WE DISCUSS THE BIOLOGY OF CERTAIN PSYCHIATRIC ISSUES

Episode Transcript

Speaker 1 (00:01):
We welcome back, folks. Today we're going to be looking
at psychological disorders and how biology plays a role in
these disorders. So when we looking at depression, what's linked
to the theory of monamine deficiency and it is a
theory hpa acxsis, hyperactivity and hippocampal atrophy that's associated with depression.

(00:21):
We'll look at schizophrena which involves dopamine over activity as
well another theory lutamate hypofunction of metricular enlargement, anxiety disorders
which show gabutus function, amignual hyperactivation, and bipolar disorder which
features neurotransmitter instability and disrupted circadian rhythms. Oh, we'll also
look at ADHD, which involves dopamine and europineferndus regulation and

(00:43):
underactive prefunal cortex. Every psychological disorder seems to have a
story written in both behavior and biology. And you got
to remember the DSM described in symptoms, that's what it
tends to do. It's really there's just symptomologies. There's no ideologies,

(01:03):
no study of the cause of it, or there is
a study of it, but there's no has of it
in our medical conditions that don't have causes either. So
we're going to look now is look at these disorders
in the brain according to biology and see what's going
on with functional MRIs and then do PET scans. Pharmacological

(01:24):
response patterns, and genetic data all feed into how we
understand and sometimes how we treat mental illness. One of
the first one again is major depressive disorder with the
monamine hypothesis. Hypothesis is an educated guests, so that's not
even a theory. A theory is based on collection of
studies to give the evidence, but also depends on the
quality of these studies determines not how good the quality

(01:46):
of that theory is right now. The mona meane hypothesis,
as some call it, is one of the oldest biological
concepts of depression that holds the deficiencies in serotonin, nor
up an, effron and dopamine contribute to low MOODI andhndonia
and hendonia is a lack of pleasure. Antidepressants, especially SSRIs
and ssn R eyes target these areas and they support

(02:09):
the idea by increasing synaptic availability of these new transmitters,
you would increase the serotonin or the other neurotransmitters. Hence
the person would feel better and balance out or hormonal deficient.
There neurotransmitter deficiencies in these areas, but the response takes weeks,
suggesting downstream neuroplastic effects may also be involved. In addition

(02:31):
to that it can take. It's only effective to about
forty fifty percent of the people who take SSRIs and SNRIs,
so it doesn't seem to be working with everybody in
their heart Studies that showed that not everybody has these deficiencies.
Some people have high levels of serotonin. We're found to
have depression anyway, but we're not going to get too

(02:52):
deep into that, but I just wanted to express that.
So back again to the EIGHTPA access disregulation. Depressed individuals
often show elevated cortisols levels, indicating overactivation of the hypothalmic
pituitary adrenal access. Remember that the fight or flight system
prolong stress response is toxic to the brain, particularly the hippocampus,
which regulates memory and stress feedback, so this causes atrophy

(03:16):
to the hippocampus. Some studies consistently find a reduced hippocampal volume,
in which with chronic depression, the longer the episode, the
greater the reduction. Now it has been shown to reverse
the synchriage. The shrinkridge can be reversed with treatment such
as psychotherapy or ssrise. And it also depends on the
type of depression because you can some people will get

(03:40):
over the depression within six to nine months without any
psychotherapy or medication. So it's interesting to see that because
you don't hear that very often. So when treating depression,
consider both neurochemical and neurotracrine factors. Medications address monamines. Therapy
and lifestyle changes help regulate the stress system, and studies

(04:03):
have shown that the combined treatment is the most effective.
Let's look at another hypothesis, which is the dopamine hypothesis
for schizophrenia, one of the most studied models. This start
theory suggests hyperactivity of dopamine transmission in the mesolimbic pathway.
In this pathways where you have the positive symptoms derived
from hallucinations delusions, while hypo activity in the mesocortical pathway

(04:27):
relates to negative symptoms. This is where they have a
flat affect right, very little emotion, evolition, no will. This
is where you take away things. The negative is a
loss of things and the positives addition to antipsychotics work
primarily by blocking dopamine D two receptors, again going off
the dopamine hypothesis, so there's too much dopamine. Also, there's

(04:51):
things there. There's another one called glutamate dysfunction. Research implicates
glutamate hype o function, so too low levels of glutamate,
particularly at NMDA receptors, and they contribute to both the
cognitive deficits and negative symptoms seen in schizophrenia. Drugs like PCP,
which block NMDA receptors induce schizophrenia like symptoms, supporting this model,

(05:14):
and we're also seeing this now with marijuana. Structural brain
abnormalities as well. MRI studies show enlarged lateral ventricles, cortical thinning,
and reduced gray matter and the prefunnel cortex hippocampus and thaumas.
These structural differences often precede symptom onset and worsen over time.

(05:35):
Genetics and risk schizophrenia is highly heritable, somewhere around seventy
to eighty percent heritability. The gas genomic wide association studies
have identified hundreds of risk loca, especially those involved in
synaptic pruning and immune system functions. Confordance is high in
monozygotic twins. Are monozygotic twins about fifty percent, so antipsychotic

(06:00):
medication targets dopamine, but treatment resistant cases may benefit from
glutamate based interventions and cognitive remediation to protect brain structure
and function. We look at anxiety soorders and we see
GAMBA dysfunction. Gamba is the brains prehentit primary inhibitory neuroor transmitter.

(06:23):
If you remember that in anxiety, gaba's signaling is often underactive,
leading to an overactive fear response. So this is when
benzodiazepines will increase GABBA and produce rapid calming effects. But
remember it's also highly addictive, So the tolerance and dependence
limit for the long term use of benzoiantopenes Amygdala hyperactivity.

(06:46):
This is the central processing part of our brain for
fear and threat is overactive in anxiety disorders, especially PTSD
and generalized anxiety disorder. This hyperactivation is evident in fMRI studies.
It correlates with symptoms severity, hippocampal and prefuntal involvement the
hippocampus which deals with contextual type of memories and pre
funnel cortex regulation of emotion fail to inhibit amgdala over

(07:10):
activity effectively in anxiety. That explains why anxious individuals may
recognize their fear is irrational but still feel it strongly.
They can't seem to control it sometimes. Treatment, of course,
is also SSRIs, which seems to indirectly reduce amgdala activation
over time. CBTs a psychotherapy that's commonly used and highly effective,

(07:35):
which strengths prefuntal regulation via cognitive restructuring and exposure. Another
one that does really well is mindfulness based type of therapies.
Now we'll look at bipolar disorder, and this is neurotransmitter imbalances.
Bi Polar disorder involves cycling dysregulation of dopamine, serotonin, and orapinephrine.

(07:55):
Mania reflects dopamine hyperactivity, while depression involves dopamine depletion. This
sensibility leads to wide mood swings. Circadian rhythm disruption, sleep
and circadian dysregulation are common triggers for manic episodes. Genes
are associated with the body's internal clock. Mood episodes often
followed sleep disruption. Travel across time zones or irregular routines

(08:20):
can also do it. Study show reduced volume in the
prefunnel cortex and the amygdala and ab normal activity in
emotion processing circuits. Functional imaging shows increased activity activation in
the limbic system, the emotional system doing manic states. Mood
stabilizers like we talked about before, like lithium, lamicdol, and

(08:41):
anti convulsions target intracellular signaling pathways. Sleep stabilization and daily
rhythm regulation are critical non pharmacological components, so sleep is
going to be really important for these individuals. And last,
but not least is ADHD. ANYHD is tied to deficits
in dopamine and orepinephrin signaling, especially in the pre funnel cortex.

(09:06):
These neurotransmitters regulate attention, inhibition and working memory. Stimulants like
methyl fenel date that we talked about before, ritalin and
amphetamine like adderall work by increasing their availability, improving focus
and impulse control. Neuroimaging shows reduced activity and volume endorsal
lateral prefunnel cortex, anterior singular cortex, and basal ganglia regions

(09:30):
for executive function. The delayed cortical maturation has also been observed.
There's also a disruption of the default mode network. Children
with ADHD show alter connectivity in the default mode network,
a brain network active during rest and internal thought. For
a regulation of this network may contribute to mind wandering
and distractability. Is this is the area where you're thinking

(09:51):
about yourself and it's an internal thought, especially during rest
or nothing is going on, so when this happens, you
can't focus. Genetics it also plays a role here where
the heritability of ADHD is high seventy to eighty percent.
Genes affecting the dopamine transpitters dapt one and receptors DRD
four and five are strongly implicated. Stimilant medications. Stimulant medications

(10:15):
are still the first line and I can't remember what
it was, but I think it was twenty thirty percent
of ADHD clients don't even get therapy. However, behavioral interventions
parent training and executive functioning, coaching, reinforce prefuntal development, sleep, nutrition,
and structure amplify the treatment effects. So you can see
the benefits of psychotherapy and especially psycho education for the

(10:38):
parents as well as the individual, depending if they're an
adult or a teenager. So the biological models of psychological
disorders are complicated in their layered they're not linear. Each
diagnosis is shaped by several factors. Neurotransmitters, circuits in the brain,
hormonal signals, gene environment interplay. Could be a moots what

(11:01):
seems like a mootswind could be a circums firing. What
feels like worry may begin in chemistry. And when you
treat behavior, you're ignoring the brain. You're engaging it. You're
not ignoring the brain, I'm sorry. When you treat behavior,
you're engaging it. So when you understand the brain, you
can bring more precision, compassion, and impact to your job
as a therapist. So we do see things being manifested

(11:25):
in the biology of these psychological disorders. We see the
neurotransmitters component. We see the structure and function, which is
a neuroscience component. We see a little bit of genetics
in there. We did not see genetics in regards to
anxiety and depression, which have a lower haretability rate compared
to schizophrenia ADHD. We definitely saw some other physiological disruptions

(11:55):
as well. Next time we're going to go switch and
talk to about sleep neurobiology and we'll see how that
affects yes, which is a big part of a lot
of my clients' success and being able to get better sleep.
You'd be surprised how much faster the recovery is. That's
it for now.