- More than 27 million Americans have some type of thyroid dysfunction and about half of them remain undiagnosed.
- The thyroid gland is located in the front central area at the base of the neck and produces thyroid hormones thyroxine (T4), triiodothyronine (T3), diiodotyronine (T2), monoiodotyronine (T1) and calcitonin.
- To build thyroid hormones the human body needs iodine and tyrosine that can be obtained from your diet.
- The lack of thyroid hormone affects the function of every cell in the body slowing down the metabolic rate.
- There is significantly more T4 hormone produced in the thyroid gland than T3. The ratio of T4 to T3 released in the blood is about 20 to 1.
- T3 is the active form of thyroid hormone whereas T4 is a pro-hormone and is metabolically inactive.
- About 80% of T3 hormone is produced through conversion from T4 in the liver, kidneys, peripheral tissues and cells.
- Up to 20% of thyroid hormone conversions from T4 to T3 takes place in the intestines but only in the presence of good bacteria.
- Only 0.5% of thyroid hormone is in a “free” metabolically active form.
10. Reverse T3 is biologically inactive and blocks the action of metabolically active thyroid hormoneT3.
11. About 30% of the body’s iodine supply is concentrated in the thyroid gland, where the amount of iodine is 20 to 40 times greater than in the blood.
12. Iodine deficiency contributes to thyroid disease, enlargement of the thyroid gland, hypothyroidism and mental abnormalities in children.
13. Hashimoto’s thyroiditis is an inflammation of the thyroid gland and sometimes also called Hashimoto’s disease, chronic lymphocytic thyroiditis or autoimmune thyroiditis.
14. In the autoimmune thyroid condition Hashimoto’s thyroiditis, Grave’s and eye thyroid diseases thyroid antibodies are significantly elevated.
15. Hashitoxicosis is a short term event with abnormally high levels of thyroid hormones caused by the destruction of the thyroid gland due to Hashimoto’s thyroiditis.
16. Goiter is an abnormal enlargement of the thyroid gland.
17. Thyroid peroxidase is an enzyme made in the thyroid gland that regulates iodine uptake.
18. Antithyroperoxidase antibodies (TPO Ab) act against thyroid peroxidise causing thyroid dysfunction.
19. Thyroglobulin is a protein that builds most of the thyroid gland and stores the thyroid hormones T3 and T4.
20. Antithyroglobulin antibodies (Tg Ab) attack thyroglobulin causing the destruction of the thyroid gland.
21. The damage to the thyroid gland through the antibodies activity is permanent.
22. Hashimoto’s thyroiditis has become the most common cause of hypothyroidism in North America and other industrialized countries.
23. Hashimoto’s thyroiditis affects between 2% and 5% of the general population in Western countries and occurs six times more frequently in women than in men.
24. Hashimoto’s thyroiditis can occur at any age. However, it is most common in women of child bearing age, during menopause and in the elderly who have a family history of thyroid disorders.
25. About 80% of the susceptibility to develop an autoimmune thyroid disease is attributed to genetic factors, while environmental factors contribute to 20%.
26. Cigarette smoking contributes to thyroid dysfunction and could trigger toxic nodular goiter, Grave’s and thyroid eye diseases or make an existing condition worse.
27. The incidence of hypothyroidism, high levels of the thyroid antibodies and autoimmune thyroid diseases has a tendency to increase with age.
28. There is a high prevalence of autoimmune thyroid disease in patients with Alzheimer’s disease and chromosomal disorders including Turner’s, Klinefelter’s and Down syndromes.
29. Currently there are several known genes associated with Hashimoto’s thyroiditis: cytotoxic T-lymphocyte associated antigen 4 (CTLA-4), human leukocyte antigens (HLA), protein tyrosine phosphatase 22 (PTPN22) and thyroglobulin receptor gene.
30. Some of these genes are specific to Hashimoto’s thyroiditis, while others are common in both Grave’s and Hashimoto’s diseases indicating that there is a shared genetic susceptibility.
31. Environmental factors such as excessive iodine, gluten, infections, drugs and pollutants can trigger Hashimoto’s thyroiditis and contribute to the disease progression in genetically predisposed individuals.
32. Celiac disease and dermatitic herpetiformis are relatively common in people with Hashimoto’s thyroiditis with a prevalence of approximately 20% to 25%, however there are many patients who are either asymptomatic or have subtle symptoms and remain undiagnosed.
33. The coexistence of dermatitis herpetiformis, celiac and Hashimoto’s diseases is partly due to a common genetic predisposition and sharing the gluten as a common trigger.
34. Infection such as Helicobacter pylori, Yersinia enterocolitica and Borellia could act as environmental triggers of autoimmune thyroid diseases such as Grave’s and Hashimoto’s.
35. Iodine containing drug amiodarone may induce thyrotoxicosis, hypothyroidism and increase levels of thyroid peroxidise antibodies in females when the treatment lasts longer than 24 months.
36. The incidence of autoimmune and non-autoimmune thyroid disorders increases in the patients treated with interferons.
37. Drug lithium inhibits release of the thyroid hormones contributing to the development of hypothyroidism, goiter and changes in the texture of the thyroid gland.
38. Over 90 synthetic chemicals were noted to interfere with thyroid function and contribute to hormonal imbalances.
39. About 25% of patients with celiac disease and Hashimoto’s thyroiditis have dermatitis herpetiformis which is a very itchy and blistering rash.
40. Prevalence of celiac disease was noted to be up to 4.5% in Grave’s and 13% in Hashimoto’s disease patients.
41. It was reported that thyroid antibodies in Hashimoto’s patients were significantly lower after 6 months and were practically non-detectable after 12 and 24 months in individuals who followed a gluten-free diet.
42. The intestinal lining is an important immune barrier that is responsible for more than 60% of the immune defence.
43. Imbalances in digestion and intestinal flora causes the immune system to malfunction and can trigger autoimmune diseases including Hashimoto’s thyroiditis.
44. High cortisol levels suppress the immune function and promote conversion of active T3 thyroid hormone in its inactive form reverse T3.
45. Bad bacteria overgrowth in the intestines can suppress the good bacteria, diminish the thyroid function and interfere with absorption of thyroid medication and nutrients.
46. Probiotics modulate both Th1 and Th2 immune responses and healthy immunity.
47. Incidence of hypothyroidism increases with age. By age 60, one out of six women is hypothyroid.
48. At hypothyroidism, the production of thyroid hormones T3 and/or T4 is decreased to abnormally low levels and TSH is increased.
49. Primary hypothyroidism occurs when the thyroid gland is unable to produce the necessary amount of thyroid hormones. About 90% of primary hypothyroidism is due to Hashimoto’s thyroiditis.
50. Secondary hypothyroidism is caused by a disorder of the pituitary or the hypothalamus, leading to decreased TSH and low levels of thyroid hormones.
51. Adrenal fatigue is the most common cause of secondary hypothyroidism. Low adrenal function often causes low thyroid function.
52. In adrenal fatigue, the cortisol level drops below normal making the body more susceptible to autoimmune and inflammatory reactions.
53. The probability to develop Hashimoto’s disease and hypothyroidism increases in women of child bearing age due to the shifts in hormonal and immune functions during and after pregnancy.
54. Increased requirements in iodine and thyroid hormones during the pregnancy often contributes to hypothyroidism.
55. Thyroid gland volume usually enlarges during pregnancy. The production of thyroid hormones increases about 50% above the level before pregnancy.
56. Postpartum thyroiditis is an autoimmune condition that affects 5 to 10% of women during the first year after delivery.
57. Pospartum thyroiditis causes high levels of thyroid antibodies, painless goiter and hypothyroidism that subside in most of women within 4 years.
58. Hypothyroidism with even a relatively small rise in TSH puts elderly women at risk of cardiovascular disease, atherosclerosis and heart attack.
59. Testing for thyroid hormones is recommended in women around menopause, after age 60, during pregnancy, after delivery and in women with unexplained high levels of cholesterol.
60. Primarily hyperthyroidism is an overactive thyroid gland that leads to excessive production of thyroid hormones T4 or T3 or both and low TSH. About 20 times more women have hyperthyroidism than men.
61. Secondary hyperthyroidism occurs due to pituitary adenomas, thyroiditis and iodine induced hyperthyroiditis.
62. Grave’s disease is responsible for hyperthyroidism in about 80% of patients. Toxic multinodular goitre, toxic adenoma and excessive thyroid replacement are other common causes of hyperthyroidism.
63. Treatments for hyperthyroidism such as radioiodine treatment, thyroidectomy as well as whole body irradiation and external radiotherapy of the head and neck could result in hypothyroidism.
64. Myxedema coma is an advanced stage of hypothyroidism that most commonly occurs in women with undiagnosed or untreated hypothyroidism or in the elderly.
65. Hypothyroidism causes decreased liver clearance, congestion of the gall bladder due to the thickening of the bile and gall stones.
66. Hypothyroidism is the second leading cause of high cholesterol after diet. When the levels of thyroid hormones drop, the liver produces an excess of cholesterol, fatty acids and triglycerides, which increase the risk of heart disease.
67. More than 70% of people taking thyroid replacement medications continue to complain of hypothyroid symptoms.
68. Underactive thyroid causes delay in the insulin release after eating carbohydrates, slows glucose absorption in the intestine and its uptake into the cells and tissues.
69. Elevated cortisol contributes to reducing the levels of DHEA, testosterone, growth hormone and TSH all of which are involved in keeping us lean.
70. With Grave’s disease the antibodies attack the thyroid gland and stimulate it to produce excessive amounts of thyroid hormones.
71. Grave’s disease is the next most common autoimmune thyroid condition after Hashimoto’s thyroiditis.
72. Grave’s disease affects women 5 to 10 times more often than men and usually occurs between the ages of 20 and 40 and around menopause.
73. Thyrotoxicosis is an increase in thyroid hormones that occurs in 2% of women.
74. About 80% of all cases of thyrotoxicosis are due to Grave’s disease.
75. Thyroid eye disease occurs in a mild form in 25 to 50% of patients with Graves’ disease, with about 3 to 5% of patients developing severe symptoms which require immunosuppression, orbital surgery or radiotherapy.
76. Autonomous toxic nodules are single thyroid nodules or lumps that independently produce too much thyroid hormone causing hyperthyroid symptoms.
77. At the toxic multinodular goiter, thyroid gland has multiple nodules that produce thyroid hormones on their own without being controlled by the pituitary gland.
78. Toxic multinodular goiter causes hyperthyroidism and symptoms of thyrotoxicosis and is usually benign.
79. A thyroid cyst is a growth within the thyroid gland that contains fluid.
80. Thyroid nodules occur 5 times more often in women than in man.
81. Non-toxic multinodular goiter does not cause hyperthyroidism and consists of non-toxic nodules that could be malignant.
82. Nodular goiter causes irregular heartbeat in 40% of patients over age 60.
83. About 10% of the nodules are diagnosed as an adenocarcinoma which is a malignant growth within the thyroid gland and involves the epithelial cells.
84. The occurrence of thyroid nodules increases with age and is estimated to form in half of the American population over the age of 50.
85. Thyroid cancer may present itself as a dominant nodule in a multinodular gland or as a single nodule. Every nodule in the diameter more than 1 cm should be evaluated.
86. Malignant nodules make thyroid cancer accountable for less than 0.5% of all cancer deaths.
87. Excess of estrogen in relation to progesterone suppresses thyroid function and reduces the amount of free active thyroid hormones contributing to hypothyroidism and increasing autoimmunity.
88. Hypothyroidism can cause a reduction of sex hormone binding globulin and increase in free testosterone that contributes to the development of PCOS symptoms.
89. Progesterone supports thyroid function assisting in the retention of zinc and potassium, which allow the thyroid hormone to enter into the cell and be converted to the active T3 form.
90. Thyroid hormone stimulates progesterone production in the ovaries.
91. Most patients with Hashimoto’s and Grave’s disease are Th1 dominant.
92. Chronic dieting suppresses thyroid function and reduces metabolic rate.
93. Leptin resistance results in cellular hypothyroidism with diminished TSH secretion, suppressed T4 to T3 conversion and an increase in reverse T3.
94. Stress, depression, anxiety, tiredness, gynaecological and hormonal symptoms can mask a thyroid imbalance.
95. Stress and inability to handle stress can trigger the thyroid imbalance.
96. Hypothyroidism does not necessarily mean that the thyroid gland has completely stopped functioning.
97. Low-grade hypothyroidism can contribute to infertility, miscarriages, fatigue and depression.
98. Both aging and low thyroid function are associated with decreased mental activity, dry skin, constipation, depression, increased incidence of atherosclerosis and high cholesterol making the diagnosis of hypothyroidism more difficult in elderly women.
99. Minimal thyroid hormone excess can contribute to bone loss and osteoporosis, which could predispose, particularly peri- and postmenopausal women to the bone fractures.
100. Atypical depression is a common form of chronic depression experienced by women with hypothyroidism that resolves with thyroid hormone treatment.
101. About 15 to 20% of severely depressed patients have an underactive thyroid function.
P.S.
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