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  • 1. Health Psychology and Aging
  • 2. Health Psychology
    • Also, “behavioural medicine”
    • Role of behaviour in promoting health, preventing and treating disease
    • New
    • Relatively little behavioural genetics work
  • 3. 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
  • 4. Obesity
    • Natural energy reserves (fatty tissue) exceeds healthy limits
    • Absolute or relative terms
    • Body mass index
      • Weight/height 2
      • Exceeds 30kg/m 2
  • 5. Co-morbidity
    • Osteoarthritis
    • Obstructive sleep apnea
    • Diabetes
    • Cancer
    • Cardiovascular disease
  • 6. Environmental Factors
    • Overeating
      • High caloric, “energy-dense” foods
      • Fast food consumption tripled and calorie intake quadrupled between 1977-1995 in North America
    • Sedentary lifestyle
  • 7. 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
  • 8. 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
  • 9. 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
  • 10. 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>
  • 11. 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
  • 12. 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
  • 13. 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
  • 14. 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
  • 15. Female Twin Studies
    • Inconsistent results
    • Heritability figures range from 0.25 to 0.55
  • 16. 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
  • 17. 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
  • 18. 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)
  • 19. 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
  • 20. 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
  • 21. Smoking
    • MZ concordance, 75%
    • DZ concordance, 63%
    • Heritability about 60% with some shared environmental effects
      • Like alcohol, less parents, more peers and siblings
  • 22. 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?
  • 23. 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
  • 24.
    • 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%)