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Dr. Ali's
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Editor,
The Journal of Integrative Medicine
Formerly, Associate Professor of Pathology (adj.), College
of Physicians
and Surgeons of Columbia University, NY
Formerly, President of Staff and Chief Pathologist,
Holy Name Hospital, Teaneck, NJ
Fellow, Royal
College of Surgeons of England -
Diplomate,
American Board of Anatomic and Clinical Pathology
Diplomate, American Boards of Environmental Medicine
Past President Capital University of Integrative
Medicine |
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OXYGEN AND ADRENAL
DYSFUNCTION
The Cushinoid-Addisonian Epidemic
The core message of this brief essay on adrenal health and
adrenal deficit is: All chronically dysoxic individuals
suffer clinically significant adrenal dysfunction. Dysox is
the state of disrupted oxygen signaling and oxygen-driven
cellular energetics. This view of adrenal deficiency is
significantly different from the prevailing thinking in
endocrinology. Endocrinologists, with rare exception,
continue to be preoccupied with named adrenal
syndrome-Cushing's syndrome, Addison's disease, Conn's
syndrome, and Sheehan's syndrome-as well as pituitary tumors
and hypothalamic disorders. Such lesions account for an
exceedingly small number of chronically ill individuals with
objectively and quantifiably detected adrenal dysfunction.
This, indeed, is one of the core messages of this column. My
assertions in this column are based on extended clinical
work with over 7,500 patients with chronic illness and on
close analysis of over 900 profiles of the 24-hour urinary
excretion of steroid compounds.
This column has nine other core points:
● First, the adrenal dysfunction of every individual
requires individualized support for the gland.
● Second, the essential "adrenal question" is
not what diagnostic label is chosen for someone with a
dysfunctional gland-people everywhere are diminished by
relentless habitat chemicalization and unrelenting
frustration and anger-but how the adrenal function of that
person can be assessed and restored.
● Third, the degrees of adrenal dysfunction are
best assessed clinically, as well as with the measurement of
24-hour urinary excretion of adrenal and gonadal
metabolites.
● Fourth, adrenal regeneration requires
spiritual equilibrium and full restoration of oxygen
homeostasis.
● Fifth, all disruptions of the bowel, blood,
and liver ecosystems must be effectively addressed for
adrenal homeostasis.
● Sixth, in my clinical experience, the direct
short-term adrenal support is optimally provided with
hydrocortisone, beginning with small doses of 2.5 mg twice
daily to larger doses of ten to twenty mg daily.
● Seventh, the adrenal gland cannot be
understood except through its inter-relationships with the
hypothalamic-pituitary axis (HPA), gonadal output, insulin
metabolism, energy economy of the body, the oxygen-driven
bioenergetics, and chronic stress.
● Eighth, there is a "Cushinoid-Addisonian
epidemic"-most people with adrenal dysfunction pass from an
initial hyperadrenergic (Cushing's syndrome-like state) to a
hypodrenergic (Addison's disease-like) state.
● Ninth, an increasing number of young people
are "gender-skewed"-females are "male-like" and males are
"female-like,"so to speak-and the adrenals play crucial
roles in the phenomenon of gender devolution. For an
in-depth discussion of these subjects, I refer the readers
to Darwin and Dysox Trilogy, the tenth, eleventh, and
twelfth volumes of The Principles and Practice of
Integrative Medicine.1-3 Before discussing the above issues,
below is an illuminating historical footnote.
The Adrenal Gland: Two
Glands in One
The adrenal glands are a pair of structures capping the two
kidneys. The word renal is an adjective for elements related
to kidneys. The adrenal glands were so named centuries ago
to refer to their relationship to the kidneys. Ad-renals for
add-ons to the kidneys so to speak.. Adrenal cortex is the
bright-yellow outer gland while adrenal m edulla accounts
for the central 20 percent of the gland and is functionally
related to the sympathetic system..The cortex includes zona
glomerulosa, zona fasciclata, and zona reticularis, Over 50
steroids have been isolated from the adrenal cortex.. Two
major types of hormones are called glucocorticoid. and
mineralocorticoid and glucocorticoid. The primary
glucocorticoid. is cortisol while the primary
mineralocorticoid is called aldosterone.
The major clinical features of adrenal deficit
include:
● Easy fatiguibility
● Persistent fatigue
● Undue cold sensitvity
● Low body temperature
● Orthostatic intolerance
● Skin discoloration, pigmentation
● Estrogen and testosterone deficit in older people
as well as younf people with chronic energy deficit states.
The major clinical features of adrenal overactivity include
obesity, hypertension, and most of the above.
Rebecca Gerschman-An Unsung Hero
The unsung hero of the field of free radical pathobiology is
Rebecca Gerschman, a physiologist at the University of
Rochester. In the early 1950s, she investigated the
relationships between oxygen toxicity and the adrenal gland,
and proposed that oxygen toxicity was mediated by free
radicals.4-7It is peculiar that Gerschman's seminal
contributions escaped the notice of most researchers and
writers interested in the energetic-molecular basis of
health and disease. She observed that adrenalectomy
protected rats from oxygen toxicity. She was aware of a 1934
report of Ozorio de Almeida,8 which documented the
histological similarity between testicular tissue injury
caused by ionizing radiation and oxygen toxicity. Gerschman
also knew of the universal theory of Michaelis,9 which held
that free radicals were intermediates in oxidation
processes. Examining the effect of adrenalectomy on certain
types of acutely injured tissues, she observed that the
procedure exerted protective effects and deduced that
adrenalectomy slowed the metabolic rate and consequently
reduced the need for oxygen-driven reactions. Considering
her findings in the larger context of the earlier work of de
Almeida and Michaelis, she concluded that oxygen toxicity
was mediated by free radicals.
The Cushingoid-Addisonian Transitions
I present the model of Cushnoid-Addisonian transitions to
underscore an essential point: The adrenal glands regularly
cope with environmental, nutritional, and anger-related
stresses with an initial Cushinoid hyperactivity response,
which is followed by Addinoid adrenal failure when
decompnsation occurs. Both the initial Cushinoid and
subsequent Addinoid responses are quantifiable.
Endocrinology textbooks and journals rarely, if ever,
address the crucial issue of the adverse effects of toxic
environment, toxic foods, and toxic thoughts on the adrenal
structure and function. Nor does the endocrinology
literature recognize the Cushinouid-Addinoid sequence
occurring in people without any of the above-mentioned
syndromes. Not surprizingly, endocrinologists act as if
their patients are immune to all environmental, dietary, and
anger-related toxicities. They limit their work to textual
models of the Cushing's syndrome, Addison's disease, Conn's
syndrome, pituitary tumors, and hypothalamic
disorders-entities which, as I show below, are exceedingly
rare-and neglect adrenal dysfunctions that occurs in all
chronically ill individuals.
The Cushing's syndrome-adrenal hyperactivity caused by
adrenal neoplasms and hyperplasia-is a rare disorder, with
an incidence of 1 per 100.000 per year, with a
female-to-male ratio of 5 to 1.10 The clinical features of
the syndrome include: fatigue, excess adipose tissue
("buffalo torso"), protein deficit, facial edema and fat
build-up ("moon face"), acne, hirsutism, skin striae,
hypokalemia and muscle weakness, adrenal diabetes,
osteoporosis, and failure to fight common infections due to
immunosuppression.
The Addisons's disease-adrenal failure putatively due to
"primary atrophy," autoimmunity, tuberculosis, and adrenal
destruction by neoplasms-is also a rare disorder. There are
no accurate statistics concerning the incidence of Addison's
disease in the United States. A British study reported the
incidence of thirty nine cases per million. The clinical
features of the syndrome include: low blood sodium and
chloride levels, excess potassium, acidosis, hypotension,
hypoglycemia, dehydration, fatigue, and immunosuppression.
Among the striking signs of adrenal deficiency in some
instances are cutaneous and mucosal pigmentation.
The Conn's syndrome (primary aldosteronism)-excess
production of mineralocorticoid aldosterdue to hyperplasia
or neoplasm of zona glomerulosa of the adrenal cortex-is
also a rare disorder. Its clinical features include:
retention of sodium and water, excessive loss of potassium,
metabolic alkalosis, muscle cramps (due to neuronal
hyperexcitability), muscle weakness (due to muscle cell
hypoexcitability), headaches, and hypertension. In 1955, the
prevalence of aldosteronism was estimated to be about one in
2,000 individuals with hypertension. Recently, substantially
higher incidences of aldosteronism have been reported in
hypertensive populations.12
I furnish the above synopsis is to make a point of crucial
clinical significance: The Cushinoid-Addinoid transitions
caused by toxicities of environment, diet, and anger produce
all possible combinations of symptom-complexes seen in
classical adrenal diseases. This is what endocrinologists
refuse to accept. Their patients pay dearly for this ethical
lapse.
Laboratory Evaluation of Cushnoid-to-Addinoid Transitions
The laboratory assessment of adrenal function presents four
special problems: (1) The adrenal glands produce about 50
steroidal moieties by complex pathways and no single steroid
can be relied upon for its functional assessment; (2) The
adrenal steroidogenesis increases initially to cope with
incremental demands followed by marked reductions, but not
in any consistent pattern in the production of specific
steroids or their metabolites; (3) Adrenal production of
androgens, estrogens, and progesterone cannot be separated
from gonadal production of these hormones; and (4) The
laboratory range of some hormones is extremely widefor
instance the value for the urinary excretion of DHEA used by
the Mayo Clinic laboratory is 21 to 2170 mcg/24 hourmaking
interpretation of the values of individual steroids
difficult. Notwithstanding these problems, a suitable
profile of steroidsthe composition of my choice is shown in
Table 1is extremely valuable.
In cases of acute and severe demands on the adrenal glands,
the glands mount a strong Cushnoid response with a marked
increase in the urinary excretion of all hormones and their
metabolites (Case 1, Table 1). The other end of the spectrum
is the Addinoid depletion (complete adrenal failure) in
which amazingly no steroids can be detected in the 24-hour
urine samples (Case 6, Table 1). Between these two ends of
the spectrum are seen examples of Cushinoid-to-Addinoid
transitional stages representing varying patterns of
overproduction of some and underproduction of other adrenal
steroids.
The problem of extremely wide laboratory reference ranges
for individual steroids, as mentioned earlier, is tedious. I
find it useful to consider the mid-point of the laboratory
range for individual hormones and metabolites rather than
merely accept the "high" and "low" designations in the
report. The data in Table 2 clarifies this point by
displaying the 24-hour urinary steroid excretion values for
26 chronically ill adult individuals. Note than when related
to the midpoints of the laboratory reference ranges, the
aggregate data for these patients were "low" for five,
"normal" for one, and "high" for two steroid compounds.
Without such an approach, the laboratory values for most
patients are designated in error as "normal," as was done by
endocrinologists who reviewed the adrenal data of my
patients.
Adrenal Therapies
I prescribe adrenal therapies for all patients with chronic
illness. The crucial issues of spiritual equilibrium and the
restoration of the bowel, blood, and liver ecosystems have
been addressed in past columns. As for providing adrenal
support until there is sufficient adrenal regeneration,
there are two approaches: (1) direct support with
hydrocortisone; and (2) indirect support with raw adrenal
extract, phytofactors, and nutrients. Below, I relate how I
concluded that direct adrenal support yields superior
clinical results in most cases.
In the mid-1980s, I investigated the clinical benefits of
bovine raw adrenal concentrate, as well as phytofactors and
nutrients for adrenal support. Among the phytofactors,
prescribed in combinations and rotations, were daily doses
of roots of licorice (500 to 1,000 mg), rehmannia (500 to
750 mg), ashwargandha (100 to 200 mg), and Chinese yam (500
to 750 mg). Among the nutrients were daily doses of
pantothenic acid (50 to 150 mg), pyridoxin (25 to 50 mg),
riboflavin (10 to 20 mg), and ascorbic acid (1,000 to 2,000
mg). These adrenal factors were prescribed concurrently with
antioxidants, minerals, and redox-restorative substances,
such as glutathione, MSM, taurine, and others.
In the early 1990s, I compared the clinical benefits of the
above factors with those of DHEA, pregnenolone, and
androstenodione in daily doses of 25 to 50 mg each for men
and for women half as much on alternate days. In the
mid-1990s, I undertook a systematic study of hydrocortisone.
Based on that experience, in my hands most patients with
adrenal deficit respond best to direct adrenal support with
hydrocortisone (daily doses of 5 to 20 mg). The short-term
use of low-dose hydrocortisone is safe, effective, and
without any adverse effects. It is widely misunderstood
because it is confused with high-dose synthetic steroid
therapy.
The subject of initial adrenal support with hydrocortisone
creates unnecessary confusion in the minds of many people
uninitiated in this therapy. They fail to see the difference
between gentle adrenal support with low-dose hydrocortisone
and massive synthetic steroid therapy in common use among
the practitioners of pharmacologic medicine.
Adrenal Regeneration and Recovery
The essential points are: (1) Clinical improvement in
adrenal function is seen with optimal integrated and
individualized plans within months in most cases; (2)
Clinical indications of improved adrenal status precede
normalization of laboratory values; (3) Some individuals
with long-standing disabling illness and severe adrenal
deficiency tolerate very low doses of hydrocortisone (1 to 3
mg daily) initially and take several months to accept larger
doses (10 t 20 mg) until eventual adrenal recovery occurs in
several months; and (4) Individuals with major depression
and posttruamatic stress syndrome sometimes show poor
clinical response despite robust efforts to support the
gland.
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