Common Thyroid Medicine Linked to Bone Loss

Common Thyroid Medicine Linked to Bone Loss

Very few studies analyzed the effect of the treatment of thyroid disorders on bone metabolism (Table 6). In one study, Faber et al. analyzed 28 postmenopausal women before and after 2 years of the treatment of subclinical hyperthyroidism with radioiodine. Authors showed that BMD at spin tended to increase after one year and the effect was stable 80 after 2 years. Similar results were found by other authors 81,97,98,99 while others failed to demonstrate a beneficial effect of the treatment of subclinical hyperthyroidism.

Your thyroid gland

• We performed on PubMed a literature search for the articles published until January 2020 by using the search terms “subclinical hyperthyroidism”, “osteoporosis”, “bone mass density”, and “subclinical hypothyroidism”.
• Most experts recommend treatment for subclinical hypothyroidism when TSH levels are above 7-10 mIU/ml.
• Indeed, these patients have increased levels of circulating TSH receptor autoantibodies that stimulate the TSH receptor.
• In consequence thyrotoxicosis leads to increased risk of fractures 8,13,20,22.

Though the study showed a link between bone loss and levothyroxine, Ghotbi stressed that it didn’t prove causation and that there are other possible explanations for the bone loss. For example, someone more likely to lose bone may also be more likely to take the medication. Patients with endogenous hyperthyroidism have reduced BMD compared with euthyroid controls. It has been shown that the treatment produced a significant increase in trabecular BMD (26). The hips and spine are the areas of most concern due to the fact that hip fractures take a long time to heal, especially in older folks. Osteoporosis in the spine typically causes loss of height and curvature or rounding of the upper back, called kyphosis.

On the contrary, subclinical hypothyroidism seems to be unrelated to the bone metabolism, again for the low number of evidences currently available. Bone is formed by osteoblasts, which are derived from mesenchymal cells in the skeletal microenvironment; they are connected by gap junctions and secrete collagen and non-collagen proteins 28. Mature osteoblasts may die by apoptosis or become osteocytes, which are embedded in the matrix or are transformed into flattened lining cells, which cover a large proportion of the bone surface. Although osteocytes may still synthesize collagen and other proteins, they have an important role in bone repair by providing active molecules for the initiation of bone remodeling at the site of bone damage. This effect is probably mediated by mechanical forces that produce a fluid shear stress in the canaliculi between osteocytes, thereby inducing intracellular signals, which result in the secretion of active molecules. Most of the molecules, including hormonal factors, act on osteoblasts for initiating bone resorption.

It’s certainly not the only risk of thyroid HRT (hormone replacement therapy), but it’s one that’s in need of some serious consideration. Before receiving levothyroxine treatment (50 individuals) or placebo (48 individuals) their pQCT results were similar. After 1 year of treatment, synthroid success the bone volume or density measured by pQCT was remained unchanged in the treatment group as compared to the placebo group.

• Deficiency or dysfunction of TRα leads to growth retardation, delayed bone age, perturbations in bone mineralisation and decreased BMD 8,14.
• Mature osteoblasts may die by apoptosis or become osteocytes, which are embedded in the matrix or are transformed into flattened lining cells, which cover a large proportion of the bone surface.
• Hyperthyroidism is a common pathology, with a prevalence of 2% in women and 0.2% in men.
• Studies in young patients with exogenous subclinical hyperthyroidism have been reported to have no effect on peak bone mass 84.

The Risk: Thyroid Hormone Replacement and Osteoporosis

• Early and continuous treatment with LT4 has been shown to promote normal growth 8, 9 and BMD or other indices of bone health 10–12 in children with congenital hypothyroidism, relative to their euthyroid peers (Fig. 1), and normal BMD in adults 13.
• Elevated serum concentrations of IL-6 are observed in people with hyperthyroidism 23,24.
• They concluded that the risk of bone fractures in both hyperthyroidism and hypothyroidism are high.31 It seems that in adult patients with hypothyroidism, bone density increases but bone quality is poor, thus this may cause increased fracture risk in these patients.
• 2Included patients who were diagnosed with osteoporosis, regardless of bisphosphonate or raloxifene prescription status.

Subclinical hypothyroidism is a common condition, especially in middle aged and older adults. Its reported prevalence is between 3.9 and 6.5% in foreign studies (19, 20) and 5.6% in Chile (21). It is twice as frequent among women as men and 3 times more frequent among white people (20). Various studies have shown that 30% of patients with subclinical hypothyroidism developed hypothyroidism within 10 years and only 4% of patients with subclinical hypothyroidism normalized their TSH values. Factors influencing the progress of hypothyroidism are levels of TSH and the presence of antimicrosomal antibodies (21).

The influence of suppressive doses of levothyroxine on bone

TSH acts directly on the TSH receptor (TSH-R) expressed on the thyroid follicular cell basolateral membrane 15. The nuclear genomic effect of thyroid hormones is mediated by the intracellular binding of T3 to nuclear receptor where it activates either thyroid hormone receptor α (TRα) or β (TRβ). TRs act as a hormone-dependent transcription factor that mediates transcriptional repression in the unliganded state. T3 binding results in the dissociation of co-repressors and the recruitment of co-activators resulting in stimulation of gene transcription 16.

Even if you are taking other medication for osteoporosis if there is not enough calcium or vitamin D in your diet and/or your bone density is reduced then you should talk to your doctor or pharmacist about taking calcium and vitamin D supplements. If you do not spend much time outdoors, consider taking a 10mcg (sometimes called 400 units) vitamin D supplement all year round. We evaluated the characteristics of the cohort participants, including age, comorbidities, Charlson comorbidity scores, comedications, and the number of health service uses, with the chi-squared test and analysis of variance (ANOVA) as appropriate. If the descriptive analyses for each variable were shown to differ significantly between the groups, we performed an additional Cochran-Armitage trend test for categorical variables or Duncan’s test for continuous variables. While further studies are needed, physicians should be concerned about potential levothyroxine overtreatment in elderly osteoporosis patients.

Thyroid Research

OP is a health issue with important implications for individuals, families and the community. Untreated OP results in unnecessary pain, restriction of function (disability), decreased quality of life, altered body image with low self-esteem, increased mortality and serious economic consequences (7, 8). And I will tell you…it’s a myth that once you start thyroid hormone replacement, you have to be on it “for life.” This is NOT true. The standard American diet contains many “foods” (I like to call them food-like substances) that are culprits in bone loss. Some of these calcium-leaching offenders are soda (one of the worst), sugar, highly processed and refined foods, coffee, alcohol, excess salt. And again, some prescription medications, including statins, blood thinners, and chemotherapy drugs.

182 patients were studied (112 experimental and 70 control), diagnosed with subclinical hypothyroidism. In the experimental group the coexistence of two or more cardiovascular risk factors was detected in 5.7% of the patients. Additionally, a study on the association between fracture risk and levothyroxine use in Korean patients has not yet been performed. Therefore, the objective of our cohort study, which employed a nationwide claims database, was to evaluate the association between levothyroxine dosage and fracture risk. Furthermore, we evaluated differences in this association according to the degree of osteoporosis. The skeleton is one of the largest organs in the body and has multiple physiological actions including the structural strength and integrity of the body, having an important role in the maintenance of normal serum level of calcium and phosphate.

Thyroid hormones are essential for normal skeletal development and normal bone metabolism in adults but can have detrimental effects on bone structures in states of thyroid dysfunction. Untreated severe hyperthyroidism influences the degree of bone mass and increases the probability of high bone turnover osteoporosis. Subclinical hyperthyroidism, defined as low thyrotropin (TSH) and free hormones within the reference range, is a subtler disease, often asymptomatic, and the diagnosis is incidentally made during screening exams. However, more recent data suggest that this clinical condition may affect bone metabolism resulting in decreased bone mineral density (BMD) and increased risk of fracture, particularly in postmenopausal women. The main causes of exogenous subclinical hyperthyroidism are inappropriate replacement dose of thyroxin and TSH suppressive L-thyroxine doses in the therapy of benign thyroid nodules and thyroid carcinoma. Available data similarly suggest that a long-term TSH suppressive dose of thyroxin may decrease BMD and may induce an increased risk of fracture.