By Alfred J. Plechner, D.V.M.
It has still not been realized that the endocrine system regulates the immune system including the regulation of amounts of IgA.
The normal production of IgA is vital to the protection of all the organ systems in the body that include mucous membranes.
Of all the antibodies produced in the body, IgM, IgG, IgD and IgE, the IgA represent 75 % of the bodies total antibody production.
IGA is thought to be produced in two forms that are either secreted or found in serum.
The measurement of levels using a blood test appears to represent the production or lack production of both serum and secretory IgA.
Proper IgA production and regulation will provide protection for the digestive, respiratory, urinary, genital tracts and associated organs and other anatomical structures.
The regulation of IgA depends upon the control of the endocrine system.
What then is the endocrine control of IgA?
The endocrine system is made up of various organs that have their own production of various hormones.
The production of these various hormones will control the production and function of the immune system including the production of IgA.
The primary endocrine organs that are involved in immune regulation are the adrenal, thyroid and hypothalamus glands and their production of their hormones.
Certainly there are other hormones involved, but in my clinical studies in animals and people these three glands tend to be the main regulators of the immune system.
Obviously the pineal body and its hormone also modulate the HPA access.
Note: further information on the pineal body will be provided in my up and coming book, "Against the Odds, Given Up for Dead" and will be available on Amazon.com.
It is also apparent that hormonal imbalances can also affect other segments and other areas of the body like cellular production and general metabolism etc.
The middle and inner layers of the adrenal cortex and their feed back or lack of feedback to the pituitary gland provides most of the regulation of the immune system.
The middle layer adrenal cortex produces a hormone called cortisol.
As the cortisol carries out many of its functions including the regulation of the immune system, the liver slowly, in a 24 hour period breaks down the cortisol for the kidneys to excrete.
As the levels of regulatory cortisol decline, a signal is sent to the hypothalamic pituitary axis for the pituitary to release its hormone called ACTH.
When this occurs, the middle layer adrenal cortex responds with an increased production of cortisol.
During this time, the IgA and other antibody production remains normal as do the other functions of the components of the immune system which includes the B and T lymphocytes.
Unfortunately the weakest link in the endocrine control of the immune system including the IgA production is the middle layer adrenal cortex.
This is the layer that becomes the most easily damaged by stress, heavy metals, toxins, radiation, chemo therapy, alcohol, drugs, anesthesia, and possibly vaccines etc.
When this occurs, the cortisol production can be decreased or damaged and the negative feedback to the pituitary no longer functions normally.
It is important to note that even if the cortisol is in the normal range without comparing it to the total estrogen you cannot tell if the cortisol is functional!
The release of the pituitary hormone ACTH can no longer be controlled by the middle layer adrenal cortex due to the fact that the cortisol is decreased or defective.
The only other adrenal cortical layer that responds to ACTH is the inner layer adrenal cortex which produces estrogen and androgen.
This increased production of ACTH causes an increased production of estrogen and androgen.
The excess production of adrenal estrogen will bind the remaining decreased cortisol and bind the receptor sites for thyroid and make the thyroid hormones unavailable to the body even with normal production of T3 and T4 and normal amounts of free T3 and free T4.
Apparently the excess adrenal estrogen creates a reverse T3 that may block the receptor sites for T3.
This binding of the thyroid receptor sites reduces the metabolism in general and may cause the patient to gain weight.
If this weight occurs, in the fatty tissue of the patient, an enzyme resides and can increase its amounts as the patient gains fat.
This enzyme is called aromatase and has the ability to convert testosterone and androgen into estrogen which further adds to the amount of damaging total estrogen that is helping to cause more disease in the body.
The excess adrenal estrogen also will deregulate the function of the B and T lymphocyte so that they cannot carry out their normal function while also losing recognition of self tissue allowing the B and T lymphocytes make anti antibodies to the self tissue. This is referred to as autoimmunity.
At the same time, the elevated estrogen can cause a reduction in the production of IgA as well as a possible reduction of all the other antibodies.
Note: In animals when this occurs, all the measured immunoglobulins will low if the IGA is low, but in humans the IGA may be low while the other immunoglobulins remain normal or high. This may be due to different subgroups of B lymphocytes and a slightly different immune regulation.
When this syndrome occurs, creating a decrease in IgA etc, protection of the mucous membranes is now challenged and the disease impact area will often be determined by the genetics of the parents and their family.
You can now see why chronic disease can occur in all these different organ systems that depend on a normal IGA to protect them.
Once this syndrome has been identified but the IgA level has dropped below a certain point, often replacement hormones, nutrients, vitamins, homeopathics and herbs experience a decreased absorption rate through the intestinal tract, so that the high adrenal estrogen can continue.
Due to the fact that the elevated estrogen has bound the thyroid receptor sites, the liver metabolism decreases and the livers breakdown of the estrogen is slowed as is the kidneys excretion rate and as the adrenal estrogen levels increase, more damage may occur.
The increase in fat, due to the slowed metabolism will also cause an increase in aromatase and conversion of testosterone and androgen into more estrogen.
This is what I call the "estrogens vicious cycle".
It is also recognized, that elevated estrogen causes inflammation of the endothelial cells of all the arteries in the body and at this juncture of time in medicine, there is a great concern about the elevated estrogen causing many of the catastrophic diseases in people and animals like severe allergies, autoimmunity and cancer.
Some human researchers believe that the inflammation of the cerebral arteries may be an important cause of Alzheimer's disease.
In animals I have found that elevated total estrogen may cause anything from severe mental problems to epilepsy.
However, total estrogen is not yet being measured.
In females only ovarian estrogen is being measured.
These measurements only include estradiol, estriol and estrone and do not include adrenal estrogen.
In males only estradiol is being measured.
I an intact human female, it is very easy to determine the different amounts of estrogen being produced by the ovaries in comparison to that being produced by the inner layer adrenal cortex.
A total estrogen should be taken at the end of the first week of the menstrual cycle when the ovarian estrogen is the lowest and then again when ovulation occurs and the ovarian estrogen is the highest.
The difference is mainly from adrenal estrogen.
Obviously, plants containing natural estrogens should be avoided particularly during the period of time that the blood is drawn.
There is an available list of plants that contain natural estrogens for your consideration on my website at www.drplechner.com.
These tests can all be done with a serum sample from the patient.
The serum sample must be handled in a refrigerated state once spun down.
It is critical to keep the sample refrigerated and performed in a refrigerated state otherwise all the values of all the hormones and antibodies being checked, will elevated and in accurate.
My hope will be one day to have a temperature stick with each blood sample that will accompany the sample from the time it is drawn from the patient, until the time it arrives and is tested at the laboratory of destination.
With animals, I was able to create national values for all the hormones and antibodies tested for in this syndrome including cortisol, total estrogen, T3, T4 and IgA, IgM and IgG.
The normal values for any test should be the same for all laboratories but unfortunately at this time this is not the case.
These are just some of my thoughts.
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