PART 1
Health Locus of Control
PART 2
CONCLUSIONS
METHODS
DISCUSSION
APPENDIXES
Part I; Belief and Health
Psychosomaticism and Psychoimmunology
The main agent mitigating in psychosomaticism is stress. The Germ Theory of disease
explains disease in terms of simple biological interactions, while the Stress Model of disease takes
into account psychic factors (Zuger, 1999). Science has given us large reservoirs of knowledge
from which we may support the former, but clearly both act concurrently. "The German blitz of
London in World War II and the 1955 Kobe earthquake in Japan both precipitated local outbreaks
of ulcer disease" remains stark evidence of the influence of stress (Zuger, 1999, p. D7). The best
known psychosomatic illnesses are: coronary heart disease, hypertension, ulcers, asthma, skin
rashes, and chronic headaches, but current research now includes bacterial and viral infections,
etc. Such conditions may occur in the absence of stress (Germ Theory), but are aggravated by it
(Stress Model) (Carlson, 1995). And it is not only the presence of germs/ viral agents and stress
which precipitates illness; the appraisal of stress is also involved: "studies have shown that ulcers
heal more slowly in anxious people" (Zuger, 1999, p. D7). But how does stress and its appraisal
translate into illness in the body?
Maybe it is all in the head:
The autonomic and neuroendocrine systems of the CNS are recognized as two main
pathways over which the mind and body interact. These systems communicate with each other
and immune cells (lymphocytes) in a complex feedback loop. The relation of cognitive
information (perception, belief, emotion) to lymphocytes is taken as evidence that they "do indeed
alter immunity" (Watkins, 1996, p 58). These alterations in immunity occur when the cognitive
information communicates the perception, belief, or feeling of stress. A disruption in the activity
of lymphocytes results in sharp declines in the number of antigens produced (those which
normally control the spread of those bothersome bacterial/ viral invaders). Even in outwardly
healthy individuals, declines in immune functioning occur during periods of high or prolonged
stress (Comer, 1998). What can result is a susceptibility to illness: "Researchers suspect that
stress can interfere with the activity of lymphocytes, slowing them down and increasing the
person's susceptibility to viral and bacterial infections (Alder, Felten, & Cohen, 1991)" (Comer,
1998, p. 355). What are the physiological processes which are involved?
The autonomic system:
I will begin by discussing the autonomic component. One theory, the Disregulation
Model, suggests that any disruption in the normal course of the negative feedback loop of the
autonomic nervous system (ANS), aggregates to raise blood pressure (Comer, 1998). This might
explain the influence of stress in the development of coronary heart disease. Another theory
names the General Adaption Syndrome as an explanation for the manifestation of illness (Comer,
1998). When continuous actual or perceived stress causes the resistance stage in the natural
stress reaction to weaken, the General Adaption Syndrome predicts exhaustion (Comer, 1998).
Such a state disrupts organs which rely on the ANS so that an overly sensitive ANS may lead to a
variety of physiological symptoms (Comer, 1998). Yet another model relies on what has been
learned about the chemical messengers of the ANS, main variables under study in
psychoimmunology research (Comer, 1998). Two types of norepinephrine (a neurotransmitter)
receptors are present on lymphocytes (Comer, 1998). Stress causes an increase in this
neurotransmitter, which at moderate levels inform lymphocytes to increase activity. But when
stress reaches a heightened or prolonged level, norepinephrine reaches a comparably heightened
level. The second norepinephrine receptors respond to these higher levels, ensuing in immune
inhibition (Comer, 1998).
The neuroendocrine system:
The hormones of the neuroendocrine system impart their own effects, also of interest to
psychoimmunologists. In response to stress, adrenal glands secrete epinephrine, norepinephrine
(also a neurotransmitter), and stress hormones (Comer, 1998). Corticosteroids, for example, are
secreted from the adrenal gland after a series of reactions starting in the hypothalamus (Carlson,
1995; Comer, 1998). While corticosteroids have a beneficial effect on initial stress (it arouses the
body into action), it eventually has an enervating effect on lymphocytes (Carlson, 1995; Comer,
1998). In fact, "Prolonged exposure to high levels of these [glucocortoids] hormones can
increase blood pressure, damage muscle tissue, lead to infertility, inhibit growth, inhibit the
inflammatory response, and suppress the immune system" (Carlson, 1995, p.322).
It's evolutionary my dear Watson:
Researches might agree that all this has an evolutionary advantage. In order to capitalize
on our human resources and energy levels, we would want to withdraw from highly stressful
situations, in lieu of more productive ones. This feedback loop basically demands withdrawal,
when attacks on our immune system render us useless.
Implications:
The influence of stress on the immune system may have long lasting physiological impact,
and pave the way for illness. In urban bus drivers, for example, neuroendocrine activity is
heightened most in those who have high absenteeism rates, cite Rydsedt, Johansson, & Evans
(1998) of previous studies. In addition, "Compared to employees in comparable professions,
urban bus drivers have higher rates of psychosomatic, cardiovascular, musculoskeletal and
gastrointestinal disorders (Evans, 1994; Winkleby, Ragland, Fisher, & Syme, 1988)" (Rydstedt et
al., 1998, p. 35). They found in their own study that changes in workload had a significant impact
on psychosomatic complaints, tending to increase the rate. Chronic stress of up to 6 months
doubles risk of getting a cold, and of over 2 years quadruples it (Brody, 1998). It would seem
that the only way to steer clear of illness, then, is to avoid high or prolonged stress or to increase
one's tolerance for the stressors.
Not only does level of arousal (stress) precipitate autonomic and neuroendocrine
variability, but specific emotional states do as well (Miller & Wood, 1997). Miller and Wood
(1997) studied asthmatic children and theorized from their results that: "the coexistence of
conflicting or mixed emotions may engender more complex autonomic patterning" (p. 674). This
extends the notion that our own perception, affect, and belief might influence the onset of disease
or the lack thereof. Perhaps certain individuals are better able to 'tolerate' stressors as based on
their beliefs. It is the influence of belief to which I will currently turn.
