L1: depression & physical health Flashcards
how does depression look in the brain? (3)
- structural: lower hippocampus, amygdala, and pfc volumes
- connectivity: higher activation of default mode network, lower activation of salience & central executive networks
- functional activation: stronger activation to negative stimuli, lower to positive stimuli in amygdala, striatum, pfc
what are the criteria of MDD aka depresion? (12)
- depressed mood
- loss of interest/pleasure
- loss of energy/fatigue
- changes in appetite/weight
- sleep problems (insomnia/hypersomnia)
- worthlessness / guilt
- psychomotor retardation / agitation
- difficulties concentrating
- suicidal thoughts
+ symptoms present for min 2 weeks, for most of the day
+ significant distress / impairment
meet min 5 (from which one has to be depressed mood or loss of interest)
what is the prevalence of depression? (3)
6-7%
- early onset
- (often) chronic course
what are the consequences of depression? (4)
- burden for society
- high comorbidity w many diseases (somatic illnesses, mortality, disability, cognitive impairment, obesity, diabetes, heart disease)
- so also higher health care costs
- treatment not effective for all
what are 5 possible explanations for the high comorbidity between depression & somatic illnesses?
- coincidence (illness + depression)
- therapy related (treatment of medical disease -> depression or vice versa like antidepressants can lead to obesity)
- behavioural (depression relates to med disease via behaviour: heart disease as consequence of reduced physical acitivity of depression, poor diet or smoking in patients w depression)
- psychosocial factor (like low SES) leads to both med disease & depression, or med disease -> depression (adjustmention disorder)
- converging biology
which biological mechanisms play a role in depression (and somatic comorbidity)? (1+5)
dysregulation in
- immune system (inflammation)
- HPA axis (cortisol)
- autonomic NS (heart rate variability)
- oxidative stress
- accelerated ageing (telomere length, brain age)
how does the HPA axis affect depression & somatic comorbidity? (1->3, 1->6)
HPA axis enables reaction to stress by mobilizing stored energy, suppressing immune function & facilitating many CNS processes (memory, learning)
but when this acitvation becomes chronic -> lots of cortisol -> atrophy of hippocampal cells, reduced neurogenesis , reduced synaptic plasticity, altered monoaminergic signalling
how does the ANS affect depression & somatic comorbidity? (1->2)
depression associated w
- more sympathetic activation (fight or flight) (but could be due to antidepressant meds)
- higher hear rate, lower RSA, shorter PEP, lower heart rate variability
how does the immune system interact w depression & somatic comorbidity? (2)
sickness behaviour
-> loss of appetite, sleepiness, withdrawal from normal social activities, fever, aching joints, and fatigue
-> shifting bodys priority to faciliate recovery
this behaviour’s also seen in depression! cause stress (depression) induces inflammatory signals to the brain (link inflammation & depression is bi directoinal) which makes u exhibit sickness behaviour
what is oxidative stress? (2+1->1)
- normally we have a balance of reactive oxygen species (ROS, important but can be damaging) & antioxidants (which protect against ROS)
- in oxidative stress theres an imbalance which can lead to physiological ageing & disease
how can oxidative stress arise? (2)
- increased ROS due to exposure to toxins/radiation, or due to chronic inflammatory conditions (stress, depression)
- decreased antioxidants due to dietery depletion of vitamins or micronutriens
how can accelerated ageing be related to depression? through what 2 mechanisms?
- ppl w depression tend to have shorter telomeres (can be helped by telomerase)
- DNA methylation leads to higher epigenetic age
how come telomere shortening is accelerated by stress and thus depression? (3)
possibilities
1. depression / stress leaves long lasting “cellular scar”
2. short telomeres are risk factor for depression & stress
3. common cause that lead to shorter telomeres & depression/stress
what are some depression subtypes (2)
depression is very heterogeneous
- melancholic depression (loss of pleasure, lack of mood reactivity, decreased appetite/weight, early morning awakening, excessive guilt, distinct quality of mood, mood worse in morning, psychomotor retardation/agitation)
- atypical depression (mood reactivity, increased appetite/weight, hypersomnia, leaden paralysis, interpersonal rejection sensitivity)
how do biological profiles differ per depression subtype (2)
atypical: more linked to obesity, inflammatory markers, and metabolic abnormalities
melancholic: HPA hyperactivity & higher levels of cortisol
