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The COVID-19 pandemic has had negative mental health outcomes in populations, but the suicide numbers in Finland have remained unchanged compared with expected levels based on the pre-pandemic period. We included all deaths from suicide verified by the official cause-of-death investigations, including forensic autopsy with analysis of forensic toxicology samples, between 1 January 2016 and 31 December 2020 in Finland. There was a decline in suicide incidence from 2016 to 2020 in men, and a declining tendency in suicide rates for every consecutive month during the COVID-19 pandemic period. The COVID-19 governmental policy responses do not seem to have led to an increase in suicide numbers.
Individuals with a later timing of circadian rhythms (evening types) tend to have unhealthier behaviors compared to those with an earlier timing (morning types). Previous studies have shown that evening types have unhealthier diets and later eating times than morning types. Furthermore, evening types bear higher odds for type 2 diabetes and weight gain (women). Circadian rhythms are controlled by clock genes which have an important role in regulating energy homeostasis. Thus far, a number of single nucleotide polymorphisms (SNP) of clock genes have been associated with metabolic disturbances, obesity and dietary habits (e.g., breakfast skipping and macronutrient intakes). Our aim was to examine chronotype associations with SNPs of the 20 known key clock genes which could help to clarify the underlying mechanisms behind chronotype phenotype.
Our data included 8558 participants (aged 25–74 years, 52% of women) from the cross-sectional population-based National FINRISK 2007 and 2012 surveys. Chronotype was assessed with a shortened six-item version of Horne and Östberg's Morningness-Eveningness Questionnaire (sMEQ) accounting for 83% of the total variance of the original questionnaire. For comparison we used a single self-evaluation question on chronotype from the questionnaire. Genotyping was done using Illumina arrays (HumanCoreExome, Omniexpress and 610K). Linear and logistic regression was used for statistical analysis with the additive genetic model. The analyses were adjusted for age, sex, batch effects and five principal components to account for population structure. The false discovery rate method by the Benjamini-Yekutieli procedure was applied to correct for multiple comparisons.
We found 27 SNPs in two clock genes that were significantly (P < 0.05) associated with chronotype when assessed with the single question. Minor allele carriers of the NR1D2 (Rev-erbβ) polymorphisms (rs4131403A, rs4858095T, rs6794922G, rs4619734A, rs4589882A, rs4321479C, rs6779476A, rs6790557A, rs13095392A, rs4858098G, rs4858567C, rs11717862G, rs7431301A, rs5023610G, rs5847265C, rs5847266G, rs6550823A, rs9882735C, rs7371944A, rs55792500G) were associated with evening type, whereas minor allele carriers of the NFIL3 polymorphisms (rs2482704T, rs2989836T, rs2482356C, rs2440589T, rs9409419G, rs2482702G, rs2482357A) were more likely morning types. Findings were similar when chronotype was assessed with sMEQ but did not reach statistical significance.
Our findings indicated novel genetic associations of chronotype with two clock genes that have previously been associated with carbohydrate and lipid metabolism (NR1D2), and with lipid absorption and export in intestinal epithelial cells and hepatic gluconeogenesis (NFIL3). These results expand our knowledge of the genetic basis of chronotype and warrant further studies to replicate these findings.
Vitamin D has been suggested to protect against depression, but epidemiological evidence is scarce. The present study investigated the relationship of serum 25-hydroxyvitamin D (25(OH)D) with the prevalence of depressive and anxiety disorders. The study population consisted of a representative sample of Finnish men and women aged 30–79 years from the Health 2000 Survey. The sample included 5371 individuals, of which 354 were diagnosed with depressive disorder and 222 with anxiety disorder. Serum 25(OH)D concentration was determined from frozen samples. In a cross-sectional study, a total of four indicators of depression and one indicator of anxiety were used as dependent variables. Serum 25(OH)D was the risk factor of interest, and logistic models used further included sociodemographic and lifestyle variables as well as indicators of metabolic health as confounding and/or effect-modifying factors. The population attributable fraction (PAF) was estimated. Individuals with higher serum 25(OH)D concentrations showed a reduced risk of depression. The relative odds between the highest and lowest quartiles was 0·65 (95 % CI 0·46, 0·93; P for trend = 0·006) after adjustment for sociodemographic, lifestyle and metabolic factors. Higher serum 25(OH)D concentrations were associated with a lower prevalence of depressive disorder especially among men, younger, divorced and those who had an unhealthy lifestyle or suffered from the metabolic syndrome. The PAF was estimated to be 19 % for depression when serum 25(OH)D concentration was at least 50 nmol/l. These results support the hypothesis that higher serum 25(OH)D concentrations protect against depression even after adjustment for a large number of sociodemographic, lifestyle and metabolic factors. Large-scale prospective studies are needed to confirm this finding.
The operational criteria for seasonal affective disorder (SAD) have undergone several changes since first proposed in 1984. SAD is currently included as a specifier of either bipolar or recurrent major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The International Classification of Diseases, Tenth Edition has provisional diagnostic criteria for SAD. The most characteristic quality of SAD is that the symptoms usually present during winter and remit in the spring. Furthermore, the symptoms tend to remit when the patients are exposed to daylight or bright light therapy. The cognitive and emotional symptoms are as in other types of depression but the vegetative symptoms are the reverse of classic depressive vegetative symptoms, namely increased sleep and increased appetite. SAD is a common condition, but the exact prevalence rates vary between different studies and countries and is consistently found to be more common in women and in youth. SAD probably possibly occurs in children although not as commonly as in young adults. Some studies have found that certain ethnic groups who live at high northern latitudes may have adapted to the long arctic winter.
Background. Impairments in verbal learning and memory, executive functions and attention are manifest in some euthymic patients with bipolar disorder (BPD). However, evidence is sparse on their putative role as aetiologically important genetic vulnerability markers for the disorder. This population-based study examined the cognitive functions of affected and unaffected individuals in families with BPD. The aim was to discover whether any cognitive function would indicate genetic liability to the disorder and could thus be regarded as endophenotypes of BPD.
Method. A diagnostic interview and a neuropsychological test battery were administered to 32 familial bipolar I disorder patients, 40 of their unaffected first-degree relatives and 55 controls, all representing population-based samples.
Results. Unaffected first-degree relatives showed impairment in psychomotor performance speed and slight impairment in executive function. Bipolar patients were impaired in verbal learning and memory compared with unaffected relatives and controls. They also differed from controls in tasks of executive functions. There were no difference between the groups in simple attention and working memory tasks.
Conclusions. Impaired psychomotor performance speed and executive function may represent endophenotypes of BPD, reflecting possible underlying vulnerability to the disorder. Verbal memory impairments appear to be more related to the fully developed disorder.
Background. Euthymic bipolar-I disorder (BP I) patients and their siblings have shown impairments in verbal learning and memory functions compared with controls, suggesting that these impairments may be genetic in origin. Reduced information-processing speed has been associated with impaired memory in the elderly, and recently in schizophrenia. The authors compared verbal learning and memory functioning in twins with BP I and co-twins to control twins, and examined whether the observed deficits are related to information-processing speed.
Method. Finnish Medical and Population Registers and Twin Cohorts were used to identify the BP I and control twins. Neuropsychological tests assessing verbal learning and memory, working memory, facial recognition, visual memory, and information-processing speed were administered to 26 BP I twins, 19 non-bipolar co-twins, and 114 controls. Group differences were analyzed by generalized estimation equation modeling.
Results. BP I patients, but not co-twins, showed impairments in all memory tests compared with controls. Female co-twins showed impairment in verbal learning and memory. Information-processing speed had a significant effect on encoding and learning efficiency.
Conclusions. This study showed for the first time that information-processing speed is related to memory functioning and verbal learning in BP I in a population-based, representative and euthymic sample. Furthermore, the data support the view that defects in verbal memory may be related to the genetic factors predisposing to BP I in females.
Impairments in cognitive functioning are common in schizophrenia, and the degree of impairment may be associated with the individual's age at onset of the disorder.
To examine the effect of age at onset on cognitive functioning using the California Verbal Learning Test, sub-tests from the Wechsler Memory Scale – Revised and sub-scales from the Wechsler Adult Intelligence Scale – Revised among families with schizophrenia.
The effect of age at onset on cognitive function in 237 people with schizophrenia from a population-based sample was examined using linear mixed effects models with family as the random effect, and age, gender, chronicity of the illness and number of affected first-degree relatives as fixed effects.
Impairment in verbal learning and memory was associated with earlier disease onset. No association was found for working memory or IQ.
In patients with early-onset schizophrenia, verbal memory functions in particular should be taken into account in neuropsychological evaluation and efforts at remediation.
In patients with bipolar disorder, admissions for manic and depressive episodes frequently display a seasonal pattern. We examined this variation and compared the patterns with the seasonal admission rates for schizophrenia.
Patients with bipolar disorder or schizophrenia were identified from the Finnish Hospital Discharge Register of in-patient admissions to all psychiatric hospitals during the years 1969–91. They were included in the analysis if the first admission had occurred before 30 years of age. A total of 295 bipolar patients were found and a sample of 295 schizophrenic patients was randomly selected for comparison.
There was no seasonal variation among all hospital admissions for bipolar disorder or schizophrenia However, the first admission for a depressive compared with a manic episode of bipolar disorder occurred significantly more often in the autumn (33% v. 21% respectively). The peak difference occurred during the week after the autumnal equinox in September.
Our findings suggest that there is no seasonal variation in bipolar disorder, although in some patients the clinical course might be influenced by the autumn, as far as the likelihood of a first admission for depression is concerned.
In patients with winter seasonal affective disorder (SAD) the onset of a depressive episode is probably associated with the decreasing amount of light during the autumn. A highly predictable onset of a recurrent depressive episode with seasonal pattern provides a rationale for testing the efficacy of bright-light treatment as a preventive measure. Twelve out-patients with winter SAD were assigned to start bright light treatment either when they were well, or not to start it until the first symptoms of depression had already emerged. The severity of depressive symptoms was prospectively rated for a parallel randomized comparison. Bright light given well in advance of the emerging symptoms prevented a depressive episode. Clinical remission was significantly more frequent in the former subgroup of the patients in January and in March. To sum up, bright light can be successfully administered as prophylactic treatment for the prevention of winter SAD.
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