Iodine is the substrate that provides the synthesis of thyroid hormones, thyroxine and triiodothyronine, in the body, which are essential for normal growth and development. The thyroid gland weighs 15-20g and contains 80% of the body’s iodine pool, about 15mg for adults. Iodide, in its ionic form, is rapidly absorbed from the gastrointestinal tract and distributed to the extracellular fluid. The general intake of iodine in healthy people is 100-200 μg per day, mostly from iodized salt (70 μg/g).
Deficiency
Iodine deficiency is caused when iodine intake is less than 20μg per day. In mild iodine deficiency, the thyroid gland becomes excessively enlarged under the influence of stimulating thyroid hormones to concentrate iodide in itself, causing mucinous goiter. Most of these patients still have normal thyroid function. Zhou Guangwen, Department of General Surgery, Shanghai Sixth People’s Hospital
Severe iodine deficiency can cause endemic mucinous edema in adults and endemic cretinism in infants. Several metabolic disorders in thyroid hormone synthesis can cause hypothyroidism in adults and infants. However, worldwide, endemic iodine deficiency remains the leading cause of hypothyroidism. Severe maternal iodine deficiency prevents fetal growth and brain development. Endemic cretinism can take one of two forms (neurological or mucinous edema) depending on the interaction of iodine deficiency and genetics.
Iodine-deficient infants are given L-thyroxine (3 μg/kg per day) for 1 week plus 50 μg of iodide to restore normal thyroid function as soon as possible. Iodide supplementation is continued. Iodine-deficient adults are given iodide at a dose of 1500 μg/day (about 10 times the RDA) for several weeks to restore iodine levels in depleted glands and to synthesize thyroxine.
Poisoning
Chronic iodine toxicity can occur when iodide intake is greater than 20 times the daily requirement, i.e., 2 mg per day. In some areas, especially in Japan, residents consume as much as 50 to 80 mg per day, causing high plasma levels. Some of these people develop goiter, but most of them still have normal thyroid function. Some people develop mucinous edema, while others paradoxically develop hyperthyroidism (Jod-Basedow phenomenon). Increased iodine intake by the thyroid gland can lead to inhibition of thyroid hormone synthesis (Wolff-Chaikoff effect), which eventually leads to iodothyroidism or mucinous edema. Very high doses of iodide, a brass-like hobby, can produce increased salivation, gastric irritation, and acne-like skin damage.
Iodine, a necessary component of thyroxine, is closely related to the health of the body. Iodine deficiency can lead to iodine deficiency disease (IDD), which includes premature birth, miscarriage, first birth, congenital malformations, endemic deafness, mental retardation, cerebral hypoplasia, and infertility caused by micro-iodine. It also includes physical and bone age developmental backwardness due to birth residence in iodine deficient areas, mild intellectual backwardness, mild neurological dysfunction, and thyroid dysfunction.
It is important to note that the human body’s intake of iodine is not as high as possible. The prevalence of iodine on goiter is clearly bidirectional, with upper and lower limit thresholds. Below the lower threshold, low iodine goiters are caused, while above the upper threshold, high iodine goiters are caused, with a “safe range” between the upper and lower thresholds and sporadic goiters.
6 types of goiter
Goiter is commonly known as thick neck disease. When it comes to this disease, many people think of eating more iodine-rich seaweed. In fact, this idea is biased. The causes of goiter are complex and are usually divided into six types.
1. endemic goiter, which mostly occurs in iodine-deficient areas.
2. physiological goiter, mostly seen in adolescent development, women during pregnancy and lactation
3. hyperiodized goiter.
4. hyperthyroidism.
5. thyroiditis.
6, goitre.
The first two types of patients are very beneficial to eat more iodine-rich foods, but the last four types of patients eating iodine-rich foods are not only unhelpful, but also can worsen the condition or bring trouble to diagnosis and treatment.
In China, there are more patients with high iodine goiter in coastal and inland low-lying saline areas. This is due to excessive consumption of iodine-rich seafood or high iodine content in drinking water for a long time. If you continue to give this “thick neck” to eat iodine-rich food, it will undoubtedly aggravate the condition and even lead to hyperthyroidism.
In patients with hyperthyroidism, the thyroid gland’s ability to take in iodine is 10 times greater than that of a normal person. A large amount of iodine can temporarily suppress thyroxine in the short term, but iodine is, after all, the raw material for thyroxine, and continued excessive intake of iodine for more than half a month can cause an increase in thyroid hormones, which in turn can worsen the symptoms of hyperthyroidism.
Excessive intake of iodine in patients with thyroiditis can cause hypothyroidism and mucinous edema. If you consume iodine-rich foods such as kelp and nori, you should not have an isotope test for 2 months, as this will affect the accuracy of the test. It is true that patients with goiter should first go to a hospital for examination and diagnosis and under the guidance of a doctor for medication or dietary treatment. Do not blindly take iodine supplements or foods rich in iodine without permission.
Goiter caused by excessive iodine intake
Goiter caused by excessive iodine intake is common in people who have been taking iodine-containing drugs for a long time due to a certain disease. (Endemic hyperthyroidism was first reported in a study of goiter and iodine metabolism in fishermen off the coast of Hokkaido, Japan, and in 1978, scholars in China also reported an epidemic of goiter in fishermen drinking highly iodized water off the coast of Bohai Bay, Hebei Province, and since then there have been increasing reports in this area.) The distinctive feature of such patients is that their symptoms can be significantly relieved or even disappear within a few weeks after stopping consumption of high iodine products or induced water. The mechanism of goiter due to high iodine is generally believed to be: firstly, excessive inorganic iodine generates too much I2, which inactivates the “active iodine” and inhibits the iodination of camptothecin in the gland; secondly, iodine inhibits the enzymes related to hormone secretion in the gland, which makes it difficult to keep the flow group of thyroid proteins in a reduced state, thus making it difficult to release thyroxine by the action of thyroid protein hydrolase, resulting in a decrease in the level of hormones in the blood. This leads to a decrease in the level of hormones in the blood and an increase in the level of thyroid stimulating hormones, causing goiter.
Causes of goiter
Goiter is one of the common clinical signs with various causes, the common causes are
1. Iodine deficiency and high iodine causing goiter: Iodine deficiency is the main cause of endemic goiter, mostly seen in the interior and mountainous areas away from the high terrain of the ocean. Adolescence, pregnancy, lactation, menopause and mental stimulation, trauma and other causes.
2, all can increase the need for thyroxine, resulting in a relative lack of iodine. When the environment is iodine deficient and the concentration of inorganic iodine in the blood is reduced, the thyroid tissue proliferates and enhances its iodine uptake function, trying to make the thyroid gland take in enough iodine from the blood in a low iodine state to ensure the synthesis of sufficient amounts of thyroid hormones to supply the physiological needs of the body tissues. However, when iodine deficiency is severe, this compensatory mechanism is still unable to maintain normal thyroid function, and the thyroid gland preferentially secretes T3, which requires less iodine but is more active, while T4 synthesis is reduced. Since the concentration of T4 in the blood is the main reason for stimulating the pituitary gland to produce thyroid stimulating hormone, a decrease in the concentration of T4 in the blood stimulates the pituitary gland to produce more thyroid stimulating hormone, resulting in an enlarged and enlarged thyroid gland. In addition, due to the long-term intake of excessive iodine, there are too many inorganic iodine ions in the thyroid tissue, which hinders the organicization process of iodine, resulting in a decrease in thyroxine synthesis.
3, to goiter substances: some people found that some food may have a certain relationship with the occurrence of enlargement of the thyroid gland. Eating a lot of cabbage for a long time can cause goiter. It has been found that the organic cyanide in cabbage can affect the oxidation of iodide, which affects the synthesis of thyroid hormones and then causes compensatory enlargement of the thyroid gland. Cassava can also cause goiter, also because it contains cyanide cyanate sugar, which produces thiocyanate after eating, preventing the thyroid gland from taking in iodine. Turnips and brassicas contain thiourea-like substances that cause goiter, which has the effect of causing goiter. The prolonged consumption of soy can also prevent the reabsorption of thyroid hormones in the intestine, resulting in increased loss of thyroid hormones in the feces, which in turn causes a relative deficiency of thyroid hormones. Infants have been found to develop an enlarged thyroid gland when fed a soy diet. When the soy component is removed, the goiter resolves on its own. Long-term consumption of peas and peanuts may also cause goiter, as they may produce a substance called 5-ethylene-2-sulfur oxazepentacyclic, which has a goiter-causing effect. The prolonged use of certain drugs such as potassium cyanide, potassium perchlorate, para-aminosalicylic acid, pau d’arco, sulfonamide and thioureas can prevent the synthesis of thyroid hormones and inhibit their release, resulting in a decrease in thyroxine and an increase in thyroid stimulating hormones in the blood, causing goiter.
4. Congenital defects in thyroid hormone synthesis: The synthesis of thyroid hormones requires the catalytic action of a variety of special enzymes to complete.
Nodular goiter is a common clinical thyroid disease and a neck lump easily found in recent years during physical examinations. The nodules are sometimes hard to the touch and cause nervousness, fearing that something “bad” has grown. In fact, most long-term goiters will develop into this disease. This is a benign thyroid disease, and surgery is often prone to recurrence, so surgery is generally not recommended. Of course, surgery should be considered when the growth is fast and there are symptoms of pressure or suspected malignancy.
The etiology of this disease is many. Considering that thyrotropin (TSH) from the pituitary gland has a proliferative effect on the thyroid gland, thyroxine is commonly used to suppress TSH in order to treat nodular goiter. It is important to emphasize that the dosage of suppression and replacement are different, as the former requires a full dose to have suppressive effect, while the latter can be used in normal doses. The former requires a full dose for suppression, while the latter can be used in normal doses. The main purpose of clinical use of thyroxine is to identify the benign and malignant nature of nodular goiter. Benign nodules can be suppressed, and the mass will shrink with the decrease of TSH after using thyroxine; malignant masses, although TSH decreases, the mass is not small or enlarged, and surgery should be considered. However, it is necessary to use thyroxine for at least 6-9 months before making a judgment.
After surgery for nodular goiter, thyroxine is commonly used for 1-2 years after which the dosage is gradually reduced. This is not replacement therapy, but the main purpose is to suppress TSH to prevent recurrence. Some patients often ask which is better: thyroid tablets or thyroxine tablets. Generally speaking, the former comes from the animal thyroid gland, which is unstable in efficacy but cheaper; the latter is synthetic thyroxine, which is stable in efficacy but more expensive in price. Some people also ask, to evaluate thyroid function, which is better, thyroxine T3 or T4, given that T4 is all but T3 is only a small part synthesized by the thyroid gland, so T4 is more valuable
Overview of thyroid nodules: Nodules on the thyroid gland may be thyroid cancer, thyroid adenoma, nodular goiter and other causes, which are collectively called thyroid nodules until their nature is clarified.
The determination of the benignity of thyroid nodules is based on medical history, physical examination, and radionuclide scan, as well as cytological examination. In terms of medical history, 50% of nodules that appear in childhood are malignant, and a single nodule that occurs in a young male should also be alerted to the possibility of malignancy. On physical examination, multiple nodules are usually benign lesions, while thyroid cancer is mostly a single isolated nodule with uneven angular palpation, hard texture, and little movement when swallowing, and sometimes even the enlarged lymph nodes in the ipsilateral neck can be palpated. On radionuclide scan, thyroid cancer is mostly “cold nodules” with faint margins. The nature of the nodule can be further clarified by puncture cytology, and the correct diagnosis rate of experienced pathologists can be over 80%.
Those with high suspicion of malignant disease should have the nodules surgically removed as soon as possible. Although multiple nodules or single adenomas are benign lesions, some patients may develop secondary hyperfunction or cancer, so early surgical treatment is also recommended.
Thyroid nodules are a common thyroid disorder
Many thyroid disorders can manifest as nodules and can be caused by a variety of pathologies such as thyroid degeneration, inflammation, autoimmunity, and neoplasia.
Thyroid nodules can be seen in both men and women of all ages, but are more common in middle-aged women. Thyroid nodules can be solitary or multiple. Multiple nodules have a higher incidence than solitary nodules, while solitary nodules have a higher incidence of thyroid cancer compared to multiple nodules. Thyroid nodules are divided into two categories: benign and malignant, with the majority being benign and less than 1% being malignant. Based on the etiology of the nodules, they can be classified as: nodular goiter, inflammatory nodules, toxic nodular goiter, thyroid cysts, and thyroid tumors. Early recognition of the nature of thyroid nodules, especially the differentiation between benign and malignant lesions, is important for the selection of treatment options and prognosis.
Nodular goiter is a common thyroid disorder. Nodular goiter is a benign disease that is most commonly seen in middle-aged women. Due to the relative deficiency of thyroid hormones in the body, the pituitary TSH secretion increases. Under the stimulation of this increased TSH for a long period of time, the thyroid gland repeatedly proliferates with various degenerative changes and eventually forms nodules.
The clinical manifestation is an enlarged thyroid gland with multiple nodules of varying sizes that can be seen or palpated, and the texture of the nodules is mostly moderately hard. There are few clinical symptoms, only discomfort in the anterior neck area. Thyroid function is mostly normal. A thyroid scan and ultrasound of the thyroid gland can make a definitive diagnosis.
Single nodular goiter needs to be excluded, thyroid tumor and multinodular goiter do not always require surgery, and can be better treated with Chinese medicine. Patients can refer to the diagnostic opinion of endocrinologists to decide whether to operate. Preoperative thyroid function and thyroid antibodies should be checked to avoid postoperative hypothyroidism.
Nodular goiter with hyperthyroidism
This disease is also known as toxic multinodular goiter and secondary hyperthyroidism. It is a type of hyperthyroidism that occurs on the basis of multinodular goiter, and multinodular goiter has often existed for many years before the onset of hyperthyroidism. It is a common result of simple goiter after a long period of illness, and the cause is unknown. The onset of the disease is slow and mild in women over 40 to 50 years of age. The symptoms of neuroexcitation are not obvious, and proptosis is rare. The thyroid gland is enlarged and multiple nodules may be palpable, with varying sizes; there is no tremor or vascular murmur. TT3 is elevated and TT4 is normal or elevated, which may be manifested as T3 hyperthyroidism. Care should be taken to avoid the term toxic nodular goiter, as it includes both toxic multinodular goiter and toxic thyroid adenoma.
What is the significance of an isotope scan in patients with thyroid nodules?
An isotope scan of a thyroid nodule, known as an ECT test, is an ancillary test that is used by physicians to diagnose the disease. The main purpose is to clarify the function of the nodule. The scan results are generally classified into four categories: hot nodules, warm nodules, cool nodules and cold nodules. A hot nodule is a nodule that takes up more iodine than the surrounding thyroid tissue and is usually a high-functioning adenoma. Warm nodules refer to nodules with the same iodine uptake as the surrounding thyroid tissue, cool nodules refer to nodules with lower iodine uptake than the surrounding thyroid tissue and are usually benign, and cold nodules refer to nodules with no iodine uptake. The latter three conditions only indicate the function of the nodule and do not determine the nature of the nodule. In the case of cold nodules, this means that the thyroid mass has no iodine uptake function at all, such as in thyroid cancer, but cold nodules can occur in a variety of thyroid diseases and are not specific to thyroid cancer. -Some benign lesions such as thyroid adenomas, cysts, hemorrhages, calcifications, and thyroiditis can manifest as cold nodules.
Why should hyperthyroidism patients not consume foods high in iodine for a long time?
Since ancient times, Chinese doctors have been using iodine-containing drugs and foods to treat gall tumors (including hyperthyroidism) with certain efficacy, but since the 1980s, as people continue to study the pathology and physiology of hyperthyroidism and accumulate clinical experience, they have gradually realized the advantages and disadvantages of iodine-containing herbs and foods for the treatment of hyperthyroidism. If the dose exceeds the limit (5 mg/day for normal people and 2 mg/day for hyperthyroidism patients), the synthesis and release of thyroid hormone will be temporarily inhibited, so that the amount of thyroid hormone in the blood will drop quickly and the patient’s symptoms will be relieved rapidly. It is important to emphasize that the inhibition of thyroid hormone synthesis and release by iodine is temporary. If you take high iodine foods (drugs) such as kelp, sea fish, jellyfish and other high iodine foods for a long time, the thyroid gland may “adapt” to the inhibition of iodine, so that the synthesis of thyroid hormone “escapes” from the inhibition of iodine. After “escaping”, the synthesis of thyroid hormone is accelerated again, so that the accumulation of thyroid hormone in the thyroid gland increases day by day, and a large amount of accumulated thyroid hormone is released into the blood, so that the concentration of thyroid hormone in the blood increases suddenly, which may cause the recurrence of hyperthyroidism, so it is inappropriate to take a large amount of high iodine food (drugs) for a long time. Therefore, it is inappropriate to take a lot of high iodine foods (drugs) for a long time. It should be noted that iodine deficiency is not the cause of hyperthyroidism, so iodine preparations and high iodine foods cannot be used as the main drugs or foods for hyperthyroidism treatment and dietary therapy.
Can hyperthyroidism patients eat foods containing iodine?
Iodine is one of the important raw materials for the synthesis of thyroid hormones by the thyroid gland. The content of thyroid hormones in the body of hyperthyroid patients is already higher than that of normal people, so if iodine-containing foods are given, the hyperfunctional thyroid gland will synthesize more hormones, which will aggravate the condition.
2. The bioavailability of iodine in the thyroid gland of hyperthyroidism patients is significantly higher than that of normal people. Even if a small dose of iodine-containing food is given, the sick thyroid gland may produce more thyroid hormones than normal, thus aggravating the condition.
3. The normal organism will excrete excess iodine after consuming too much iodine-containing food to avoid producing excessive thyroid hormones. However, hyperthyroid patients with abnormally hyperactive thyroid gland and dysfunctional self-protection mechanism will not only fail to remove the excess raw materials, but will instead make excessive use of this iodine to synthesize a large amount of thyroid hormones, which will worsen their condition.
Therefore, not only should hyperthyroidism patients not take iodine-containing food supplements, but they should also avoid any iodine-containing food and medication as much as possible. The highest iodine content is found in seafood, especially kelp, jellyfish, nori, seaweed and mussels.
What is the principle of radioactive iodine treatment for hyperthyroidism?
Radioactive 131 iodine was first used as a treatment for hyperthyroidism in 1942 and is an effective anti-thyroid drug. Thyroid cells have a special affinity for iodide, and after a certain amount of 131 iodine is taken orally, it can be absorbed by the thyroid gland in large quantities, and the radioactive 131 iodine with damaging effects can be seeded into the thyroid tissue. 131 iodine, when decaying into 131 xenon, can radiate beta rays (99% of the total) and gamma rays (1% of the total). The former has an effective range of only 0.5 to 2 mm, and can selectively destroy the epithelium of the thyroid vesicles without affecting the adjacent tissues. Therefore, some people call 131 iodine treatment for hyperthyroidism “internal thyroid surgery”.