The Endocrine Research Project
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.
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)