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]).