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

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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%)