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PSYCHONEUROIMMUNOLOGY · Understanding the Brain

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  Speaker 1: Well, welcome back to that. We're going to be talking
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  Speaker 1: about the psychoneuromineology. So how psychooneuroimmunology, So it's how it's
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  Speaker 1: the intersection of psychology, neurology, and immunology, and how it
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  Speaker 1: bridges it all together together. You see, the stress activates
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  Speaker 1: the HPA access which we talked about before, and the
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  Speaker 1: sympathetic nervous system leading to ctcholamine release. This creates what
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  Speaker 1: they call it alostatic load, which we'll look at later,
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  Speaker 1: contributing to inflammation, suppressed immunity, and chronic mental health disorders.
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  Speaker 1: The immune system influences mood and cognition through cytokine signaling.
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  Speaker 1: It is bidirectional. So when you look at the nervous system,
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  Speaker 1: the endocrine system, and the immune system, they communicate with
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  Speaker 1: each other. The P and I psychooneuroimmunology from now we'll
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  Speaker 1: call it P and I emphasizes that the brain, indocrine system,
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  Speaker 1: and immune system are in constant conversation. The nervous system
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  Speaker 1: senses a threat and coordinates responses through neurotransmitters and electrical signals.
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  Speaker 1: The endocrine system releases hormones like cord isol, adrenaline, and oxytocin.
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  Speaker 1: Remember those are traveling through the bloodstream. The immune system
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  Speaker 1: responds with cytokines, signaling proteins that can trigger or suppress
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  Speaker 1: inflammation and alter brain function. These systems, though, are not separate.
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  Speaker 1: They use chemical messengers, for example, into Leuken's six IL
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  Speaker 1: six and tumor necrosis factor alpha tn F. Cytokines that
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  Speaker 1: are released by the immune cells can produce The can
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  Speaker 1: cross the blood brain barrier and affect mood, producing sickness
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  Speaker 1: behavior like fatigue, social withdrawal, and anhedonia. Lack of pleasure.
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  Speaker 1: Chord is al secreted during stress affects immune cells, decreasing
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  Speaker 1: inflammation in the short term, but weakening defenses when chronically
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  Speaker 1: elevated and increasing inflammation. Stress begins with perception. When a
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  Speaker 1: threat is detected real or imagine, physical or non physical,
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  Speaker 1: the amygdalis signals the hypothemist to activate the two systems
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  Speaker 1: which we've talked about before. The sympathetic adrenalmdullary system SAM
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  Speaker 1: releases adrenaline or per nephron from the adrenal medullah example,
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  Speaker 1: as a client with generalized anxiety disorder might experience heightened
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  Speaker 1: sympathetic activity, leading to increased heart rate, blood pressure, and breathing.
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  Speaker 1: The fight or flight response is triggered by the threat,
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  Speaker 1: such as it's maybe worrying about a work presentation. The
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  Speaker 1: hypothalmis and peterritory adrenal access the HPA. The HPA the
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  Speaker 1: hypothalmis releases remember CRH, stimulating the ptary gland to release
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  Speaker 1: act which again stimulates the adrenal cortex to release cortisol
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  Speaker 1: and PTSD. Chronic HPA access this regulation can lead to
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  Speaker 1: elevated cortisol levels, mobilizing energy, suppressing inflammation, and altering memory
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  Speaker 1: and emotion circuits. These systems are adaptive in the short term,
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  Speaker 1: but they help you respond quickly to danger, but they
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  Speaker 1: were designed for only short bursts, not the long haul
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  Speaker 1: stress of modern life. Allostatic load the biological cost of
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  Speaker 1: stress is the body's ability to adapt to stress and
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  Speaker 1: maintain stability through chain change. But when chronic stress. When
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  Speaker 1: stress is chronic, are repeated to careers, wear and tear
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  Speaker 1: on the body physiologically and psychologically, and that is the
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  Speaker 1: alostatic load. The physiological effects of alistatic load include elevated
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  Speaker 1: baseline cortisol. A client with major depressed that has ordered
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  Speaker 1: may exhibit elevated baseline cortisol due to prolonged stress from
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  Speaker 1: financial difficulties, leading to hippocampal volume loss, so memory problems
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  Speaker 1: and increased vulnerability to inflammation. Prolonged stress disrupts immune regulation
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  Speaker 1: through three main mechanisms. Immunosuppression chronic cortisol dampens immune cell production.
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  Speaker 1: A client with chronic stress from caregiving might show immunosuppression,
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  Speaker 1: leading to slower wound healing, increase infection risk, and poor
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  Speaker 1: vaccine response, also exacerbating feelings of helplessness, a core belief
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  Speaker 1: and CBT. Pro inflammatory cytokine activation. Stress triggers release of
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  Speaker 1: IL one, il sex, and tn F in the absence
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  Speaker 1: even in the absence of infection and bipolar disorder. Pro
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  Speaker 1: inflammatory cide kinds contribute to chronic inflammation, a factor in
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  Speaker 1: heart disease, diabetes, and mood and stability feedback disruption. Normally,
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  Speaker 1: cortisol shuts off inflammation and chronic stress cell and chronic stress,
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  Speaker 1: though cells down regulate cortisol receptors, blunting the feedback loop.
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  Speaker 1: So a person with chronic pain and stress might experience
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  Speaker 1: persistent inflammation due to down regulated cortisol receptors, which then
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  Speaker 1: worsens anxiety disorders and contributes to a cycle of pain
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  Speaker 1: and emotional distress. Some of the stress and psychological disorders
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  Speaker 1: or depression often features elevated pro inflammatory markers reduced neurogenesis
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  Speaker 1: in the hippocampus, so I climb with depression might have
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  Speaker 1: high IL six levels linked to adonia and memory issues
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  Speaker 1: treatable with CBT and PTSD. A veteran with PTSD might
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  Speaker 1: show amignal hyperactivity during trauma recall, leading to r predifferent
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  Speaker 1: spikes and sleep disturbances, manageable though with exposure therapy. PTSD
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  Speaker 1: has often character by altered cortisol regulation, heightened sympathetic activity,
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  Speaker 1: and amigula hyperactivity and anxiety. It shows no repineferent activity
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  Speaker 1: and reduced parasympathetic tone. A climb with panic disorder in
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  Speaker 1: my experience, neuropenefferent surges during panic attacks alleviated by mindfulness
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  Speaker 1: to restore parasympathetic tone. Finally, bipolar disorder manic states are
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  Speaker 1: associated with reduced sleep, increase inflammatory markers and dopamine hypersensitivity
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  Speaker 1: with reduced sleep, so you might see somebody with bipolar
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  Speaker 1: in omatic phase have elevated inflammatory markers due to sleep
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  Speaker 1: loss are treatable with mood stabilizers. The biological mechanisms of
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  Speaker 1: stress reduction techniques include mindful meditation, which reduces cortisol levels
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  Speaker 1: and lowers blood pressure, and it increases great matter density
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  Speaker 1: in the hippocampus and the prefunnel cortex. So a client
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  Speaker 1: with GAD GAD practicing mindfulness might lower cortisol, reduced anxiety,
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  Speaker 1: and improve cognition. According to studies, aerobic exercise downrange regulates
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  Speaker 1: expression of inflammatory genes as well via the NFkB pathway.
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  Speaker 1: It reduces systemic inflammation and lowers IL six and CRP levels,
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  Speaker 1: So a client with major depressive disorder engaging in aerobic
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  Speaker 1: Wilbeck exercise might increase b the nf RAIN derived neurotrophic factor,
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  Speaker 1: enhancing neuroplasticity. This isn't just the theory. Clients who sleep better,
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  Speaker 1: move more, and reframe their thoughts show measurable biological changes
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  Speaker 1: lower blood pressure, normalized cortisol, and better immunity. On the
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  Speaker 1: E triple P, you look for the connections between stress
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  Speaker 1: physiology and psychological function elaborations on bolded terms, so you
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  Speaker 1: know if you're looking at again the lass static load,
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  Speaker 1: it's the cumulative wear and trry on the body from
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  Speaker 1: chronic stress adaptation. The relevance for the E triple ps
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  Speaker 1: evaluating chronic illness cases, inflammations, immune systems response their injury
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  Speaker 1: or infection connect to mood disorders. Another one at cytokines
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  Speaker 1: for the E triple P link to six must behavior
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  Speaker 1: and depression because it's signaling proteins that mediate inflammation and mood.
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  Speaker 1: Mindfulness is part of evidence based intervention for anxiety. That's
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  Speaker 1: what you need to know for the E triple P
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  Speaker 1: exercise as well. Recommended for depression management. Social collection connection
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  Speaker 1: is address isolation and therapy stress markers of physiological indicators
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  Speaker 1: of stress monitor. For E triple P, it's relevance is
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  Speaker 1: monitor and stress related disorders. Cortisol is a key in
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  Speaker 1: HPA access dysfunction and if you look at cr act
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  Speaker 1: H those are part of the HPA access feedback and
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  Speaker 1: link to stress physiologies. You want to make sure you
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  Speaker 1: keep that in your mind as well as the neurotrophic factor,
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  Speaker 1: the protein supporting neuron growth. It's enhancing depression treatment. So
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  Speaker 1: that's it for now. Let's see if we get you
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  Speaker 1: some questions. Actually in fact, so the first question is
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  Speaker 1: a client with chronic stress report it's persistent fatigue, social withdrawal,
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  Speaker 1: and difficulty concentrating. Which of the following best explains these
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  Speaker 1: symptoms in the context of psychoneermiology, increased IL levels and
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  Speaker 1: two minocrosis crossing the blood brain barrier, reduced cortisol production,
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  Speaker 1: elevated dopamine levels, or activation of the parasympathetic system. If
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  Speaker 1: you said in psychoneurimiology, the correct answer is be chronic
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  Speaker 1: stress can lead to the release of these pro inflammatory
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  Speaker 1: cytokines IL, SEX and TNF. And the next question, a
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  Speaker 1: psychologist is working with a client diagnosed with PTSD who
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  Speaker 1: exhibits hyper arousal and memory flashbacks. Which component of the
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  Speaker 1: stress response pathway is most likely disregulated A the SAM system,
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  Speaker 1: B the HPA axis see the parasympathetic If you said
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  Speaker 1: the HPA is often disregulated leading to altered quartisol regulation,
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  Speaker 1: you got it right. And last question, a client with
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  Speaker 1: generalized anxiety disorder reports frequent panic attacks with increased heart
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  Speaker 1: rate and breathing. Which stress related mechanism is primarily responsible
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  Speaker 1: for these physiological responses A release of oxytocin B, activation
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  Speaker 1: of the SAM system, C down regulation of cortisol or
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  Speaker 1: d increased paya sympathetic. If you said B the SAM
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  Speaker 1: system which releases adrenaline and nora imperdifferent from the adreno mendula,
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  Speaker 1: you are right. That's it for now