Some information about sluggish thyroid (hypothyroidism)

What is sluggish thyrrhoid

The thyroid gland is located in the front of the neck just below the larynx. It secretes hormones controlling and mostly enhancing metabolism.These are thyroxine (T4) and triiodothyronine (T3). Metabolism is the activity of breaking down nutrients to release energy used for internal and external work, and to keep the body temperature. By this condition the thyroid gland does not produce enough thyroid hormone.

Therefore sluggish thyrrhoid results in a decreased metabolic rate. That means that most important basic chemical processes in the body are slowed down. Fat and sugar consumed is not broken down fast enough to yield enough energy for the bodily activities. Instead much of the nutrients are just stored. The body does not either build up proteins and other complex molecules fast enough. All symptoms of sluggish thyrrhoid are related to the slow rate of chemical processes.

The earliest symptoms to occur will be a direct consequence of lack of available energy and of nutrients stored as fat instead of being used to do work. The body's normal functioning rate slows down, causing mental and physical sluggishness and an over-weight also develops.

Later on there will be symptoms related to lack of molecules for the development of body tissue and to repair body tissue from injuries, and symptoms from a defective immune systems that lack important molecular tools for its work, like anti-bodies.

sluggish thyrrhoid may cause a variety of symptoms and may affect all body functions. The symptoms may vary from mild to severe, which is called myxedema.


Symptoms occuring early are:

-weakness
-fatigue of physical and mental type
-intolerance against cold
-constipation, even with food containing much fibres, like whole corn bread vegatables, fruit and the like.
-weight gain, even without excessive eating.
-thin and brittle hair
-pale color
-depression
-joint or muscle pain
-thin, brittle fingernails


Later the following symptoms may occur:

-decreased taste and smell
-thinning of eyebrows
-hoarseness
-abnormal menstrual periods
-slow speech
-dry flaky skin
-skin thickening
-puffy face, hands and feet


Because the thyroid hormones regulates, and mostly increases the metabolic functions of the body, a lot of other secundary symptoms may occure, because normal bodily processes occur to slowly.

-overall swelling
-muscle spasms (cramps)
-muscle pain
-muscle atrophy
-uncoordinated movement
-absent menstruation
-joint stiffness
-hair dryness
-extremity swelling
-short stature
-separated sutures
-delayed formation of teeth
-absence of teeth
-hair loss
-facial swelling
-drowsiness
-appetite loss


The causes and variants of sluggish thyroid

Hashimoto's thyroiditis - Sluggish thyrrhoid is most often caused by Hashimoto's thyroiditis, a disease of the thyrhoid gland where the body's immune system attacks the gland. By this disease the immune system attacks an enzyme used in the production of thyroid hormones, thyroid peroxidase, and the proteins used to store the hormones, thyreoglobulines. The disease involves attack by antibodies and  invasion by cells like leucocytes in the thyroid gland.  By the disease follickles in the throid gland are destroyed, but the thyroid gland does not shrink.

Ord's thyroiditis - Sluggish thyroid is also often caused by anothor form of auto-immune attack on the thyroid gland, Ord's thyroiditis. Also by this disease there is an attack from the immune system at enzymes like thyroid peroxidase and at the thyreoglobulines. Also this disease involves attack by antibodies and  invasion by cells like leucocytes in the thyroid gland. By this disease the thyroid gland can react with increased hormone production a time before the production of hormones drops. The disease is characterized by a shrinking of the thyroid gland.  It differs accordingly from Hashimoto's disease by the exact symptoms and the exact chemical nature of the antibodies.

Subacute thyroiditis - Subacute hypothyroidism is an inflammation in the thyroid gland that causes mild hypothyroidism that usually heals by itself after some time. It occurs often as a reaction to upper respiratory tract infection.

Postpartum thyroiditis - Postpartum hypothyroidism occurs in women after pregnancy. It is probably caused by antibodies against the thyroid tissue that are present allready before and during pregnancy and the pregancy probably aggavate this condition so that overt symptoms of hypothyroidism develop. This kind of hypothyroidism will often be chronic.

Congenital sluggish thyroid - There is a variant called congenital sluggish thyrrhoid that one can detect by screening tests of newborn.

Secundary thyroiditis - caused by failur in the hypothalamus or pituitary - The hypothalamus (a part of the brain) and the pituitary gland regulate the secretion of T3 and T4. The hypothalamus produces a hormone that goues downt to the pituitary below and stimulates the pituitary to secrete the hormone thyreotropin. Thyreotropine released into the blood strem stimulates again the thyroid gland to produce its hormones.

Abnormalities of the pituitary or hypothalamus may thus also cause thyroid secretion disorders. Failure of the pituitary gland to secrete a hormone to stimulate the thyroid gland (secondary hypothyroidism) is however a less common cause of sluggish thyrrhoid.

Hypothyroiditis after medical treatment - Surgical removal of the thyroid gland or parts of it or irradiation of the gland can cause hypothyroidism.


Risk factors for hypothyroiditis

Risk factors include age over 50 years, female gender, obesity, thyroid surgery, and exposure of the neck to x-ray or radiation treatments.


Findings by physical examinations

A physical examination shows delayed relaxation of muscles during tests of reflexes, pale and yellow skin, loss of the outer edge of the eyebrows, thin and brittle hair, coarse facial features, brittle nails, firm swelling of arms and legs. One may note mental slowness. Vital signs symptoms are slow heart rate, low blood pressure, and low temperature.

The heart may be enlarged, which is detected by x-ray.

Laboratory tests to determine thyroid function include:

-T4 test (low)
-serum TSH (high in primary sluggish thyrrhoid, low or low-normal in secondary sluggish thyrrhoid)


Additional laboratory abnormalities may include:

-increased cholesterol levels
-increased liver enzymes
-increased serum prolactin
-low serum sodium
-a complete blood count (CBC) that shows anemia


Complications of an ineffective thyroid gland and insufficient thyroid hormone production

Complications of hypothyroidism are heart disease, increased risk of infection, infertility, and miscarriage.

Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection, illness, exposure to cold, or certain medications in an individual with untreated sluggish thyrrhoid. Symptoms of myxedema coma include unresponsiveness, decreased breathing, low blood pressure, low blood sugar, and below normal temperature.


Traditional measures for the treatmen of hypothyroidism

By the conevtional approach, sluggish thyrrhoid is seldome treated before it has developed into a serious disease.

The purpose of treatment is to replace the deficient thyroid hormone levels by drugs containing some variant of the thyroid hormones. Levothyroxine is the most commonly used medication. The lowest dose effective in relieving symptoms and normalizing the TSH is used. Life-long therapy is the norm and medication is thus continued even when symptoms subside. Thyroid hormone levels must be monitored yearly after a stable dose of medication is determined.

However, this treatment may result in symptoms of to much thyroid activity (hyperthyroidism), which as restlessness, rapid weight loss, and sweating, when the mediaction is not totrated to the right amount.

Myxedema coma is treated with intravenous thyroid replacement and steroid therapy. Supportive therapy of oxygen, assisted ventilation, fluid replacement, and intensive-care nursing may be indicated. Treatment restores normal state as long as one manages to titrate the medication doses to right level. The medication is lifelong.


Natural treatment for sluggish thyrrhoid

On the market you can find supplements to treat hypothyroidism naturally. These natural means to cure sluggish thyrrhoid attack he lack of thyroid hormons from several angles:

- They may supply the body with raw materials that the tyroid gland use to make the hormones, like thyrosine or thyrosine derivates and iodine.

- They may supply herbs or other ingredients that stimulate the thyroid gland to higher hormone production, like for exaple aspartate, the element manganese and a battery of vitamins

- They may give ingredients that stimulate the thyroid tissue to repair iteslf from damage, like the elements manganese, magnesium and zink.

- They may contain igredients that alleviate inflammation, and thereby take away inflamamtory processes in the thyroid gland that destroy tissue.

- They may contain measures to help the body against the consequences of a sluggish thyroid, for example the element potassium.

A diet that decreases inflammation in the body and supplies the body with nutrients important for the function and repair of the thyroid gland, is also a useful means to help cure sluggish thyrrhoid. Such a diet contain fatty acids that are known to have anti-inflamamtory actions like omega-3 polyinsaturated acids and mono-unsaturated acids. Such acids are found in nutrients like olive oil, flax oil, rape oil, fish, almonds and seafood.

Great amount of fatty acids that stimulate inflammatory processes should also be avoided, like omega-6 polyunsaturated fatty acids and trans fat. Nutrients to be avoided in great amounts are soy oil, corn oil pal oil, margarine an dready made food containing these fat types.


THE PRODUCTION AND ACTION OF THE THYROID HORMONS IN THE BODY

The primary function of the thyroid is production of the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin. Up to 80% of the T4 is converted to T3 by peripheral organs such as the liver, kidney and spleen. T3 is about ten times more active than T4.


Production of the thyroid hormones

Thyroxine is synthesised by the follicular cells from free tyrosine and on the tyrosine residues of the protein called thyroglobulin (TG). Iodine, captured with the "iodine trap" by the hydrogen peroxide generated by the enzyme thyroid peroxidase (TPO)[2] 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 proteolytically cleave the iodinated tyrosines from TG, forming T4 and T3 (in T3, one iodine is absent compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3[3]. Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3[1].


Action of the thyroid hormones

Cells of the brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play a particularly crucial role in brain development during pregnancy[4]. A transport protein (OATP1C1) has been identified that seems to be important for T4 transport across the blood brain barrier[5]. A second transport protein (MCT8) is important for T3 transport across brain cell membranes.

In the blood, T4 and T3 are partially bound to thyroxine-binding globulin, 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.



Regulation of the thyroid hormone production

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, and vice versa. 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.


The hormone Calcitonin

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, but not the parathyroids.

It may be used diagnostically as a tumor marker for a form of thyroid cancer (medullary thyroid adenocarcinoma), in which high calcitonin levels may be present and elevated levels after surgery may indicate recurrence. It may even be used on biopsy samples from suspicious lesions (e.g. swollen lymph nodes) to establish whether they are metastasis of the original cancer.

Calcitonin can be used therapeutically for the treatment of hypercalcemia or osteoporosis.


The role of iodine

In areas of the world where iodine (essential for the production of thyroxine, which contains four iodine atoms) is lacking in the diet, the thyroid gland can be considerably enlarged, resulting in the swollen necks of endemic goitre.

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; conversely, administering thyroxine will trigger metamorphosis.

In humans, children born with thyroid hormone deficiency will have physical growth and development problems, and brain development can also be severely impaired, in the condition referred to as cretinism. Newborn children in many developed countries are now routinely tested for thyroid hormone deficiency as part of newborn screening by analysis of a drop of blood. Children with thyroid hormone deficiency are treated by supplementation with synthetic thyroxine, which enables them to grow and develop normally.

Because of the thyroid's selective uptake and concentration of what is a fairly rare element, it is sensitive to the effects of 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. While biological researchers making compounds labelled with iodine isotopes do this, in the wider world such preventive measures are usually not stockpiled before an accident, nor are they distributed adequately afterward. One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.

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 mandatory. Potassium iodide and Sodium iodide are the most active forms of supplemental iodine




Image showing the thyroid gland and the parathyroid glands - glandula thyroidea and glanadulae parathyroideae. The information and image in this article are mostly fetched from Wikipedia.org, and it is therefore free to copy and reuse.