An innovative cancer therapy that saves animals can it help humans as well? - Cortisol Imbalances

Townsend Letter for Doctors and Patients, Feb-March, 2004 by Alfred J. Plechner

Introduction

Cancer is not just a people killer. Dogs develop the disease at about the same rate as humans and it accounts for almost half of canine deaths over the age of ten years. Felines have a lower incidence but tumors tend to be more malignant.

Cancer has many causes. In my clinical practice I have identified a common, yet unrecognized endocrine immune disturbance that acts as an "enabling mechanism" for multiple diseases, including cancer. I reported on this mechanism--"Chaos in the Cortex"--in the April 2003 issue of Townsend Letter. During the last 30 years I have routinely tested many thousands of sick patients for endocrine-immune imbalances and found a similar pattern of disturbance in each and every case of cancer. The imbalances originate with defective, excessively bound, or otherwise deficient cortisol. Cortisol is an essential adrenal hormone with a paramount regulatory influence over immune and inflammatory activity in the body.

I have found that a cortisol defect triggers a domino effect of problems, among them a profound destabilization of the immune system. The system loses its ability to prevent abnormally mutating weak cancer cells from growing rapidly. In one animal the proliferation of cells may develop into a skin tumor such as squamous cell in the jaw or mouth. In another, mammary cancer, lymphoma, fibrous sarcoma, or leukemia may develop. The impact area varies from animal to animal, however these are the same cancers that occur in people.

I have successfully treated many cases by addressing this cortisol defect, in my opinion a major causal factor. I have corrected imbalances in very young dogs from families in which cancer has already killed littermates. These "corrected" animals have gone on to live healthy lives for as long as they were maintained on a cortisol replacement program. Some may have developed cancer at eleven, twelve, or thirteen years of age, or some not at all. Similarly, I have been able to save patients considered terminal and given little time to live. In many such advanced cases, the cortisol replacement program I developed has often worked to extend the lives of otherwise doomed animals.

Cortisol-based endocrine-immune imbalances represent a major unsuspected cause of cancer in pets. I believe that such imbalances may be significantly involved in human cancer as well. Exploring the cortisol connection may offer profound insights not only for veterinarians but for physicians who face the challenging task of helping cancer patients.

The nature of cortisol imbalances

The typical endocrine-immune imbalances I see in cancer patients start with a deficit of cortisol and subsequently involve elevated total estrogen, impaired thyroid (T3/T4) function, and low IgA, IgG, and IgM levels.

Cortisol, a steroid hormone, is produced from cholesterol through an enzymatic process in the middle layer of the adrenal cortex--the zona fasciculata. Hormones secreted by the hypothalamus and pituitary in the brain govern this activity.

Much has been written about the immunosuppressive properties of elevated cortisol and powerful cortisone drugs, but little about defective/bound/deficient cortisol that can lead to an unresponsive immune system. A normal level of cortisol appears necessary for proper immune and inflammatory responses (see Fig. 1). At a basal level this hormone regulates molecular mediators that turn on or turn off activity related to immunity and inflammation.

A lack of active cortisol disturbs the hypothalamus-pituitary-adrenal feedback loop (see Fig. 2) that governs cortisol production. To increase a lesser cortisol level, the pituitary steps up adrenocorticotropic hormone (ACTH) secretion. This hormone stimulates cortisol release.

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However, when the adrenal cortex is unable to produce enough cortisol, or for some reason the cortisol is bound, or otherwise inactive, and thus not recognized by the system, the pituitary continues to produce ACTH in order to extract more cortisol.

One consistent consequence of this activity that I have not seen reported elsewhere is the generation of a physiologically significant increase of estrogen compounds into the system. The added endogenous estrogen may come from ACTH-stimulated androgens, produced by the inner layer of the cortex (zona reticularis), which convert in part to estrogens in peripheral tissue, (1) or from "interface" cortical tissue that may directly secrete estrogen compounds. (2) (3) I routinely measure elevated estrogen in all animals with the endocrine-immune disturbance-male and female, intact or neutered-and thus the excess cannot be attributed to ovarian activity. It is possible, however, that environmental estrogenic compounds in industrial chemicals and in food (such as soybeans) contribute to increased estrogen as well.

Elevated estrogen disturbs the immune system in a number of ways, including interference with the thymus gland, (4) and has been implicated in the initiation of autoimmune processes. (5) Moreover, too much estrogen in the system may impair the synthesis of cortisol (6) as well as bind active cortisol, thus further exacerbating a cortisol abnormality. It is interesting to note that researchers have discovered that phytoestrogens (estrogen compounds) in tofu and soy-based food decrease cortisol production and increase androgens, some of which convert to estrogen and raise the total estrogen level in the body. (7) When considered together, these factors indicate a vicious cycle of destabilizing cortisol-estrogen interactions.