Can Synthroid Taken for Hypothyroidism Cause Osteoporosis?

Once the level of thyroid hormone in your body has been reduced to a normal level the rate of bone loss will no longer be so rapid and the bone strength may improve. Some people, however, will have or continue to have bone loss, with or without thyroid disease. If you have had a long period of untreated hyperthyroidism and have other risk factors for osteoporosis and bone fractures, a bone density scan two to three years after you start thyroid treatment will help assess your risk. If a bone density scan shows osteoporosis then this can be treated with osteoporosis medication.

TRα1 is considered as a main functional mediator of triiodothyronine in skeleton 5,11,12. Deficiency or dysfunction of TRα leads to growth retardation, delayed bone age, perturbations in bone mineralisation and decreased BMD 8,14. Studies that analyzed the effect of endogenous subclinical hyperthyroidism on lumbar spine bone mass density and femoral bone mass density. The study group included 81 euthyroid levothyroxine users (32 men, 49 women) and 364 non-users (148 men, 216 women), with a median age of 73 and TSH levels of 2.35 at the initial visit. Other risk factors like age, gender, height, weight, race, medications, smoking history and alcohol use were considered in propensity score matching of levothyroxine users versus non-users. During the study period, we considered comorbidities and comedications as the confounding factors of the association between levothyroxine use and fracture risk.

Common Thyroid Medicine Linked to Bone Loss

• However, it has been shown in children with congenital hypothyroidism that bone density is lower than normal children.39 In children with subclinical hypothyroidism, bone qualities by using of quantitative ultrasound were studied.
• If we’ve neglected to accumulate adequate bone mass during our formative years, including childhood, adolescence, and early adulthood, we’re at increased risk of full-fledged osteoporosis.
• Before receiving levothyroxine treatment (50 individuals) or placebo (48 individuals) their pQCT results were similar.
• Gonzalez-Rodriguez et al. did not find any association between hypothyroidism and decreased bone mineral density or vertebral and non-vertebral fractures among 400 women suffering from hypothyroidism 44.
• Overt hypothyroidism is defined as increased TSH together with T3 and T4 below the lower limit of the reference range.

The results showed that with increasing concentrations of TSH, calculated osteo sono-assessment index is reduced.40 This study showed that the hypothyroidism affects the bone structure. Subclinical hypothyroidism is defined by experts as a condition of mild thyroid failure characterized by normal levels of T3 and T4 with moderately elevated serum TSH between 5 and 10 mU/L (15, 16). Increased access to serological tests for TSH have resulted in an increase in the number of patients with abnormal thyroid function, but not necessarily symptomatic. This has led to a series of disputes among experts regarding the management and diagnosis of these patients (17, 18).

What is the link between thyroid disease and osteoporosis?

Other controlled studies show no changes in BMD with synthroid rxlist suppressive therapy (27). However, if you are prescribed levothyroxine you should have regular blood tests, at least once a year, to ensure your thyroid hormone levels are not too high. Continuous high thyroid hormone levels may lead to developing or worsening of low bone density and osteoporosis. We calculated the incidence rates among the total elderly women in our dataset, the eligible cohort participants, and each subgroup stratified by osteoporosis statuses and daily levothyroxine dose groups. Furthermore, these incidence rates were standardized to the age distribution of all Korean elderly women in 2005.

• At the moment, there are no clear data that demonstrate any relationship between BMD in adults and hypothyroidism.
• Long-term treatment with high doses of LT4 may be administered to suppress the activity of residual thyroid tumour cells after total thyroidectomy for well-differentiated thyroid carcinoma (see chapter, “Levothyroxine and Cancer”).
• However, the most pronounced effects of thyroid hormones on bone in adults are seen in hyperthyroidism.
• Authors showed that BMD at spin tended to increase after one year and the effect was stable 80 after 2 years.
• But if you’re concerned about taking levothyroxine, experts suggest speaking to your doctor before making any changes.

Data Source and Ethical Considerations

The conversion of vitamin D into its active form is also reduced by low parathormone thus reducing gastrointestinal calcium absorption and resultant fecal calcium losses. 182 patients were studied (112 experimental and 70 control), all diagnosed with subclinical hypothyroidism in the age range between 14 and 65 inclusive (Table 1). There exist criteria for referral for cases that require the patient to be referred to other levels of care. Once the sample was selected its members were summoned to complete a clinical questionnaire and undergo a bone density scan with a validated measuring device. Levothyroxine, marketed under multiple brand names including Synthroid, is a synthetic version of a hormone called thyroxine and is commonly prescribed to treat the condition hypothyroidism, or underactive thyroid.

If we’ve neglected to accumulate adequate bone mass during our formative years, including childhood, adolescence, and early adulthood, we’re at increased risk of full-fledged osteoporosis. The aim of this study is to review the current literature concerning the role of thyroid hormones on bone metabolism. You can help keep your bones healthy by eating a well-balanced diet containing calcium-rich foods, maintaining normal vitamin D levels, avoiding smoking, keeping your alcohol drinking to within recommended limits, and exercising regularly. High-impact exercise, such as running or power walking, helps strengthen bones. Weight bearing exercise, such as gardening or stair climbing may be useful in improving balance, therefore reducing the risk of falls which could break bones.

• In adults, overt hyperthyroidism leads to acceleration of bone turnover and loss of mineral density in 10-20%, mainly in cortical bone 8,13,19.
• Ultrasonography, particularly in the calcaneous, is a rapid procedure, which does not use X-rays and may predict fracture risk.
• Persistent increase in bone turnover in Graves’ patients with subclinical hyperthyroidism was observed in other studies.
• The description of qualitative data was done in absolute frequencies and percentages and the quantitative data as mean standard deviation, median, minimum and maximum.
• On the other hand, another study reported no effect of rhTSH on serum osteoprotegerin and RANKL 26.

Any increase in the number of resorption sites produces decreased bone mass together with changes in skeletal microarchitecture, since the mechanism of resorption requires a much shorter time than that of bone formation in the bone remodeling cycle. Thus, the amount of bone formation decreases with age, leading to a more fragile skeleton. Although many variables may be involved in this process, decrease in bone formation may also be due to an age-related decline in skeletal growth factors 3. It is estimated that about 75% of bone loss during the first 15 years after menopause is attributed to estrogen deficiency rather than to aging 4. The bone loss is more evident in vertebral bodies since the trabecular component is metabolically very active and decreases significantly when estrogen is deficient.

The influence of suppressive doses of levothyroxine on bone

TRα1 is considered as a main functional mediator of triiodothyronine in skeleton 5,11,12. Deficiency or dysfunction of TRα leads to growth retardation, delayed bone age, perturbations in bone mineralisation and decreased BMD 8,14. T3 stimulates the IL-6 and IL-8, intensifies the effects of IL-1 and IL-6, augments the synthesis of osteocalcin, collagen type 1, increases proliferation, differentiation and apoptosis of osteoblasts 8. Only TRβ2 is connected with hypothalamus and pituitary, where inhibits the secretion of TRH and TSH 8,9. Osteoblasts and chondrocytes exert the expression of both TRα and TRβ 5,6,10, but concentration of TRα1 is ten times larger than TRβ1 4,5.

How can I reduce my chance of osteoporosis?

The application of TSH-suppressive doses of LT4 has raised concern over its effects on bone health, given the known association between hyperthyroidism, osteoporosis and increased risk of fractures, as described above. Indeed, many clinical studies have applied various measures of bone mineral density or other markers of skeletal function to post-surgical, athyroid patients receiving TSH-suppressive therapy. Conflicting results of the effects of TSH suppression were reported in pre-menopausal women (adverse effect 30–41, or no clear adverse effect 42–47), or post-menopausal women (adverse effect 40, 48, 49 or no clear adverse effect 31, 45, 47, 50–53). An absence of marked effects on bone health was also observed in studies in which pre-menopausal women 71–74, post-menopausal women 71, 74, 75 or mixed populations 76, 77 received less intensive TSH-suppressive therapy for benign thyroid nodules, or for goitre. Untreated hypothyroidism in childhood leads to growth retardation or even growth arrest, disturbances of endochondral ossification, delayed bone age and persistent short stature 8,13,19.

Thyroid hormones are also essential for skeletal maturation and have an important physiological role in the maintenance of adult bone structure and strength. The action of thyroid hormones is mediated by thyroid hormone receptors (TR), which are encoded by THRA and THRB genes 4. They are localized not only on thyrocytes, but also on majority human tissues and cells. Only TRβ2 is connected with hypothalamus and pituitary, where inhibits the secretion of TRH and TSH 8,9. Their expression in bone directly means that this tissue is under the influence of thyroid hormones. Osteoblasts and chondrocytes exert the expression of both TRα and TRβ 5,6,10, but concentration of TRα1 is ten times larger than TRβ1 4,5.