A synthesis of evidence for policy from behavioural science during COVID-19

Scientific evidence regularly guides policy decisions1, with behavioural science increasingly part of this process2. In April 2020, an influential paper3 proposed 19 policy recommendations (‘claims’) detailing how evidence from behavioural science could contribute to efforts to reduce impacts and end the COVID-19 pandemic. Here we assess 747 pandemic-related research articles that empirically investigated those claims. We report the scale of evidence and whether evidence supports them to indicate applicability for policymaking. Two independent teams, involving 72 reviewers, found evidence for 18 of 19 claims, with both teams finding evidence supporting 16 (89%) of those 18 claims. The strongest evidence supported claims that anticipated culture, polarization and misinformation would be associated with policy effectiveness. Claims suggesting trusted leaders and positive social norms increased adherence to behavioural interventions also had strong empirical support, as did appealing to social consensus or bipartisan agreement. Targeted language in messaging yielded mixed effects and there were no effects for highlighting individual benefits or protecting others. No available evidence existed to assess any distinct differences in effects between using the terms ‘physical distancing’ and ‘social distancing’. Analysis of 463 papers containing data showed generally large samples; 418 involved human participants with a mean of 16,848 (median of 1,699). That statistical power underscored improved suitability of behavioural science research for informing policy decisions. Furthermore, by implementing a standardized approach to evidence selection and synthesis, we amplify broader implications for advancing scientific evidence in policy formulation and prioritization

Tiroide e selenio

Breve revisione dei dati in letteratura sugli effetti del selenio in patologia tiroide

Iodine status assessment in Campania (Italy) as determined by urinary iodine excretion.

Mild iodine deficiency was first documented in Campania in the 1990s. We assessed the urinary iodine nutritional status of schoolchildren in Campania before the introduction of legislation for salt iodization and compared the findings with previous results to evaluate to what extent "silent" iodine prophylaxis, which accompanies socioeconomic advances, affects iodine status. METHODS: We examined 10552 schoolchildren aged 9-13 y from the five Campania provinces. The study was conducted from April 1999 to October 2002. Urinary iodine excretion was measured in morning urine samples with the AutoAnalyzer 3, an automated system based on the Sandell-Kolthoff reaction. Data were interpreted according to World Health Organization criteria. RESULTS: The median urinary iodine excretion level in Campania was less than 100 micromicrog/L, which indicates insufficient iodine intake. Mild iodine deficiency was identified in all provinces, namely Napoli, Salerno, Caserta, Avellino, and Benevento, with median urinary iodine excretions of 87, 81, 72, 64, and 61 microg/L, respectively. Overall, the analysis of frequency distribution showed values below 50 and 100 microg/L in 32% and 61% of children, respectively. These values were lower than those previously reported for Campania. CONCLUSION: This study confirms that Campania is a mild iodine deficiency area. The decrease in iodine deficiency versus previous studies indicates that silent prophylaxis plays a relevant role in this condition, but it is not sufficient to eradicate it. Our data will serve as a basis for future evaluations of iodine status in Campania

Five New Families with Resistance to Thyroid Hormone not Caused by Mutations in the Thyroid Hormone Receptor β Gene1

Resistance to thyroid hormone (RTH) is a syndrome of variable tissue hyposensitivity to TH. In 191 families, the RTH phenotype has been linked to mutations located in the ligand-binding or hinge domains of the TH receptor (TR) β gene. The defective TRβ molecules interfere with the function of the normal TRs to produce dominantly inherited RTH. Of the 65 families with RTH studied in our laboratory, 59 had mutations in the mutagenic region of the TRβ gene that encompasses exons 7–10. Isolation of a TRβ PAC (P1 derived artificial chromosome) clone provided the intronic sequences necessary to amplify and sequence the entire TRβ gene from genomic DNA. Not a single nucleotide substitution, deletion, or insertion was found in all coding and noncoding TRβ1- and TRβ2-specific and common exons of the five families with RTH reported herein. Furthermore, linkage analysis using polymorphic markers excluded involvement of the TRβ and TRα genes in two and three of the five families, respectively. The phenotype of RTH in patients without TRβ gene defects was not different from that in patients with RTH due to TRβ gene mutations in terms of clinical presentation and reduced responsiveness of the pituitary and peripheral tissues to TH. However, the degree of thyrotroph hyposensitivity to TH appeared to be among the more severe, similar to that of patients with mutant TRβs that have more than 50-fold reduction of T3 binding affinity and strong dominant negative effect. In these five families and another with non-TRα/non-TRβ RTH, previously identified in our laboratory, evidence for dominant inheritance was secured in two families, and the appearance of a new defect or recessive inheritance was found in the remaining four families. RTH without a structural TRβ defect occurs in about 10% of families expressing the classic phenotype of TH hyposensitivity, and TRβ and TRα gene involvement has been excluded in 5%. We postulate that a cofactor that interacts with TR is potentially responsible for the manifestation of RTH in these families. As affected subjects are not infertile, the high prevalence of putative neomutations and the low rate of transmission in this non-TR form of RTH may be due to reduced survival of embryos harboring the defect

Search for Abnormalities of Nuclear Corepressors, Coactivators, and a Coregulator in Families with Resistance to Thyroid Hormone without Mutations in Thyroid Hormone Receptor β or α Genes1

The syndrome of resistance to thyroid hormone (RTH) is characterized by decreased tissue responsiveness to thyroid hormones. Inheritance is usually autosomal dominant due to mutations in the ligand-binding domain or adjacent hinge region of the thyroid hormone receptor β (TRβ) gene. Six of 65 families with the RTH phenotype studied in our laboratory had normal TRβ1 and TRβ2 gene sequences. Their clinical characteristics were not different from those of subjects with TRβ gene mutations. Four of the 6 families were amenable to linkage analysis, and TRα involvement was excluded. Candidate genes were then evaluated for their possible involvement in the RTH phenotype in these 4 families: 2 coactivators [NCoA-1 (SRC-1) and NCoA-3 (AIB-1)], 2 corepressors (NCoR and SMRT), and a coregulator (RXRγ). DNA was obtained from 8 affected subjects and 41 of 45 living first degree relatives. In 2 of the 4 families, the mode of inheritance could be determined by pedigree analysis and was found to be autosomal dominant. Linkage analyses were performed using polymorphic markers near or within the 5 candidate genes. When analyses were not informative or linkage could not be excluded, direct sequencing of the genes in question was performed. Involvement of NCoA-1 was excluded in all four families assuming autosomal dominant inheritance. Roles for NCoR, SMRT, and NCoA-3 were excluded in three and a role for RXRγ was excluded in two of the four families. However, if the two families without proven dominant mode of inheritance were compound heterozygous, only the involvement of NCoA-1 could be excluded in both. Roles for NCoR, SMRT, and RXRγ were excluded in one of these two families. Thus, NCoA-1 and RXRγ genes were not found to be the cause of RTH in subjects without TR gene mutations even though the absence of NCoA-1 and RXRγ is the cause of RTH in mice. Involvement of other candidate genes in the mediation of thyroid hormone action as well as intracellular hormone transport needs to be explored in these families with non-TRβ, TRα RTH