GE Blok 5.docx

GE Interplay – Study Guide Block 5 Lecture 10: BMI and personality Body weight and obesity Weight is often determined by body mass index (BMI) 𝐵𝑀𝐼 = weight (𝑘𝑔) / height2 (𝑚2 ) A heritability of about 70 percent has been found across eight European countries despite average differences in weight, wi...

GE Interplay – Study Guide Block 5 Lecture 10: BMI and personality Body weight and obesity Weight is often determined by body mass index (BMI) 𝐵𝑀𝐼 = weight (𝑘𝑔) / height2 (𝑚2 ) A heritability of about 70 percent has been found across eight European countries despite average differences in weight, with some suggestion of greater shared environmental influence for women. No heritability of weight at birth and during the first months. The environment is more important for those early differences. Genes influence eating behavior too like the enjoyment of food, slowness in eating, satiety responsiveness, and food responsiveness. Animal studies They provide clues on the biological mechanisms behind obesity. An obese strain of mice have the mutation (allele) ob/ob. The ob/ob mouse is always hungry and does not stop eating. The gene’s product, a hormone called leptin, was shown to reduce weight in mice by decreasing appetite and increasing energy use. However, with rare exceptions, obese humans do not appear to have defects in the leptin gene. Obesity-related traits are highly complex and are likely to be regulated by multiple genes that impact many systems, and these genes are likely to interact not only with one another but also with environmental stimuli. The obesity epidemic Obesity and overweight are becoming more widespread and are worldwide clinical and public health burdens. The current obesity epidemic cannot be caused by genes because the frequency of genes in a population does not change this quickly! The mean population increase in weight is probably due to the increased availability and reduced costs of energy-dense food, increased portion sizes, increased consumption of added sugars, and a reduction in physical activity. However, despite our increasingly “obesogenic” environments, a wide range of variation in weight remains — many people are still thin. Obesogenic environments could shift the entire distribution upward while the causes of individual differences, including genetic causes, could remain unchanged. The role of gene-environment interplay in the risk for obesity can be seen, for example, in the fact that heritability estimates may vary depending on certain environmental factors, like income or physical exercise. Over the years: At the low end of the distribution of food availability (famine), not much change. But at the high-end, BMI increased. Same genotype interacting with different environments (like the mouse study with enriched environments). Same environment interacting with different genotypes. Personality – Distinctive and relatively stable pattern of behavior, thoughts, motives, and emotions that characterizes an individual. Personality has always been the major domain for studying the normal range of individual differences, with the abnormal range being the provenance of psychopathology. Some psychopathology may be the extreme of normal variation in personality. Genes make a major contribution to individual differences in personality whereas shared environment does not; environmental influence on personality is almost entirely of the nonshared variety. The big five Genetic research on personality has focused on five broad dimensions of personality, called the Five-Factor Model (FFM or the Big Five), under the acronym OCEAN: Openness to experience (culture) vs resistance to new experience. Conscientiousness (conformity, will to achieve) vs. impulsivity. Extraversion (sociability, impulsiveness, and liveliness) vs introversion. Agreeableness (likability, friendliness) vs impulsivity. Neuroticism (moodiness, anxiousness, and irritability) vs emotional stability. Although the Big Five traits are fairly stable, changes do occur over the life span. Neuroticism is highest among young adults and then declines, whereas conscientiousness is lowest among young adults and then steadily increases. Heritabilities in the 30 to 50 percent range are typical of personality results. Heritabilities explained by common SNPs are low (10%). As expected, based on what we talked about the missing heritability. Heritability of personality is not visible at birth. Heritability in childhood is higher than in adulthood (heritability of personality decreases with age). Gene-enviroment interplay in life events Saudino, 1997 – life events: Controllable events (e.g., getting married or divorced). Uncontrollable events (e.g., serious illness in child or death of spouse). Desirable events (e.g., major improvement in financial status or making a new acquaintance). Undesirable events (e.g., major deterioration in financial status or death child). Heritable components for all of these (except for uncontrollable). And the effect was related to genes for personality traits. Genes→Personality→Life events. Well-being Research suggests, perhaps unsurprisingly, that lower subjective well-being is associated with chronic health problems, depression, poorer quality of life, increased health care costs, early retirement, and mortality. Positive well-being, on the other hand, is related to longevity and may add several years to the life span. Twin studies suggest that about 35 percent of the variance in subjective well-being is due to genetic influences. Consequently, it appears that self-rated health and subjective well-being are likely to be due to the contribution of multiple genes of small effect rather than a few genes of major effect. The well-being spectrum polygenic score predicted well-being, but it did not predict any of the environmental correlates, no gene-environment correlation was found. Personality and social psychology Social psychology focuses on the behavior of groups, whereas individual differences are in the spotlight for personality research. Sexual orientation Not necessarily a “pure choice”! But not genetically determined either! Higher MZ correlation than DZ correlation for being gay. Also, discordant MZ pairs. The heritability (based on twin studies) of sexual orientation is about 35%. SNP-based heritability was estimated to be 8 to 25% of the variation in female and male same-sex sexual behavior, in which the range reflects differing estimates by using different analysis methods. There is a misconception that “the more someone is attracted to the same-sex the less they are attracted to the opposite-sex”. This finding suggests that on the genetic level, there is no single dimension from opposite-sex to same-sex preference. Religiousness The trait of believing strongly in a particular religion and obeying its laws and practices. Many aspects are related to religiousness. And heritability can differ as a function of such aspects, as age. Thus, many factors are involved in individual differences in the degree of religiousness. Research suggests that the heritability of religiousness increases and shared environmental influence decreases from adolescence to adulthood. Political behavior Although it is recognized that social factors are not solely responsible for attitudes, it has been a surprise to find that genetics makes a major contribution to individual differences in attitudes. Genetic research extends beyond political attitudes to political behaviors. Heritability is clear for all political ideologies. This is an example of the cafeteria model: “We may view this as a kind of cafeteria model of the acquisition of social attitudes. The individual does not inherit his ideas about fluoridation, royalty, women judges, and nudist camps; he learns them from his culture. But his genes may influence which ones he elects to put on his tray. Different cultural institutions—family, church, school, books, television—like different cafeterias, serve up somewhat different menus, and the choices a person makes will reflect those offered him as well as his own biases.” (Loehlin, 1997, p. 48). Lecture 11: Mental disorders Genetic correlation – a statistic indexing the extent to which genetic influences on one trait are correlated with genetic influences on another trait independent of the heritabilities of the traits. It can be estimated with family studies and/or GWAS. Test for shared genetics by looking for correlations in effect sizes (for example, of SNPs) across traits. A positive genetic correlation is considered when the higher the trait 1, the higher the trait 2. On the opposite way – the higher the trait 1, the lower the trait 2 – is a negative genetic correlation. In humans, most lifestyle risk factors of disease, as well as the diseases themselves, are at least partially heritable; genetic correlation estimates help to describe their complex relationships, which, particularly in the context of disease traits, may be unrecognized. Understanding horizontal pleiotropy may lead to a better understanding of biological processes that are common between traits. Vertical pleiotropy can inform on causality for intervention strategies for disease prevention. Mental disorder – any behaviour or emotional state that causes a person to suffer, is self-destructive; seriously impairs the person’s ability to work or get along with others; or endangers others or the community Autism Causes In 1950s and 1960s: Autism was thought to be fully environmentally caused by cold and rejecting parents “Refrigerator Mother Theory”. From 1970s: Twin studies start building up of evidence refuting the cases from parenting style. These twin studies show that autism has many genetic influences. ASD has a very high heritability! Genetic studies support the idea of a continuum of traits, with diagnosed ASD being the tail end. Relatives of individuals with autism show increased rates of social deficits, impairments in communication and language, a preference for routines, and difficulty with change. Almost zero C (shared environment). So, it’s extremely unlikely that parenting styles play a role in autism! Twin heritability is estimated in 0.95, while SNP heritability in 0.12. It is not caused by vaccination!!! Taken together, metal study with discordant twins supports the hypothesis that prenatal and early childhood disruption (excess or deficiency) of multiple metals during critical developmental windows is associated with ASD, and suggests a role for elemental dysregulation in the etiology of ASD. (Arora et al., 2017; https://www.nature.com/articles/ncomms15493) Attention-deficit/hyperactivity disorder Causes Results suggest that heritability is greater for ADHD than for other childhood disorders except autism. Also, the heritability is stable over development. Suggests that the same genes are in common at different time points. Twin heritability is estimated at around 73%, and SNP heritability as 22% For ADHD (as opposed to ASD), the genetic correlations with intelligence, grades, and college completion match the cognitive deficits commonly found in ADHD (at the trait level). Studies conclude that the associations between parent characteristics and offspring outcomes in childhood are mainly to be attributable to the effects of genes that are shared by parents and children. Major depressive disorder (MDD) Depression is heritable, estimated at around 38%. Kendler et al. (2013) study supports the idea that there are multiple forms of major depression and that each may have different genetic underpinnings (https://jamanetwork.com/journals/jamapsychiatry/article-abstract/1679421). “The DSM-IV syndrome of MD does not reflect a single dimension of genetic liability. Rather, these criteria reflect 3 underlying dimensions that index genetic risk for cognitive/psychomotor, mood, and neurovegetative symptoms.“ Depression and anxiety Overlap in genes & unique environment. Genetic correlation of 1.0 !!! between the two disorders, indicating that the same genes affect depression and anxiety. Drug use Genes play a role in all drug addictions. Overlap for drugs: Phenotypic overlap. Genetic overlap: 2 general genetic factors (legal and illegal drugs) and specific genetic factors. 60% genetic overlap for alcohol, nicotine and cannabis addiction. Influence of genes may differ for different phases in drug use and can be different in different environments. Koopmans et al. (1999) study shows supporting evidence for the social control hypothesis. Religiosity appears to moderate the genetic effects on problem alcohol use during adolescence, but not during early adulthood. The reduced genetic variance for problem alcohol use in adolescence may be the consequence of greater social control in adolescence than in young adulthood.