Mothers’ Babies, Fathers’ Maybes: Paternal Discrepancy and Its Effect on Male Immunological Functioning

Keith R. Fluegge
University of Michigan - Flint

Keywords: paternal, discrepancy, paternity, biphasic, stress, immunity.

Abstract

Who’s your daddy? This is a question most of us would answer without much deliberation. However, with the increasing rate of paternity testing, such knowledge becomes fleeting and has contributed to the phenomenon known as paternal discrepancy (PD). Fathers who may suspect PD are greeted by medical officials who shrug such stressing suspicions and by familial forces that seek to reinforce a child’s paternal resemblance. Fathers may feel forced to suppress such suspicions, and this cognitive tool has been documented to have suppressive immunological effects. This research paper seeks to understand the potential endocrinological and immunological effects among male caretakers suspecting PD. The current hypothesis supports the biphasic model of stress and immunity that has been posited by previous researchers.

Mothers’ Babies, Fathers’ Maybes: Paternal Discrepancy and Its Effect on Male Immunological Functioning

One biological certainty this study is based upon is that every human being is conceived from the reproductive capacities of a mother and a father. This construct is non-negotiable. However, a stark increase in paternity testing in the United States has spurred a phenomenon known as paternal discrepancy. “In the United States, rates [of paternity testing] more than doubled to 310,490 between 1991 and 2001" (Reinberg, 2005, qtd. Bellis, 2002, p. 1). That this statistic has been increasing significantly indicates that paternal discrepancy, or “...when a child is believed to have been fathered by the husband [or partner] but is actually the progeny of another man,” (Bellis, Hughes, Hughes, & Ashton, 2005, p. 749) is becoming a pervasive familial conflict that may very well be hard to diagnose. In the Journal of Epidemiology and Community Health, Mark A. Bellis et al. (2005) report that “…rates vary between studies from 0.8% to 30%...” (p. 749). That fathers have this need to believe the child to whom they are devoting their resources is their own biological progeny is a facet of human nature that has fascinated evolutionary psychologists for decades.

Just how bothersome this uncertainty can be is hard to conceptualize, as Bellis et al. offer that “... little is understood about the consequences to parents or children of the father suspecting PD but not having this established or refuted. Many [consequences] are likely to be similar to having PD confirmed (that is, stress...)” (2005, p. 752). Amid paternity suspicions, fathers are greeted by medical officials who shrug such suspicions (Lucassen & Parker, 2001) and by familial forces that seek to reinforce a child’s paternal resemblance (Regalski & Gaulin, 1993; Bressan, 2002). Such exposure can be overwhelming and persuade paternal investment (Apicella & Marlowe, 2004; Platek, Critton, Burch, Frederick, Myers, & Gallup, 2003). This uncontrollable environment can induce a great deal of stress on the father, potentially leading to immunosuppression (Sieber, Rodin, Larson, Ortega, & Cummings, 1992).

For decades, researchers have been documenting the physiological effects stress can have. Much of this research has focused upon the effects of acute, laboratory stress. But, as the preceding paragraphs have mentioned, paternal discrepancy is a phenomenon that pervades all aspects of the father’s life and, tantamount to many other chronic stressors, may force him to restructure his identity or social roles (Segerstrom & Miller, 2003). Moreover, chronic stressors have a stability characteristic, in which a person is unsure whether the stressor will ever end. This chronic state of arousal perpetuates shifts in three bodily systems: the nervous, endocrine, and immune system. These three systems communicate intimately, and as such, have formed the burgeoning field that is psychoneuroimmunology. In the following section, the researcher discusses the role of each system.

Discussion

Psychological Pressures

Just how an individual appraises stress is unique and is dependent, oftentimes, on an individual’s personality and coping styles. One such coping style spotlighted by Petrie, Booth, & Pennebaker (1998) is thought suppression. “Suppression of emotional thoughts, particularly those thoughts that arouse negative emotions, is often invoked as a way of regulating mood and reducing stress” (p. 1264). Cited earlier, fathers suspecting paternal discrepancy are greeted socially and interpersonally with countering messages from significant others and medical officials. These interactions may shove fathers into a suppressive state, in which suspicions of paternal discrepancy are tucked away but not altogether forgotten. Suppressing such suspicions may bode well for the offspring and the significant others, who now come to rely upon the father for financial and emotional support. As Petrie et al. (1998, p. 1272) have demonstrated, the physiological ramifications of thought suppression was evident, as it can “...[lead] to a reduction in certain circulating lymphocyte populations [and] is associated with a significant increase in sympathetic nervous system activation” (Gross & Levenson, 1993, 1997; Wegner et al., 1990). As such, thought suppression, a cognitive mechanism, has been documented to have both endocrinological and immunological effects, systems to which the discussion shall now turn.

Endocrinological Equation

Exposure to stressors has been shown to activate the sympathomedullary axis (SMA) and the hypothalamic-pituitary-adrenocortical (HPA) system (Renard, Suarez, Levin, Rivarola, 2005). The former has been found to release catecholamines (namely, norepinephrine [NE] and epinephrine [EPI]). Concurrently, corticotropin releasing hormone (CRH) is secreted by the hypothalamus which, then, orders the pituitary gland to release adrenocorticotrophic hormone (ACTH); furthermore, ACTH acts upon the adrenal gland, secreting corticosteroids such as cortisol into the blood during stressful bouts. If, however, stress is not overcome, as may be the case with chronic stress, elevated NE, EPI, and cortisol levels parade the plasma where they can latch onto lymphocytes, a prime component of the immune system.

Immunological Issues

The immune system is composed of a natural and specific immune response. Natural immunity is a response in which no particular pathogen is attacked; rather, cells attack a number of pathogens within a short period of time. The immune cells employed in this natural line of defense are granulocytes, which are further divided into monocytes, neutrophils, and natural killer (NK) cells. On the other hand, specific immunity mounts a premeditated attack against a specific pathogen. Lymphocytes assigned to this process are T cells (thymus derived) and B cells (derived in bone marrow and spleen). T-cells are further subdivided: T helper cells, which produce cytokines that activate the rest of the immune response, and T cytotoxic cells, which identify and lyse infected or malignant cells. B cells, on the other hand, produce soluble proteins called antibodies, which are the key ingredients in the fight against specific pathogens (Segerstrom & Miller, 2003). With this briefing, we now turn to how stress can modulate these components.

Neurochemicals, including catecholamines (epinephrine and norepinephrine) among others, are released during bouts of stress. Prolonged periods of stress keep neurochemicals circulating in the blood where they can modulate immune function (Marsland, Bachen,& Cohen, 2002). The key component of the immune system that is targeted by these neurochemicals are called lymphocytes. Born and bred in primary (bone marrow, or B cells, and thymus derived, or T-cells) and secondary (spleen and lymph nodes) lymphoid tissues, lymphocytes then migrate throughout the body through lymphatic vessels and plasma. It is here, in the body’s periphery, that these lymphocytes collide with the stress hormones. These neurochemicals stimulate the alpha (NE) and beta (EPI) adrenergic receptors present on all lymphocytes. The class of cells of particular interest in this study is natural killer (NK) cells, which play a part in cancer surveillance (Kiecolt-Glaser, Robles, Heffner, Loving, & Glaser, 2002). Not only do these cells man malignant cells, they also have high density and high affinity beta (NE) adrenergic receptors (Segerstrom & Miller, 2003), which makes this class susceptible to the presence of adrenal hormones. The ensuing cAMP messenger system can initiate an activation of a series of protein kinases, eventually leading to activation of other immune cells via cytokine production. Cytokines are communication molecules, released by macrophages in the natural immune response and released by T-helper cells in the specific immune response. In its latter role, cytokines serve as immune activators in either a cellular response or humoral immune response. In the cellular response, a set of T helper cells, called Th1, produce cytokines that activate NK cells, T cytotoxic cells, and macrophages to combat intracellular pathogens. In the humoral response, another set of T helper cells, called Th2, activate another group of cytokines which activate B cells and mast cells to combat extracellular pathogens. This physiological explanation reasons the heightened immune reactivity, usually seen after acute stressors.

If stressors become chronic in nature, glucocorticoids (namely, cortisol) tyrannize the immune trajectory. As noted previously, catecholamines, via the cAMP second messenger system, elevate T cytotoxic and NK cell levels, via cytokine expression. These cells, now numerous in supply, are greeted by glucocorticoids (e.g., cortisol). Lymphocytes now undergo direct gene activation, a process detailed in Marieb’s classic medical physiology text (2004):

This lipid-soluble steroid (cortisol) diffuses through the plasma membrane of the target cell and binds to a receptor–chaperonin complex in the nucleus. Once the hormone is bound, the chaperonin dissociates from the receptor and the hormone receptor complex is activated by phosphorylation and binds to a specific receptor protein on the chromatin, thus initiating transcription of a certain gene. The messenger RNA formed migrates into the cytoplasm, where it directs synthesis of a specific protein (p. 608).

This gene activation immunosuppression, which can assume many articulations, is corroborated in the literature. During chronic stress, the Th1 cytokines (namely, interleukin 2 [IL-2] and interferon gamma [IFNy]) are suppressed, while the Th2 cytokines (namely, interleukin 4 [IL-4] and interleukin 10 [IL-10]) proliferate and exacerbate the humoral response by inducing the secretion of an immense amount of irregular immunoglobulin from B cells, potentially resulting in many autoimmune diseases (Segerstrom & Miller, 2005). What this model suggests is that when Th1 cytokines are suppressed as a result of chronic stress, the ability to activate T cytotoxic and NK cells is also stunted (Zorrilla, Luborsky, McKay, Rosenthal, Houldin, Tax, McCorkle, Seligman, & Schmidt, 2001). Thus, glucocorticoids are thought to not only reduce the number of lymphocytes but also transform their function. Summarily, it is believed that neurohormones (NE and EPI) elevate the number of lymphocytes present, while glucocorticoids (e.g. cortisol) may directly alter gene expression in these lymphocytes, inducing eventual immunosuppression; such a summary is a founding tenet of the popular biphasic model of stress and immunity.

Summary

The purpose of this proposal is to detect whether endocrinological and immunological functioning is altered among men suspecting paternal discrepancy. Research on the subject of paternal discrepancy has hinted at the potential health consequences of all parties involved (Bellis et al., 2005). Yet, no study has examined this potentiality in its entirety, and therefore guiding references are slim. However, that this study’s purpose has focused exclusively on the men suspecting PD may extend previous findings that gender may moderate the effects of stress. That is, “... men are considered to be more biologically vulnerable (Maes, 1999), and they may be more psychosocially vulnerable (e.g., Scanlan, Vitaliano, Ochs, Savage, & Borson, 1998)” (Segerstrom & Miller, 2003, p. 619). Moreover, Renard et al. (2005) inform us that SMA activity is dependent on gender because males showed higher NE and EPI concentrations than females. Realizing such gender differences may predict this study’s results.

To conduct this correlational study, three fatherly cohorts ought to be assimilated: biological fathers, adoptive fathers, and those fathers suspecting paternal discrepancy. Stratifying the population of fathers into these three cohorts allows one to isolate the health effects of paternal discrepancy. Dependent measures of immunologic functioning (i.e., T cell, NK cell) ought to be taken as well as endocrinological assays of hormone (i.e., NE, EPI, cortisol) levels during a baseline period and after many observed interactions with the child. The motivation behind this methodology is corroborated by Petrie et al. (1998), who found that suppressing emotional thoughts (PD) for a period (interaction with child) resulted in a “rebound effect,” in which the suppressed thought increased in frequency after the suppression period and physiological activity (i.e., NE, EPI) increased as well. It is during this “rebound effect” the researcher hopes to measure each father’s physiological activity. With this procedure in mind, the researcher hypothesizes that chronic stressors, in this case suspecting paternal discrepancy (PD), may ultimately decrease a man’s immunocompetence quantitatively and functionally by altering a lymphocyte’s genetic expression via steroidal saturation.

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