PSYCHONEUROIMMUNOLOGY

Episode Transcript

Speaker 1 (00:00):
Well, welcome back to that. We're going to be talking
about the psychoneuromineology. So how psychooneuroimmunology, So it's how it's
the intersection of psychology, neurology, and immunology, and how it
bridges it all together together. You see, the stress activates
the HPA access which we talked about before, and the
sympathetic nervous system leading to ctcholamine release. This creates what

(00:24):
they call it alostatic load, which we'll look at later,
contributing to inflammation, suppressed immunity, and chronic mental health disorders.
The immune system influences mood and cognition through cytokine signaling.
It is bidirectional. So when you look at the nervous system,
the endocrine system, and the immune system, they communicate with
each other. The P and I psychooneuroimmunology from now we'll

(00:49):
call it P and I emphasizes that the brain, indocrine system,
and immune system are in constant conversation. The nervous system
senses a threat and coordinates responses through neurotransmitters and electrical signals.
The endocrine system releases hormones like cord isol, adrenaline, and oxytocin.
Remember those are traveling through the bloodstream. The immune system
responds with cytokines, signaling proteins that can trigger or suppress

(01:10):
inflammation and alter brain function. These systems, though, are not separate.
They use chemical messengers, for example, into Leuken's six IL
six and tumor necrosis factor alpha tn F. Cytokines that
are released by the immune cells can produce The can
cross the blood brain barrier and affect mood, producing sickness
behavior like fatigue, social withdrawal, and anhedonia. Lack of pleasure.

(01:33):
Chord is al secreted during stress affects immune cells, decreasing
inflammation in the short term, but weakening defenses when chronically
elevated and increasing inflammation. Stress begins with perception. When a
threat is detected real or imagine, physical or non physical,
the amygdalis signals the hypothemist to activate the two systems
which we've talked about before. The sympathetic adrenalmdullary system SAM

(02:00):
releases adrenaline or per nephron from the adrenal medullah example,
as a client with generalized anxiety disorder might experience heightened
sympathetic activity, leading to increased heart rate, blood pressure, and breathing.
The fight or flight response is triggered by the threat,
such as it's maybe worrying about a work presentation. The
hypothalmis and peterritory adrenal access the HPA. The HPA the

(02:22):
hypothalmis releases remember CRH, stimulating the ptary gland to release
act which again stimulates the adrenal cortex to release cortisol
and PTSD. Chronic HPA access this regulation can lead to
elevated cortisol levels, mobilizing energy, suppressing inflammation, and altering memory
and emotion circuits. These systems are adaptive in the short term,

(02:46):
but they help you respond quickly to danger, but they
were designed for only short bursts, not the long haul
stress of modern life. Allostatic load the biological cost of
stress is the body's ability to adapt to stress and
maintain stability through chain change. But when chronic stress. When
stress is chronic, are repeated to careers, wear and tear
on the body physiologically and psychologically, and that is the

(03:07):
alostatic load. The physiological effects of alistatic load include elevated
baseline cortisol. A client with major depressed that has ordered
may exhibit elevated baseline cortisol due to prolonged stress from
financial difficulties, leading to hippocampal volume loss, so memory problems
and increased vulnerability to inflammation. Prolonged stress disrupts immune regulation

(03:28):
through three main mechanisms. Immunosuppression chronic cortisol dampens immune cell production.
A client with chronic stress from caregiving might show immunosuppression,
leading to slower wound healing, increase infection risk, and poor
vaccine response, also exacerbating feelings of helplessness, a core belief
and CBT. Pro inflammatory cytokine activation. Stress triggers release of

(03:51):
IL one, il sex, and tn F in the absence
even in the absence of infection and bipolar disorder. Pro
inflammatory cide kinds contribute to chronic inflammation, a factor in
heart disease, diabetes, and mood and stability feedback disruption. Normally,
cortisol shuts off inflammation and chronic stress cell and chronic stress,

(04:12):
though cells down regulate cortisol receptors, blunting the feedback loop.
So a person with chronic pain and stress might experience
persistent inflammation due to down regulated cortisol receptors, which then
worsens anxiety disorders and contributes to a cycle of pain
and emotional distress. Some of the stress and psychological disorders

(04:32):
or depression often features elevated pro inflammatory markers reduced neurogenesis
in the hippocampus, so I climb with depression might have
high IL six levels linked to adonia and memory issues
treatable with CBT and PTSD. A veteran with PTSD might
show amignal hyperactivity during trauma recall, leading to r predifferent

(04:54):
spikes and sleep disturbances, manageable though with exposure therapy. PTSD
has often character by altered cortisol regulation, heightened sympathetic activity,
and amigula hyperactivity and anxiety. It shows no repineferent activity
and reduced parasympathetic tone. A climb with panic disorder in
my experience, neuropenefferent surges during panic attacks alleviated by mindfulness

(05:16):
to restore parasympathetic tone. Finally, bipolar disorder manic states are
associated with reduced sleep, increase inflammatory markers and dopamine hypersensitivity
with reduced sleep, so you might see somebody with bipolar
in omatic phase have elevated inflammatory markers due to sleep
loss are treatable with mood stabilizers. The biological mechanisms of

(05:39):
stress reduction techniques include mindful meditation, which reduces cortisol levels
and lowers blood pressure, and it increases great matter density
in the hippocampus and the prefunnel cortex. So a client
with GAD GAD practicing mindfulness might lower cortisol, reduced anxiety,
and improve cognition. According to studies, aerobic exercise downrange regulates

(06:00):
expression of inflammatory genes as well via the NFkB pathway.
It reduces systemic inflammation and lowers IL six and CRP levels,
So a client with major depressive disorder engaging in aerobic
Wilbeck exercise might increase b the nf RAIN derived neurotrophic factor,
enhancing neuroplasticity. This isn't just the theory. Clients who sleep better,

(06:22):
move more, and reframe their thoughts show measurable biological changes
lower blood pressure, normalized cortisol, and better immunity. On the
E triple P, you look for the connections between stress
physiology and psychological function elaborations on bolded terms, so you
know if you're looking at again the lass static load,
it's the cumulative wear and trry on the body from
chronic stress adaptation. The relevance for the E triple ps

(06:45):
evaluating chronic illness cases, inflammations, immune systems response their injury
or infection connect to mood disorders. Another one at cytokines
for the E triple P link to six must behavior
and depression because it's signaling proteins that mediate inflammation and mood.
Mindfulness is part of evidence based intervention for anxiety. That's

(07:08):
what you need to know for the E triple P
exercise as well. Recommended for depression management. Social collection connection
is address isolation and therapy stress markers of physiological indicators
of stress monitor. For E triple P, it's relevance is
monitor and stress related disorders. Cortisol is a key in
HPA access dysfunction and if you look at cr act

(07:34):
H those are part of the HPA access feedback and
link to stress physiologies. You want to make sure you
keep that in your mind as well as the neurotrophic factor,
the protein supporting neuron growth. It's enhancing depression treatment. So
that's it for now. Let's see if we get you
some questions. Actually in fact, so the first question is

(07:57):
a client with chronic stress report it's persistent fatigue, social withdrawal,
and difficulty concentrating. Which of the following best explains these
symptoms in the context of psychoneermiology, increased IL levels and
two minocrosis crossing the blood brain barrier, reduced cortisol production,
elevated dopamine levels, or activation of the parasympathetic system. If

(08:21):
you said in psychoneurimiology, the correct answer is be chronic
stress can lead to the release of these pro inflammatory
cytokines IL, SEX and TNF. And the next question, a
psychologist is working with a client diagnosed with PTSD who
exhibits hyper arousal and memory flashbacks. Which component of the
stress response pathway is most likely disregulated A the SAM system,

(08:45):
B the HPA axis see the parasympathetic If you said
the HPA is often disregulated leading to altered quartisol regulation,
you got it right. And last question, a client with
generalized anxiety disorder reports frequent panic attacks with increased heart
rate and breathing. Which stress related mechanism is primarily responsible

(09:09):
for these physiological responses A release of oxytocin B, activation
of the SAM system, C down regulation of cortisol or
d increased paya sympathetic. If you said B the SAM
system which releases adrenaline and nora imperdifferent from the adreno mendula,
you are right. That's it for now