Wednesday, September 30, 2015

ROLE OF HOMEOPATHIC MEDICINES IN ALTERING REVERSET3 DOMINANCE [ ongoing research

Research methodology a new perspective -2 [ second part of the NOTE posted in 2011]

ROLE OF HOMEOPATHIC MEDICINES IN ALTERING REVERSET3 DOMINANCE [ ongoing research]

[copyright 2015 Serenity Global Homeopathy - SGH All rights reserved ]


Introduction & Background
Thyroxin (T4) and triiodothyronine (T3), together referred to as thyroid hormones, play an important role in
basal metabolism and the functioning of almost all tissues and systems in the body.
Untreated hypothyroidism can lead to increased body weight, cognitive dysfunction, fatigue, abnormal serum
Lipids, coronary heart disease, and for women recurrent miscarriage, infertility, and possibly delayed cognitive development
in their children. This is not a research paper to be published .But an article to substantiate the relevance of extensive research in autoimmune thyroiditis illustrating my clinical findings and ongoing research details.

 Hashimoto’s thyroiditis:
Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes, causing primary hypothyroidism. It was the first disease to be recognized as an autoimmune disease. It was first described by the Japanese specialist Hakaru Hashimoto in a paper published in Germany in 1912.There are many symptoms that are attributed to Hashimoto's thyroiditis or Hashimoto's disease.
       The most common symptoms include the following: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy.
          Hashimoto’s disease is about seven times more common in women than in men. Hashimoto disease is a common thyroid gland disorder. It can occur at any age, but is most often seen in middle-aged women. It is caused by a reaction of the immune system against the thyroid gland. The disease begins slowly. It may take months or even years for the condition to be detected. Chronic thyroiditis is most common in women and in people with a family history of thyroid disease.
         In rare cases, Hashimoto disease may be related to other hormone problems caused by the immune system. This condition can occur with adrenal insufficiency and type 1 diabetes. In these cases, the condition is called type 2 polyglandular autoimmune syndrome (PGA II).Less commonly, Hashimoto disease occurs as part of a condition called type 1 polyglandular autoimmune syndrome (PGA I), along with:
Adrenal insufficiency (poor function of the adrenal glands)
Fungal infections of the mouth and nails
Hypo parathyroidism (under active parathyroid gland)
·                                  

Risk factors

A family history of thyroid disorders is common, with the HLA-DR5 gene most strongly implicated conferring a relative risk of 3 in the UK. In addition Hashimoto's thyroiditis may be associated with CTLA-4 (Cytotoxic T-lymphocyte Antigen-4) gene polymorphisms that result in reduced functioning of the gene's products, which are associated with negative regulation of T-lymphocyte activity.

Pathophysiology

There are multiple suggested mechanisms by which the pathology of Hashimoto's thyroiditis develops.
Various auto antibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors.  Antibody-dependent cell-mediated cytotoxicity is a substantial factor behind the apoptotic fall-out of Hashimoto's thyroiditis.
           Activation of cytotoxic T-lymphocytes (CD8+ T-cells) in response to cell-mediated immune response affected by helper T-lymphocytes (CD4+ T-cells) is central to thyrocyte destruction. As is characteristic of type IV hypersensitivities, recruitment of macrophages is another effect of the helper T-lymphocyte activation, with Th1 axis lymphocytes producing inflammatory cytokines within thyroid tissue to further macrophage activation and migration into the thyroid gland for direct effect.
            Gross morphological changes within the thyroid are seen in the general enlargement which is far more locally nodular and irregular than more diffuse patterns (such as that of hyperthyroidism). While the capsule is intact and the gland itself is still distinct from surrounding tissue, microscopic examination can provide a more revealing indication of the level of damage.
Histologically, the hypersensitivity is seen as diffuse parenchymal infiltration by lymphocytes, particularly plasma B-cells, which can often be seen as secondary lymphoid follicles (germinal centers, not to be confused with the normally present colloid-filled follicles that constitute the thyroid). Atrophy of the colloid bodies is lined by Hürthle cells, cells with intensely eosinophilic, granular cytoplasm, a metaplasia from the normal cuboidal cells that constitute the lining of the thyroid follicles. Severe thyroid atrophy presents often with denser fibrotic bands of collagen that remains within the confines of the thyroid capsule.
Diagnosis

Diagnosis is usually made by detecting elevated levels of anti-thyroid peroxidase antibodies in the serum.

Testing for thyroid-stimulating hormone (TSH), free T3, free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies can help obtain an accurate diagnosis.

Reference of this section
  • medlineplus

  • wikipedia----

LITERATURE REVIEW – on role of stress as a trigger of thyroid autoimmunity

Stress as a trigger of autoimmune disease.

Author information

Abstract

The etiology of autoimmune diseases is multifactorial: genetic, environmental, hormonal, and immunological factors are all considered important in their development. Nevertheless, the onset of at least 50% of autoimmune disorders has been attributed to "unknown trigger factors". Physical and psychological stress has been implicated in the development of autoimmune disease, since numerous animal and human studies demonstrated the effect of sundry stressors on immune function. Moreover, many retrospective studies found that a high proportion (up to 80%) of patients reported uncommon emotional stress before disease onset. Unfortunately, not only does stress cause disease, but the disease itself also causes significant stress in the patients, creating a vicious cycle. Recent reviews discuss the possible role of psychological stress, and of the major stress-related hormones, in the pathogenesis of autoimmune disease. It is presumed that the stress-triggered neuroendocrine hormones lead to immune dysregulation, which ultimately results in autoimmune disease, by altering or amplifying cytokine production. The treatment of autoimmune disease should thus include stress management and behavioral intervention to prevent stress-related immune imbalance. Different stress reactions should be discussed with autoimmune patients, and obligatory questionnaires about trigger factors should include psychological stress in addition to infection, trauma, and other common triggers.

Stress and thyroid autoimmunity.

Author information

Abstract

While many studies have shown a connection between stress and autoimmune disease, most of the evidence for stress contributing to the onset and course of autoimmune disease is circumstantial and the mechanisms by which stress affects autoimmune disease are not fully understood. The best circumstantial evidence for an effect of stress on autoimmune thyroid disease is the well-known relationship between the onset of Graves' hyperthyroidism and major stress but even this is debated. However, most of the recent case-control studies have supported stress as a factor that affects the onset and clinical course of Graves' disease. On the other hand, there have been few reports concerning the possible relationship between stress and Hashimoto's thyroiditis. Because the onset and course of Hashimoto's thyroiditis is generally insidious, the effect of stress on Hashimoto's thyroiditis might be overlooked. Numerous human and animal studies have demonstrated that psychological and physiologic stressors induce various immunologic changes. Stress affects the immune system either directly or indirectly through the nervous and endocrine systems. These immune modulations may contribute to the development of autoimmunity as well as the susceptibility to autoimmune disease in genetically predisposed individuals. Stress can be one of the environmental factors for thyroid autoimmunity.

Reference




Purpose and significance of the study

ROLE OF RT3 DOMINANCE IN HASHIMOTO’S THYROIDITIS AND EFFECT OF HOMEOPATHIC MEDICINES IN REVERSING THE CHANGE

 T3 is the active thyroid hormone and every cell in the body has molecular docking stations for T3.
 T4 is made by the thyroid, circulates and eventually ends up in the liver where it is converted to T3 and a tiny amount of a substance called Reverse T3 (RT3). RT3 has no action on the cell, except that it binds with the receptor sites, the tiny docking stations, and blocks the action of T3. However, in the normal situation, T3 dominates and RT3 is no problem.
                  However, when a person experiences prolonged stress, the adrenal glands respond by manufacturing a large amount of cortisol. Cortisol inhibits the conversion of T4 to T3 and favors the conversion of T4 to RT3. If stress is prolonged, a condition called Reverse T3 Dominance occurs and persists even after the stress passes and cortisol levels fall. Apparently, RT3 itself acts like cortisol and blocks the conversion of T4 to T3. Reverse T3 Dominance is the cause of hypometabolism because too many receptor sites are blocked by RT3 and the chemical reactions of life slow down. This is because the reverse T3 continues to inhibit the conversion of T4 to T3, perpetuating production of the inactive T3 hormone. Prolonged stress is the major cause of reverse T3 dominance. Reverse T3 has the same molecular structure as T3 however it is a mirror image of T3 and therefore fits into the receptor upside down. This prevents the active T3 from binding to the receptor site and activating the appropriate thyroid response
Reverse T3 slows metabolism and causes the typical signs & symptoms of hypothyroidism .
A specific measurement of reverse T3 is valuable in identifying excessive levels of reverse T3,   ----------Reverse T3 Dominance.

High levels of stress, toxicity, adrenal exhaustion, hypoglycemia and/or low sex hormone levels are the key factors that lead to reverse T3 dominance.


Factors increasing cortisol levels

·                    Viral infections increase cortisol levels through activation of the HPA axis by cytokines.
·                    Caffeine may increase cortisol levels.
·                    Sleep deprivation
·                    Intense (high VO2 max) or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose;however, cortisol declines to normal levels after eating (i.e., restoring a neutral energy balance)
·                    The Val/Val variation of the BDNF gene in men and the Val/Met variation in women are associated with increased salivary cortisol in a stressful situation.
·                    Hypoestrogenism and melatonin supplementation increase cortisol levels in postmenopausal women.
·                    Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods.
·                    Subcutaneous adipose tissue regenerates cortisol from cortisone by the enzyme 11-beta HSD1.
·                    Anorexia nervosa may be associated with increased cortisol levels.
·                    The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men.
·                    Severe calorie restriction causes elevated baseline levels of cortisol.
·                    Posing in low-power nonverbal displays through close, contractive postures can increase cortisol levels.
·                    Smelling androstadienone has been found in one study to raise cortisol levels in women; as well as, in other studies, to affect mood .


RESEARCH 

RESEARCH PROBLEM:  BY Dr  Sanjana VB . BHMS , DBRM.

Can homeopathic medicines alter the neuroimmunoendocrine modulations of thyroid   resulting from stress  ?

Abstract

Objective:

HASHIMOTO’S thyroiditis being an autoimmune disease  having multifactorial causation  and having  various explanations for the pathogenesis  we find stress as one of the multiple factors causing the disease in genetically susceptible populations.The role of cortisol and RT3 in slowing down metabolism  needs further extensive research for finding out a solution to alter  the RT3 dominance which persists despite cortisol withdrawal .We want to study the effects of a few homeopathic medicines in  reversing RT3 DOMINANCE and thus making biologically active T3 available for metabolic functions to establish euthyroid state.

Clinical findings
Homeopathic medicines which have found to be effective in my clinical  practice in the order of maximum effectivity are:

Natrum muriaticum  1M onwards
Lycopodium  1M
Baryta muriatica 200
Calcarea carbonica 1M
Bromium 1M
Calcarea fluorica 200
Thyroidinum 3x

Compared to the conventional medical  hormone therapy with levothyroxine  which helps only in achieving euthyroid state homeopathic medicines could achieve euthyroid state along with better quality of life with respect to their physical and mental symptoms.

The extra benefit  of homeopathic treatment include the following
  • Emotional stability+++++++++++++
  • Reduced sleepiness
  • Liveliness
  • Reduced oedema,dryness of skin

Lab findings
After treatment an apparent increase in T3 AND T4 was noticed  with the symptomatic recovery.It was evident with respect to T3  bcoz manysymptomatic patients who had subclinical or overt hypothyroidism had low T3 Level compared to t4.As we mentioned earlier T3 is the biologically active  thyroid hormone  although T4 is the determinant of hypo or hyperthyroidism in clinical diagnosis.

All these point out that the metabolic slowing due to T3 reduction is  positively altered by homeopathic medicines.
we [homeopaths]want to know if it is due to the  receptor level action of medicine in altering RT3 dominance.
We also want to know does our medicines alter
1] anti TPO ANTIBODY levels,
2] cortisol negative feedback with TSH,
3]  T3 ,reverseT3 conversion.

Conclusion: It needs extensive research on the above mentioned parameters.


Dr Sanjana VB
HV HOMEOPATHY/sgh
Ramanattukara,calicut,kerala
serenityinternational academy of homeopathic medical science and research
[SIAHMSR]

serenitysiahms@gmail.com                                                                       [ copyright 2015 Serenity Global Homeopathy - SGH All rights reserved ]





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ROLE OF HOMEOPATHIC MEDICINES IN ALTERING REVERSET3 DOMINANCE [ ongoing research

Research methodology a new perspective -2 [ second part of the NOTE posted in 2011] ROLE OF HOMEOPATHIC MEDICINES IN ALTERING REVERSET3...