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Summary Exam 2 Current Topics: Stress in Health and Disease UvA Year 3
- Instelling
- Universiteit Van Amsterdam (UvA)
Summary of Current Topics: Stress in Health and Disease Exam 2
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W1.1ARTICLE BY PENNINX (2016) – DEPRESSION AND CARDIOVASCULAR
DISEASE: EPIDEMIOLOGICAL EVIDENCE ON THEIR LINKING MECHANISMS
The article investigates causal mediating
mechanisms of depression and cardiovascular
disease (CVD)
Residual confounding hypothesis: Even after
adjusting for known factors like age, gender,
socioeconomic status and baseline health
conditions, there may still be inadequately
accounted-for variables that influence the
relationship between depression and CVD
Unhealthy lifestyle behaviours → Depression is
linked to higher rates of smoking, alcohol
consumption, poor diet, physical inactivity and less
adherence to medical treatments → Meta-analyses show that even after adjusting for
unhealthy behaviours, the risk remains high, suggesting that unhealthy behaviours do not fully
explain the link between depression and cardiovascular problems
Biological dysregulation:
1. Autonomic dysregulation
- Polyvagal theory: Depression is hypothesised to involve more sympathetic and
less parasympathetic activation because depression involves reduced social
engagement and a less flexible behavioural response to environmental change,
lowering vagal activity (= the functioning of the vagus nerve, the main
component of the parasympathetic nervous system)
- Heart rate variability (HRV): Reflects an individual’s capacity for
parasympathetic inhibition of autonomic arousal – Heart rate consistency is a
sign of stress; heart rate variability is a sign of health → Many studies have
found that depressed individuals have significantly reduced HRV, but some
studies found no consistent differences in HRV between depressed and non-
depressed individuals, suggesting that depression’s impact on autonomic
regulation may vary based on individual characteristics and stress levels
- Tricyclic antidepressants are shown to reduce HRV, contributing to a higher
cardiovascular risk profile
2. HPA-axis dysregulation
- Hyperactivity of the HPA-axis may lead to alterations of the mineralocorticoid
and glucocorticoid receptors, resulting in atrophy of hippocampal cells,
reduced neurogenesis, reduced synaptic plasticity and altered monoaminergic
signalling, all of which may lead to a depressive state
- Salivary measures are used to assess HPA-axis activity → Depressed
individuals have increased cortisol levels, particularly in the morning
- An increased cortisol awakening response has been found in both currently and
previously depressed individuals, as well as in non-depressed offspring of
, depressed patients, suggesting that HPA-axis hyperactivity may be a genetic
vulnerability marker or endophenotype rather than a temporary state
3. Metabolic dysregulation
- Metabolic syndrome: A clustering of risk factors including abdominal obesity,
elevated blood glucose and high blood pressure, which indicates a preclinical
state for CVD and diabetes → Several studies indicate a bidirectional
association between depression and metabolic syndrome
- Possible mechanisms linking metabolic dysregulation and depression:
- Inflammation → White adipose tissue, particularly abdominal fat,
releases inflammatory cytokines and hormones like leptin, which can
affect brain structure and function
- Cerebrovascular damage → Vascular depression hypothesis: Suggests
that vascular damage can lead to depression, especially in older adults
- Shared pathways → There are interconnections between depression and
metabolic dysregulation, particularly inflammation
4. Immuno-inflammatory dysregulation
- Meta-analyses have found elevated levels of inflammatory markers in drug-
naïve depressed individuals – Chronic, low-grade inflammation has been
linked to higher risks of CVD
- The relationship between depression and inflammation is bidirectional:
1. Depression can lead to inflammation through inactivity and unhealthy
dietary choices, which can contribute to weight gain + Depression
increases inflammation by turning tryptophan into kynurenine instead
of producing serotonin, resulting in less serotonin, worsening both
depression and inflammation
2. When the body experiences inflammation, it releases pro-inflammatory
cytokines (i.e. IL-6 and TNF-α), which enter the brain either directly,
by crossing the blood-brain barrier, or indirectly, by activating brain
immune cells called microglia – Once inside the brain, cytokines
reduce neurogenesis, particularly in areas that regulate mood, like the
hippocampus
Two distinct depression subtypes:
1. Melancholic depression: Characterised by appetite- and weight loss, insomnia and
early morning awakening – Pathophysiological dysfunction is mostly hyperactivity of
the HPA-axis in this subtype – 46% of cases
2. Atypical depression: Marked by increased appetite, weight gain and leaden paralysis –
Pathophysiological dysfunction is mostly elevated levels of inflammatory markers and
metabolic abnormalities such as higher BMI and abdominal obesity – 25% of cases
Iatrogenic effects linking depression and CVD → Antidepressants may have subtle effects on
cardiovascular physiology, but there is insufficient evidence to definitively link their use to
increased CVD risk
Third factor explanations for the link between depression and CVD:
, 1. Childhood maltreatment → Emotional, physical or sexual abuse is a strong risk factor
for both depression and CVD
2. Traits such as neuroticism, introversion and Type D personality are associated with
both depression and CVD
3. Genetic pleiotropy: The phenomenon where shared genetic risk factors predispose
individuals to seemingly unrelated traits or conditions
LECTURE W1.1
Brain differences between depressed and non-depressed individuals:
- Structural: Lowered volume of the hippocampus, amygdala and PFC
- Connectivity: Higher activation of the default mode network, and lower activation for
the salience and central executive networks
- Functional: Stronger response to negative stimuli and a lower response to positive
stimuli in the amygdala, striatum and PFC
Explanations for the comorbidity of depression and somatic disease:
1. Coincidence
2. Iatrogenic factors (E.g.: antidepressant use)
3. Behavioural factors (E.g.: unhealthy lifestyle behaviours)
4. Psychosocial factors
- A medical disease leading to depression when resilience is low (E.g.:
adjustment disorder)
- Social factors leading to both depression and a somatic disease (E.g.:
childhood trauma)
5. Converging biology
DEPRESSION-RELATED BIOLOGICAL DYSREGULATIONS
HPA-axis:
- Cortisol awakening response: A natural spike in cortisol levels where they rise rapidly
within 20 to 30 minutes after awakening, after which they gradually decrease
throughout the day – Considered a normal part of the body’s circadian rhythm and
plays a role in preparing the body for the day ahead by increasing alertness and energy
levels → Increased in people with current or previous depression
Autonomic nervous system:
- Heart rate → Higher heart rate equals more sympathetic activity
- Respiratory sinus arrythmia (RSA): Variation in heart rate during the breathing cycle
where it increases during inhalation and decreases during exhalation → Lower RSA
equals more sympathetic activity
- Pre-ejection period (PEP): A measurement of how long it takes for the heart to
generate enough pressure to open the valve and start pumping blood → Shorter PEP
equals more sympathetic activity
- Heart rate variability → Heart rate consistency is a sign of stress; heart rate variability
is a sign of health → Lower heart rate variability in people with depression may be
partially explained by antidepressant use
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