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

Author(s):  
Karen Hodgson ◽  
Russell A Poldrack ◽  
Joanne E Curran ◽  
Emma E Knowles ◽  
Samuel Mathias ◽  
...  
2018 ◽  
Author(s):  
Lisa Ronan ◽  
Nenad Medic ◽  
Paul C Fletcher

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.


2007 ◽  
Vol 10 (5) ◽  
pp. 703-711 ◽  
Author(s):  
Ellen L. Goode ◽  
Stacey S. Cherny ◽  
Joe C. Christian ◽  
Gail P. Jarvik ◽  
Mariza de Andrade

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.


2018 ◽  
Vol 43 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Victoria Garfield ◽  
Ghazaleh Fatemifar ◽  
Caroline Dale ◽  
Melissa Smart ◽  
Yanchun Bao ◽  
...  

2001 ◽  
Vol 25 (1) ◽  
pp. 132-137 ◽  
Author(s):  
J Kaprio ◽  
J Eriksson ◽  
M Lehtovirta ◽  
M Koskenvuo ◽  
J Tuomilehto

2021 ◽  
Vol 12 (1) ◽  
pp. 130-135
Author(s):  
Rawaa Hadi Shareef ◽  
Basim A. Abd ◽  
Zahraa Fathi Sharba

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.


2019 ◽  
Author(s):  
Alfredo Santovito ◽  
Gabriella Galli ◽  
Stefano Ruberto

ABSTRACTBackgroundlongevity is considered the result of interactions between environmental and genetic factors.Aimwe investigated the possible association of body mass index and the frequencies ofAPOE, ACE, eNOS, andFTOgene polymorphisms with longevity.Subjects and Method1,100 healthy volunteers aged 10-100 were recruited. We genotyped subjects forAPOE, ACE, eNOS, andFTOgene polymorphisms. Data about height and weight were also collected. The sample was split in four age groups: 1-24, 25-49, 50-85 and 86-100.Resultssignificant differences were found in BMI values between age groups, with exception of 1-24 with respect to 86-100. A significant decrease of theAPO E4, eNOS 393andFTO Aand allele frequencies was observed in the 86-100 age group with respect to younger groups. ForACEgene, no significant differences were found in the allele frequencies between groups. A similar trend was also observed subdividing the sample in two main age groups: 1-85 and 86-100.Conclusionthis study provides evidences for a role ofAPOE, eNOS, andFTOgene polymorphisms in longevity. It has been estimated that the number of centenarians worldwide will double each decade until 2100, making population data about gene polymorphisms relevant for further studies about longevity.


NeuroImage ◽  
2019 ◽  
Vol 199 ◽  
pp. 261-272 ◽  
Author(s):  
James T. Kennedy ◽  
Serguei V. Astafiev ◽  
Semyon Golosheykin ◽  
Ozlem Korucuoglu ◽  
Andrey P. Anokhin

2019 ◽  
Vol 215 (01) ◽  
pp. 428-433 ◽  
Author(s):  
Francesca Solmi ◽  
Marina Carbo Mascarell ◽  
Stanley Zammit ◽  
James B. Kirkbride ◽  
Glyn Lewis

BackgroundRecent studies suggest psychotic and eating disorders can be comorbid and could have shared genetic liability. However, this comorbidity has been overlooked in the epidemiological literature.AimsTo test whether polygenic risk scores (PRS) for schizophrenia are associated with disordered eating behaviours and body mass index (BMI) in the general population.MethodUsing data from the Avon Longitudinal Study of Parents and Children and random-effects logistic and linear regression models, we investigated the association between PRS for schizophrenia and self-reported disordered eating behaviours (binge eating, purging, fasting and excessive exercise) and BMI at 14, 16 and 18 years.ResultsOf the 6920 children with available genetic data, 4473 (64.6%) and 5069 (73.3%) had at least one disordered eating and one BMI outcome measurement, respectively. An s.d. increase in PRS was associated with greater odds of having binge eating behaviours (odds ratio, 1.36; 95% CI 1.16–1.60) and lower BMI (coefficient, −0.03; 95% CI, −0.06 to −0.01).ConclusionsOur findings suggest the presence of shared genetic risk between schizophrenia and binge eating behaviours. Intermediate phenotypes such as impaired social cognition and irritability, previously shown to be positively correlated in this sample with schizophrenia PRS, could represent risk factors for both phenotypes. Shared genetic liability between binge eating and schizophrenia could also explain higher rates of metabolic syndrome in individuals with schizophrenia, as binge eating could be a mediator of this association in drug-naïve individuals. The finding of an association between greater PRS and lower BMI, although consistent with existing epidemiological and genetic literature, requires further investigation.Declaration of interestNone.


Twin Research ◽  
2001 ◽  
Vol 4 (5) ◽  
pp. 365-370 ◽  
Author(s):  
John B. Whitfield ◽  
Susan A. Treloar ◽  
Gu Zhu ◽  
Nicholas G. Martin

AbstractBirthweight affects neonatal mortality and morbidity and has been used as a marker of foetal undernutrition in studies of prenatal effects on adult characteristics. It is potentially influenced by genetic and environmental influences on the mother, and effects of foetal genotype, which is partially derived from the maternal genotype. Interpretations of variation in birthweight and associated characteristics as being due to prenatal environment ignore other possible modes of materno-foetal transmission. Subjects were adult twins recruited through the Australian Twin Registry, aged 17 to 87 years, and the sample comprised 1820 men and 4048 women. Twins reported their own birthweight as part of a health questionnaire. Body Mass Index (BMI) was calculated from self-reports of height and weight. Correlations between co-twins' birthweights were high for both monozygotic (r = 0.77) and dizygotic (r = 0.67) pairs, leading to substantial estimates of shared environmental effects (56% of variance) with significant additive genetic (23%) and non-shared environmental (21%) components. Adult BMI was mainly influenced by genetic factors, both additive (36% of variance) and nonadditive (35%). The correlation between birthweight and BMI was positive, in that heavier babies became on average more obese adults. A bivariate model of birthweight and adult BMI showed significant positive genetic (rg = 0.16, p = 0.005) and environmental (re = 0.08, p = 0.000011) correlations. Intra-uterine environmental or perinatal influences shared by cotwins exercise a strong influence on birthweight, but the factors which affect both birthweight and adult BMI are partly genetic and partly non-shared environmental.


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