C O R T I S O L A B N O R M A L I T Y, E L E VAT E D E S T R O G E N, A N D IMMUNE D E S TA B I L I Z AT I O N
changes associated with a pre-cancerous process in
the uterus. Treatment with cortisone (dexamethasone)
in ovariectomized rats given estradiol reverses
these abnormalities.33
I routinely find the combination of abnormal cortisol
and elevated estrogen in animals with histories of
infertility and miscarriage, suggesting that reproductive
failures may be caused by inflamed and immune-deregulated
reproductive tract tissue. Such failures are routinely
corrected by proper hormone therapy, enabling
animals to conceive and produce healthy offspring.
Over decades of clinical experience, William Jefferies,
an emeritus clinical professor at the University of
Virginia, has reported that patients with cortisol insufficiency
and histories of ovarian dysfunction, infertility,
and failed pregnancies achieve significantly improved
conception and birth rates on low-dosage cortisone
therapy.34
Common variable immunodeficiency (CVID)
appears to be a grossly underdiagnosed enabling mechanism
for a multiplicity of disorders in humans just as it
is in animals, giving rise to chronic infections, autoimmune
conditions, an increased risk of cancer, and poor
response to immunization. In both humans and animals,
CVID is characterized by low IgA, IgG, and IgM
levels and abnormal T cell counts. In humans, the precise
trigger for such immune dysfunction is unknown.
Researchers have not linked CVID or other so-called
immunodeficiency mechanisms to hormones. I suggest
that exploring this connection, and looking specifically
at cortisol activity, may generate major clues for diagnosis
and treatment.
My clinical success and the growing clinical applications
of low-dosage cortisone therapy for humans
strongly argue for sustained research into the nature,
magnitude, and impact of cortisol defects, including an
associated estrogen-immune problem, in the etiology of
disease. While it is now recognized that the hypothalamic-
pituitary-adrenal axis, as part of the neuroendocrine
system, has central importance to immune
homeostasis,35 we still don’t understand the countless
details and interactions.
Estrogen measurements are generally assumed to
be expressions of ovarian function. This seems an
invalid assumption, since a deficit of active cortisol—
from genetics, stress, toxicity, or phytoestrogens—can
initiate a significant estrogen buildup—estrogen
dominance—independent of the ovaries. Estrogen
dominance not only causes inflammation of many of
the arteries, but it also binds active cortisol and active
thyroid, and deregulates the immune system. It can
also contribute to such ailments as cancer, autoimmunity,
and hypersensitivity diseases. It will contribute
to loss of homeostasis, deregulated immune
function, and increased risk of disease among females
with or without ovaries as well as neutered or intact
males. In other words, none are exempt.
In humans, routine testing for a cortisol deficit and
consequential hormonal-immune abnormalities, followed
by an appropriate low-dosage, remedial steroid
therapy program, may provide breakthrough strategies
in the perpetual battle against disease.
21

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22
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2. Ibid.
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28. Personal communication with David Brownstein, M.D.,
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REFERENCES
Phil