Skip to main content

Postpartum depression in maternal thyroidal changes

Abstract

Evidence in the literature has suggested that there may be an association between thyroid antibodies and depression during pregnancy and in the postpartum period. Thus, this study aims to conduct a systematic review on the prevalence of postpartum depression (PPD) in women with thyroid abnormalities during pregnancy or in the postpartum period. For this review, we used four databases (PubMed, Lilacs, Scielo, and Scopus). Fifteen studies were selected; one study used a case–control design, four used a cross-sectional design and ten utilized prospective cohort designs. All studies were restricted to up to 1 year postpartum, and 46.7% focused on a period between immediate postpartum and 6 months postpartum. Estimates of the prevalence of PPD in pregnant women with thyroid disorders ranged between 8.3% and 36.0%. For follow-up studies, the cumulative incidence of self-reported depression from the primary episode in the first postpartum year was 6.3% in a high-city survey. Although some authors consider the status of positive anti-TPO antibodies to be a possible marker of vulnerability to depression , it is not yet possible to conclude whether thyroid function in the pregnancy-puerperal cycle is involved with the development of PPD.

Introduction

Depression, one of the most frequent mental disorders after childbirth, is considered a severe and current health problem due to its high prevalence and the negative impact that it has on both the mother's health and the development of her child [1]. The postpartum period, considered one of the most complex experiences of human life [2], is characterized by an emotional vulnerability that, associated with physiological, psychological, social, and cultural changes, promotes the appearance of maternal mental disorders. PPD is defined as a mood disorder that usually manifests itself in the first four weeks after delivery and usually reaches its maximum intensity in the first six months after delivery.

Epidemiological studies on PPD suggest a multiplicity of risk factors involved in its genesis, among which are endocrinopathies [3, 4]. Thyroid disorders are the endocrine diseases that have been most researched to identify an association with postpartum depression. During pregnancy, the maternal immune system undergoes many changes to accommodate the development of the fetus [5] and tries to return to its prepregnancy state in the postpartum period. These modifications include changes in the production of autoantibodies that target thyroid antigens, such as thyroid peroxidase (anti-TPO) [6]. Anti-TPO is the most common type of thyroid autoantibody found in euthyroid individuals and is associated with various forms of thyroid dysfunction [7].

Several studies have shown a positive association between the thyroid peroxidase antibody and the development of mood disorders, with a high prevalence of positive anti-TPO antibodies among patients with bipolar and unipolar disorders. However, this association between positive thyroid antibody and postpartum depression has not been replicated in other studies. Menna et al. [8] and Le Donne et al. [9] concluded that there is insufficient evidence to confirm an association between PPD and postpartum thyroiditis or positive anti-TPO antibodies (in euthyroid women who did not develop postpartum thyroiditis).

The relationship between thyroid dysfunction and PPD cannot yet be considered consistent [10, 11] and requires further study. Therefore, the present study aims to assess the potential of thyroid biomarkers as predictors for the development of PPD through a systematic review. Our working hypothesis is that one or more thyroid markers can predict the risk of developing PPD in pregnant/puerperal women, and these markers may be related to worse disease.

Methods

Review question

Can thyroid markers predict the risk of developing PPD in pregnant/puerperal women?

Inclusion and exclusion criteria

As an inclusion criterion, the publication should contain original data, and the research must be carried out with humans, not including literature reviews, editorials, perspectives, letters, commentaries, and abstracts from meetings. No other exclusion criteria, such as language, year limit, sample sizes, or diagnostic tools for PPD, were used.

Search strategy

This study was based on a systematic review of scientific articles published in indexed journals until the date of January 24, 2022. The PubMed, Lilacs (Latin American and Caribbean Literature in Health Sciences) SciELO (Scientific Electronic Library Online), and Scopus databases were searched, according to Table 1. For the outcome (thyroid changes), the terms “thyroid dysfunction”, “thyroid hormones”, “TPO protein, human”, “thyroid peroxidase antibody”, “hypothyroidism” and “hyperthyroidism” were used. As terms of exposure (PPD), the terms “depression, postpartum” and “perinatal depression” were used. In the Lilacs and SciELO databases, the terms “postpartum depression” and “postnatal depression” were used to determine if they were present in the articles, according to Health Sciences Descriptors (DeCS).

Table 1 Structured search strategy carried out in databases. The search followed the structure of each database

All references were managed in EndNote X7 software (Thomson Reuters, New York, NY, US). Initially, duplicate references were excluded. Titles and abstracts were independently screened based on the aforementioned inclusion and exclusion criteria by two reviewers (PMSS and AL). The screened lists were compared, and in case of disagreement, a consensus was reached by discussion. When a consensus was not achieved, a third reviewer decided if the article should be included (AMA). After the initial screening of titles and abstracts, full articles were evaluated by the same two reviewers. In addition to an electronic search, the reviewers also performed a hand search in the reference lists of all included studies. Predefined data collection worksheets were used for the data extraction of each selected publication. This systematic review followed the PRISMA statements, with some adjustments [12].

Data extraction

The titles and abstracts of the studies were initially analyzed. For the full evaluation, publications with original results on the prevalence or incidence of PPD in women/pregnant women with previous thyroid evaluation were selected (Fig. 1). A secondary search was also carried out in the bibliographic list of the articles initially evaluated to identify other important references not captured by the initial search.

Fig. 1
figure 1

Flow chart analysis of the articles selected in the PubMed, LILACS, Scielo and Scopus databases (January 24, 2022)

In addition to data on thyroid assessment and PPD, information was collected on methodological aspects that could have some influence on the results of suspected or diagnosed cases of PPD, such as the study design, sociodemographic profile of the population evaluated, gestational and postpartum period used and blood analysis method and criteria.

The process of searching, extracting, and tabulating the selected articles was performed independently by two reviewers (PMSS and AL) to be submitted to descriptive analysis. Cases of disagreement were handled as described above. Both reviewers also manually searched the reference section of each relevant article and independently assessed and collected all other articles identified as eligible. A meta-analysis of the data was not feasible, given the absence of agreement in the literature to date.

Statistical analysis

We chose not to meta-analyze data from eligible studies because significant heterogeneity exists across studies in terms of the assays used to measure anti-TPO and the cutoffs used to determine anti-TPO (i.e., normal or abnormal levels), the methods used to define depression, and the timing of assessment for both TPO-AB status and depression. Consistent timing in the measurement of TPO-AB and thyroid hormones during pregnancy is required for valid meta-analysis given the changing immune milieu of this period of life [13, 14].

Results

Our initial searches yielded 1768, 272, 38, and 54 studies in the PubMed, Lilacs, SciELO, and Scopus databases, respectively (Fig. 1). Twenty-one full text articles were examined as they were thought to contain data that could address our objective (associations between anti-TPO during pregnancy or the puerperium or postnatal depression). However, only 15 original articles suggested the presence, in the full text, of data on the frequency of PPD and thyroid assessment [9, 15,16,17,18,19,20,21,22,23,24,25,26,27,28]. The selected articles were published between 1992 and 2019.

The characteristics and results of the studies included in this review can be found in Table 2. The sample sizes in these studies ranged from 31 [15] to 1075 [16]. One study used a case–control design [17], four used a cross-sectional design [9, 18,19,20], and ten utilized prospective cohort designs [15, 16, 21,22,23,24,25,26,27,28].

Table 2 Summary of selected studies on maternal thyroid disorder and postpartum depression

Of these studies, seven reported on the relationships between anti-TPO during pregnancy and postnatal depression [16, 20,21,22,23,24,25], and five investigated the links between anti-TPO during the postpartum period and postnatal depression [9, 17,18,19, 26].

Of these, one study used a cutoff value of 19.6 kIU/l [23], two studies each utilized cutoffs of 20 IU/ml [16, 25], and one utilized 27 IU/ml [17], 34 IU/ml [9], 49 kIU/l [18], and 50 U/ml [24]. One study used a cutoff value of 525 U/ml of microsomal antibodies [21], and one study identified women as anti-TPO (TPO-AB +) if they detected any level of microsomal antibodies at 32 weeks of gestation [22]. Two studies also examined TPO-AB as a continuous measure [9, 17].

Estimates of the prevalence of PPD in pregnant women with thyroid disorders ranged from 8.3% [17] to 59.0% [24]. For follow-up studies, the cumulative incidence of self-reported depression from the first episode in the first postpartum year was 6.3% in a high-city survey (n = 1075) [16]. The incidence of depression at 3 days postpartum and 4 weeks postpartum was 14.58% and 7.29%, respectively [28]. Among other findings, women in the postpartum period (24–48 h) with positive anti-TPO had a five times greater risk of hypothyroidism [17]. Clinical thyroid dysfunction occurred in 19% of patients with postpartum psychosis compared to only 3% of the control group [15].

Anti-TPO and anti-TG levels were significantly higher in women at risk for PPD [9]. In a study by Groer and Vaughan [25], anti-TPO positive women had significantly higher scores for depression, anger, and total scores of mood disturbance postpartum than anti-TPO negative women, regardless of the development of postpartum thyroiditis (n = 25).

In another study, after adjustment for previous psychiatric contact, smoking during pregnancy, prepregnancy BMI and sleep, TSH levels above 4.0 mU/L were associated with an increased risk of depressive symptoms at six months postpartum [26]. Lower concentrations of TGB at the end of pregnancy also proved to be a strong predictor for perinatal syndromic depression, as well as a history of trauma [27].

The postnatal period in which maternal depressive symptoms were assessed varied between the selected studies (Table 3). Although all studies were restricted to up to 1 year postpartum, eight studies (53,3%) covered some period between the immediate postpartum period and 6 months postpartum [9, 18,19,20, 25,26,27,28], and seven publications (46,7%) carried out a maternal mental health assessment after 6 months [15,16,17, 21,22,23,24]. A follow-up after 1 year of the postpartum period was not performed by any of the studies.

Table 3 Instruments for diagnosis/screening of postpartum depression

Concerning the detection instruments used for PPD screening or diagnosis (Table 3), nine studies (60,0%) used the Edinburgh Postnatal Depression Scale (EPDS), of which they made exclusive use of the EPDS 5 surveys (33,3%) [16, 17, 19, 26, 28]. The Research Diagnostic Criteria, RDC, was exclusively used in two publications (13,3%) [22, 24], and in only one publication (6,7%), the clinical interview (SCI) was used to characterize PPD [15].

The cutoff values for the EPDS also varied between studies from 9 to more than 12 points (Table 3). Only one publication used different cutoff points for the gestational trimesters and the postpartum period: 1st trimester ≥ 11, 2nd and 3rd trimester ≥ 10 and postpartum ≥ 13 [16].

Discussion

From this systematic review of the literature to clarify the relationship between maternal thyroid changes and postpartum depression, based on our search criteria, it was observed that the studies on the subject are heterogeneous in terms of study size, population studied, design (prospective, case–control, transversal), psychometric scale, and the evaluation of thyroid hormones (different analysis methods and different cutoff points). However, for some authors, the status of thyroid peroxidase antibodies has become considered a marker of vulnerability to depression. It is observed that studies have been concerned with assessing PPD and thyroid changes throughout the gestational period and in the postpartum period through longitudinal studies. Most studies followed the participants over a certain period, with periodic measurements of postnatal depressive symptoms, thus obtaining an estimate of the incidence of the condition. The studies that showed a relationship between PPD and thyroid function suggested that thyroperoxidase antibodies (anti-TPO) may be a possible target in the search for a biomarker to predict the development of emotional disorders, including PPD [16, 17, 21, 23,24,25].

Ruschi et al. [19] and Kuijpens et al. [24] showed that the frequency of PPD was high, without an association between PPD and thyroid alterations. Multiple studies examining associations between thyroid hormones and depression during the perinatal period have suggested a link [20, 26, 27, 29, 32,33,34]. However, a consensus does not exist as to whether clinical syndromes of thyroid dysfunction (e.g., hyper- and/or hypothyroidism) are linked to depression in the perinatal period [23, 35,36,37,38].

Regarding TSH, our research shows few studies directly correlating TSH levels and PPD [26, 28]. Zhang et al. [28] found no significant difference in the occurrence of PPD between the TSH groups > 2.5 mUI/L and TSH ≤ 2.5 mUI/L. However, for serum T4, a meta-analysis article with low heterogeneity conducted with population-based studies showed that serum T4 was positively correlated with depressed mood, while TSH was negatively associated with depressed mood [39]. A study by Sylvén et al. [26] suggested that there was no significant association between PPD and TSH levels at five days or six weeks after delivery. However, after adjustment for previous psychiatric contact, smoking during pregnancy, prepregnancy BMI and sleep, TSH levels above 4.0 mU/L were associated with an increased risk of depressive symptoms at six months postpartum.

The findings of our study showed heterogeneity in the methods used to investigate both thyroid alterations and PPD (Tables 2 and 3). According to Lewandowski et al. [33], when they evaluated baseline concentrations of free T4, free T3, and TSH at 30-min intervals in 110 healthy pregnant women, in a significant number of patients, the diagnosis of subclinical thyroid dysfunction could be misdiagnosed, not as a result of "disease", but as a result of physiological variation in TSH concentrations. Additionally, in 2021, Xing et al. [29] found that the TSH reference range was significantly influenced by sex, age, iodine intake, sample size, region and test methods and manufacturers. Therefore, for the reliability of the thyroid alteration in a sample, each laboratory must validate an appropriate TSH reference interval based on local conditions and based on the physiological variations of pregnant women, postpartum women and the postpregnancy period.

Lambrinoudaki et al. [22] investigated whether thyroid function within the normal range affects the incidence of postpartum mood disorders. The findings indicated an association between the occurrence of postpartum mood disorders and prenatal thyroid function. Within normal limits, lower levels of free T3 and free T4 were associated with an increased incidence of mood disorders in the first postpartum week.

However, Albacar et al. [27] did not observe any association between thyroid function and PPD. All women who scored 9/10 on the EPDS at 8 weeks and 32 weeks postpartum were defined as likely cases of major depression. Among the 1053 women evaluated in the study, 8.3% were depressed. Although 14.4% had high levels of anti-TPO and slightly elevated TSH concentrations with normal free T4, no association was found between thyroid function and PPD. It was concluded that thyroid function at 48 h after delivery does not predict the risk of PPD. However, it may be that the observed anti-TPO positivity worsens thyroid function and that subsequent anti-TPO positivity may be associated with PPD, requiring additional investigations at multiple postpartum intervals. For Le Donne et al. [18], the risk of PPD and alexithymia is directly associated with thyroid autoimmunity. The risk of postpartum depression and alexithymia had a significant correlation with positive anti-TPO, suggesting that these mood disorders may have neurobehavioral consequences of an autoimmune attack (because of the anti-TPO circulation in the CSF and its possible cross-reactivity with brain autoantigens) [18, 32].

After analysis, we found that higher prevalence and incidence rates of depression and/or more severe complaints of depression have been reported in antithyroperoxidase antibody (TPOAb)-positive women by some authors [16, 21, 23,24,25,26], while others could not demonstrate such an association [17,18,19,20, 26]. Sylven et al. [26] evaluated depressive symptoms during each trimester and at four postpartum moments (6 weeks, 4 months, 8 months, and 12 months). A positive anti-TPO state was associated with an increased risk of self-reported depression of a single onset at four months postpartum but not at other postpartum time points. The longitudinal pattern of self-reported postpartum depression in the positive anti-TPO group was similar to the typical course of anti-TPO in the postpartum period. This suggests an overlap in the etiology of PPD and autoimmune thyroid dysfunction. By analyzing these results, we can assess thyroid function in women with PPD. Similarly, the results of Groer and Vaughan [25] suggest that the presence of positive anti-TPO in pregnant women and euthyroid mothers increases the possibility of a negative dysphoric mood, especially of depressive symptoms that cannot be explained by stress or demographic factors.

It is noteworthy that among the studies included in this work, the reference value for anti-TPO positivity varied; for example, levels above 19.6 KIU/L [23] and serum levels above 50 IU/mL [24]. For the reference values ​​for TSH, the most indicated for the reliability of anti-TPO positivity is to compare the patient’s anti-TPO value with that of the local laboratory reference. However, the studies found do not refer to adjustment for this possible confounding factor.

For the PPD detection or screening instruments, we found that the most used scale was the Edinburgh Postnatal Depression Scale (EPDS), with cutoff values between 9 and more than 12 points (Table 3); nevertheless, in some studies, there was the use of other associated scales, such as the Montgomery-Asberg Depression Rating Scale, the Toronto Alexithymia Scale, the Hamilton Anxiety Scale, the Modified MINI Plus 5.0.0., the Perceived Stress Scale and the Mood States Profile Questionnaire [17,18,19, 21, 22], and even when used alone, the cutoff point differed between studies. The standardization of a gold diagnostic method is essential to guarantee the validity of the diagnosis of PPD in a population sample. The absence of this standardization in the studies found should be considered a limitation for the correct diagnosis of PPD.

Another limitation that should be considered in the studies addressed by this systematic review is the influence of the social conditions of pregnant women with PPD, since the development of PPD is also influenced by social factors, and these factors can have a more significant impact than a slight increase in anti-TPO. According to Zhang et al. [28], the most cited risk factors for PPD in the literature over the last 5 (five) years were lack of family or partner support, unplanned pregnancy, family or personal history of psychiatric illness, low education and being a minor. The research also concludes that social and emotional factors have more influence on the prevalence of PPD than economic factors.

Indeed, dysregulation of various endocrine systems has been implicated in the pathophysiology of both antenatal and postnatal depression [40, 41]. Research suggests that the etiology of perinatal depression involves a combination of social [42, 43], psychological [44, 45], and biological factors [40, 41, 46].

In summary, the studies comprising this systematic review suggest that associations may exist between anti-TPO-positive status during gestation and postpartum depression. However, further studies are needed that consider the aforementioned limitations and analyze different stages of the period because Anti-TPO fluctuates throughout gestation and the postpartum period [13, 14].

Conclusion

After analyzing these results, it is clear that the association between anti-TPO antibodies and PPD was previously examined with contradictory results. The studies carried out are heterogeneous in terms of study size, population studied, design (prospective, case–control, transversal), psychometric scale, and anti-TPO measures (different analysis methods and different cutoff points). Although some authors consider the status of positive anti-TPO antibodies to be a possible marker of vulnerability to depression (Fig. 2), it is not yet possible to conclude which are the mechanisms of thyroid function involved in the pregnancy-puerperal cycle and PPD.

Fig. 2
figure 2

Our main finding is that there is no definition in the literature about the function of the thyroid gland and the development of PPD in pregnant/puerperal women. However, most studies that showed a relationship between PPD and thyroid function suggest that thyroperoxidase antibodies (anti-TPO) may be a possible target in the search for a biomarker to predict the development of PPD

Availability of data and materials

None.

References

  1. Gelaye B, Rondon MB, Araya R, Williams MA. Epidemiology of maternal depression, risk factors, and child outcomes in low-income and middle-income countries. Lancet Psychiatry. 2016;3(10):973–82.

    PubMed  PubMed Central  Google Scholar 

  2. Yim IS, Tanner Stapleton LR, Guardino CM, Hahn-Holbrook J, Dunkel SC. Biological and psychosocial predictors of postpartum depression: systematic review and call for integration. Annu Rev Clin Psychol. 2015;11:99–137.

    PubMed  PubMed Central  Google Scholar 

  3. Ghaedrahmati M, Kazemi A, Kheirabadi G, Ebrahimi A, Bahrami M. Postpartum depression risk factors: A narrative review. J Educ Health Promot. 2017;6:60.

    PubMed  PubMed Central  Google Scholar 

  4. Theme Filha MM, Ayers S, da Gama SG, Leal MoC. Factors associated with postpartum depressive symptomatology in Brazil: The Birth in Brazil National Research Study, 2011/2012. J Affect Disord. 2016;194:159–67.

    PubMed  Google Scholar 

  5. Zenclussen AC. Adaptive immune responses during pregnancy. Am J Reprod Immunol. 2013;69(4):291–303.

    CAS  PubMed  Google Scholar 

  6. Balucan FS, Morshed SA, Davies TF. Thyroid autoantibodies in pregnancy: their role, regulation and clinical relevance. J Thyroid Res. 2013;2013:182472.

    PubMed  PubMed Central  Google Scholar 

  7. Galofre JC, Haber RS, Mitchell AA, Pessah R, Davies TF. Increased postpartum thyroxine replacement in Hashimoto’s thyroiditis. Thyroid. 2010;20(8):901–8.

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Meena M, Chopra S, Jain V, Aggarwal N. The Effect of Anti-Thyroid Peroxidase Antibodies on Pregnancy Outcomes in Euthyroid Women. Journal of clinical and diagnostic research. JCDR. 2016;10(9):QC04-QC7.

    CAS  PubMed  PubMed Central  Google Scholar 

  9. Le Donne M, Mento C, Settineri S, Antonelli A, Benvenga S. Postpartum Mood Disorders and Thyroid Autoimmunity. Front Endocrinol. 2017;8:91.

    Google Scholar 

  10. Abalovich M, Amino N, Barbour LA, Cobin RH, De Groot LJ, Glinoer D, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007;92(8 Suppl):S1-47.

    CAS  PubMed  Google Scholar 

  11. Keshavarzi F, Yazdchi K, Rahimi M, Rezaei M, Farnia V, Davarinejad O, et al. Post partum depression and thyroid function. Iran J Psychiatry. 2011;6(3):117–20.

    PubMed  PubMed Central  Google Scholar 

  12. Moher D, Liberati A, Tetzlaff J, Altman DG, Group P. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. J Clin Epidemiol. 2009;62(10):1006–12.

    Google Scholar 

  13. Glinoer D, Riahi M, Grün JP, Kinthaert J. Risk of subclinical hypothyroidism in pregnant women with asymptomatic autoimmune thyroid disorders. J Clin Endocrinol Metab. 1994;79:197–204.

    CAS  PubMed  Google Scholar 

  14. Stagnaro-Green A, Roman SH, Cobin RH, El-Harazy E, Wallenstein S, Davies TF. A prospective study of lymphocyte-initiated immunosuppression in normal pregnancy: evidence of a T-cell etiology for postpartum thyroid dysfunction. J Clin Endocrinol Metab. 1992;74:645–53.

    CAS  PubMed  Google Scholar 

  15. Bergink V, Kushner SA, Pop V, Kuijpens H, Lambregtse-van den Berg MP. Prevalence of autoimmune thyroid dysfunction in postpartum psychosis. Br J Psychiatry. 2011;198(4):264–8.

    PubMed  Google Scholar 

  16. Wesseloo R, Kamperman AM, Bergink V, Pop VJM. Thyroid peroxidase antibodies during early gestation and the subsequent risk of first-onset postpartum depression: A prospective cohort study. J Affect Disord. 2018;225:399–403.

    CAS  PubMed  Google Scholar 

  17. Albacar G, Sans T, Martin-Santos R, Garcia-Esteve L, Guillamat R, Sanjuan J, et al. Thyroid function 48h after delivery as a marker for subsequent postpartum depression. Psychoneuroendocrinology. 2010;35(5):738–42.

    CAS  PubMed  Google Scholar 

  18. Kent GN, Stuckey BGA, Allen JR, Lambert T, Gee V. Postpartum thyroid dysfunction: Clinical assessment and relationship to psychiatric affective morbidity. Clin Endocrinol (Oxf). 1999;51:429–38.

    CAS  Google Scholar 

  19. Ruschi GEC, Chambô-filho A, A. SJVL, Zandonade E, Mattar R. Alteração tireoidiana: um fator de risco associado à depressão pó s-parto? Rev Bras Saude Mater Infant. 2009;9:6.

    Google Scholar 

  20. Lambrinoudaki I, Rizos D, Armeni E, Pliatsika P, Leonardou A, Sygelou A, et al. Thyroid function and postpartum mood disturbances in Greek women. J Affect Disord. 2010;121(3):278–82.

    CAS  PubMed  Google Scholar 

  21. Harris B, Othman S, Davies JA, Weppner GJ, Richards CJ, Newcombe RG, et al. Association between postpartum thyroid dysfunction and thyroid antibodies and depression. BMJ. 1992;305:152–6.

    CAS  PubMed  PubMed Central  Google Scholar 

  22. Pop VJ, de Rooy HA, Vader HL, van der Heide D, van Son MM, Komproe IH. Microsomal antibodies during gestation in relation to postpartum thyroid dysfunction and depression. Acta Endocrinol (Copenh). 1993;129:26–30.

    CAS  Google Scholar 

  23. Lazarus JH, Hall R, Othman S, Parkes AB, Richards CJ, McCulloch B, et al. The clinical spectrum of postpartum thyroid disease. QJM. 1996;89:429–35.

    CAS  PubMed  Google Scholar 

  24. Kuijpens JL, Vader HL, Drexhage HA, Wiersinga WM, van Son MJ, Pop VJ. Thyroid peroxidase antibodies during gestation are a marker for subsequent depression postpartum. Eur J Endocrinol. 2001;145:579–84.

    CAS  PubMed  Google Scholar 

  25. Groer MW, Vaughan JH. Positive thyroid peroxidase antibody titer is associated with dysphoric moods during pregnancy and postpartum. J Obstet Gynecol Neonatal Nurs. 2013;42(1):E26-32.

    PubMed  Google Scholar 

  26. Sylvén SM, Elenis E, Michelakos T, Larsson A, Olovsson M, Poromaa IS, et al. Thyroid function tests at delivery and risk for postpartum depressive symptoms. Psychoneuroendocrinology. 2013;38(7):1007–13.

    PubMed  Google Scholar 

  27. Pedersen C, Leserman J, Garcia N, Stansbury M, Meltzer-Brody S, Johnson J. Late pregnancy thyroid-binding globulin predicts perinatal depression. Psychoneuroendocrinology. 2016;65:84–93.

    CAS  PubMed  Google Scholar 

  28. Zhang L, Li C, Wu S, Wang L, Qiao C. Maternal thyroid function during late pregnancy is not a risk factor for postpartum depression. Psychiatry Res. 2019;279:387–8.

    PubMed  Google Scholar 

  29. Pedersen CA, Johnson JL, Silva S, Bunevicius R, Meltzer-Brody S, Hamer RM, et al. Antenatal thyroid correlates of postpartum depression. Psychoneuroendocrinology. 2007;32:235–45.

    CAS  PubMed  Google Scholar 

  30. Spitzer RL, Endicott J, Robins E. Research diagnostic criteria: rationale and reliability. Arch Gen Psychiatry. 1978;35(6):773–82.

    CAS  PubMed  Google Scholar 

  31. Goldberg DP, Hillier VF. A scaled version of the General Health Questionnaire. Psychol Med. 1979;1979(9):139–45.

    Google Scholar 

  32. Abou-Saleh MT, Ghubash R, Karim L, Krymski M, Bhai I. Hormonal aspects of postpartum depression. Psychoneuroendocrinology. 1998;23:465–75.

    CAS  PubMed  Google Scholar 

  33. Ijuin T, Douchi T, Yamamoto S, Ijuin Y, Nagata Y. The relationship between maternity blues and thyroid dysfunction. J Obstet Gynaecol Res. 1998;24:49–55.

    CAS  PubMed  Google Scholar 

  34. Saleh ES, El-Bahei W, El-Hadidy MA, Zayed A. Predictors of postpartum depression in a sample of Egyptian women. Neuropsychiatr Dis Treat. 2012;9:15–24.

    PubMed Central  Google Scholar 

  35. Basraon S, Costantine MM. Mood disorders in pregnant women with thyroid dysfunction. Clin Obstet Gynecol. 2011;54:506–14.

    PubMed  Google Scholar 

  36. Lucas A, Pizarro E, Granada ML, Salinas I, Sanmarti A. Postpartum thyroid dysfunction and postpartum depression: are they two linked disorders? Clin Endocrinol (Oxf). 2001;55:809–14.

    CAS  Google Scholar 

  37. Pop VJ, de Rooy HA, Vader HL, van der Heide D, van Son M, Komproe IH, Essed GG, et al. Postpartum thyroid dysfunction and depression in an unselected population. N Engl J Med. 1991;324:1815–6.

    CAS  PubMed  Google Scholar 

  38. Walfish PG, Meyerson J, Provias JP, Vargas MT, Papsin FR. Prevalence and characteristics of post-partum thyroid dysfunction: results of a survey from Toronto. Canada J Endocrinol Invest. 1992;15:265–72.

    CAS  PubMed  Google Scholar 

  39. Williams MD, Harris R, Dayan CM, Evans J, Gallacher J, Ben-Shlomo Y. Thyroid function and the natural history of depression: findings from the Caerphilly Prospective Study (CaPS) and a meta-analysis. Clin Endocrinol (Oxf). 2009;70(3):484–92.

    CAS  Google Scholar 

  40. Meltzer-Brody S. New insights into perinatal depression: pathogenesis and treatment during pregnancy and postpartum. Dialogues Clin Neurosci. 2011;13:89–100.

    PubMed  PubMed Central  Google Scholar 

  41. Serati M, Redaelli M, Buoli M, Altamura AC. Perinatal major depression biomarkers: A systematic review. J Affect Disord. 2016;193:391–404.

    CAS  PubMed  Google Scholar 

  42. Beck CT. Predictors of postpartum depression: an update. Nurs Res. 2001;50:275–85.

    CAS  PubMed  Google Scholar 

  43. Lancaster CA, Gold KJ, Flynn HA, Yoo H, Marcus SM, Davis MM. Risk factors for depressive symptoms during pregnancy: a systematic review. Am J Obstet Gynecol. 2010;202:5–14.

    PubMed  PubMed Central  Google Scholar 

  44. Bunevicius R, Kusminskas L, Mickuviene N, Bunevicius A, Pedersen CA, Pop VJM. Depressive disorder and thyroid axis functioning during pregnancy. World J Biol Psychiatry. 2009;10:324–9.

    PubMed  Google Scholar 

  45. Zeng Y, Cui Y, Li J. Prevalence and predictors of antenatal depressive symptoms among Chinese women in their third trimester: a cross-sectional survey. BMC Psychiatry. 2015;15:66.

    PubMed  PubMed Central  Google Scholar 

  46. Skalkidou A, Hellgren C, Comasco E, Sylvén S, Poromaa IS. Biological aspects of postpartum depression. Women’s Heal. 2012;8:659–71.

    CAS  Google Scholar 

Download references

Acknowledgements

Not applicable

Funding

This work was supported by Brazilian agencies and grants: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq 429570/2018–0) and INCT — Excitotoxicity and Neuroprotection (465671/2014–4).

Author information

Authors and Affiliations

Authors

Contributions

MSc P.M. da S. Schmidt and MSc PhD A. Longoni shared authorship by both conducting the search, data extraction, and quality assessment, as well as sharing the work of writing the draft of the paper. Professor R.T. Pinheiro and Professor A.M. de Assis contributed to the manuscript planning and revision. All authors have approved the manuscript.

Corresponding author

Correspondence to Adriano Martimbianco de Assis.

Ethics declarations

Ethics approval and consent to participate

The authors confirm that all of the research meets the ethics guidelines, including adherence to the legal requirements of the country where the study was performed.

Consent for publication

All authors give consent for publication.

Competing interests

The authors report no potential conflicts of interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Schmidt, P.M.d.S., Longoni, A., Pinheiro, R.T. et al. Postpartum depression in maternal thyroidal changes. Thyroid Res 15, 6 (2022). https://doi.org/10.1186/s13044-022-00124-6

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s13044-022-00124-6

Keywords

  • Thyroid
  • Thyroid peroxidase antibodies
  • Pregnancy
  • Postpartum depression
  • Perinatal depression