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Cortisol Abnormality- Estrogen Part 1

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    Cortisol Abnormality- Estrogen Part 1


    Part 1 of 2
    Cortisol Abnormality as a Cause of Elevated
    Estrogen and Immune Destabilization
    ©Alfred J. Plechner, D.V.M.
    To be published in Medical Hypotheses, 2003
    Ihave long regarded adrenal dysfunction as a wellspring
    of excess estrogen which may contribute to hormonal
    imbalances, immune destabilization, and
    increased vulnerability to disease. As a practicing clinician,
    I have consistently found elevated total estrogen
    as part of an endocrine-immune derangement present
    in many common diseases of dogs and cats. Ninety
    percent of these cases involve spayed females and
    neutered or intact males, so the elevated estrogen cannot
    be attributed to ovarian activity. Sick and intact
    females, tested outside their estrus period, frequently
    have an elevated estrogen level as well.
    The pattern of derangement identified in thousands
    of cases over three decades involves insufficient cortisol,
    high estrogen, and abnormally low IgA, IgG, and IgM
    levels. This pattern undermines homeostasis and sets the
    stage for malabsorption and digestive disorders, allergies,
    lung and urinary tract problems, sluggish liver function,
    strange or aggressive behavior, epilepsy, obesity, deadly
    viral and bacterial infections, periodontitis, vaccine complications,
    autoimmunity, and cancer. Moreover, the
    same set of imbalances is often present as an underlying
    enabling mechanism in multiple illnesses.
    The adrenal cortex produces a variety of vital
    hormones. Among them is cortisol, the primary
    glucocorticoid made in the middle cortex layer (zona
    fasciculata). Endogenous cortisol controls inflammation,
    1 a function that inspired the development of cortisone
    drugs, pharmaceutical versions of cortisol. A profound
    loss of cortisol can lead to a critical state of
    deranged metabolism and an inability to deal with stress
    and infections. Cortisol exerts a discriminating regulatory
    effect on molecular mediators. These mediators
    trigger activity related to both immunity and inflammation.
    A normal level of cortisol seems to be required
    for healthy responses.2 Cortisol deficiency may result
    in an unresponsive immune system, whereas too
    much cortisol—like too much cortisone medication—
    suppresses immune responses.
    Adrenocorticotropic hormone (ACTH) from the pituitary
    stimulates cortisol production. ACTH is
    controlled in turn by the hypothalamic corticotropicreleasing
    factor (CRF) in a classical feedback loop.
    When cortisol blood concentrations rise to a certain
    level, CRF secretion slows, inhibiting ACTH and subsequent
    cortisol secretion.
    The androgens dehydroepiandrosterone (DHEA)
    and dehydroepiandrosterone sulfate (DHEAS) are the
    most abundant circulating hormones in the body. These
    substances, known as prohormones because they metabolize
    into other hormones, are primarily made in the
    zona reticularis of the adrenal cortex. Through enzymatic
    actions, they convert to androstenedione, androstenediol,
    testosterone, and further to the estrogen compounds
    estrone and estradiol.3 Androstenedione is the
    most important precursor of estrone, the most abundant
    circulating estrogen in postmenopausal women.
    Androstenediol has inherent estrogenic activity. 4
    The exact biological function of adrenal androgens
    and the mechanisms underlying their control is still
    the object of debate. However, it is well known that
    both may have androgenic and estrogenic effects.5
    Veterinary researchers have found numerous genetic
    defects resulting from contemporary linebreeding and
    inbreeding practices.6 Since the 1970s I have reported a
    cortisol defect in cats and dogs.7 I believe this stems
    largely from questionable breeding practices.
    Other potential causes for cortisol deficiency include
    prolonged stress and toxicity, which may be a significant
    acquired cause of adrenal cortical dysfunction. Harvey
    states that the adrenal gland is the most vulnerable
    organ in the endocrine system for toxins, and within the
    adrenal gland “the majority of effects” have been
    observed in the cortex. Such disturbances can
    “fundamentally affect the whole body physiology and
    biochemistry.”8
    When the zona fasciculata cannot make enough cortisol,
    or for some reason the cortisol is excessively bound

    E N D O C R I N E - IMMUNE ME C H A N I S M S A N D HU M A N HE A LT H I M P L I CAT I O N S
    (inactive) and thus not recognized by the hypothalamuspituitary
    system, the pituitary continues to release
    ACTH in order to stimulate more cortisol. The zona
    reticularis also responds to ACTH. This part of the adrenal
    gland, as noted above, produces androgens that can
    convert to the estrogen compound estrone, or to testosterone,
    which may then convert in part to the more
    potent estrogen compound estradiol.
    Some researchers say that an interface or transition
    zone of tissue between the zona fasciculata and reticularis
    of the adrenal cortex is capable of directly producing sex
    hormones, including estrogen compounds.9, 10 Excess
    estrogen promotes CRF release from the hypothalamus
    and ACTH from the pituitary, and contributes to
    hormonal imbalances and deleterious effects in the body.
    Researchers working in the field of rheumatoid arthritis
    and autoimmune rheumatic diseases believe that hormone
    balance is a crucial factor in the regulation of
    immune and inflammatory responses. Generally, estrogen
    in physiologic concentrations enhances humoral
    immune responses and depresses cellular-mediated
    responses. At higher and pharmacological concentrations
    the hormone has a number of inhibitory actions.
    Elevated estrogen, for instance, is associated with atrophy
    of the thymus gland. Androgens, by contrast, tend to
    suppress both humoral and cellular types of mechanisms.
    11 An examination of the endocrinology literature
    reveals, however, that mechanisms through which sex
    hormones regulate immune and inflammatory responses
    are poorly understood.12
    POSSIBLE ROLES OF ADRENAL ESTROGEN
    I have developed an endocrine-immune blood test
    that measures cortisol, total estrogen, T3 and T4, and
    IgA, IgG, and IgM antibody levels. The measurement for
    estrogen includes all estrogen compounds in the body,
    that is estradiol, estrone, and estriol.
    The test shows a consistent link between clinical
    signs of various illnesses and total estrogen outside of a
    normal range. Intact female animals are not tested
    during their estrus period. In out-of-estrus females, intact
    males, and neutered pets, normal levels are as follows:
     Males: 20-25 pg/ml
     Females: 30-35 pg/ml
    Elevated estrogen appears to contribute to a number
    of negative effects:
     Cortisol impairment. Studies have shown that estrogen
    inhibits cortisol synthesis by specific interference
    with enzyme activity,13 thereby exacerbating a cortisol
    deficiency and initiating hormonal imbalances.
     Thyroid hormone impairment. Estrogen causes an
    increase in serum thyroxine-binding globulin, which
    may slow the entry of thyroxine into cells and
    thereby reduce thyroid hormone action in tissue.14
    Elevated estrogen may also directly inhibit thyroid
    glandular release.15 Cortisol appears to be involved in
    the normal transference of T4 to T3, and the entry of
    T3 into cells.16 By interfering with cortisol synthesis,
    estrogen may indirectly impair thyroid function.
    These combined effects may slow the overall metabolism
    and interfere with many basic physiologic
    functions.
     Inflammation. My patients’ blood tests consistently
    show an association between inflammatory conditions
    and the pattern of low cortisol, high estrogen,
    and low antibody levels. Studies have shown that cortisol
    inhibits the production and accumulation of
    excess histamine in tissue17 and the synthesis of
    prostaglandins, mediators of the inflammatory
    response.18
     Cancer. In humans, estrogens are involved in the
    development of breast and endometrial cancer.19 All
    the dogs and cats I test and treat for cancer have
    impaired cortisol and high estrogen, along with
    deregulated immune cells.
     Autoimmunity. The same abnormal hormonal pattern
    is found in pets with autoimmune conditions.
    Immune cells are suppressed and appear to be
    stripped of normal regulation and the ability to distinguish
    between host tissue and foreign matter.
    Lahita has reported that recent data indicates
    “increased estrogen levels might initiate autoimmune
    diseases in many women and men.”20
     Aggressive behavior. Many unpredictable and
    aggressive animals have the endocrine-immune
    disturbance. In humans, Finkelstein provides
    evidence suggesting “that estrogen may play a
    significant role in the production of aggressive
    behavior in both sexes.”21
    TREATMENT
    I initiate corrective therapy when testing indicates
    the presence of imbalances. The protocol involves the
    use of various cortisone medications, either standard
    pharmaceutical compounds or a natural bio-identical
    preparation made from an ultra extract of soy. All
    18

    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
    plant material—the part of soy which increases body
    estrogen levels—has been removed. The compound is
    administered at low, physiologic dosages sufficient to
    compensate for deficient cortisol and re-regulate the
    immune system. These therapeutic dosages are significantly
    lower than standard pharmacologic levels used
    for short-term treatment and are usually needed for the
    duration of the patient’s life.
    This innovative use of a standard medication consistently
    restores lost immune competence. Most canine
    conditions require additional T4 thyroid medication.
    For some species-specific reason, most affected felines
    require only steroid replacement. This treatment
    approach has proven to be effective, safe, and free from
    side effects in thousands of cases.
    After two weeks of therapy, patients are retested.
    There is usually a clear normalization of the key
    endocrine-immune markers along with parallel clinical
    improvements, indicating that a significant healing
    process is underway. In general, animals recover and
    maintain good health as long as the program is maintained.
    A supportive hypoallergenic diet eliminates the
    risk of food reactions which can nullify the therapy.
    This clinical experience demonstrates the potent regulatory
    influences of cortisol and estrogen in immune
    function. It shows, perhaps for the first time, how an
    adrenal combination of abnormal cortisol and high
    estrogen interact to substantially deregulate and weaken
    immunity and contribute to multiple diseases.
    For decades, William Jefferies, M.D., clinical professor
    emeritus at the University of Virginia School of
    Medicine, has used low-dosage steroid replacement for
    human patients with “adrenocortical deficiency” and
    reported improvement for allergies, autoimmune disorders,
    and chronic fatigue.22 The medical community
    has largely ignored his clinical research because of an
    ingrained fear of using cortisone long-term under any
    circumstances. A similar fear exists in veterinary medicine.
    At conventional pharmacologic dosages, cortisone
    does indeed create side effects. In the past practitioners
    often shuddered at any suggestion of long-term cortisone,
    and, as the old saying goes, “threw the baby out
    with the bathwater.”
    Recently, resistance to long-term physiologic doses
    of cortisone appears to be eroding. Medical researchers
    have reported successful applications of low-dosage cortisone
    in rheumatoid arthritis,23 polymyalgia rheumatica—
    a systemic inflammatory disorder of the aged24 —
    and sepsis.25 However, none of these studies link specific
    conditions to an overall mechanism wherein an
    abnormality of cortisol triggers excess estrogen, HPA
    destabilization, interference with thyroid, and deregulation
    of the immune system. I believe that this pattern of
    hormone-immune imbalance is a widespread but largely
    unrecognized mechanism among pets, and may contribute
    to various human illnesses.
    TESTING THE HYPOTHESIS IN HUMANS
    The presence of such imbalances in humans could
    most readily be tested among symptomatic men and
    postmenopausal (non-ERT) women. First, a baseline
    blood test would be taken to measure cortisol, total
    estrogen, T3/T4, and IgA, IgG, and IgM antibody levels,
    along with a 24-hour urine test for active hormones
    and other relevant markers. The urine test permits the
    clinician to compare results against the blood test. This
    is an important evaluation because some blood values
    (such as cortisol and thyroid) may appear normal in a
    blood test but in fact involve excessively bound, inactive
    hormone fractions. Blood tests alone may not indicate
    whether or not the hormone is working. The urine test
    helps answer this question and contributes to a more
    accurate assessment and effective treatment.
    Jefferies’ clinical experience with human patients
    suggests that low-dosage cortisol replacement therapy
    could be applied to symptomatic patients who are tested
    and found to have the endocrine-immune imbalances
    described in this article. If their health status improves
    and retesting shows a reduction in total estrogen, one
    could conclude that a hypocortisol syndrome with wide
    systemic impact has been clinically corrected. Such a
    result would argue for further investigation of this
    testing and therapy method for various illnesses.
    Even though post-menopausal women are deficient
    in estradiol, their estriol and estrone are often very high
    not only from the possible interface layer but because
    the tissue enzyme aromatase converts DHEA and
    DHEAS and other androgens into total estrogen.
    Gruber states that estrogen synthesis increases in
    non-ovarian tissues as a function of age and body
    weight even though little is known about the factors
    that regulate estrogen production in the postmenopausal
    population.26 Longcope and colleagues
    observed a “marked increase in the ratio of estrogens to
    androgens in acute illness” among postmenopausal
    women. Conditions included heart attack, unstable
    angina, respiratory illnesses, and congestive heart
    failure.27 One physician with whom I have been
    19

    E N D O C R I N E - IMMUNE ME C H A N I S M S A N D HU M A N HE A LT H I M P L I CAT I O N S
    communicating commented that his sickest postmenopausal
    (non-ERT) patients have the highest total
    estrogen levels and the lowest immunoglobulins.28
    Estradiol alone, and not total estrogen, is currently
    the standard measurement in patients, yet in postmenopausal
    women, estrone is the major estrogen.29
    Estriol, generally considered to be a weaker compound
    than estradiol and estrone, is present in significantly
    greater concentration in premenopausal
    women,30 and may have significant though currently
    unidentified biological activity. I believe that total
    estrogen, including estrone and estriol, is a more
    meaningful indicator of estrogen activity than estradiol
    alone.
    The presence of xenoestrogens and phytoestrogens,
    chemicals which mimic estrogen and which can
    potentially trigger androgen-estrogen imbalance, complicate
    the process of assessing serum estrogen status.
    Such compounds appear in the environment and in
    food. Ubiquitous estrogenic compounds, including
    industrial chemicals, pesticides, and surfactants, affect
    wildlife and laboratory animals’ immune systems.
    Further studies are needed to determine the immune
    response in humans. These compounds may affect
    humans in similar ways.31 Hence, the need to measure
    total estrogen.
    Mesiano, demonstrated in 1999 that dietary phytoestrogen
    compounds found in soy decrease cortisol production
    and, as a result, increase androgens. Such consumption,
    he suggests, may indirectly increase total
    estrogen by raising DHEA and DHEAS levels. In his
    opinion it is “possible that some of the estrogenic actions
    of dietary phytoestrogens may be mediated via their
    stimulation of adrenal androgen synthesis.”32
    One way to determine the influence of dietary phytoestrogens,
    at least in men and postmenopausal
    women, would be to eliminate soy from the diet of
    patients who test high in total estrogen, then retest the
    patient again after several weeks. A clear drop in estrogen
    level could indicate a dietary effect. An unchanged
    or insignificantly changed level would indicate a source
    for estrogen unrelated to diet.
    Xenoestrogens include birth control pills and chemicalized
    estrogen drugs. Can these contribute to a disturbance
    of cortisol and thyroid, and contribute to the disease
    process? It seems plausible that exogenous estrogen,
    or even androgen supplements (such as DHEA, which
    can convert to estrogen in the body) could indeed contribute
    to imbalances and disease.
    My male patients’ test results make a strong argument
    for hypocortisolism as a primary cause of elevated
    estrogen. In symptomatic males with endocrineimmune
    imbalances, high estrogen occurs almost exclusively
    as a consequence of a cortisol abnormality. The
    rare exception is the animal whose endocrine-immune
    status normalizes spontaneously without any treatment
    after moving to another area. I assume in such cases that
    a significant toxic or xenoestrogenic compound, perhaps
    ingested or inhaled, was present in one area and not in
    the other.
    IMPLICATIONS FOR HUMANS
    Elevated estrogen participates in a broad syndrome of
    hormonal-immune imbalances contributing to multiple
    diseases in animals. Is estrogen similarly involved in
    human conditions?
    Is an unsuspected excess of estrogen involved in
    AIDS? Veterinarians regard diseased cats infected with
    feline immunodeficiency virus (FIV), a retrovirus
    similar to HIV, as untreatable. Yet I have a 70 percent
    recovery rate among symptomatic FIV patients. These
    animals have a typical pattern of low cortisol, high
    estrogen, and disturbed immune function. Low-dosage
    steroid therapy corrects the underlying imbalances and
    restores natural immunity. Cats remain disease-free as
    long as they are kept on the therapy. The results raise a
    number of questions.
    Does the virus cause the disease or do the imbalances
    weaken the immune system and give the virus free rein?
    Do the imbalances also accelerate the disease process by
    deregulating the immune system so that immune cells
    attack both viruses and host tissue? Is it not possible that
    in humans cortisol-estrogen-immune status may dictate
    whether a person develops AIDS symptoms after being
    exposed to the HIV virus? My clinical experience with
    animals suggests that HIV-positive humans be tested for
    endocrine-immune imbalances. If present, appropriate
    hormone replacement might offer a significant prevention
    and therapy strategy.
    All of my cancer patients have the same general
    pattern of endocrine-immune disturbance. Based on
    this experience I would suggest that human cancer
    patients be tested for similar imbalances. If they exist,
    appropriate hormone replacement therapy might
    offer an effective treatment strategy for humans just
    as it does for animals, even in advanced cases.
    According to Gunin estrogen generates proinflammatory
    responses as well as proliferative
    20

    Phil

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    Yes phil xenoestrogens are becoming more popular, but have they come up of a way to measure them accurate? I am thinking 24 hour urine would be the best route of measuring them through daily exposures.

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