Stress Response: SNS and HPA Axis

Stress Response Systems

• The sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis are essential in the body's reaction to stress.
• SNS and HPA work in conjunction to prepare the body for a "fight or flight" response when a threat is perceived.

Sympathetic Nervous System (SNS)

• Activates the adrenal medulla to release adrenaline (epinephrine) and noradrenaline (norepinephrine) into the bloodstream.
• SNS is part of the autonomic nervous system.
• SNS functions in the immediate, short-term response to stress by initiating rapid physiological changes that prepare the body for swift action.
• Increases heart rate to supply more oxygen and nutrients to muscles and vital organs.
• Increases blood pressure as blood vessels constrict to maintain blood flow to the heart and brain.
• Dilates pupils to enhance environmental awareness through improved vision.
• Dilates airways, widening the bronchi in the lungs to increase oxygen intake that helps meet higher metabolic needs.
• Increases glucose release, where the liver provides energy for muscles through increased glucose in the bloodstream.
• Inhibits non-essential functions like digestion and immune reaction to prioritize survival.

Hypothalamic-Pituitary-Adrenal (HPA) Axis

• Contributes to long-term stress response by regulating the body during prolonged stress to maintain homeostasis involving hormone signaling.
• Hypothalamus activation occurs, where the hypothalamus signals the release of corticotropin-releasing hormone (CRH) when the brain identifies stress.
• Pituitary gland stimulation occurs, where CRH leads to the anterior pituitary gland releasing adrenocorticotropic hormone (ACTH) into the bloodstream.
• Adrenal gland response involves ACTH stimulating the adrenal cortex to release cortisol, a key stress hormone.
• Cortisol increases glucose availability by promoting gluconeogenesis in the liver.
• Cortisol has anti-inflammatory effects that temporarily suppress immune responses.
• Cortisol regulates the circadian rhythm and manages long-term energy needs.
• Cortisol supports the body during stress by enhancing alertness and memory.
• Operates through a negative feedback loop, where high cortisol levels reduce CRH and ACTH release, decreasing cortisol production.

SNS and HPA Axis Coordination

• SNS mobilizes energy and redirects resources for quick responses during acute stress, enabling the immediate "fight or flight" reaction.
• SNS is an immediate reaction
• HPA axis manages prolonged or chronic stress and ensures the body meets the increased energy demands, regulating less important functions.
• HPA is a gradual response

Interplay between the SNS and HPA Axis

• SNS Activation can trigger the HPA axis as hormonal changes like cortisol enhance the SNS's reaction to stress.
• Chronic Stress causes the HPA axis to become dysregulated, resulting in persistently high cortisol that then leads to immune suppression, sleep disturbances, and mental health conditions.
• Chronic SNS activation leads to high blood pressure, cardiovascular issues, and gastrointestinal problems.

The Development of Mental Illness

• Chronic stress response significantly impacts the brain and body by dysregulating stress hormones, like cortisol and adrenaline, which can be damaging when persistently elevated.

Impacts of Chronic Cortisol Release on Brain Regions

• Cortisol as a stress hormone regulates energy and the immune system but becomes harmful to areas involved in mood regulation, memory, and decision-making when persistently elevated.

Hippocampus

• Critical for memory formation and emotional regulation
• Shrinks with Chronic exposure to high cortisol, impairing memory and learning, and raising vulnerability to depression and anxiety.
• Cortisol inhibits the production of brain-derived neurotrophic factor (BDNF) which impairs neurogenesis.

Prefrontal cortex (PFC)

• Involved with higher cognitive functions like planning, decision-making, and emotional regulation.
• Impaired PFC functioning through chronic stress reduces emotional management and effective decision-making, which causes impulse control issues and heightened vulnerability to depression and anxiety.
• Mechanism: Chronic cortisol release disrupts the connectivity between the PFC and other brain regions, disrupting emotional responses and coping mechanisms.

Amygdala

• Responsible for processing emotions, especially fear.
• Increased Amygdala activation due to chronic stress leads to hyper-responsiveness to threats, heightened anxiety, paranoia, and emotional dysregulation.
• Contributes to the development of anxiety disorders (PTSD) and panic attacks.

Dysregulation of the HPA Axis

• HPA axis is responsible for controlling cortisol levels and other aspects of the stress response
• Dysregulation occurs with chronic stress in individuals lacking response to feedback mechanisms that regulate the axis.

Consequences of HPA Axis Dysregulation

• Hyperactivity includes an overactive HPA axis which then causes consistently elevated cortisol, commonly seen in depression.
• Hypoactivity can cause an underactive HPA axis, resulting in an inadequate cortisol response; associated with PTSD.
• HPA Axis dysregulation creates a feedback loop, increasing susceptibility to mental health disorders.

Neuroinflammation and the Immune System

• Linked particularly to depression, inflammation causes elevated pro-inflammatory cytokines that causes symptoms of depressive disorders.
• Chronic stress creates increased inflammation that impacts the brain and body that contributes to mental health disorders.
• Inflammation has been implicated in the development of several mental health disorders,

Cytokines and Depression

• Inflammation leads to elevated levels of pro-inflammatory cytokines, disrupting neurotransmitter systems, and causing symptoms of depressive disorders.

Neuroinflammation and Anxiety

• Neuroinflammation impacts the hippocampus and amygdala, by increasing emotional stress responses that lead to anxiety, panic, and PTSD.

Altered Neurotransmitter Systems

• Disruptions are central to many mental health conditions
• Chronic stress leads to imbalances of serotonin, dopamine, and norepinephrine that then affect mood regulation.

Serotonin

• Reduces levels or impairs function, which can lead to depression, anxiety, and OCD.
• Critical for emotional stability that when deficient, can impact hopelessness, mood swings, and irritability.

Dopamine

• Dysfunction leads to low motivation (anhedonia) that is a hallmark of depression
• Involved in reward processing

Norepinephrine

• High levels can lead to increased arousal, hypervigilance, and heightened anxiety.
• Dysregulation is often found in PTSD and generalized anxiety disorder (GAD).

Sleep Disturbances and Mental Health

• Leads to sleep disturbances that creates a cycle of stress and can exacerbate mental health issues.

Cognitive Impairment from Sleep Issues

• Lack of restorative sleep impairs functions like attention, memory, and emotional regulation that increases vulnerability to anxiety and depression.

Emotional Dysregulation from Sleep Issues

• Sleep deprivation impacts the amygdala, making it more reactive and worsening mood disorders.

Impact on Coping Mechanisms and Behavior

• Chronic stress weakens effective coping mechanisms for mental issues
• Can cause avoidance of situations which reinforces depression
• Can cause substance abuse as self-medication

Chronic Activation

• Alters brain structures, dysregulating neurotransmitter systems, promoting neuroinflammation, and increasing vulnerability to mood disorders.

Schizophrenia

• It is a multifaceted mental disorder that affects thought, emotion, and behavior with a mix of diverse symptoms
• Can can be described as positive, negative, and cognitive

Positive Symptoms

• Hallucinations: false perceptions that occur without an external stimulus.
• Delusions: false beliefs
• Disorganized Thinking (Speech): thoughts that are fragmented and illogical.
• Disorganized or Abnormal Motor Behavior: includes a range of behaviors that are disruptive or bizarre

Negative Symptoms

• Represent the absence of normal functioning that is very debilitating affecting everyday life.
• Avolition: lack of motivation.
• Alogia: reduces speech.
• Anhedonia: diminished ability to experience pleasure.
• Flat Affect: reduced emotional expression.
• Social Withdrawal: lack of interest in interacting with others

Cognitive Symptoms

• Affects impairments in memory, attention that is essential for day to day task.
• Impaired Attention: difficulty focusing
• Working Memory Deficits: problems with short-term memory.
• Impaired executive functioning: high level cognitive problems.
• Slow processing speed: effects interactions.
• Impaired insight: difficulty recognizing

Treatment

• Positive symptoms are typically treated with antipsychotics medications
• Negative symptoms need psychosocial interventions
• Cognitive symptoms need cognitive remediation therapy

Alterations

• It is a complex disorder that alters neurotransmitter signaling in the neuro anatomy of the brain.
• Dopamine hypothesis suggestes Dopamine dysregulation plays a role Glutomate, serotonin and GABA, also add to the disorder.

Dopamine deregulation

• Excessive dopamine actives certain areas, while a diffeciency others contribute to other symptoms.
  Mesolimbic pathway: overstimulates to positive symptoms.
• Mesocortical pathway: reduced dopamine actions, causing cognitive deficits.
• Nigrostriatal pathway: motor control
• Tuberoinfundibular pathway: regulates prolactin release.

Glutamate disfunction

• Is a primary excitatory neurotransmiter
• Hypofuntion if NMDA contributes to cognitive and negative symptoms
• NMDA receptor helps with cognitive function and synaptic plasticity

Serotonin dysregulation

• Is more complex, it affects both positive and negative symptoms
• Serotonin helps affect dopamine release

GABA

• IS PRIMARY INHIBOTORY
• helps balance excitatory
• Reduced leads to disfunction

Brain Abnormalities

• Changes the structure
• Enlarged Ventricles: most consistant
• Gray Matter Loss: reduces volume of gray matter
• Hippocampus effects cognitive and negative symptoms
• Impaired Connectivity: disrupts the brain networks

Mood disorders

• Genetic predisposition of multiple genes affecting neurotransmitters
• Genetic variations that affect serotonin has an increase in the risk

Bipolar

• Has a stronger genetic component

Major Depressions

• Mood= Persistent depressed mood
• Cognition= inpaired thinking
• Physical= fatique

Risk Factors for Substance Use

• Complex conditions that arise from three factors
• Development for multiple risk factors,
• Greater likelihood of development of said factors

Genetic History

• Having a first degree increases risks.
• Variants that predispose vulnerability to adiction
• Low base line to dopamine compensate
• Adaptaion can cause tollerance

Mental Health

• The substances can help self medicate symptoms
• Lack of control

Factors with Substance Risk

• Trauma
• Poor coping
• Influence
• Stressors
• High impulsivity

SUD and Brain function

• Affects brain structure
• Leads to neuroadaptaions
• Is related to reward
• HPA is active
• Amygdala overactive
• Impairs cognition
• Alters behaviors

Manifestation of substance use disorders (SUDs)

• compulsive use
• craving
• tolarence
• With-drawls
• Reltapse
• Impaired judgment

Personality Disorder

• Individuals often use food as a way to cope with negative emotions.
• It is also linked to a body dismorphia and low self esteme

Treatment

• There is a need to have 4 types of therapy
• Cognative
• Nutrituanal

Factors That are a Risk: In Anorexia

• Perfectionism
• Bullying
• Trauma

Factors That are a Risk: In Blimia

• A history of deiting
• Influence of peers
• Social media