Hypersensitivity: Looking Through the Oxygen Prism
Introduction
In my clinical experience, daily
administration of oxygen by mask with hydrogen peroxide foot soaks
often reduces the frequency and
intensity
of hypersensitivity reactions. What may be the mechanism of action
in this context? I have also commonly observed that therapeutic
measures directed at 'bowel cleansing' and 'liver detox' reduce
the frequency and intensity of hypersensitivity reactions—or
eliminate them altogether under certain circumstances. What might
be the operant mechanisms there? Why do some antigens trigger hypersensitivity
responses at some times but not others in the same atopic individual?
Why does the same antigen evoke strong responses under one set
of conditions but very weak reactions under another? For the same
individual,
why does antigen immunotherapy provide near-complete relief of
allergy symptoms at some time but not others? Why does the spectrum
of symptom-complex
induced by antigenic stimuli vary over a broad range? None of those
questions can be answered with the established knowledge of the
Gell and Coombs or any other recognized types of hypersensitivity
reactions.
Eczema lesions in the same person flare more during some weeks
than in others. In the same asthma sufferer, lifestyle stressors
exaggerate
bronchospasm more on some days than on others. Symptoms of Crohn's
colitis and ulcerative colitis remit and relapse for no apparent reason
in most instances. Food sensitivity reactions vary over a broad range
in the same individual. Allergic rhinitis becomes more intense on some
days when pollen counts are low and abates on days when pollen counts
are high. The phenomenon of "spreading sensitivity reactions" (long
vigorously denied by IgE researchers) is increasingly recognized
in chronic fatigue syndrome, fibromyalgia, and multiple chemical
sensitivity
syndrome. The molecular explanation of the above cannot be understood
on the basis of the known immunologic responses.
The oxidizing capacity of Earth is steadily increasing, and so is the
cumulative burden of particulate matter and other pollutants in the
ambient air. How do those changes affect the physiological and pathological
inflammatory responses that are integral to all immunologic hypersensitivity
reactions? In this column, looking through the prism of oxygen homeostasis,
I explore those questions and offer some explanations. In my view,
some aspects of pathophysiology of oxygen homeostasis and redox equilibrium
are not only crucial in understanding the wide range of clinically
recognized hypersensitivity responses, but also for formulating a rational
and scientifically sound integrative management plan for hypersensitivity
disorders.
Looking through the Oxygen Prism
In 1993, with the writing of Spontaneity
of Oxidation and Aging,1 I began my
clinical, biochemical, and pathologic studies with the central
purpose of looking at the health/dis-ease/disease continuum through
the prism of oxygen homeostasis. In 1998, in an article entitled "Oxidative
Regression to Primordial Cellular Ecology (ORPEC),"2 I presented
a large body of data to support my hypothesis that progressive and
unrelenting oxidative stress eventually creates cellular conditions
that simulate primordial, predominantly glycolytic metabolism. Later,
in an article entitled "Darwin, Oxidosis, Dysoxygenosis, and
Integration," I extended the ORPEC concept by focusing on impaired
mitochondrial function and respiratory-to-fermentative shift in ATP
production in patients with persistent energy states, including fibromyalgia,
chronic fatigue syndrome, and chronic fatigue following chemotherapy
for cancer.3
In 2000, I presented the oxidative-dysoxygenative (OD) model of IgE-mediated
allergy in Current Opinion in Otolaryngology.4
The OD model of atopy is a unifying model that integrates diverse clinical,
biochemical,
morphologic, and experimental observations in the following three areas:
(1) classical studies of IgE-mediated atopic response and, to a lesser
degree, the other three types of Gell and Coombs hypersensitivity responses;
(2) an ecologic view of clinical allergy that includes sensitivity
to environmental agents independent of the dose of the excitant;
(3)
an expanded, integrative perspective of hypersensitivity responses
that focuses on oxidative-dysoxygenative dysfunction (OD), which profoundly
influences sensitivity reactions included in the first two categories.
In 2000, I also proposed that oxidative coagulopathy is a major pathogenetic
mechanism of hypersensitivity disorders in an article published in
Environmental Management and Health.5
My focus there was on oxidative-dysoxygenative phenomena in the circulating
blood that provide an important mechanism
for turning local chemical sensitivity responses into the complex and
yet well-characterized systemic symptom complexes.
Human external and internal ecosystems are under increasing oxidative
stress. The oxidizing capacity of the planet Earth is increasing.6
The ozone layer is thinning and is oxidizing.7 Global anoxia is increasing
and is oxidizing.8 Ever-increasing levels of fossil fuel burning is
increasing oxidant stress. Industrial pollution is increasing, and
most pollutants are oxidizing. The greenhouse effect is oxidizing.
Ten thousand years ago the estimated average temperature of Earth was
50 degrees F,9 and it has been steadily rising. From January to July
1998, average temperatures consistently broke previous monthly records,
with temperatures rising to 124 degrees F in India, claiming 3,000
deaths.10 The total oxidizing burden of the above natural and anthropogenic
elements on human ecosystems has increased enormously in recent decades.
As for the various body organ ecosystems in environmental medicine,
oxygen transport and utilization in chemical sensitivity is impaired,
as evidenced by increased urinary excretion of toxic organic acids
(such as tartaric acid) that inhibit the Krebs cycle.11 Clinical evidence
for that is furnished by the pervasive sense of "air hunger" among
patients with environmental illness and clinical benefits of oxygenative
therapies for such patients.12 The bowel ecology disrupted by massive
sugar overload and extended antibiotic use (which feeds yeast and primordial
flora) is oxidizing.13 Lactic acidosis and dehydration, almost invariably
seen in advanced environmental illness, is oxidizing by interfering
with the Krebs cycle as well as hepatic enzyme detoxification pathways.
This subject has been recently discussed at length.14
The integrative oxidative-dysoxygenative model has a strong explanatory
power for many hitherto poorly understood aspects of clinical allergy.
Beyond that, this model provides a scientifically sound basis for adding
specific antigen immunotherapy to nutritional, antioxidant, detoxification,
and oxygenative therapies to enhance clinical benefits. To provide
a historical frame of reference for presenting this subject, I include
below some brief comments about the classical atopic and clinical ecology
perspectives.
The Classical Atopic Perspective
In 1902, Charles Robert Richet ushered
in the age of experimental study of hypersensitivity phenomena with
his description of anaphylactic
reaction.15 Four years later, Von Pirquet introduced the
term allergy (derived from the Greek words allos [other] and ergia
[energy]) for
an altered state of immune responsiveness or "changed reactivity" of
an individua1.16 In 1911, Noon introduced specific antigen
immunotherapy.17
In 1923, Coca and Cooke proposed the term atopy (derived from the
Greek word atopos, meaning strange or uncommon) for an abnormal state
of hypersensitivity in an individual, rather than a hypersensitive
response in a healthy individual, and believed that such sensitivity
could not be transferred to animals or humans.18 In 1921,
Prausnitz and Kustner laid the cornerstone for immunologic investigation
of
allergic phenomena in humans by documenting the presence of a transferrable
skin-sensitizing factor in the serum of allergic individuals.19 In
1964, Gell and Coombs proposed their classification of four mechanisms
of allergic reactions, Type-I reaction being the response mediated
by the reaginic antibody.20 In the mid-1960s, Ishizaka
established the IgE as a new unique immunoglobulin on the basis of
the following
three principal criteria: its ability to bind the specific antigen,
its unique antigenic determinants, and its correlation with biologic
activity, as demonstrated by the P-K technique.21 In 1966,
Wide et al.22 described the radioallergosorbent test (RAST)
for semi-quantitative measurement of allergen-specific IgE antibodies,
and ushered in the
era of in vitro diagnosis of allergy. In 1979, my colleagues and
I demonstrated local IgE production in plasma cells in nasal mucosa
of atopic persons23 and in nasal polyps.24 The same year, my colleague,
Madhava Ramanarayanan, and I described micro-ELISA assays for allergen-specific
IgE and IgG antibodies and, to achieve a higher level of assay sensitivity
and specificity, developed a methodology for accounting for a range
of variability in the nonspecific binding among individual antigens.25,26
Employing that assay, Hurst and colleagues demonstrated the local
production of allergen-specific IgE antibodies in the middle ear
mucosa and firmly established such mucosa as the primary target of
the atopic response.27
The Ecologic Perspective
The discipline of clinical ecology evolved to focus on clinically verifiable
patterns of hypersensitivity reactions that could not be explained
on the basis of any of the Gell and Coombs immunologic sensitivity
mechanisms. Clinical ecology was defined as the study of the effects
of the environment upon the individual by the pioneers of the field,
including Randolph,28 Rea,29 Waickman,30 and others. Chemical sensitivity
was defined as an adverse response of an individual to environmental
chemicals at levels that are generally considered safe. Thus, chemical
sensitivity is independent of the dose of excitant. The core concept
of chemical sensitivity holds that clinical expression of an adverse
reaction is determined by the following:
(1) the body tissue or organ
involved;
(2) the chemical nature of the excitant trigger;
(3) the
biochemical individuality of the person (the individual susceptibility
of the person to a given excitant);
(4) the length of the exposure;
and
(5) the existence of concurrent but unrelated stressors as well
as synergism among them (the concept of total load).
Four general
principles that govern the cause-and-effect relationships in clinical
ecology are:
(1) total load;
(2) adaptation (first described by
Selye31 and including masking or acute toxicologic tolerance);
(3)
bipolarity
(consisting of an initial stimulatory phase followed by a depressive
phase); and
(4) biochemical individuality.
The
core tenets of clinical ecology represent crucially important conceptual
advances beyond the classical atopy because they explain
a broad spectrum
of clinical manifestations not accounted for by the latter. The
IgE researchers continued to focus on issues of single-allergen
sensitivity
and consequences of specific immunotherapy in such disorders.
The ecologists, while recognizing the theoretical merit of such work,
found those findings
to be of very limited clinical value, since allergic persons
invariably
suffer from multiple sensitivities. After decades of doubt and
denial,32 the existence of multiple chemical sensitivity
syndrome was finally
acknowledged and its relevance to the management of the classical
allergy understood.33
During the 1970s and early 1980s, many pathologic, biochemical,
and clinical observations convinced me of the need to look
at the bowel
as an ecologic system. (See www.majidali.health for nearly 30
of my articles on the subject). That academic interest also
led me
to investigate
the role of altered states of the bowel ecosystem on the clinical
manifestations of hypersensitivity reactions. For example, a
marked improvement in
symptoms of atopic dermatitis was observed in many patients with
empirical therapies that putatively "restored the bowel health." Relief
of constipation was associated with relief of sinusitis headache
in others. Symptoms of allergic rhinitis often subsided with
antifungal therapies. All those considerations allowed me to
introduce the
concept
of altered states of bowel ecology as the basis for heightened
hypersensitivity states.
Particulate Matter, Pollutants, and Hypersensitivity
Particulate matter (PM) in ambient
air inflicts oxidative injury and induces inflammation in microecologic
cellular and organ-system macroecologic
systems. Such injury involves myriad prooxidant and proinflammatory
pathways, as well as antioxidant and antiinflammatory systems.34-37
Examples of the former include cellular heme oxygenase-1 (HO-1),
NADPH cytochrome P-450 reductase (P-450 reductase), nitric synthase,
sulfates, nitrates, organic hydrocarbons, metallic compounds, and
prooxidant transition metals, such as copper, vanadium, chromium,
nickel, cobalt, and iron. The counteractive antioxidant/antiinflammatory
responses evoked include superoxide dismutase, catalase, glutathione
peroxidase, and antioxidants.
Those changes have been closely examined in the pulmonary and cardiovascular
systems and other microecologic cellular and tissue-organ macroecologic
systems. The uptake of PM in macrophages and epithelial cells and induction
of oxidative stress is affected by differences in the size—coarse
particles (2.5-10 microns), fine particles (< 2.5 microns), and
ultrafine particles (UFP, < 0.1 micron)—and composition of
such matter. UFPs are the most potent inducer of cellular heme oxygenase-1
(HO-1) expression and depletion of intracellular glutathione. Furthermore,
HO-1 expression is directly correlated with the high organic carbon
and polycyclic aromatic hydrocarbon (PAH) content of UFPs.34 What increases
the biological potency of UFPs markedly is their localization in mitochondria.35
Diesel exhaust particles (DEP) in ambient air contain redox cycling
organic chemicals with potent prooxidative and proinflammatory responses.
Such effects are associated with a documented increase in the production
of over 30 proteins—a number that will definitely increase with
time. Technologies in current use for such studies include matrix?assisted
laser desorption/ ionization-time of flight mass spectrometry and electrospray
ionization liquid chromatography-mass spectrometry. In doses ranging
from 10-100 µg/ml, organic DEP extracts induce incremental impairment
of cellular glutathione systems—a decline in glutathione/oxidized
glutathione (GSH/GSSG) ratio, in parallel with a linear increase in
newly expressed proteins. Other antioxidant enzymes and proteins produced
in response to DEP (in addition to the above-mentioned heme oxygenase-1)
are catalase, proinflammatory components (p38MAPK and Rel A), and products
of intermediary metabolism regulated by oxidative stress. At DEP extract
doses of over 50 µg/ml, a steep decline in cellular viability
has been documented.36
The biologic effects of PM and DEP are inhibited by a variety of antioxidants
and antioxidant enzyme systems, including N-acetylcysteine (NAC), superoxide
dismutase (SOD), and others, by a variety of mechanisms.35,36 For
instance, N-acetylcysteine (NAC), which directly complexes to electrophilic
DEP
chemicals, suppresses DEP-induced effects. Not unexpectedly, such responses
to pollutants also evoke responses from certain oxidant-generating
enzymes, such as NADPH cytochrome P-450 reductase (P-450 reductase),
which has been detected mainly in ciliated cells in the respiratory
passages. By contrast, CuZn-SOD and Mn-SOD have also been found in
the airway epithelium. Another important system induced by DEP is constitutive
NO synthase (cNOS) in the airway epithelium and inducible NO synthase
(iNOS) in the macrophages. Pretreatment with NG-monomethyl-L-arginine,
a nonspecific inhibitor of NO synthase, significantly decreases DEP-induced
bronchial hyper-responsiveness.
The increasing amounts of minerals generally increase the degree of
oxidative stress in biologic systems. This issue has also been examined
in the case of PM- and DEP-induced responses. For instance, the degree
of chemiluminescence—an indicator of oxidative stress—shows
a strong association between such stress and the amounts of iron, manganese,
copper, and zinc in the lung and with iron, aluminum, silicon, and
titanium in the heart.37
In a recent issue, Science reported that particulate matter is estimated
to kill more than 500,000 people each year.38 What can be made of that
number when one realizes that one of every four children in New York
City carries an inhaler to school? PM comprises solid and liquid particles
derived from industrial and vehicular exhaust, smokestacks, forest
fires, windblown soil, road dust, volcanic emissions, and sea spray39–41
Ultrafine particulates are largely derived from combustion of fossil
fuel and have a core of elemental carbon coated with layers of chemicals,
such as sulfates, nitrates, organic hydrocarbons, and metallic compounds.42
The prooxidative/proinflammatory effects of many components of PM are
well established. Organic hydrocarbons, including polycyclic aromatic
hydrocarbons, quinones, and transition metals (copper, vanadium, chromium,
nickel, cobalt, and iron) also play a role.43,44 PM serves
as a template for electron transfer to molecular oxygen in redox cycling
events involved
in the above.45 Additional oxyradicals are also produced
in target cells (bronchial epithelial cells, macrophages, and others)
when contacted
by PM. Of special interest in this context are oxyradicals produced
in response to particle uptake by biologically catalyzed redox reactions
in the matrix, biomembranes, and mitochondria.46-48 The oxyradical-inflicted
damage includes that affecting:
(1) cellular proteins (especially those
involved in intracellular signaling cascades);
(2) lipids;
(3) complex
sugars;
(4) DNA;
(5) molecular species of epigenetic regulatory mechanisms;
(6) cytokines and transcription factors, such as NFk-B49 and eventually
cytokine and chemokine genes.44,45,50-52
These products are produced
locally in target tissues as well as systemically and lead to widespread
proinflammatory effects remote from site of damage.
Oxidative Regression to Primordial Cellular Ecology
In an earlier column, I briefly described the phenomenon of oxidative
regression to primordial cellular ecology (ORPEC).2 Briefly, it is
a dysox state in which persistent oxidosis, acidosis, and dysoxygenosis
create cellular metabolic conditions that closely simulate those
existing in the primordial era, before there were biologically significant
amounts of oxygen in the ambient era. The ORPEC state is associated
with overgrowth of anaerobic species in the bowel, blood, and other
tissue.
In my clinical experience, indolent hypersensitivity states—those
caused by any of the Gell and Coombs hypersensitivity responses, as
well as dose-independent chemical sensitivity—are nearly always
associated with the ORPEC state. Furthermore, clinically significant
reduction in the frequency and intensity of those reactions was achieved
with the use of dietary, herbal, and antifungal agents. Those observed
clinical responses shed further light on the contributory roles of
the ORPEC state in the pathogenesis and perpetuation of hypersensitivity
states. This subject is presented at length in Dysoxygenosis
and Oxystatic Therapies, the third
volume of The Principles and Practice of Integrative Medicine.53
Pathogenesis of Chemical Sensitivity: Oxidative-Dysoxygenative Dysautonomia?
Chemical sensitivity is a state of
exquisite sensitivity in which a person reacts strongly to exposure
to chemicals in amounts that are
tolerated by nonsensitive subjects without any ill effects. A classical
example of chemical sensitivity is a person who develops headache,
confusion, and tachycardia within minutes of exposure to formaldehyde
in a hospital laboratory, when others in the facility feel no discomfort.
I cite here an illustrative example of a variant of this disorder.
One of my associate pathologists could tolerate exposure to formaldehyde
fixative used for preserving surgical specimens without headache
when she processed such samples on two noncontiguous days of the
week. However, when unexpected schedule changes compelled her to
process formalized specimens on two contiguous days of the week,
she developed severe headache, illustrating the concept of cumulative
total load of chemicals. The clinical symptom-complexes of chemical
sensitivity have been comprehensively described and its pathogenesis
discussed at length. For detailed information, I highly recommend
William Rea's four-volume classic on the subject entitled Chemical
Sensitivity: Tools of Diagnosis and Methods of Treatment.
54
What are the primary pathogenetic mechanisms involved in chemical
sensitivity? This question can be answered in only a conceptual mode
at this time.
My own sense is that chemical sensitivity is an electrochemical derangement
in which the neurotransmitter dynamics are initially altered by substantial
cumulative initial injury and later perpetuated by what may seem to
be minor triggering exposures. The essential nature of that neurotransmitter
disruption is hyper-responsiveness, the brunt of which is borne by
the autonomic nervous system. Thus, oxidative-dysoxygenative dysautonomia—in
my view—is the principal pathogenetic mechanism of chemical sensitivity.
I saw objective evidence for that view in autonomic dysfunction delineated
by power spectral scan studies of R-R wave variability in all of my
patients with chemical sensitivity. I have presented this subject at
length in Integrative Cardiology,
the sixth volume of The Principles and Practice of Integrative
Medicine.55
As for the treatment, chemical sensitivity is one of the most exasperating
disorders. Infrequently I have seen patients who made a seemingly complete
recovery following periods of disabling illness. It seemed to me that
such cases had responded more to therapies designed to restore oxygen
homeostasis and redox equilibrium through restoration of the bowel,
blood, and liver ecosystems. As a rule, however, persons with long-standing
chemical sensitivity show a modest to moderate degree of clinical responses
and relapses are common following common deoxygenizing threats, such
as exposure to mycotoxins, infectious processes, emotional stresses,
and chemical insults.
Not surprisingly in view of incremental stress on human oxygen homeostasis,
the incidence of chemical sensitivity is rising—and can be expected
to continue to do so, as I previously pointed out.
Mold Desensitization and Antifungal Therapies
Mold-induced ill health—in my view—is
the most crucial aspect of all types of hypersensitivity reactions.56,57
For that reason,
proper diagnosis and desensitization with clinically relevant mold
antigens and optimally administered antifungal regimens should be deemed
as the central part of an integrative management plan. The spectrum
of mold-related illness includes:
(1) classical allergic reactions
caused by mold antigens with specificity for IgE antibodies;
(2) mold-induced
non-Ige-mediated immunologic responses;
(3) symptoms triggered by mycotoxins;
(4) bowel symptom-complexes caused by mold (yeast) overgrowth;
(5)
increased gut permeability secondary to mold overgrowth;
(6) biologic
consequences of the ORPEC state; and
(7) vulnerability to yeast infections
due to any combination of the above factors.
Needless to point out,
all of the above mold (yeast)-related derangements put oxygen homeostasis
and redox equilibrium in jeopardy, directly or indirectly.
The details of the diagnosis and desensitization with mold antigen
for long-term clinical benefits—including but not confined to
normalization of Th1 and Th2 functionalities—have been furnished
in Integrative Immunology, the
fourth volume of The Principles and Practice of Integrative
Medicine.58
The Enterohepatic Therapies for Preventing Food Reactions
I consider therapies for bowel cleansing
and liver detoxification essential for integrative treatment plans
of hypersensitivity disorders of
all ilk. I have marshaled extensive biochemical, morphologic, and
clinical evidence for my view in Integrative
Nutritional Medicine—Looking
Through the Prism of Oxygen Homeostasis,
the fifth volume of The Principles and Practice of Integrative
Medicine.59
In that volume,
I also provide specific information about nutrient-herbal formulations
as well as detoxification procedures, the efficacy of which I have
validated with extensive clinical work.
Empirically validated therapies for bowel cleansing and liver detoxification
comprised the core of therapeutic regimens for all chronic illnesses
in the ancient Ayurvedic, Chinese, and classical Greek treatises. The
focus of the indigenous African therapies—taught essentially
by oral tradition—was also on remedies that we now know affect
the bowel and the liver. Those healing arts were preserved by the naturopathic
community during the intervening centuries. The reader is referred
to The History and Philosophy of Integrative Medicine,
the second volume of The Principles and Practice of Integrative
Medicine,60
in which
I establish the connectedness of the healing arts practiced in different
parts of the world in those earlier eras. It is heartening to see that
an ever-growing number of the so-called allopathic physicians are now
beginning to adopt many of those 'naturopathic' therapies.
In Table 1, I furnish guidelines for dosage schedules for nutrients
my colleagues at the Institute and I prescribe to support our programs
for patients with hypersensitivity syndromes.
Table 1. General Guidelines for Nutrient and
Redox-Restorative Supplements for Atopic Patients With and Without
Indolent Immune Disorders
(74KB .pdf, requires Adobe Reader
to view.)
Oxystatic Therapies
I liberally prescribe direct oxystatic
therapies to restore oxygen homeostasis and redox equilibrium for all
my patients with hypersensitivity
syndromes. Such therapies include oxygen by mask (3 to 5 liters per
minute for 30 to 60 minutes), hydrogen peroxide soaks and baths,
intravenous infusions of hydrogen peroxide and ozone, and topical
ozone injection therapies (discussed in my May 2005 column). For
detailed information of such protocols, see Dysoxygenosis
and Oxystatic Therapies, the
third volume of The Principles and
Practice of Integrative Medicine.61
Healing Chemical Sensitivity: A Case History
In February 2002, a 36-year-old woman consulted me for a progressive
and incapacitating chemical sensitivity of a three year duration.
Prior to developing chemical sensitivity, for three years she had
suffered disabling chronic fatigue, persistent diffuse myalgia, frequent
sore throat, recurrent yeast vaginitis, and air hunger. Her body
weight had fallen from 123 to 100 pounds. During the first year of
integrative management with antigen-specific immunotherapy, vigorous
oxystatic therapies, bowel and liver detox measures, and endocrine
support, she showed steady and satisfactory improvement in all her
symptoms except those of chemical sensitivity. Then she received
doxycycline for putative Lyme disease from another practitioner and
had a full blown relapse. A psychiatrist prescribed paroxetine. In
February 2005, she participated in a special healing prayer session
at her church. The following are excerpts of her conversation during
a visit on June 1, 2005:
"I am back on my full schedule. I could not wash any dishes or do laundry
for over three years, nor could I go grocery shopping. Since the February
prayer period, I have been making steady progress. Now I am back to
my full household schedule. Doing dishes and laundry would mean nothing
to another person but for me it was uplifting. It means I'm normal
again. I am not tired and have little, if any, tissue pain. I have
gained 13 pounds. I was so sick I nearly died.
"I am a woman of the word . . . the word of God. I have always believed
God as a healer. It doesn't matter to me who He heals me through.
I work on being a receiver. I try to do my part. If I had not gotten
better in another three years, I wouldn't have lost my faith.
In 2002, my 6-year-old daughter wrote the following for the Xmas wish.
'I pray that my mom gets better and that I go to Disney World.' Would
you believe that my daughter's class got picked up by Disney
World to go there and dance. Would you believe we are going to Disney
World with her?
"I believe that if I had been healed suddenly, I would have gone back
to the old ways of unhealthy eating and unhealthy home environment.
What would I say to a doctor who is skeptic of my healing story? Well,
I almost died. I was really sick. I was desperate. I would tell him
this: I know some of my doctors didn't believe I was sick. If
you as a physician can heal, why can't God heal? Doctors are
really in God's business. They should recognize that."
Closing Comments
In 2000, I put forth the oxidative-dysoxygenative
model of hypersensitivity to provide scientific basis and rationale
for integrating prevailing
immunotherapeutic measures with naturopathic oxystatic therapies
for improved clinical outcome. Chronic hypersensitivity disorders
can be exasperating and dispiriting, both for the patient and the
physician. Chronic stress of unrelenting reactions eventually leads
to anxiety and depression of varying degrees. This is especially
true of chemical sensitivity, which regrettably continues to be labeled
as 'psychiatric illness' by many. Two elements are important
to recognize in this context:
(1) Persons with hypersensitivity illnesses
are not immune to the tyranny of neurotransmitters and the misconduct
of genes, thus setting the stage for otherwise unexplained sadness
and/or depression; and
(2) unrelenting suffering creates its own
pattern of disrupting neurotransmitter functionalities. Together,
those two elements wreak havoc on many victims of hypersensitivity
disorders.
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