First-degree Relatives Of Individuals Research Articles

Community-Based Pilot Study of a Screening Program for Gastric Cancer in a Chinese Population.

A majority of gastric cancer cases in China are diagnosed at advanced stages, chiefly due to lack of an established routine nationwide screening program. This study evaluated the effectiveness of a novel screening program for gastric cancer. Seven geographic communities were randomly selected, and residents ages 40-69 years were screened. Serologic tests of Helicobacter pylori antibodies and pepsinogens, and positive family history of gastric cancer in first-degree relatives (FDR), were used to differentiate individuals for further gastroscopic examination and gastric mucosal biopsies. Among 7,773 individuals who underwent examination of serum markers, gastric cancer was detected in 14 (1.8%; 10 men). The rate in terms of gastric cancer cases per 100 gastroendoscopies was 1.6% (14/872), which was greater than 0.87% previously reported. Eleven of 14 patients with gastric cancer (78.6%) were FDRs of patients with gastric cancer. Two-thirds of the subjects with cardia gastric cancer were FDRs of individuals with gastric cancer rather than cardia gastric cancer. Comparative analysis indicated that the gastric cancer subjects were significantly more likely to be FDRs of patients with gastric cancer, in contrast to those without gastric cancer. All the individuals with gastric cancer were aged ≥50 years. After conducting a reverse analysis, we propose a novel screening program for gastric cancer. In conclusions, the populations most vulnerable to gastric cancer are those with positive family history of gastric cancer in FDRs, male gender, and aged 50 years or older. This screening program using fewer serum markers combined individual risk factors, mainly FDRs, is novel for identification of high-risk individuals for further gastroscopy in detecting early gastric cancer.

Hereditary or Not? Understanding Serrated Polyposis Syndrome.

To present the current understanding of the diagnosis, management, and potential genetic causes of serrated polyposis syndrome. The clinical criteria for serrated polyposis syndrome was recently updated and now includes individuals with five or more serrated polyps proximal to the rectum that are 5 mm in size or greater and at least two that are 10 mm in size of greater as well as individuals with 20 or more serrated polyps throughout the colon with at least five proximal to the rectum. There is a significant risk for colon cancer in first-degree relatives of individuals with serrated polyposis syndrome. However, less than 3% of serrated polyposis syndrome cases are explained by identifiable germline mutations, with mutations in RNF43 being the only currently validated genetic cause. Serrated polyposis syndrome is rarely explained by identifiable germline mutations, but there remains an increased risk for colorectal cancer in first-degree relatives. Referral for genetic counseling and testing is recommended for individuals with serrated polyposis syndrome and a personal history of coexisting adenomatous polyposis or with a concerning family history and can be considered for all individuals with serrated polyposis syndrome. Close endoscopic surveillance of those with serrated polyposis syndrome and their first-degree relatives is recommended. Continued efforts at identifying hereditary causes of serrated polyposis are needed.

Lifetime Risk and Heritability of Amyotrophic Lateral Sclerosis

Heritability describes the proportion of variance in the risk of developing a condition that is explained by genetic factors. Although amyotrophic lateral sclerosis (ALS) is known to have a complex genetic origin, disease heritability remains unclear. To determine the extent of ALS heritability and assess the association of sex with disease transmission. A prospective population-based parent-offspring heritability study was conducted from January 1, 2008, to December 31, 2017 to assess ALS heritability, and was the first study to assess heritability in the context of known gene mutations of large effect. A total of 1123 incident cases of ALS, diagnosed according to the El Escorial criteria and recorded on the Irish ALS register, were identified. Ninety-two individuals were excluded (non-Irish parental origin [n = 86] and familial ALS [n = 6]), and 1117 patients were included in the final analysis. Annual age-specific and sex-specific standardized ALS incidence and mortality-adjusted lifetime risk were determined. Sex-specific heritability estimates were calculated for the overall study cohort, for those known to carry the C9orf72 (OMIM 614260) variant, and for those with no known genetic risk. A total of 32 parent-child ALS dyads were identified during the study period. Affected offspring were younger at the onset of disease (mean age, 52.0 years; 95% CI, 48.8-55.3 years) compared with their parents (mean age, 69.6 years; 95% CI, 62.4-76.9 years; P = .008). Lifetime risk of developing ALS in first-degree relatives of individuals with ALS was increased compared with the general population (1.4% [32 of 2234] vs 0.3% [2.6 of 1000]; P < .001). Mean lifetime heritability of ALS for the overall study cohort was 52.3% (95% CI, 42.9%-61.7%) and 36.9% (95% CI, 19.8%-53.9%) for those with no known genetic risk. Heritability estimates were highest in mother-daughter pairings (66.2%; 95% CI, 58.5%-73.9%). This population-based study confirms that up to 50% of variance in ALS has a genetic basis, and that the presence of the C9orf72 variant is an important determinant of heritability. First-degree relatives of individuals with ALS without a known genetic basis remain at increased risk of developing ALS compared with the general population. A higher heritability estimate in mother-daughter pairings points to a sex-mediated effect that has been previously unrecognized.

Is schizotypic maternal personality linked to sensory gating abilities during infancy?

Schizotypy is a personality dimension within the general population elevated among schizophrenia-spectrum patients and their first-degree relatives. Sensory gating is the pre-attentional habituation of responses distinguishing between important and irrelevant information. This is measured by event-related potentials, which have been found to display abnormalities in schizophrenic disorders. The current study investigated whether 6-month-old infants of mothers with schizotypic traits display sensory gating abnormalities. The paired-tone paradigm: two identical auditory tones (stimulus 1 and stimulus 2) played 500 ms apart, was used to probe the selective activation of the brain during 15-minutes of sleep. Their mothers completed the Oxford and Liverpool Inventory of Feelings and Experiences-Short Form as an index of schizotypy dimensionality, categorized into: infants of control, and infants of schizotypic, mothers. The findings revealed that although the infants’ P50 components displayed significant differences between stimulus 1 and stimulus 2 in the paired-tone paradigm, there was no clear difference between infants of schizotypic and infants of control mothers. In contrast, all mothers displayed significant differences between stimulus 1 and stimulus 2, as observed in the infants, but also significant differences between their sensory gating ability correlated with schizotypy dimensionality. These findings are consistent with sensory processes, such as sensory gating, evidencing impairment in schizophrenia-spectrum disorders. The present research supports the idea that first-degree relatives of individuals who identify on this spectrum, within the sub-clinical category, do not display the same deficit at 6 postnatal months of age.

Coaggregation of Major Psychiatric Disorders in First-Degree Relatives of Individuals With Attention-Deficit/Hyperactivity Disorder: A Nationwide Population-Based Study.

Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable mental illness that is easily passed from one generation to the next. Studies have shown that first-degree relatives (FDRs; ie, parents, offspring, and siblings) of individuals with ADHD had a higher risk of also having ADHD. However, the familial coaggregation of ADHD with other major psychiatric disorders, specifically schizophrenia (ICD-9-CM code 295), bipolar disorder (ICD-9-CM cods 296 except codes 296.2, 296.3, 296.9, and 296.82), major depressive disorder (ICD-9-CM codes 296.2 and 296.3), and autism spectrum disorder (ASD; ICD-9-CM code 299), remains unclear. Among the entire Taiwanese population in 2010, there were 220,966 parents of children with ADHD (ICD-9-CM code 314), 174,460 siblings of children with ADHD, and 5,875 children of parents with ADHD. Matched control individuals who did not have FDRs with ADHD (1:4) were selected based on age, sex, and their relation to family members. FDRs (parents, offspring, siblings, and twins) of ADHD-diagnosed individuals had higher relative risks (95% CI) of major psychiatric disorders than the controls: 1.69 (1.60-1.79) for schizophrenia, 2.21 (2.10-2.32) for bipolar disorder, 2.08 (2.02-2.13) for major depressive disorder, 4.14 (3.90-4.39) for ASD, and 6.87 (6.73-7.01) for ADHD. These results show that ADHD coaggregated with other major psychiatric disorders, specifically schizophrenia, bipolar disorder, major depressive disorder, and ASD, within families. The results suggest that public health officials and psychiatrists should closely monitor and follow the mental health of FDRs of ADHD-diagnosed individuals, such as parents and siblings of children with ADHD.

Neurocognitive deficits in obsessive-compulsive disorder: A selective review.

Obsessive–compulsive disorder (OCD) is a debilitating mental illness characterized by an early onset and chronic course. Evidence from several lines of research suggests significant neuropsychological deficits in patients with OCD; executive dysfunction and nonverbal memory deficits have been reported consistently in OCD. These deficits persist despite controlling potential confounders such as comorbidity, severity of illness, and medications. Neuropsychological impairments are independent of illness severity, thus suggesting that the neuropsychological deficits are trait markers of the disease. In addition, these deficits are seen in first-degree relatives of individuals with OCD. These reports suggest that neuropsychological deficits are potential endophenotype markers in OCD. Neuropsychological studies in pediatric OCD are limited; they show impairments of small effect size across multiple domains but with doubtful clinical significance. Preliminary evidence shows that different symptom dimensions of OCD may have unique neuropsychological deficits suggestive of discrete but overlapping neuroanatomical regions for individual symptom dimensions. Overall, neuropsychological deficits further support the role of frontostriatal circuits in the neurobiology of OCD. In addition, emerging literature also suggests the important role of other areas, in particular parietal cortex. Preliminary evidence suggests the possible role of neuropsychological deficits to be markers of treatment response but needs to be examined in future. Longitudinal studies with examination of patients at different time points and examination of their potential utility as predictors of treatment response are needed in future.

Metabolic and genetic profiling of young adults with and without a family history of premature coronary heart disease (MAGNETIC). Study design and methodology.

IntroductionFirst-degree relatives of individuals with premature coronary artery disease (CAD) are at increased risk of CAD. The research hypothesis of this project assumes that there are differences in the metabolic profiles between individuals with and without a positive family history (FH) of premature CAD.Material and methodsThe study group will comprise healthy patients (n = 500) aged 18–35 years with a FH of premature CAD, and the control group (n = 500) will consist of healthy subjects without a FH of premature CAD. Blood tests assessing the lipid profile will be carried out. Patients will respond to a questionnaire regarding FH and dietary habits. Measurement of carotid intima media thickness will be performed. Analysis of single-nucleotide polymorphisms (SNPs) associated with premature CAD will be carried out for every patient. Metabolomic profiling will be performed using a high-sensitivity Bruker AVANCE II 600 MHz NMR spectroscope.ResultsThe results of this study will include a comparison of metabolic profiles assessed by 1H-NMR spectroscopy in the study and control groups and the results of analyses of the relationship between the metabolic profiles and genetic risk score calculated based on evaluated SNPs associated with premature CAD.ConclusionsThis study will deepen our knowledge of the aetiopathogenesis of atherosclerosis by identifying metabolic patterns associated with a positive FH of premature CAD. Obtaining a detailed FH will enable adjustments for major risk factors of premature CAD in the proband’s first-degree relatives. This research project also provides a chance to discover new biomarkers associated with the risk of premature CAD.

Cognitive Performance in First-Degree Relatives of Individuals With vs Without Major Depressive Disorder

Findings of cognitive impairment in major depressive disorder (MDD), including remitted MDD, raise the question whether impaired cognition is part of preexisting vulnerability rather than a consequence of MDD or its treatment. To our knowledge, no meta-analyses have been published on cognitive impairment in first-degree relatives of individuals with MDD. To compare cognitive performance between individuals with and without family history of MDD. Medline/PubMed, PsycINFO, and Embase using combinations of search terms for depression, first-degree relatives, and cognition from January 1, 1980, to July 15, 2018. Original articles that reported data on cognition in first-degree relatives of individuals with MDD compared with controls with no family history of major mental illness. Means and SDs were extracted, and standardized mean differences (SMD) between relatives and controls were calculated for each measure of cognitive performance. The relative-control differences in overall cognition and in specific cognitive domains were synthesized in random-effects meta-analyses with robust variance estimation that allows including multiple correlated measures of cognition within each study. Heterogeneity was quantified with τ2. Publication bias was assessed with funnel plots and Egger intercept. Performance on cognitive tests. Across 284 measures of cognition in 54 nonoverlapping samples including 3246 relatives of people with MDD (mean age 15.38 years, 57.68% females) and 5222 controls (mean age 14.70 years, 55.93% females), relatives of people with MDD performed worse than controls across all measures of cognition (SMD = -0.19; 95% CI, -0.27 to -0.11; P < .001). Domain-specific meta-analyses showed similar size of relative-control difference in most domains of cognition, including Full-Scale IQ (SMD = -0.19), verbal intelligence (SMD = -0.29), perceptual intelligence (SMD = -0.23), memory (SMD = -0.20), academic performance (SMD = -0.40), and language (SMD = -0.29). Study characteristics were not significantly associated with observed between-group differences. There was no evidence of publication bias. A general impairment in cognition is a feature of familial disposition for MDD. Cognition may contribute to early identification of risk for depression and may be examined as potential target for early intervention.

Instrument-based assessment of motor function yields no evidence of dyskinesia in adult first-degree biological relatives of individuals with schizophrenia and schizoaffective disorder

There is accruing evidence of spontaneous dyskinesia in individuals with schizophrenia that is independent of medication exposure. Dyskinetic motor behavior is also present in individuals who are at high risk of schizophrenia and appears to have prognostic value for the development of psychosis. Nonetheless, it remains unclear whether dyskinesia is present in first-degree relatives of individuals with schizophrenia and thus associated with genetic liability for schizophrenia (i.e., an endophenotype), or whether the motor abnormality is a biomarker specific to the disease state spectrum. There is also limited information about links between dyskinesia and clinically relevant phenomena such as symptoms and cognition. Because dyskinesia marking genetic liability is likely to be subtle, we used sensitive instrument-based measurement of handwriting fluency to quantify dyskinesia in medicated individuals with schizophrenia or schizoaffective disorder, unaffected first-degree biological relatives of individuals with schizophrenia and schizoaffective disorder, and control participants. Results indicated that medicated individuals with schizophrenia or schizoaffective disorder exhibited more dyskinesia than both relatives and controls, with no difference between relatives and controls. Dyskinesia in individuals with schizophrenia or schizoaffective disorder was unrelated to current antipsychotic medication dosage, but associated with worse working memory function and greater positive formal thought disorder. These results provide evidence that dyskinesia is not associated with unexpressed genetic liability for schizophrenia.

Daily-life stress differentially impacts ventral striatal dopaminergic modulation of reward processing in first-degree relatives of individuals with psychosis

Emerging evidence shows that stress can impair the ability to learn from and pursue rewards, which in turn has been linked to motivational impairments characteristic of the psychotic disorder. Ventral striatal dopaminergic neurotransmission has been found to modulate reward processing, and appears to be disrupted by exposure to stress. We investigated the hypothesis that stress experienced in the everyday life has a blunting effect on reward-induced dopamine release in the ventral striatum of 16 individuals at a familial risk for psychosis compared to 16 matched control subjects. Six days of ecological momentary assessments quantified the amount of daily-life stress prior to [18F]fallypride PET imaging while performing a probabilistic reinforcement learning task. Relative to the controls, individuals at a familial risk for psychosis who encountered more daily-life stress showed significantly diminished extent of reward-induced dopamine release in the right ventral striatum, as well as poorer performance on the reward task. These findings provide the first neuromolecular evidence for stress-related deregulation of reward processing in familial predisposition to psychosis. The implication of daily-life stress in compromised modulation of reward function may facilitate the design of targeted neuropharmacological and ecological interventions.

Temporal lobe thickness and verbal memory in first-degree relatives of individuals with schizophrenia

Cortical thinning in frontal and temporal regions has been reported in individuals diagnosed with schizophrenia and, less consistently, among their unaffected first-degree relatives. Likewise, first-degree relatives demonstrate attenuated differences in neurocognitive performance relative to healthy controls, indicating that neurocognitive performance may be an important endophenotype of the disorder. Less is known about how cortical thickness relates to neurocognitive performance in these individuals. Given the robust nature of temporal structural abnormalities in schizophrenia, this study aimed to identify how temporal lobe cortical thickness might relate to verbal memory in first-degree relatives. Unaffected parents and siblings of individuals with adult-onset schizophrenia (N=62) and individuals in healthy control families (N=70) participating in the UCLA Family Study received a structural MRI and completed a battery of neurocognitive tests. Cortical thickness was estimated across the cortex and thickness measures of all regions in the temporal lobe were summed, averaged, and residualized for age and sex to produce a variable. A verbal learning factor was derived from two common tests of verbal learning and memory, the CVLT-II and Logical Memory of the WMS-III. Results demonstrated a significant interaction between group and verbal learning in relationship to temporal lobe thickness. Post-hoc analyses revealed significant correlations between verbal learning and cortical thickness in the relatives of schizophrenia patients which were driven by immediate recall scores on the CVLT-II and Logical Memory. These findings indicate that cortical thickness in the temporal cortex may represent a structural correlate for encoding verbal information in unaffected relatives of individuals with schizophrenia.

Self-Stigma in Relatives of people with Mental Illness scale: development and validation.

Serious mental illness (SMI) is profoundly stigmatised, such that there is even an impact on relatives of people with SMI. Aims To develop and validate a scale to comprehensively measure self-stigma among first-degree relatives of individuals with SMI. We conducted group interviews focusing on self-stigma with first-degree relatives (n = 20) of people with SMI, from which 74 representative quotations were reframed as Likert-type items. Cognitive interviews with relatives (n = 11) identified 30 items for the Self-Stigma in Relatives of people with Mental Illness (SSRMI) scale. Relatives (n = 195) completed the scale twice, a month apart, together with four external correlate scales. The 30-item SSRMI was reliable, with scores stable over time. Its single-factor structure allowed generation of a 10-item version. Construct validity of 30- and 10-item versions was supported by expected relationships with external correlates. Both versions of the SSRMI scale are valid and reliable instruments appropriate for use in clinical and research contexts. Declaration of interest None.

Intact striatal dopaminergic modulation of reward learning and daily-life reward-oriented behavior in first-degree relatives of individuals with psychotic disorder.

Abnormalities in reward learning in psychotic disorders have been proposed to be linked to dysregulated subcortical dopaminergic (DA) neurotransmission, which in turn is a suspected mechanism for predisposition to psychosis. We therefore explored the striatal dopaminergic modulation of reward processing and its behavioral correlates in individuals at familial risk for psychosis. We performed a DA D2/3 receptor [18F]fallypride positron emission tomography scan during a probabilistic reinforcement learning task in 16 healthy first-degree relatives of patients with psychosis and 16 healthy volunteers, followed by a 6-day ecological momentary assessment study capturing reward-oriented behavior in the everyday life. We detected significant reward-induced DA release in bilateral caudate, putamen and ventral striatum of both groups, with no group differences in its magnitude nor spatial extent. In both groups alike, greater extent of reward-induced DA release in all regions of interest was associated with better performance in the task, as well as in greater tendency to be engaged in reward-oriented behavior in the daily life. These findings suggest intact striatal dopaminergic modulation of reinforcement learning and reward-oriented behavior in individuals with familial predisposition to psychosis. Furthermore, this study points towards a key link between striatal reward-related DA release and pursuit of ecologically relevant rewards.

High risk of conversion to diabetes in first-degree relatives of individuals with young-onset type 2 diabetes: a 12-year follow-up analysis.

Family history of diabetes is an established risk factor for Type 2 diabetes, but the impact of a family history of young-onset diabetes (onset < 40 years) on future risk of diabetes among first-degree relatives is unclear. In this prospective study, we examined the influence of family history of late- versus young-onset diabetes on the development of diabetes in a young to middle-aged Chinese population. Some 365 siblings identified through probands with Type 2 diabetes and 452 participants from a community-based health awareness project (aged 18-55 years) who underwent metabolic assessment during the period 1998-2002 were followed to 2012-2013 to determine their glycaemic status. Multivariate logistic regression was performed to investigate the association of family history of diabetes presented at different age categories with development of diabetes. In this cohort, 53.4% (n = 167) of participants with a family history of young-onset diabetes, 30.1% (n = 68) of those with a family history of late-onset diabetes and 14.4% (n = 40) of those without a family history developed diabetes. Using logistic regression, family history of diabetes presented at ages ≥ 50, 40-49, 30-39 and < 30 years, increased conversion to diabetes with respective odds ratios of 2.4, 5.8, 9.4 and 7.0 (P < 0.001 for all), after adjustment for socio-economic status, smoking, obesity, hypertension and dyslipidaemia. Among participants without diabetes at baseline, risk association of family history of late-onset diabetes with incident diabetes was not sustained, whereas that of family history of young-onset diabetes remained robust on further adjustment for baseline glycaemic measurements. First-degree relatives of people with Type 2 diabetes, especially relatives of those with young-onset diabetes, are at high risk for diabetes.

Runs of homozygosity, copy number variation, and risk for depression and suicidal behavior in an Arab Bedouin kindred.

Inbreeding increases the probability of homozygosity of deleterious alleles. Inbreeding and runs of homozygosity (ROH) are associated with an increased risk for disease phenotypes, including schizophrenia and other psychiatric disorders. The effects of inbreeding, ROH, homozygous deletions, and other copy number variations (CNVs) on risk for depression and suicide attempt (SA) were quantified in an Arab Bedouin Kindred. We carried out genetic analyses of 439 individuals from an Arab kindred with high rates of depression and suicidal behavior. We obtained complete ascertainment of SAs and first-degree relatives of individuals who have attempted or died by suicide. We found extensive regions of ROH. On average, 5% of the genome is covered by ROH for these individuals, two-fold higher than ROH rates for individuals from populations of European ancestry. Inbreeding and total length of ROH were not associated with risk for depression or attempt. For CNVs, an increased number of duplications more than 500 kb was associated with an increased risk for attempt (odds ratio: 2.9; P=0.01; 95% confidence interval: 1.3-6.6). Although not significant after correction for multiple testing, the risk for SA appears to increase with copy number for a CNV on chromosome 9p24.1. This possibility is intriguing because the CNV covers GLDC, which encodes glycine dehydrogenase that binds to glycine, a co-agonist at N-methyl-D-aspartate glutamate receptors, and is involved in glutamatergic neurotransmission. Our findings add to the growing evidence of genetic risk factors that act pleiotropically to increase the risk for several neuropsychiatric disorders, including depression and SA, irrespective of ancestry.

Cognitive abilities in first-degree relatives of individuals with bipolar disorder

BackgroundAlthough the study of cognition in first degree relatives (FDRs) is not new, findings in this group are still somewhat inconsistent and much of the research examining FDR populations include individuals under the age of 25, who are arguably still at significant risk to go on to develop BD. The present study aimed to establish the value of cognitive performance as a genuine endophenotypic marker of familial risk for bipolar disorder (BD), by examining cognition in FDRs aged 25 years or older. MethodsThe current study compared the cognitive performance of 27 unaffected FDRs to 47 healthy controls (HCs) and 28 BD patients using the MATRICS Consensus Cognitive Battery (MCCB). ResultsResults indicated that FDRs had impaired verbal learning performance, as well as selective impairments on a measure of speed of processing; and a measure of spatial working memory compared to HC. LimitationsLimitations relate to the potential insensitivity of some of the tests in the MCCB for detecting cognitive deficits that have been previously noted in BD and FDR samples using other batteries. ConclusionsFindings from this study implicate verbal learning, processing speed and working memory performance as promising candidate endophenotypes of familial risk for BD.

Prevention of cardiovascular disease in patients with familial hypercholesterolaemia: The role of PCSK9 inhibitors.

Familial hypercholesterolaemia is an autosomal dominant inherited disorder characterised by elevated low-density lipoprotein cholesterol levels and consequently an increased risk of atherosclerotic cardiovascular disease (ASCVD). Familial hypercholesterolaemia is relatively common, but is often underdiagnosed and undertreated. Cardiologists are likely to encounter many individuals with familial hypercholesterolaemia; however, patients presenting with premature ASCVD are rarely screened for familial hypercholesterolaemia and fasting lipid levels are infrequently documented. Given that individuals with familial hypercholesterolaemia and ASCVD are at a particularly high risk of subsequent cardiac events, this is a missed opportunity for preventive therapy. Furthermore, because there is a 50% chance that first-degree relatives of individuals with familial hypercholesterolaemia will also be affected by the disorder, the underdiagnosis of familial hypercholesterolaemia among patients with ASCVD is a barrier to cascade screening and the prevention of ASCVD in affected relatives. Targeted screening of patients with ASCVD is an effective strategy to identify new familial hypercholesterolaemia index cases. Statins are the standard treatment for individuals with familial hypercholesterolaemia; however, low-density lipoprotein cholesterol targets are not achieved in a large proportion of patients despite treatment. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have been shown to reduce low-density lipoprotein cholesterol levels considerably in individuals with familial hypercholesterolaemia who are concurrently receiving the maximal tolerated statin dose. The clinical benefit of PCSK9 inhibitors must, however, also be considered in terms of their cost-effectiveness. Increased awareness of familial hypercholesterolaemia is required among healthcare professionals, particularly cardiologists and primary care physicians, in order to start early preventive measures and to reduce the mortality and morbidity associated with familial hypercholesterolaemia and ASCVD.

The Relationship between Compulsions, Worry, and Academic Performance among United Arab Emirates University Students

&lt;p&gt;The cognitive approaches of obsessive-compulsive disorder consider negative appraisal of beliefs and thoughts to be the core factor for the onset of this disorder. The present study was aimed at investigating the relationship between compulsions and worries (anxious thoughts), and between compulsions and academic performance in a sample of 461 university students aged between 18 and 30 years (mean age=21.2 years). Male participants represented 31.2% of the total sample while female participants represented 68.8% of the sample. The Anxious Thoughts Inventory and the Compulsion Checklist were administered. Results showed that worries were positively related to compulsions. Meta-worry was the strongest predictor of compulsions. First-degree relatives of individuals with history of obsessive-compulsive symptoms significantly reported more symptoms of compulsions compared to their counterparts. Academic performance (GPA) was not related to compulsion but it was related to worry. Further, older participants expressed less social worry and less compulsive symptoms compared to younger ones. The results were discussed in relation to relevant theoretical framework and in light of findings of previous studies. This study will provide researchers, practitioners and readers with an understanding of the relationship between worry, academic performance and compulsions in this part of the world.&lt;/p&gt;&lt;strong&gt;&lt;em&gt;Keywords&lt;/em&gt;&lt;/strong&gt;: Compulsions, Meta-worry, Social Worry, Health Worry, Academic Performance

Su1728 - Risk of Colorectal Neoplasms in First-Degree Relatives of Individuals with Non-Advanced Adenomas: A Cross-Sectional Study

Su1728 - Risk of Colorectal Neoplasms in First-Degree Relatives of Individuals with Non-Advanced Adenomas: A Cross-Sectional Study

M91. Temporal Lobe Thinning and Verbal Learning in First-Degree Relatives of Individuals With Schizophrenia

M91. Temporal Lobe Thinning and Verbal Learning in First-Degree Relatives of Individuals With Schizophrenia