scholarly journals The Role of Eating Behaviours in Genetic Susceptibility to Obesity

2020 ◽  
Vol 9 (4) ◽  
pp. 512-521
Author(s):  
Moritz Herle ◽  
Andrea D. Smith ◽  
Alice Kininmonth ◽  
Clare Llewellyn
Keyword(s):  
Genetic Susceptibility ◽  
Genetic Risk ◽  
Genetic Research ◽  
Twin Studies ◽  
Eating Behaviours ◽  
Genetic Liability ◽  
The Past ◽  
Uncontrolled Eating ◽  
Shared Genetic

Abstract Purpose of Review Eating behaviours are hypothesised to be the behavioural expression of genetic risk of obesity. In this review, we summarise findings from behavioural genetic research on the association between genetic risk for obesity and validated psychometrics measures of eating behaviours in children and adults (published in the past 10 years). Recent Findings Twin studies have produced some evidence for a shared genetic aetiology underlying body mass index and eating behaviours. Studies using measured genetic susceptibility to obesity have suggested that increased genetic liability for obesity is associated with variation in obesogenic eating behaviours such as emotional and uncontrolled eating. Summary More research on this topic is needed. Especially longitudinal studies using genetically sensitive designs to investigate the direction of genetic pathways between genetic liability of eating behaviours to weight and vice versa, as well as the potential subsequent link to eating disorders.

Bipolar Disorders and Their Clinical Management, Part I: Epidemiology, Etiology, Genetics, and Neurobiology

2019 ◽  
Author(s):  
Vladimir Maletic ◽  
Bernadette DeMuri-Maletic
Keyword(s):  
Autistic Spectrum Disorder ◽  
Relevant Literature ◽  
Genetic Research ◽  
Bipolar Disorders ◽  
Major Depressive ◽  
Disease Evolution ◽  
The Past ◽  
Endocrine Disturbances ◽  
Brain Changes

The concept of bipolar disorders has undergone a substantial evolution over the course of the past two decades. Emerging scientific research no longer supports the notion of bipolar disorder as a discrete neurobiologic entity. Most likely, there are a number of different biotypes with similar phenotypical manifestations. Advancements in genetic research suggest that bipolar disorders have a polygenetic pattern of inheritance, sharing common genetic underpinnings with a number of other psychiatric disorders, including schizophrenia, autistic spectrum disorder, and major depressive disorder. Contemporary etiological theories are discussed in some detail, inclusive of the role of immune disturbances, oxidative stress, and changes in neuroplasticity and neurotransmission, which underpin functional and structural brain changes associated with bipolar disorders. Contemporary epidemiologic research and understanding of disease evolution are discussed from the perspective of its clinical relevance. Our review provides a succinct summary of relevant literature. This review contains 4 figures, 2 tables, and 80 references. Key Words: bipolar disorders, endocrine disturbances, epidemiology, genetics, glia, immunity, neurobiology, neuroplasticity, neurotransmitters

Bipolar Disorders and Their Clinical Management, Part I: Epidemiology, Etiology, Genetics, and Neurobiology

2019 ◽  
Author(s):  
Vladimir Maletic ◽  
Bernadette DeMuri-Maletic
Keyword(s):  
Autistic Spectrum Disorder ◽  
Relevant Literature ◽  
Genetic Research ◽  
Bipolar Disorders ◽  
Major Depressive ◽  
Disease Evolution ◽  
The Past ◽  
Endocrine Disturbances ◽  
Brain Changes

The concept of bipolar disorders has undergone a substantial evolution over the course of the past two decades. Emerging scientific research no longer supports the notion of bipolar disorder as a discrete neurobiologic entity. Most likely, there are a number of different biotypes with similar phenotypical manifestations. Advancements in genetic research suggest that bipolar disorders have a polygenetic pattern of inheritance, sharing common genetic underpinnings with a number of other psychiatric disorders, including schizophrenia, autistic spectrum disorder, and major depressive disorder. Contemporary etiological theories are discussed in some detail, inclusive of the role of immune disturbances, oxidative stress, and changes in neuroplasticity and neurotransmission, which underpin functional and structural brain changes associated with bipolar disorders. Contemporary epidemiologic research and understanding of disease evolution are discussed from the perspective of its clinical relevance. Our review provides a succinct summary of relevant literature. This review contains 4 figures, 2 tables, and 80 references. Key Words: bipolar disorders, endocrine disturbances, epidemiology, genetics, glia, immunity, neurobiology, neuroplasticity, neurotransmitters

scholarly journals Genotype and phenotype in Alzheimer's disease

2002 ◽  
Vol 180 (2) ◽  
pp. 131-134 ◽  
Author(s):  
Clive Holmes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Factors ◽  
Clinical Phenotype ◽  
Genetic Research ◽  
Twin Studies ◽  
Common Variants ◽  
Clinical Expression ◽  
Presenilin 2

BackgroundPatients with Alzheimer's disease show a wide variation in clinical phenotype. Genetic research has been largely concerned with the role of mutations or common variants as risk factors for the disease. Do genetic factors also influence clinical phenotype?AimsTo examine the evidence that genetic factors influence the clinical expression of the disease in addition to influencing risk.MethodA selective review was made of the key literature.ResultsMutations in three genes, coding for amyloid precursor protein, presenilin-1 and presenilin-2, and a common variation (ε4) in another gene, APOE, have been shown to lead to an earlier development of the disease. More recently, genetic association and twin studies have suggested a role for genetic factors in the development of other aspects of clinical phenotype, notably the appearance of non-cognitive symptoms.ConclusionsIn Alzheimer's disease genetic variation influences a number of aspects of clinical phenotype.

scholarly journals Polygenic risk for schizophrenia, disordered eating behaviours and body mass index in adolescents

2019 ◽  
Vol 215 (01) ◽  
pp. 428-433 ◽  
Author(s):  
Francesca Solmi ◽  
Marina Carbo Mascarell ◽  
Stanley Zammit ◽  
James B. Kirkbride ◽  
Glyn Lewis
Keyword(s):  
Body Mass Index ◽  
Binge Eating ◽  
Disordered Eating ◽  
Body Mass ◽  
Outcome Measurement ◽  
Eating Behaviours ◽  
Genetic Liability ◽  
Polygenic Risk ◽  
Intermediate Phenotypes ◽  
Shared Genetic

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.

scholarly journals The Role of Genetics in Risk Stratification of Thoracic Aortic Aneurysm Dissection

Hearts ◽  
2020 ◽  
Vol 1 (2) ◽  
pp. 50-61
Author(s):  
Jotte Rodrigues Bento ◽  
Josephina A.N. Meester ◽  
Ilse Luyckx ◽  
Aline Verstraeten ◽  
Bart L. Loeys
Keyword(s):  
Genetic Risk ◽  
Thoracic Aortic Aneurysm ◽  
Elective Surgery ◽  
Aortic Aneurysms ◽  
Risk Markers ◽  
Additional Risk ◽  
Thoracic Aortic Aneurysms ◽  
The Past ◽  
Aneurysm Dissection

Thoracic aortic aneurysms are prevalent in the Western population and are often caused by genetic defects. If undetected, aneurysms can dissect or rupture, which are events associated with a high mortality rate. Hitherto no cure exists other than elective surgery if aneurysm dimensions reach a certain threshold. In the past decades, genotype-phenotype associations have emerged that enable clinicians to start stratifying patients according to risk for dissection. Nonetheless, risk assessment is—to this day—confounded by the lack of full comprehension of underlying genetics and modifying genetic risk factors that complicate the yet established genotype-phenotype correlations. Further research that focuses on identifying these additional risk markers is crucial.

scholarly journals Susceptibility Genes in Thyroid Autoimmunity

2005 ◽  
Vol 12 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Yoshiyuki Ban ◽  
Yaron Tomer
Keyword(s):  
Genetic Susceptibility ◽  
Thyroid Autoimmunity ◽  
Twin Studies ◽  
Epidemiological Data ◽  
Susceptibility Genes ◽  
Autoimmune Response ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Genome Screening ◽  
Shared Genetic

The autoimmune thyroid diseases (AITD) are complex diseases which are caused by an interaction between susceptibility genes and environmental triggers. Genetic susceptibility in combination with external factors (e.g. dietary iodine) is believed to initiate the autoimmune response to thyroid antigens. Abundant epidemiological data, including family and twin studies, point to a strong genetic influence on the development of AITD. Various techniques have been employed to identify the genes contributing to the etiology of AITD, including candidate gene analysis and whole genome screening. These studies have enabled the identification of several loci (genetic regions) that are linked with AITD, and in some of these loci, putative AITD susceptibility genes have been identified. Some of these genes/loci are unique to Graves' disease (GD) and Hashimoto's thyroiditis (HT) and some are common to both the diseases, indicating that there is a shared genetic susceptibility to GD and HT. The putative GD and HT susceptibility genes include both immune modifying genes (e.g. HLA, CTLA-4) and thyroid specific genes (e.g. TSHR, Tg). Most likely, these loci interact and their interactions may influence disease phenotype and severity.

scholarly journals Genetic Factors of Autoimmune Thyroid Diseases in Japanese

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Yoshiyuki Ban
Keyword(s):  
Genetic Susceptibility ◽  
Twin Studies ◽  
Epidemiological Data ◽  
Susceptibility Genes ◽  
Thyroid Diseases ◽  
Autoimmune Response ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Genome Screening ◽  
Shared Genetic

Autoimmune thyroid diseases (AITDs), including Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), are caused by immune response to self-thyroid antigens and affect approximately 2–5% of the general population. Genetic susceptibility in combination with external factors, such as smoking, viral/bacterial infection, and chemicals, is believed to initiate the autoimmune response against thyroid antigens. Abundant epidemiological data, including family and twin studies, point to a strong genetic influence on the development of AITDs. Various techniques have been employed to identify genes contributing to the etiology of AITDs, including candidate gene analysis and whole genome screening. These studies have enabled the identification of several loci (genetic regions) that are linked to AITDs, and, in some of these loci, putative AITD susceptibility genes have been identified. Some of these genes/loci are unique to GD and HT and some are common to both diseases, indicating that there is a shared genetic susceptibility to GD and HT. Known AITD-susceptibility genes are classified into three groups: HLA genes, non-HLA immune-regulatory genes (e.g., CTLA-4, PTPN22, and CD40), and thyroid-specific genes (e.g., TSHR and Tg). In this paper, we will summarize the latest findings on AITD susceptibility genes in Japanese.

Bipolar Disorders and Their Clinical Management, Part I: Epidemiology, Etiology, Genetics, and Neurobiology

2019 ◽  
Author(s):  
Vladimir Maletic ◽  
Bernadette DeMuri-Maletic
Keyword(s):  
Autistic Spectrum Disorder ◽  
Relevant Literature ◽  
Genetic Research ◽  
Bipolar Disorders ◽  
Major Depressive ◽  
Disease Evolution ◽  
The Past ◽  
Endocrine Disturbances ◽  
Brain Changes

The concept of bipolar disorders has undergone a substantial evolution over the course of the past two decades. Emerging scientific research no longer supports the notion of bipolar disorder as a discrete neurobiologic entity. Most likely, there are a number of different biotypes with similar phenotypical manifestations. Advancements in genetic research suggest that bipolar disorders have a polygenetic pattern of inheritance, sharing common genetic underpinnings with a number of other psychiatric disorders, including schizophrenia, autistic spectrum disorder, and major depressive disorder. Contemporary etiological theories are discussed in some detail, inclusive of the role of immune disturbances, oxidative stress, and changes in neuroplasticity and neurotransmission, which underpin functional and structural brain changes associated with bipolar disorders. Contemporary epidemiologic research and understanding of disease evolution are discussed from the perspective of its clinical relevance. Our review provides a succinct summary of relevant literature. This review contains 4 figures, 2 tables, and 80 references. Key Words: bipolar disorders, endocrine disturbances, epidemiology, genetics, glia, immunity, neurobiology, neuroplasticity, neurotransmitters

scholarly journals Shared genetic risk underlies the co-occurrence of ADHD and other psychiatric symptoms

2020 ◽  
Keyword(s):  
Psychiatric Disorders ◽  
Genetic Risk ◽  
Psychiatric Symptoms ◽  
Twin Studies ◽  
Genetic Risks ◽  
Shared Genetic

Data from twin studies suggest that the co-occurrence of ADHD with other psychiatric disorders is due, in part, to shared genetic risks.

Bipolar Disorders and Their Clinical Management, Part I: Epidemiology, Etiology, Genetics, and Neurobiology

2019 ◽  
Author(s):  
Vladimir Maletic ◽  
Bernadette DeMuri-Maletic
Keyword(s):  
Autistic Spectrum Disorder ◽  
Relevant Literature ◽  
Genetic Research ◽  
Bipolar Disorders ◽  
Major Depressive ◽  
Disease Evolution ◽  
The Past ◽  
Endocrine Disturbances ◽  
Brain Changes

The concept of bipolar disorders has undergone a substantial evolution over the course of the past two decades. Emerging scientific research no longer supports the notion of bipolar disorder as a discrete neurobiologic entity. Most likely, there are a number of different biotypes with similar phenotypical manifestations. Advancements in genetic research suggest that bipolar disorders have a polygenetic pattern of inheritance, sharing common genetic underpinnings with a number of other psychiatric disorders, including schizophrenia, autistic spectrum disorder, and major depressive disorder. Contemporary etiological theories are discussed in some detail, inclusive of the role of immune disturbances, oxidative stress, and changes in neuroplasticity and neurotransmission, which underpin functional and structural brain changes associated with bipolar disorders. Contemporary epidemiologic research and understanding of disease evolution are discussed from the perspective of its clinical relevance. Our review provides a succinct summary of relevant literature. This review contains 4 figures, 2 tables, and 80 references. Key Words: bipolar disorders, endocrine disturbances, epidemiology, genetics, glia, immunity, neurobiology, neuroplasticity, neurotransmitters

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