Association and Predictive Accuracy of High TSH Serum Levels in First Trimester and Adverse Pregnancy Outcomes

The effect of thyroid malfunction in pregnancy and on subsequent pregnancies and infant outcomes is a subject of interest and controversy (1). In vitro studies suggest that thyroid hormones contribute directly to early placental development, stimulating angiogenesis and promoting invasion and differentiation of embryonic cells (2, 3). Thyroid hormone (T3) receptors are present in the trophoblast, and thyroid hormone transporters are significantly reduced in pregnancies with intrauterine growth restriction (4). These findings attest to a possible effect of abnormal levels of thyroid hormones on the pathological pathways to adverse pregnancy outcomes.

Fetal T4 production does not occur until 8–10 wk gestation; therefore, the fetus depends upon maternal thyroid hormone transfer in early pregnancy for normal brain development (5, 6). Neurological impairment in children has been associated with maternal overt hypothyroidism (7) and hypothyroxinemia (8). Subclinical hypothyroidism is diagnosed in women with TSH above a statistically defined upper limit of a reference range but normal levels of free T4 (fT4) (9). Although some studies have reported increased rates of pregnancy loss (10, 11), placental abruption (12), preterm delivery (12), and preeclampsia (13) in women with elevated TSH levels, other studies have not identified a significant association with any adverse pregnancy outcome (14, 15).

These inconsistent findings have led to conflicting support for screening asymptomatic women for high TSH levels in early pregnancy. Furthermore, studies suggest that screening and treating women with subclinical hypothyroidism would be cost-effective if this resulted in improved child neurodevelopment (16, 17). First trimester screening would also provide an ideal opportunity to identify at-risk pregnancies and may be incorporated into existing routine antenatal testing when preventive interventions may be a realistic option. Despite these potential benefits and a recent study that found that screening and treating pregnant women with subclinical hypothyroidism was beneficial (18), current clinical guidelines of the American Thyroid Association indicate that there is insufficient evidence to recommend it (19). There is also little information on the predictive accuracy of screening for TSH to identify pregnancies at risk.

The aim of this study was to evaluate the association between high maternal TSH levels measured at 10 to 14 wk of gestation and the risk of adverse pregnancy outcomes, and to assess the predictive accuracy of TSH in predicting adverse outcomes in an unselected pregnant population.

Subjects and Methods

Study population and data sources

The study population included pregnant women who had first trimester Down syndrome screening between July and October 2006 by The Pacific Laboratory Medicine Services (PaLMs), a pathology screening service in New South Wales (NSW), Australia. This was the state’s only public screening service, and it received samples from throughout NSW. A total of 3103 serum samples were collected from women undergoing screening at 10–14 wk gestation, and all samples were archived at −80 C.

Serum TSH levels were measured by automated immunoassay system (Siemens IMMULITE 2000; Siemens Medical Solutions Diagnostics, Los Angeles, CA). The inter- and intraassay coefficient of variation was less than 8%, and the reported analytic sensitivity of the immunoassay was 0.004 IU/liter. The samples were analyzed blind to the clinical outcomes.

Pregnancy and birth information for mothers and babies was ascertained from birth and hospital data, and individual data were record-linked to each woman’s corresponding laboratory (Down syndrome and TSH) results. Birth information was obtained from the NSW Perinatal Data Collection, a statuary collection of all live births and stillbirths in NSW of at least 400-g birth weight or at least 20-wk gestation. It contains demographic, medical, and obstetric information on the mother and information on the labor, delivery, and condition of the infant. Hospital data were obtained from the NSW Admitted Patient Data Collection, a census of hospital discharges from all NSW public and private hospitals and day procedure centers. It includes demographic, administrative, and clinical information for each hospital admission. Information includes reason for admission, significant comorbidities and complications, and procedures performed during the admission. Up to 20 diagnosis and procedure fields were available for each admission and were coded according to the 10th revision of the International Classification of Diseases–Australian Modification (ICD10-AM) and the 5th edition of the Australian Classification of Health Interventions, respectively.

In Australia, unique identifiers are not available for record linkage of unit record data from multiple datasets ( Consequently, probabilistic linkage methods were used. This involves a complex process of blocking and matching combinations of selected variables (such as name, date of birth, address, and hospital) using record-linkage software (21). Probability weights are calculated, adjusted for incomplete and missing data, and used to determine correct matches. The validity of the probabilistic record linkage is extremely high, with less than 1% of records having an incorrect match (23). The NSW Centre for Health Record Linkage conducted the record linkage, and identifying information was removed before the release of data for analysis. The study was approved by the NSW Population and Health Services Research Ethics Committee.

Explanatory variables applied in this study included: maternal age, parity (nulliparous/multiparous), smoking during pregnancy (yes/no), maternal weight (kilograms), and free β-human chorionic gonadotropin (β-hCG) (corrected for gestational age at testing and maternal weight) collected at Down syndrome screening. Only factors that are well and accurately reported were included in the analyses (26, 27). Maternal weight was missing for 550 (20%) of the records. We conducted a sensitivity analysis by comparing original model results attained when we assigned women with a missing weight records the mean weight of the population rather than excluding them from the analysis. Because no significant difference between results was found, mean weight was applied to those missing values and included in the analyses. Other missing data were infrequent. There were no records with missing maternal age or parity. Smoking was missing in 58 records (2.1%), and there were four missing records for free β-hCG (0.1%) that were excluded from the analysis. Only SGA analyses were affected by the missing data exclusions, but importantly, there were no SGA cases with missing data.

Statistical analysis

We compared women with each study outcome to those without the adverse outcome. Descriptive statistics were calculated, and differences between groups were tested using χ2 and Fisher’s exact test for categorical variables and Student’s t test for continuous variables. Given a nonlinear distribution of the serum levels of TSH, a nonparametric Kruskal-Wallis test was used to determine differences among medians of gestational age at testing grouped in weeks, and the Wilcoxon rank-sum test to determine differences in median TSH serum levels between mothers with and without each outcome of interest.

Because TSH differed by gestational week at testing, we standardized TSH levels using multiple of the median (MoM), as described by Cuckle and Wald (28). A regression model was fitted to the medians for each week of gestation at testing for the unaffected group, and each individual value was divided by its regressed value to calculate each MoM. Multivariable logistic regression was used to determine the association between maternal TSH (MoM) and adverse pregnancy outcomes. TSH (MoM) levels were dichotomized to identify mothers with high values of TSH using percentile cutoffs above the 95th (2.92; n = 140) and 97.5th (3.74; n = 70) percentiles. Backward elimination method was then used to fit models with only significant explanatory variables retained. Results are reported as adjusted odds ratios (aOR) with 95% confidence intervals (CI).

The diagnostic performance of significant outcomes was assessed by examining the area under the receiver operating characteristic (ROC) curves (AUC), derived from logistic regression analysis, and using the TSH (MoM) 97.5th centile cutoff because this was considered to be more clinically meaningful. AUC was calculated for both univariate and multivariable models, and results examined whether the test performed better than chance (0.5). A standardized scale was used to assess the AUC result (29), where an AUC of 1 represents a perfect test; 0.9 to less than 1, an excellent test; 0.8 to less than 0.9, a good test; 0.7 to less than 0.8, a fair test; 0.6 to less than 0.7, a poor test; and 0.5 to less than 0.6, a worthless test. Finally, estimates of predictive accuracy were calculated, including sensitivity, specificity, positive and negative predictive values with exact binominal CI (, based on the population prevalence of each outcome. Statistical analysis was performed using SAS software 9.2 (SAS Institute Inc., Cary, NC), and a P value of <0.05 was considered statistically significant.

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In total, 2801 women were included in the analysis. Table 1 presents the maternal characteristics by pregnancy outcome. The mean maternal age was 32.8 (sd, 4.7) yr, 1266 (45.2%) women were nulliparous, and 168 (6.1%) smoked during pregnancy. There were 218 (7.8%) SGA infants, 142 (5.1%) preterm births, 73 (2.6%) women diagnosed with preeclampsia, 42 (1.5%) women who had miscarriages, and 12 (0.4%) stillbirths. The median TSH level for the total population was 0.84 IU/liter (5th to 95th centile range, 0.08–2.37 IU/liter) and for TSH (MoM) was 1.02 (5th to 95th centile range, 0.11–2.92). Compared with unaffected pregnancies, median TSH levels were significantly higher in women with SGA infants below the 10th centile (P < 0.01) and in women who had a preterm birth (<37 wk) (P < 0.05) (Table 1).


Our study indicates that women with high TSH levels at 10 to 14 wk of pregnancy are at increased risk of experiencing an adverse pregnancy outcome, especially of having a SGA infant (<10th centile), preterm birth (<37 wk), or miscarriage. However, we found no significant association for more severe outcomes of SGA below the 3rd centile, very preterm birth (<34 wk), preeclampsia, or stillbirth. Moreover, our results indicate that the predictive accuracy of high TSH levels was poor. Inclusion of additional maternal information and serum biomarker, β-hCG did not improve results.

Overall, our findings do not support routine screening for high TSH levels to identify adverse pregnancy outcomes. Application of our results to a general maternity population of 10000 women with an estimated 10% prevalence of SGA infants reveals that screening for high levels of TSH in the first trimester would identify 4698 women at risk, but only 711 would truly have a SGA infant. A total of 3987 would be falsely labeled, and a further 289 would be missed altogether. This is supported by a recent trial comparing universal screening for TSH with a high-risk, case-finding approach for the detection and treatment of thyroid hormone dysfunction in pregnancy. The trial found no significant difference in adverse pregnancy outcomes between groups, although women from the universal screening group that were low-risk, hypothyroid, and treated had less adverse pregnancy outcomes compared with women from the case-finding group that were low-risk, hypothyroid (nonidentified), and nontreated (18). These findings, as well as our own results, suggest that the majority of women having adverse pregnancy outcomes do not have elevated TSH and are euthyroid. Thus, TSH screening is likely to fail to identify the majority of women at risk because high TSH levels may represent only one specific pathological pathway, and the causes of adverse pregnancy outcomes are heterogeneous and multifactorial (31).

To date, there have been a number of studies investigating the association between high TSH levels and adverse pregnancy outcomes, and findings have been inconsistent. Although, our results suggest some evidence of an increased risk of SGA below the 10th centile and preterm birth (<37 wk), these may have been chance findings because we did not find any relationship for more severe cases, sga below the 3rd centile, and very preterm birth (<34 wk); however, numbers were small. strong association between high tsh levels miscarriage has reported by previous studies but should be replicated in future studies. a study of euthyroid pregnant women with autoimmune thyroid disease found reduction rates group treated levothyroxine compared nontreated that had higher levels, suggesting determinant risk factor (32). Also, two studies have found increased risk of fetal loss, which included miscarriages and/or stillbirths (10, 11). Overall, our findings suggest that there is significant association between high TSH levels and some adverse pregnancy outcomes examined. Variation in study findings may be explained by differences in study design, population sample size, or representativeness of the clinical population, ranging from case-control studies of 167 women to large cohort studies testing over 17,000 women, and differences in demographic characteristics such as maternal age, racial origin, or parity.

Serum TSH was also variable across studies. We identified a 95th percentile cut point of 2.37 IU/liter; although a degree of mild iodine deficiency has been reported in NSW (33), results are consistent with an iodine-replete population and reference intervals reported for first trimester of pregnancy in Western Australia (34). However, other studies have used various (95th and 97.5th centiles) cut points to define high TSH levels, ranging from 2.78 to 4.8 IU/liter (12, 14, 3436). These differences suggest significant variability in distribution of TSH serum levels that may be explained by different levels of iodine status in populations, different immunoassay used in the analysis, or underlying ethnic differences (37).

Strengths of this study were the assessment of a large sample and unselected consecutive cohort of women attending first trimester screening. Record linkage of laboratory to birth and hospital data ensured follow-up and ascertainment of pregnancy outcomes with only minimal missing information.

Missing health and pregnancy information was mostly attributable to women residing in bordering towns and giving birth in hospitals out of state. Nevertheless, women with missing health information had similar characteristics compared with those included in the study. Another strength was that the exposure was measured independently of the outcome and was adjusted for β-hCG, with testing performed blinded to outcome. Low β-hCG has been identified as a risk factor or marker for miscarriage, preterm delivery, and fetal growth restriction (26, 38); and maternal TSH function in pregnancy can be influenced by the thyrotrophic activity of β-hCG. Both hormones have similar structure, sharing a common α-subunit, and a reduction in TSH secretion in response to rising β-hCG levels in the first trimester of pregnancy has been previously reported (1, 39). However, one of the limitations of our study was the lack of clinical information such as supplementation use in pregnancy. Nevertheless, women in our study appeared to be healthier, reflected by the lower prevalence of adverse pregnancy outcomes compared with the maternity population in NSW (5.1 vs. 5.9% preterm birth, 7.8 vs. 10% SGA infants, 2.6 vs. 3.1% preeclampsia) (20). Finally, miscarriages were underrepresented because these were limited to only those occurring after 10 wk gestation, and not all women are admitted to hospital for such an event.

In our study, women were not tested for fT4; therefore, it was only possible to categorize women as having high TSH levels but not to separate women with subclinical (high TSH and fT4 within normal range) and clinical hypothyroidism (high TSH with fT4 <5th centile). women with tsh levels greater than 10 iuliter, irrespective of their ft4 levels, are considered to have clinical hypothyroidism (19). In our population, only four women had TSH levels greater than 10 IU/liter; consequently, it was not considered significant enough to conduct a subanalysis in the group. Thyroid antibody presence (thyroid peroxidase antibody or triglyceride antibody) was also not tested in our study. A recent meta-analysis of studies (41) found that miscarriage and preterm birth were associated with the presence of thyroid antibodies and that antibody-positive women have, on average, higher TSH levels compared with antibody-negative women. However, the predictive usefulness of high TSH levels for miscarriage is questionable due to the very limited time to intervention.

Overall, our findings suggest that elevated TSH levels are associated with an increased risk of adverse pregnancy outcomes. Despite the positive associations, the poor predictive accuracy of our models suggests that widespread screening for high levels of TSH in the first trimester of pregnancy would not efficiently identify women at risk of adverse pregnancy outcomes.


We thank the NSW Department of Health and the NSW Centre for Health Record Linkage, for record linkage and for access to the population health data; Cyrille Guilbert, for preparation of samples; and Samantha Lain, for preparation of data for linkage.

This work was funded by a National Health and Medical Research Council (NHMRC) Project Grant (no. 632653). C.L.R. is supported by a NHMRC Senior Research Fellowship (no. 457078) and N.N. by a NHMRC Career Development Fellowship (no. 632955).

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Disclosure Summary: There is no conflict of interest to declare.




— Update: 19-03-2023 — found an additional article Thyroglobulin Antibody Normal Range + High Levels from the website for the keyword hypothyroidism tsh 4.8ui l toohigh.

Hypothyroidism tsh 4.8ui l toohigh

Your body creates thyroglobulin antibodies when it mistakes thyroglobulin as a threat. Testing the levels is useful in thyroid cancer patients and those with other thyroid disorders. Learn about the causes and effects of high levels + factors that reduce them.

What is Thyroglobulin Antibody?

In order to understand what thyroglobulin antibodies (TgAb) are, we first have to talk about thyroglobulin (Tg) itself.

Thyroglobulin is a protein the thyroid gland uses to create T3 and T4 or thyroid hormones. Doctors often check thyroglobulin levels in people who received thyroid cancer treatment [1].

The immune system may mistakenly identify thyroglobulin as a harmful substance. In turn, it produces antibodies to attack thyroglobulin, otherwise known as TgAb [1].

According to some estimates, about 10% of the general population produces at least some TgAb. This rate goes up to 80% in those with thyroid disorders, such as in Hashimoto’s or Graves’ disease. That’s why TgAb are used as a marker of autoimmune thyroid problems [1, 2, 3].

Thyroglobulin antibodies can bind to thyroid cells, but it’s not entirely clear if they cause damage. These antibodies mostly become a problem when trying to measure thyroglobulin, as they skew thyroglobulin test results [1, 3, 4, 5].

Thyroglobulin Antibody Test

Why is it Ordered?

Detecting Autoimmune Thyroid Disorders

The TgAb test can help pinpoint autoimmune thyroid disorders, such as Graves’ disease and Hashimoto’s Thyroiditis. Your doctor may order the test if you have signs or symptoms of a thyroid disorder. Some symptoms of hypo- and hyperthyroidism may overlap. For example, both can cause thyroid gland enlargement and neck swelling [3, 4, 6].

The following symptoms point to an underactive thyroid (hypothyroidism) [6]:

  • Weight gain
  • Fatigue and lethargy
  • Depression
  • Dry skin
  • Cold intolerance

On the other hand, typical symptoms of an overactive thyroid (hyperthyroidism) include [6]:

  • Weight loss
  • Anxiety or nervousness
  • Increased sweating
  • Diarrhea
  • Heart palpitations
  • Muscle weakness
  • Heat intolerance

The TgAb test requires a blood sample. Results are reported as a number in units of IU/mL.

Monitoring Thyroid Cancer

Thyroglobulin antibody (TgAb) tests are usually performed alongside thyroglobulin tests to monitor thyroid cancer patients and check for cancer recurrence after surgery [1, 7].

These two tests are done together because TgAb interferes with thyroglobulin measurements, resulting in falsely low levels. TgAb testing helps doctors determine the extent of interference. However, since this interference varies from person to person, estimating the true thyroglobulin levels can still be challenging [8, 9].

Normal Range

The body should not be producing any TgAb [5].

However, even people without any thyroid issues may produce someTgAb. In healthy people, TgAb does not cause any problems [5].

Often times, the TgAb results will come back as 1.0 IU/mL. This may be the actual TgAb level, or it could be that the test isn’t sensitive to detect levels lower than that.

General population

TgAb levels below 20 IU/mL are typically considered normal for the general population (those without any thyroid issues). However, the normal range can greatly vary depending on the test manufacturer [10].

People with Thyroid Issues

The optimal range for people with thyroid conditions is even less clear. Higher levels point to autoimmune thyroid disorders. Research also suggests TgAb levels above 40 IU/mL may be associated with an increased risk of thyroid cancer [11].

People Who Had Thyroid Cancer

In people who had thyroid cancer, thyroglobulin levels should be as low as possible. Any increases suggest the cancer is coming back or there is leftover thyroid tissue. Newer studies suggest that thyroglobulin antibody levels should also be as low as possible [12].

According to a recent study, thyroid cancer survivors with TgAb levels that fall by 50% (or more) by one year after treatment are at a lower risk of the cancer coming back. Patients whose TgAb levels didn’t change or increased over this period of time had higher rates of cancer recurrence [12].

Connection to Thyroid Peroxidase Antibody (TPOAb)

Thyroid peroxidase antibody (TPOAb) is very similar to TgAb: it is also an antibody that mistakenly attacks the thyroid gland. While TgAb targets thyroglobulin, TPOAb targets an important thyroid enzyme called thyroid peroxidase. TPOAb can increase oxidative stress and may damage the thyroid [5].

The TBOAb test is also sometimes called the Antithyroid Microsomal Antibody Test (or just antimicrosomal antibodies test).

The same conditions that cause TgAb to increase usually also raise TPOAb. In fact, TPOAb may be a better indicator of autoimmune thyroid disorders than TgAb [5, 13].

About 90-95% of people with autoimmune thyroid disorders have detectable TPO antibodies, while only 70-80% of them have detectable thyroglobulin antibodies. Therefore, your test results may come back as normal TgAb and detectable TPOAb even if you have autoimmune thyroid issues [5].

TPOAb assays vary in sensitivity. Older assays may not detect TPO antibody levels more sensitive assays would. If your TPOAb came back normal (undetectable) and your TgAb high, you should probably repeat the TPO test with a more sensitive assay [14+].

People without thyroid problems may also test positive for TPOAb. According to some estimates, about 10 to 15% of the general population produce TPOAb [13].

Another big difference between these two types of antibodies is that TPOAb does not interfere with thyroglobulin tests like TgAb does. This means a TPOAb test would not be helpful for determining thyroglobulin levels [5].

High Thyroglobulin Antibody Levels

TgAb levels are a marker of thyroid health. Low or high levels don’t necessarily indicate a problem if there are no symptoms or if your doctor tells you not to worry about it.


High TgAb alone do not cause any symptoms. For example, TgAb does not cause any problems in healthy people with normal thyroid function [5].

If you have an underlying thyroid condition, high thyroglobulin antibodies may be associated with the symptoms of that condition. According to one study, those with high TgAb and Hashimoto’s thyroiditis will experience more [15]:

  • Face and eye swelling
  • Fragile hair
  • Voice changes

Potential Causes & Associated Conditions

1) Autoimmune Diseases

Autoimmune diseases occur when the body’s immune system mistakenly attacks its own tissues [16].

A number of autoimmune conditions can elevate TgAb, particularly those affecting the thyroid gland [16].

For instance, TgAb is found in about 80% of people with Hashimoto’s thyroiditis, the most common autoimmune thyroid disorder. This condition causes thyroid gland inflammation, eventually leading to hypothyroidism [3].

Graves’ disease is another autoimmune disorder that attacks the thyroid and results in hyperthyroidism. About 20-40% of people with Graves’ disease have high TgAb levels [4].

Non-thyroid autoimmune disorders may also trigger the production of TgAb [16].

According to several studies, over 50% of systemic sclerosis patients and 30% of rheumatoid arthritis patients have high TgAb levels. Systemic sclerosis is a rare autoimmune disease in which too much collagen and other proteins are produced [16, 17, 18].

Another example is in Sjogren’s syndrome, an autoimmune disorder that attacks the glands that produce tears and saliva. People with Sjogren’s are 9x more likely to have a thyroid-related autoimmune disorder, which is likely to raise TgAb [19, 20].

2) Hives

Hives are a type of skin rash caused by an allergic reaction or infection. The exact cause often remains unknown and may involve autoimmunity [21].

According to a large review of over 14k cases, people with hives are much more likely to have high TgAb. In another study of 144 people with hives, about 26% tested positive for TgAb [21, 22].

3) Sleep Apnea

Obstructive sleep apnea, the most common form of sleep apnea, is caused by blockages to the upper airway during sleep. Curiously, this type of sleep apnea is linked to autoimmune diseases [23, 24].

In one study of 245 people with normal thyroid hormone levels and suspected obstructive sleep apnea, almost 50% were diagnosed with Hashimoto’s thyroiditis due, in part, to high TgAb levels. Those with worse sleep apnea symptoms were more likely to be positive for TgAb [24].

Gender appears to play a role as well. In general, women are 10 times more likely to be affected by Hashimoto’s than men. But men are more likely to develop apnea-related Hashimoto’s than women [25, 24].

4) Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a hormonal disorder that leads to irregular or no menstrual periods, acne, and difficulty getting pregnant [26].

These symptoms are due to high levels of androgens (male sex hormones) in women. But some researchers think PCOS may have an autoimmune basis. They discovered a strong link between PCOS and autoimmune thyroid conditions [26, 27].

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For example, one study of 343 women revealed that about 27% of those with PCOS test positive for thyroid antibodies [28].

5) Vitamin D Deficiency

When most people think of vitamin D, they think of its benefits to bone health. Some know it’s good for mood as well. But this vitamin also plays a key role in the immune system. Deficiencies in vitamin D are linked to immune disorders, including autoimmunity [29].

In a study of 540 people, those with lower levels of vitamin D had higher levels of TgAb. Other studies have found similar results [30, 31].

6) High Doses of Iodine

Iodine is vital to thyroid gland health. Your thyroid uses it to create the thyroid hormones T3 and T4 [32].

In fact, iodine deficiency is one of the leading causes of hypothyroidism worldwide [32].

But more is not always better with iodine. In a trial of 752 people, high doses of iodine (1.53 mg each week) increased levels of TgAb [33].

On the flip side, low dose iodine (200 micrograms daily) actually reduces TgAb levels [33].

7) Dental Amalgam (Mercury) Fillings

Dental amalgams may trigger an autoimmune response and increase TgAb. These “silver” dental fillings are made from a mix of metals, including mercury, silver, and copper. Their use in the U.S. is declining, but they are still the most common type of dental filling in Canada today [34].

People with dental amalgams may have elevated TgAb levels, according to one study. Average TgAb levels were cut in half after removing the fillings, but only in those who tested positive for mercury hypersensitivity. Up to 15% of the population is highly sensitive to chemical toxins like mercury [34, 35].

8) Exposure to Heavy Metals

As with mercury-containing dental fillings, environmental exposure to other heavy metals like lead and cadmium may disrupt immune and thyroid health [36, 35].

In a study of over 5,600 Chinese adults, women exposed to more cadmium had higher thyroglobulin antibody levels. Interestingly enough, heavy metal exposure did not affect TgAb levels in men [36].

9) Turner’s Syndrome

Women with Turner’s syndrome are completely or partially missing an X chromosome. This leads to a number of health problems, including thyroid dysfunction [37].

In a study of 89 girls, thyroid antibodies were detected in about 52% of those with Turner’s syndrome. Girls with more severe forms of the disorder were more likely to have high TgAb [38].

Other studies voice the same results: one discovered thyroid antibodies in over 60% of Turner’s patients [39, 37].

10) Hepatitis C

Hepatitis C is a viral infection that attacks the liver. Research suggests an important link between hepatitis C and the risk of autoimmune thyroid disorders [40].

According to a review of 12 studies, people with hepatitis C are 2.4x more likely to test positive for TgAb [41].

11) Genetics

Your genes may affect your thyroglobulin antibodies and thyroid health [42].

One study explored this genetic effect by looking at 686 sets of twins. They discovered that the influence of genetics on TgAb levels is about 39% in men and 75% in women [42].

12) Certain Drugs

Several medications may raise TgAb. Many of these drugs are cancer treatments that alter the immune system in some way.

Some examples of drugs that can raise TgAb levels include:

  • Interferon-α (Multiferon) [43]
  • Nevirapine (Viramune) [44]
  • Nivolumab (Opdivo) [45]
  • Triptorelin (Trelstar) [46]
  • Radioactive iodine therapy [47]

Health Effects

1) Worse Autoimmune Thyroid Symptoms

TgAb probably doesn’t trigger autoimmune problems, since it does not attack thyroid cells. But high levels may worsen autoimmunity [3, 5].

A study of 290 people with Hashimoto’s thyroiditis revealed that higher levels of TgAb are associated with an increased number and severity of symptoms [15].

2) Thyroid Nodules

Thyroid nodules are small lumps that can form in the thyroid gland (near the base of the neck) [48].

For the most part, these nodules are harmless and don’t cause any symptoms. However, a small percentage of thyroid nodules are cancerous [48, 49].

In one study of 1,271 adults, those with higher levels of TgAb were at a higher risk of developing thyroid nodules. The association was stronger in women [49].

On top of that, thyroid nodules are more likely to be cancerous in those with high TgAb [50].

3) May Increase the Risk of Thyroid Cancer

Thyroglobulin antibodies are commonly used as a lab marker to monitor treatment effectiveness in thyroid cancer patients. These antibodies may be a risk factor to begin with [51, 11, 50].

According to a study of over 1,600 people, high levels of TgAb (≥40 IU/mL) are linked to increased rates of thyroid cancer (differentiated thyroid carcinoma) [11].

As mentioned in the previous section, TgAb may also increase the risk of cancerous thyroid nodules [50].

4) Worse Outcomes for In Vitro Fertilization

In vitro fertilization (IVF) is the process of fertilizing a human egg in the lab. The procedure is a great option for couples with fertility issues.

However, women who test positive for thyroid antibodies may want to do additional screenings if considering IVF.

Based on a study of 766 women, those who have thyroid antibodies have worse IVF outcomes. This includes lower fertilization and pregnancy rates, as well as a higher risk of miscarriages [52].

5) Lower Birth Weights in Newborns

TgAb levels may influence normal pregnancies as well.

Mothers who are positive for TgAb give birth to infants with lower birth weights, according to a study of over 7,600 women [53].

Women with TgAb may also be more likely to have their “water break” prematurely, a condition known as prelabor rupture of membranes [53].

Factors that Lower Tg Antibodies

Improving your TgAb levels won’t necessarily cause improvement in thyroid health, but it can be used as a biomarker. The following is a list of complementary approaches to support the thyroid that may also balance high TgAb levels.

Though studies suggest various dietary and lifestyle factors may lower TgAb levels, additional large-scale studies are needed. Remember to talk to your doctor before making any major changes to your day-to-day routine.

1) Vitamin D

Vitamin D deficiencies are associated with thyroid dysfunction and higher levels of TgAb [31, 30].

One clinical trial gave 50,000 IU of vitamin D for a week to 42 women with Hashimoto’s thyroiditis. After 3 months, vitamin D supplementation reduced TgAb levels by an average of 50 IU/mL [54].

Another study using a smaller vitamin D dose of 2,000 IU daily found a similar (but smaller) reduction in TgAb [55].

The best way to increase your vitamin D levels is to get more sun. Beyond vitamin D, sun exposure can balance the immune system and provide you with a number of other benefits. Studies have yet to examine its effects on TgAb, though [56].

2) Optimal Iodine Intake

Iodine is essential for proper thyroid function, but too much can be harmful [57].

For example, weekly iodine doses of 1.53 mg increased TgAb levels [33].

On the other hand, a much lower dose of 200 micrograms daily (equivalent to 0.2 mg) significantly reduces TgAb [33].

Some good dietary sources of iodine include [58]:

  • Seafood
  • Seaweed
  • Dairy products
  • Iodized salt

3) Selenium

Similar to iodine, selenium is an essential micronutrient. Many enzymes – including the ones in your thyroid – require it [59].

According to a study of 88 women, a selenium dose of 200 micrograms each day decreases TgAb levels [60].

However, a dose of 100 micrograms had a weaker effect that diminished over time [60].

Other studies suggest selenium supplementation may reduce thyroid size and inflammation as well [61, 62].

Some good sources of selenium include [63]:

  • Brazil nuts
  • Seafood
  • Whole grains

4) Low-Carb Diet

Diet plays an important role in many conditions, and thyroid disorders are no exception.

A recent study revealed that a low-carb, protein-rich diet reduces TgAb levels by about 40% [64].

It also had the added benefit of weight loss: participants lost about 5% of their body weight after 3 weeks of the diet [64].

5) Amalgam Dental Fillings Removal

Dental amalgam fillings may trigger a rise in TgAb and autoimmunity [34].

One study reveals that removing this type of metal filling decreases TgAb levels in people who are hypersensitive to mercury [34].

Have a talk with your dentist and doctor to weigh the potential benefits of replacing your amalgam fillings with mercury-free ones.


Emerging research suggests TgAb plays an important role in thyroid disorders, but studies remain limited [5].

The effects TgAb has on healthy people or on those with a thyroid disorder are not fully understood. TgAb is associated with many conditions, but it’s not always clear if high TgAb levels are a causal factor or result of thyroid disorders [5, 65].


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