Presentation on theme: "An unsuspected, underdiagnosed Endocrine Immune mechanism causing disease in animals and humans. PART I."— Presentation transcript:
An unsuspected, underdiagnosed Endocrine Immune mechanism causing disease in animals and humans. PART I
I have studied and treated as many as 50,000 endocrine-immune cases in dogs, cats and horses.
What I have found is underdiagnosed or perhaps unrecognized, or an unsuspected mechanism that creates disease.
These cases vary from simple allergies to autoimmunity and cancer.
It appears that a similar syndrome is found in humans called CVID (Common Variable Immunodeficiency).
CVID appears to vary from allergies to autoimmunity and cancer.
EI patients that I have treated all have (a).Deficient or bound cortisol (b).Elevated total estrogen (c).Deficient or bound T3T4 (d).Immunodeficient or immunoderegulation of B & T cells
Is there a first domino that falls allowing for EI Syndrome or possible CVID Syndrome?
In animals, the 1st domino to fall is Cortisol.
What causes this Zona Fasciculata failure? (a). Genetic damage (b). Acquired damage
This EI Syndrome can be diagnosed with blood tests in puppies, kittens & foals as early as 4 to 6 weeks of age!
The parents of the offspring can be tested and identified as the culprits before Breeding, enabling the prevention of EI Syndrome in the offspring.
Acquired damage to the Zona Fasciculata may occur due to toxicological sensitivity of this layer. (+/- environmental toxins, vaccines, anesthesia, ingested pharmaceuticals).
In animals, it is rare to see complete adrenal cortex damage! Usually it is the cortisol level that is affected either temporarily or permanently.
Quote Harvey on the toxicological sensitivity of the adrenals and particularly the cortex as an unappreciated factor. According to British toxicology expert Philip Harvey, in The Adrenals in Toxicity: Target Organ and Modulator of Toxicity, 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.
In personal communication, Harvey has told me that surveys of toxicity within the endocrine system indeed reveal that the adrenal cortex is a very common target and factors predisposing this are at its large blood supply per unit mass, Lipophilicity and it is also rich in cytochrome P450 enzymes.
Hans Selyes work on stress, recognized in General Adaptation Syndrome that chronic stress would cause adrenal exhaustion and lead to an EI Syndrome. I also published these findings in animals in 1978. In this published paper, I theorized that in the production from dopa to norepinephrine, cortisol appeared to be used as a catalyst.
Selye prescribed cortisol to help people, which was successful for a while, but then moved into an over adaptation phase which often recreated the original syndrome with the chronic stress it caused.
In Dogs with chronic stress, thyroid supplementation with cortisol for the EI Syndrome will be necessary for improvement. Without thyroid supplementation, the syndrome would improve temporarily but eventually return, due to cortisol replacement going from a physiological dose level into a pharmacological dose level, leading to over adaptation.
What is occurring with a defective zona fasciculata?
What then does excess estrogen do? (a).Acts like histamine – Therefore causing inflammation (b).Binds T3T4 (c).Binds cortisol (bound cortisol disallows transferance from T4 – T3 (d).Deregulates B + T Cells
REMEMBER, THE ENDOCRINE SYSTEM REGULATES THE IMMUNE SYSTEM IN ANIMALS. USUALLY THESE SYSTEMS DO NOT ACT INDEPENDENTLY.
If you find similarities between an EI Syndrome on CVID common variable syndrome, then your measuring stick is identifying factual B cell antibody levels and correcting them and the disease with proper hormone therapy. Remember, each patient will and should be different.
I had to create my own clinical norms for IgG, IgM & IgA. You will need to do this also.
The IgA level will determine if malabsorption is present and whether oral hormone replacement will effectively normalize the immune system.
T cell regulation usually accompanies B cell regulation.
Some of you here are familiar with the concept of low-dosage, long term cortisone. Others may be appalled by any thought of long-term cortisone.
Among us here is William Jefferies, M.D., who has pioneered for decades the practice of long-term, low-dosage cortisone replacement that is both safe and hugely effective for allergies, chronic fatigue, and rheumatoid conditions. Other physicians have started to realize as well that cortisone, at low dosage, can be a major long term therapy modality. At pharmacologic dosages, it is indeed immunosuppressive. However, at physiologic low- dosage level, in the presence of a cortisol deficiency, which I believe is extremely common among people because of a combination of genetic, toxicity, and prolonged stress, this great healing medicine.
Drs Barnes and Hertoghe Identified the importance of thyroid therapy in humans.
With my EI syndrome in animals, in particular dogs, I have found that proper thyroid supplementation will guarantee keeping cortisol supplementation at a physiological regulatory level and correct this EI Syndrome.
The next hour will discuss clinical testing and supplementation of the EI Syndrome.
An unsuspected, underdiagnosed Endocrine Immune mechanism causing disease in animals and humans. PART II
Phase 1 protocol – Blood MALE: Blood Cortisol TSH T3 T4 Total Estrogen Testosterone (total & free) IgA, IgM, IgG FEMALE: Blood Cortisol TSH T3 T4 Total Estrogen Progesterone Testosterone (total & free) Ferritin IgA, IgM, IgG
Phase 1 protocol – Urine MALE: 24 hour urine collection 1. Active Cortisol 2. Free T3 3. Free T4 FEMALE: 24 hour urine collection 1. Active Cortisol 2. Free T3 3. Free T4
Phase 1 protocol – Basal Metabolic Temperature MALE: Upon waking, place thermometer in axilla for 10 minutes before getting up. Normal temperature should be 97.8 – 98.2 degrees. FEMALE: Upon waking, place thermometer in axilla for 10 minutes before getting up. Normal temperature should be 97.8 – 98.2 degrees. Only accurate in a menstruating woman from 2nd to 4th day.
In my experience with dogs, I have found that a physiological dose level of cortisol may become a pharmacological dose level if used without thyroid supplementation.
If this fact is true, then what happens to any hormone supplementation? In canines and humans, that must be a concern about a pharmacological build up of a particular hormone causing various hormone cycles resulting in damage to our patients.
If with CVID – common variable immunodeficiency syndrome, how do you determine a normal immune measuring stick with the different laboratory normals that are now available?
I analyzed reference ranges from 15 major human medical labs. Many laboratories used the same lab kits for the immunoglobulin, yet there are wide discrepancies in what these laboratories regard as normal.
These are the variable ranges for normal ranges according to each to each laboratory:
IgG results from various human laboratories
IgM results from various human laboratories
IgA results from various human laboratories
Based upon these results, you definitely need an international standardized reference range on an international basis that you create!
By removing the high & low and possibly removing 10% of the lower and higher levels, your immune measuring stick may be closer to being accurate.
Obviously, as you normalize your patients, these values will be modified based on your clinical results.
This is merely an attempt to show you that depending on the variability of the lab test results your patient may be normal or highly abnormal, which would lead to improper therapy based upon inaccurate laboratory results.
My EI Syndrome and possibly your CVID Syndrome relates from simple allergies to all autoimmune disorders and all cancers in animals.
Finally, remember, in all animals with cancer, there is deficient or bound cortisol, elevated total estrogen, deficient transfer defect or bound T3T4 and deregulated B & T cells.
Fortunately, you and I practice for our patient first, and our profession second.