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Cancer, Depression, Hair Loss, Vertigo, & Infertility Correlate
with Low Thyroid Levels
TSH Levels Fluctuate and often
do not Reflect Thyroid Levels
Osteoporosis, Gum Disease &
Bad Teeth are not from Low TSH
High Blood Sugar & Insulin Resistance Correlate with High T3
Thyroid Blood Tests to Diagnose a
Thyroid or Hormone Imbalance
Thyroid Lab Results are Affected
by the Time of your Last Dose
Thyroid Reference Ranges are too Broad; What is Healthy / Optimal?
Thyroid Hormone Medications:
T4, T3, or Desiccated (T4 + T3)
Thyroid Hormone Requires
Iron, Cortisol, Selenium, Iodine
Hyperthyroid Symptoms (Anxiety, Tachycardia), Hypothyroid Labs
Adrenal Fatigue or Low Cortisol: Hydrocortisone (HC) Side Effects
Reverse T3: Side Effects of T3-only
(or why you need T4 too)
Insomnia, Incontinence, &
Vaginal Dryness Resolve with BHRT
Low Testosterone in Aging Men:
TRT for Andropause
Saw Palmetto, Stinging Nettle, and OTC Men’s Supplements
Asthma, Eczema, Allergies, Hives, and Yellow #5 (Tartrazine)
Antithyroid drugs + Levothyroxine
High Altitude Sickness: Headache, Insomnia, and Hypothyroid?
Books I Recommend
Who Writes TiredThyroid?
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Osteoporosis, Osteopenia, Gum Disease & Bad Teeth are not from Low TSH, but can be from Low (or High) Thyroid Levels
Thyroid’s effect on bones
Osteoporosis, osteopenia, or bone loss can be caused by thyroid levels (Free T3 and Free T4) that are too high. A low TSH is often found with high thyroid levels and can be diagnostic for hyperthyroidism. It is for this reason that doctors are reluctant to prescribe enough thyroid hormone for the patient to feel well. They will only prescribe enough to bring the TSH into range. Desiccated thyroid usually suppresses TSH close to zero at a dose of 2 grains or more. In one study, doses of 3 grains or higher of natural desiccated thyroid resulted in a lower combined cortical thickness (CCT), which is a measure of bone health (a higher value is desirable). Subjects on 4 grains had a lower CCT than the subjects on 3 grains, while those on 2 grains had a higher CCT. 
Osteoporosis can also be caused by low thyroid levels (low Free T3 and Free T4), which are not always reflected in the TSH. [TSH levels do not reflect thyroid levels] High thyroid levels upregulate the genes involved with bone resorption or bone loss. But thyroid hormone also upregulates the genes involved with bone matrix formation and collagen maturation (bone generation), so if thyroid levels are kept too low, bone generation is impaired.  Healthy bone metabolism requires thyroid levels that are neither too high nor low. Doctors believe that a low TSH always indicates a hyperthyroid state and will thus lead to osteoporosis. There are, however, many exceptions to this TSH rule, and many with a low TSH actually have low thyroid levels. Because of the misleading TSH, patients are often maintained on a thyroid replacement dose that is so low they still remain hypothyroid, and with time, they eventually develop low thyroid symptoms such as osteoporosis, osteopenia, gingivitis, periodontitis, high cholesterol, heart disease, depression, etc.
A study of mice that lacked thyroid hormone receptors illustrates the dangers of thyroid levels that are too high or too low. Without specific thyroid receptors, thyroid hormone (T3 or T4) may have no effect. Mice that were thyroid receptor alpha deficient developed osteosclerosis (abnormal hardening of the bone) and reduced osteoclastic bone resorption, a form of skeletal hypothyroidism, even though thyroid hormone and TSH levels were normal. Mice that were thyroid receptor beta deficient had elevated TSH and thyroid hormone levels, and developed osteoporosis with evidence of increased bone resorption. These mice displayed skeletal thyrotoxicosis without a suppressed TSH, which means elevated thyroid hormone levels, not a low TSH, caused osteoporosis.  This is another reason why both Free T3 and Free T4 need to be monitored, not the TSH.
To determine the relative importance of T3 and TSH in bone, the skeletal properties of two mouse models with congenital hypothyroidism were compared. One type of mouse had a 1900-fold increase in TSH, a normal TSH Receptor, and undetectable T3 and T4 levels. The other had a 2300-fold elevation of TSH, a nonfunctional TSH Receptor, and a T4 that was 95% lower than wild mice. Both types of mice displayed skeletal hypothyroidism: delayed ossification (new bone formation), reduced cortical bone (the stronger, outer part), a trabecular bone remodeling defect (old bone must be resorbed to make way for new bone), reduced bone mineralization (where calcium is added to bone), and impaired osteoblast T3 target gene expression (bone building cells are not activated).  Because one type of mouse had a normal TSH receptor and the other did not, it stands to reason that TSH is not the major determinant of skeletal development, since both types of mice had skeletal hypothyroidism with ample TSH. The lack of T3 would be more likely. Also, TSH did not influence primary osteoblast (bone building) or osteoclast (bone clearing) differentiation and functional activity in vitro (in a lab). Earlier mice studies support these conclusions: low T3 levels caused reduced bone mineralization and delayed ossification.
Female human thyroid cancer patients who received thyroidectomies and then suppressive doses of T4 medications (TSH near zero) were compared to normal controls to examine the effects on bone mineral density. When the patients were separated into premenopausal and postmenopausal groups, bone mineral density in both the femoral neck and lumbar spine was similar between patients and controls. The proportion of women with normal bone mass density, osteopenia and osteoporosis in patient and control groups was similar in the pre- and postmenopausal groups. Long-term TSH suppressive T4 treatment did not appear to affect skeletal integrity in these women.  In other words, even though TSH was kept at an undetectable level in the thyroid cancer patients, their bone health was not different from normal women of their age. This study points to age and menopausal status as the primary determinants of bone health, not TSH. Lower levels of estrogen are normal in menopause, and there are numerous studies that implicate estrogen deficiency in osteoporosis.  In this case, lack of TSH cannot be said to be the primary cause of poor bones.
Thyroid’s effect on teeth
Gingivitis, periodontitis, gum disease, bad teeth, dentures at age 25, and root canals at age 12 have been reported by members of thyroid internet forums. Like bones, there is a definite connection between dental health and optimal thyroid levels.
is the inflammation / infection of the
gums (gingivitis) that leads to inflammation / infection of the bones
support the teeth, which can cause the teeth to become loose and
fall out. A study
of nearly 14,000
people in the US who had received a periodontal exam found that severe
periodontitis is associated with the metabolic syndrome in middle-aged
of the metabolic syndrome are similar to the symptoms of hypothyroidism: central obesity, high
triglycerides, low HDL
cholesterol, hypertension, and insulin resistance. 
If low thyroid levels are the root cause of
the metabolic syndrome, then they would also be implicated in
fact, one study found that low normal Free T4 levels were
significantly associated with increased insulin resistance and with
five metabolic syndrome traits. 
Tooth loss that results from root resorption from orthodontic procedures (braces) is an occasional unfortunate side effect of orthodontia. Rats treated with thyroid hormone (who had orthodontic appliances inserted) displayed significantly less force-induced root resorptive lesions compared with a control group.  Another study confirmed these findings--hypothyroidism significantly increased periodontitis-related bone loss, as a function of an increased number of resorbing cells.  In other words, low thyroid levels can affect the bones that support your teeth. The results from the rats that had orthodontics suggest that orthodontia is not a good idea if one is hypothyroid, because it may result in tooth loss.
To see what effect thyroid levels had on titanium implants, rat tibiae (leg bones) were implanted with titanium screws. The hyperthyroid rats had significantly more newly formed bone around the implants, whereas the hypothyroid rats had significantly less.  This suggests that dental implants may not be successful if the patient is still hypothyroid, which could be the cause of tooth loss in the first place.
Thyroid Treatments such as T3-only and Hydrocortisone (HC) May Cause OsteoporosisOsteoporosis can be caused by thyroid hormone deficiency, as discussed earlier in this section. At the other end of the spectrum, excessive thyroid hormones, especially T3, can lead to elevated SHBG (sex hormone binding globulin) levels , and elevated SHBG levels are a major risk factor for osteoporosis.  SHBG can be affected by other factors like age, weight, sex steroids, and insulin, to name just a few, but there is a strong positive correlation of high T3 with high SHBG, and high SHBG is correlated with poor bone mineral density and osteoporotic fractures of the vertebra and peripheral bones, especially the femur (thigh bone).  Hip fractures are also associated with higher levels of SHBG, independent of bioavailable estradiol and testosterone levels.  SHBG appears to have a bone wasting effect on post-menopausal women, while estradiol has a bone preserving effect.  SHBG should be used in conjunction with symptoms and other thyroid lab tests, like Free T3, to determine when thyroid levels are too high.
Hydrocortisone (HC) supplementation to treat adrenal fatigue, at excessive levels, can also lead to osteoporosis. Hydrocortisone is the bioidentical replacement for the hormone cortisol, but because cortisol has a circadian rhythm and rises and falls on its own in response to stress, it is nearly impossible to replicate by manual dosing. If cortisol levels throughout the day were depicted graphically, it would look like a downward sloping curve--highest in the early morning, and lowest at night. Manual HC dosing would show as multiple, decreasing mountain peaks, with cortisol levels above the normal level after a dose, and then below the normal level before the next dose. These high cortisol peaks are behind the high cortisol physical signs of moon face, buffalo hump, “Buddha belly,” and general weight gain. Bones may also be adversely affected, because corticosteroids not only decrease bone formation, they also increase bone resorption.  A hydrocortisone dose no higher than 20 mg/day is sufficient, according to some studies. In fact, one study had patients reduce their 20-30 mg daily hydrocortisone doses to 10-15 mg/day. None of the patients reported low cortisol symptoms. Instead, 10/11 subjects lost weight (specifically abdominal fat), total cholesterol and triglycerides decreased, and Quality of Life scores improved.  Another study that compared the effects of 15, 20, and 30 mg of daily hydrocortisone found no difference in Quality of Life between the doses, but a negative correlation with osteocalcin (a protein involved with bone formation) as the hydrocortisone dose was increased. In other words, as the HC dose increased, bone formation decreased. Since bone loss would be induced at a daily hydrocortisone dose of 30 mg, the study recommended 15 to 20 mg of HC instead.  Bone density scans are recommended while on hydrocortisone, and Vitamin D levels should also be tested and treated if low. 
The T3-only protocol combined with hydrocortisone supplementation may have adverse effects on bone health and bone density scans are highly recommended.
Getting your thyroid tested
If you'd like to have your thyroid levels tested, please ask for these thyroid tests, and note where your levels are in the thyroid lab ranges compared to healthy people. If you do not ask for these specific tests, your doctor will most likely just run a TSH test, which sadly, does not catch many cases of hypothyroidism. [TSH levels do not reflect thyroid levels]
[reference links inactivated for search engines; copy and paste the url at the end of each reference into your browser to view the reference]
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© 2011-2014 by Barbara Lougheed. All rights reserved.