Research methodology a new perspective -note2
Efficacy of homeopathic medicines in altering
AntiTPO ab Titre-research study
AntiTPO ab Titre-research study
-A study for substantiating the relevance of researching on RT3dominance and homeopathic drug efficacy.
VB SANJANA·WEDNESDAY, SEPTEMBER 30, 2015
[copyright 2015 Serenity Global Homeopathy - SGH &SIAHMSR All rights reserved ]
[copyright 2015 Serenity Global Homeopathy - SGH &SIAHMSR All rights reserved ]
Introduction
Thyroxin
(T4) and triiodothyronine (T3), together referred to as thyroid hormones, play
an important role inbasal
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 only a research paper .But an article to substantiate the relevance of extensive research in
autoimmune thyroiditis illustrating my clinical findings and ongoing research
details.
but it includes my clinical research findings on the role of homeopathic medicines in altering antiTPO ab titre and T3.
but it includes my clinical research findings on the role of homeopathic medicines in altering antiTPO ab titre and T3.
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
Hypoparathyroisism
·
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
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
- 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 EFFICACY 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 .
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.
·
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.
·
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 PAPER
BY Dr Sanjana VB . BHMS , DBRM.
Can homeopathic
medicines alter the neuroimmunoendocrine modulations of thyroid resulting from stress ?
Background
Abstract
Abstract
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 efficacy of homeopathic medicines in altering AntiTPO antibodies and hence controlling autoimmunity is studied in fifty cases.the improvement in T3 levels also measured .
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 .
keywords
hashimotos thyroiditis,antitpo ab,T4,T3.RT3.
autoimmunity
conflict of interest- not applicable.nil
methodology and procedure:
inclusion &exclusion criteria
age group 13-40 male and females are included .
pregnant and psychiatrical illness group,very old people excluded.
design: Retrospective study.
fifty cases of HV homeopathy which were studied had undergone usg and antitpo ab test to confirm the disease under study. they were treated with different homeopathic medicines chosen based on the principles of classical homeopathy.the outcome of the study is dependent on the findings on alterations made by the drug in T3,T4 and Anti TPO ab titres.as the study indirectly measures RT3 dominance through T3 in the study T3 is given more emphasis.
RESULT &;conclusion
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 .
keywords
hashimotos thyroiditis,antitpo ab,T4,T3.RT3.
autoimmunity
conflict of interest- not applicable.nil
methodology and procedure:
inclusion &exclusion criteria
age group 13-40 male and females are included .
pregnant and psychiatrical illness group,very old people excluded.
design: Retrospective study.
fifty cases of HV homeopathy which were studied had undergone usg and antitpo ab test to confirm the disease under study. they were treated with different homeopathic medicines chosen based on the principles of classical homeopathy.the outcome of the study is dependent on the findings on alterations made by the drug in T3,T4 and Anti TPO ab titres.as the study indirectly measures RT3 dominance through T3 in the study T3 is given more emphasis.
RESULT &;conclusion
1.Homeopathic
medicines which have found to be effective in my clinical practice in the order of maximum effectivity
are:
Natrum
muriaticum 1M
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
It is found that homeopathic drugs alter ANTITPO ab titres.The efficacy varies with the duration of illness since diagnosed .advanced pathology failed to make significant alteration in Thyroxine levels although it could alter antibody titre.
After treatment an
apparent increase in T3 AND T4 were noticed
with the symptomatic recovery.It was evident with respect to T3 bcoz many symptomatic 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.
further extensive research is needed to understand if it is due to the
receptor level action of medicine in altering
. RT3 dominance.
. RT3 dominance.
. cortisol negative feedback with TSH,
. t3 ,reverseT3 conversion.
Dr Sanjana VB
HV HOMEOPATHY/sgh
serenityinternational
academy of homeopathic medical science and research
[SIAHMSR]
email:
serenitysiahms@gmail.com [
copyright 2015 Serenity Global Homeopathy - SGH All rights reserved ]
