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Emotional neglect means that the child’s emotional and developmental needs are not fulfilled by the parents or other caregivers. Adverse childhood events (ACEs) are a risk factor for mental health problems and impaired parenting skills. The objective here was to examine whether parents’ ACEs increase the child’s risk of experiencing emotional neglect.
The participants in the present study were members of the Northern Finland Birth Cohort 1986 (NFBC1986). Emotional neglect experiences were measured in 190 members of this cohort by means of the Trauma and Distress Scale (TADS), and ACEs in both parents were measured with a specific questionnaire. A linear regression model was used to examine the association between parents’ ACEs and the children’s emotional neglect scores.
The children’s mean emotional neglect score was 8.11 on a scale from 5 to 25. There was no significant difference between males (mean 8.01) and females (mean 8.19). Only father’s ACEs were associated with child’s emotional neglect score. In the linear regression model, the children’s emotional neglect scores increased by 0.3 points for father’s ACE.
Our findings suggest that father’s ACEs may increase the child’s risk of experiencing emotional neglect. It seems that childhood adversities are transferred from parents to children, but larger samples would be needed to confirm these findings.
People with severe mental illness (SMI) have an elevated risk of obesity but the causes and mechanisms are unclear. We explored the familial association between parental SMI and body mass index (BMI) in middle-aged offspring. Our objective was to determine if the offspring of either parent with SMI have an increased risk for obesity.
The Northern Finland Birth Cohort 1966 is a cohort study of offspring with expected date of birth in 1966. The data include originally 12 068 mothers and 12 231 children from the provinces of Lapland and Oulu in Finland. The final study sample included 5050 middle-aged offspring. Parental SMI was used as exposure in the study. BMI measured at the age of 46 years was used as a primary outcome.
Risk for obesity was elevated in the offspring of mothers with SMI [overweight: adjusted odds ratio (OR) 1.93 (1.29–2.90), obese class I: 1.97 (1.20–3.25), obese classes II–III: 2.98 (1.67–5.33)]. For the offspring of either parent with SMI, statistically significant results were found in obese class I and obese classes II–III [overweight: adjusted OR 1.21 (0.94–1.54), obese class I: 1.52 (1.03–1.08), obese classes II–III: 1.53 (1.01–2.32)].
We found an elevated risk of obesity in the middle-aged offspring of either parent with SMI, especially in the offspring of mothers with SMI. Thus, there might be a common familial pathway leading to the co-occurrence of obesity and SMI.
Studies on the transmission of suicide risk have focused on parental history of suicide attempts (SAs), overlooking when the attempt happened. This study examined how the offspring's risk of attempting or dying by suicide varied by the timing of a first parental SA and the sex of the parent who attempted suicide.
Participants were 59 469 members of the 1987 Finnish Birth Cohort. The Finnish Hospital Discharge and Cause of Death Registers were the sources for parental and offspring SAs and offspring suicide. Timing of parental SA was coded as before (pre-pregnancy and pregnancy) and after the child's birth [infant/toddler years (0–2 years), childhood (3–11 years), adolescence (12–17 years), and young adulthood (18–26 years)].
In the multivariate models, having a parent who attempted suicide increased the offspring's risk of attempting suicide (odds ratio (OR) = 1.77, 95% confidence interval (CI) 1.39–2.25), but not of dying by suicide. Compared to unexposed offspring, those exposed after child's birth were at higher risk of attempting suicide (OR = 1.90, 95% CI 1.46–2.47), specifically when the parent attempted during offspring's childhood, adolescence, and young adulthood. A first maternal SA increased offspring's risk of attempting suicide regardless of the timing.
The impact of a parental SA on offspring's risk of attempting suicide differed depending on the timing and sex of the parent who attempted suicide, suggesting that the transmission of suicide risk may occur through genetic as well as environmental factors. Our findings call for an intergenerational approach in suicide risk assessment.
Psychoses, especially schizophrenia, are often preceded by cognitive deficits and psychosis risk states. Altered metabolic profiles have been found in schizophrenia. However, the associations between metabolic profiles and poorer cognitive performance and psychosis risk in the population remain to be determined.
Detailed molecular profiles were measured for up to 8976 individuals from two general population-based prospective birth cohorts: the Northern Finland Birth Cohort 1986 (NFBC 1986) and the Avon Longitudinal Study of Parents and Children (ALSPAC). A high-throughput nuclear magnetic resonance spectroscopy platform was used to quantify 70 metabolic measures at age 15–16 years in the NFBC 1986 and at ages 15 and 17 years in ALSPAC. Psychosis risk was assessed using the PROD-screen questionnaire at age 15–16 years in the NFBC 1986 or the psychotic-like symptoms assessment at age 17 years in ALSPAC. Cognitive measures included academic performance at age 16 years in both cohorts and general intelligence and executive function in ALSPAC. Logistic regression measured cross-sectional and longitudinal associations between metabolic measures and psychosis risk and cognitive performance, controlling for important covariates.
Seven metabolic measures, primarily fatty acid (FA) measures, showed cross-sectional associations with general cognitive performance, four across both cohorts (low density lipoprotein diameter, monounsaturated FA ratio, omega-3 ratio and docosahexaenoic acid ratio), even after controlling for important mental and physical health covariates. Psychosis risk showed minimal metabolic associations.
FA ratios may be important in marking risk for cognitive deficits in adolescence. Further research is needed to clarify whether these biomarkers could be causal and thereby possible targets for intervention.
The evidence of the effect of the age at introduction of new foods during infancy on the development of asthma and allergic rhinitis is inconsistent and scarce. We set out to study these associations. A prospective birth cohort of infants with increased HLA-DQB1-conferred risk for type 1 diabetes was recruited in 1996–2000. The families completed at home a record on the age at introduction of new foods. Persistent asthma and allergic rhinitis were assessed at the age of 5 years with an International Study of Asthma and Allergies in Childhood-type questionnaire. The Cox proportional hazards regression analyses were adjusted for parental asthma and allergic diseases, and several perinatal and sociodemographical factors. Out of the 1293 children, 77 (6·0 %) developed persistent asthma; and out of the 1288 children, 185 (14·4 %) developed allergic rhinitis by the age of 5 years. Early age at introduction of oats was associated with a reduced risk of persistent asthma (hazard ratio (HR; 95 % CI) for the first and mid-tertiles compared with the latest tertile was 0·36 (0·15, 0·85) and 0·37 (0·22, 0·62), respectively, P < 0·001). Early age at introduction of fish was dose dependently associated with a decreased risk of allergic rhinitis (HR (95 % CI) for the first and mid-tertiles compared with the latest tertile was 0·34 (0·22, 0·54) and 0·45 (0·28, 0·70), respectively, P < 0·001). The present finding that age at introduction of oats is inversely and independently associated with development of persistent asthma is novel. We confirmed the earlier observation that the age at introduction of fish is inversely related to the risk of allergic rhinitis. Clinical implications remain to be determined.
Although schizotypal traits, such as anhedonia and aberrant perceptions,
may increase the risk for schizophrenia-spectrum disorders, little is
known about early-life characteristics that predict more pronounced
To examine whether birth size or several other early-life factors that
have been previously linked with schizophrenia predict schizotypal traits
Participants of the Northern Finland 1966 Birth Cohort Study
(n = 4976) completed a questionnaire on positive and
negative schizotypal traits at the age of 31 years.
Lower placental weight, lower birth weight and smaller head circumference
at 12 months predicted elevated positive schizotypal traits in women
after adjusting for several confounders (P<0.02).
Moreover, higher gestational age, lower childhood family socioeconomic
status, undesirability of pregnancy, winter/autumn birth, higher birth
order and maternal smoking during pregnancy predicted some augmented
schizotypal traits in women, some in men and some in both genders.
The results point to similarities in the aetiology of schitzotypal traits
and schizophrenia-spectrum disorders.
Recent interest has focused on the association between cannabis use and risk
of psychosis. In the largest unselected population-based study on this topic
to date, we examined cannabis use and prodromal symptoms of psychosis at age
15-16 years among 6330 adolescents. Those who had tried cannabis (n=352;
5.6% of the total sample) were more likely to present three or more
prodromal symptoms even after controlling for confounders including previous
behavioural symptoms (OR=2.23; 95% CI 1.70-2.94). A dose-response effect was
seen. We conclude that cannabis use is associated with prodromal symptoms of
psychosis in adolescence.
Subtle motor, emotional, cognitive and behavioural abnormalities are often present in apparently healthy individuals who later develop schizophrenia, suggesting that some aspects of causation are established before overt psychosis.
To outline the development of schizophrenia.
We drew on evidence from The Northern Finland 1966 Birth Cohort supplemented by selected findings from other relevant literature.
The main known risk factors in development of schizophrenia are genetic causes, pregnancy and delivery complications, slow neuromotor development, and deviant cognitive and academic performance. However, their effect size and predictive power are small.
No powerful risk factor, premorbid sign or risk indicator has been identified that is useful for the prediction of schizophrenia in the general population.
The aim was to give estimates of the incidence of different mental disorders from a Finnish prospective epidemiological follow-up study, the UKKI Study.
The original probability sample consisted of 1000 persons, aged 15–64 years. The baseline survey took place in 1969–71, and follow-up surveys were conducted 5 and 16 years after the baseline survey. The research methods included a personal psychiatric interview and data collection from different registers. The diagnostic system was based on the ICD–8 classification.
The estimated annual incidence of all mental disorders was close to 15 per 1000 both between baseline and the 5-year follow-up as well as between the 5-year and the 16-year follow-up. During the entire 16-year follow-up period the annual incidence of all disorders was 14 per 1000 in men and 17 per 1000 in women. The annual incidence of neurotic disorders was 10 per 1000 in men and 14 per 1000 in women, and that of psychotic disorders 2 per 1000.
In the literature, there are huge differences in the results concerning incidence of mental disorders. The results of the present study were rather close to those of the Swedish Lundby Study, but nowhere near the results of the American ECA Study.
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