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Not common terminology but occasionally brought up at the veterinarians office, so I felt this was a good time to help with a distinction between these diseases. If you hear this at the doctor office, you will have a better understanding of their significance. Even though we don’t hear these terms very often, it is important to understand them as there is a direct relationship with Catastrophic Disease in our pets so of course you want to have at least a basic understanding with the connection of the terms.

Please keep in mind that the body produces 30-35 mg of “active” cortisol “naturally”, in the Adrenal Glands, on a daily basis so if you or your dog CANNOT produce this or what is being produced is bound or defective then there is a cortisol deficiency causing an imbalance which can cause major consequences. If you did not know, cortisol is a “steroid” and is also a hormone. My point here is that in this day and age there is a tremendous fear and bad reputation of steroids but in reality, it’s ABUSE and a misunderstanding of its importance and its use, that is the problem and it’s important that you understand that a certain amount of cortisol is produced naturally and is needed by the body and in essence, it’s all about BALANCE.

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The medical profession is treating the effects of Cancer and Auto-Immunity aggressively, and is making gains. However did you ever wonder what caused cancer and auto-immunity?

Every patient I have been involved with, whether dogs, cats, horses or people, all have an identifiable, hormonal antibody imbalance. Every one of these patients with either cancer or auto-immunity has an active cortisol imbalance and elevated adrenal estrogen, with ovarian estrogen, if the patient is still going through ovulation. The elevated estrogen level, not only blocks the available use of thyroid hormones, but deregulates the immune system, so that these cells not only do not protect the body, but lose recognition of self tissue and turn against the body’s own tissue.

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In the past few years, a new disease has been identified called Sudden Acquired Retinal Degeneration Syndrome (SARDS).

The disease manifests itself as a loss of vision which may be slow to occur, but because the patient has such a great ability to adapt, vision loss is usually unnoticed by the owner until the patient become almost completely blind.

For the most part, the veterinary profession believes there is no cure or control for SARDS.

Since this is a fairly new disease and early research is limited in its scope, there has been very little teaching about this disease done in schools of higher veterinary learning as of yet.

My own clinical studies, over the past 46 years, have allowed me to find a control and possible cure for SARDS.

SARDS, is an autoimmune disease that is caused by a measurable hormone imbalance and loss of control of the immune system.

The deregulated immune system not only lost its recognition of self-tissue in the eye, but also has lost its ability to create protective antibodies for the eyes.

This deregulation also allows for anti-antibody production against many other types of tissues in the body so the autoimmunity usually does not stop just with the eyes and without proper hormone antibody regulation of a SARDS patient, they will often develop allergies, autoimmunity and cancer.

So there is an urgency to get the SARDS controlled even if the sight does not return.

There is also an urgency to get a SARDS patient treated properly as soon as possible so some sight can be achieved before permanent retinal damage has occurred.

The blood test that will determine why SARDS has occurred is very simple to do, but the sample needs to be handled in a special manner and sent to the only veterinary laboratory that is doing this kind of work at this time.

All of this information is available at www.drplechner.com.

The blood test itself measures cortisol, total estrogen, T3, T4 and IgA, IgM and IgG.

What I have from found from blood test results with SARDS patients, is that the majority of them are producing large amounts of defective or bound cortisol which often are perceived by the veterinary profession as high level, active cortisol and therefore thought that the patient has Cushing Syndrome which SARDS patients normally do not have.

The high level, inactive cortisol is either defective or bound and not recognized by the pituitary gland and therefore is unable to fund the negative feedback between the cortisol producing middle layer of the adrenal cortex and the pituitary gland.

Therefore, the pituitary gland keeps releasing more of its hormone called ACTH in hopes of causing release of active cortisol which will not occur.

Instead, the inner layer adrenal cortex responds with a direct feedback to the pituitary gland and causes the production and release of elevated amounts of adrenal estrogen.

The elevated amounts of estrogen not only deregulates the immune system and allows for anti-antibodies to develop in this case against retinal tissue but also decreases the amount of protective antibody throughout the patient including the mucous membrane antibody that protects the eyes which is immunoglobulin A.

One other feature that the elevated adrenal estrogen causes is its ability to bind the receptor sites of the thyroid hormones.

This is the basic hormone antibody imbalance that causes the pathology that occurs with SARDS.

This imbalance may be genetic and or acquired.

The following are 3 SARDS case studies for your consideration.


The SARDS affected a 4 year old, spayed, miniature poodle which had a history of allergies including warts and sebaceous cysts.

After several visits to a number of different veterinarians, SARDS was finally diagnosed.

Upon examination, I suggested doing my endocrine immune blood test and here are the results.

TEST RESULTS                                            NORMAL LEVELS

Cortisol = 6.5 ug/dL                                   1 to 2.5 ug/dL

Total estrogen = 35.17 pg/ml                  30 to 35 pg/ml

T3 = 72 ug/dL                                              100 to 200 ug/dL

T4 = .95 ig/dL                                              2 to 4.5 ug/dL

IgA = 52 ug/dL                                            70 to 170 ug/dL

IgM = 80 ug/dL                                           100 to 200 ug/dL

IgG = 820 ug/dL                                          1000 to 2000 ug/dL


The elevated cortisol being defective or bound has caused the pituitary gland to over-stimulate the inner layer adrenal cortex and cause the elevated adrenal estrogen.

If the elevated cortisol were active like with Cushing Syndrome, the pituitary ACTH would be decreased and the total estrogen would be below 30 in a female and below 20 in a male which it is not.

The elevated estrogen is binding the thyroid receptor sites in combination with the thyroid gland itself producing decreased amounts of T3 and T4.

The elevated adrenal estrogen also has reduced the production of protective mucous membrane antibody in the gut and when the IgA level is below 58, oral steroids cannot be absorbed.

In this case, this patient will need 3 injections of a combination short and long acting steroid in the muscle at a 10 day interval.

Oral steroids can usually be given 10 days after the last injection.

Oral thyroid hormone needs to be given immediately twice daily upon receiving the test results.

The test can be repeated either at the time of the last injection to make sure the IgA has reached 58 and if not, one more injection may be needed or if the patient is doing well, then repeat the test 2 weeks after oral steroids have begun to determine if there needs to be any modification of those hormone supplements the patient is taking.

This was all done with this patient, and not only did the allergy subside but so did the SARDS and in this instance, the disease had not gone on too long and her sight did return.

All hormone antibody levels returned to normal with proper hormone supplementation and once the immunoglobulins (IgA, M and G) became normal, the protective function of the immune system followed.


This SARDS patient was an 8 years old, neutered male Pug with chronic mast cell tumors and feeling quite badly in general.

Upon testing, his blood test indicated the following;

TEST LEVELS                                                 NORMAL LEVELS

Cortisol = 4.2 ug/dL                                            1 to 2.5 ug/dL

Total estrogen = 25.20 ug/dL                           20 -25 pg/ml

T3 = 120 ug/dL                                                    100 -200 ug/dL

T4 = 2.4 ug/dL                                                     2 to 2.5 ug/dL

IgA = 57 ug/dL                                                     70 to 170 ug/dL

IgM = 81 ug/dL                                                    100 to 200 ug/dL

IgG = 901 ug/dL                                                   1000 to 2000 ug/dL


His blood test indicated a defective cortisol leading to high adrenal, estrogen deregulating his immune system.

His thyroid hormones were normal but bound by the high estrogen so he was put on a thyroid hormone twice daily.

Since his IgA was close to 58, he received only one injection of the combination steroid and began oral steroid 10 days later.

Unfortunately his SARDS has not been diagnosed for over a year and his sight never returned however his mast cell tumors did stop developing after the remaining tumors were removed.

All his hormone antibody levels returned to normal with proper hormone supplementation.


This was a SARDS case in a 6 years old, spayed female, miniature Dachshund.

Outside of her sight impairment, she had lost her appetite and did not want to go on walks on her favorite trails which she and her owner had done for the past 5 years.

Her test results are as follows;

TEST RESULTS                                              NORMAL LEVELS

Cortisol = 9.1 ug/dL                                           1 to 2.5 ug/dL

Total estrogen = 35.17 pg/ml                          30 to 35 pg/ml

T3 = 90 ug/dL                                                      100 to 200 ug/dL

T4 =1.50 ug/dL                                                    2 to 4.5 ug/dL

IgA = 54 ug/dL                                                     70 to 170 ug/dL

IgM = 80 ug/dL                                                    100 to 200 ug/dL

IgG = 910 ug/dL                                                   1000 to 2000 ug/dL


With an IgA of 54, she needed only 2 injections of the steroid combination, and then oral steroids 10 days after her last injection.

Thyroid hormone began immediately, twice daily.

She is back again hiking on her trails and not only feels well again but has gained some peripheral vision.

All her hormone antibody levels had returned to normal on proper hormone supplementation.

Each case may be different, but they all seem to have this basic endocrine immune imbalance with a damaged or bound cortisol.

Note: Both humans and our animals produce 30 to 35 units of natural, active cortisol everyday of their lives if we are to remain healthy.

Please realize that once this basic mechanism has been identified for a patient, other forms of natural therapy can be tried as long as the therapy works quickly to try to avoid permanent, retinal damage.

Please also remember, by trying to enhance the production of cortisol through natural supplements may only increase the amount of defective or bound cortisol and make the SARDS worse.

Just remember, if you are told there is no treatment for SARDS, you now know there is a treatment.

Because its cause has never been found before, does not mean its cause does not exist.

I believe that the world will find one day, that the secret to good health in both animals and people will come from a normal ratio between active cortisol and total estrogen and the subsequent regulation of the immune system.

These are only my thoughts, and I do hope they will help.


Dr. AL Plechner


For more information, Michael can be reached @ Michael@HealthyPetNetwork.org . Please visit the main site @ www.healthypetnetwork.org or through their informational blog @ www.healthypetnetwork.net

Ball-and-stick model of the cortisol (hydrocor...
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This is a common syndrome in animals and people that has never been diagnosed before.

This syndrome involves the production of a deficient or defective cortisol from the middle layer of the adrenal cortex, with the pituitary gland producing ACTH to insure the production of more active cortisol.

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When I first graduated from the veterinary school at the University of California at Davis, I became aware that many of the animals I was seeing appeared to have some sort of allergies, ranging from skin problems to bowel problems etc.

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