Allergy, hypersensitivity and stress
The traditional view of allergy is that allergenic substances are essentially harmless and allergic reactions are a “mistake” by the immune system. In recent decades, there is growing support for an alternative “toxin hypothesis” in which allergy is seen as an important defense mechanism that protects the host from harmful environmental substances, i.e., venoms, toxins, irritants and substances produced by biting insects[9]. More recent research continues to support this hypothesis, and it has been proposed that this response may also promote avoidance of some microbes[1,10].
Palm et al[9] describes how the high sensitivity of IgE-mediated responses may have evolved to allow anticipation of dangerous exposures and thus cause avoidance of noxious substances. Experiments in mice and rats sensitized to a specific allergen have shown stress/anxiety effects and avoidance behavior associated with trace amounts of allergen in their cages[1,9]. Stress-related neuropsychiatric disorders have also been associated with allergic reactions in humans[11,12].
The PHM hypothesis proposes that PHM-associated antigens would also produce a stress response. Thus, the observed stress effects (e.g., increased anxiety, sleep disruption, elevated heart rate, and lower heart rate variability) that occur in a wide range of diseases could be at least partly due to frequent elicitation of the stress response by exposures to PHM and other sources of allergens.
Thus, greater levels of physiological stress could be due to a higher level of PHM colonization, leading to a higher level of response to PHM and cross-reacting allergens/antigens inside and outside of the body. Chronic exposure to known or unknown allergens, including some PHM, could lead to elevated cortisol, damaging inflammation, elevated heart rate and hypertension.
In support of this view, there is increasing published evidence for IgE-mediated bacterial and fungal allergy, auto-allergy (IgE against self-tissue), and IgE responses that appear to be protective against pathogens. And these pathogens are not limited to parasites. Studies have suggested that anti-microbial IgE antibodies may help inhibit HIV-1 disease progression and may play a role in anti-Borrelia burgdorferi immunity[13]. These findings are compatible with microbial allergy being an evolved defensive mechanism against infection as well as a potentially important contributor to allergic/hypersensitivity reactions. Cross-reactions between microbial antigens and self-tissue could account for the IgE against self-tissue in auto-allergy. The fact that selective IgE deficiency is associated with increased asthma, chronic sinusitis, otitis media, autoimmune disease and cancer suggests that IgE responses might be protective and may be a response to potentially harmful substances/microbes (for additional references, see[1]).