Canine skin cancer

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.

Medical science regards the hypothalamic-pituitary-adrenal axis, which is part of the neuroendocrine system, as exerting a primary influence on immune function, (8) however researchers are still in the dark about much of the countless details and interactions. My clinical impression over the years has been that cortisol and estrogen have an intimate relationship that affects the homeostasis of the neuroendocrine system. If the relationship goes awry, as it obviously has in the animals I test and treat, the immune system becomes deregulated and disease protection is lost.

The combination of deficient cortisol and excess estrogen not only destabilizes the immune system but also has considerable potential to interfere with thyroid function and cause a slowdown of the metabolic rate. Cortisol-estrogen imbalances can impact thyroid function by binding thyroid hormones, decreasing transference of T4 to T3, and impairing cellular uptake of T3. (9-11)

In the common endocrine-immune derangement I have identified there appears to be no discernible involvement of the outer adrenal cortical layer (the zona glomerulosa), where aldosterone is manufactured. This hormone helps maintain blood pressure and water and salt balance in the body. In Addison's Disease, a rare condition that affected President Kennedy, there is both a deficiency of cortisol and aldosterone.

From my perspective, several primary factors appear to cause the cortisol deficit I see in animals:

1. Genetics. Pets are predominantly inbred to attain a structure and appearance based on human notions of cosmetic perfection. Many animals, and particularly dogs, are no longer bred for function and work, such as hunting, herding, tracking, and retrieving. This has caused a harmful narrowing of gene pools along with major health problems.

Most popular dog breeds have been bred almost exclusively "to look good," Time reported in a 1994 cover article, and this "obsessive focus on show-ring looks is crippling, sometimes fatally, America's purebred dogs." (12) Time noted that that there are more than 300 different genetic disorders that may subject animals to enormous pain and suffering. "The astonishing thing," the magazine article reports, "is that despite the scope of these diseases, veterinary researchers know next to nothing about what causes them or how to cure them."

The cortisol-based endocrine-immune disorder I have identified in pets may be largely the result of such breeding practices. However, this and other genetic problems are not limited to purebreds. Mating between animals of different breeds has thoroughly spread genetic defects throughout the dog and cat world. Today, genetic defects are widely established among all breeds--pure or mixed.

Many veterinarians are concerned about a sharp rise in cancer among younger animals. I treat dogs and cats with cancer as young as one or two years of age, something I never encountered when I started practicing in 1966. This phenomenon is probably related to the proliferation and intensification of genetic defects that include endocrine-immune imbalances.