drob31
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I'm copying this straight from "Why Do I still Have Thyroid Symptoms? When My Lab Tests Are Normal..."
By: Kharrazian, Datis
Note: these are all backed by the literature. If you notice, your blood work can be totally normally, but things like autoimmune conditions, Lyme, HPA-axis issues, methylation, missing co-factors, hormonal imbalances, etc, lead to hypothyroid symptoms.
By: Kharrazian, Datis
Note: these are all backed by the literature. If you notice, your blood work can be totally normally, but things like autoimmune conditions, Lyme, HPA-axis issues, methylation, missing co-factors, hormonal imbalances, etc, lead to hypothyroid symptoms.
TWENTY-TWO PATTERNS OF LOW THYROID FUNCTION
1. Hypothalamus paraventricular defect relates to central nervous system deficiency of serotonin, leading to low TSH341 342 343 344 345 The hypothalamus is the part of the brain that directs hormone function, including that of the thyroid, via the pituitary gland. Dysglycemia (hypoglycemia, insulin resistance, and diabetes) is the most common cause of a serotonin deficiency, which hampers communication between the brain and thyroid gland. People with this type of low thyroid function will have symptoms of serotonin deficiency, a TSH below the functional range of 1.8, and a T4 below 6.
2. Hypothalamus paraventricular defect relates to central nervous system deficiency of dopamine, leading to low TSH346 347 348 349 The hypothalamus is the part of the brain that directs hormone function, including that of the thyroid, via the pituitary gland. Dysglycemia (hypoglycemia, insulin resistance, and diabetes) is the most common cause of a dopamine deficiency, which hampers communication between the brain and thyroid gland. Also, the importance of methylation cannot be overlooked with a dopamine deficiency and should be addressed as well. People with this type of low thyroid function have symptoms of dopamine deficiency, a TSH below the functional range of 1.8, and T4 below 6.
3. Hypothalamus paraventricular defect promoted by cytokines, leading to low TSH350 351 352 353 354 355 Inflammation from gut infections, chronic viral infection, Lyme disease, food intolerances, molds, or environmental compounds can damage the hypothalamus and affect its ability to communicate with the thyroid gland. These patients typically will have low white blood cell counts, a TSH below the functional range of 1.8, and a T4 below 6.
4. Hypothalamus paraventricular defect promoted by elevated prolactin356 357 358 359 The hormone prolactin is very sensitive to shifts of dopamine, thyroid hormones, progesterone, and serotonin. These shifts can elevate prolactin, suppressing both TSH, and the luteinizing hormone (LH), leading to depression of the sex hormones in women and men. Prolactinoma, a benign pituitary tumor, may also elevate prolactin, again suppressing TSH.
5. Pituitary suppression from cortisol leading to low TSH360 361 362 363 364 365 This pattern (See Chapter Four) occurs when elevated cortisol from adrenal stress suppresses pituitary function and thus TSH levels. These patients will have a TSH below the functional range of 1.8, and T4 below 6. The main causes for this pattern are active infection, dysglycemia, unrelenting stress, and, most commonly, hypoglycemia or insulin resistance.
6. Thyroid tissue disorder related to thyroid peroxidase (TPO) autoimmune response: 366 TPO is the enzyme in the thyroid responsible for the production of thyroid hormones and is a common site for autoimmune attacks. A positive TPO antibody test suggests Hashimoto’s disease.
7. Thyroid tissue disorder related to thyroglobulin (TGB) autoimmune response367 368 TGB is produced in the thyroid gland and is used to produce thyroid hormones. It is also a common site for autoimmune attacks. A positive TGB antibody tests suggests Hashimoto’s.
8. Down-regulated TPO activity related to progesterone deficiency Progesterone increases TPO activity. 369 This is why a woman’s body temperature is higher when she ovulates — progesterone surges at ovulation, stimulating TPO activity and overall metabolism. Low progesterone can lead to low thyroid hormones, although their levels of TSH, T4, and T3 will not fall outside of normal lab ranges. Dysglycemia is a common culprit for low progesterone.
9. Down-regulated TPO from deficiency of cofactors370 371 372 373 374 Various nutrients are important for the manufacture and function of adequate levels of TPO, which is responsible for thyroid hormone production. Poor diet and gut function can lead to a deficiency in these nutrients (See Chapter Four).
10. Down-regulated 5’ deiodinase activity from deficiency of cofactors375 376 377 378 379 380 381 382 383 384 The 5’ deiodinase enzyme is responsible for converting T4 to T3, the only form of thyroid hormone the body can use. Poor diet and gut function can lead to a deficiency in the nutrients responsible for adequate function of this enzyme.
11. Down-regulated 5’ deiodinase from gastrointestinal dysbiosis and lipopolysaccharides385 386 387 About 20 percent of the body’s T3 depends on healthy gut flora for conversion. Dysbiosis and bacterial infections down-regulate the 5’ deiodinase enzyme, which hampers this conversion.
12. Down-regulated 5’ deiodinase activity from elevated cytokines388 389 390 391 392 Inflammation from gut infections, chronic viral infection, Lyme’s disease, food intolerances, molds, or environmental compounds can disrupt the conversion of T4 to T3. Inflammation elevates the levels of cytokines, which down regulates the 5’ deiodinase enzyme. Because T3 levels do not affect TSH levels, it should be standard to measure T3. Normal TSH, normal T4, and a depressed T3 strongly suggest down-regulation of the 5’ deiodinase enzyme.
13. Down-regulated 5’ deiodinase activity from elevated cortisol393 394 395 Elevated cortisol from chronic stress down-regulates the 5’ deiodinase enzyme, inhibiting the conversion of T4 to T3. In the past it was believed T4 was shunted into irreversible and inactive T3. New research shows that there is not an increase in reverse T3, but rather poor clearance of reverse T3 due to elevated cortisol. 396 397 398
14. Down-regulated 5’ deiodinase activity from peripheral deficiencies of serotonin399 Serotonin influences the hypothalamus-pituitary-thyroid axis, as well as T3 conversion. Peripheral serotonin deficiency down-regulates these functions.
15. Down-regulated 5’ deiodinase activity from peripheral deficiencies of dopamine400 Dopamine influences the hypothalamus-pituitary-thyroid axis as well as T3 conversion. Peripheral dopamine deficiency down regulates these functions.
16. Up-regulated 5’ deiodinase activity from elevated testosterone401 Elevated levels of testosterone in women create this pattern of too much T4 being converted into T3. The excess production of T3 overwhelms the cells and they develop a resistance to the thyroid hormone. This pattern is most often found in women with insulin resistance and PCOS or in men who use testosterone creams.
17. Elevations of thyroid binding globulin (TGB) leading to decreased production of thyroid hormones TGB is the protein responsible for transporting thyroid hormones. When TGB levels increase, the percentage of free-faction thyroid hormones drop. This is evidenced by a depressed T3 uptake or low free thyroid hormones, despite a normal TSH. This pattern is typically due to a source of exogenous estrogens, particularly oral contraceptives or Premarin. 402 403 404 405
18. Depression of thyroid-binding globulin (TGB) leading to increased production of thyroid hormones and resistance When TGB drops, the amount of free thyroid hormones rises. In this pattern, the TSH is normal. The free thyroid hormone elevation is typically subtle and does not create hyperthyroid symptoms. Instead, the person develops symptoms of hypothyroidism due to thyroid receptor-site resistance. This pattern is typically caused by elevations of estrogens associated with insulin resistance and may also be promoted by high testosterone, 406 such as occurs in women with insulin resistance or in men who use testosterone creams and medications. 407 408
19. Thyroid resistance promoted by an elevation of cytokines Pro-inflammatory TH-1 cytokines have been shown to decrease a cell’s sensitivity to thyroid hormones, causing symptoms of hypothyroidism. 410 411 412 413 This is especially apparent with people on thyroid replacement hormone medication who are still suffering from symptoms of low thyroid activity. The effect of a chronic inflammatory immune response on thyroid receptor sites should be considered in this case. 20. Thyroid resistance promoted by elevations of cortisol414 415 416 Chronic elevations in the adrenals hormone cortisol have been shown to decrease the sensitivity of cellular receptor sites to thyroid hormones.
21. Thyroid resistance promoted by deficiencies of vitamin A417 Thyroid hormone receptor sites must be sufficient in vitamin A in order to activate thyroid hormone. A deficiency in vitamin A hampers receptor site function so that the cell is resistant to thyroid hormones, leading to hypothyroidism symptoms. Vitamin A deficiency should be suspected with anemia, liver disease, cirrhosis, and alcoholism. The key clinical symptom of vitamin A deficiency is difficulty with night vision not related to astigmatism.
22. Thyroid resistance promoted by homocysteine418 Elevated homocysteine has been shown to dampen the expression of thyroid hormones at the receptor site. Elevated homocysteine should always be considered in individuals who take antacid medications, oral contraceptives, and estrogen, or who have hypochlorydria and H.pylori infections. This pattern is difficult to identify since the patient has hypothyroid symptoms but normal blood tests. Since elevated homocysteine produces no symptoms, a blood test should be run to identify this pattern.
