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

Link to article that explains how chronic fatigue syndrome, anorexia nervosa and major depression result from ACTH autoantibodies

Link to article about an effective influenza treatment

Link to article about viral carriers

Welcome to our web pages.


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:

Alternative Treatment Considerations in Anorexia Nervosa

R. Wheatland

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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)

[Link to Full Text] [Link to Abstract on PubMed]

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)

[Link to Full Text] [Link to Abstract on PubMed]

This article describes how chronic fatigue syndrome, anorexia nervosa and major depression are the result of chronic ACTH autoantibodies and can be effectively treated with corticosteroids:

Chronic ACTH Autoantibodies are a Significant Pathological Factor in the Disruption of the Hypothalamic-Pituitary-Adrenal Axis in Chronic Fatigue Syndrome, Anorexia Nervosa and Major Depression

R. Wheatland

Summary Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is a commonly recognized feature of many pathological conditions. Abnormal adrenal responses to experimental manipulation have been well documented in patients suffering from chronic fatigue syndrome, anorexia nervosa and major depression. Yet no defect of any single organ, gland or brain region has been identified as a cause of these abnormalities. The disruption of the HPA axis that occurs in these conditions can be understood if an interfering factor is present in these patients. Evidence indicates that this interfering factor is adrenocorticotropin hormone (ACTH) autoantibodies. Chronic high levels of ACTH autoantibodies will significantly disrupt the HPA axis and force the body to compensate for an impaired cortisol response. The resulting effect of chronic ACTH autoantibody interference is the manifestation of adrenocortical insufficient symptoms and psychological disturbances. Some symptoms of chronic fatigue syndrome, anorexia nervosa and major depression, such as anxiety, are the adverse effects of mechanisms compensating for less effective ACTH due to autoantibodies. Furthermore, these patients engage in extraordinary behaviors, such as self-injury, to increase their cortisol levels. When this compensation is inadequate, symptoms of adrenocortical insufficiency appear. Corticosteroid supplements have been demonstrated to be an effective treatment for chronic fatigue syndrome, anorexia nervosa and major depression. It allows the patients to have the corticosteroids they require for daily functioning and daily stressors. This therapy will relieve the patients of their symptoms of adrenocortical insufficiency and permit their cortisol-stimulating mechanisms to operate at levels that will not cause pathological problems. (Med Hypotheses 2005;65(2):287-95)

[Link to Full Text] [Link to Abstract on PubMed]

This article describes why corticosteroids should be used to treat influenza and other viral infections:

Effective Influenza Treatment

R. Wheatland

Summary An effective treatment is the best response to an infectious epidemic. Currently, for influenza and many other viral infections, corticosteroids are the best treatment. In fact, corticosteroids have been used successfully in the treatment of influenza for over 50 years. The reason that corticosteroids are such an effective treatment is that they directly relieve the symptoms caused by influenza. But most importantly, corticosteroid therapy does not just reduce a patient's suffering, corticosteroids keep patients alive. Corticosteroid treatment has been shown to be an effective therapy for influenza and other viral infections. Includes excerpts of medical journal articles describing the good results attained by using corticosteroids in the treatment of viral respiratory illnesses.

[Link to Full Text]

This article describes how viruses set themselves up in hosts to be carried:

Viral Carrier Status is Instilled by Viral Regulatory Particles

Rand Wheatland

Summary Human viral carriers are important agents in the periodic resurgence of many pathogens. Instillation of virus in human carriers explains several of the unusual epidemiological features of viral epidemics, such as where viruses linger between epidemics and how epidemics can arise without an apparent source. By inactivating itself, a virus can easily reside in a host for months or years without being noticed by the immune system, enabling the virus to be dispersed inconspicuously in the future and into new regions. When this silent activity of human carriers is appreciated, it is easier to understand the dynamics of viral epidemics, such as the explosive appearance of influenza epidemics.

During viral illnesses, virus in infected cells is put into a latent state by regulatory sequences delivered by particles produced by other virus-infected cells. These regulatory particles are similar to the virus’s virion but contain specific subsets of the viral genome and cannot replicate in cells that are not infected by the complete viral genome. Regulatory particles have previously been referred to as defective interfering particles, noninfective viruses, inactive viruses, incomplete viruses, satellite viruses, and defective viruses.

There are still many unanswered questions regarding viral carrier creation and the role human carriers play in the pathology and epidemiology of viral diseases. Some of these questions are presented and discussed in relation to regulatory particles, possible investigations and how carrier status may affect the health of the carrier.

Viral regulatory particles limit the extent of viral infections and shift the active infection to a latent infection. Just as multicellular creatures use hormones as chemical messengers to coordinate cellular functions, viruses utilize regulatory particles to coordinate viral modes among infected cells within a host. Many viruses depend on these particles for their continued existence. If we wish to comprehend and effectively treat viral infections, we must secure a thorough understanding of viral regulatory particles. (Med Hypotheses 2010;74(4):688-91)

[Link to Full Text] [Link to Abstract on PubMed]

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Last changed: 09/28/2010, 15:17:10