Hypothyroidism is a common endocrine disorder caused by a deficiency of thyroid hormone. Primary hypothyroidism occurs when the thyroid gland fails to produce thyroid hormones necessary to meet the body’s metabolic needs.
A disorder of the pituitary gland or hypothalamus are the main causes of secondary hypothyroidism:
- Pituitary gland fails to secrete thyroid-stimulating hormone (TSH) leading to deceased synthesis of thyroid hormones.
- Hypothalamus does not release appropriate levels of the thyroid-releasing hormone (TRH) causing the thyroid gland produce inadequate amount of thyroid hormones.
A variety of disorders could be a cause of secondary hypothyroidism including pituitary adenomas and side effects of their treatments such as surgery and radiotherapy.
The main cause of primary hypothyroidism is an autoimmune thyroid condition called Hashimoto’s disease which affects women 3 to 5 times more often than men. Genetic predisposition and environmental factors could trigger Hashimoto’s thyroiditis causing the immune system to malfunction. The thyroid antibodies attack and destroy the thyroid gland leading to inflammation and hypothyroidism.
Pregnancy could cause hypothyroidism due to the shifts in hormonal and immune functions during and after pregnancy. Pregnant women become Th2 dominant in the third trimester. Later on the immune system shifts to Th1 dominance and can trigger Hashimoto’s disease and cause hypothyroidism.
Both postpartum thyroiditis and silent thyroiditis are a form of chronic autoimmune thyroiditis and could be a possible cause of hypothyroidism. Postpartum thyroiditis occurs during the first year after delivery. This autoimmune condition affects from 5 to 10% of women who give birth and is characterized by high levels of thyroid antibodies and painless goiter. Postpartum thyroiditis often causes temporary mild hypothyroidism that could last up to 4 years and in most cases subside later on.
Silent thyroiditis is also a temporary condition where thyroid gland becomes over reactive initially. About half of affected women progress to transient hypothyroidism which normally subsides within a couple of months. Hypothyroidism becomes permanent only in about 5% of women.
Birth control pills, fluctuations of estrogen during the perimenopause and menopause and hormonal imbalances especially estrogen dominance could trigger Hashimoto’s disease and hypothyroid symptoms in women. Excess estrogen inhibits thyroid action, lowers the rate of metabolism and contributes to hypothyroidism. In the opposite case, progesterone supports thyroid function.
Polycyctic ovary syndrome (PCOS) and Hashimoto’s diesease drive each other. A high proportion of women with PCOS have elevated levels of thyroid antibodies and show damage to the tissue of the thyroid gland.
An adequate amount of iodine is necessary for the thyroid gland to function and produce thyroid hormones. Both excess and deficiency of iodine are common causes of hypothyroidism, enlargement of the thyroid gland and also can trigger Hashimoto’s disease. When not enough iodine comes from the diet then the person may become hypothyroid or subclinical hypothyroid.
Excessive iodine can trigger autoimmune thyroid disease Hashimoto’s thyroiditis in genetically susceptible individuals and cause permanent damage to the thyroid gland. Excess of iodine in the diet can stimulate the immune system to create antibodies that attack the thyroid gland.
As a result, the thyroid starts to produce less hormones and with time it can be a possible cause of progression to hypothyroidism. More information on how high iodine affects thyroid function can be found in the FREE e-mail course Nutritional guide for Hashimoto’s disease and hypothyroidism.
High iodine intake through the diet has been found to increase the incidence of clinical hypothyroidism. Iodine is concentrated in the thyroglobulin within the thyroid gland. After the ingestion of large amounts of iodine with the diet the production of pro-inflammatory free radicals significantly increases and the synthesis of hormones within the thyroid gland becomes impaired.
Overuse of iodine supplements and high dietary intake of iodine can be a frequent cause of transient hypothyroidism. The best way to evaluate if iodine is a cause of your thyroid problems is to perform a reliable iodine test.
The modern American diet is very acidic: most people consume far more dietary acids than bases. This imbalance is called metabolic acidosis can result in some serious long-term health and physique problems and contribute to mild hypothyroidism.
Liver detoxification problems and impaired clearance of hormones from the liver can cause mild hypothyroidism. Liver and thyroid are closely connected. Without a properly functioning liver thyroid hormone conversions can be diminished and result in low T3 and hypothyroid symptoms.
Intestinal dysbiosis is a deficiency or absence of good bacteria in the intestinal flora that can also lead to an abnormally high level of bacterial infections in the small intestine such candida overgrowth. Both this conditions can trigger increased thyroid autoimmunity and result in Hashimoto’s disease, impaired T4 to T3 conversion and multiple hypothyroid symptoms in women.
Gluten is another common dietary factor that can trigger Hashimoto’s disease. Recent studies show that people with Hashimoto’s have some degree of gluten sensitivity or full-blown celiac disease due to common genetic predisposition shared between these two health conditions.
People with digestive disorders, IBD, celiac disease and leaky gut show malabsorption of many nutrients. Some of these nutrients are necessary for thyroid hormones production and metabolism. Nutritional deficiencies, for example low selenium levels is a well-known factor that can result in hypothyroidism, elevated thyroid antibodies and selenium deficiency induced Hashimoto’s disease.
People who have Hashimoto’s and hypothyroidism and go gluten free have shown to reduce their levels of thyroid antibodies and dose of thyroid drugs in many cases. In addition, celiac disease affects thyroid autoimmunity due to impaired absorption of selenium and other nutrients.
Contamination of food and water supplies with chemical agent perchlorate could contribute to thyroid problems in susceptible individuals. Perchlorate blocks iodine uptake in the thyroid gland and may increase the risk for subclinical hypothyroidism especially in the women with low iodine levels. Toxicity is one of often overlooked factors that contributes to hypothyroidism.
Radioiodine treatment and thyroidectomy used for treatment of hyperthyroidism are less common causes of underactive thyroid in women. Whole body irradiation and external radiotherapy of the head and neck could cause damage to the thyroid gland and result in permanent hypothyroidism.
Use of various drugs are well-known side effects that can cause hypothyroidism. Common medication for bipolar disorder lithium inhibits the release of the thyroid hormones contributing to the development of hypothyroidism and goiter. Lithium and interferons could also initiate chronic autoimmune thyroiditis with hypothyroidism. The iodine containing drug amiodarone and contract agents have been also shown to cause hypothyroidism.
Overtraining and a wrong type of exercise can contribute to hypothyroidism, autoimmunity and make an existing health condition worse. It is important to make sure that your exercise program makes you feel good.
According to Dr. D.Kharrazian, there are about 22 thyroid defects that can be a hidden cause of hypothyroidism. You can get more information about it in the article Thyroid Defects Most Doctors Don’t Know About
If you would like to know more on how iodine and diet affect your thyroid function get your FREE e-mail course Nutritional guide for Hashimoto’s disease and you will also receive free blog updates for OutsmartDisease.com
Why do I still have thyroid symptoms? When my lab tests are normal: A revolutionary breakthrough in understanding Hashimoto’s disease and hypothyroidism by Dr. Datis Kharrazian, Morgan James Publishing, 2010
Hypothyroidism – new aspects of an old disease. Hippokratia. 2010 Apr;14(2):82-7.