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WE DISCUSS THE BIOLOGY OF CERTAIN PSYCHIATRIC ISSUES · Understanding the Brain

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  Speaker 1: We welcome back, folks. Today we're going to be looking
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  Speaker 1: at psychological disorders and how biology plays a role in
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  Speaker 1: these disorders. So when we looking at depression, what's linked
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  Speaker 1: to the theory of monamine deficiency and it is a
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  Speaker 1: theory hpa acxsis, hyperactivity and hippocampal atrophy that's associated with depression.
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  Speaker 1: We'll look at schizophrena which involves dopamine over activity as
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  Speaker 1: well another theory lutamate hypofunction of metricular enlargement, anxiety disorders
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  Speaker 1: which show gabutus function, amignual hyperactivation, and bipolar disorder which
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  Speaker 1: features neurotransmitter instability and disrupted circadian rhythms. Oh, we'll also
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  Speaker 1: look at ADHD, which involves dopamine and europineferndus regulation and
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  Speaker 1: underactive prefunal cortex. Every psychological disorder seems to have a
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  Speaker 1: story written in both behavior and biology. And you got
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  Speaker 1: to remember the DSM described in symptoms, that's what it
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  Speaker 1: tends to do. It's really there's just symptomologies. There's no ideologies,
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  Speaker 1: no study of the cause of it, or there is
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  Speaker 1: a study of it, but there's no has of it
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  Speaker 1: in our medical conditions that don't have causes either. So
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  Speaker 1: we're going to look now is look at these disorders
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  Speaker 1: in the brain according to biology and see what's going
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  Speaker 1: on with functional MRIs and then do PET scans. Pharmacological
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  Speaker 1: response patterns, and genetic data all feed into how we
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  Speaker 1: understand and sometimes how we treat mental illness. One of
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  Speaker 1: the first one again is major depressive disorder with the
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  Speaker 1: monamine hypothesis. Hypothesis is an educated guests, so that's not
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  Speaker 1: even a theory. A theory is based on collection of
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  Speaker 1: studies to give the evidence, but also depends on the
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  Speaker 1: quality of these studies determines not how good the quality
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  Speaker 1: of that theory is right now. The mona meane hypothesis,
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  Speaker 1: as some call it, is one of the oldest biological
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  Speaker 1: concepts of depression that holds the deficiencies in serotonin, nor
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  Speaker 1: up an, effron and dopamine contribute to low MOODI andhndonia
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  Speaker 1: and hendonia is a lack of pleasure. Antidepressants, especially SSRIs
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  Speaker 1: and ssn R eyes target these areas and they support
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  Speaker 1: the idea by increasing synaptic availability of these new transmitters,
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  Speaker 1: you would increase the serotonin or the other neurotransmitters. Hence
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  Speaker 1: the person would feel better and balance out or hormonal deficient.
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  Speaker 1: There neurotransmitter deficiencies in these areas, but the response takes weeks,
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  Speaker 1: suggesting downstream neuroplastic effects may also be involved. In addition
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  Speaker 1: to that it can take. It's only effective to about
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  Speaker 1: forty fifty percent of the people who take SSRIs and SNRIs,
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  Speaker 1: so it doesn't seem to be working with everybody in
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  Speaker 1: their heart Studies that showed that not everybody has these deficiencies.
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  Speaker 1: Some people have high levels of serotonin. We're found to
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  Speaker 1: have depression anyway, but we're not going to get too
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  Speaker 1: deep into that, but I just wanted to express that.
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  Speaker 1: So back again to the EIGHTPA access disregulation. Depressed individuals
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  Speaker 1: often show elevated cortisols levels, indicating overactivation of the hypothalmic
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  Speaker 1: pituitary adrenal access. Remember that the fight or flight system
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  Speaker 1: prolong stress response is toxic to the brain, particularly the hippocampus,
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  Speaker 1: which regulates memory and stress feedback, so this causes atrophy
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  Speaker 1: to the hippocampus. Some studies consistently find a reduced hippocampal volume,
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  Speaker 1: in which with chronic depression, the longer the episode, the
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  Speaker 1: greater the reduction. Now it has been shown to reverse
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  Speaker 1: the synchriage. The shrinkridge can be reversed with treatment such
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  Speaker 1: as psychotherapy or ssrise. And it also depends on the
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  Speaker 1: type of depression because you can some people will get
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  Speaker 1: over the depression within six to nine months without any
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  Speaker 1: psychotherapy or medication. So it's interesting to see that because
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  Speaker 1: you don't hear that very often. So when treating depression,
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  Speaker 1: consider both neurochemical and neurotracrine factors. Medications address monamines. Therapy
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  Speaker 1: and lifestyle changes help regulate the stress system, and studies
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  Speaker 1: have shown that the combined treatment is the most effective.
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  Speaker 1: Let's look at another hypothesis, which is the dopamine hypothesis
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  Speaker 1: for schizophrenia, one of the most studied models. This start
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  Speaker 1: theory suggests hyperactivity of dopamine transmission in the mesolimbic pathway.
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  Speaker 1: In this pathways where you have the positive symptoms derived
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  Speaker 1: from hallucinations delusions, while hypo activity in the mesocortical pathway
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  Speaker 1: relates to negative symptoms. This is where they have a
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  Speaker 1: flat affect right, very little emotion, evolition, no will. This
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  Speaker 1: is where you take away things. The negative is a
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  Speaker 1: loss of things and the positives addition to antipsychotics work
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  Speaker 1: primarily by blocking dopamine D two receptors, again going off
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  Speaker 1: the dopamine hypothesis, so there's too much dopamine. Also, there's
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  Speaker 1: things there. There's another one called glutamate dysfunction. Research implicates
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  Speaker 1: glutamate hype o function, so too low levels of glutamate,
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  Speaker 1: particularly at NMDA receptors, and they contribute to both the
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  Speaker 1: cognitive deficits and negative symptoms seen in schizophrenia. Drugs like PCP,
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  Speaker 1: which block NMDA receptors induce schizophrenia like symptoms, supporting this model,
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  Speaker 1: and we're also seeing this now with marijuana. Structural brain
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  Speaker 1: abnormalities as well. MRI studies show enlarged lateral ventricles, cortical thinning,
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  Speaker 1: and reduced gray matter and the prefunnel cortex hippocampus and thaumas.
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  Speaker 1: These structural differences often precede symptom onset and worsen over time.
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  Speaker 1: Genetics and risk schizophrenia is highly heritable, somewhere around seventy
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  Speaker 1: to eighty percent heritability. The gas genomic wide association studies
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  Speaker 1: have identified hundreds of risk loca, especially those involved in
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  Speaker 1: synaptic pruning and immune system functions. Confordance is high in
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  Speaker 1: monozygotic twins. Are monozygotic twins about fifty percent, so antipsychotic
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  Speaker 1: medication targets dopamine, but treatment resistant cases may benefit from
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  Speaker 1: glutamate based interventions and cognitive remediation to protect brain structure
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  Speaker 1: and function. We look at anxiety soorders and we see
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  Speaker 1: GAMBA dysfunction. Gamba is the brains prehentit primary inhibitory neuroor transmitter.
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  Speaker 1: If you remember that in anxiety, gaba's signaling is often underactive,
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  Speaker 1: leading to an overactive fear response. So this is when
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  Speaker 1: benzodiazepines will increase GABBA and produce rapid calming effects. But
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  Speaker 1: remember it's also highly addictive, So the tolerance and dependence
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  Speaker 1: limit for the long term use of benzoiantopenes Amygdala hyperactivity.
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  Speaker 1: This is the central processing part of our brain for
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  Speaker 1: fear and threat is overactive in anxiety disorders, especially PTSD
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  Speaker 1: and generalized anxiety disorder. This hyperactivation is evident in fMRI studies.
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  Speaker 1: It correlates with symptoms severity, hippocampal and prefuntal involvement the
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  Speaker 1: hippocampus which deals with contextual type of memories and pre
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  Speaker 1: funnel cortex regulation of emotion fail to inhibit amgdala over
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  Speaker 1: activity effectively in anxiety. That explains why anxious individuals may
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  Speaker 1: recognize their fear is irrational but still feel it strongly.
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  Speaker 1: They can't seem to control it sometimes. Treatment, of course,
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  Speaker 1: is also SSRIs, which seems to indirectly reduce amgdala activation
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  Speaker 1: over time. CBTs a psychotherapy that's commonly used and highly effective,
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  Speaker 1: which strengths prefuntal regulation via cognitive restructuring and exposure. Another
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  Speaker 1: one that does really well is mindfulness based type of therapies.
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  Speaker 1: Now we'll look at bipolar disorder, and this is neurotransmitter imbalances.
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  Speaker 1: Bi Polar disorder involves cycling dysregulation of dopamine, serotonin, and orapinephrine.
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  Speaker 1: Mania reflects dopamine hyperactivity, while depression involves dopamine depletion. This
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  Speaker 1: sensibility leads to wide mood swings. Circadian rhythm disruption, sleep
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  Speaker 1: and circadian dysregulation are common triggers for manic episodes. Genes
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  Speaker 1: are associated with the body's internal clock. Mood episodes often
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  Speaker 1: followed sleep disruption. Travel across time zones or irregular routines
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  Speaker 1: can also do it. Study show reduced volume in the
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  Speaker 1: prefunnel cortex and the amygdala and ab normal activity in
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  Speaker 1: emotion processing circuits. Functional imaging shows increased activity activation in
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  Speaker 1: the limbic system, the emotional system doing manic states. Mood
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  Speaker 1: stabilizers like we talked about before, like lithium, lamicdol, and
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  Speaker 1: anti convulsions target intracellular signaling pathways. Sleep stabilization and daily
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  Speaker 1: rhythm regulation are critical non pharmacological components, so sleep is
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  Speaker 1: going to be really important for these individuals. And last,
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  Speaker 1: but not least is ADHD. ANYHD is tied to deficits
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  Speaker 1: in dopamine and orepinephrin signaling, especially in the pre funnel cortex.
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  Speaker 1: These neurotransmitters regulate attention, inhibition and working memory. Stimulants like
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  Speaker 1: methyl fenel date that we talked about before, ritalin and
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  Speaker 1: amphetamine like adderall work by increasing their availability, improving focus
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  Speaker 1: and impulse control. Neuroimaging shows reduced activity and volume endorsal
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  Speaker 1: lateral prefunnel cortex, anterior singular cortex, and basal ganglia regions
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  Speaker 1: for executive function. The delayed cortical maturation has also been observed.
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  Speaker 1: There's also a disruption of the default mode network. Children
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  Speaker 1: with ADHD show alter connectivity in the default mode network,
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  Speaker 1: a brain network active during rest and internal thought. For
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  Speaker 1: a regulation of this network may contribute to mind wandering
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  Speaker 1: and distractability. Is this is the area where you're thinking
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  Speaker 1: about yourself and it's an internal thought, especially during rest
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  Speaker 1: or nothing is going on, so when this happens, you
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  Speaker 1: can't focus. Genetics it also plays a role here where
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  Speaker 1: the heritability of ADHD is high seventy to eighty percent.
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  Speaker 1: Genes affecting the dopamine transpitters dapt one and receptors DRD
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  Speaker 1: four and five are strongly implicated. Stimilant medications. Stimulant medications
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  Speaker 1: are still the first line and I can't remember what
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  Speaker 1: it was, but I think it was twenty thirty percent
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  Speaker 1: of ADHD clients don't even get therapy. However, behavioral interventions
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  Speaker 1: parent training and executive functioning, coaching, reinforce prefuntal development, sleep, nutrition,
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  Speaker 1: and structure amplify the treatment effects. So you can see
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  Speaker 1: the benefits of psychotherapy and especially psycho education for the
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  Speaker 1: parents as well as the individual, depending if they're an
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  Speaker 1: adult or a teenager. So the biological models of psychological
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  Speaker 1: disorders are complicated in their layered they're not linear. Each
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  Speaker 1: diagnosis is shaped by several factors. Neurotransmitters, circuits in the brain,
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  Speaker 1: hormonal signals, gene environment interplay. Could be a moots what
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  Speaker 1: seems like a mootswind could be a circums firing. What
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  Speaker 1: feels like worry may begin in chemistry. And when you
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  Speaker 1: treat behavior, you're ignoring the brain. You're engaging it. You're
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  Speaker 1: not ignoring the brain, I'm sorry. When you treat behavior,
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  Speaker 1: you're engaging it. So when you understand the brain, you
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  Speaker 1: can bring more precision, compassion, and impact to your job
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  Speaker 1: as a therapist. So we do see things being manifested
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  Speaker 1: in the biology of these psychological disorders. We see the
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  Speaker 1: neurotransmitters component. We see the structure and function, which is
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  Speaker 1: a neuroscience component. We see a little bit of genetics
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  Speaker 1: in there. We did not see genetics in regards to
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  Speaker 1: anxiety and depression, which have a lower haretability rate compared
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  Speaker 1: to schizophrenia ADHD. We definitely saw some other physiological disruptions
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  Speaker 1: as well. Next time we're going to go switch and
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  Speaker 1: talk to about sleep neurobiology and we'll see how that
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  Speaker 1: affects yes, which is a big part of a lot
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  Speaker 1: of my clients' success and being able to get better sleep.
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  Speaker 1: You'd be surprised how much faster the recovery is. That's
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  Speaker 1: it for now.