ABSTRACT
OBJECTIVES: This study aimed to (1) explore the changes in conspiracy mentality across the four waves of the COVID-19 pandemic; (2) assess the relationship between conspirative mentality and psychological/behavioural variables; (3) identify the predictors of conspirative mentality; and (4) explore the effect of conspirative mentality on COVID-19 protective behaviour. STUDY DESIGN: This was a multiwave survey. METHODS: A total of 10,013 Italian individuals, aged 18-70 years, were assessed across the four waves (from January to May 2021) through online survey. We collected information about the sociodemographic characteristics of participants, personal experiences of COVID-19 infection, trust, COVID-19 protective behaviours, COVID-19 risk perception, arousal, auto-efficacy, resilience and well-being. Conspiracy mentality was assessed with the Conspiracy Mentality Questionnaire. The statistical analyses included exploratory factorial analyses, Pearson correlations and multiple linear regressions. RESULTS: The conspiracy mentality score during the COVID-19 pandemic was medium-high (mean 59.0 on a 0-100 scale) and slightly increased from 58.2 to 59.9 across months, in parallel with a slight decrease in trust in health institutions and scientific informational sources. Individuals aged >35 years, poorly educated and particularly scared about their financial situation were at risk of showing higher levels of conspirative mentality. Higher levels of conspirative mentality were risk factors for low levels of COVID-19 protective behaviours. CONCLUSIONS: Clear and effective communication may improve trust in health institutions and informational sources, decrease conspirative theories and increase compliance with protective behaviour.
Subject(s)
COVID-19 , Pandemics , Humans , COVID-19/epidemiology , Health Behavior , Italy/epidemiology , TrustABSTRACT
BACKGROUND AND AIMS: Carotid intima-media thickness (IMT) and arterial stiffness parameters, including aortic augmentation index (AIx) and pulse wave velocity (PWV), are independent predictors of stroke and cardiovascular disease. Genetic effects on these traits were never explored in a Mediterranean country. The present study aims to quantify the contribution of genes, environment and age to carotid IMT and aortic Aix and PWV. METHODS AND RESULTS: The twin design was used. A total of 348 adult twins from the Italian Twin Register underwent measurements of carotid IMT and aortic PWV and AIx in three university hospitals located in Rome, Padua and Perugia. Carotid IMT was measured by B-mode ultrasound, aortic PWV and AIx by Arteriograph. Genetic modelling was performed to decompose total variance of traits into genetic, shared and unshared environmental and age components. For each phenotype, the best-fitting model included additive genetic, unshared environmental and age effects. For IMT, heritability was 0.32 (95% confidence interval (CI): 0.25-0.38), unshared environmental component was 0.25 (0.18-0.32) and age contribution was 0.44 (0.39-0.49). For AIx and PWV, heritabilities were 0.42 (0.29-0.55) and 0.49 (0.35-0.62), unshared environmental components were 0.31 (0.22-0.44) and 0.37 (0.26-0.51) and age contributions were 0.27 (0.16-0.39) and 0.14 (0.06-0.24), respectively. CONCLUSION: This study shows substantial genetic and unshared environmental influences on carotid intima-media thickness and arterial stiffness and confirms the relevant role of age in the aetiology of these traits. Further support is provided for prevention and health promotion strategies based on modifiable factors.
Subject(s)
Carotid Intima-Media Thickness , Gene-Environment Interaction , Vascular Stiffness/genetics , Adult , Aged , Aorta/metabolism , Body Mass Index , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/genetics , Carotid Artery, Common/diagnostic imaging , Female , Genetic Predisposition to Disease , Humans , Italy , Male , Middle Aged , Pulse Wave Analysis , Risk FactorsABSTRACT
Until early 2000, permanent and transient neonatal diabetes mellitus (NDM), defined as diabetes with onset within 6 weeks from birth that requires insulin therapy for at least 2 weeks, were considered exceedingly rare conditions, with a global incidence of 1:500,000-1:400,000 live births. The new definition of NDM recently adopted, that includes patients with diabetes onset within 6 months of age, has prompted studies that have set the incidence of the permanent form alone between 1:210,000 and 1:260,000 live births. Aim of the present work was to ascertain the incidence of NDM (i.e. permanent + transient form) in Italy for years 2005-2010. Patients referred to the Italian reference laboratory for NDM between years 2005 and 2010 and screened for mutations in common NDM genes (KCNJ11, ABCC8, and INS) and for uniparental isodisomy of chromosome 6 (UDP6) were reviewed. A questionnaire aimed at identifying NDM cases investigated in other laboratories was sent to 54 Italian reference centers for pediatric diabetes. Twenty-seven patients with NDM born between 2005 and 2010 were referred to the reference laboratory. In this group, a mutation of either KCNJ11, ABCC8 or INS was found in 18 patients, and a case with UDP6 was identified. Questionnaires revealed 4 additional cases with transient neonatal diabetes due to UDP6. Incidence of NDM was calculated at 1:90,000 (CI: 1:63,000-1:132,000) live births. Thus, with the definition currently in use, about 6 new cases with NDM are expected to be born in Italy each year.
Subject(s)
Diabetes Mellitus, Type 1/epidemiology , Infant, Newborn, Diseases/epidemiology , Diabetes Mellitus, Type 1/genetics , Female , Humans , Incidence , Infant , Infant, Newborn , Infant, Newborn, Diseases/genetics , Italy/epidemiology , Live Birth , Male , MutationABSTRACT
AIMS/HYPOTHESIS: The aim of this study was to investigate the genetic aetiology of permanent diabetes mellitus with onset in the first 12 months of age. METHODS: We studied 46 probands with permanent, insulin-requiring diabetes with onset within the first 6 months of life (permanent neonatal diabetes mellitus [PNDM]/monogenic diabetes of infancy [MDI]) (group 1) and eight participants with diabetes diagnosed between 7 and 12 months of age (group 2). KCNJ11, INS and ABCC8 genes were sequentially sequenced in all patients. For those who were negative in the initial screening, we examined ERN1, CHGA, CHGB and NKX6-1 genes and, in selected probands, CACNA1C, GCK, FOXP3, NEUROG3 and CDK4. The incidence rate for PNDM/MDI was calculated using a database of Italian patients collected from 1995 to 2009. RESULTS: In group 1 we found mutations in KCNJ11, INS and ABCC8 genes in 23 (50%), 9 (19.5%) and 4 (8.6%) patients respectively, and a single homozygous mutation in GCK (2.1%). In group 2, we identified one incidence of a KCNJ11 mutation. No genetic defects were detected in other loci. The incidence rate of PNDM/MDI in Italy is estimated to be 1:210,287. CONCLUSIONS/INTERPRETATION: Genetic mutations were identified in ~75% of non-consanguineous probands with PNDM/MDI, using sequential screening of KCNJ11, INS and ABCC8 genes in infants diagnosed within the first 6 months of age. This percentage decreased to 12% in those with diabetes diagnosed between 7 and 12 months. Patients belonging to the latter group may either carry mutations in genes different from those commonly found in PNDM/MDI or have developed an early-onset form of autoimmune diabetes.
Subject(s)
Diabetes Mellitus/etiology , Diabetes Mellitus/genetics , ATP-Binding Cassette Transporters/genetics , Diabetes Mellitus/epidemiology , Female , Genetic Predisposition to Disease , Germinal Center Kinases , Humans , Infant , Infant, Newborn , Insulin/genetics , Male , Mutation , Potassium Channels, Inwardly Rectifying/genetics , Protein Serine-Threonine Kinases/genetics , Receptors, Drug/genetics , Sulfonylurea ReceptorsABSTRACT
BACKGROUND: Metals are suspected of being involved in the pathogenesis of various neurologic diseases. We previously found a complex imbalance in serum chemical elements and oxidative status in patients with clinically definite multiple sclerosis (CDMS). OBJECTIVE: To understand whether this imbalance affects people with clinically isolated syndrome (CIS) and, if so, whether it predicts conversion to CDMS. METHODS: We studied 22 chemical elements and the oxidative status in 49 patients with CIS, 49 patients with CDMS, and 49 healthy donors (HD). Univariate and multivariate approaches were used to identify profiles for each group. A logistic regression analysis was used to identify the predictive potential of baseline data (elements, oxidative status, and MRI findings) for conversion to CDMS over 36 months. RESULTS: Several elements and oxidative status values differed significantly among the 3 groups. Discriminant analysis revealed a major contribution of Ca, Fe, Sn, Zn, serum antioxidant capacity, and serum oxidative status, which resulted in distinct profiles (the prediction of group membership was 96% [cross-validated 92%] for HD, 92% [cross-validated 92%] for CDMS, and 90% [cross-validated 86%] for CIS). A weighted combination of element concentrations and oxidative status values, adjusting for all other predictors, would predict a reduction in the risk of conversion to CDMS within 3 years (odds ratio 0.37; 95% confidence interval 0.18-0.76; p = 0.007), thereby proving more effective than MRI at baseline. CONCLUSIONS: The peculiar imbalance in serum elements and oxidative status that characterizes patients with CIS and may predict conversion to CDMS warrants studies on larger sample sizes.
Subject(s)
Demyelinating Diseases/blood , Demyelinating Diseases/diagnosis , Oxidative Stress/physiology , Trace Elements/blood , Adolescent , Adult , Biomarkers/blood , Demyelinating Diseases/epidemiology , Female , Humans , Longitudinal Studies , Male , Middle Aged , Predictive Value of Tests , Young AdultSubject(s)
Crohn Disease/genetics , Adolescent , Adult , Female , Gene Frequency , Genetic Predisposition to Disease/genetics , Haplotypes/genetics , Humans , Male , PhenotypeABSTRACT
PURPOSE: The study goal was to assess teratogenic effects of antiepileptic drugs (AEDs) through the use of a surveillance system (MADRE) of infants with malformations. METHODS: Information on all malformed infants (1990-1996) with maternal first-trimester drug exposure was collected by the International Clearinghouse for Birth Defects and Monitoring Systems (ICBDMS). Cases were defined as infants presenting with a specific malformation, and controls were defined as infants presenting with any other birth defect. Exposure was defined by the use of AEDs during the first trimester of pregnancy. The association of AEDs with malformations was then estimated by calculating the odds ratios with 95% confidence intervals and testing their homogeneity among registries. RESULTS: Among 8005 cases of malformations, 299 infants were exposed in utero to AEDs. Of those exposed to monotherapy, 65 were exposed to phenobarbital, 10 to methylphenobarbital, 80 to valproic acid, 46 to carbamazepine, 24 to phenytoin, and 16 to other AEDs. Associations were found for spina bifida with valproic acid. Infants exposed to phenobarbital and to methylphenobarbital showed an increased risk of oral clefts. Cardiac malformations were found to be associated with phenobarbital, methylphenobarbital, valproic acid, and carbamazepine. Hypospadias was associated with valproic acid. Porencephaly and other specified anomalies of brain, anomalies of face, coarctation of aorta, and limb reduction defects were found to be associated with valproic acid. CONCLUSIONS: Using the MADRE system, we confirmed known teratogenic effects of AEDs. We also found increased risks for malformations that had never been reported associated with AEDs or for which the association was suggested by case reports.
Subject(s)
Abnormalities, Drug-Induced/epidemiology , Anticonvulsants/adverse effects , Databases, Factual/statistics & numerical data , Epilepsy/drug therapy , Abnormalities, Drug-Induced/etiology , Anticonvulsants/therapeutic use , Female , Global Health , Humans , Pregnancy , Product Surveillance, Postmarketing/statistics & numerical data , Registries/statistics & numerical data , Risk Factors , World Health OrganizationABSTRACT
BACKGROUND: The age-adjusted incidence of breast cancer in the San Francisco Bay Area has consistently been higher than that in other regions of the United States. The distribution of established risk factors for breast cancer (i.e., parity, age at first full-term pregnancy, breast-feeding, age at menarche, and age at menopause) and probable risk factors (e.g., alcohol consumption) also differs across geographic regions. PURPOSE: A study was planned to explore the extent to which differences in the regional distribution of established and probable risk factors could explain the increased incidence of breast cancer in the San Francisco Bay Area. METHODS: Age-adjusted breast cancer incidence rates for January 1978 through December 1982 were obtained for the San Francisco Bay Area and other regions from the Surveillance, Epidemiology, and End Results (SEER) Program. Risk factor data from January 1980 through December 1982 were computed from the Cancer and Steroid Hormone Study, a population-based, case-control study of women 22-55 years of age who resided in eight SEER regions. Two different statistical methods were used to compute the relative risk (RR) of breast cancer associated with residence in the San Francisco Bay Area versus other regions, after adjusting for regional differences in known risk factors. RESULTS: Substantial differences in the distribution of breast cancer risk factors were found between the San Francisco Bay Area and other regions. Nearly all of these differences would be expected to lead to an elevated incidence of breast cancer in the San Francisco Bay Area. With the use of incidence rates adjusted only for age, the RR for San Francisco Bay Area residence from January 1978 through December 1982 compared with residence in seven other SEER areas was 1.14 for white women and 1.10 for black women. Depending on the statistical method used, the RR was reduced to approximately 0.96-0.99 for white women and 0.75-0.83 for black women, after further adjusting for established and probable risk factors (parity, age at first full-term pregnancy, breast-feeding, age at menarche, age at menopause, and alcohol consumption). Without adjustment for alcohol consumption, the corresponding results were 0.97-1.02 for white women and 0.77-0.88 for black women. CONCLUSIONS: Among both white women and black women, the elevated breast cancer incidence rate in the San Francisco Bay Area can be completely accounted for by regional differences in known risk factors.