When the Body Says No: The Cost of Hidden Stress (16 page)

Eating patterns are directly connected with emotional issues arising both from childhood and from current stresses. The patterns of how we eat or don’t eat, and how much we eat, are strongly related to the levels of stress we experience and to the coping responses we have developed in face of life’s vicissitudes. In turn, dietary habits intimately affect the functioning of the hormones that influence the female reproductive tract. Anorexics, for example, will often stop menstruating.

Jerilynn Prior, a Vancouver endocrinologist with a special interest in women’s health issues, found that subtle hormonal disruptions can occur even among women who report regular periods and no symptoms. She wrote in the
Canadian Journal of Diagnosis:
“Approximately one-third of regular, asymptomatic menstrual cycles of healthy women will have disturbances of ovulation that, based on biologic principles, could lead to significant health risks.”
¹⁵

The commonest cause of failed ovulation in Dr. Prior’s study was insufficient stimulation of the ovaries by the hypothalamus and pituitary due to “an imbalance or incoordination in the signals sent from the hypothalamus and pituitary gland to the ovarian follicle.” These disturbances, wrote Dr. Prior, “are caused by adaptions related to life cycle, changes in weight, psychosocial stresses, excessive exercise, or illness.”

Malignancies of the hematological (blood-cell producing) system such as leukemia and lymphoma are also hormone dependent, being profoundly affected by cortisol produced in the adrenal gland. Adrenal corticoid hormones inhibit the division and spread of leukemia and lymphoma cells. Thus, hematological malignancies may, in part, result when blood and lymph cells escape from normal inhibition owing to a chronically unbalanced HPA system. The available research points to emotional stress as a significant dynamic in the lives of adults with these diseases.

At the University of Rochester, a fifteen-year study of people who developed lymphoma or leukemia reportedly found that these malignancies were “apt to occur in a setting of emotional loss or separation which in turn brought about feelings of anxiety, sadness, anger or hopelessness.”
¹⁶

Synthetic analogues of the stress hormone cortisol are important components of the treatment of leukemia and lymphoma. Interestingly, the amount of cortisol-like hormone needed to block the replication of leukemic cells is only a little higher than what should normally be functionally available in the body. In the case of leukemia, episodes of acute stress in which the cortisol levels temporarily rise are sometimes enough to induce a remission. Such is thought to have happened during the illness of the composer Béla Bartók.

We need to recall here that the temporary elevation of cortisol that occurs in episodes of
acute
stress is healthy and necessary. Not healthy are the chronically elevated cortisol levels in chronically stressed persons.

Bartók, in exile from his native Hungary and stricken with leukemia, was commissioned by the conductor of the Boston Symphony Orchestra, Serge Koussevitsky, to write a new piece. The composer went into spontanous remission, which lasted until the work was completed. Quite likely, HPA-triggered cortisol and several other elements of the PNI system contributed to this famous remission, which made possible the creation of Bartók’s
Concerto for Orchestra
, a classic of twentieth-century music.

Apart from their direct effects on hormone-dependent malignancies, hormones regulated by the stress-sensitive HPA axis and by limbic areas of the brain act on other tissues in the body to influence the development of cancers. Chief among these hormone-sensitive tissues is the immune system.

It is customary to conceive of cancer as an invader against whom the body—like a country under foreign attack—must wage war. Such a view, while perhaps comforting in its simplicity, is a distortion of reality. First, even when there is an external carcinogen like tobacco, the cancer itself is partially an outcome of internal processes gone wrong. And, of course, for most cancers there is no such identified carcinogen. Second, it is the internal environment, locally and throughout the entire organism, that plays the major role in deciding whether the malignancy will
flourish or be eliminated. The malignant transformation of normal cells, in other words, is a process determined by many factors that have at least as much to do with the biopsychosocial state of the organism as with the type of cancer itself.

Once a cancer reaches the stage where its cell surfaces display molecules different from the normal body proteins, it ought to be destroyed by immune responses of many different kinds. T-cells should attack it with noxious chemicals; antibodies should be formed against it; specialized blood cells should chew it up. Under conditions of chronic stress, the immune system may become either too confused to recognize the mutated cell clones that form the cancer or too debilitated to mount an effective attack against them.

Also implicated in the growth and development of tumours are a large number of locally produced chemicals, some secreted by the cancer cells themselves. Such chemicals include growth factors, inhibitory substances and messenger molecules of many kinds. A complicated balance among them will tilt the process toward either tumour suppression or tumour growth. Suffice it to say here that this intricate biochemical cascade is profoundly influenced by the PNI system, particularly through hormones and other information substances.

Finally, emotional states are of great potential significance in the prevention or encouragement of cancer metastasis, the movement of malignant cells from the original tumour site to other areas of the body.

In popular mythology, cancer has to be “caught early” before it has a chance to spread. The biological reality is quite different: by the time a tumour becomes detectable, spread has, in many cases, already occurred. “A high proportion of early cancers have already thrown off occult metastases by the time the primary tumour is diagnosed,” the British oncologist Basil Stoll has pointed out.
¹⁷
However, most metastases either die or lie dormant for a long time.

Doubling time—the amount of time needed for a tumour mass to double in size—varies from one cancer type to another, and there are great variations within individual cancer types. For a tumour to become clinically noticeable, even on an easily accessible body tissue like the skin or the breast, it has to become about half a gram in size, comprising about five hundred million cells. A single cell with a malignant mutation would have to double about thirty times to reach such dimensions.
¹⁸
In
breast cancer, doubling time has been calculated to range from a few days to one and one-half years, with an average of about four months. “If a tumour cell were to grow constantly at the last rate, it would take about eight years to become clinically evident, and some sources suggest an even longer doubling time with a time span of about 15–20 years to become clinically evident.”
¹⁹

In the real life of a tumour, there is probably no steady doubling rate. Rather, there are broad fluctuations in growth rate depending on what is happening in the life of the host. We recall the history of Michelle, whose breast lump, which had been present for seven years, changed dramatically after a period of acute stress.

Since breast cancers have the potential to metastasize by the time they are a little over half a millimetre in diameter, “if a tumor is going to metastasize, in general it will already have done so by the time [it] is clinically detectable.”
²⁰
Microscopic spread of malignant cells seems to happen in many cases of breast cancer without ever causing clinical problems. In other cases, the metastatic deposit may lie dormant in distant tissues for years and then, unexpectedly, declare itself in the form of symptoms. The same dynamic operates with prostate cancer, which is why spread has already occurred in 40 per cent of prostate malignancies by the time the diagnosis is made. In fact, in a striking similarity with prostate cancer, autopsy studies on women indicate that as many as 25 to 30 per cent of all women have microscopic breast malignancies, “far in excess of the number ever actually manifested.”
²¹

The issue, therefore, is not simply the prevention of spread, but why and under what conditions in some people already existing dormant deposits convert into clinical cancer. Tumour dormancy is affected by many hormonal and immunological influences, all of them functions of the PNI system and all of them highly susceptible to life stresses.

There are dramatic fluctuations in tumour growth rates from one patient to the next. Also evident is a high degree of inconsistency in the appearance of metastatic disease and of survival times among patients who, clinically, are diagnosed with exactly the same type of cancer at the same stage of severity. For example, there are “many cases where incompletely excised breast cancers never recur, or where secondary deposits lie dormant in the host tissues for up to 30 years before finally manifesting.”
²²
Such individual differences, it would seem, are due not
to the autonomous behaviour of the malignancy but to factors in the body’s internal environment that inhibit the growth of cancer or, conversely, encourage it. That internal milieu is profoundly affected by the stressors acting on people’s lives and also by the highly variable ways in which individuals cope with stress.

In numerous studies of cancer, the most consistently identified risk factor is the inability to express emotion, particularly the feelings associated with anger. The repression of anger is not an abstract emotional trait that mysteriously leads to disease. It is a major risk factor because it increases physiological stress on the organism. It does not act alone but in conjunction with other risk factors that are likely to accompany it, such as hopelessness and lack of social support. The person who does not feel or express “negative” emotion will be isolated even if surrounded by friends, because his real self is not seen. The sense of hopelessness follows from the chronic inability to be true to oneself on the deepest level. And hopelessness leads to helplessness, since nothing one can do is perceived as making any difference.

One study dealt with healthy women who had no symptoms, only an abnormal Pap smear on a routine physical examination. Without any knowledge of the results of the Pap smear, the researchers “were able to predict with almost 75 per cent accuracy those individuals who had early cancer, simply by utilizing a questionnaire which differentiated between various emotional states. They found that cancer was most apt to occur in those women with a ‘helplessness-prone personality,’ or some sense of helpless frustration which could not be resolved in the preceding six months.”
²³

The researchers in Cvrenka had also predicted who among their nearly fourteen hundred subjects would likely develop cancer and die of it, based on the psychological characteristics of rationality/anti-emotionality (repressed anger) and a long-lasting sense of hopelessness. When they checked the death records ten years later, they found they had been right in 78 per cent of cases. “It seems to us,” they commented, “that the importance of psychosomatic risk factors is likely to have been grossly underestimated in many studies.”

The influence of psychological risk factors is poignantly illustrated in the life history of Gilda Radner. Radner’s maternal aunt and two
cousins died of ovarian cancer, and her mother was successfully treated for breast cancer. Gilda faced a genetic risk, but was she absolutely fated to die of ovarian cancer? There is no reason to think so.

For most women who develop ovarian cancer, heredity does not figure heavily among the risk factors. For a few, it is highly significant. About 8 per cent of women with ovarian cancer carry one of the genetic mutations known to increase risk. In fact, these are the same BRCA genes implicated in breast cancer. Depending on which strand of DNA is involved, those with the mutation in one gene could have a 63 per cent risk of developing cancer by age seventy. Those women whose mutation is in the other gene have a 27 per cent risk of ovarian cancer by age seventy-five.
²⁴
For women without the mutation but who have a first-degree relative—mother, sister or daughter—with ovarian cancer, the risk is about 5 per cent. Here again, we see that genes by themselves do not tell the whole story. Even in these high-risk categories, not everyone is ordained to develop cancer.

Gilda Radner sparkled with manic energy and a zest for experience, but she carried the psychological burdens of a highly stressful and self-negating life. The eating disorder she suffered from likely affected her hormonal balance. She was also infertile, due probably to the type of hypothalamic-pituitary dysfunction discussed earlier in this chapter.

The slim star of
Saturday Night Live
was bulimic. By her own description, she had been an “unhappy, fat and mediocre” child. She characterized her childhood as a “nightmare.” “My brother and I ate ourselves into little balloon children,” she wrote in her memoir. “We looked like no-neck monsters. My parents sent me to summer camp every year and every year I was scapegoated…. In the ‘princess game’ there would be controlling girls and pretty girls. The controlling girls would make the pretty girl the princess, and the controlling girls would be the advisors to the princess. The fat girl would be the servant or something, and that would be me.”
²⁵

Gilda’s relationship with her mother appears to have been intensely negative, and apparently marked by competition for her father’s attention. Gilda maintained that her father had been “the love of my life.” His death of brain cancer, when she was twelve, was an irreparable loss.

All her adult life, Gilda, out of sheer desperation, promiscuously sought male love and acceptance. “To a great extent my life has been
controlled by the men I loved,” she wrote. She attempted to make herself into whatever woman she thought the man in her life preferred.