scholarly journals Pleiotropic effects drive correlation between body mass index and cortical myelination

2018 ◽  
Author(s):  
Lisa Ronan ◽  
Nenad Medic ◽  
Paul C Fletcher
Keyword(s):  
Body Mass Index ◽  
Genetic Correlation ◽  
Causal Relationship ◽  
Body Mass ◽  
Genetic Factors ◽  
Monozygotic Twins ◽  
Pleiotropic Effects ◽  
Phenotypic Correlation ◽  
Neurocognitive Decline ◽  
Shared Genetic

AbstractBackgroundEpidemiological studies have reported significant associations between obesity and neurocognitive decline. Understanding these associations will require deeper analyses of how body mass index (BMI) and brain structure are related. Here we explore the extent to which shared genetic factors (pleiotropy) govern the association between BMI and cortical myelination.MethodsStatistical models of bivariate heritability were applied to structural MR image data from a cohort of monozyogotic and dizygotic twins. Estimates of phenotypic and genetic correlation between BMI and cortical myelination were derived. A co-twin control design based on monozygotic twins was used to test the hypothesis of a causal relationship between BMI and myelination. The variation in the genetic correlation across the cortex was compared with the average statistical enrichment of genes associated with obesity derived from data from the Allen brain atlas.ResultsStatistically significant phenotypic and genetic correlation between BMI and cortical myelination was observed across the cortex. Taking the heritability of each trait into account, approximately 80% of the phenotypic correlation between the traits was accounted for by shared genetic factors.Intra-pair differences between traits in monozygotic twins failed to support a causal relationship. Moreover, variation in genetic correlation across the cortex was significantly associated with the statistical enrichment of genes related to obesity.ConclusionsThese results support the hypothesis that pleiotropic effects drive the association between BMI and cortical myelination. This observation may help to explain the co-occurrence of obesity in neurocognitive decline and mental health disorders characterized by changes in myelination and oligodendrocyte function.

scholarly journals Shared Genetic Factors Influence Head Motion During MRI and Body Mass Index

2016 ◽  
Author(s):  
Karen Hodgson ◽  
Russell A Poldrack ◽  
Joanne E Curran ◽  
Emma E Knowles ◽  
Samuel Mathias ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Genetic Factors ◽  
Head Motion ◽  
Shared Genetic

Heritability of Longitudinal Measures of Body Mass Index and Lipid and Lipoprotein Levels in Aging Twins

2007 ◽  
Vol 10 (5) ◽  
pp. 703-711 ◽  
Author(s):  
Ellen L. Goode ◽  
Stacey S. Cherny ◽  
Joe C. Christian ◽  
Gail P. Jarvik ◽  
Mariza de Andrade
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Genetic Factors ◽  
Significant Proportion ◽  
Lipoprotein Cholesterol ◽  
Equation Modeling ◽  
Shared Environment ◽  
Significant Contributor ◽  
Age Related ◽  
Over Time

AbstractBody-mass index (BMI), total cholesterol (TC), lowdensity lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG) levels are known to be highly heritable. We evaluated the genetic and environmental relationships of these measures over time in an analysis of twin pairs. Monozygotic (235 pairs) and dizygotic (260 pairs) male twins were participants in the National Heart Lung and Blood Institute Veteran Twin Study, and were followed with three clinical exams from mean age 48 years to mean age 63 years. Structural equation modeling (SEM) with adjustment forAPOEgenotype (a significant contributor to TC and LDL-C) was used to assess longitudinal patterns of heritability. Results indicated a contribution of genetic factors to BMI, TC, LDL-C, HLD-C, and TG. Modest increases over time were observed in the heritability of BMI (from 0.48 to 0.61), TC (from 0.46 to 0.57), LDL-C (from 0.49 to 0.64), and HDL-C (from 0.50 to 0.62), but this trend was not present for TG. There was a corresponding decrease in shared environmental influences over time for these traits, although shared environment was a significant contributor only for HDL-C. Moreover, we observed that genetic influences for all measures were significantly correlated over time, and we found no evidence of age-specific genetic effects. In summary, longitudinal analyses of twin data indicate that genetic factors do not account for a significant proportion of the variation in age-related changes of BMI or lipid and lipoprotein levels.

A genomewide study of body mass index and its genetic correlation with thromboembolic risk

2014 ◽  
Vol 112 (11) ◽  
pp. 1036-1043 ◽  
Author(s):  
Geórgia Pena ◽  
Andrey Ziyatdinov ◽  
Alfonso Buil ◽  
Sonia López ◽  
Jordi Fontcuberta ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Genetic Correlation ◽  
Body Mass ◽  
Thromboembolic Disease ◽  
Thromboembolic Risk ◽  
Genetic Components ◽  
Genome Wide ◽  
Thrombosis Risk ◽  
Bivariate Linkage Analysis ◽  
Genome Wide Scan

SummaryThrombosis and obesity are complex epidemiologically associated diseases. The mechanism of this association is not yet understood. It was the objective of this study to identify genetic components of body mass index (BMI) and their possible role in the risk of thromboembolic disease. With the self-reported BMI of 397 individuals from 21 extended families enrolled in the GAIT (Genetic Analysis of Idiopathic Thrombophilia) Project, we estimated the heritability of BMI and the genetic correlation with the risk of thrombosis. Subjects were genotyped for an autosomal genome-wide scan with 363 highly-informative DNA markers. Univariate and bivariate multipoint linkage analyses were performed. The heritability for BMI was 0.31 (p= 2.9×10–5). Thromboembolic disease (including venous and arterial) and BMI had a significant genetic correlation (ρG= 0.54, p= 0.005). Two linkage signals for BMI were obtained, one at 13q34 (LOD= 3.36, p= 0.0004) and other at 2q34, highly suggestive of linkage (LOD= 1.95). Bivariate linkage analysis with BMI and thrombosis risk also showed a significant signal at 13q34 (LOD= 3), indicating that this locus influences at the same time normal variation in the BMI phenotype as well as susceptibility to thrombosis. In conclusion, BMI and thrombosis are genetically correlated. The locus 13q34, which showed pleiotropy with both phenotypes, contains two candidate genes, which may explain our linkage pleiotropic signal and deserve further investigation as possible risk factors for obesity and thrombosis.

scholarly journals Assessing potential shared genetic aetiology between body mass index and sleep duration in 142,209 individuals

2018 ◽  
Vol 43 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Victoria Garfield ◽  
Ghazaleh Fatemifar ◽  
Caroline Dale ◽  
Melissa Smart ◽  
Yanchun Bao ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Sleep Duration ◽  
Body Mass ◽  
Shared Genetic

scholarly journals Assessment of a causal relationship between body mass index and atopic dermatitis

2021 ◽  
Vol 147 (1) ◽  
pp. 400-403 ◽  
Author(s):  
Ashley Budu-Aggrey ◽  
Sarah H. Watkins ◽  
Ben Brumpton ◽  
Mari Løset ◽  
Jess Tyrrell ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Atopic Dermatitis ◽  
Causal Relationship ◽  
Body Mass

scholarly journals Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium

2019 ◽  
Vol 49 (07) ◽  
pp. 1218-1226 ◽  
Author(s):  
Renato Polimanti ◽  
Roseann E. Peterson ◽  
Jue-Sheng Ong ◽  
Stuart MacGregor ◽  
Alexis C. Edwards ◽  
...  
Keyword(s):  
Major Depression ◽  
Alcohol Dependence ◽  
Genetic Correlation ◽  
Causal Relationship ◽  
Causal Effect ◽  
Uk Biobank ◽  
Genome Wide ◽  
Genome Wide Data ◽  
Genetic Mechanisms ◽  
Shared Genetic

AbstractBackgroundDespite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC.MethodsLinkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals).ResultsPositive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10−6). There was no evidence for reverse causation.ConclusionThis study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.

scholarly journals Heritability of leptin levels and the shared genetic effects on body mass index and leptin in adult Finnish twins

2001 ◽  
Vol 25 (1) ◽  
pp. 132-137 ◽  
Author(s):  
J Kaprio ◽  
J Eriksson ◽  
M Lehtovirta ◽  
M Koskenvuo ◽  
J Tuomilehto
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Genetic Effects ◽  
Shared Genetic

scholarly journals Impact of different blood groups on body mass index and blood pressure

2021 ◽  
Vol 12 (1) ◽  
pp. 130-135
Author(s):  
Rawaa Hadi Shareef ◽  
Basim A. Abd ◽  
Zahraa Fathi Sharba
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Blood Group ◽  
Body Mass ◽  
Genetic Factors ◽  
Blood Groups ◽  
Blood Type ◽  
Lower Percentage ◽  
Chronic Medical Condition ◽  
The Impact

Obesity is considered as a public health problem that affects all age groups in the population. Genetic factors are considered as one of the non-modifiable risk factors, causing obesity. Hypertension is a chronic medical condition that is associated with vague symptoms. The ABO blood type is one of the fundamental genetic factors that can give important information for early detection of risky population. This study aimed to evaluate the impact of different blood groups on body mass index and blood pressure. The design of this study is a cross-sectional study, included 250 participants (144 males and 106 females), aged between 18-70 years were selected from the population of Al-Najaf Governorate, Iraq, through a period which extends from October 2019 to February 2020.  The blood groups were determined for each participant; blood pressure and body mass index were also measured. The results of a current study revealed that from this 250 participants there was 115 were obese person, 82 were overweight person, 51 were normal weight, and 2 were underweight persons. In the obese group, the blood group B has the highest percentage (45.2% ) followed by blood group A and O that were found to have the same percentage (22.6%), while the blood group AB has the lower percentage (9.6%). On the other hand, there was no significant relationship between hypertension and ABO blood groups.

scholarly journals Association between premorbid body mass index and amyotrophic lateral sclerosis: causal inference through genetic approaches

2019 ◽  
Author(s):  
Ping Zeng ◽  
Xinghao Yu ◽  
Haibo Xu
Keyword(s):  
Body Mass Index ◽  
Amyotrophic Lateral Sclerosis ◽  
Causal Relationship ◽  
Body Mass ◽  
European Population ◽  
Sensitivity Analyses ◽  
Genome Wide Association Studies ◽  
Inverse Association ◽  
Standard Deviation Increase ◽  
Lateral Sclerosis

Background: Inverse association between premorbid body mass index (BMI) and amyotrophic lateral sclerosis (ALS) has been discovered in observational studies; however, whether this association is causal remains largely unknown. Methods: We employed a two-sample Mendelian randomization approach to evaluate the causal relationship of genetically increased BMI with the risk of ALS. The analyses were implemented using summary statistics obtained for the independent instruments identified from large-scale genome-wide association studies of BMI (up to ~770,000 individuals) and ALS (up to ~81,000 individuals). The causal relationship between BMI and ALS was estimated using inverse-variance weighted methods and was further validated through extensive complementary and sensitivity analyses. Findings: Using 1,031 instruments strongly related to BMI, the causal effect of per one standard deviation increase of BMI was estimated to be 1.04 (95% CI 0.97~1.11, p=0.275) in the European population. The null association between BMI and ALS discovered in the European population also held in the East Asian population and was robust against various modeling assumptions and outlier biases. Additionally, the Egger-regression and MR-PRESSO ruled out the possibility of horizontal pleiotropic effects of instruments. Interpretation: Our results do not support the causal role of genetically increased or decreased BMI on the risk of ALS.

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