Oxygen Model of Environmental Medicine
In 2000, I published an article
in the journal Environmental Management and Health.
Entitled " Oxidative Coagulopathy In Environmental
Illness" (Volume 11, pgeas 175-191). I presented
data to support my hypothesis that oxidative
coagulopathy is a major pathogenetic mechanism for
illness related to environmental triggers. This
report of a part of a series of articles on
molecular biology of oxygen and the clinical
applications of oxygen. Inow offer brief comments
about oxygen signaling and then reproduce texts from
my earlier article in Environmental Management and
Health to underscore the salient features of the
Oxygen Model of Environmental Illness.
In 1998, I introduced the term
dysox—short for dysoxygenosis—for a state of
fundamental failure of energy generation and detox
in the cells. I showed that dysox is
caused by impaired function of enzymes involved in
oxygen-driven chemistry ("oxyenzymes") and leads to
buildup of acids and toxins in the body. Soon after
I defined dysox as energy and detox failure, I
recognize other biochemical defects (and their
clinical consequences) caused by blocked oxygen
functions in the body, including:
*Oxygen-driven cellular development and
Oxygen-driven removal of cellular grease (oxygen’s
Oxygen-activation of the enzyme systems of the body,
Oxygen-driven cellular detox mechanisms.
In 1998, my primary purpose in
introducing the term dysox was to compel the readers
to reach beyond the then-prevailing practice of
naming diseases—choosing a diagnostic labels that
reveal nothing about the real underlying causes—to
justify the use of the so-called "drugs of choice."
Later studies of molecular biology of oxygen led me
to a broader view of oxygen homeostasis.
Specifically, I recognized that the derangements of
the primary oxystatic and energetic
mechanisms set the stage for all subsequent
autonomic, endothelial, inflammatory, autoimmune,
and environmentally-induced disorders.
High-Resolution Phase-Contrast mircoscopy of
In the above-cited article, I
reported my observations with freshly prepared,
unstained peripheral blood smears of fifty patients
with chronic environmental illness. Of these,
forty-six of fifty patients showed clear microscopic
evidence of advanced oxidative injury to all
elements of circulating blood. As observed with
high-resolution (15,000x) phase-contrast and
darkfield microscopy, morphologic patterns of
oxidative injury to blood components have been
designated oxidative coagulopathy, a state of
circulating blood comprising: (1) structural
abnormalities involving erythrocytes and
granulocytes and zones of congealed plasma in its
early stages; (2) fibrin clots and thread formation
with platelet entrapment in the intermediate stages;
and (3) microclot and microplaque formation in late
stages. Moderate to advanced changes of oxidative
coagulopathy were seen in only two of fifteen
healthy control subjects. Oxidative coagulopathy
begins with oxidative activation of plasma enzymes
and leads to oxidative permutations of plasma
lipids, proteins, and sugars, and is not merely
confined to oxidative activation of recognized
coagulation pathways. It is proposed that oxidative
coagulopathy represents one of the core pathogenetic
mechanisms of homeostatic dysregulation seen in
environmental illness and leads to oxidative injury
to intracellular matrix, cell membranes, and
intracellular organelles such as mitochondria. The
observed cellular and plasma changes shed
considerable light on many aspects of the
macroecologic toxicants and their cellular targets
as well as the microecologic oxidants and their
molecular targets. Oxidative coagulopathy is a
powerful explanation of the production of
symptom-complexes characteristically encountered in
Toxicity Versus Chemical Sensitivity
While clinical patterns of
environmental illness are quite well recognized and
established among physicians who practice
environmental medicine,1-8 this subject
remains controversial.9-12 The primary
reason for this is the nonlinear dynamics of
clinical disease caused by ecologic factors.13
Thus, unlike chemical toxicity, chemical sensitivity
in most cases is not dose-related, and the range of
susceptibility of environmentally sensitive persons
to ecologic chemicals is so wide as to make the
traditional approaches for establishing
cause-and-effect relationships exceedingly
difficult. Moreover, the lack of morphologic or
biochemical abnormalities in the results of commonly
performed laboratory tests in environmental illness
has further hampered progress in understanding
clinical ecologic illness.
During nearly two decades of the
author's clinical work, he has investigated redox
dysregulation in patients with environmental illness
with biochemical tests and high-resolution,
phase-contrast microscopic studies. Specifically, he
has focused on the following: (1) the fundamental
oxygen order of human biology14; (2)
spontaneity of oxidation in nature and its impact on
pathogenesis of illness15; (3) oxidative
injury to elements of circulating blood called
oxidative coagulopathy16; (4) oxidative
injury to intracellular matrix, cell membranes, and
mitochondria previously designated AA oxidopathy17;
(5) clinical consequences of anoxia, acidosis, and
accumulation of toxic organic acids18 ;
(6) oxidative regression to primordial cellular
ecology (ORPEC) that favors proliferation of
anaerobes under primordial conditions18;
and (7) clinical entities caused by, or associated
with, oxidative coagulopathy, AA oxidopathy, and the
ORPEC state.19-22 In this paper,
morphologic evidence of accelerated oxidative injury
to circulating blood in environmental illness is
presented as an extension of the previous studies.
and Clinical Diagnostic Criteria for Environmental
There were 31 females and 19
males in the study. The ages ranged from 15 to 67
years for females (average, 42.5) and from 17 to 61
years for males (average, 40.5). For this study, the
following clinical criteria for the diagnosis of
environmental illness were used: (1) no history of
organic or psychiatric illness before the onset of
environmental illness; (2) persistence of symptoms
for a minimum of twelve months; and (3) a clear
pattern of clinical symptomatology characteristic of
environmental illness elicited by a physician
experienced in the diagnosis and management of
environmental illness. Thirty-three patients also
met diagnostic criteria of chronic fatigue syndrome
(21), fibromyalgia (12), or both.
Blood Morphology Examined with High-Resolution
Phase-Contrast and Darkfield Microscopy
Freshly prepared, unstained
peripheral blood smears of patients were examined
with a high-resolution (15,000x) microscope with
phase-contrast and darkfield optics (American
Biologics, Chula Vista, CA). The procedural details
of such microscopy have been described.18
The peripheral blood morphology with such microscopy
is distinctly different from that studied with
ordinary bright-light microscopy. The following
brief comments about peripheral blood morphology in
healthy subjects are included here to provide a
frame of reference for presenting features and
degrees of oxidative coagulopathy in environmental
illness. Erythrocytes appear as pliable round cells
that readily change their shape to ovoid,
triangular, dumbbell, or irregular outlines to
squeeze past other erythrocytes in densely populated
fields. Such cells resume their regular rounded
contour as soon as they find open space (Figure
1).Most granulocytes were observed to show amoeboid
movements, their locomotion provided by streaming of
their granules into little protrusions of cytoplasm
which grew in size to become the "legs" of the
cells. Such cells continuously changed their
configurations as they appeared to explore their
microenvironment. Not uncommonly, active
phagocytosis of bacteria and cellular debris by some
cells is observed. Lymphocytic details seen included
fine cytoplasmic granules and finer detail of the
nuclear chromatin. The platelets appear as dark
round-to-ovoid poorly circumscribed bodies with
poorly visualized granules. Some fields show
clumping. However, platelet agglutination and
degranulation is only infrequently seen. There is
little tendency toward plasma congealing in their
vicinity. Indeed even when smears are allowed to
stand for 15 to 30 minutes, platelets remain
discrete and do not cause congealing of fields of
plasma that surround them in the central portions of
the smears. The peripheral parts of the smear
commonly show cellular damage as a processing
Patterns of Oxidative Coagulopathy
In previous studies of peripheral
blood morphology in clinical entities characterized
by accelerated oxidative stress, the author and his
colleague, Omar Ali, have described the following
salient morphologic features of oxidative
coagulopathy: (1) erythrocyte and leukocyte membrane
deformities; (2) diaphanous congealing of plasma;
(3) platelet aggregation and lysis; (4) filamentous
coagulum (fibrin needles); (5) lumpy coagulum; (6)
microclots; and (7) microplaques.17,18 In
the present study,
the following observations were
made in environmentally sensitive patients.
Erythrocytic Morphology in Environmental Illness
The most common abnormalities
observed in environmental illness involved
erythrocytes and consisted of lack of erythrocyte
membrane plasticity, irregularities of its outlines,
and clumping. Many erythrocytes showed surface
wrinkling, teardrop deformity, sharp angulations,
and spike formations. In later stages, zones of
plasma congealing were seen around many
erythrocytes. In more advanced cases, an increasing
number of erythrocytes showed shrinkage and
filamentous outgrowths extending from their
membranes, such filamentous outgrowths covering the
entire surface of cells to produce a Medusa-like
appearance. Other cells appeared as ghost outlines.
Zones of congealed plasma surrounded many cells.
Granulocytic Morphology in Environmental Illness
The earliest changes involving
granulocytes were clumping and loss of locomotion,
with cells lying limp in pools of plasma with
absence of granular streaming and amoeboid
cytoplasmic protrusions. In later stages,
granulocyte cytoplasm showed vacuolation, zones of
increased density, and disintegrating membranes.
Congealed plasma surrounded ruptured cells. Clear
evidence of granulocytic phagocytic dysfunction was
observed in the majority of smears. Even when
actively motile, phagocytic leukocytes failed to
actively engulf and digest primordial life forms
(yeast-like organisms). Interestingly, leukocytes in
such situations were observed to approach clusters
of primordial organisms, shrink back, and move away.
(For illustrated details of such altered
predator-prey dynamics of granulocytic phagocytes
and microbes in peripheral smears, see reference
Morphology in Environmental Illness
The dominant morphologic
alteration of lymphocytes involved enlargement. and
lymphoblastic transformation. In mild to moderate
degrees of oxidopathy, lymphocyte nuclei lost their
normal intense basophilic appearance and exhibited
pale blue staining. Cytoplasmic vacuolation was an
uncommon feature. In most advanced stages, up to 90%
of lymphocytes in most smears showed abnormal
cytologic characteristics with a majority of cells
in lymphoblastic transformation.
Morphology in Environmental Illness
The earliest changes involving
platelets were platelet clumping and loss of
membrane detail. Enlarged platelets were seen
frequently. With increasing intensity of
coagulopathy, degranulation and lysis were common.
Zones of congealed plasma, the beginning of soft
clots, were pronounced, and often extended to
erythrocytes and leukocytes in the vicinity. Fibrin
deposits occurred both as fibrin needles and
amorphous masses surrounding lysed platelets and
Morphology in Environmental Illness
Zones of congealed plasma in
close vicinity of platelets, erythrocytes,
granulocytes, and lymphocytes, as described in the
preceding paragraphs, were encountered in all
cases. Such zones of plasma solidification were also
commonly observed surrounding microbes (coccal and
bacillary microbes as well as primordial life forms
described fully previously18); this
phenomenon was most pronounced in the vicinity of
the latter. Congealed plasma also surrounded
microcrystals encountered in oxidative coagulopathy
(presumably composed of oxalates, urates,
cholesterol and other substances precipitated by
acidosis associated with oxidative coagulopathy).
While congealed areas were small and discrete in
mild cases, large and confluent areas of plasma
consolidation were seen in nearly every microscopic
field in advanced cases.
and Microplaque Formation in the Circulating Blood
in Environmental Illness
In earlier descriptions of
oxidative coagulopathy in ischemic coronary artery
disease, a microclot was defined as a discrete zone
of clotting of plasma components with entrapped
blood corpuscles, with or without visible fibrin
crystals. Microclots seen in this study ranged from
20 to 150 microns or larger. Microclots were
observed as loose ("soft") with poorly delineated
edges or as firm ("hard") with rather circumscribed
boundaries. A microplaque in that report was defined
as a compacted microclot with a clearly definable
inner structure composed of fibrin needles,
amorphous masses, and discrete layers of thrombotic
material. The morphology of microclots and
microplaques is illustrated in Figures 2-6.
Semiquantitative Assessment of Abnormal Peripheral
Blood Morphology in Environmental Illness
In Table 1, semiquantitative data
for microscopic features observed in freshly
prepared peripheral blood smears of fifty patients
with environmental illness are compared with similar
data for fifteen apparently healthy subjects.
Microscopy was performed within five minutes of the
preparation of smears. The semiquantitative
assessment of cellular and plasma abnormalities was
done by examination of a minimum of 100 microscopic
fields in each case.
The scale of scoring
abnormalities was as follows: 0=abnormal feature
absent; 1+=abnormal features present in less than
one in ten microscopic fields; 2+=abnormal features
present in at least one in five fields; 3+=abnormal
features present in about one-half of fields; and
4+=abnormal features present in nearly all fields.
Table 1: Semiquantitative
Scores of Morphologic Abnormalities Observed
in Oxidative Coagulopathy in 50 Patients
with Environmental Illness.
RBC membrane rupture
Diminished WBC granules
Diminished WBC motility
WBC membrane rupture
Microclots per 20 fields
Microplaques per 20 fields
Crystals per 20 fields
* See scale of scores in the
paragraph preceding the table.
Toxic environmental compounds
adversely affect a host of crucial physiologic
processes of humans.23-26 The critical
aspects of toxicant-cell dynamics are the following:
(1) exposure to toxicant (concentration and route of
entry); (2) uptake; (3) transport; (4) storage; (5)
direct toxicity; (6) metabolism of toxicant
(including Phase-I involving oxidation, reduction,
or hydrolysis and phase II involving various
conjugation reactions); (7) secondary and tertiary
tissue responses; and (8) excretion. All of the
above are complex issues. For instance, uptake of
the toxicant by the cells involves complex dynamics
between the cell membrane and the xenobiotics,
including: (a) passive diffusion through spores or
relevant spaces of lipid-protein-sugar bilayers; (b)
facilitated transport that requires water-soluble
substances "carried" by fat-soluble moities; and (c)
lipophility of the toxicant. Moreover, each of the
above elements is profoundly influenced by the
concentration and tension of oxygen, pH,
temperature, humidity, light, and the availability
(as well as lack) of redox-active nutrients. While
many advances in our understanding of the above
factors have been made in plant and animal models,26-28
little, if any, progress has been made in this
field as regards human ecologic illness. The primary
reason is that plant and animal ecotoxicity
experiments are designed to culminate in sacrifice
of the living organisms, which, of course, cannot be
planned for human subjects. To such difficulties
must be added the previously noted lack of
biochemical and morphologic abnormalities in the
traditional diagnostic laboratory tests in clinical
environmental illness. It is in this context that
the changes of oxidative coagulopathy observed in
the present study not only open up the possibility
of an expedient laboratory method of assessing the
degree of oxidative stress in environmental illness
but also provide valuable insight into the
pathogenesis of its symptom-complexes.
To provide a framework for
considering the role of oxidative coagulopathy in
the pathogenesis of symptom-complexes of
environmental illness, brief comments about the
following aspects of human redox regulation seem
necessary: (1) spontaneity of oxidation and disease;
(2) clotting-unclotting dysequilibrium in
environmental illness; (3) redox dynamics of
oxidative coagulopathy; (4) primary pathologic
processes triggered or perpetuated by oxidative
coagulopathy; and (5) oxidative injury to matrix,
membranes, and mitochondria.
of Oxidation and Disease
In 1983, the author proposed that
spontaneity of oxidation in nature is the core
pathogenetic mechanism of the aging process and all
diseases. bbbb That one basic mechanism
should be the basis of molecular injury in all
diseases seems implausible at first blush. However,
extensive review fails to provide any evidence to
the contrary.15-19 Specifically, in 1988,
the author proposed that spontaneity of oxidation
provides the molecular basis of environmental
illness in the sense that all agents causing
environmental illness are oxidizing in nature and
that oxidizing injury once initiated perpetuates
itself. (Spontaneity of oxidation, then, becomes the
essential mechanism that flames the oxidative fires
and perpetuates molecular injury.) In 1990,
following the study of peripheral blood morphology
of several hundred patients with chronic fatigue
syndrome, the oxidative nature of the erythrocyte
abnormalities observed in patients with chronic
fatigue syndrome was established by demonstrating
the reversibility of changes by ascorbic acid.18
In 1991, the author established the oxidative
nature of platelet aggregation and clot formation by
the addition of ascorbic acid and
ethylenediaminetetraacetic acid (EDTA) to platelet
aggregates induced by oxidizing agents such as
collagen, epinephrine, ADP, and ristocetin. Both
ascorbic acid and EDTA can readily break up platelet
aggregates formed by addition of various aggregating
agents.19 In 1995, accelerated oxidative
molecular injury was recognized as the core
pathogenetic mechanism of chronic fatigue syndrome20.
In 1997, oxidative coagulopathy was proposed as the
core pathogenetic mechanism of ischemic coronary
Abnormal coagulative phenomena
within the circulating blood occur in diverse
clinicopathologic entities such as eclampsia,
anaphylaxis, localized and generalized Shwartzman
reactions, hemorrhagic diathesis in clinical and
experimental acute viral in fections, bacterial
endotoxic shock and others.21 However,
until recently, intravascular clotting was regarded
as a homeostatic dysregulation of interest only in
life-threatening acute illnesses. The essential role
of such homeostatic dysregulation in chronic illness
has only recently been recognized.23-26
Clotting-Unclotting Dysequilibrium (CUD) in
(CUE) is, in the author's view, the second most
critical homeostatic requirement in health, the
first being the redox equilibrium. The present study
adds to the author's previously published evidence
for this view. Notable in those investigations are
the studies documenting reversibility of the early
changes of oxidative coagulopathy by antioxidants
such as ascorbic acid,29,30 vitamin E,31
taurine and others.31 Accelerated
oxidative molecular injury, regardless of its
origin, disrupts the CUE of health and causes CUD of
disease.18 It is noteworthy that all
oxidants operant on the circulating blood contribute
to oxidative coagulopathy.
Human external and internal
ecosystems are under increasing oxidative stress.
The oxidizing capacity of the planet earth is
increasing.32 The ozone layer is thinning
and is oxidizing. 33 Global anoxia is
increasing and is oxidizing.34
Ever-increasing levels of fossil fuel burning is
increasing oxidant stress. Industrial pollution is
increasing, and most pollutants are oxidizing. Ten
thousand years ago, the estimated average
temperature of Earth was 500 F, 35
and it has been steadily rising. From January
to July 1998, average monthly temperatures
consistently broke previous monthly records, with
temperatures rising to 1240 F in India,
claiming 3,000 lives.36 The greenhouse
effect is oxidizing. All of the above natural and
anthropogenic oxidizing elements contributing to the
increasing oxidizing burden on human ecosystems have
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.37
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.18
The bowel ecology disrupted by massive sugar
overload and extended antibiotic use (which feeds
yeast and primordial flora) is oxidizing.18
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 length18
Dynamics of Oxidative Coagulopathy in Environmental
Not unexpectedly, erythrocytes
were found to be more vulnerable to oxidative injury
than other blood corpuscles since such cells
transport oxygen, the most important oxidizer in the
body. Furthermore, unlike the leukocyte cell
membrane which is sturdy and uniquely equipped with
enzymatic antioxidant defenses against oxidative
stresses of microbial invaders, the erythrocyte
membrane is more permeable to oxygen (to facilitate
uptake and delivery of oxygen). Erythrocyte lysis
leads to the release of free hemoglobin in plasma.
Free hemoglobin has been considered a dangerous
protein—a biological Fenton catalyst.38
It rapidly quenches free radicals in a highly
oxidizing environment and becomes oxidized, thus
turning into a potent oxidant. It is readily
degraded by H2O2 to release
free iron, which initiates and propagates several
free radical reactions.39,40 Hemoglobin
reacts with H2O2 to produce a
protein-bound oxidizing species capable of causing
lipid peroxidation. 41 Free hemoglobin
also avidly binds with nitric oxide radicals and
induces vasospasm, triggering yet other oxidizing
events which, in turn, feed the oxidative fires of
Not unexpectedly, granulocytes
also play critical roles in the initiation and
perpetuation of oxidative coagulopathy.42,43
In health, such cells produce bursts of
oxidizing species for microbial killing as well as
for oxidative neutralization of toxins. In oxidative
coagulopathy, granulocytes are activated by
increasing oxidant stress and, in turn, feed the
oxidative flames by their own increased generation
of toxic oxidative species that degrade other
intracellular and extracellular molecular species,
inflict peroxidative injury to cytoplasmic and
organelle membranes, enhance polymorphonuclear
leukocyte-endothelial adhesion, and increase
Evidently, all of those factors can initiate,
perpetuate and intensify oxidative phenomena in
environmental illness. Some oxidizing molecular
species elaborated by granulocytes increase
capillary permeability and enhance
The cytoplasmic granules of human granulocytes
are rich in many enzymes, including proteases such
as elastase, which is capable of degrading proteins
in intracellular as well as extracellular fluids.48
Oxidative cell membrane injury may be expected
to result in escape of proteases from granulocytes
into the circulating blood. The destructive capacity
of granulocytes represents an exaggerated
physiologic response in which bursts of potent
oxidative molecular species are produced during
inflammatory and repair responses. Specifically,
hydroxyl radicals (OH.) derived from
superoxide radicals (O2-) produced by
granulocytes are a major cause of cellular injury.
Granulocytic myeloperoxidase generates hypochlorite
radicals when exposed to H2O2
following phagocytic activation.49
Hypochlorite, in turn, oxidizes protease inhibitors,
thus leading to increased proteolytic tissue damage.
Pathologic Processes Initiated or Perpetuated by
Oxidative coagulopathy initiates
and perpetuates the following seven primary
pathologic processes that feed upon each other and
serve as core pathogenetic mechanisms for various
symptom-complexes of environmental illness: (1)
impaired perfusion, (2) increased free radical
activity; (3) anoxia; (4) acidosis; (5) impaired
enzymatic functions; (6) matrix, membrane, and
mitochondria dysfunctions; and (7) autoimmune
injury. It is proposed that oxidative coagulopathy
triggers all of the recognized
symptom-complexes of environmental illness.
Oxidative coagulopathy impairs
perfusion by the following mechanisms: (a) increased
viscosity and impaired rheology of the blood; (b)
vasospasm induced by increased free radical actvity;
(c) occlusion of capillaries and arterioles by
microclots and microplaques; (d) diminished
antithrombotic characteristics of the endothelium.
Clear evidence for all of those factors is
vasodiltation by intravenous infusion of EDTA, which
arrests oxidative coagulopathy and increases
Oxidative coagulopathy, initially
triggered by oxidative stress, is known to
facilitate free radical generation by all known
mechanisms operant in the circulating blood.17
Specifically, it causes lysis of erythrocytes and
releases into the plasma free autoxidation of
glucose, oxidatively damages plasma proteins, and
accelerates activation of myriads of redox-active
Oxidative coagulopathy causes
anoxia, both by impaired perfusion and increased
free radical activity. Anoxia, in turn, leads to yet
greater free radical activity, as is amply
demonstrated by reperfusion studies,51,52
and further fires the oxidative flames of
coagulopathy. Thus, perfusion deficits, increased
free radical activity, and anoxia feed upon each
other, setting off reverberating cycles of
Oxidative coagulopathy causes
acidosis by the following mechanisms: (1)
accumulation of lactic acid due to impaired tissue
perfusion; (2) accumulation of other organic acids
due to accumulated oxyradicals; and (3) anoxia.
Intracellular acidosis results in compensatory
alkalosis in peripheral blood, which further impairs
oxygen transport to tissues by shifting to the right
the oxygen dissociation curve.
Oxidative coagulopathy, if
allowed to persist, leads to autoimmune injury by
all of the mechanisms that cause impaired tissue
perfusion, increased free radical activity, anoxia,
Significance of Oxidative Coagulopathy in
The symptom-complexes of
environmental illnesses have been delineated in
numerous clinical studies.1-6,53-54. One
or more of the seven primary pathologic processes of
oxidative coagulopathy listed above trigger or
perpetuate almost all of the molecular mechanisms
that underlie such symptom-complexes. Many of those
mechanisms have been recently reviewed.55
However, the precise initial molecular events that
render patients exquisitely sensitive to minute
amounts of chemicals that do not cause symptoms in
subjects without chemical sensitivity have not been
fully elucidated. Notwithstanding, the phenomenon of
oxidative coagulopathy illuminates well the
pathogenesis of the following symptom-complexes.
dysfunctions, including indigestion,
malabsorption, abdominal bloating and
cramps, and cycles of constipation and
disorders including easy fatiguability,
diminished endurance, and, in advanced
cases, disabling fatigue.
dysfunction, including temperature
dysregulation, palpitations, cardiac
arrythmias, and vasculitis.
thyroid, and pancreas functional disorders,
including cold sensitivity, dry skin, rapid
hyperglycemic-hypoglycemic shifts, and
hyperadrenergic episodes. Clear laboratory
evidence of such dysfunctions was seen in
the majority of patients in this study.
diasthessis, asthma, bronchospastic
episodes, and air hunger.
myalgia, and soft tissue pain syndromes.
PMS, lack of libido, and related
dysregulation of sex hormones,
pituitary-hypothalamus axis, and the limbic
system. The common disorders of mood, memory
and mentation in environmental illness are
also included in this category.
It is noteworthy that accelerated
oxidative injury (which triggers, and is fed by,
oxidative coagulopathy) is the common denominator in
all pathophysiologic derangements that underlie the
pathogenesis of clinical symptom-complexes in
environmental illness. Why some symptom-complexes
predominate in some patients while other symptoms
predominate in others, is in the author's view, is a
matter of genetic predisposition.
Occurrence and intensity of
oxidative coagulopathy in fifty chemically sensitive
patients are described. Such coagulopathy is
recognized as the core homeostatic dysregulation in
environmental illness. It is triggered by oxidative
stressors operant in our internal and external
environments. Seven major pathologic processes
triggered and perpetuated by oxidative coagulopathy
are highlighted and are shown to cause all of the
established symptom-complexes of environmental
illness. High-resolution phase-contrast microscopy
is identified as a useful laboratory method for
assessing the degree of oxidative stress in
environmental illness as well as for monitoring the
efficacy of therapies employed in the recently
described model of integrative medicine.56,57
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