The Thyroid Web
Cheryl Kasdorf, ND
The thyroid is the central gear in the complex web of metabolism and extremely sensitive to minor imbalances in other areas of physiology. An astute clinician should always ask what else is going wrong, as a result and cause, when they identify a thyroid imbalance.
Datis Kharrazian, DC, DHSc, MS, MNeuro Sci1
We as NDs are taught to view things holistically, to see the pattern of the complex web of physiology and beyond. In this article, I intend to fill in pieces of that pattern relating to thyroid function with clinical pearls from two perspectives. One view is the consequence of metabolic disturbance in many body systems when there is low thyroid hormone status. The other is metabolic disturbances that tip us off to evaluate thyroid function.
We also must do a discerning job of evaluating the thyroid function, deciding which blood tests will give us the information we want. An understanding of thyroid physiology as well as an understanding of the applications of the tests is essential to successful treatment. These clinical pearls may give a few hints to that evaluation as well.
Whenever a patient has an elevated thyroid-stimulating hormone (TSH) on a blood test or is diagnosed with hypothyroidism, test for thyroid antibodies. In this case, specifically test thyroid peroxidase antibody (TPOAb) and thyroglobulin antibodies (TgAb).
In the United States, the most common cause of hypothyroidism is secondary to Hashimoto’s thyroiditis.2 Successful treatment is dependent upon addressing the immune component, not just thyroid hormone replacement.
In patients with chronic inflammation, evaluating thyroid function with a standard TSH test may be misleading. Useful information comes from comparing the patient’s TSH before onset of the chronic illness, as well as evaluating other parameters including free triiodothyronine (T3).
In these instances, the thyroid gland itself is not dysfunctional, but there are chemical imbalances which disturb thyroid hormone metabolism. This results in a blood TSH level that may be within the wide “normal” range, but is reduced compared to values demonstrated before the inflammation started.3-5 In addition, immune messengers have been shown to disrupt the peripheral conversion of thyroxine (T4) to T3.6,7
Look to optimizing thyroid hormone function in patients, especially older adults, with chronic inflammation and for maintaining optimal immune system lymphocyte counts.
Thyroid hormone concentration in a study of healthy subjects 55 to 70 years old was positively correlated with markers for inflammation, and inversely associated with early lymphocyte apoptosis.8
If a patient presents with depression, especially if reporting not being helped by selective serotonin re-uptake inhibitors (SSRIs), evaluate the thyroid function. Treatment may include T3 supplementation even in patients testing normal, but possibly having trouble converting T4 to T3.
Triiodothyronine has been shown to increase cerebral bioenergic metabolism, which has been reported low in patients with major depressive disorder.9 Hypothyroid patients not treated with thyroid replacement had reduced systemic serotonin platelet biomarkers when compared with hypothyroid patients taking thyroid hormones.10 A 2006 study showed that treating with T3 helped to relieve depressive symptoms in non-hypothyroid major depressive disorder patients who failed to respond to a standard course of SSRI antidepressants.11
Thyroid hormones are used to modulate acetylcholine activity. Thyroid hormone deficiency may lead to acetylcholine depletion. Symptoms of acetylcholine deficiency in the brain are memory lapses, decreased visual and verbal memory, slower mental response and comprehension, difficulty calculating numbers and recognizing objects and faces, and decreased creativity. Hypothyroid patients often have these symptoms. Consider thyroid testing and treatment.
When gastric ulcers or intestinal permeability issues are diagnosed, check thyroid function.
Both thyroxine and triiodothyronine have been shown to protect the mucosal lining from stress-induced ulcer formation.12 Thyroxine has been shown to prevent intestinal inflammation due to over-expression of intestinal intraepithelial lymphocytes.13
In patients diagnosed with gallstone and common bile duct stone formation and sluggish contraction of the gallbladder, consider hypothyroidism.
On cholecystography, hypothyroid patients often have a distended gallbladder that contracts sluggishly.14 Thyroxine has been shown to relax the sphincter of Oddi to facilitate emptying of the biliary tract; gallbladder and common bile duct stones tend to form in hypothyroid patients.15,16
In patients with imbalanced gastrointestinal (GI) microorganisms along with an immune challenge, hypothyroid symptoms may be evident with no damage to the thyroid gland. Instead, the low thyroid function may be due to underconversion to the active T3 and other mechanisms. Testing may show decreased TSH and T3 levels, and an increased rT3.
Lipopolysaccharides (LPS) from gram-negative bacteria in the GI tract may activate an immune response when coupled with other agents which together impact thyroid physiology. Studies showed that healthy subjects given LPS resulted in lower blood levels of T4, free T3, and TSH and increased inactive rT3 when compared with controls.17,18
In patients presenting with ovarian cysts, especially those that are younger and who do not have dysglycemia and are of normal weight, it is prudent to evaluate thyroid function.
In most cases, insulin surges related to hypoglycemia and insulin resistance upregulate the activity of the enzyme 17,20-lyase and promote androgen excess and ovarian cyst formation. However, in the absence of this pattern in girls with longstanding uncompensated primary hypothyroidism, ovarian cysts commonly develop. Restoration of normal thyroid function resolves these ovarian cysts.19
Low thyroid status may lead to increased homocysteine and development of arterial plaque deposits, signs of increased risk for cardiovascular disease. This can be reversed with treatment of the thyroid.
Research has found that patients with subclinical hypothyroidism had severe endothelial destruction independent of blood lipid levels which was reversed with levothyroxine supplementation.20 In addition, T3 enhances endothelial function.21
On blood testing, whenever a lipid profile shows hypercholesterolemia, check first for hypothyroid symptoms and run a complete thyroid profile.
A decrease in degradation of blood lipids in hypothyroidism leads to an elevated total cholesterol, triglycerides, and LDL (low-density lipoprotein). Management of the blood lipids is dependent on correction of the thyroid disorder, as it will usually bring the lipids back within normal ranges.22
Cheryl Kasdorf, ND maintains a private practice in Cottonwood, Ariz. Her specialties include homeopathy and Unda drainage, Bowen technique and craniosacral therapy, as well as lifestyle counseling. Her passion is to assist others in activating the healing process with the least amount of outer resources, and tapping into the greatest of one’s inner resources. To that end, she teaches The Ishayas’ Ascension. She finds these techniques are the gentlest, most easily achieved, most effective and most natural method of meditation.
- Kharrazian D. Mastering the Thyroid. Seminar. Apex Energetics Educational Services, 2009.
- Baskin HJ, Cobin RH, Duick DS, et al; American Association of Clinical Endocrinologists. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8(6):457-469.
- Corssmit EP, Heyligenberg R, Endert E, Sauerwein HP, Romijn JA. Acute effects of interferon-alpha administration on thyroid hormone metabolism in healthy men. J Clin Endocrinol Metab. 1995;80(11):3140-3144.
- van der Poll T, Romijn JA, Wiersinga WM, Sauerwein HP. Tumor necrosis factor: a putative mediator of the sick euthyroid syndrome in man. J Clin Endocrinol Metab. 1990;71(6):1567-1572.
- Stouthard JM, van der Poll T, Endert E, et al. Effects of acute and chronic interleukin-6 administration on thyroid hormone metabolism in humans. J Clin Endocrinol Metab. 1994;79(5):1342-1346.
- Molnár I, Balázs C, Szegedi G, Sipka S. Inhibition of type 2,5’-deiodinase by tumor necrosis factor alpha, interleukin-6 and interferon gamma in human thyroid tissue. Immunol Lett. 2002;80(1):3-7.
- Nagaya T, Fujieda M, Otsuka G, Yang JP, Okamoto T, Seo H. A potential role of activated NF-kappa B in the pathogenesis of euthyroid sick syndrome. J Clin Invest. 2000;106(3):393-402.
- Hodkinson CF, Simpson EA, Beattie JH, et al. Preliminary evidence of immune function modulation by thyroid hormones in healthy men and women aged 55-70 years. J Endocrinol. 2009;202(1):55-63.
- Iosifescu DV, Bolo NR, Nierenberg AA, Jensen JE, Fava M, Renshaw PF. Brain bioenergetics and response to triiodothyronine augmentation in major depressive disorder. Biol Psychiatry. 2008;63(12):1127-1134.
- Stipcevic T, Kusacic-Kuna S, Dezeljin M, et al. Platelet serotonin concentration and monoamine oxidase activity in hypothyroid patients. Horm Res. 2009;71(4):207-212.
- Abraham G, Milev R, Stuart Lawson J. T3 augmentation of SSRI resistant depression. J Affect Disord. 2006;91(2-3):211-215.
- Koyuncu A, Aydintu S, Koçak S, et al. Effect of thyroid hormones on stress ulcer formation. ANZ J Surg. 2002;72(9):672-675.
- Wang J, Klein JR. Hormone regulation of murine T cells: potent tissue-specific immunosuppressive effects of thyroxine targeted to gut cells. Int Immunol. 1996;8(2):231-235.
- Laukkarinen J, Sand J, Saaristo R, et al. Is bile flow reduced in patients with hypothyroidism? Surgery. 2003;133(3):288-293.
- Laukkarinen J, Kiudelis G, Lempinen M, et al. Increased prevalence of subclinical hypothyroidism in common bile duct stone patients. J Clin Endocrinol Metab. 2007;92(11):4260-4264.
- Inkinen J, Sand J, Nordback I. Association between common bile duct stones and treated hypothyroidism. Hepatogastroenterology. 2000;47(34):919-921.
- van der Poll T, Endert E, Coyle SM, Agosti JM, Lowry SF. Neutralization of TNF does not influence endotoxininduced changes in thyroid hormone metabolism in humans. Am J Physiol. 1999;276(2, pt 2):R357-R362.
- van der Poll T, Van Zee KJ, Endert E, et al. Interleukin-1 receptor blockade does not affect endotoxin-induced changes in plasma thyroid hormone and thyrotropin concentrations in man. J Clin Endocrinol Metab. 1995;80(4):1341-1346.
- Sharma Y, Bajpai A, Mittal S, Kabra M, Menon PS. Ovarian cysts in young girls with hypothyroidism: follow-up and effect of treatment. J Pediatr Endocrinol Metab. 2006:19(7):895-900.
- Taddei S, Caraccio N, Virdis A, et al. Impaired endothelium-dependent vasodilatation in subclinical hypothyroidism: beneficial effect of levothyroxine therapy. J Clin Endocrinal Metab. 2003;88(8):3731-3737.
- Napoli R, Guardasole V, Angelini V, et al. Acute effects of triiodothyronine on endothelial function in human subjects. J Clin Endocrinol Metab. 2007;92(1):250-254.
- Oge A, Sozmen E, Karaoglu AO. Effect of thyroid function on LDL oxidation in hypothyroidism and hyperthyroidism. Endocr Res. 2004;30(3):481-489.