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From the Townsend Letter
December 2008


Letter from the Publisher
by Jonathan Collin, MD

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Hans Selye
The unfolding financial debacle on Wall Street and Main Street is unwittingly subjecting the population en masse to a physiological stress experiment. We need look no further than at the work of Canadian endocrinologist Hans Selye to understand the biologic response most humans are now experiencing. Selye's work, done primarily at the University of Montreal from the 1940s through the 1970s, focused on the reaction of the body to stress. His theory of general adaptation syndrome (GAS) was based on observing the nearly uniform changes that occurred in mice after exposure to poisonous chemicals and agents. Selye published over 1700 research articles and authored 15 monographs and seven books. One article, a classic paper originally published in Nature in 1936, described the adaptation syndrome and the response of the organism to chronic unrelieved stress.1 That paper, "A Syndrome Produced by Diverse Nocuous Agents," characterized the reaction to stress, which develops in three stages, in the following way: an initial physiologic reaction to the stress, the homeostatic adaptation to ongoing stress, and, finally, the exhaustive reaction to persistent, unrelieved stress. The three phases observed by Selye and his co-workers in numerous experiments remain a cornerstone of understanding adrenal physiology.

Selye's work found that regardless of the stress, be it chemical or physical, biologic or psychological, the stress reaction always had an initial emergency response, then general adaptation, and, finally, exhaustion ultimately leading to organ failure. The description by Selye in 1936 of these three phases deserves being retold in 2008:

This syndrome develops in three stages: during the first stage, 6-48 hours after the initial injury, one observes rapid decrease in size of the thymus, spleen, lymph glands, and liver; disappearance of fat tissue; edema formation, especially in the thymus and loose retroperitoneal connective tissue; accumulation of pleural and peritoneal transudate; loss of muscular tone; fall of body temperature; formation of acute erosions in the digestive tract, particularly in the stomach, small intestine, and appendix; loss of cortical lipoids and chromaffin substances from the adrenals; and sometimes hyperemia of the skin, exophthalmos, [and] increased lachrymation and salivation. In particularly severe cases, focal necrosis of the liver and dense clouding of the crystalline lens are observed.

In the second stage, beginning 48 hours after the injury, the adrenals are greatly enlarged but regain their lipoid granules, while the medullary chromaffin cells show vacuolization; the edema begins to disappear, numerous basophiles appear in the pituitary; the thyroid shows a tendency towards hyperplasia (more marked in the guinea pig); general body growth ceases, and the gonads become atrophic; in lactating animals, milk secretion stops. It would seem that the anterior pituitary ceases production of growth and gonadotrophic hormones and prolactin in favor of increased elaboration of thyrotrophic and adrenotrophic principles, which may be regarded as more urgently needed in such emergencies.

If the treatment [noxious agent] be continued with relatively small doses of the drug or relatively slight injuries, the animals will build up such resistance that in the later part of the second stage the appearance and function of their organs returns practically to normal; but with further continued treatment, after a period of one to three months (depending on the severity of the damaging agent), the animals lose their resistance and succumb with symptoms similar to those seen in the first stage; this phase of exhaustion being regarded as the third stage of the syndrome.1

Selye's monographs display photographs of the gross anatomy of the adrenal glands in each of the three phases of the syndrome. In the first stage, the initial insult, the adrenal gland appears almost the same as in a non-stressed stage, but there are minor changes in size and coloration. In the second stage, with persistent stress, the adrenal balloons in size dramatically, but the enlargement is tissue hyperplasia (enlargement), not edema. The final stage of chronic exhaustion due to unrelenting stress is, perhaps, most eye-opening. The adrenal gland has lost all of its tone, shrunken to nearly half the size of its normal state, and appears to be non-functioning. The monograph photographs demonstrate this same series of events in animals of differing species and with predictable outcomes based on exposure to ongoing stress. When one beholds the photographs of Selye's animal experiments, there are no doubts that his work is correct; the tag line at the conclusion of most papers that additional research is needed would be inappropriate here.

The financial crises and natural disasters unfolding in 2008 portend very serious risk to every individual. Whether the individual's adrenal response is benign and adapts well or is pathologic and deteriorates progressively depends on the resiliency of each individual's adrenal system. As practitioners, we need to understand Selye's model to be able to prevent stress adaptation from becoming adrenal exhaustion.

Roger J. Williams
Around the same time period that Selye conducted his first experiments with stress, a chemist named Roger Williams was initiating his own experimentation with stress. Williams noticed that organisms deprived of certain nutritional factors were unable to tolerate stress as well as nourished organisms. These observations led to Williams' discovery of the B-vitamin pantothenic acid. Like thiamine's relationship to beriberi and niacin's relationship to pellagra, pantothenic acid deficiency caused a nutritional deficiency state. Roger Williams characterized human pantothenic acid deficiency as an unrecognized medical condition:

According to the broader view of nutrition, the following are among the effects of nutritional deficiency [of pantothenic acid]: (1) decreased growth of young; (2) decreased reproductive ability; (3) decreased length of life; (4) decreased stamina; (5) decreased vigor as evidenced by loss of physical activity and playfulness; (6) decreased food efficiency; (7) impaired appetite; (8) impaired "body wisdom" with respect to food choices (deficient animals consume by choice more sugar and more alcohol then well nourished animals); (9) loss of learning ability; (10) loss of memory, and probably many other losses. None of the above effects is associated with any easily recognized lesions in any specific tissue; yet every one may be important in the realm of health and well-being. The incidence of such human nutritional impairments may be high.2

Roger Williams' nutritional work led to his study of alcoholism. When animals were subject to persistent stress and were fed a chow deprived in pantothenic acid, most animals opted to drink the water diluted with alcohol rather than drink plain water. Similar results were noted with other induced vitamin-deficiency states. However, Williams' studies argued strongly against the psychological theories that alcohol consumption stemmed from habit and behavioral conditioning. The fact that B-vitamins could play a role in modifying the adaptive response to stress was a fundamental tenet in Williams' approach to health and disease prevention. He developed the theory of biochemical individuality, which held that individual organisms may share nutritional requirements, but the extent of nutritional need would vary depending on general health, genetics, nutritional status, and level of stress. Williams would strive to prevent the development of adrenal exhaustion by supplying higher level of nutrients, such as pantothenic acid. In the 1960s, Williams collaborated with associates to form the Clayton Foundation in the Department of Chemistry at the University of Texas at Austin. In 1966, Williams authored a short history of the collaborative efforts of the investigators at the Clayton Foundation. The paper provides a bibliography of seven hundred studies examining the effects of B-vitamins and other nutritional factors on physiology. Williams' work provides the basis for much of the mega-vitamin treatment employed in orthomolecular and nutritional medicine. That conventional medicine disagrees with the use of mega-vitamin therapy is evidence that Williams' work has gone largely unrecognized.

1. Selye H. A syndrome produced by diverse nocuous agents. Nature. 138: July 4, 1936.
2. Williams RJ. The Clayton Foundation Biochemical Institute: A Short History. University of Texas at Austin. 1966. Available at: http://bioinst.cm.utexas.edu/williams/CFBI%20Short%History.htm.

Nenah Sylver on Hypothyroidism
One of the more gratifying aspects of practicing medicine is the successful treatment of a previously untreated hypothyroid patient. The treatment of hypothyroidism is surprisingly easy – a tablet of dessicated thyroid hormone or synthetic thyroxine is typically the only treatment needed to reverse this disorder. The problem with hypothyroidism treatment is not determining the therapy but establishing the diagnosis. Most patients who need thyroid treatment do not have abnormal serum thyroid hormone studies, but their clinical picture fits the profile of underactive thyroid functioning. Whereas conventional endocrinology draws a line in the sand and permits the diagnosis of hypothyroidism only when the patient has a lab test abnormality confirming the disorder, most alternative practitioners and naturopaths accept the diagnosis of hypothyroidism without such a lab test.

Nenah Sylver examines hypothyroidism in this issue of the Townsend Letter. Her article is based on the best-selling book Hypothyroidism: Type 2 by Mark Starr, MD. Starr differentiates between Type 1 hypothyroidism, which is the classic disorder diagnosed with serum thyroid testing, and Type 2 hypothyroidism, which cannot be diagnosed with blood or urine testing. Sylver outlines the theoretical differences of Type 1 and Type 2 hypothyroidism and devotes the bulk of the article to understanding Type 2 disorder. Sylver's review of hypothyroidism reminds us that this disorder may be involved in a great many differing medical pathologies and conditions. The article emphasizes the fact that the treatment of undiagnosed hypothyroidism may offer clinical support, if not symptom resolution, to a diverse group of conditions from fatigue and depression to atherosclerosis and possibly cancer. Sylver's article also provides a number of "before" and "after" photographs; it is difficult to recognize the same individual after thyroid treatment has been administered.

Alfred Plechner on Adrenal Dysfunction
Veterinarian Alfred Plechner has been a vocal proponent of the under-diagnosis of hypoadrenalism and hypothyroidism in animals. He has observed that reproductive failure in dogs, cats, horses, and other animals is frequently the direct result of insufficient thyroid and adrenal hormones. Plechner has observed that excess estrogen aggravates the deficiency of thyroid and adrenal hormones and interferes with the fertilization process. Moreover, Plechner has observed that deficiency of thyroid and adrenal hormones as observed on blood studies is often accompanied by excess estrogen and decreased immunoglobulins, especially IgA.

Beyond the obvious implications in treating unfertile animals as well as dogs and cats debilitated by aging and fatigue, Plechner makes the case that humans suffer the same age-related hormone deficiencies. Plechner cites the work of William Jeffries, MD, who used low-dose cortisol to support fatigue, allergies, and inflammatory disorders. Plechner writes in this issue that his use of low-dose cortisol in animals has not led to serious adverse effects typical of high-dose, long-term steroid therapy.

Also please take a look at Dr. Majid Ali's report on the use of hormones in treating adrenal dysfunctioning. Ali's work focuses on the important relationship between hormone levels and oxygen utilization in adrenal disorders.

Jonathan Collin, MD

 

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