Many research studies have shown a strong association between low TSH and low bone mineral density or osteoporosis.
As a result, many guidelines strongly caution against the risk associated with low TSH. Some doctors and thyroid patients have jumped to the conclusion that a low TSH “causes” osteoporosis.
Some even believe a low TSH must be avoided at all costs during thyroid therapy, even if lowering their thyroid hormone dose causes chronic hypothyroid symptoms in a patient!
But as of 2019, has science proven that lack of TSH “causes” harm to bones?
Surprisingly, the answer is NO!
Correlation is not causation. It is scientifically incorrect to believe that a low or suppressed TSH is a sufficient “cause” of osteoporosis. There is only a statistical association that depends on various factors that the TSH risk association research never covers.
And the research is full of holes. Big holes.
In this post I summarize and quote the literature that has examined this question of TSH cause and effect most comprehensively.
I do not emphasize the statistical risk association research, but rather the perspective of molecular endocrinologists Bassett and Williams, who investigate the direct action of thyroid hormones and TSH on bone cells.
It’s a crucial topic because the misapplication and misunderstanding of research is causing daily suffering — I have in mind the many patients on support forums whose hypothyroid symptoms worsen when thyroid medication doses are reduced only for the sake of raising their TSH.
A cause-effect role for TSH concentrations?
TSH and thyroid hormones’ effect on bone has been a contentious and deep area of research, especially since the 1990s.
During the 1990s, endocrinologists had to defend T4 monotherapy from the charge that this therapy in general, not low TSH in particular, was causing osteoporosis and other harms in patients treated with thyroid hormone.
The result of that research proved that not only is T4 hormone generally safe to bones when it is dosed properly, but that even dosing standard thyroid therapy to the point of suppression does not necessarily cause harm to bones.
Leese, et al, 1992:
“There was no increase in risk for overall fracture, fractured neck of femur or breast carcinoma in those on thyroxine with suppressed or normal TSH.”
— No matter how much or how little TSH they had, there were no clear risk associations.
“There was no excess of fractures in patients on L-thyroxine even if the TSH is suppressed.”
Low TSH did not “cause” fractures.
The decade of the 2000s then saw a lot of research that clarified a lot about how thyroid hormones and/or TSH caused osteoporosis.
It is true that TSH receptors are found in bone cells and that they have some effects on some cells. However, bone cells interact in complex ways. The interactions between TSH, T3 and T4 in bone cells and in relationship to bloodstream concentrations is also complex. Therefore, the relationship between low TSH and osteoporosis is complex.
J. H. Duncan Basset, a “molecular endocrinology” researcher who focuses on direct thyroid hormone effects on bone, was lead author of a 2007 article whose title should have made the cause-effect relationship loud and clear:
“Thyroid hormone excess rather than thyrotropin [TSH] deficiency induces osteoporosis in hyperthyroidism.”
In this article, Bassett and his team directed people in 2007 to stop obsessing over TSH and focus on the direct effects of T3 hormone in inducing osteoporosis by means of its exclusive activity in thyroid receptors in bone.
Since 2010, basic research and population risk research has been ongoing, but more and more reviews of this literature have been published to help clinicians interpret its findings.
In 2014, a review of research aptly concluded that
“it is still unclear if bone changes observed in state of thyrotoxicosis are related to lack of TSH or to excess of thyroid hormones or both of them.”
Listen: they say there’s “unclear” cause-effect relationships!
Bolanowski et al, 2015, in an article on hypopituitary disorders, wrote
“The mechanisms underlying the association between either ACTH [Adrenocorticotropic hormone] or TSH deficiency and lower BMD [bone mineral density] are not clarified.”
In 2018, Van Vliet et al, studying this TSH – bone association stated
“we found no evidence for a causal effect of circulating TSH on BMD [bone mineral density].”
No evidence for cause and effect.
Finally, in a massive chapter of a 2018 genetics textbook Bassett and Williams, the molecular endocrinologists re-confirmed that no causal role for TSH, either low or high, could be proven as a factor in bone health:
“Studies have been conflicting regarding the relative roles of thyroid hormone and TSH.“
Studies are conflicting. Is cause A more important than cause B, and do you need A+B?
To summarize: As of 2019, a low TSH level has merely a statistically determined risk association with osteoporosis. Various studies have found an increased risk of harm to bones in various populations of people who have a low or suppressed TSH.
However, a statistical risk can never be a “sufficient cause” of harm occurring to the body at the present time, or even anywhere in the near future, but that appears to be the way that some doctors are treating a low TSH, as a sufficient cause of thyrotoxicosis.
Saying that a low TSH is a cause of thyrotoxicosis would be the equivalent of saying that high cholesterol level is currently building up plaque in your arteries right now and will certainly cause you a heart attack in the next 20 years.
There are many reasons why TSH is not sufficient as a cause of osteoporosis.
How much excess thyroid hormone can bones handle?
In the scientific literature, there is no doubt that excess thyroid hormone T3 signaling at the site of bone cells causes harm to bones.
Bassett and Williams write
“In adults, thyrotoxicosis is an established cause of secondary osteoporosis.”
Notice the word is thyrotoxicosis, not hyperthyroidism, and there’s an important distinction even though TSH is often low or suppressed in both cases.
The most biologically accurate definition of thyrotoxicosis is found in the official endocrinology textbook Werner and Ingbar’s The Thyroid, edited by Braverman and Cooper, in its 10th edition as of 2013:
“We use the term thyrotoxicosis to mean the clinical syndrome of hypermetabolism and hyperactivity that results when the serum concentrations of free thyroxine (T4), free triiodothyronine (T3), or both, are elevated.”
TSH is not mentioned in this definition for a good reason. It has no place at the core of this definition because its physiological role in tissue thyrotoxicosis is indirect.
It is not the level of TSH, but the excess supply of either or both hormone, that can cause thyrotoxicosis.
Also, thyrotoxicosis is not synonymous with the biochemical state of T4 or T3 concentration excess. If you look at the grammar in the quotation above, the elevated serum concentrations of thyroid hormone are a circumstantial requirement but are not a sufficient cause because excess metabolism and signaling must also occur.
Not merely T4 and T3 levels in blood, but excess T4-T3 conversion (“hypermetabolism”) and excess T3 signaling within bone cells (“hyperactivity”) are the causes of “thyrotoxicosis” in tissues.
Tissues can only become thyrotoxic when their thyroid hormone receptors are experiencing excess occupancy levels.
This is not mere semantics. This is a fact about thyroid hormone biology. A lot can happen to T3 before it binds to a nuclear receptor within a cell. (See our review post, “Thyrotoxicosis vs. Low TSH“)
In cases with mild isolated elevations of T3 hormone in blood, the body has a built-in defense system. Excess levels of T3 hormone can be deactivated before reaching nuclear receptors and mitochondria. Deiodinase type 3 (D3) enzyme performs this role. D3 is expressed in bones to help locally regulate T3 levels and get rid of excess Free T3 entering cells from bloodstream.
But when circulating T4 hormone levels are also high or high-normal — alongside high T3 levels, as they are in most cases of autoimmune hyperthyroidism and T4 therapy overdose — D3 in bone cells may not be able to solve the problem. D3 enzyme may be overwhelmed by all the hormone entering cells that must be deactivated.
Bone tissue thyrotoxicosis is more of a problem when T4 is excessive at the same time that T3 is in excess.
D3 enzyme has a priority system. Its primary “substrate” is T3, which means it focuses its activity on making T3 into inactive T2, even while it also converts T4 to Reverse T3. In most hyperthyroid people, there’s a lot more Free T4 in circulation (in absolute pmol/L units) than there is Free T3 in circulation. That’s a lot of extra work on D3’s desk. Because of D3’s priority to take apart T3, it’s a lot easier for D3 to deactivate an isolated excess of T3 alone.
In addition, bone cells express D2 enzyme, which converts T4 to T3 within cells. Even if many bone cells express D3 enzyme, neighboring D2-expressing cells do not necessarily stop expressing their D2. Therefore, some excess T4 may inevitably convert to excess T3 in bone.
Can you predict the balance of D2 and D3 within bone cells by using the TSH alone or by saying “your T3 or T4 is mildly over reference” ? No.
This is especially true in borderline cases of subclinical hyperthyroidism (isolated low TSH) and cases where T3 levels are above reference while T4 is simultaneously in the bottom half of reference or lower (as in cases of desiccated thyroid or T3 hormone treatment).
The degree to which D2 or D3 is active in bone during a thyroid hormone excess cannot be measured, considering the complex ways in which these two enzymes are upregulated, downregulated, and expressed (bones do not have a strong D1 expression).
The individual’s risk cannot be assessed by a series of research studies that focused on one hormone more than others and did not look at multiple relevant factors in synergy, which is the way hormone metabolism works in living tissues.
TSH secretion is a local, organ-specific response of the pituitary and hypothalamus.
Ultimately, TSH concentrations can’t speak for thyroid hormone levels in bone cells. They can only speak for thyroid hormone signaling in the pituitary and hypothalamus.
Modern thyroid science has proven that every single organ and tissue metabolizes T4 to T3 at a different rate, the pituitary included.
This means that even TSH is a localized, organ-specific response to thyroid hormone levels in blood.
The pituitary does not send out tendrils with sensors to every other organ and tissue in the body to bring back data on their T3 supply to cells, but it appears that some doctors imagine pituitary TSH has god-like omniscience over thyroid hormone supply everywhere in the body!
In addition, TSH is wired to ignore low T3 levels in the presence of elevated T4 during T4 monotherapy. TSH will not rise to signal a T3 deficiency whenever T4 is above the person’s metabolic set point. Doctors who measure T3 during this therapy will know this, and the incorrect conclusion is to say “oh well, if the TSH is not rising, then the low T3 must not be a bad thing!”
The fact of TSH’s blindness to low T3 is continually proven by all patients who experience “non-thyroidal illness” and all patients who experience a Free T3 deficit during T4 monotherapy. Their TSH will not elevate, even past the point at which other organs start to show the signs and symptoms of hypothyroidism from the loss of T3.
As I have shown in this series of posts on low TSH, this pituitary secretion is hypersensitive to multiple factors in addition to thyroid hormone (such as fasting, TSAb antibodies, hCG hormone, circadian TSH rhythms). A multitude of factors may over-suppress TSH long, long before thyroid hormone levels reach concentrations that are capable of creating thyrotoxic responses in any organ.
Given this knowledge of the pituitary’s TSH response as of 2019, it is completely unscientific to assume that the pituitary’s secretion of TSH is an extremely accurate measure of how much T3 is reaching a person’s bone cells, or heart cells, or eyes, or the tip of their left big toe.
Here’s another reason why one must question low-TSH risk associations in thyroid therapy:
An “intact” HPT axis clouds the distinction between low TSH and high thyroid hormones.
Bassett and Williams put their finger on why it is impossible to prove low TSH concentration in blood is the cause of harm to bone in most human studies.
“Importantly, this issue cannot be resolved when the HPT-axis remains intact and the reciprocal relationship between thyroid hormones and TSH is maintained.”
In other words, you can’t use people with an “intact” HPT axis to determine the degree to which TSH or thyroid hormones (such as T4 and T3) cause direct harm to bone.
This is because thyroid hormone has a direct inverse relationship with TSH when this axis is intact. TSH’s amplified inverse mirroring of excess T4 and T3 makes it unclear whether the pituitary hormone or the thyroid hormones, or both, are responsible for causing action in bones.
That’s why mouse models are often used in studies. Researchers can “knock out” certain genes in mice or rats so that their HPT axis is distorted in different ways. Doing so reveals interactions you can’t see otherwise.
The distorted HPT axis in thyroid therapy
According to some recent research, treated thyroid patients do not have a normal HPT axis when it comes to FT3 – FT4 – TSH hormone relationships. Including the Free T3 enables one to see the distortions that may otherwise be less evident. Excluding FT3 from HPT axis modeling has resulted in the common misconception that the HPT axis is not broken or harmed by primary hypothyroidism. It is. Some patients’ HPT axis will be more distorted than others.
At the point of complete TSH suppression, a T4-monotherapy treated patient’s Free T3 level can be anywhere below, within, or above reference range (Larisch et al, 2018, scatterplot). Researchers call this the TSH-T3 disjoint in thyroid therapy.
This is unnatural!
FT3 levels must behave normally in relation to FT4 levels and TSH levels for the HPT axis to be intact.
Outside of thyroid therapy, it is almost impossible for T3 and TSH both to be low except in central hypothyroidism, a category of conditions that compromise TSH secretion.
This TSH-T3 disjoint is one of the most significant distortions of the HPT axis found within thyroid therapy. The clinical importance of this distortion to human health should not be minimized or overlooked by overemphasizing the patient’s TSH at the expense of the most potent signaling thyroid hormone, T3.
Research has found that after T4 dosing has achieved complete suppression, further escalation of the dose will elevate Free T4. However, escalating the T4 dose past the point of TSH suppression may or may not also elevate Free T3. In some patients, T4 rises and TSH falls while FT3 remains in the lower half of reference or below.
The “normal” rise in FT3, if any, entirely depends on how well the patient converts T4 hormone.
Individual response to T4 hormone therapy is highly variable. Some people are “poor converters” of T4 to T3 — their bodies are less able to process their T4 medication into the active hormone (Midgley et al, 2015).
Research on a large population of thyroidless patients on T4 therapy proved that the symptoms of thyrotoxicosis are entirely absent until Free T3 hormone levels exceed the statistical average found in healthy controls, which is mid-reference range. (Larisch et al, 2018)
The wide human variation among patients’ response to T4 therapy may indeed be responsible for keeping some patients out of a state of “thyrotoxicosis” despite having a suppressed TSH. In fact, it may render some patients hypothyroid despite a low or suppressed TSH.
When the patient’s entire body is not in a thyrotoxic state of hypermetabolism as proven by their clinical presentation and their low-normal or low FT3 levels, why would their bones alone be in a state of thyrotoxicosis?
And if the patient’s FT3 is low while TSH is low, how could their bones be thyrotoxic, while their heart is hypothyroid? Low T3 levels are associated with higher death rates in cardiovascular disease. (See the recent research on low T3 in ischemic heart disease.)
Studies on untreated populations’ TSH
Every TSH risk association study excludes certain populations, but few pay attention to these important exclusions.
Most TSH-osteoporosis studies have excluded people with diagnosed thyroid disease and all people taking thyroid hormone medications.
Therefore, when those researchers study “hyperthyroidism” they don’t mean the thyroid levels seen in thyroid therapy. They usually mean the type of hyperthyroidism that is caused by antibody-stimulation of the thyroid gland, which presents with elevations in both T4 and T3 into the upper part of reference long before one or both hormones elevates above reference.
Studies only on people dosed with T4 monotherapy
Of course, there are also studies of low TSH and osteoporosis that have focused on people with thyroid disease and therapy.
These studies tend to focus only on people treated with T4 hormone alone. They are also people who have had total thyroidectomies after thyroid cancer and whose TSH is therapeutically kept low or suppressed to prevent cancer regrowth.
A person whose TSH is purposely suppressed may well be more likely to be overdosed than a person who is treated to remove signs and symptoms of hypothyroidism, whose TSH just happens to drop a bit low. Perhaps their TSH dropped low due to the patient’s experimentation with fasting, or TSH fell low during the blood draw in mid afternoon, or TSH was tested on a day in the middle of their menstrual cycle when estrogen was low and less thyroid hormone was bound and more was free.
Therefore, three bodies of “Low-TSH risk” research should never be applied to populations of treated thyroid patients their researchers did NOT study:
- A body of research largely based on healthy, untreated patients’ low TSH can’t apply to a population that has a modified and broken HPT axis. People with thyroid disease who are on thyroid therapy have an artificially regulated HPT axis that can result in unusual T3 and T4 ratios and levels at a suppressed TSH.
- Risk calculations in populations of thyroidless patients after thyroid cancer will be skewed by the exclusion of all autoimmune thyroid disease patients and anyone with with partial gland function. These results should not be applied to patients with partial thyroid gland function nor to autoimmune thyroid patients who may have TSH-oversuppressing TSHR antibodies.
- Studies of the risk of TSH suppression in T4-monotherapy treated thyroid patients have never examined people treated wholly or partially with T3 hormone. Therefore, they are entirely incapable of proving their very different T3:T4 levels and ratios put them at risk or not when TSH is low or suppressed.
I must emphasize the third point — these studies of risk should not be applied to the low TSH found in T3-based therapies like desiccated thyroid and T3 monotherapy.
T3-treated patients are especially vulnerable to having a lower TSH while total thyroid hormone supply is low or normal, due to what I call the “T3 dosing effect.”
When a person is dosing T3 even to euthyroid levels, their TSH responds differently than if they were secreting T3 and converting T3 gradually 24/7, because there will be intermittent peaks in FT3. This dosing effect is commonly seen when T3 is included in full thyroid-replacement doses of desiccated thyroid.
Consider that euthyroid desiccated thyroid treatment commonly involves a FT4 at or below the midpoint of the reference range. Now add their higher-normal FT3 to their FT4. How much of their low-normal FT4 can potentially become T3 in cells? Even if dosing makes Free T3 peak above reference two and a half to three hours post-dose, the peak is brief and quickly cleared and metabolized, primarily by D3. These patients carry a net T3 and T4 “load” in bloodstream that is not necessarily thyrotoxic despite the pharmaceutical side-effect on TSH secretion.
Omitting the measurement of FT3 as a continuous variable
This point leads to a final fatal flaw in the vast majority of TSH-risk research, the exclusion not of a patient group but of a crucial hormone:
- Studies of TSH suppression in thyroid patients are severely compromised in their ability to discern cause and effect whenever they don’t measure Free T3.
The T3 hormone is the most powerful thyroid hormone, so it is entirely illogical to omit its measurement if you want to know if a patient is likely thyrotoxic in bone.
Omitting FT3 from research is a way of forcing TSH, rather than FT3, to be the most significant factor in risk association studies.
Omitting FT3 from studies cheats us all. It is like disqualifying the fastest horse from running the race.
Yet these Low-TSH-risk studies routinely exclude Free T3 hormone measurement; it exists in perhaps 1% of studies on this question.
Even in studies that do measure Free T3, it is incorrectly viewed as an entirely separate hormone to be judged in isolation from Free T4, which is not physiological: it is not how the body judges it. The FT3:FT4 ratio should be a variable in addition to FT3.
In addition, the individual human body does not judge FT3 levels by reference range boundaries. Studies that arbitrarily group patients according to reference boundaries are establishing arbitrary, nonphysiological boundaries. Examining FT3 as a continuous variable is the best way to overcome this handicap in research.
If you don’t measure Free T3, then as a researcher you are blind both to the T3 level and to the T3:T4 ratio and how they influence health.
The human body is not blind to T3 levels and T3:T4 ratios, as you will see if you gather all the studies you can find to date on the T3:T4 ratio (which I have done, and I encourage others to do). This is why it also makes sense to consider FT3 in the context of symptoms and signs of thyrotoxicosis.
Bassett and Williams’ conclusions
Before I offer my own conclusion, let’s look at one section of Bassett and Williams’ chapter’s “conclusions” section. It would be here, not in inconclusive literature reviews, that one would expect to find their recommendations for the path forward for research and clinical practice:
“These data establish a new field of research and further highlight the fundamental importance of understanding the mechanisms of T3 action in cartilage and bone, and its role in tissue maintenance, response to injury, and pathogenesis of degenerative disease.
Precise determination of the cell molecular mechanisms of T3 and TSH actions in the skeleton in vivo will require cell-specific conditional gene targeting approaches in individual bone cell lineages.
Combined with genome-wide gene expression analysis, these approaches will determine key target genes and downstream signaling pathways and the potential to identify new therapeutic targets for skeletal disease.”
Do they recommend against TSH suppression in thyroid therapy? This would be the place to do it. No, they do not, nether in this passage nor in the conclusion as a whole.
Do you see anything in there that says low TSH has been conclusively identified as the cause of damage to bone? No? This would be the place to emphasize it. Not in the entire conclusion.
Do you see anything in there that implies that T4 levels anywhere are at issue? No. Hmm, the hormone emphasized in therapy today is not even given honorable mention. T4 is only indirectly alluded to in their phrase “thyroid hormone” in other parts of their conclusion.
Do you see anything in there that says particular blood levels or ranges of T3 and TSH are thresholds for adverse effects on bone? Again and again, no.
Do they recommend always forbidding Free T3 or Free T4 to rise above reference during thyroid therapy? No.
Do they recommend against using T3 in hormone in therapy due to osteoporosis risk? No.
Interestingly, they do discuss T3 hormone therapy in studies on mice and rats, where it has sometimes proven the beneficial effects of T3 supplementation alone to correct hypothyroidism.
Given what Bassett and Williams teach, thyrotoxicosis in bone cannot be judged by isolating Free T3 and Free T4 hormone concentrations and judging them separately by where they are in their reference ranges.
The closest you can come to protecting bone is to assess both T3 and T4 thyroid hormone levels together in the context of signs and symptoms of hypermetabolism in a variety of bodily systems and tissues.
Given what we know in 2019 about thyrotoxicosis, bloodstream levels of thyroid hormone, and thyroid hormone action in bone, it is more likely that both FT4 and FT3 must be higher in reference range, as they often are in untreated endogenous hyperthyroidism, for a risk of osteoporosis to be significant.
Given what we know in 2019 about the statistical risk of low TSH in association with osteoporosis, the risk associations are largely inapplicable to treated thyroid patients who bear the brunt of the low-TSH prohibition policy because our hormones are vulnerable to medical manipulation. The vast majority of studies have either excluded thyroid patients from study or excluded Free T3 measurement in the patients studied, or both.
When we apply these low-TSH statistical risk associations to treated thyroid patients, we are misapplying the vast majority of research on the topic.
Vulnerable people pay the price of incomplete, biased research. Treated patients’ hormones are vulnerable to medical manipulation and doctors are persuaded they are always helping us when they forbid us from having a low TSH or suppressed TSH.
Where are the studies on the bone health of treated patients with central hypothyroidism?
Where are the studies of bone health in patients whose TSH receptor blocking antibodies prevent their normal or high TSH from stimulating TSH receptors in bone?
Where are the studies of bone health in patients dosed with T3-inclusive hormone therapies — patients whose FT4 does not have to be as abnormally high as it is in most patients on T4 monotherapy?
Where are the studies of bone health in patients who have spent years with no T4 in circulation while on an euthyroid dose of T3 monotherapy that suppresses TSH?
Discretion and critical thinking is required when interpreting research, and when interpreting an individual patient’s TSH in context with both of the thyroid hormones and symptoms and signs.
Even if you wait 10 more years for more research to be done, the fact will remain — merely an isolated low TSH is never going to be a sufficient “cause” of harm to bones.
See References for Thyrotoxicosis vs. Low TSH series
Bassett, J. H. D., O’Shea, P. J., Sriskantharajah, S., Rabier, B., Boyde, A., Howell, P. G. T., … Williams, G. R. (2007). Thyroid hormone excess rather than thyrotropin deficiency induces osteoporosis in hyperthyroidism. Molecular Endocrinology (Baltimore, Md.), 21(5), 1095–1107. https://doi.org/10.1210/me.2007-0033
Bassett, J. H. D., & Williams, G. R. (2018). Chapter 31 – Thyroid Hormone in Bone and Joint Disorders. In R. V. Thakker, M. P. Whyte, J. A. Eisman, & T. Igarashi (Eds.), Genetics of Bone Biology and Skeletal Disease (Second Edition) (pp. 547–569). https://doi.org/10.1016/B978-0-12-804182-6.00031-9
Bhatnagar, S., Srivastva, R. K., Jahan, S., & Ranjan, R. (2017). Multiple Effects of Hypothyroidism on Bone Mineral Density and Its Association with Vitamin D, Serum Calcium: A Cross-sectional Study. International Journal of Scientific Study, 5(6), 120–124.
Bolanowski, M., Halupczok, J., & Jawiarczyk-Przybyłowska, A. (2015). Pituitary Disorders and Osteoporosis [Research article]. https://doi.org/10.1155/2015/206853
Friesema, E. C. H., Jansen, J., Jachtenberg, J., Visser, W. E., Kester, M. H. A., & Visser, T. J. (2008). Effective Cellular Uptake and Efflux of Thyroid Hormone by Human Monocarboxylate Transporter 10. Molecular Endocrinology, 22(6), 1357–1369. https://doi.org/10.1210/me.2007-0112
Krause, G., & Hinz, K. M. (2017). Thyroid hormone transport across L-type amino acid transporters: What can molecular modelling tell us? Molecular and Cellular Endocrinology, 458, 68–75. https://doi.org/10.1016/j.mce.2017.03.018
Leese GP, Jung RT, Guthrie C, Waugh N. Morbidity in patients on l-thyroxine: a comparison of those with a normal TSH to those with a suppressed TSH. Clin Endocrinol (Oxf). 1992;37(6):500-503. doi:10.1111/j.1365-2265.1992.tb01480.x
Mackawy, A. M. H., Al-ayed, B. M., & Al-rashidi, B. M. (2013). Vitamin D Deficiency and Its Association with Thyroid Disease. International Journal of Health Sciences, 7(3), 267–275.
Tuchendler D, Bolanowski M. The influence of thyroid dysfunction on bone metabolism. Thyroid Res. 2014;7. doi:10.1186/s13044-014-0012-0
van Vliet NA, Noordam R, van Klinken JB, et al. Thyroid Stimulating Hormone and Bone Mineral Density: Evidence From a Two-Sample Mendelian Randomization Study and a Candidate Gene Association Study. J Bone Miner Res Off J Am Soc Bone Miner Res. March 2018. doi:10.1002/jbmr.3426
Williams, G. R. (2013). Thyroid Hormone Actions in Cartilage and Bone. European Thyroid Journal, 2(1), 3–13. https://doi.org/10.1159/000345548
Zevenbergen, C., Meima, M. E., Lima de Souza, E. C., Peeters, R. P., Kinne, A., Krause, G., … Visser, T. J. (2015). Transport of Iodothyronines by Human L-Type Amino Acid Transporters. Endocrinology, 156(11), 4345–4355. https://doi.org/10.1210/en.2015-1140
6 thoughts on “As of 2019, still no proof that low TSH causes harm to bones”