HOMOEOPATHIC PERSPECTIVE OF THYROID DISORDERS

R. K. Manchanda1, Archana Narang2,

Saurav Arora3, Latika Nagpal3
For Correspondence:
1
Deputy Director, Directorate of ISM & H, New Delhi
2
Medical Officer, SHMC & H, Nanak Pura, Moti Bagh, New Delhi
3
SRF, SHMC & H, Nanak Pura, Moti Bagh, New Delhi
E mail id: shmc.thyroidclinic@gmail.com

Abstract

Homoeopathy is a unique system of medicine based on individualization and symptom

similarity of the patient. It treats every sickness of a man as a whole and individualised entity.
The homoeopathic literature is loaded with vast examples of thyroid diseases and their cure
with homoeopathy. There are numerous examples of clinical and therapeutic studies done on
thyroid disorders but there are few peer reviewed controlled design studies in Homoeopathy.
Homoepathic medicines play an important role in immuno modulation at the cellular level
and can cure cases of sub clinical & mild hypothyroidism and hyperthyroidism.
Homoeopathic Medicines due to their infinitesimal light isotopic forms are capable of
penetrating the Hypothalamus-Pituitary Axis. The need of the hour is to carry out scientific,
evidence based studies and case documentation to prove the potential role of homeopathy in
reversing the functional & immune disturbances of thyroid gland.

Keywords: Homoeopathy and thyroid disorders, research in homoeopathy, autoimmune

thyroiditis, goiter, immuno-modulation

FROM THE HISTORY1

Goiter was first described in China in 2700 BC. Da Vinci described thyroid as a thing that is
designed to fill empty spaces in the neck. According to Parry – thyroid works as a buffer to
protect the brain from surges in blood flow. Roman physicians have reported thyroid
enlargement as a sign of puberty. In 500 AD Abdul Kasan Kelebis Abis performed the first
goiter excision in Baghdad, the procedure remained unknown. In 1200’s AD advancements in
goiter procedures included applying hot irons through the skin and slowly withdrawing them
at right angles. The remaining mass or pedicled tissue was excised. Patients were tied to the
table and held down to prevent unwanted movement, but most died from haemorrhage or
sepsis. In 1646 AD Wilhelm Fabricus performed a thyroidectomy with standard surgical
scalpels, for which he was imprisoned. In 1656 thyroid was first identified by the anatomist
Thomas Wharton. In 1808 AD Guillaume Dupuytren performed a total thyroidectomy, but
the patient died postoperatively of “shock”. In 1820 AD Johann Straub and Francois Coindet
found that use of seaweed (iodine) reduced goiter size and vascularity. In 1830 AD Graves
and von Basedow describe a toxic goiter condition they referred to as “Merseburg Triad” –
goiter, exopthalmos, and palpitations. In 1866, Samuel David Gross said, “If a surgeon
1
should be so foolhardy as to undertake it [thyroidectomy] … every step of the way will be
environed with difficulty, every stroke of his knife will be followed by a torrent of blood, and
lucky will it be for him if his victim lives long enough to enable him to finish his horrid
butchery.” In 1883, Theodor Kocher while addressing the German Medical Congress stated,
“the thyroid gland in fact had a function”. In the same year Kocher’s performed a
retrospective review on 5000 career thyroidectomies. The thyroxine was discovered
somewhere in 19th century and a remarkable turning point started with this in management of
thyroid disorders by allopathic counterparts.

REFERENCES FROM THE LITERATURE2

The homoeopathic literature is loaded with vast examples of thyroid diseases and their cure
with homoeopathy. It was the insight of our great masters that they have so beautifully
described thyroid related disorders and their management in Homoeopathy. In his great work,
Master Samuel Hahnemann has quoted, “What action is exerted on the skin by certain
diseases of the glands with an internal secretion (thyroid gland, ovaries, testicles, supra-renal
capsules, pituitary gland, etc.) must remain reserved for future research. So much, however,
is established to-day to prove that some of these disturbances (Addison's disease) cause
considerable alternations of the skin.” Below are some of the references from the history
regarding thyroid disorders and their Homoeopathic cure.

CASE STUDIES PRESENTED SO FAR2

• Journal of Homoeopathic Clinics, Vol 3, Sep N’1, Case 458, 1869-1870: A 19 years
old female with large swelling of the thyroid gland was treated with Bromine3,
several times a day following by Calc Carb 3 and was relieved in three weeks of time.

• International Hanhnemannian Association 1902: A case of thyrotoxicosis was treated

by Homoeopathically chosen remedies: China, Lach., Sul.

• Clinical Illustrations Homoeopathician (A Journal Of Pure Homoeopathy) 1914:

presented 3 cases of thyroid enlargement with thyroid dysfunction and were reported
cured by Iodum and Baryta carb.

• International Hahnemannian Association 1919: “Our knowledge of the endocrine

remedies is as yet in a formative stage, but the therapeutic use of the ductless glands is
steadily growing. We know more of the thyroid gland and of its therapeutic
applications, than of any of the other ductless glands.” There is also a case presented
which was treated using 2x and 3x trituration of thyroidinum.

• International Foundation for Homoeopathy: Case Conference Proceedings 1995: A

case of primary hypothyroidism aged 30 female was presented by Dr. George Guess.

2
 • Master F. J. , 1995: A case of a lady aged 51 years with migraine of 15 years standing,
hypothyroidism since 10 years and leucoderma since 5 years and a diagnosed as a
case of Hypothyroidism was given Staphisgaria.

REFERENECES FROM MATERIA MEDICA2

• Blackwood A. L. Manual of materia medica therapeutics: “A normal thyroid has

much to do with the function of the ovaries; with a hypothyroid condition, although
the ovaries and uterus are normal, menstruation may not appear and the patient
becomes obese, the skin dry; should the pituitary show disturbance, the skin will be
moist and soft”.

• American Homoeopath described the concept of Hypothyroidism, cancer and clinical

depression.

• Boericke W. Pocket manual of homoeopathic materia medica: Kali Carb: “Pain in

small spot on left side Hypothyroidism”. Thryroidinum: “Marked sensitiveness to
cold, Hypothyroidism after acute diseases, i.e. weakness.

• Grand Georage D. The spirit of homoeopathic medicines: “At times the remedy is
suggested by hypertrophied glands or the beginning of goiter. Homeopathic treatment
will remedy a slight disorder in the glandular system, but when the disorder is too
great, hormonal treatment will be necessary.

• Lesser O. Textbook of Homoeopathic Materia Medica: “If the alkali and earthy alkali
metals, Na, K, Mg, Ca, as cations determine the drug picture, then they shape it as
hydrogenoid, cold, sensitive to cold, relaxed torpid lymphatic constitutional types
stigmatized along the side of the parasympathetic system. Seen from an endocrine
side, they tend toward the hypothyroid side, the function of the lymphocytic apparatus
(thymus) is increased.”

• Master F. J. The bed side Organon of Medicine: “Never give thyroidinum as a routine
or specific for all patients who come with thiroid problem.”

REFERENCES FROM REPERTORY3

There are 32 references in the forms of rubrics and subrubrics given in Synthesis treaure
edition. Where as Kents repertory, Murphy repertory and Complete repertory consists of 9,
13 and 37 rubrics in relation of thyroid and other rubrics and vice versa respectively.

THYROID GLAND

DEVELOPMENTAL CONSIDERATIONS4

The thyroid gland starts developing by 3-4 weeks of gestation, appearing as an epithelial
proliferation in the floor of the pharynx. Follicles of the thyroid begin to make colloid in the
by 12th week of gestation and thus contribute in development of physical and neurological

3
features. Failure of synthesis of hormones and TSH by thyroid gland may result in arrested or
abnormal growth of the fetus. At birth, a cold-stimulated short-lived TSH surge is observed,
followed by a TSH decrease until day 3 or 4 of life by T4 feedback inhibition.

ANATOMY OF THYROID GLAND5

Source: Grant’s Atlas of Anatomy

FUNCTIONS OF THYROID GLAND6

The thyroid gland is one of the most important endocrine gland which secrets two major
hormones, thyroxine and triiodothyronine. It is situated in anterior part of neck just above the
lower part of trachea, situated in between cricoid cartilage and suprasternal notch. Normally
it is not palpable but may be palpated in conditions in which it is enlarged. Enlargement of
the gland may not be a sign of its under or over functioning, but association of goiter with
thyroid function status and other investigative modalities helps us to understand disease in a
better term. Goiter is assessed by palpation by fingers of both hands for size, consistency and
presence of nodules if any.

Thyroid palpation method

4
Thyroxine (T4) and tri-iodothyronine (T3) are two major hormones which are secreted in
pulsatile manner under feed back mechanism controlled by hypothalamic-pitautory-thyroid-
pituatory axis.

DIAGNOSING VARIOUS THYROID DISORDERS

The diagnosis of thyroid disorder is primarily done on following points:

• Complete homoeopathic case taking.

• Family history of systemic disorders particularly thyroid and autoimmune disorders. It

is seen that the individuals who have family history positive of thyroid dysfunction
are at more risk of developing thyroid disorders.

• Consistancy and size of thyroid gland, as it may give us some hint about the
underlying pathology, e.g. firm gland are suggestive of hashimoto’s thyroiditis, goiter
in high grades can induce pressure symptoms on trachea and other adjacent tissues,
painful gland suggests acute or subacute inflammatory condition.

• Presence of anti thyroid antibodies, may suggest some of the thyroid dysfunction.

• Other investigations also help in arriving at diagnosis of thyroid disorders. Some of

the investigations are: Radio active iodine uptake (RAIU), Technicium scan (Tc
Scan), Fine needle biopsy (FNB). These investigations are condition specific and are
to be advised as per requirement of the case. The detailed description of these
investigative modalities is described later in the following text.

The ultimate and ground level workers in thyroid-body axis are the two hormones secreted by
thyroid gland. These hormones are responsible for various activities in almost the entire
body. Every organ and tissue thus needs these hormones (particulary T3) for proper

5
functioning. Thyroid hormones acts by crossing the cell membrane and binding to
intracellular receptors (α1, α2, β1 and β2), which act alone, in pairs or together with the
retinoid X-receptor as transcription factors to modulate DNA transcription and thus various
metabolic and other functions are performed. There are two variants of thyroid hormones
circulating in body, free and bounded hormones, as hormones are circulated along the body in
protein bounded form. These proteins are majorly thyroid binding globulins (TBG) and less
commonly albumin. According to extensive research studies done on this revelas that free
hormone assay is more reliable as bounded hormones level may vary in conditions in which
there is pooling of TBG in body eg.

• Pregnancy

• Estrogen therapy

• Oral contraceptive pills

• Acute viral hepatitis

• Primary biliary cirrhosis

• Hepatocellular cancer

• Collagen vascular disease

On the other hand TBG in decreased in

• Glucocorticoids

• Androgens

• Nephrotic syndrome

• Protein-losing enteropathy

• Cirrhosis

• Critical illness/starvation

T4 (thyroxine) is the major circulating hormone whereas T3 is more biologically active. Both
T3 and T4 give a feed back to pituatory to release of suppress secretion of TSH. TSH is
ultrasensitive to even smaller amouts of circulating T3 and T4 levels, this phenomenon is to
be understood at the ground level to understand the diagnosing and follow up cases of thyroid
disorders. This can be understood by the following simple yet informative flow chart:

6
TSH is the one of the most reliable marker of thyroid disorders along with FT4 estimation.
Other diagnostic modalities used to diagnose various thyroid dysfunctions are given below
with their advantages and desription:

MARKER/INVESTIGATION BRIEF UTILITY

TSH Most reliable marker to asses thyroid dysfunction
with FT4 as TSH is the precursor of release of
FT3 & FT4
Free T3, T4 Circulating un-bounded hormone assays depicts
the actual level of thyroid hormones thus
prognosis can further be made along with the
clinical and confirmed diagnosis.
Antibodies: Anti-TPO, Anti-TSHr Presence of antibodies may sometime help us to
understand the natural history of thyroid
functions, as their presence confirms the
undergoing pathological conditions.
Thyroid ultrasonography Thyroid Ultrasonography is done to see the
consistency of thyroid gland. It is also done to
rule out the presence of nodules. Ultrasonography
can also be suggestive of congenital anomalies
e.g. absence of one or both lobes of thyroid gland.
RAIU Scintillation counter measures radioactivity after
I123 administration. Uptake varies greatly by
iodine status, e.g. Indigenous diet (normal uptake
10%).
Elevated RAIU with hyperthyroid symptoms may
be presented in:
• Graves
• Toxic goiter
Low RAIU with hyperthyroid symptoms is used
to distinguish:
7

Technetium scan (Tc Scan)
Final Needle Biopsy (FNB)
• Thyroiditis (Sub acute, Active
Hashimoto’s)
• Hormone ingestion
• Excess I- intake in Graves’
(Jod-Basedow effect)
• Ectopic thyroid carcinoma (Struma ovarii)
The RAIU technique is also used as a therapy to
suppress the hyperactive gland in thyrotoxicosis
and hyperthyroidism.
Technetium scan is also based on the uptake
phenomenon of Tc by thyroid gland which is then
use to differentiate various nodules and hyper
functioning and hyper active thyroid gland.
FNB is used to study the morphological and
pathophysiology of glandular tissue. By this
technique we can differentiate various types of
carcinomas, dysplasia, and chronic lymphatic
infiltration.

SUMMARY

• TSH is a good screening test to assess thyroid function in an outpatient setting.

• If TSH is abnormal, the diagnosis is confirmed with thyroid hormone levels.

• Change in thyroid binding proteins could alter total thyroid hormone levels.

• 99% of thyroid hormones are protein bound.

• In order to assess the thyroid hormone levels unaffected by the binding proteins, free
thyroid hormone levels assessment is more reliable.

• T4 is the major thyroid hormone in circulation, therefore assessing T4 status alone is

usually sufficient to assess the thyroid hormone status.

• In certain situation, T3 level becomes abnormal without changes in T4, as in T3

thyrotoxicosis where there are elevated levels of T3 along with normal T4 levels and
low TSH level.

• Acute illnesses can alter thyroid function tests without thyroid disease as they tend to
increase binding proteins, also TSH can also be influenced by stress and anxiety.

• Thyroglobulin is a good cancer marker for papillary and follicular cancer after total
thyroidectomy.

• Thyroid antibodies can assess the risk of developing autoimmune thyroid diseases.

SPECTRUM OF THYROID DISORDERS7

8
GOITER

Chronic enlargement of the thyroid gland not due to neoplasm is called as goiter.

• Endemic goiter-Areas where > 5% of children of 6-12 years of age have goiter, very
common in China and central Africa.
• Sporadic goiter -Areas where < 5% of children 6-12 years of age have
goiter.Multinodular goiter in sporadic areas often denotes the presence of multiple
nodules rather than gross gland enlargement.
• Familial
Etiology:
1. Hashimoto’s thyroiditis
• Early stages only, late stages show atrophic changes
• May present with hypo, hyper, or euthyroid states
2. Graves’ disease-Due to chronic stimulation of TSH receptor
3. Diet -Brassica (cabbage, turnips, cauliflower, broccoli),Cassava,Lithium
prevents release of hormone, causes goiter in 6% of chronic users
4. Neoplasm
5. Chronic Iodine excess-Iodine excess leads to increased colloid formation and
can prevent hormone release.If a patient does not develop iodine leak, excess
iodine can lead to goiter.

9
THYROID NODULES

• Prevalence

– Palpable: 4-7%

– Non-Palpable: >50%

– Cancer in nodules: 5%

• Women affected more than men

• Most subjects are euthyroid and/or asymptomatic

• Prevalence is less than 1% with thyrotoxicosis

• Historical Red Flags are defined as:

– Male

– Extremes of age (<20 or >65)

– Rapid Growth

– Symptoms of local invasion (hoarseness, dysphagia, neck pain)

– History of radiation to the head or neck dispose an individual to develop

nodules

– Family history of Thyroid Cancer or Polyposis

SOLITARY THYROID NODULE

• More likely to be malignant in men, patients over 60 and patients with

a h/o head or neck irradiation are at more risk.

• No growth for years almost always indicative of benign nodule as it is

not a nodule that appears suddenly (likely a cyst or adenoma hemorrhage)

• Malignant nodule develops in weeks to months.

• Virtually all patients with thyroid carcinoma are euthyroid as are those
with benign nodules. Nodule of >1.5 cm are usually detectable on examination
and are confirmed in the Ultrasonography. Lifetime risk for developing a
nodule is 5-10%. Studies show 50% of people during autopsy has either single
or multiple nodules. 5-10% of clinically detectable hypofunctioning (cold)
nodules can be malignant. The laboratory/Imaging techniques used are: TSH,
Calcitonin, Ultrasound, FNB for characterization of Nodules, Nuclear Scan to
see whether nodule is “Hot” or “Cold.” If FNB is suggestive of malignancy
then surgery is advised, and if it is supscpicious or negative then a follow up

10
 of few months is given to the patient with repeat investigations. In case there
are Indeterminant reports then FNB is repeated, if still indeterminant, surgery
is recommended.

PRIMARY HYPOTHYROIDISM

Definition - disorder of the thyroid gland causing decreased thyroid hormone production and
secretion. It is the most common disorder of thyroid dysfunction. The factors attributed to
these are:

• Worldwide - iodine deficiency is most common cause.

• Iodine depleted areas - chronic autoimmune thyroiditis is commonly present in these

areas.

• Associated with elevated serum cholesterol, CPK, AST and LDH

SECONDARY HYPOTHYROIDISM

Definition – It is caused by decreased thyroidal stimulation by TSH.

• Also referred to as central or hypothyrotropic hypothyroidism.

• Caused by either pituitary or hypothalamic diseases.

• Very uncommon.

• TSH is usually low or inappropriately normal.

Symptoms of hypothyroidism

It includes - Fatigue, lethargy, mental impairment, depression, cold intolerance, hoarseness,

dry skin, decreased perspiration, weight gain, decreased appetite, constipation, menstrual
irregularities, arthralgias, and parasthesias.

Signs

Slow movements, slow speech, hoarseness, bradycardia, dry skin, non-pitting edema,
hyporeflexia, delayed relaxation of reflexes are some of the signs of hypothyroidism.

N. B.: Older patients tend to have fewer signs and symptoms of hypothyroidism and those
they have tend to be less specific.

Diagnosis

• Low FT4, High TSH (Primary, antibodies estimation suggested)

• Low FT4, Low TSH (Secondary or Tertiary, TRH stimulation test, MRI)

11
HASHIMOTO’S THYROIDITIS

• It is the most common cause of hypothyroidism.

• It is due to action of auto- antibodies to TPO, TBG thus by inhibiting/diminishing the

production and secretion of thyroid hormones.

• Commonly presents in subjects from 30-50 yrs, female affected more than males.

• It is usually non-tender and asymptomatic.

• Lab values

• High TSH

• Low T4

• Anti-TPO Ab, Anti-TBG Ab

SILENT THYROIDITIS (POST-PARTUM THYROIDITIS)

Silent thyroiditis is termed post-partum thyroiditis if it occurs within one year of

delivery.Patient comes with Hyperthyroid symptoms.Soon there is progression to
euthyroidism followed by hypothyroidism for up to 1 year.Later on Hypothyroidism
generally resolves.

SUBACUTE THYROIDITIS (DEQUERVAIN’S, GRANULOMATOUS)

It is the most common cause of painful thyroiditis.It often follows a URI.FNA may reveal
multinuleated giant cells or granulomatous change.

Course

– It starts with pain and thyrotoxicosis (3-6 weeks) followed by asymptomatic

euthyroidism.

– Then there is period of Hypothyroid state.(weeks to months)

– It is followed by phase of recovery (complete in 95% after 4-6 months).

Diagnosis

– Elevated ESR

– Anemia (normochromic, normocytic)

– Low TSH, Elevated T4 > T3, Low anti-TPO/Tgb

12
 – Low RAI uptake (same as silent thyroiditis)

– Graves’ disease may occasionally develop as a late sequellae

ACUTE THYROIDITIS

Causes:

– 68% Bacterial (S. aureus, S. pyogenes)

– 15% Fungal

– 9% Mycobacterial

It May occur secondary to Pyriform sinus fistulae, Pharyngeal space infections, Persistent
Thyroglossal remnants, Thyroid surgery wound infections (rare) and in HIV.

Diagnosis:

– Warm, tender, enlarged thyroid

– FNA to drain abscess, obtain culture

– RAIU normal (versus decreased in DeQuervain’s)

– CT or US if infected TGDC suspected

Recovery is usually complete

RIEDEL’S THYROIDITIS

It is a rare disease involving fibrosis of the thyroid gland

Diagnosis:

– Thyroid antibodies are present in 2/3

– Painless goiter “woody”

– Open biopsy often needed to diagnose

– Associated with focal sclerosis syndromes (retroperitoneal, mediastinal,

retroorbital, and sclerosing cholangitis)

THYROTOXICOSIS

Definition - refers to clinical syndrome of hyper metabolism resulting from increased

serum concentration of T4 and/or T3, regardless of cause. Not synonymous with

13
 hyperthyroidism. Hyperthyroidism - increased thyroid hormone biosynthesis and
secretion by the thyroid gland.

Symptoms - nervousness, fatigue, weakness, increased perspiration, heat intolerance,

tremor, hyperactivity, palpitation, change in appetite, weight change, menstrual
irregularities.

Signs - hyperactivity, tachycardia, atrial arrhythmia, systolic hypertension, stare, eyelid

retraction, tremor, hyperreflexia, muscle weakness.

*Older patients - have fewer signs and symptoms of sympathetic activation and more
cardiovascular dysfunction.

GRAVES’ DISEASE

It is the most common cause of thyrotoxicosis in the industrialized world.It is Autoimmune

condition with anti-TSHr antibodies.Onset of disease may be related to severe stress which
alters the immune response.

Diagnosis:

– TSH, T4, T3 to establish toxicosis

– RAIU scan to differentiate toxic conditions

– Anti-TPO, Anti-TSAb, FT3 if indicated

RAIU in Hyperthyroid States

High Uptake Low Uptake
Graves’ Sub acute Thyroiditis
Toxic MNG Iodine Toxicosis
Toxic Adenoma Thyrotoxicosis factitia

HOMOEOPATHIC MANAGEMENT

There are various types of thyroid disorders which we commonly encounter in our day to day
practice. These disorders are attributed at different levels, viz:-

• Dynamic- Euthyroid autoimmune thyroiditis.

• Functional- initial stages of autoimmune/hashimoto thyroiditis, Subclinical

hypothyroidism and Subclinical hyperthyroidism.

• Patho-physiological- Goitre, Hashitoxicosis, Chronic lymphocytic infiltration of

thyroid, Non-malignant Nodules.

14
 • Pathological- Hypothyroidism, Graves’ disease, Thyrotoxicosis.

• Descructive- Malignancies, toxic nodules.

The understanding of these levels helps us to define the prognostic and management plan for
the individual. Also it helps us to define the therapeutic guidelines to treat a case of thyroid
dysfunction. If we clearly perceive this concept we can avoid claiming false cures, as we
cannot go against nature’s law of cure. If destruction has started we can only stop its
progression, but cannot revive new cells. Once destruction has set in and the functional units
of gland are non functional, no medicine can revive it or grow it, but on the other hand
medicine will save rest of the cells. This is the reason why we encounter many patients in our
practise who do not respond to best selected homoeopathic remedies according to
Homoeopathic principles. This occurs in cases where there is either disease has progressed to
non revertible changes or there is/are some other obstacles to cure. These obstacles to cure
can be:

• Other systemic disorders e.g. Diabetes mellitus, Hypertension, Metabolic syndrome,

dyslipidemia etc

• Autoimmune disorders e.g. SLE, vitiligo,

• Any history of previous thyroid disorders e.g. hashimoto thyroiditis, thyroid nodules,
autoimmune thyroiditis, etc

• Other endocrinal disorders e.g. PCOS, prolactinoma, Cushing syndrome, etc.

Association of thyroid dysfunction with these disorders make the condition what we read in
Organon as “Complex diseases”. The treament plan of these cases is done according the laws
embedded in Organon of Medicine8.

15
In aphorism 3 of Organon of Medicine8 fifth edition, Hahnemann states that, “If the physician
clearly perceives what is to be cured in diseases, that is to say, in every individual case of
disease (knowledge of disease, indication),……” the first homework to be done by a
physician is to understand the disease and its component, then only he can see the finer
shades of individulization, difference between common and uncommon symptoms,
understaning an individual as a whole and not a diseased part or organ, diagnosis and
prognosis of this state etc. The natural history of any disease helps us to manage a disease and
to intervene it with judicial employment of medicines. For example cases in which
irreversible pathological changes have occurred, remedies having specific actions in low to
moderate doses are usually advised. In cases where there are dynamic or functional
abnormalities remedies with moderate to high potency are advised.

LEVELS OF PREVENTION OF THYROID DISORDERS:

PRIMORDIAL PREVENTION

Health promotion:

Educate the family regarding lifestyle measures, good food habits, positive attitude to be
inculcated in young child

Specific protection:

• Regular exercise

• Desirable BMI

• Health promotive measures and attitude

• Identifications and elimination of exciting or precipitating factors, if any.

PRIMARY PREVENTION
16
 • Early diagnosis and treatment.

• Reinforce primary and preventive measures.

• Identifications and elimination of exciting or precipitating factors, if any.

SECONDARY PREVENTION

Aggressive reinforcement of:

• Primary and secondary risk intervention.

• Secondary prevention: lipid profile within normal limits

• Aggressive and effective control of disease.

TERTIARY PREVENTION

• Disability limitation

• Rehabilitation

TREATMENT GUIDELINES FOR PHYSICIANS

Although it has been a matter of debate regarding the exact guidelines to treat various thyroid
disoders especially diseases which are in their subclinical states, a general line of treatment
can be sought out if one knows the basic facts about thyroid disorders. Moreover one needs to
be updated regarding the latest techniques and research going on. For a very long period of
time the subclinical hypothyroidism and subclinical hyperthyroidism conditions were treated
as full blown cases of hypo or hyper thyroidism. As the studies in these areas advanced, it
was seen that one needs to clearly define the line and justification of treatment. Treatment
only upon biochemical anomaly and in absence or minimal symptoms needs to be justified
and scientfically reasoned. Also the term subclinical sometime seems arbitrary when there are
symptoms but biochemically anomalies are minimal and vice versa. Thus a physician’s
discretion at this point of time should be critical and justified.

As Hahnemann has rightly said that there are patient in disease and not the disease in patient.
Therefore, a holistic approach is needed to treat the patients. A detailed case taking with
psyco somatic approach should be adapted during the case taking. It should include
investigation of emotional and psychological factors such as stress, repressed emotions,
mental shock, grief, anger, dreams, delusions, and all other factors affecting the mind along
with past, family history and intellectual and physical aspects of the patient. Hahnemann in
aphorism 2nd has stated that, “The highest ideal of cure is rapid, gentle and permanent
restoration of the health, or removal and annihilation of the disease in its whole exten.” Such
a choosen remedy on the basis of individualization as stated in aphorism 7 works at deeper
levels especially on pituatory hypothalamic axis and sets right the basic imbalance of
hormones in the body.
17
In cases of sub clinical & mild hypothyroidism and hyperthyroidism Homoeopathic treatment
has been found to be very efficacious. Homoeopathic Medicines have their impact on
Hypothalamus-Pituitary Axis. Homoeopathy can delay the progression of malfunctioning of
the thyroid gland. As the thyroid and its hormones effects each and every organ of the body
including mental and physical growth, early detection and treatment with Homoeopathy in
children can lead to prevention of complications. As homoepathic medicines are selected on
the basis of constitution of the patient, it plays an important role in immuno modulation at the
cellular level and therefore helps in annihilation of auto antibodies. Theses are the
observations which authors have drawn during the past years in OPD at INMAS, NHMC &
SHMC.

WHEN TO CONSULT AN ENDOCRINOLOGIST

For Patients with:

• Grave’s disease

• Multinodular goiter

• Single palpable nodule

• Central disease (pituitary or hypothalamic)

• Patients resistant to therapy

STUDIES ON HOMOEOPATHY AND THYROID DISORDERS

There are numerous examples of clinical and therapeutic studies done on thyroid disorders,
examples of which are discussed in short in historical perspective elsewhere in this article.
Following are some of the peer reviewed controlled design studies in Homoeopathy apart
from clinical and therapeutic studies.

• Does a homeopathic ultramolecular dilution of Thyroidinum 30cH affect the rate of

body weight reduction in fasting patients? A randomised placebo-controlled double-
blind clinical trial. (Homeopathy, 2002; 91(4):197-206 (ISSN: 1475-4916)
Schmidt JM; Ostermayr B, Krankenhaus für Naturheilweisen, Munich, Germany.9

• Homeopathically prepared dilution of Rana catesbeiana thyroid glands modifies its

rate of metamorphosis. (Homeopathy, 2004; 93(3):132-7 (ISSN: 1475-4916)
Guedes JR; Ferreira CM; Guimarães HM; Saldiva PH; Capelozzi VL
Laboratory of Molecular Pathology, University of São Paulo School of Medicine, SP,
Brazil.10

18
 • THYROIDINUM, A PROVING (HYGANTHROPHARMACOLOGY). J Am Inst
Homeopath. 1964; 57:201-7 (ISSN: 0002-8967) PANOS M; ROGERS R;
STEPHENSON J.11

• Pharmacologic and alternative therapies for the horse with chronic laminitis. Vet Clin
North Am Equine Pract. 1999; 15(2):495-516, viii (ISSN: 0749-0739) Sumano
López H; Hoyas Sepúlveda ML; Brumbaugh GW.
Departamento de Fisiología y Farmacologiá, Facultad de Medicina Veterinaria y
Zootecnia, Universidad Nacional Autónoma de México, México DF, México.12

• To evaluate the efficacy of homoeopathic treatment in sub clinical hypothyroidism

(SCH). A single blind case control 18 months follow-up pilot study at NHMC &
Hospital and Institute of Nuclear Medicine & Allied Sciences, Delhi, India under Dilli
Homoeopathic Anusandhan Parishad (DHAP) revealved remarkable results about
management of children on subclinical hypothyroidism.13

In continuation of this scientific spirit another research study on, “Effect of Homoeopathic
treatment on natural history of autoimmune thyroiditis” is undergoing at Dr. B. R. Sur
Homoeopathic Medical College, Hospital & Research Centre, Nanak Pura, Moti Bagh, New
Delhi (Govt of NCT of Delhi) in collaboration with Institute of Nuclear Medicine & Allied
Sciences (INMAS), Timarpur, Delhi – 54 (under ministry of Defence). The project is under
EMR scheme of AYUSH.

ACKNOWLEDGEMENT

The authors express their thankfulness to Maj. Gen. Dr. R. K. Marwaha, Addl. Director,
Institute of Nuclear Medicine, Timarpur, Delhi, Dr. V. K. Khanna, Ex-Principal, NHMC &
H, Defence colony, New Delhi and Dr. V. K. Chauhan, Principal SHMC & H, Nanak Pura,
Moti Bagh, New Delhi for their timely support, help and guidance. The authors are also
thankful to the staff of INMAS-Mr. Kuntal Bhadra, Mr. Baig, and Mr. Satwir Singh for their
assistance in various activities at screening, investigations and OPD setups.

REFERENCES

1. V. Leoutsakos, A short history of the thyroid gland, Dept of Surgery Athens

University School of Medicine, Athens, 115 27 Greece.
2. Encyclopedia Homeopathica, Version 2.2.2
3. RADAR 10, Apex Version.
4. Thyroid gland development and defects, Kratzsch J, Pulzer F., Institute of Laboratory
Medicine, Clinical Chemistry and Molecular Diagnostics, University Hospital, Paul-
List-Str. 13-15, D-04103 Leipzig, Germany.
5. Grant's Atlas of Anatomy, Twelfth edition, Anne M. R. Agur
6. Guyton & Hall Textbook Of Medical Physiology 11th_Edition
7. Harrisons textbook of medicine, 17th edition.

19
8. Organon of Medicine, Samuel Hahnemann, 5th edition, Publisher B. Jain.
9. http://www.sciencedirect.com
10. http://www.ncbi.nlm.nih.gov/pubmed/15287432
11. http://www.ncbi.nlm.nih.gov/pubmed/14178448
12. http://www.find-health-articles.com/rec_pub_10472124-pharmacologic-alternative-
therapies-horse-chronic-laminitis.htm
13. http://www.delhihomeo.com/clinical_hypothyroidism.htm

20