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Speaker 1: Well, welcome back to that. We're going to be talking

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about the psychoneuromineology. So how psychooneuroimmunology, So it's how it's

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the intersection of psychology, neurology, and immunology, and how it

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bridges it all together together. You see, the stress activates

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the HPA access which we talked about before, and the

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sympathetic nervous system leading to ctcholamine release. This creates what

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they call it alostatic load, which we'll look at later,

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contributing to inflammation, suppressed immunity, and chronic mental health disorders.

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The immune system influences mood and cognition through cytokine signaling.

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It is bidirectional. So when you look at the nervous system,

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the endocrine system, and the immune system, they communicate with

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each other. The P and I psychooneuroimmunology from now we'll

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call it P and I emphasizes that the brain, indocrine system,

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and immune system are in constant conversation. The nervous system

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senses a threat and coordinates responses through neurotransmitters and electrical signals.

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The endocrine system releases hormones like cord isol, adrenaline, and oxytocin.

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Remember those are traveling through the bloodstream. The immune system

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responds with cytokines, signaling proteins that can trigger or suppress

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inflammation and alter brain function. These systems, though, are not separate.

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They use chemical messengers, for example, into Leuken's six IL

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six and tumor necrosis factor alpha tn F. Cytokines that

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are released by the immune cells can produce The can

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cross the blood brain barrier and affect mood, producing sickness

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behavior like fatigue, social withdrawal, and anhedonia. Lack of pleasure.

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Chord is al secreted during stress affects immune cells, decreasing

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inflammation in the short term, but weakening defenses when chronically

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elevated and increasing inflammation. Stress begins with perception. When a

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threat is detected real or imagine, physical or non physical,

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the amygdalis signals the hypothemist to activate the two systems

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which we've talked about before. The sympathetic adrenalmdullary system SAM

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releases adrenaline or per nephron from the adrenal medullah example,

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as a client with generalized anxiety disorder might experience heightened

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sympathetic activity, leading to increased heart rate, blood pressure, and breathing.

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The fight or flight response is triggered by the threat,

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such as it's maybe worrying about a work presentation. The

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hypothalmis and peterritory adrenal access the HPA. The HPA the

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hypothalmis releases remember CRH, stimulating the ptary gland to release

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act which again stimulates the adrenal cortex to release cortisol

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and PTSD. Chronic HPA access this regulation can lead to

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elevated cortisol levels, mobilizing energy, suppressing inflammation, and altering memory

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and emotion circuits. These systems are adaptive in the short term,

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but they help you respond quickly to danger, but they

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were designed for only short bursts, not the long haul

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stress of modern life. Allostatic load the biological cost of

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stress is the body's ability to adapt to stress and

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maintain stability through chain change. But when chronic stress. When

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stress is chronic, are repeated to careers, wear and tear

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on the body physiologically and psychologically, and that is the

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alostatic load. The physiological effects of alistatic load include elevated

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baseline cortisol. A client with major depressed that has ordered

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may exhibit elevated baseline cortisol due to prolonged stress from

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financial difficulties, leading to hippocampal volume loss, so memory problems

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and increased vulnerability to inflammation. Prolonged stress disrupts immune regulation

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through three main mechanisms. Immunosuppression chronic cortisol dampens immune cell production.

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A client with chronic stress from caregiving might show immunosuppression,

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leading to slower wound healing, increase infection risk, and poor

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vaccine response, also exacerbating feelings of helplessness, a core belief

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and CBT. Pro inflammatory cytokine activation. Stress triggers release of

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IL one, il sex, and tn F in the absence

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even in the absence of infection and bipolar disorder. Pro

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inflammatory cide kinds contribute to chronic inflammation, a factor in

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heart disease, diabetes, and mood and stability feedback disruption. Normally,

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cortisol shuts off inflammation and chronic stress cell and chronic stress,

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though cells down regulate cortisol receptors, blunting the feedback loop.

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So a person with chronic pain and stress might experience

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persistent inflammation due to down regulated cortisol receptors, which then

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worsens anxiety disorders and contributes to a cycle of pain

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and emotional distress. Some of the stress and psychological disorders

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or depression often features elevated pro inflammatory markers reduced neurogenesis

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in the hippocampus, so I climb with depression might have

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high IL six levels linked to adonia and memory issues

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treatable with CBT and PTSD. A veteran with PTSD might

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show amignal hyperactivity during trauma recall, leading to r predifferent

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spikes and sleep disturbances, manageable though with exposure therapy. PTSD

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has often character by altered cortisol regulation, heightened sympathetic activity,

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and amigula hyperactivity and anxiety. It shows no repineferent activity

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and reduced parasympathetic tone. A climb with panic disorder in

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my experience, neuropenefferent surges during panic attacks alleviated by mindfulness

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to restore parasympathetic tone. Finally, bipolar disorder manic states are

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associated with reduced sleep, increase inflammatory markers and dopamine hypersensitivity

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with reduced sleep, so you might see somebody with bipolar

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in omatic phase have elevated inflammatory markers due to sleep

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loss are treatable with mood stabilizers. The biological mechanisms of

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stress reduction techniques include mindful meditation, which reduces cortisol levels

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and lowers blood pressure, and it increases great matter density

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in the hippocampus and the prefunnel cortex. So a client

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with GAD GAD practicing mindfulness might lower cortisol, reduced anxiety,

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and improve cognition. According to studies, aerobic exercise downrange regulates

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expression of inflammatory genes as well via the NFkB pathway.

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It reduces systemic inflammation and lowers IL six and CRP levels,

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So a client with major depressive disorder engaging in aerobic

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Wilbeck exercise might increase b the nf RAIN derived neurotrophic factor,

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enhancing neuroplasticity. This isn't just the theory. Clients who sleep better,

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move more, and reframe their thoughts show measurable biological changes

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lower blood pressure, normalized cortisol, and better immunity. On the

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E triple P, you look for the connections between stress

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physiology and psychological function elaborations on bolded terms, so you

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know if you're looking at again the lass static load,

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it's the cumulative wear and trry on the body from

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chronic stress adaptation. The relevance for the E triple ps

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evaluating chronic illness cases, inflammations, immune systems response their injury

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or infection connect to mood disorders. Another one at cytokines

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for the E triple P link to six must behavior

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and depression because it's signaling proteins that mediate inflammation and mood.

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Mindfulness is part of evidence based intervention for anxiety. That's

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what you need to know for the E triple P

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exercise as well. Recommended for depression management. Social collection connection

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is address isolation and therapy stress markers of physiological indicators

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of stress monitor. For E triple P, it's relevance is

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monitor and stress related disorders. Cortisol is a key in

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HPA access dysfunction and if you look at cr act

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H those are part of the HPA access feedback and

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link to stress physiologies. You want to make sure you

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keep that in your mind as well as the neurotrophic factor,

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the protein supporting neuron growth. It's enhancing depression treatment. So

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that's it for now. Let's see if we get you

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some questions. Actually in fact, so the first question is

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a client with chronic stress report it's persistent fatigue, social withdrawal,

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and difficulty concentrating. Which of the following best explains these

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symptoms in the context of psychoneermiology, increased IL levels and

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two minocrosis crossing the blood brain barrier, reduced cortisol production,

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elevated dopamine levels, or activation of the parasympathetic system. If

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you said in psychoneurimiology, the correct answer is be chronic

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stress can lead to the release of these pro inflammatory

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cytokines IL, SEX and TNF. And the next question, a

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psychologist is working with a client diagnosed with PTSD who

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exhibits hyper arousal and memory flashbacks. Which component of the

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stress response pathway is most likely disregulated A the SAM system,

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B the HPA axis see the parasympathetic If you said

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the HPA is often disregulated leading to altered quartisol regulation,

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you got it right. And last question, a client with

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generalized anxiety disorder reports frequent panic attacks with increased heart

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rate and breathing. Which stress related mechanism is primarily responsible

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for these physiological responses A release of oxytocin B, activation

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of the SAM system, C down regulation of cortisol or

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d increased paya sympathetic. If you said B the SAM

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system which releases adrenaline and nora imperdifferent from the adreno mendula,

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you are right. That's it for now