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Individuality: The Trees in the ForestPNI research has several goals. One of these is to understand how the mind-body interaction works and then to apply what has been learned to prevent or lessen the grip of disease. Ultimately, we need to remember that psychosocial support treats an individual, not a group. One size does not fit all. Cause and effect is sometimes difficult to determine in the behavioral sciences. Many of the psychological concepts such as stress and depression, mood and affect are nebulous in practice. Although scales have been routinely used to measure such parameters in experimental protocols, it is still unclear what physiological correlates may be involved in a given individual. Individuals are stochastic (, ) and together we make up a set of probabilities. By stochastic we mean that actions of an individual compared to the population appear to be random or the opposite of deterministic. If we were deterministic creatures, the same input to any member of our species would always yield the same output. Instead, that any one of us will experience and react in a predictable fashion is based upon how closely we fit to that norm. And that is a product of genes, psychosocial environment, and choices we have made and continue to make that reflect our individuality. All scientific studies have norms and outliers. Although we may not mention the implications of these outlying data points, it is well to remember that they represent individual human beings. Sometimes investigation of these folks who fall on the ends of the curves may reveal much more than we at first believe. Nature vs. nurture in various guises is a universal and timeless theme in science. In the present context, we might recall that genetic factors most often determine susceptibility to disease, not the development of the disease. Environmental variables may be the precipitating factors. Race and ethnicity may be manifestations of gene pools in which certain disease susceptibility and resiliency genes may reside. The effects of these genetic influences on immunity, emotions and ultimately on health may be difficult to tease out of the influences of culture, socioeconomic classes, and health practices (, , ). That is not to say that there is not a contribution of genetics that seems to follow race and ethnic lines especially for autoimmune diseases (). That we represent considerable biochemical diversity can be easily seen when we look at the range of normal values within many of the standard laboratory tests. These ranges represent not only normal interindividual variations but also intraindividual changes. Intraindividual values for some indices may vary in circadian or ultradian rhythms. Laboratory values will also vary depending upon instrumentation, methods, and laboratory techniques (, ). Nevertheless, significant differences are seen related to sex, ethnicity, and age (). Even normal levels of elements have been shown to vary (). Nevertheless, ranges tend to hold across these variables. One potential source for the wide variation in disease susceptibility is the genetic makeup of individuals, which can either afford a measure of protection from a disease or make someone susceptible to a disease. Protection against one disease may make someone vulnerable to another disease (e.g. sickle cell trait). Individual differences in behavior and susceptibility to different psychopathologies may be influenced by differences in neuroendocrine response to stress (, ). Individual differences in expression of stress-related genes have been documented in humans (). There seems to be a strong genetic component to perception of chronic stress (, , ). And common polymorphisms of the glucocorticoid receptor have been shown to have an impact on cortisol response to psychosocial stress (). That is, normal variations in the form of a receptor for the hormone cortisol (a powerful modulator of the immune system), may vary in mediating influences of psychosocial stressors on immune responses. Yet psychosocial influences on individual human stress responses are extremely difficult to ferret out of studies that are not controlling for those variables (, ). As we look at the literature relating to PNI, it should become quite clear that the pathways for translating psychosocial stressors into changes at the cellular level are largely unknown. This is not for lack of attempts at exploration but rather the complexity of the problem. Take for example the problem with a mainstay in PNI research: monitoring cortisol levels. Cortisol has a considerable influence on our immune system, and often varies with our levels of stress. However, for several reasons, caution should be exercised in interpreting the relevance of plasma levels of cortisol. Most importantly, cortisol may or may not be elevated in the serum but that does not necessarily reflect the utilization or turnover in the specific tissues (). Cortisol receptors in lymphocytes appear to be modulated by more influences than just circulating cortisol and vary with psychological state (, ) and by sex and age in adolescents (), and maybe not by sex but by age in adults (). Not only does cortisol sensitivity vary between individuals, but it also varies from tissue to tissue and by season in peripheral blood mononuclear cells (). Individual reactions to stress of sampling blood may make results difficult to interpret (). As a consequence, increasing numbers of PNI-related research studies have switched to salivary monitoring of cortisol. Salivary cortisol varies with psychosocial factors (), and correlations between salivary and serum cortisol are generally considered to be established (). However, these correlations may not be clear-cut (). And, over the counter medications, collection, storage, and handling methods can have a dramatic influence on accuracy of cortisol measurements (). Caffeine (), alcohol (), tobacco (), and sleep () may also influence cortisol levels. It is naïve to assume that looking at a couple of molecules will tell us very much useful information about our individual stress responses. From a research standpoint, probably the best way to look at individuality in stress related immune responses is to look at expression of various stress-related genes. This could take the tactic of using molecular biology techniques of quantitative real-time polymerase chain reaction (qRT-PCR) to analyze the amount of expression of various genes into messenger RNA (mRNA). Or it could take the form of epigenetic research. That is looking at the proteins that are the final products of our inheritance. The latter is far more complex as there are many more proteins produced than there are numbers of genes. This is true because after the DNA is transcribed into mRNA, the further steps of translating RNA into polypeptides and post-translational processing may produce many proteins from one mRNA. From a practical standpoint, we have a way to go before a panel of relevant tests could be designed to give us a meaningful picture of individual reactions and susceptibilities to the stress of life’s challenges. So, that leaves us with the best we can do at this point. And, that may be to acknowledge that we are individuals and as such we will have unique reactions to stress. Perhaps with that knowledge we can do our best to minimize our potential to turn disease susceptibility into inevitability. |
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