone from three thousand miles away. And what happened was a microcosm of a central problem with technology—that a lab test can only be used correctly in the context of the patient’s symptoms.
“This cardiologist was looking at the fact that the whole heart muscle was not contracting well—something that occurs in people with viral infections of the heart muscle—and he was making a misdiagnosis because he was forgetting that you had told him you were also having symptoms of angina. And people with viral heart disease do not get any symptoms of pressure, tightness, or pain—what you were having between your shoulder blades—they simply develop shortness of breath.
“So he misread the echocardiogram because he forgot the fundamentals—he forgot about you. You start with the patient’s story, and the tests you run are only valuable if they add dimension to that story. But they do not let you be seduced away from the story.”
Rich talks for a while about what Phil and Jerry have been talking about: the ways technology has lured physicians toward quick-fix procedures, and away from the primary source of diagnostic information, and why, because this is happening, we are often kept from knowing what is really going on. He declares that I would not have been able to benefit from the incredible technological advances we do have at our disposal—bypasses, coronary care units, revolutionary medications—if people wedded to technology had had the final say.
“What has happened, it seems to me,” Rich says, “is that the diagnostic acumen of the physician at the bedside, on the phone, or in the office has been severely compromised because the mindset now—and this is also the main reason medical costs keep going up—has become, ‘Well, the tests will tell me anyway, so I don’t have to spend a lot of time listening. I can just run a battery of tests, and the tests will tell me the diagnosis.’
“First the nurse said, ‘Why don’t we just schedule you for a full exam,’ and then you had a diagnosis of asthma, and then you had a diagnosis of ‘Well we don’t know,’ and then you had a diagnosis of a heart attack, and then you had the doctor saying, ‘No, there’s no heart attack, but we have a viral cardiomyopathy,’ and all the while the symptoms are progressing, you’re hanging on by a single artery which is itself hanging by a thread, and something catastrophic is about to occur. Let me say it again, Jay. There is no question in my mind that we wouldn’t be sitting here today if you hadn’t gone to high school with the right guys.”
In our talks in Palos Verdes, we return frequently to what we talked about in the days immediately following my surgery: what we do and don’t know about heart disease.
“Theories have come and gone,” Rich says, “yet we are no closer to a true understanding of the causes of atherosclerosis—of what happened to you—than we were a generation ago. We do, however, know that smokers are several times more likely to develop heart disease than nonsmokers.
“The evidence is unequivocal there. We know that people with really high cholesterol levels are more likely to develop heart disease. The same is true for patients with hypertension, or with diabetes, or for patients who are obese—we have very strong statistical correlations in these instances. But if you compare what we know to what happened when medicine first became scientific—when Pasteur made his discovery of the germ theory: that germs cause infectious disease—and when Koch provided the scientific standard for proving cause and effect with respect to these diseases—we come up short. Statistics have almost nothing to do with cause and effect—they only show associations— and we cannot yet show cause and effect when it comes to atherosclerosis.
“If you give antibiotics to one hundred people who have pneumococcal pneumonia, all one hundred will be cured. Nothing like that exists regarding atherosclerosis—though we do know the causes of other heart diseases, such as rheumatic valve disease, which is caused by streptococcus.”
According to Koch’s postulates, an organism must be present in every instance of a particular disease; it must be capable of being isolated in pure form from the disease lesion and possess the capacity to reproduce the disease in a healthy animal through inoculation with a pure culture; and the same organism must then be capable of being retrieved from the inoculated animal—in the lesions of the artificially produced disease—and of being cultured anew.*
The assumption, and hope, still with us 120 years after Koch formalized his postulates in 1882—as we see in the immoderate rhetoric that accompanies much recent genetic and biomedical research and drug company advertising—is that each disease will be shown to have a specific causative agent, and that once this agent has been discovered and isolated, we will be able to control and cure the disease.*
But the world of biology and disease is rarely this simple. Even when we do find what appear to be single causative genetic abnormalities, as with Huntington’s chorea, Friedreich’s ataxia, sickle cell anemia, cystic fibrosis, and muscular dystrophy, developing means for controlling such agents (in these instances, defective genes) frequently eludes us.
“Phil was right when he said that except for the possible genetic link with your father, you had at very most only minor risk factors,” Rich continues. “Now, for people who have a strong family history of coronary disease, particularly early-age coronary disease—if, say, your father had had a heart attack at age thirty-eight or forty-two—then that would make the genetic link, and the danger, much more likely.”
I say that after hearing my stories of how the common early warning signs and symptoms for the illnesses Robert and I had (schizophrenia, coronary artery disease) were largely absent, people have usually responded by saying, “Oh, then it must be genetic.” Rich agrees that “It must be genetic” is simply another way of saying “We don’t know why these things happen”—and that the use of a scientific term such as genetic does somehow reassure people.
It is much the same, I say, with diagnoses. For years, when people would ask what my brother’s diagnosis was, and I said “manicdepressive,” or “schizophrenic,” or schizo-affective”—whatever the most recent diagnosis happened to be—people would nod knowingly, and then move on to another topic of conversation.
I had come to group such responses under the heading of “The Consolation of Diagnosis,” and had taken to following up with questions of my own: “So now that I’ve given you a word—a clinical term—what does it tell you about my brother?” I’d ask. “What do you know about him now that you didn’t know before—when you met him, or heard me talk about him, or read about him—?” I would, that is, use the question as an occasion to talk about Robert as a man with an idiosyncratic personality, a complex history, an unenviable series of breakdowns and hospitalizations, and an identity at least as unique as anyone else’s.
In point of fact, it turns out that the genetic basis for coronary artery disease, as for the major mental illnesses, is modest. Twin studies of coronary artery disease show a concordance rate between identical twins of 19 percent, and of 8 percent for nonidentical twins.* (Compare this, for example, to a rate of 50 percent for identical twins in insulin-dependent diabetes, and of nearly 100 percent in non-insulin-dependent diabetes.)
I ask what high blood pressure (where the genetic factor is also modest, the concordance rate for identical twins being only 30 percent) does to the arteries that makes it a risk factor.
“You ask the right questions,” Rich says. “But again, though theories abound—perhaps it weakens the walls of the arteries, or it induces dysfunctions in the endothelium, which is the innermost layer of blood vessels and is critical in determining the contractile state of the underlying smooth muscle, or it may reduce the activity of nitric oxide, which has anti-atherosclerotic effects—the real answer is that we don’t know.
“What we do know is that high blood pressure is statistically associated with higher rates of heart disease and heart attacks, though labile hypertension—the condition you evidenced—so-called white coat syndrome, where your pressure goes up when you’re in the doctor’s office and see the white lab coat in front of you—is not anything like the risk factor other, more repeatable and predictable patterns are.
“And all of this is why I keep saying that you are living evidence, my friend, of a much larger point.”
Which is? I ask.
“That we simply don’t know what causes atherosclerosis. But remember—these statistical correlations do have great importance from a preventive point of view, because a lot of information shows that people with severe elevations of cholesterol who lower them with diet, drugs, or exercise have lower rates of atherosclerosis. People who take aspirin have fewer coronary events, and if you stop smoking, treat your high blood pressure, your obesity, et cetera, your risk will go down—statistically—and this is important. But it is by no means conclusive.
“Because the average temperature in Palos Verdes on August 21 is sixty-eight degrees, doesn’t mean that it will be sixty-eight degrees today. Because it might be sixty-eight degrees in Northampton today doesn’t mean that every flower that blooms here can bloom there. Because, let’s say, we discover that most cardiologists who own fancy cars also play tennis well doesn’t mean that being a cardiologist and owning a fancy car will make you a good tennis player. As I said to you when you were at Yale, when ‘n’ equals one—when it comes to each individual instance: to the patient we are treating—associations and statistics break down.”
Arthur and I have talked about this—yes, an airplane is statistically the safest way to travel, he says, unless you happen to get on the wrong plane—and I quote him to Rich now, Arthur saying that it used to be “Neugie died of a heart attack,” but now it’s “Neugie died of a heart attack because he ate too many Mallomars…or too many eggs, or because he didn’t exercise enough.”
Rich laughs, and says that what is true for heart disease—that we don’t really know why somebody with few if any risk factors dies, and somebody with a multitude of risk factors lives to a ripe old age—is also true for cancer.
“Heart disease and cancer—in our time, these are the two biggies,” he says.
The reading I’ve been doing in evolutionary medicine, or what is sometimes called Darwinian medicine, has, with regard to these two killers, been instructive, I say. What those who work in this discipline, most notably, Paul W. Ewald, with whom I’ve talked about this (he teaches at Amherst College across town from the University of Massachusetts), believe is that medical research and practice could be significantly enhanced if questions of adaptation and historical causation were routinely taken into account along with questions of more proximate physical and chemical causation.
Evolutionary biologists ask intriguing questions: for example, If evolution by natural selection can shape mechanisms as sophisticated as the eye, heart, and brain, why hasn’t it shaped ways to prevent nearsightedness, heart attacks, and Alzheimer’s disease?* If our immune system can recognize and attack millions of foreign, harmful pathogens and proteins, why do we still get sick?
Since we know that smoking and excessive exposure to the sun are implicated in causing lung and skin cancer, why hasn’t natural selection eliminated the genes (if genes they are) that make us crave cigarettes and sunshine? And why can’t our bodies repair clogged arteries, sun-damaged skin, and brain lesions the way they repair bruises and skin abrasions, and nerve and muscle damage?
When placing present infirmities within evolutionary contexts—taking a long historical view—researchers such as Ewald begin with a fundamental observation: that the bodies and immune systems we now possess have come into being over the course of millions of years, most of which—perhaps 90 percent of the years since we became recognizable as the species we are today—we spent as hunter-gatherers living in small groups on the plains of Africa. Natural selection, therefore, has not in many instances had the time, or the biological wherewithal, to enable us to accommodate to more recent conditions of environment and history.
The gene that causes sickle cell anemia, for example, also prevents malaria—useful on the plains of Africa, but not on the streets of New York. Most of the genes we believe may predispose us to heart disease were harmless until certain other events occurred—the availability of fats, sweets, and tobacco, the migration to densely populated cities, and the public health measures and medical innovations that enable us to have markedly longer average life spans than we did only a hundred years ago.
This is so because natural selection does not select for health, but only for reproductive success. It has no plan, no intent, no direction; survival, that is, increases fitness only insofar as it increases later reproductive capabilities, and fitness leads to survival only when it has aided reproductive success.
Since the gene for Huntington’s chorea, for example, causes little harm before the age of forty, and so cannot decrease the number of children born to someone who later develops this disease, natural selection does not eliminate the gene. In a similar way, it would seem, since cancer and heart disease commonly occur after the age of reproduction, natural selection has not eliminated those genes that may predispose us to cancer or heart disease.*
From an evolutionary point of view, we age and we die in the ways that we do, then, not because we have done something wrong (eaten too many Mallomars), but because the diseases that, in our time, generally do us in are those that occur after the age of reproduction. What evolution seems to care about—the pathetic fallacy writ large in the example I offer to Rich—is not Rich or Neugie, but simply being able to produce another Rich or Neugie.
Seen from this perspective, we are only, as Richard Dawkins suggests, vessels created by genes for the replication of genes, and thus may be discarded when the genes are through with us.
In addition, as Ewald points out, from an evolutionary perspective it makes no sense that our immune systems would suddenly, early in the twentieth century, begin malfunctioning on their own in a higher and higher proportion of people.
Conversely, after thousands of years of exposure to disease agents such as smallpox and tuberculosis, one would expect natural selection to have produced a population of individuals all of whom were resistant to these diseases. But this has not happened, Ewald explains, because “natural selection obtains its power from the differences in the survival and reproduction of competitors within a species, which in turn determine differences in the passing on of the genetic instructions that individuals house.” That is where one must look if one wishes to understand why infectious diseases are the way they are and what we can do to control them, because that is where the strategies of pathogens are being shaped.
What evolutionary biologists thus recommend to researchers as holding promise for significant progress in the understanding and treatment of disease is, first of all, the investment of greater resources in investigating those selective processes that favor increased or decreased virulence of viral strains.
The race, they submit, is between what Ewald calls “the biological weaponry” our bodily defenses impose on pathogens, and the pathogens’ resistance to them. And, as we know from the increasing resistance to antibiotics, or the decreasing potency of many antiretrovirals—most pathogens evolve much more swiftly, and ingeniously, than we can create medications capable of eliminating, suppressing, or moderating their effects.
Consider, for example, streptococcus. Here is a bacterium that has evolved along with us for millions of years. When we create antibodies that attack strep, these antibodies, which are capable of imitating the codes of our cells, are prone to attack our own tissues too, and while we produce a new generation of Neugies and Riches every twenty years or so, strep evolves and produces a new generation of pathogens every hour or so. Until now, antibiotics have generally proven capable of dealing with these newly evolved variants. But as we know from the alarming rise in the presence and lethal power both of new infectious diseases (AIDS, ebola, legionnaires’ disease) and of reemerging diseases (tuberculosis, malaria, streptococcal pneumonia), this may be only a temporary blessing. By the late 1970s, Laurie Garrett informs us in The Coming Plague, “strep B was the most serious life-threatening disease in neonatal units all over the industrialized world, and 75 percent of all infections in babies under two months of age were fatal, despite aggressive antibiotic treatment.”* And by the year 2000, the New York Times reports, fourteen thousand people were dying each year from drug-resistant infections contracted in hospitals.
Researchers first began studying the inflammatory process in atherosclerosis in the 1820s, first proposed infectious causation of atherosclerosis in the 1870s, and found evidence that chlamydia was implicated in arterial disease in the 1940s. Evolutionary biologists now contend that atherosclerosis is most probably an inflammatory disease of infectious origin, and the arguments and evidence they present in support of this view are persuasive. Until very recently, they maintain, it was mostly in order to develop a consensus that other medical researchers and cardiologists shied away from statements of causation in favor of a much less informative concept, that of risk factors—high cholesterol, high blood pressure, smoking, obesity, lack of exercise, genetics, et cetera.
None of the risk factors for atherosclerosis, though, appears to be a primary risk factor—for each risk factor, that is, many of us are found who do not have it, yet still have atherosclerosis.* In fact, as we have known for some time, and as Ewald reminds us, if you add up all the known noninfectious risk factors, they still explain only about half the risk of acquiring atherosclerosis, a finding corroborated by Dr. Joseph B. Muhlestein, director of research at the cardiac catherization laboratory, and a professor of medicine at the University of Utah Medical School. “Although much is known about the pathologic process whereby atherosclerotic plaque develops,” Dr. Muhlestein writes, “in many cases, the underlying cause remains unclear. Certain risk factors associated with the development of atherosclerosis are well defined, including diabetes mellitus, hypertension, hyperlipidemia, tobacco abuse, and a positive family history. These risk factors, however, combine to account for only about 50% of the observed incidence of atherosclerosis. Additionally, these risk factors generally are only associations, and the exact mechanism by which they may contribute to the development of atherosclerosis is not known.”
Moreover, as Lewis Thomas observed more than thirty years ago, and as Ewald argues now, most major achievements in medicine have resulted from principles of primary causation: this holds for large theoretical discoveries such as the germ theory of disease, as well as for practical interventions such as surgery, antimicrobial drugs, vaccines, and improved nutrition and hygiene.*
Rich agrees. The efficacy—and genius—of vaccines is due not so much to the medications themselves, but more to our ability to make use of what we know about the human immune system. As to risk factors for atherosclerosis, Rich compares each new risk factor put forth as the key risk factor to the old flavor-of-the month posted at our local ice cream parlors; and with regard to each such risk factor heralded as “the ultimate bad guy,” he likes to tell the story of the cop who comes upon a drunk crawling around on his hands and knees under a lamppost. The cop asks him what he’s doing, and the drunk says he’s looking for his wallet. “Where did you lose it?” the cop asks. “Oh, I lost it inside the bar,” the drunk says. “Then why are you looking for it under the lamppost?” the cop asks. “Because,” the drunk replies, “the light’s better here.”
Still, Rich says, the prevailing theory among cardiologists these days does corroborate Ewald’s hypothesis. In fact, he goes on, he and his team at the University of California at Irvine contributed to the discussion of the possible inflammatory origins of atherosclerosis with work they did in the mid-nineties.
“The entire process of atheroma formation is complex and difficult to pin down because, among other things, lots of elements seem to play a role,” he says.* “But what I have believed for years, as you know, is that it is not the atheroma itself—the fatty deposits in the walls of the arteries—that kills people, but the rupture of the atheroma, and if we could identify what causes the rupture, and find ways to prevent it, we would make a huge impact on the prevention of heart attacks.
“We have a lot of indirect and experimental evidence to explain the process that leads to coronary disease, and from coronary disease to heart attacks,” Rich explains, “and it all seems to indicate that something happens to the inner layer—the endothelium—of the coronary blood vessel. An abnormality develops, which in turn allows cells carrying the bad cholesterol—the LDL—to seep through and get caught up in the artery’s wall. When that process matures, cholesterol deposits leak out of the cells and, essentially, form masses, and these masses protrude back into the opening of the artery—the lumen—causing a partial obstruction.
“Sometimes nothing happens—even severe blockages cause at most only three out of every ten heart attacks—and sometimes the obstruction reaches a point where it interferes with the amount of blood flowing through the passageway of the artery. And when the heart is under stress because the oxygen it needs exceeds the ability of the blocked coronary artery to supply it—you’re exerting yourself more than usual: swimming, walking fast, playing tennis—this imbalance causes the symptoms of angina pectoris. But the most dangerous thing that can occur is for the atheroma to rupture into the blood vessel itself, causing a clot to form.
“This is the same kind of clot you get when your skin is cut—it’s nature’s way of healing us—and when these atheroma rupture, their surfaces are very sticky, and platelets bind to them. But the clot closes off the artery and the coronary artery becomes occluded. Suddenly, an area of heart muscle is starved of oxygen, and if this is not relieved quickly enough, that area of the heart dies—in other words, a heart attack occurs. If the area is large enough, you don’t survive it.”
Rich talks about the experiment he and his research team performed, in collaboration with the local coroner’s office and pathology researchers, in which they studied the hearts and arteries of people who had died in automobile accidents, and compared them with the hearts and arteries of people who had died of heart attacks.
“What we found,” he says, “was that the people who died of heart attacks had huge collections of macrophages—white blood cells—in their atheroma. More importantly, these macrophages secreted substances with the fancy term of matrix metalloproteinases, which are enzymes that digest proteins.
“What these enyzmes were doing was digesting away tissue that contained the fatty deposits, thus weakening the walls of the arteries, and making them susceptible to rupture. And we found something else that was fascinating—and totally unexpected. When we looked at other arteries in the patients whose atheroma had ruptured—at the arteries that had not ruptured—we found the same collection of lesions containing macrophages and metalloproteinases.
“Yet this was not the case in those people with atheroma where no rupture had occurred. This strongly suggests that the process is systemic—in other words, that the inflammatory process is not taking place only in the one susceptible atheroma.
“Add to this recent studies that have shown that people with elevated levels of C-reactive protein—which are nonspecific markers of inflammation circulating in the blood—are much more susceptible to heart attacks, and that high levels of C-reactive protein, even in the absence of high cholesterol, are fairly reliable indicators of heart disease and of potential heart attacks, and you can see why infectious and inflammatory disease explanations make sense.* In addition, it now seems that aspirin and the statins, which we thought were effective against coronary heart disease because they reduced clotting and/or lowered cholesterol, may owe a large part of their effectiveness to the fact that they reduce inflammation.
“All of which suggests that there is some kind of total body inflammatory process involved in triggering heart attacks, and that this process is triggered for reasons no one understands.”
My researches confirm much of what Rich tells me. Ewald’s hypotheses about the infectious causes of heart disease, along with evidence that he and other evolutionary biologists present—that there are significant associations between atherosclerosis and both Chlamydia pneumoniae and gingivitis (Porphyromonas gingivalis); that treatment of bypass patients with antibiotics improves their recovery; and that an inflammatory hypothesis makes sense since it does not specify whether the atherosclerotic damage is caused directly by the infectious organism or indirectly through the organism’s stimulation of an inflammatory response—these arguments are reiterated, reinforced, and expanded upon in an abundance of medical journal articles.
Here, for example, is the simple declarative sentence with which Dr. Russell Ross begins a January 1999 article in the New England Journal of Medicine: “Atherosclerosis is an inflammatory disease.”*
After taking us through a substantial body of evidence to support this proposition, Ross concludes that “atherosclerosis is clearly an inflammatory disease, and does not result simply from the accumulation of lipids.
“If we can selectively modify the harmful components of inflammation in the arteries and leave the protective aspects intact,” he adds, “we may create new avenues for the diagnosis and management of disease in the 50 percent of patients with cardiovascular disease who do not have hypercholesterolemia.”
“From a clinical standpoint, chronic inflammation, as evidenced by elevated levels of C-reactive protein, has been shown to be directly associated with the development as well as progression of coronary artery disease,” Dr. Joseph Muhlestein writes in an article published a year later, in January 2000.*
After reviewing research from a sizable number of studies linking various infectious diseases to coronary artery disease, Muhlestein concludes that “the infectious agents with the most evidence to support a causative role in atherosclerosis” include Chlamydia pneumoniae, cytomegalovirus (a member of the herpesvirus genus), Helicobacter pylori (implicated in causing peptic ulcer disease), and several bacterial agents (including Porphyromonas gingivalis) associated with periodontal disease.
Although we may, thanks to the research that lends these propositions their plausibility, be getting closer to understanding the underlying cause or causes of atherosclerosis, what we do not know, Rich maintains, is still infinitely greater than what we do know.
He remains highly skeptical of anyone who claims to know, definitively, what can either cause or cure coronary heart disease, and outraged by the ways those claiming such knowledge go directly to the consumer with sales pitches for their products, as in the extensive campaigns to sell us cholesterol-lowering medications.
“I mean, why don’t they just put the stuff in the well water and be done with it?” he asks at one point, and here again, everything I read lends credence to his skepticism.
Is Zocor really going to help me “live a longer healthier life”? Has Pravachol really been “proven to help prevent heart attacks in people with high cholesterol or heart disease”? Should I, like Dan Reeves, make taking Zocor “an important part of my game plan”—and will it not only lower my cholesterol by 29 to 45 percent, but enable me to “stay beautiful on the inside”?
In an article in Science (March 30, 2001), Gary Taubes, a three-time winner of the Science-in-Society Award from the National Association of Science Writers, reassesses much of what we know about the relation of a diet high in fat to cholesterol and heart disease, and demonstrates that “by the 1970s, each individual step of this chain from fat to cholesterol to heart disease had been demonstrated beyond reasonable doubt, but the veracity of the chain as a whole had never been proven” (italics in original).
Nor has it been proven since. In 1991, a study funded by the U.S. Surgeon General’s Office determined that cutting fat consumption in the United States would delay forty-two thousand deaths each year. The key word, however, as Taubes points out, is delay.
“To be precise,” he explains, “a woman who might otherwise die at 65 could expect to live two extra weeks after a lifetime of avoiding saturated fat.* If she lived to be 90, she could expect 10 additional weeks.”
The proposition that reducing fat consumption, whether by diet or drugs, prevents heart disease and leads to longer, healthier lives is, at best, inconclusive, and at worst, as many medical experts maintain, the result of an enormous, often greed-inspired hoax. Rich talks frequently (and is writing about) what he considers unethical collusion between doctors, hospitals, and pharmaceutical firms.* (Corroborating what he has witnessed firsthand, an article in the January 2, 2002, issue of the Journal of the American Medical Association reports that nearly nine out of ten medical experts who write guidelines for treating conditions such as heart disease, depression, and diabetes have financial ties to the pharmaceutical industry, and that these ties are rarely if ever disclosed; moreover, approximately six out of every ten medical experts have financial ties to companies whose medications they either considered or recommended in the guidelines they wrote.)
Although more than 80 percent of the money spent on the promotion of prescription drugs is still directed to health-care professionals, annual spending on direct-to-consumer advertising for prescription drugs tripled between 1996 and 2000, when it went from 791 million dollars (9 percent of annual spending), to just under 2.5 billion dollars (16 percent).*
Taubes reviews not only the research concerning the relation of dietary fat to heart disease, but the history of the ways in which the general public, encouraged by drug companies, politicians, and the media, has come to accept as axiomatic what has never been proven.
Despite the existence of many trials that “showed no evidence that men who ate less fat lived longer or had fewer heart attacks,” Taubes cites Time magazine, for example, declaring, in its headline to a feature story (on the magazine’s cover, below a plate of bacon and eggs arranged so as to resemble a doleful face, “CHOLESTEROL: AND NOW THE BAD NEWS”)—“Sorry, It’s True. Cholesterol Really Is a Killer.”*
“Snatching victory from the jaws of defeat of the verdict of the [cholesterol] trials,” James LeFanu, a London physician and author (a regular columnist for the London Times, and Daily and Sunday Telegraph), writes in an examination of the subject in his book, The Rise and Fall of Modern Medicine, “dozens of expert committee reports had persuaded most people that ‘Western food is the chief reason for our modern epidemic of heart disease.’* This in turn had been the Trojan Horse by which millions had been prescribed cholesterol-lowering drugs.”
LeFanu subjects the claims of the pharmaceutical industry to close analysis—in one instance, when they assert that according to a “landmark study” there is “conclusive proof” that taking the drug cholestyramine reduces the chances of dying from a heart attack by 25 percent, he sorts through the data of a seven-year study used in support of such a claim.
“After seven years…thirty out of the 1,900 taking cholestyramine had had a fatal heart attack compared to thirty-eight of the similar number in the control group,” he informs us.* “This indeed can be interpreted as ‘reducing the chances of dying from a heart attack by 25 percent…’ But put another way, almost 2,000 men took cholestyramine for seven years to increase their chances of not having a heart attack by less than half of 1 percent. This seems a modest enough achievement, except that overall cholestyramine made no difference at all, as the total number of deaths in the ‘intervention’ and ‘control’ groups were exactly the same, with the modest reduction in heart disease mortality in those taking cholestyramine being balanced by an increased risk of death ‘from other causes.’”
“It is much easier to promote a drug on the grounds that it reduces the ‘risk of a heart attack by 25 percent,’” LeFanu observes, “than by pointing out that ruining one’s meals with cholestyramine for seven years increases one’s chances of not having a heart attack by 0.5 percent, at the price of chronic bowel symptoms, depression and increased risk of death from other causes.”
The enormous number of studies on the relation of dietary fat to heart disease validate Rich’s assertion: that while reducing cholesterol levels, especially LDL (the so-called bad cholesterol), for individuals who have already had heart disease, or are considered to be at high risk for heart disease, is probably wise, there is a distinct absence of evidence to persuade one that otherwise healthy individuals with normal or borderline cholesterol levels need to take what will, in most instances, become lifetime medications.
“The ideal way to treat atherosclerosis,” Rich says, “would be to give patients a pill that would be a medical roto-rooter and ream out the blocked arteries. But we don’t have that pill, and we won’t have it, if ever, for a good while. In the meantime, we have millions of people taking these medications because Dan Reeves or their doctors tell them to—and taking these meds is not like taking an antibiotic for an infection.
“You take an antibiotic for ten days to two weeks and the bug is killed and that’s the end of it,” Rich goes on. “Yes, when you need these cholesterol meds, of course you should take them. But these are lifetime medications, remember, and every pill that has ever been manufactured by humankind has its own side effects, and nobody really knows what the effects of these medications will be in your body over the course of a lifetime.”
While Rich is exceptionally knowledgeable about the many useful technologies available for the treatment of heart disease (and is himself responsible for the early and ongoing development of several of these technologies, including nuclear cardiology, cardiac electrophysiology, angioplasty, and the use of calcium channel-blocker drugs to treat coronary artery spasm and hypertension), in recent years he has become more attuned to, and passionate about, the role that non-technological elements play in the healing process.
Increasingly, his life, and his work, have become informed by a range of activities—daily meditation, reading and study of Eastern thought and philosophy (especially, as with Arthur, the writings of the Dalai Lama), and his own writing—that explore experiences that cannot be fully understood or explained rationally.
In one of the books he is working on, he tells the stories of patients whose experiences of, and recoveries from, heart disease cannot be accounted for by conventional scientific reasoning or observation.
“After a lifetime of caring for sick people, there is no question in my mind that belief is a powerful force for those good, bad, or indifferent things that happen to people, whether in what we call ordinary life, or in things pertaining specifically to health,” he says. “And I think an awful lot of what happens has to do with what has come to be called the mind/body connection.”
When I recount some of what I’ve been reading about placebos, and the placebo effect, Rich shakes his head sideways, and laments the fact that the word placebo has become synonymous with worthless.
“The placebo effect is enormously powerful, and enormously healing,” he says, “and should be mobilized to the max, in addition to whatever else we may bring to bear on a specific condition. But the placebo effect is only valuable to the extent that a patient believes it’s valuable.”
What I wonder about, I say, is this: If the doctor-patient relationship continues to be seriously weakened and devalued—if, increasingly, we and our doctors become strangers to one another—what happens to all those conditions that have no apparent organic cause, yet are ameliorated by the simple act of going to a doctor one knows and trusts?
“Well, we know very little about the causes of illnesses that would appear to have obvious chemical, biological, genetic, or environmental origins,” Rich says. “And we know even less about the mysterious interactions between the mind and the body—and these interactions are crucial in enabling the body to heal itself, and to modify the course of illness. Thus the great danger if we lose sight of the doctor’s ability to make use of the body’s natural power to heal itself.
“But let me be more specific, and talk about something I call paragenetics,” he continues. “Now we know that genes per se are rarely the sole or even decisive cause of most common diseases, but if your father died of a heart attack at age fifty-nine, that festers in your mind, and through the mind/body connection, in your body as well. You’re forty-eight, and then fifty, and then you reach fifty-nine and something starts to happen.
“Now we know that genetics usually confer a propensity—a potential vulnerability. But will the heart attack that got your dad land on the same part of the time clock for you? Of course not. Still, your mind is programming your body in some way to believe that it will, and what I think about more and more is the power of the patient-doctor relationship to reset the mind/body clock—something that has largely been lost in the hoopla of technology all around us.
“And there’s also this: in the absence of a healthy doctor-patient relationship—when somebody gets an impersonal lab coat doing all the stuff instead of a caring doctor like Phil or Jerry, or gets a different doctor for each visit—then fear kicks in, and becomes an element that itself inhibits the mind/body’s ability to heal itself. And we should never underestimate the role fear and apprehension play in a patient’s ability to deal with illness, and to recover from illness.
“So what we’re really talking about here, I think, are questions of medical responsibility,” he continues. “What I’ve been teaching for years, for example, is that if you have a patient who is not taking medications, it’s your responsibility to see that he does. It is because you have not sat down and adequately explained the urgency, or if there are side effects, because you have not given your patient the space—the comfort, the confidence, the necessary trust—to talk with you so that you can look for a suitable alternative. People don’t want to talk about the cost of drugs or side effects with a doctor, often, because they’re embarrassed, or they’re ashamed, and so, here and in myriad other ways, I find that there is tremendous power in the doctor-patient relationship to help in the healing process—but only if we value it, encourage it, and understand its potential both for ill and for good.
“Excellence matters too, of course. Whether it’s managing a hotel or a cardiology program, there has to be a commitment to excellence and to care, and that starts at the top, with leadership. In the case of Massachusetts General Hospital, for example, ever since Paul Dudley White, who was Eisenhower’s personal physician, was in charge, there has been a standard of excellence there in cardiology and cardiac care that has been passed down from one generation to the next.
“The way I see it, there is content and there is context. The content is the expertise—how good technically are the surgeons and the angiographers, and how up-to-date are they, and so forth. But then there’s the context. And the context is: Does the care work? Because the context, you see, is the caring, the wisdom, and the judgment about employing the knowledge and power we do have—this vast array of medications, treatments, and technologies—to best serve individual patients in the way that we were able to serve you, my friend.”