Considering Genetics/Heredity

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Considering Genetics/Heredity How do biological factors contribute to the development of alcohol abuse and dependence? Considering Genetics/Heredity

Some Behavioral Genetics Basics: Genotype ≈ combination of genes Identical twins have same set of genes Phenotype ≈ how genes are expressed genes + environment (shared+ unique) Even identical twins are never identical Endophenotypes (per Gottesman & Gould, 2003): Genetically-influenced phenotype Identifiable before a disorder develops Associated with high risk of developing a disorder Endophenotype = not the disorder, but an intermediate expression of genes that increases/decreases likelihood of developing disorder Schucket describes 4 endophenotypes that meet these criteria and have been associated with AUD outcomes

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Low response to alcohol Disinhibited, impulsive, externalizing temperament Psychiatric comorbidity (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Beverage Alcohol Acetic acid, CO2, HzO  ADH  acetaldehyde  ALDH  ADH1B*2 variant speeds up process Flushing, nausea, Vomiting, headache The ADH1B*2 variant speeds up the process, causes acetaldehyde to build up Adverse effects = flushing, nausea, vomiting, headache PROTECTIVE – this variant lower in alcoholics than controls (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Lower levels, less aversive Beverage Alcohol Acetic acid, CO2, HzO  ADH  acetaldehyde  ALDH  ADH1C*2 variant slows process ADH1C*2 is less active polymorphism, RISK FACTOR for alcohol dependence (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Beverage Alcohol Acetic acid, CO2, HzO  ADH  acetaldehyde  ALDH  ALDH2*2 variant slows metabolism (may have 1 allele or 2) Flushing, nausea, Vomiting, headache Having the inactive form of ALDH causes acetaldehyde to build up in blood, leading to aversive physical effects PROTECTIVE factor Homozygous (2 mutated alleles) = least likely to develop AUDs because of strong flushing response Heterozygous (1 mutated allele only) = some flushing but not as protective (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Low response to alcohol always able to “hold my liquor” less cognitive/motor impairment seen in COAs, Native Americans ability to drink heavily and develop tolerance (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Low response to alcohol Disinhibited, impulsive, externalizing temperament nonspecific to drinking heavier drinking, more problems early onset of AUDs gene x environment interaction (more later) (Schuckit, 2009)

4 known sources of genetic influence on likelihood of developing AUDs: Variations in alcohol-metabolizing enzymes Low response to alcohol Disinhibited, impulsive, externalizing temperament Psychiatric comorbidity (cf. Hasin et al., 2007) Antisocial personality (adj OR = 1.7, lifetime AD) Bipolar mood disorder (adj OR = 2.1, lifetime AD) Schizophrenia (Schuckit, 2009)

Heritability = proportion of observable differences between individuals that is due to genetic differences Varies according to how much variability is attributable to the environment heritability is specific to a population in a given environment Cf Rose & Dick (2004/2005) FinnTwin findings on differences between urban and rural twins Gene x environment interaction Heritability could increase if genetic variability increases, or if environmental variability decreases (in islamic countries); therefore heritability is specific to a population in a given environment. Genetic influences on drinking frequency stronger among urban twins than rural twins– why? The more that sociodemographic factors facilitated drinking (lots of young adults, more social mobility [less stability], higher alcohol sales/availability) the greater the expression of genetic risk Conversely, strong environmental influences that protect against access to alcohol and restrict excessive drinking, the less genetic influence we will be able to detect.

Take away messages about the genetics of alcohol use disorders Genes explain ~ 50% vulnerability (Schuckit, 2009) Similar genetic contributions in both sexes AUDs are polygenic AUDs are multifactorial: Genes x environments Gene-environment correlations

Likely gene-environment correlations in alcoholism (Searles, 1988) Passive: Environment is not independent of genes prenatal exposure to alcohol Parenting, parent/sib role models Reactive/evocative: certain temperaments precede AUDs and evoke responses from parents, teachers, peers, etc. high activity level / behavioral undercontrol emotionality / low soothability / neuroticism poor attention span / persistence sociability / extraversion (Tarter & Vanyukov, JCCP, 1994)

Likely gene-environment correlations in alcoholism - cont’d Active (niche seeking): People actively seek environments that complement/support their genotype self-selection into “partying” social groups selection of mates self-selection away from alcohol involvement (e.g., flushing response) Genetic influences change over life course Several pathways to development of AUDs

Cloninger’s Typology Type II : Type I: Affects both men and women Age of onset after age 25 Periodic binge drinking, guilt about drinking Progressive severity Both genetic and environmental influences Type II : Affects primarily men Early age of onset (before age 25) Inability to abstain, assoc.with fights and arrests Severity usually not progressive Primarily genetic Cloninger Type 1-2 distinction based on a cross-fostering adoption study in Sweden (862 men, 913 women); Type 1 = 76%, most common type has substantial environmental influence Type 2 = 24%; men and women have different patterns demonstrates multiple pathways to alcohol problems