Week 6 lec 1 (suicide and intro to anxiety)

Mortality of suicidality

2x more than homocides

5x more than HIV/aids

Gender in suicide

-males are more likely to complete due to violent methods

-Females are more likely to attempt

Suicide risk factors

-preexisting psychological disorder

-past suicidal behavior

-suicide within family

-plans to acess lethal methodes

-experiencing stressful/humiliating events

suicide predisposing risk factors

-genetics

-biological factors

-personality (impulsivity)

suicide precipitating factors

-Method availability

-humiliating life event

Klonsky 3 step model

1) theres pain and hopelessness

2)pain is overwhelming connectedness

3) is there capability of suicide

research gaps

-who is at risk

-measuring the suicidal mind

problems with measuring whos at risk

-low base rate behavior

-multidimensional factors

problems with measuring the suicidal mind

-laboratory measurements are limited

-phenomina is transient

-self reporting isnt reliable

How do we measure whos at risk?

-large data sets

-machine learning and sophisticated modeling

so whos at risk

-minorities

-high school + college aged individuals

-increase in plans, ideation, and attempt for preexisting disorders

-^ impulse control and SUD have high plans and ideation

-mental disorders tend to predict transition from ideation to attempt

How is the suicidal mind measured?

-IAT

-real time monitering

-neuro imaging

IAT

-computerized test that uses reaction time to measure strength of association between death and self

-resistant against ‘fake good’

-reliable

-positive score= more association between self and death

IAT findings

-more death bias=6x increase in suicide attempts

-more death bias=5x increase in self harm

-less grey matter in dopamaneric regions in reward and imupulisivity (more death bias)

Real time monitering

-can be passive or active

-less recall bias

-more relaibly

Real time monitering results

-odolescents, rested, listened to music when having suicidal thoughts or NSSI thoughts

-NSSI was used to escape aversive states (anxiety, sadness, bad memories)

-in younger people NSSI/suicidal thoughts coaccoured

-teens often socialized/worked to curveball thoughts (in adults socializing reduced ideation while work amplified it)

suicidal thoughts are transient and triggeref by many feelings

-hopelessness, burdensomeness and lonlieness usually correalate with suicidal ideation

-sadness, tension and boredom tended to predict thoghts within hours

Post mortem neuroimaging in suicidality

-inconsistent results, heterogeneity across people and differing characteristics

Functional MRI in suicidality

depresed adolescents→ less connectivity in regions involved in error monitering, salience, and self referential thinking= more ideation

Structure MRI in suicidality

less grey matter in OFC and white matter connecting the OFC with the amygdala in BP attempters

Fear

response to immenent threat

Anxiety

-prepares us to meet challanges posed by threats

-varies in severity and frequency

-response to the anticipation of a future threat

what happens when we are anxious

-suddent attention to ‘danger/threat’

-theres absence of a real ‘threat’, rather the attention is to negative aspects of the enviorment

Why does the body react the way it does when anxious ?

-activation of the autonomic sympathetic nervous system, mediated by norepinephrine

The HPA axis

-what happens in the BRAIN during anxiety

-CRH is released by the hypothalamus→

-CRH stimulates pituitary gland→

-The pituitary releases ACTH→

-ACTH stimulates adrenal cortex→

-cortisol (stress hormone) and norepinephrine are released

when functioning has a negative feedback loop

Treatments for an overactive HPA

-generally a result of not enough GABA (inh neurotransmitter)

-Benzodiazepines

-Norepinephrine antagonist (beta blockers)

Benzodiazepines

Enhance GABA by binding to GABA receptor

Beta blockers

-Norepinephrine antagonist

-blocks peripheral receptors

Anxiety v. stress

-Anxiety is increased sensitivity to stress (its a behavioral condition)

-Anxiety continues even after the stressor goes away

-stress activates CRH (aka CRF)

-^ when activated repeatedly and uncontrollably, anxiety is induced

Amygdala in stress and anxiety

-in stress responses and presentation of anxiety

-has high norephinephrine input and high CRF/CRH levels

-animals with lesions to this structure lack stress and anxiety responses