Do flame retardants increase risk of thyroid disease?

Women who have been exposed to polybrominated diphenyl esters (PBDEs)—common chemicals used as flame retardants—may have a higher risk of thyroid disease, according to results of a study in Environmental Health. The association may be enhanced, the authors said, by the altered estrogen levels in menopause.

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To test the association between the chemicals and thyroid disease in women, the researchers used serum PBDE concentrations for BDEs 47, 99, 100, and 153, which were part of the National Health and Examination Survey (NHANES) and reports on thyroid problems, which had been a part of the NHANES 2003-2004 cycle. Multivariate logistic regression models were used to calculate odds ratios (ORs), while controlling for thyroid medication, alcohol consumption, smoking, education, age, and body mass index. Menopause status was identified using self-reported absence of menstruation in the previous 12 months.

Women who were in the highest quartile of BDE 47, 99, and 100 exposure showed increased odds of currently having thyroid disease (ORs: 1.5, 1.8, 1.5, respectively) when compared to those who were in the first and second quartiles combined. When the analysis was restricted to just postmenopausal women, the association was stronger (ORs: 2.2, 3.6, 2.0, respectively).

The researchers concluded that exposure to BDEs 47, 99, and 100 can increase the risk of thyroid disease. As for the stronger association in postmenopause, they hypothesized that the change in estrogen levels during menopause may disrupt thyroid signaling by PBDEs. The authors suggested additional research to confirm their findings, particularly when new NHANES data become available.

NEXT: Maternal smoking and schizophrenia

Maternal smoking and schizophrenia

A first-of-its-kind study of a biomarker for nicotine exposure suggests that there may be a link between maternal smoking and schizophrenia in offspring. The results, published in The American Journal of Psychiatry, are from a population-based analysis by Finnish researchers.

For the nested case-control study, the authors examined the relationship between prenatal nicotine exposure (or cotinine level) in archived maternal sera and schizophrenia in the women’s offspring. All live births in Finland between 1983 and 1998 were represented. The 997 cases of schizophrenia identified in a national registry were matched 1:1 to controls based on date of birth, sex, and residence. Data on serum levels of cotinine were from a national biobank and the samples were drawn from early- to mid-gestation and measured prospectively using quantitative immunoassay.

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Increased odds of schizophrenia were associated with a higher maternal cotinine level (odds ratio=3.41, 95% confidence interval, 1.86-6.24). Categorically defined heavy maternal nicotine exposure was associated with a 38% increase in the risk of schizophrenia. The findings were not altered by adjustment for maternal age, maternal or paternal psychiatric disorders, socioeconomic status, or other covariates. Weight for gestational age also did not appear to affect the association.

The study, the authors said, is the first to look at the relationship between a biomarker for maternal smoking and schizophrenia. Their findings, they believe, suggest that preventing smoking during pregnancy may decrease the incidence of schizophrenia and they are the most definitive evidence to date of the association.

NEXT: Using telephone therapy to improve sleep quality in menopausal women

How telephone therapy can improve sleep quality in menopausal women

Women who are menopausal may be able to improve their sleep quality if they have access to telephone-based cognitive behavioral therapy for insomnia (CBT-I), according to results from a single-site, randomized clinical trial in JAMA.

From September 2013 to August 2015, the researchers looked at women in western Washington State aged 40 to 65 years who were perimenopausal or postmenopausal who had moderate insomnia symptoms and 2 or more daily occurrences of vasomotor symptoms. Assessments were blinded and conducted at baseline, 8 weeks, and 24 weeks following randomization. Intent-to-treat analysis was also conducted. The 106 women underwent either 6 telephone sessions of CBT-I or menopause education control (MEC) sessions over 8 weeks that provided information about menopause and women’s health.

After those 8 weeks, Insomnia Severity Index (ISI) scores had fallen by 9.9 points in the 53 women who received CBT-I (mean [SD] age, 55.0 [3.5] years) and by 4.7 points among the women in the control group (age, 54.7 [4.7] years), representing a 5.2-point difference between the groups (95% CI, –6.1 to –3.3; P < .001). Using the Pittsburgh Sleep Quality Index, the scores decreased 4.0 points in women who received CBT-I and 1.4 points in the control group, representing a between-group difference of 2.7 points (95% CI, –3.9 to –1.5; P < .001). At 24 weeks, the significant group differences were sustained.

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At 8 weeks, 33 of 47 (70%) in the CBT-I therapy had an ISI score in the non-insomnia range and 10 of 41 (24%) in the control group had a score in the non-insomnia range. At 24 weeks, 37 of 44 (84%) in the CBT-I group had an ISI score in the non-insomnia range versus 16 of 37 (43%) in the control group.

No between-group differences were seen in the frequency of daily vasomotor symptoms. However hot flash interference was significantly less at 8 weeks in the intervention group (–15.7; 95% CI, –20.4 to –11.0) when compared to the control group (–7.1; 95% CI, –14.6 to 0.4) (P = .03). After 24 weeks, the differences were maintained in the intervention group (–22.8; 95% CI, –28.6 to –16.9) and the control group (–11.6; 95% CI, –19.4 to –3.8) (P = .003).

The researchers concluded that the telephone-based therapy did help women in menopause with their insomnia and vasomotor symptoms. They believe that their results support further testing and development of CBT-I for insomnia in menopause.