Hypothyroidism

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Hypothyroidism
Classification and external resources

Thyroxine (T4) normally produced in 20:1 ratio to

triiodothyronine (T3)
ICD-10 E03.9
ICD-9 244.9
DiseasesDB 6558
eMedicine med/1145
MeSH D007037

Hypothyroidism (pronounced /ˌhaɪpɵˈθaɪrɔɪdɪzəm/) is the disease state in humans and in

vertebrates caused by insufficient production of thyroid hormones by the thyroid gland.
Cretinism is a form of hypothyroidism found in infants.

Contents
[hide]

 1 Signs and symptoms

o 1.1 Early
o 1.2 Late
o 1.3 Uncommon
 2 Causes
o 2.1 General psychological associations
 3 Diagnosis
 4 Treatment
o 4.1 Treatment controversy
o 4.2 Subclinical hypothyroidism
o 4.3 Alternative treatments
  5 See also
 6 References
 7 Further reading
 8 External links

[edit] Signs and symptoms

In adults, hypothyroidism is associated with the following symptoms:[1][2][3]

[edit] Early

 Poor muscle tone (muscle hypotonia)

 Fatigue
 Cold intolerance, increased sensitivity to cold
 Constipation
 Depression
 Muscle cramps and joint pain
 Goiter
 Thin, brittle fingernails
 Coarse hair
 Paleness
 Decreased sweating
 Dry, itchy skin
 Weight gain and water retention[4][5][6]
 Bradycardia (low heart rate – fewer than sixty beats per minute)

[edit] Late

 Slow speech and a hoarse, breaking voice – deepening of the voice can also be noticed,
caused by Reinke's Edema.
 Dry puffy skin, especially on the face
 Thinning of the outer third of the eyebrows (sign of Hertoghe)
 Abnormal menstrual cycles
 Low basal body temperature

[edit] Uncommon

 Impaired memory[7]
 Impaired cognitive function (brain fog) and inattentiveness.[8]
 A slow heart rate with ECG changes including low voltage signals. Diminished cardiac
output and decreased contractility.
 Reactive (or post-prandial) hypoglycemia[9]
 Sluggish reflexes
 Hair loss
  Anemia caused by impaired haemoglobin synthesis (decreased EPO levels), impaired
intestinal iron and folate absorption or B12 deficiency[10] from pernicious anemia
 Difficulty swallowing
 Shortness of breath with a shallow and slow respiratory pattern.
 Increased need for sleep
 Irritability and mood instability
 Yellowing of the skin due to impaired conversion of beta-carotene[11] to vitamin A
 Impaired renal function with decreased glomerular filtration rate
 Elevated serum cholesterol
 Acute psychosis (myxedema madness) (a rare presentation of hypothyroidism)
 Decreased libido[12] due to impairment of testicular testosterone synthesis
 Decreased sense of taste and smell (anosmia)
 Puffy face, hands and feet (late, less common symptoms)
 Gynecomastia

[edit] Causes
About three percent of the general population is hypothyroid.[13] Factors such as iodine
deficiency or exposure to Iodine-131 (I-131) can increase that risk. There are a number of causes
for hypothyroidism. Iodine deficiency is the most common cause of hypothyroidism worldwide.
[citation needed]
In iodine-replete individuals hypothyroidism is generally caused by Hashimoto's
thyroiditis, or otherwise as a result of either an absent thyroid gland or a deficiency in
stimulating hormones from the hypothalamus or pituitary.

Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all
women within a year of giving birth.[citation needed] The first phase is typically hyperthyroidism; the
thyroid then either returns to normal, or a woman develops hypothyroidism. Of those women
who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop
permanent hypothyroidism requiring life-long treatment.

Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.[citation
needed]

Hypothyroidism is also a relatively common disease in domestic dogs, with some specific breeds
having a definite predisposition.[14]

Temporary hypothyroidism can be due to the Wolff-Chaikoff effect. A very high intake of iodine
can be used to temporarily treat hyperthyroidism, especially in an emergency situation. Although
iodine is substrate for thyroid hormones, high levels prompt the thyroid gland to take in less of
the iodine that is eaten, reducing hormone production.

Hypothyroidism is often classified by association with the indicated organ dysfunction (see
below):[15][16]

Type Origin Description

Primary Thyroid gland The most common forms include Hashimoto's thyroiditis (an
 autoimmune disease) and radioiodine therapy for hyperthyroidism.
Occurs if the pituitary gland does not create enough thyroid-
stimulating hormone (TSH) to induce the thyroid gland to produce
Secondary Pituitary gland enough thyroxine and triiodothyronine. Although not every case of
secondary hypothyroidism has a clear-cut cause, it is usually caused by
damage to the pituitary gland, as by a tumor, radiation, or surgery.[1]
Results when the hypothalamus fails to produce sufficient thyrotropin-
releasing hormone (TRH). TRH prompts the pituitary gland to produce
Tertiary Hypothalamus
thyroid-stimulating hormone (TSH). Hence may also be termed
hypothalamic-pituitary-axis hypothyroidism.

[edit] General psychological associations

Hypothyroidism can be caused by lithium-based mood stabilizers, usually used to treat bipolar
disorder (previously known as manic depression).[citation needed] In fact, lithium has occasionally
been used to treat hyperthyroidism.[17]

In addition, patients with hypothyroidism and psychiatric symptoms may be diagnosed with:[18][19]

 Atypical depression (which may present as dysthymia)

 Bipolar spectrum syndrome (including bipolar I or bipolar II disorder, cyclothymia, or
premenstrual syndrome)
 Inattentive ADHD or sluggish cognitive tempo
 Anxiety and/or panic disorder is also a symptom of Hypothyroidism.

[edit] Diagnosis
To diagnose primary hypothyroidism, many doctors simply measure the amount of thyroid-
stimulating hormone (TSH) being produced by the pituitary gland. High levels of TSH indicate
that the thyroid is not producing sufficient levels of thyroid hormone (mainly as thyroxine (T4)
and smaller amounts of triiodothyronine (T3)). However, measuring just TSH fails to diagnose
secondary and tertiary hypothyroidism, thus leading to the following suggested blood testing if
the TSH is normal and hypothyroidism is still suspected:

 Free triiodothyronine (fT3)

 Free levothyroxine (fT4)
 Total T3
 Total T4

Additionally, the following measurements may be needed:

 24-Hour urine-free T3[20]

 Antithyroid antibodies — for evidence of autoimmune diseases that may be damaging the
thyroid gland
 Serum cholesterol — which may be elevated in hypothyroidism
  Prolactin — as a widely available test of pituitary function
 Testing for anemia, including ferritin
 Basal body temperature

[edit] Treatment
Main article: Medical use of thyroid hormones

Hypothyroidism is treated with the levorotatory forms of thyroxine (L-T4) and triiodothyronine
(L-T3). Both synthetic and animal-derived thyroid tablets are available and can be prescribed for
patients in need of additional thyroid hormone. Thyroid hormone is taken daily, and doctors can
monitor blood levels to help assure proper dosing. There are several different treatment protocols
in thyroid replacement therapy:

T4 only
This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is
currently the standard treatment in mainstream medicine.[21]
T4 and T3 in combination
This treatment protocol involves administering both synthetic L-T4 and L-T3
simultaneously in combination.[22]
Desiccated thyroid extract
Desiccated thyroid extract is an animal based thyroid extract, most commonly from a
porcine source. It is also a combination therapy, containing natural forms of L-T4 and L-
T3.[23]

[edit] Treatment controversy

A 2000 paper suggested "clear improvements in both cognition and mood" from combination
therapy,[22] [24] and another in 2001 concluded that combined treatment seemed to be more
effective than treatment with T4 alone on eight main symptoms of hypothyroidism.[23]

However, more recent studies have shown no improvement in mood or mental abilities for those
on combination therapy, and possibly impaired well-being from subclinical hyperthyroidism.[25]
Another 2006 study which looked at the correlation between free T3 and free T4 levels and
psychological well-being in a randomized controlled trial of combined treatment found a strong
correlation for free T4, but none for T3.[26]. A 2007 metaanalysis of the nine controlled studies so
far published found no significant difference in the effect on psychiatric symptoms.[27].

In addition, a metaanalysis of 11 randomized controlled trials which looked at a wider range of

symptoms including: bodily pain, anxiety, fatigue, body weight and a range of other factors,
found no difference between the combined treatment and therapy with T4 alone.[28]

There is also concern among some practitioners about the use of T3 due to its short half-life. T3
when used on its own as a treatment results in wide fluctuations across the course of a day in the
thyroid hormone levels, and with combined T3/T4 therapy there continues to be wide variation
throughout each day.[29]
[edit] Subclinical hypothyroidism

Subclinical hypothyroidism occurs when thyrotropin (TSH) levels are elevated but thyroxine (T4)
and triiodothyronine (T3) levels are normal.[13] Prevalence estimates range 3–8%, increasing with
age; incidence is more common in women than in men.[30] In primary hypothyroidism, TSH
levels are high and T4 and T3 levels are low. TSH usually increases when T4 and T3 levels drop.
TSH prompts the thyroid gland to make more hormone. Hypothyroidism is sub-clinical if it has
no discernible adverse effect on cellular metabolic rates (and ultimately the body's organs). The
levels of the active hormones will be within the laboratory reference ranges. There is a range of
opinion on the biochemical and symptomatic point at which to treat with levothyroxine, the
typical treatment for overt hypothyroidism. Reference ranges have been debated as well. The
American Association of Clinical Endocrinologists (ACEE) considers 0.45–4.5 mIU/L, with the
ranges down to 0.1 and up to 10 mIU/L requiring monitoring but not necessarily treatment.[31]
There is always the risk of overtreatment and hyperthyroidism. Some studies have suggested that
subclinical hypothyroidism does not need to be treated. A meta-analysis by the Cochrane
Collaboration found no benefit of thyroid hormone replacement except "some parameters of lipid
profiles and left ventricular function."[32] A more recent metanalysis looking into whether
subclinical hypothyroidism may increase the risk of cardiovascular disease, as has been
previously suggested,[33] found a possible modest increase and suggested further studies be
undertaken with coronary heart disease as an end point "before current recommendations are
updated."[34]

[edit] Alternative treatments

Alternative practitioners may combine conventional serum tests with less conventional tests to
assess thyroid hormone function, or simply look at symptoms[citation needed]. Many[who?] have found
that compounded slow release T3 used in combination with T4 may help to mitigate many of the
symptoms of functional hypothyroidism and improve quality of life, although this is still
controversial and is rejected by the conventional medical establishment.[35]

Alternative treatments for hypothyroidism consist of natural food and supplements which aid the
thyroid or support the body by giving help where normally the thyroid would. An example of
one natural treatment is coconut oil. The use of coconut oil has been proven in clinical studies to
increase metabolism.[36]. Although it does not directly affect the thyroid, it aids the body's
metabolism which has slowed down due to hypothyroidism.

[edit] See also

 Subacute lymphocytic thyroiditis
 Hyperthyroidism
 Risk factors in pregnancy

[edit] References
Thyroid
From Wikipedia, the free encyclopedia
Jump to: navigation, search
thyroid

Thyroid and parathyroid.

Latin glandula thyroidea
Gray's subject #272 1269
System Endocrine system
Thyroid diverticulum (an extension of
Precursor
endoderm into 2nd Branchial arch)
MeSH Thyroid+Gland
Dorlands/Elsevier Thyroid gland

In vertebrate anatomy, the thyroid gland or simply, the thyroid, is one of the largest endocrine
glands in the body, and is not to be confused with the "parathyroid glands" (a completely
different set of glands). The thyroid gland is found in the neck, inferior to (below) the thyroid
cartilage (also known as the 'Adam's Apple') and at approximately the same level as the cricoid
cartilage. The thyroid controls how quickly the body uses energy, makes proteins, and controls
how sensitive the body should be to other hormones.

The thyroid gland participates in these processes by producing thyroid hormones, principally
triiodothyronine (T3) and thyroxine (T4). These hormones regulate the rate of metabolism and
affect the growth and rate of function of many other systems in the body. T3 and T4 are
synthesized utilizing both iodine and tyrosine. The thyroid gland also produces a hormone called
'calcitonin', which plays a role in calcium homeostasis.
The thyroid gland is controlled by the hypothalamus and pituitary (specifically, the anterior
pituitary). The thyroid gland gets its name from the Greek word for "shield", after the shape of
the related thyroid cartilage. The most common problems of the thyroid gland consist of an over-
active thyroid gland, referred to as 'hyperthyroidism', and an under-active thyroid gland, referred
to as 'hypothyroidism'.

Contents
[hide]

 1 Anatomy
o 1.1 Embryological development
o 1.2 Histology
 2 Disorders
o 2.1 Hyperthyroidism
o 2.2 Hypothyroidism
o 2.3 Initial hyperthyroidism followed by hypothyroidism
o 2.4 Enlargement of the thyroid
o 2.5 Cancers
o 2.6 Non-cancerous nodules
o 2.7 Seasonal Aggravation
 3 Physiology
o 3.1 T3 and T4 production and action
o 3.2 T3 and T4 regulation
3.3 Thyroid function laboratory tests - normal ranges[20]
o
o 3.4 Significance of iodine
 4 Treatment for Hyperthyroidism
 5 History
 6 In other animals
 7 Additional images
 8 See also
 9 References
 10 External links

[edit] Anatomy
The thyroid gland is a butterfly-shape organ and is composed of two cone-like lobes or wings,
lobus dexter (right lobe) and lobus sinister (left lobe), connected via the isthmus. The organ is
situated on the anterior side of the neck, lying against and around the larynx and trachea,
reaching posteriorly the oesophagus and carotid sheath. It starts cranially at the oblique line on
the thyroid cartilage (just below the laryngeal prominence, or 'Adam's Apple'), and extends
inferiorly to approximately the fifth or sixth tracheal ring.[1] It is difficult to demarcate the gland's
upper and lower border with vertebral levels because it moves position in relation to these during
swallowing.
The thyroid gland is covered by a fibrous sheath, the capsula glandulae thyroidea, composed of
an internal and external layer. The external layer is anteriorly continuous with the lamina
pretrachealis fasciae cervicalis and posteriorolaterally continuous with the carotid sheath. The
gland is covered anteriorly with infrahyoid muscles and laterally with the sternocleidomastoid
muscle also known as sternomastoid muscle. On the posterior side, the gland is fixed to the
cricoid and tracheal cartilage and cricopharyngeus muscle by a thickening of the fascia to form
the posterior suspensory ligament of Berry.[2][3] The thyroid gland's firm attachment to the
underlying trachea is the reason behind its movement with swallowing.[4] In variable extent,
Lalouette's Pyramid, a pyramidal extension of the thyroid lobe, is present at the most anterior
side of the lobe. In this region, the recurrent laryngeal nerve and the inferior thyroid artery pass
next to or in the ligament and tubercle.

Between the two layers of the capsule and on the posterior side of the lobes there are on each
side two parathyroid glands.

The thyroid isthmus is variable in presence and size, and can encompass a cranially extending
pyramid lobe (lobus pyramidalis or processus pyramidalis), remnant of the thyroglossal duct.
The thyroid is one of the larger endocrine glands, weighing 2-3 grams in neonates and 18-
60 grams in adults, and is increased in pregnancy.

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the
external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and
sometimes by the thyroid ima artery, branching directly from the brachiocephalic trunk. The
venous blood is drained via superior thyroid veins, draining in the internal jugular vein, and via
inferior thyroid veins, draining via the plexus thyroideus impar in the left brachiocephalic vein.

Lymphatic drainage passes frequently the lateral deep cervical lymph nodes and the pre- and
parathracheal lymph nodes. The gland is supplied by parasympathetic nerve input from the
superior laryngeal nerve and the recurrent laryngeal nerve.

[edit] Embryological development

In the fetus, at 3–4 weeks of gestation, the thyroid gland appears as an epithelial proliferation in
the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula
linguae at a point latter indicated by the foramen cecum. The thyroid then descends in front of
the pharyngeal gut as a bilobed diverticulum through the thyroglossal duct. Over the next few
weeks, it migrates to the base of the neck. During migration, the thyroid remains connected to
the tongue by a narrow canal, the thyroglossal duct.

Thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) start being

secreted from the fetal hypothalamus and pituitary at 18-20 weeks of gestation, and fetal
production of thyroxine (T4) reach a clinically significant level at 18–20 weeks.[5] Fetal
triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks of gestation, and increases
to 50 ng/dL at term.[5] Fetal self-sufficiency of thyroid hormones protects the fetus against e.g.
brain development abnormalities caused by maternal hypothyroidism.[6] However, preterm births
can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones due their own
thyroid being insufficiently developed to meet their postnatal needs.[7]

The portion of the thyroid containing the parafollicular C cells, those responsible for the
production of calcitonin, are derived from the 4th pharyngeal pouch endoderm. This is first seen
as the ultimobranchial body, which joins the primordial thyroid gland during its descent to its
final location in the anterior neck.

[edit] Histology

At the microscopic level, there are three primary features of the thyroid:[8]

Feature Description
The thyroid is composed of spherical follicles that selectively absorb
iodine (as iodide ions, I-) from the blood for production of thyroid
hormones. Twenty-five percent of all the body's iodide ions are in the
Follicles thyroid gland. Inside the follicles, colloid serve as a reservoir of materials
for thyroid hormone production and, to a lesser extent, act as a reservoir
for the hormones themselves. Colloid is rich in a protein called
thyroglobulin.
The follicles are surrounded by a single layer of thyroid epithelial cells,
Thyroid epithelial cells which secrete T3 and T4. When the gland is not secreting T3/T4
(or "follicular cells") (inactive), the epithelial cells range from low columnar to cuboidal cells.
When active, the epithelial cells become tall columnar cells.
Scattered among follicular cells and in spaces between the spherical
Parafollicular cells
follicles are another type of thyroid cell, parafollicular cells, which
(or "C cells")
secrete calcitonin.

[edit] Disorders
Disorders of the thyroid gland fall into the following categories:

[edit] Hyperthyroidism

Hyperthyroidism in an overactive thyroid. It is the overproduction of the "thyroid hormones" (T3

and T4) by the thyroid gland to which hyperthyroidism refers. The most common cause of
hyperthyroidism is a disease called "Graves' Disease". Graves' Disease is a 'diffuse toxic goiter'
in which the thyroid gland enlarges as a result of the thyroid glands' overproduction of the T3 &
T4 hormones.

Graves' disease is considered to be an autoimmune disease and is the most common cause of
thyroid gland overactivity (hyperthyroidism). Graves' disease is much more common in women
than in men. Graves' Disease results from excess stimulation of the thyroid gland and usually
presents with symptoms in the 2-3rd decade of life. Symptoms include: An enlarged thyroid
(goitre), protruding eyes (exopthalmos), palpitations, excess sweating, diarrhea, weight loss,
muscle weakness and unusual sensitivity to heat. Treatment of Grave's disease involves the
patient taking an oral dose of radioactive iodine, resulting in permanent destruction of cells in the
thyroid, thus rendering them permanently inactive. The patient may then be treated with daily
replacement hormone therapy as a result of a new found hypothyroidism.

[edit] Hypothyroidism

Hypothyroidism is the underproduction of "thyroid hormones" (T3 and T4). Hypothyroid

disorders occur when the thyroid gland is inactive or underactive as a result of improper
formation from birth, or the removal in whole or the removal in part of the thyroid gland.

Symptoms include: abnormal weight gain, tiredness, baldness, temperature intolerance (both heat
and cold), and palpitation.

[edit] Initial hyperthyroidism followed by hypothyroidism

This is the overproduction of T3 and T4 followed by the underproduction of T3 and T4. There
are two types: "Hashimoto's Thyroiditis" and "Postpartum Thyroiditis".

Hashimoto's thyroiditis is an autoimmune disorder whereby the body's own immune system
reacts with the thyroid tissues. At the beginning, the gland is overactive, and then becomes
underactive as the gland is destroyed resulting in too little thyroid hormone production or
hypothyroidism. Hashimoto's is most common in middle-age females and tend to run in families.
Also more common in individuals with hashimoto's thyroiditis are type 1 diabetes and celiac
disease.[9]

Postpartum thyroiditis occurs in some females following delivery. The gland gets inflamed and
the condition initially presents with over activity of the gland followed by under activity. In some
cases, the gland does recover with time and resume its functions.

[edit] Enlargement of the thyroid

An enlarged thyroid gland can exist and not be considered "hyperthyroidism". The term "Non-
toxic goiter" (or simply 'Goiter') is used when enlargement of the thyroid gland occurs-but only
if the enlargement is not as a result of hyperthyroidism (not due to the overproduction of a
thyroid hormone), nor due to a malignancy. Only then can the condition be deemed a "Non-toxic
Goiter" (or simply 'Goiter') for short. This enlargement, the 'goiter', can occur when iodine is not
in the diet in sufficient amounts. Goiter due to iodine deficiency is uncommon in developed
countries as various food items come standard with added iodine (i.e.: Seasoning-type table salt
is supplemented with iodine). Iodine deficiency is still observed in some developing parts of the
world.

Additionally, enlargement of the thyroid can also occur as a result of a bacterial infection or a
viral infection. When this occurs it is deemed 'Thyroiditis'.

Goiter typically takes many years to present.

[edit] Cancers

Cancers do occur in the thyroid gland and, in general, are more common in females. In most
cases, the thyroid cancer presents as a painless mass in the neck. It is very unusual for the thyroid
cancers to present with symptoms, unless it has been neglected. One may be able to feel a hard
nodule in the neck. Diagnosis is made using a needle biopsy and various radiological studies. All
thyroid cancers are treated with surgery.[10]

[edit] Non-cancerous nodules

Many individuals may find the presence of small masses (nodules) in the neck. The majority of
these thyroid nodules are benign (non cancerous). The presence of a thyroid nodule does not
mean one has thyroid disease. Most thyroid nodules do not cause any symptoms, and most are
discovered on an incidental exam. Doctors usually perform a needle aspiration biopsy of the
thyroid to determine the status of the nodules. If the nodule is found to be non-cancerous, no
other treatment is required. If the nodule is suspicious then surgery is recommended..

[edit] Seasonal Aggravation

Limited research shows that seasonal allergies may trigger episodes of hypo- or hyperthyroidism.
[11][12]

[edit] Physiology
The primary function of the thyroid is production of the hormones triiodothyronine (T3),
thyroxine (T4), and calcitonin. Up to 80% of the T4 is converted to T3 by peripheral organs such
as the liver, kidney and spleen. T3 is several times more powerful than T4, which is largely a
prohormone, perhaps four[13] or even ten times more active.[14]

[edit] T3 and T4 production and action

The system of the thyroid hormones T3 and T4.[15]

Thyroxine (T4) is synthesised by the follicular cells from free tyrosine and on the tyrosine
residues of the protein called thyroglobulin (Tg). Iodine is captured with the "iodine trap" by the
hydrogen peroxide generated by the enzyme thyroid peroxidase (TPO)[16] and linked to the 3' and
5' sites of the benzene ring of the tyrosine residues on Tg, and on free tyrosine. Upon stimulation
by the thyroid-stimulating hormone (TSH), the follicular cells reabsorb Tg and cleave the
iodinated tyrosines from Tg in lysosomes, forming T4 and T3 (in T3, one iodine atom is absent
compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3.[17]
Thyroid hormones that are secreted from the gland is about 80-90% T4 and about 10-20% T3.[13]
[14]

Cells of the brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play
a particularly crucial role in brain maturation during fetal development.[18] A transport protein
that seems to be important for T4 transport across the blood-brain barrier (OATP1C1) has been
identified.[19] A second transport protein (MCT8) is important for T3 transport across brain cell
membranes.[19]

Non-genomic actions of T4 are those that are not initiated by liganding of the hormone to
intranuclear thyroid receptor. These may begin at the plasma membrane or within cytoplasm.
Plasma membrane-initiated actions begin at a receptor on the integrin alphaV beta3 that activates
ERK1/2. This binding culminates in local membrane actions on ion transport systems such as the
Na(+)/H(+) exchanger or complex cellular events including cell proliferation. These integrins are
concentrated on cells of the vasculature and on some types of tumor cells, which in part explains
the proangiogenic effects of iodothyronines and proliferative actions of thyroid hormone on
some cancers including gliomas. T4 also acts on the mitochondrial genome via imported
isoforms of nuclear thyroid receptors to affect several mitochondrial transcription factors.
Regulation of actin polymerization by T4 is critical to cell migration in neurons and glial cells
and is important to brain development.

T3 can activate phosphatidylinositol 3-kinase by a mechanism that may be cytoplasmic in origin

or may begin at integrin alpha V beta3.

In the blood, T4 and T3 are partially bound to thyroxine-binding globulin (TBG), transthyretin,
and albumin. Only a very small fraction of the circulating hormone is free (unbound) - T4 0.03%
and T3 0.3%. Only the free fraction has hormonal activity. As with the steroid hormones and
retinoic acid, thyroid hormones cross the cell membrane and bind 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[1].

[edit] T3 and T4 regulation

The production of thyroxine and triiodothyronine is regulated by thyroid-stimulating hormone

(TSH), released by the anterior pituitary. The thyroid and thyrotropes form a negative feedback
loop: TSH production is suppressed when the T4 levels are high. The TSH production itself is
modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and
secreted at an increased rate in situations such as cold (in which an accelerated metabolism
would generate more heat). TSH production is blunted by somatostatin (SRIH), rising levels of
glucocorticoids and sex hormones (estrogen and testosterone), and excessively high blood iodide
concentration.

An additional hormone produced by the thyroid contributes to the regulation of blood calcium
levels. Parafollicular cells produce calcitonin in response to hypercalcemia. Calcitonin stimulates
movement of calcium into bone, in opposition to the effects of parathyroid hormone (PTH).
However, calcitonin seems far less essential than PTH, as calcium metabolism remains clinically
normal after removal of the thyroid (thyroidectomy), but not the parathyroids.

[edit] Thyroid function laboratory tests - normal ranges[20]

Test Abbreviation Normal ranges

Serum thyrotropin/thyroid-stimulating
TSH 0.3–3.0 μU/ml
hormone
Free thyroxine FT4 7–18 ng/l = 0.7–1.8 ng/dl
800 ng/l – 1.8 μg/l = 80–
Serum triiodothyronine T3
180 ng/dl
Radioactive iodine-123 uptake RAIU 10–30%
Radioiodine scan (gamma camera) N/A N/A - thyroid contrasted images
Free thyroxine fraction FT4F 0.03–0.005%
Serum thyroxine T4 46–120 μg/l = 4.6–12.0 μg/dl
Thyroid hormone binding ratio THBR 0.9–1.1
Free thyroxine index FT4I 4–11
Free triiodothyronine l FT3 230–619 pg/d
Free T3 Index FT3I 80–180
Thyroxine-binding globulin TBG 12–20 ug/dl T4 +1.8 μg
TRH stimulation test Peak TSH 9–30 μIU/ml at 20–30 min.
Serum thyroglobulin l Tg 0-30 ng/m
Thyroid microsomal antibody titer TMAb Varies with method
Thyroglobulin antibody titer TgAb Varies with method

 μU/ml = mU/l, microunit per milliliter

 ng/dl, nanograms per deciliter
 μg, micrograms
 pg/d, picograms per day
 μIU/ml = mIU/l, micro-international unit per milliliter
 See [2] for more information on medical units of measure

[edit] Significance of iodine

In areas of the world where iodine is lacking in the diet the thyroid gland can become
considerably enlarged, a condition called 'endemic goitre'. Pregnant women who have diet which
is severely deficient of iodine can give birth to infants who can present with thyroid hormone
deficiency, manifesting in problems of physical growth and development as well as brain
development (a condition referred to as 'endemic cretinism'), and is one cause of congenital
hypothyroidism. In many developed countries newborns are routinely tested for congenital
hypothyroidism as part of newborn screening. Children with congenital hypothyroidism are
treated supplementally with levothyroxine, which facilitates normal growth and development.

Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom.
Among amphibians, for example, administering a thyroid-blocking agent such as
propylthiouracil (PTU) can prevent tadpoles from metamorphosing into frogs; in contrast,
administering thyroxine will trigger metamorphosis.

Because the thyroid concentrates this element, it also concentrates various radioactive isotopes of
iodine produced by nuclear fission. In the event of large accidental releases of such material into
the environment, the uptake of radioactive iodine isotopes by the thyroid can, in theory, be
blocked by saturating the uptake mechanism with a large surplus of non-radioactive iodine, taken
in the form of potassium iodide tablets. One consequence of the Chernobyl disaster was an
increase in thyroid cancers in children in the years following the accident.[21]

The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic
cretinism in most developed countries, and some governments have made the iodination of flour,
cooking oil, and salt mandatory. Potassium iodide and sodium iodide are typically used forms of
supplemental iodine.

As with most substances, either too much or too little can cause problems. Recent studies on
some populations are showing that excess iodine intake could cause an inceased prevelence of
autoimmune thyroid disease resulting in permanent hypothyroidism.[22]
[edit] Treatment for Hyperthyroidism
Beta blockers are used to decrease symptoms like fast heart rate, tremors, anxiety and chest
palpitations, and are sometimes anti thyroid drugs used to block thyroid hormones, particularly
in the case of Graves' disease. These medications take several months to take full effect and have
side effects like skin rash or a drop in white blood cell count, which decreases the ability of the
body to fight off infections. Sometimes these drugs involve frequent dosing (such as one pill
each 8 hours) and require frequent doctor visits (blood tests) to track impacts and progress and
sometimes may be ineffective at free. Because of the side effects and treatment protocol of
drugs, many patients choose to undergo surgery or more commonly the use of radioactive iodine
131, a type of radioiodine. Sometimes, radioiodine is administered under a thyroid ablation
procedure to severely restrict or altogether destroy the gland; the radioactive iodine is selectively
taken up by the gland and gradually thins out producing cells and destroys the tissues. The
treatment has been noted to be safe and effective.

Individuals that have underactivity of the thyroid gland require hormone replacement therapy.
Several types of thyroid hormone replacements are available and all are very safe but need to be
taken for the rest of one's life. Thyroid hormone treatment is given under the care of a physician
and may take a few weeks to become effective.[23]

Surgery is sometimes used to treat overactive thyroid, thyroid nodules, and often for thyroid
cancers. The surgery is quite effective but can have a few side effects or risks:

 The nerves controlling the vocal cords can be damaged.

 The parathyroid glands that produce parathyroid hormone (PTH) can be destroyed and
one can develop bleeding.
 If the entire thyroid gland is removed, one develops hypothyroidism, which entails taking
hormone supplements for the rest of one's life.[24]

[edit] History
There are several findings that evidence a great interest for thyroid disorders just in the Medieval
Medical School of Salerno (12th century). Rogerius Salernitanus, the Salernitan surgeon and
author of "Post mundi fabricam" (around 1180) was considered at that time the surgical text par
excellence all over Europe. In the chapter "De bocio" of his magnum opus, he describes several
pharmacological and surgical cures, some of which nowadays are reappraised quite scientifically
effective.[25]

In modern times, the thyroid was first identified by the anatomist Thomas Wharton (whose name
is also eponymised in Wharton's duct of the submandibular gland) in 1656.[26]

Thyroxin was identified only in the 19th century.

[edit] In other animals

The thyroid gland is found in all vertebrates. In fish, it is, in general, located below the gills and
is not always divided into distinct lobes. However, in some teleosts, patches of thyroid tissue are
found elsewhere in the body, associated with the kidneys, spleen, heart, or eyes.[27]

In tetrapods, the thyroid is always found somewhere in the neck region. In most tetrapod species,
there are two paired thyroid glands - that is, the right and left lobes are not joined together.
However, there is only ever a single thyroid gland in most mammals, and the shape found in
humans is common to many other species.[27]

In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the
gut, and associated with the larva's filter-feeding apparatus. In the adult lamprey, the gland
separates from the gut, and becomes endocrine, but this path of development may reflect the
evolutionary origin of the thyroid. For instance, the closest living relatives of vertebrates, the
tunicates and Amphioxus, have a structure very similar to that of larval lampreys, and this also
secretes iodine-containing compounds (albeit not thyroxine).[27]

[edit] Additional images

Section of the neck at Muscles of the neck.

Position of the Thyroid
about the level of the Anterior view.
in Males and Females
sixth cervical vertebra.

Superficial dissection of
Diagram showing Sagittal section of
The arch of the aorta, the right side of the neck,
common arrangement nose mouth, pharynx,
and its branches. showing the carotid and
of thyroid veins. and larynx.
subclavian arteries.
Muscles of the pharynx, The position and relation Section of thyroid The thymus of a full-
viewed from behind, of the esophagus in the gland of sheep. X 160. term fetus, exposed
together with the cervical region and in the in situ.
associated vessels and posterior mediastinum.
nerves. Seen from behind.

Thyoid histology

[edit] See also

 Thyroid disease
 Academy of Clinical Thyroidologists

[edit] References

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We have seen that cells are designed to run at -20 millivolts.  Cells need -50 millivolts to make
new cells to heal.  Chronic disease occurs when voltage drops below -20 millivolts.  As voltage
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2. 2.Chronic pain is caused by low voltage.

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 4. 4.With anaerobic metabolism, one unit of fat makes only two molecules of ATP
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5. 5.With anaerobic metabolism, microorganisms begin to grow and put out toxins to
dissolve our cells so they can eat us.

The Biomodulator can measure the voltage in the organs so you know whether the organ is
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the voltage in the cells to -50 millivolts so they can heal.

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