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Health Psychology and Aging Health Psychology • Also, “behavioural medicine” • Role of behaviour in promoting health, preventing and treating disease • New • Relatively little behavioural genetics work Body Weight • Genetic factors account for majority of variance in weight – – – – – – MZ, reared together = 0.8 MZ, reared apart = 0.72 DZ, reared together = 0.43 Biological parents & offspring = 0.26 Biological parents & adopted away offspring = 0.23 Adoptive parents & adopted offspring = 0.01 • Heritability about 70% • Shared environment effects low Obesity • Natural energy reserves (fatty tissue) exceeds healthy limits • Absolute or relative terms • Body mass index – Weight/height2 – Exceeds 30kg/m2 Co-morbidity • • • • • Osteoarthritis Obstructive sleep apnea Diabetes Cancer Cardiovascular disease Environmental Factors • Overeating – High caloric, “energy-dense” foods – Fast food consumption tripled and calorie intake quadrupled between 1977-1995 in North America • Sedentary lifestyle Genetics • Prader-Willi syndrome – 7 gene deletion, chromosome 15q • Bardet-Biedl syndrome – 12 genes, chromosome 11 or 16 – BBS proteins • MOMO syndrome – Extremely rare (1 in 100 million births); seems to be autosomal dominant mutation • Leptin receptor mutations – Regulates adipose-tissue mass • Melanocortin receptor mutations – G-protein coupled receptors; account for 6% of early-onset obesity • Single-locus mutations only account for 7% of all cases of obesity Neurobiological Mechanisms • Leptin – Produced by adipose tissue – Signals fat storage reserves in body – Mediates long-term appetite controls (eat more when fat stores low, less when stores are high) • Ghrelin – Produced by stomach – Modulates short-term appetite control (eat when empty, stop when stretched) • Both produced peripherally, but act on CNS, primarily hypothalamus Hypothalamus • Several circuits contribute to hypothalamus’ involvement in appetite • Melanocortin pathway – Arcuate nucleus (AN) --> lateral hypothalamus (LH) and ventromedial hypothalamus (VMH) • LH = brain’s feeding centre VMH = brain’s satiety centre – When AN neurons activated --> appetite – Neurons inhibited by circulating leptin and ghrelin Leptin • Leptin originally discovered 1950s; homozygous mutation --> obese mice • But, not the primary cause of obesity in humans • Over 240 other mouse genes identified in weight <wikipedia.org/wiki/Image:Fatmouse.jpg> FTO • Obesity risk allele – 10 SNPs in first intron of FTO; chromosome 16 • About 39,000 Europeans studied (Frayling et al. (2007)) • Versus individuals with no variant copy: – One copy, average 1.2kg heavier; 30% increased risk of obesity – Two copies (16% of subjects), average 3kg heavier, 70% increased risk of obesity • Ethnic differences in copy variant frequencies – 45% West/Central Europeans; 52% West African; 14% Chinese and Japanese Addictions • Typically, some form of chemical use • Substance alters body physiology and/or neurochemistry – Recurring compulsion • Questions about other addictions – E.g., food, gambling, sex – Suggestions that these may be components of obsessive compulsive disorder, not addictions, per se Alcoholism • Runs in families • 40% and 20% risk for first degree male and female relatives of alcoholic proband, respectively – 20% and 5% for general male and female population, respectively • Assortative mating for alcohol use high (0.38) – Could be inflating shared environment estimates Male Twin Studies • Moderate heritability for males, modest for females • E.g., Concordances: MZ ~ 50%, DZ ~35% • Heritability ~0.6 • Early onset and more severe alcoholism is more heritable Female Twin Studies • Inconsistent results • Heritability figures range from 0.25 to 0.55 Shared Environment • Related to initial alcohol use in teens and young adults, but not to later alcohol abuse • Effect on siblings, not parents and offspring • Correlation for alcohol abuse in parents and biological teens 0.3, but only 0.04 for adopted teens • Correlation for alcohol abuse in unrelated adopted siblings 0.24 (0.45 for same sex, 0.01 for opposite sex) • Sibling and/or peer effects more important than parent effects in adolescence Genotype-Environment Interaction • Genetic risk for alcoholism greater in more permissive environments • Heritability lower for: – – – – Married individuals People with strong religious upbringing People from stricter and closer families Regions with lower alcohol sales Animal Models • Long sleep (LS) and short sleep (SS) mice • Inbred strain • After 18 generations LS mice “slept” for average of 2 hours post alcohol; SS mice only for about 10 minutes – Lot of variation in LS (1.2 - 4.4 hours); less in SS (0 - 0.65 hours) Alcohol Response Polygenic • Suggests many genes involved – Steady divergence over 18 generations (1 or 2 genes would have stabilized much sooner) – Variability in sleep times for LS and SS – Different responses by LS & SS strains to other drugs (e.g., cocaine, morphine) • QTL mapping and knockout studies identify 5 genes for dopamine D2 receptor – Each gene accounts for 20 minutes of sleep; five about 130 minutes of total 170 minute difference between LS and SS mice • Dopamine D4 receptor knockout --> supersensitivity to alcohol, cocaine, methamphetamine • Serotonin receptor knockout --> increased alcohol consumption Humans • Ethnic differences • Mutant ALDH2 allele – Inactivates key enzyme in alcohol metabolism – 25% Chinese, 40% Japanese, almost no Caucasians • But, this and other genes don’t show consistent effects even within ethnic groups Smoking • MZ concordance, 75% • DZ concordance, 63% • Heritability about 60% with some shared environmental effects – Like alcohol, less parents, more peers and siblings Aging • Tricky • Older individuals vary greatly biologically and psychologically • So, grouping into “elderly” for analysis not very effective • Relatively little behavioural genetics work on second half of lifespan – Traditional nurturist/behaviourist carry-over? Effects • Specific types (e.g., Alzheimer’s) • General cognitive decline – Various tests, e.g., Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) • Differences in abilities – Fluid abilities decline (e.g., spatial) – Crystallized abilities improve (e.g., vocabulary) – Both equally heritable • Personality traits remarkably stable across adult lifespan; large genetic effect here • Heritabilities of late life psychopathology and personality disorders very similar to younger rates • Longevity only has modest genetic effects (heritability about 25%)