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Hypothalamic dysfunction

Hypothalamic-pituitary dysfunction is a term to describe a nonorganic relative inactivity of the gonadotropin-releasing hormone (GnRH) system of the hypothalamus and its dependent pituitary gonadotrophs that normally produce follicle stimulating hormone, FSH, and luteinizing hormone, LH. The condition occurs during the reproductive years and leads to hypogonadotropic hypogonadism. Women will experience primary or secondary amenorrhea and men lack of sexual interest and impotence. more...

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Hypothalamic dysfunction

The immediate cause is a decease or lack of GnRH pulses. This may occur idiopathic, or as a result of stress or lack of caloric support. Eating disorders may lead to hypothalamic-pituitary dysfunction. Measurements of FSH and/or LH tend to show low or undetectable values, and sex hormones produced by the gonads show low levels as well. Hyperprolactinemia as well as a number of lesions in the hypothalamic or pituitary area may also lead to hypogonadotropic hypogonadism and need to be excluded before the diagnosis of hypothalamic-pituitary dysfunction can be made.

Treatment may need to address issues of hypogonadism, infertility, and osteoporosis.


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Adrenal-thyroid-immune dysfunction as a cause of reproductive failure in pets: does a veterinary syndrome offer testing and treatment insights for infertility
From Townsend Letter for Doctors and Patients, 12/1/04 by Alfred J. Plechner

As a clinical veterinarian, I repeatedly resolve infertility and miscarriages in dogs and cats by correcting a common but overlooked syndrome of hormonalimmune dysfunction originating with defective or deficient production of cortisol. The key ingredient in the corrective program involves a standard medicine used in a different way, and this approach may possibly offer insights for exploring an alternative, inexpensive treatment for reproductive failures in humans.

In the 50 plus years since first appearing in the medical marketplace, the pharmaceutical derivatives of cortisol--that is, cortisone (steroid) compounds--have become prominent mainstream medicines because of their clinically important anti-inflammatory and immune suppression applications. Over the years we have also learned a great deal about the side effects of these compounds--and come to fear them--when used at typically powerful, pharmacologic dosages. For that reason steroids are usually prescribed for the short-term and avoided for prolonged use.

This development has discouraged interest in the pivotal physiologic roles of cortisol and applications of low-dosage cortisone as a "hormone replacement" for cortisol deficiency. Such deficiencies tend to be off the radar screen of most practitioners even though common among both animals and humans as a result of genetic and/or acquired factors including toxicity and prolonged stress. This is a major omission. Research tells us that immunity appears to be regulated by the hypothalamic-pituitary-adrenal (HPA) axis, (1) thus making normal health and reactions to stress and infections critically dependent on the ability of the adrenal glands to produce a proper quantity of cortisol.


In thousands of feline and canine cases, I have consistently identified a cortisol defect that kindles a domino effect of hormonal disturbances leading to immune deregulation and systemic dysfunction. (2-4) This "disabling" mechanism sets the stage for multiple disorders ranging from chronic allergies and viral diseases to autoimmunity and cancer. The innovative blood tests I conduct to demonstrate the presence of this pattern of disturbance are usually quite revealing in animals--including horses who have been tested--with a history of infertility and miscarriages.

The signature pattern involves an initial deficiency of active cortisol plus elevated total estrogen, bound thyroid hormones, and low concentrations of immunoglobulins IgA, IgG, and IgM. I find this same pattern in intact or neutered male and female animals. I believe that the elevated estrogen stems from disturbance of the HPA feedback loop. The adrenal cortex, unable to produce adequate cortisol, causes prolonged release of pituitary ACTH. This in turn stimulates estrogen directly from the adrenal cortex or from adrenal androgen conversion to estrogen in peripheral tissue.

The combination of deficient cortisol and excess estrogen destabilizes the immune system but also has considerable potential to interfere with thyroid function. The medical literature contains considerable data linking thyroid function and reproduction. Indeed many cases of infertility are treated with thyroid medication. However, thyroid hormones--both endogenous and as medication--may be rendered ineffective to some degree by abnormal levels of cortisol and estrogen that can bind thyroid compounds in the body, impair their cellular uptake, and interfere with T4>T3 transference. (5-7) Thus, a slowing of metabolism can occur that might affect reproduction and even the body's ability to remove excess estrogen.

Low thyroid function in males is associated with impotence, loss of sperm production and motility, and abnormal morphology. I often see this in intact male dogs and cats with endocrine-immune imbalances who are infertile.

Intact female dogs and cats with the same pattern of imbalances frequently develop endometriosis, cystic ovaries, and periods of excess hemorrhaging, an apparent result of elevated estrogen. During a normal pregnancy period of 62 to 65 days, such animals may miscarry. Sometimes gross fetal abnormalities develop, including small, mummified fetuses, followed by resorption. Could this be due to an estrogen-induced inflammation of the uterine lining? In these female animals estrus is often not noticeable. There is no vaginal engorgement or bleeding, a condition referred to as "silent heat."

Standard blood tests of affected male and female animals often indicate normal levels of thyroid hormones but the action of these hormones appear to be bound, blocked, or otherwise hampered by elevated estrogen and low cortisol.

The hormonal disturbances compromise the immune system in general. Locally, the ability of the uterus to protect itself appears to be weakened. The blood tests I conduct consistently reveal a low IgA level. Most practitioners pay little attention to IgA, yet IgA is the most abundant antibody and is especially important in mucosal immunity. It is an essential protective factor against infectious agents, allergens and foreign proteins that enter the body via the mouth, nose and upper respiratory tracts, the intestines, and reproductive tract. IgA deficiency is the most frequent immunodeficiency in humans. (8)

Clinically, I regard a low IgA test score as a marker of impaired immunity in the mucous membranes, including the uterus and ovaries. The low value makes it evident to me why these tissues are vulnerable to inflammation and infections, and less able to "host" normal reproduction.

In veterinary medicine, the cause of such pathology is frequently attributed to an infected male carrying brucella canis, a bacteria that can cause infertility and abortion. However, these microorganisms are usually not found.

In dealing with a case of reproductive complications (and health disorders in general), I first draw blood for the endocrine-immune test I developed some 30 years ago. It measures cortisol, total estrogen, T3 and T4, and IgA, IgG, and IgM levels. Except for T4, the elements of this panel are not routinely tested for in veterinary medicine. I thus developed my own range of normal values based on continuing clinical experience (see table 1). Both males and females are tested. However, females are not tested when in heat to avoid the influence of ovarian estrogen.

In the syndrome of imbalance that I have identified, cortisol and thyroid hormones are bound to varying degrees, and their individual values in a blood test may or may not appear normal. For this reason I compare the relationships of hormone and antibody levels rather than relying on isolated single values. In my experience, the clear markers of cortisol-based imbalance are elevated estrogen and low IgA, IgG, and IgM.

Once the combination of clinical signs and testing determines the presence of imbalances, I initiate a correction process involving long-term, low-dosage synthetic cortisone or a natural cortisol hormone replacement made from soy. The exact type and amount of replacement depends on the weight and health status of a particular animal. I retest patients after two weeks into the therapy to determine if any modification of dosage is required. Decreased estrogen and increased antibodies indicate the effectiveness of this hormonal "re-regulating" approach.

During more than 30 years of practice, I have found that most imbalanced dogs also require T4 medication such as Soloxine. Steroid replacement promotes transference of T4 to T3. Initially I combined T3/T4 medication in dogs but found that TSH and natural T3 and T4 production were suppressed. I subsequently found that T4 alone was sufficient. Most imbalanced cats do not require thyroid replacement, unless they are outright hypothyroid or have a condition known as feline infectious peritonitis (FIP). Other than those exceptions, only cortisone/cortisol replacement is needed.

In my therapy program I give special attention to IgA level. I have found that IgA levels below 60 mg/dl reflect dysfunctional intestinal mucosa, meaning probable inflammation and malabsorption, including an inability to absorb medication. I find that low IgA is often the overlooked basis for inflammatory bowel disease. When IgA is moderately or substantially low I do not take a chance with oral medication, and instead utilize an intramuscular injection, including both immediate and long-acting steroids. This approach often returns the IgA level to near normal or normal within a few weeks, after which I am usually able to switch patients to an oral steroid. I treat each animal individually, using the lowest possible amount of cortisone to correct the deficiency and restore the missing equivalency of cortisol. In almost all cases, deficient animals need daily replacement for a lifetime.

Typical daily oral medication dosages

* Medrol or Prednisolone: 1 mg per 10 pounds of body weight.

* Vetalog (triamcinilone): .125 mg per 10 pounds.

* Natural hydrocortisone: .5 mg daily per 1 pound of body weight.

* Soloxine (T4): .10 mg per 10 pounds of body weight twice daily.

By correcting endocrine-immune imbalances in animals with reproduction complications I have successfully restored fertility and prevented subsequent miscarriage in more than 90% of cases. Both male and female animals who are imbalanced and who are to be bred, need to be corrected.

Is a similar approach applicable to human reproduction failure? In humans, the use of low-dosage cortisol or cortisone medications to compensate for common, yet widely overlooked, mild deficiencies of cortisol has been reported since the mid-1950s by endocrinologist William Jefferies, MD, an emeritus clinical professor at the University of Virginia Medical School. During this time, Jefferies has used this approach for patients with chronic fatigue, allergies, autoimmune conditions, as well as for infertility and miscarriages where he has found cortisol deficiency. In reports largely published more than 35 years ago, he cites consistent and significant improvement among patients, including improved conception and birth rates for many women with histories of ovarian dysfunction, infertility, and failed pregnancies.



Jefferies, now nearly 90, has long and steadfastly championed the medical benefits of physiologic replacement of deficient cortisol, and lamented the fact that such use has been stymied by the seemingly indelible reputation of cortisone to produce side effects. Such side effects, he has repeatedly pointed out, occur only with large pharmacologic dosages of cortisone and do not develop with low-dosage physiologic levels when given to patients with adrenal insufficiency. "There is no evidence that patients who have taken physiologic dosages for over 40 years have experienced any harmful effects, nor that children born to women taking physiologic dosages have any increased incidence of congenital defects or other difficulties," he states. (9)

My experience with animals is similar. Jefferies also notes that the treatment has had an "impressive" preventive effect against postpartum depression and thyroid disorders.

As an aside, it is interesting to note that low-dosage cortisone therapy appears to be gaining wider acceptance. Medical researchers have reported using this approach with success for patients with rheumatoid arthritis, (10) polymyalgia rheumatica, a systematic inflammatory disorder of the aged, (11) and sepsis. (12)

In respect to reproductive applications, many of Jefferies' observations with low-dosage cortisol replacement parallel my veterinary experience. Such observations include:

* Females who have difficulty conceiving also have a high incidence of miscarriages. When low-dosages of steroids are administered, and continued throughout the pregnancy to correct deficient steroid metabolism or a possible autoimmune disorder that interferes with conceiving, the incidence of miscarriages is no larger than that of women who have no difficulty conceiving.

* Excess estrogen can impair spermatogenesis. The estrogen can be brought down with small dosages of steroids, which then improves sperm count.

* Not only ovarian, but adrenal and thyroid function as well should be normal before conception can occur.

* When properly administered, safe physiologic dosages of cortisol replacement (with thyroid medication, if necessary) seem to be an effective treatment option for ovarian dysfunction and infertility.

Current treatment of fertility and miscarriage problems involves a variety of highly sophisticated and expensive methods. Exploring hormonal and immune imbalances caused by abnormal cortisol may yield new understanding and less expensive treatment options for reproductive failure, and should be comprehensively investigated.


1. Cutolo M. et al. Altered neuroendocrine immune (NEI) networks in rheumatology. Annals of the New York Academy of Sciences, June 2002, 966: xvii.

2. Plechner AJ. An effective veterinary model may offer therapeutic promise for human conditions: roles of cortisol and thyroid hormones. Medical Hypotheses. 2003, 60 (3): 309-314.

3. Plechner AJ. Chaos in the cortex: An unrecognized adrenal-immune disturbance in pets offers therapeutic insights for multiple human disorders. Townsend Letter for Doctors and Patients, April 2003; 58-61.

4. Plechner AJ. Treating unrecognized cortisol-based imbalances offers major healing benefits for multiple disorders. Journal of the American Holistic Veterinary Medical Association, 2004, 22 (4): 9-14.

5. Arafah BM. Increased need for thyroxine in women with hypothyroidism during estrogen therapy. New England Journal of Medicine, 2001, 344 (23): 1743-1749.

6. Gross HA, et al. Effect of biologically active steroids on thyroid function in man. Journal of Clinical Endocrinology and Metabolism, 1971, 33: 242-248.

7. Jefferies WMcK. Safe Uses of Cortisol. Springfield: Charles C. Thomas Publisher, 1996; 160, 181.

8. Primary immunodeficiency diseases. Clinical and Exp. Immunology, 1999, 118 (supplement 1): 17.

9. Jefferies W McK. Op. cit., 67-90.

10. Hickling P, et al. Joint destruction after glucocorticoids are withdrawn in early rheumatoid arthritis. British Journal of Rheumatology, 1998, 37: 930-936.

11. Cutolo M, et al. 2002. Cortisol, dehydroepiandrosterone sulfate, and androstenedione levels in patients with polymyalgia rheumatica during twelve months of glucocorticoid therapy. Annals of the New York Academy of Sciences, June 2002, 966: 91-96.

12. Klaitman V. Almog Y. Corticosteroids in sepsis: A new concept for an old drug. Israeli Medical Association Journal, 2003; 5 (1): 51-54.

by Alfred J. Plechner, DVM


Alfred J. Plechner, DVM

California Animal Hospital

1736 S. Sepulveda Blvd., Suite C

Los Angeles, California 90025 USA


Dr. Plechner's latest book, Pets at Risk, was published by NewSage Press ( in 2003.

COPYRIGHT 2004 The Townsend Letter Group
COPYRIGHT 2004 Gale Group

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