The Endocrine Research Project
Link to article about the TSH test
Link to article about an alternative treatment for Anorexia Nervosa
Link to article about an effective treatment for SARS and influenza
Welcome to our web pages.
Purpose
The Endocrine Research Project was established to explore better ways to diagnose and treat endocrine diseases. Currently, our focus is on thyroid and cortisol deficiency.
This article is an analysis of the TSH test's diagnostic effectiveness and recommendation for the best method for diagnosing hypothyroidism:
Should the TSH Test be Utilized in the Diagnostic Confirmation of Suspected Hypothyroidism?
Rand Wheatland
Summary Hypothyroidism is an insidious disease that manifests a great number of non-specific symptoms. The prompt, accurate diagnosis of hypothyroidism will improve the quality of life for patients while controlling healthcare costs. Therefore, it is crucial that the protocol for diagnosing hypothyroidism has been properly evaluated. Its methods must be the best available to ensure that the resulting diagnoses will be as reliable as possible. When a patient presents with signs and symptoms of hypothyroidism and a medical history indicating hypothyroidism, a TSH test result is frequently utilized to assist in the diagnostic confirmation of hypothyroidism. In these circumstances, not only is performing the TSH test a waste of resources, utilizing the result will lead to a decrease in diagnostic certainty. The TSH test should not be utilized in the diagnostic confirmation of hypothyroidism because the diagnostic accuracy of the TSH test in confirming hypothyroidism is unknown, several aspects of the TSH test indicate its poor diagnostic utility and thyroid hormone trial therapy is the best method for achieving diagnostic certainty. Diagnostic confirmation of suspected hypothyroidism should be accomplished by evaluating the patient's response to a trial administration of thyroid hormone supplements. If the patient's chronic symptoms are relieved soon after beginning thyroid hormone supplements, it is very likely that the treatment is compensating for hypothyroidism. (Med Hypotheses 2010;75(5):458-63)
[Link to HTML Full Text] [Link to PDF Full Text] [Link to Abstract on PubMed]
Our first publication concerns unrecognized cortisol deficiency in people suffering from anorexia nervosa and its effective treatment:
R. Wheatland
Summary Endocrinological factors underlying the etiology of anorexia nervosa are relevant to its treatment. It appears that sufferers of anorexia nervosa perform their weight-limiting behaviors in an attempt to compensate for adrenocortical insufficiency. Hypoglycemia stimulates the secretion of cortisol. In response to severe malnutrition, blood cortisol levels also rise due to increased cortisol half-life and a decrease in its metabolic clearance rate. If an adrenocortical-insufficient individual goes on a severe diet, one effect will be a significant increase in their blood cortisol levels, which will alleviate their adrenocortical insufficiency and its symptoms. This response is a powerful positive reinforcement for continuing their weight-limiting behaviors. Sufferers of anorexia nervosa commonly exhibit two other behaviors that can raise their cortisol levels: excessive exercise and self injury. Treatment of the underlying adrenocortical insufficiency with cortisol supplements has been shown to be effective in five previously published cases of diagnosed anorexia nervosa. (Med Hypotheses 2002;59(6):710-5)
This article describes how the influenza virus and SARS evade the immune system and induce symptoms, which accounts for the effectiveness of treating these infections with corticosteroids:
Molecular mimicry of ACTH in SARS - implications for corticosteroid treatment and prophylaxis
R. Wheatland
Summary For a virus to survive and replicate in an organism, it must employ strategies to evade and misdirect the host's immune response. There is compelling evidence that the primary immunoevasive strategy utilized by the SARS virus, like influenza, is to inhibit its host's corticosteroid stress response. This is accomplished by viral expression of amino acid sequences that are molecular mimics of the host's adrenocorticotropin hormone (ACTH). When the host produces antibodies against these viral antigens, the antibodies also bind to the host's own ACTH, which limits the host's stress response by interfering with ACTH's ability to stimulate the secretion of corticosteroids. This inadequate corticosteroid response provokes symptoms as a result of a relative adrenocortical insufficiency. Treatment with corticosteroids can relieve the patient's symptoms of adrenocortical insufficiency and give them the corticosteroid levels needed to fight their infection. Similarly, by taking moderate daily doses of corticosteroids as a prophylactic, it may be possible to avoid clinical infection with SARS. If SARS's ACTH mimic strategy never has an opportunity to get started, SARS's ability to evade its host's immune system while its viral load is low will be significantly impaired. In this article, amino acid sequences from the SARS and influenza viruses representing likely homology to human ACTH are identified. Evidence demonstrating that ACTH autoantibodies are produced during influenza infection is also presented. Early treatment with corticosteroids should lower the dose necessary to counteract SARS's ACTH autoantibody mechanism. If corticosteroid treatment is delayed until inflammatory cytokine levels are causing serious injury, only high doses of corticosteroids are likely to be effective. (Med Hypotheses 2004;63(5):855-62)