W6: Vulnerabilities and Predispositions Flashcards
What is vulnerability (in health)? (2) + examples
- Predispositions that may lead to poor health
- E.g. Genetics, life events (e.g, trauma), environment and stress
Why do we study vulnerability? (2) - importance
“At risk people”
- Identify those “at-risk” for poor health
- Provide “at risk” with pre-emptive treatment and interventions
Why do we study vulnerability? (2)
Among those seeking treatment
- Inform the type of treatment
- Escalate intensity of treatment if needed if we know they are the “ at risk group”
Some may have the resiliency to poor health (Another side to vulnerability) - (2)
- Predispositions that reduce the likelihood of unhealthy behaviours
- Healthy vs unhealthy personalities types - certain personalities more likely to engage in healthy/unhealthy behaviours
Process of health psychology theories
- Ask broad research questions (basic research) - (2)
- Understand what factors which promote poor health
- Mechanisms (e.g., stress, genetics)
Process of health psychology theories
- do health behaviours differ in their origin? - (2)
- E.g.,Is stress more likely to promote certain behaviours?
- Understand the unique processes for each behaviour
Process of health psychology theories
- Development of interventions (2)
- How can we prevent or change maladaptive health behaviours?
- This is Applied research (e.g., outside of the lab)
Process of health psychology theories
- Individual Differences (2)
- Identify vulnerabilities for specific health behaviours
- Informs individualized treatment and targets at-risk populations
Stages of process of health psychology theories (4)
- Broad RQ
- Do health behaviours differ in their origin?
- Development of interventions
- Individual Differences
Different types of vulnerabilities (4)
- Developmental
- Genetics
- Enzyme production
- Tolerance/sensitivty
Development influence
Exposure to toxins during adolescence (2)
- E.g., smoking, alcohol
- Leads to greater likelihood of poor health during adulthood
Graph of the likelihood for developing AUD - Alcohol Use Disorder (2)
- Found that if people drank alcohol before the age of 13, more likely to develop alcohol use disorder later in life on average than those who drank alcohol after 13
- Across all age ranges
Likelihood for developing AUD across all age ranges (2)
- Before ages of 13,15,17 people drank alcohol then more greater likelihood of developing AUD
- If you drank alcohol after 17 less likelihood of developing AUD
Age of Onset of Drinking (Age of first drink) and Freq of Alcohol (any drinking) + Freq of Binge Drinking (2)
- Younger of the onset of drinking the more frequently you drink at any time and also frequently you binge drink at later in life
- Early exposure lead to unhealthy behaviours later on
Smoking - Chassin et al. (1990) - (4)
- Look at people who regularly smoked as an adolescent, ex-smoker (smoked as kid and quit), trier (smoked once) or never smoke to see if they continue to smoke later in life
- Never smoke did not smoke later on in life.
- Triers (one - exposure in adolescence) greater tendency to smoke later in life
- Those who are regular smokers had a significant likelihood to smoke later in life
Development influence - gateway hypothesis (4)
- That legal drugs as a child lead to illicit and esclated drug use later in life
- Try alcohol and cigarettes (legal drugs) and go later on to smoke cannabis
- Cannabis as the link between legal and illegal drug use
- Cannabis lead to more addictive substances (e.g. cocaine, heroin)
Do licit drugs really lead to illicit drug use? (2)
Other explanation
Environmental influence = the same environment which led to licit drug use early on will naturally guide someone to more potent and illicit drugs
Developmental influence
Neural pruning (3)
- Neural pruning (loss of gray matter volume)
- Common process during adolescent to shed off excessive brain cells we were born with
- Increasing in white matter volume
Brain Areas that do not fully develop until late adolescence may explain risky health behaviours during adolescence
What areas are linked with inhibition and sustained attention?
PFC and areas linked to inhibition and sustained attention
Disrupting this brain development process (neural pruning) can lead to reduced growth of PFC and brain areas linked to inhibition and sustained attention
What disrupts the process? (3)
- Stress
- Environment
- Toxins (e.g, drug, alcohol)
What biological predispositions lead to poor health ? - (4)
- Enzyme production
- Sensitivity (e.g., natural tolerance)
- Receptor variations
- Rate of metabolization
Biological predispositions lead to poor health –> Receptor variations
Acetylcholine receptor polymorphism (alleles) - (2)
Nicotinic receptors (tobacco)
Linked to vulnerability of developing nicotine dependence
Biological predispositions lead to poor health –> Receptor variations
Genes that encode enzymes for drug metabolism (4)
Alcohol dehydrogenase (breaks down alcohol)
Protective against developing an alcohol use disorder
Individuals can vary in the release of these enzymes
Influences likelihood that drinking will lead to future use!
Genetic risks
Certain alleles may influence stress response - (2)
- People vary in their release of CRH/CRF and cortisol in periphery ( HPA axis)
- This can be a risk factor for stress-induced health behaviors and self-control failure
Biological predispositions lead to poor health –> Receptor variations
Acetaldehyde (2)
Metabolite of alcohol via alcohol dehydrogenase (ADH)
Accumulation leads to facial flushing and nausea
Biological predispositions lead to poor health –> Receptor variations
Aldehyde dehydrogenase (ALDH) (4)
Enzyme which breaks down acetaldehyde
Certain alleles generate a non-functional enzyme…
If someone has 2 of these defective alleles, it can lead to intense flushing and nausea if alcohol is consumed
Common among Asian populations
Biological predispositions lead to poor health –> Receptor variations
Too much of a deterrent research (2)
Subjective self-assesssment of effects of alcohol by 16 men homozygous for ALDH2 and 14 men with ALDH21/ALDH2 genotype at different times after a single dose of alcohol
Thos with heterozygous alleles rated the effects of alcohol more intense than those with homozygous ALDH2
Genetic risks
Alleles may also change how we process information - (2)
Certain genes are linked to poor health behaviours as may encod rewarding stimuli more rewarding
Assessed via P3 event-related potential after cue exposure during EEG
Sensitivity measured when understanding vulnerability
What is sensitivity? (2)
Amount of drug needed to experience effects
Sensitivity is usually genetically influenced (receptor variability, enzyme production) and environmental influence (tolerance from previous experiences)
Sensitivity Results
- Less sensitivity (more tolerance you have to substance like alcohol) is linked to development of AUD, more likely to experience negative consequence of drinking, higher quantity of drinking and linked to higher frequency of binge drinking
EEG P3 or P300 (3)
- Relevant to health behaviours
- P3/P300 assess motivational or emotional relevance
- P3/P300 is correlated with craving (elicited while viewing alcohol stimuli)
Namkoong et al. (2004) = (5)
Alcohol dependent vs control participants
Shown alcohol-related versus neutral pictures
Measured P3 response to images via EEG
Control = no difference in P3 response between pictures
Alcohol dependent had higher P3 response to alcohol than neutral
