N THE FIRST EDITION OF HIS CLASSIC Principles and Practice of Medicine, published in 1892, William Osler suggested that rheumatoid arthritis has “in all probability, a nervous origin.” In present- day language, Osler was referring to psychoemotional stress.
He noted “the association of the disease with shock, worry, and grief.”
No obscure theoretician, William Osler was the best-known medical doctor in the English-speaking world. According to Sherwin B. Nuland, himself a physician and author, Osler “may have been the greatest clinical teacher of any day, and any country.” He taught at McGill University in Montreal, Johns Hopkins University Medical School, Baltimore, and at Oxford. In England he was knighted for his contributions to the healing arts.
His widely used textbook underwent sixteen editions—the last one in 1947, twenty-eight years after his death.
In 1957 C. E. G. Robinson, a Vancouver internal medicine specialist, cited Osler’s words in a brief article in the Canadian Medical Assocation Journal. “I have also been impressed,” he wrote,
“by the frequency with which chronic or prolonged stress may precede the development of rheumatoid disease…. I think that the emotional and psychological aspect of many rheumatoid patients is of rst importance.”1
Dr. Robinson’s medical education was still informed by Osler’s humane and holistic approach. Now, at the beginning of the twenty- rst century, one may search in vain through the mainstream medical texts for any mention of stress in relationship to rheumatoid arthritis or to its fellow autoimmune conditions, all of them characterized by a civil war of the immune system against the body. The omission, tragic for millions of human beings su ering rheumatoid disease of one type or another, is all the more unjusti able since research has long since established the stress- autoimmune connection and has given us an understanding of many of its potential physiological pathways.
The large and overlapping set of medical conditions called rheumatic diseases include rheumatoid arthritis, scleroderma, ankylosing spondylitis and systemic lupus erythematosus (SLE). In these disorders, and in many others, a disturbed immune system reacts against the body’s own tissues, particularly against connective tissues like cartilage, tendon sheaths, the lining of joints and the walls of blood vessels. These illnesses are characterized by various patterns of in ammation that strikes the joints of the limbs or the spine; or surface tissues like skin or the lining of the eyes; or internal organs such as the heart or the lungs or—in the case of SLE—even the brain.
Characteristic of many persons with rheumatoid diseases is a stoicism carried to an extreme degree, a deeply ingrained reticence about seeking help. People often put up silently with agonizing discomfort, or will not voice their complaints loudly enough to be heard, or will resist the idea of taking symptom-relieving medications.
Celia, a woman in her thirties, experienced an episode of arteritis, or generalized in ammation of the arteries, another autoimmune process. Her pain was severe. “For two days I was in so much pain that I was throwing up from the amount of Tylenol and Ibuprofen I was ingesting. My girlfriend said, ‘Do you give up yet?’ and she took me to emergency.”
“‘Do you give up yet’—what does that mean?” I wonder.
“I’m stubborn. Whenever I’m sick, I always have this underlying fear that I won’t be believed or that I’ll be seen as a hypochondriac.”
“So here you are, not able to move because of agonizing pain, and you’re worried people will think you’re a hypochondriac. Let’s reverse this situation for a moment. Imagine it was a friend, or your husband, or your child who was su ering such pain. Would you not have acted much more quickly?”
“Yes.”
“Why the double standard?”
“I don’t know. It goes back a long way, probably. Back to the way I grew up.”
The non-complaining stoicism exhibited by rheumatoid patients is a coping style acquired early in life. Celia’s anxieties have always been focused on others. Although she herself was abused as a child, her concern was to protect her mother from a series of abusive partners. She was afraid the family would not have enough money or that the outside world would nd out about the family violence.
“Mostly I was very worried about my brother becoming a juvenile delinquent or horrible things happening to him.”
“What about you?”
“I always felt I somehow could manage it and get through it. I don’t want to accept how really upsetting things are. I rationalize it to a point where I can accept it and deal with it. I minimize.”
An intensive medical-psychiatric study of people with rheumatoid arthritis conducted for the Maryland Chapter of the Arthritis and Rheumatism Foundation in 1969 concluded that “despite the diversity in the group, the patients’ psychological characteristics, vulnerabilities and life con icts were remarkably similar.”2 One common characteristic was a pseudo-independence, described by the authors as a compensating hyperindependence. Celia’s rigid belief that she could get through everything by herself was a
coping mechanism, a compensation for emotional needs ignored in childhood. A child in her situation survives by pretending to herself, and to the world, that she has no needs she cannot take care of herself. One aspect of that pretence is to reduce the perception of emotional stresses to a child-friendly size, a habit that may then last for a lifetime.
Compensating hyperindependence originating in early role reversal between parent and child also explains Celia’s teeth- gritting endurance of physical pain, to the point that a friend had to drag her to the emergency ward with “Do you give up yet?”
In 1969 the British psychiatric researcher John Bowlby published Attachment, the rst volume of his classic trilogy exploring the in uence of parent-child relationships on personality development.
“The reversal of roles between child, or adolescent, and parent, unless very temporary, is almost always not only a sign of pathology in the parent,” he wrote, “but a cause of it in the child.”3 Role reversal with a parent skews the child’s relationship with the whole world. It is a potent source of later psychological and physical illness because it predisposes to stress.
Other traits identi ed in the psychological investigations of people with rheumatoid disease include perfectionism, a fear of one’s own angry impulses, denial of hostility and strong feelings of inadequacy. As we have seen, similar traits are said to be associated with the “cancer personality” or with personalities at risk for MS, ALS, or any other chronic condition. None of these traits represent innate features of a person, nor are they irremediably xed in the individual.
“In the developmental history of these patients a striking nding was the early e ective loss of one or both parents,” according to the Maryland study. The reader will have noticed how often in the personal histories related in this book there was early separation of the parents, abandonment or even the death of a mother or father. Even more universal is emotional deprivation, another commonly repeated theme in the research literature. A 1967 Australian study of people with systemic lupus erythematosus
reported that: “More patients than controls reported emotional deprivation in childhood associated with a disturbed parent-child relationship within ‘unbroken’ families.”4
Like compensatory hyperindependence, the repression of anger is a form of dissociation, a psychological process originating in childhood. The young human being unconsciously banishes from awareness feelings or information that, if consciously experienced, would create unsolvable problems. Bowlby calls this phenomenon
“defensive exclusion.” “The information likely to be defensively excluded is of a kind that, when accepted for processing in the past, has led the person concerned to su er more or less severely.”5 In other words, the angry child got into trouble and experienced rejection. The anger and the rejection had to be de ected inside, against the self, in order to preserve the attachment relationship with the parent. That, in turn, leads to the “strong feelings of inadequacy and a poor self-concept” researchers have recognized in people with rheumatoid disease. “Not infrequently anger is redirected away from an attachment gure who aroused it and aimed instead at the self,” Bowlby explains. “Inappropriate self- criticism results.”6
In autoimmune disease, the body’s defences turn against the self.
In the life of a society—the body politic—such behaviour would be denounced as treason. Within the individual organism, physical mutiny results from an immunologic confusion that perfectly mirrors the unconscious psychological confusion of self and non- self. In this disarray of boundaries, the immune cells attack the body as if the latter were a foreign substance, just as the psychic self is attacked by inward-directed reproaches and anger.
The cross-confusion re ects disruptions of the interconnected body/mind mechanisms within the emotional-nervous-immune- hormonal super-system, which we have called the PNI system.
Emotions precisely parallel and complement the other components of the PNI network: like the immune and nervous systems, emotions safeguard the organism from external threat;
like the nervous system and the hormones, they assure the satisfaction of indispensable appetites and needs; and, like all
these systems together, they help maintain and repair the internal milieu.
Emotions—fear, anger, love—are as necessary for the organism’s survival as nerve impulses, immune cells or hormonal activity.
Early on in the process of evolution, primitive responses of attraction or repulsion became essential to the life and reproduction of living creatures. Emotions, and the physical cells and tissues that make them possible, evolved as part and parcel of the apparatus of survival. It is no wonder, then, that the basic molecules that connect all the body systems of homeostasis and defence also participate in emotional reactions. Messenger substances, including endorphins, may be found in the most primitive of creatures who lack even a rudimentary nervous system. It is not that the organs of emotion interact with the PNI system—they form an essential part of this system.
In chapter 7 we noted that cytokines, messenger molecules produced by immune cells, can bind to receptors on brain cells to cause changes in body states, mood and behaviour. That emotions induce changes in immune activity is only the other side of the same coin. To illustrate the parallel and complementary protective duties of the emotional system and the immune apparatus, we can compare the role of immune cells with that of an emotion such as, say, anger.
Why do we have anger? In the animal world, anger is not a
“negative emotion.” An animal experiences anger when some essential need is either threatened or frustrated. Although animals lack conscious knowledge of emotional phenomena, they do feel emotion and experience the physiological changes of Emotion I.
And, of course, they manifest the behavioural displays classi ed as Emotion II. The speci c purpose of Emotion I biological changes is to prepare the creature for ght or ight responses. But since ight or ght both demand great expenditures of energy and impose risks of injury or death, the Emotion II displays serve a crucial intermediary function: they often settle the con ict without any of the participants having to get hurt.
A cornered animal turns to face his pursuer with a erce display of rage. Anger may save his life, either by intimidating the hunter or by enabling the prey to resist successfully. Or anger is aroused in an animal when a stranger of the same species, from outside the family or pack or troop, intrudes on his territory. If the two creatures immediately engaged in physical battle over the disputed territory, one or both would likely become injured. Nature provides a resolution by prompting both of them to mount anger displays:
teeth bared, menacing bodily motions, threatening sounds. The more convincing display often wins the day, avoiding harm to either contestant.
For anger to be deployed appropriately, the organism has to distinguish between threat and non-threat. The fundamental di erentiation to be made is between self and non-self. If I don’t know where my own boundaries begin and end, I cannot know when something potentially dangerous is intruding on them. The necessary distinctions between what is familiar or foreign, and what is benign or potentially harmful, require an accurate appraisal of self and non-self. Anger represents both a recognition of the foreign and dangerous and a response to it.
The rst essential task of the immune system, too, is distinguishing self from non-self. Thus immunity also begins with recognition. Recognition is a sensory function, performed in the nervous system by the sensory organs. We may rightly say that the immune system is also a sensory organ. Any failure of the immune system in its responsibility of recognition would expose us to as much danger as we would face if our capacities to see, hear, feel or taste were impaired. Another function of the nervous system is memory. The immune system must also have memory: it needs to recall what in the external world is benign and nourishing, what is neutral and what is potentially toxic.
Under the watchful eyes of the parent, the infant and toddler explore the environment, learning what is edible and what is not, what is comfortable or a source of pain, what is hazardous or safe.
The acquired information is stored in the developing brain’s memory banks. Immunity is also a matter of learning. Memory is