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THE BIOLOGY OF SLEEP · Understanding the Brain

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  Speaker 1: Welcome back, everybody. We're gonna be talking about sleep today,
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  Speaker 1: and we'll also be looking at the neurobiology of sleep. Really,
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  Speaker 1: that's kind of what we're going to be focusing on.
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  Speaker 1: So sleep cycles through what they call nr EM stages
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  Speaker 1: N one through N three, that's ends and nancy and
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  Speaker 1: rem in ninety minute intervals. That's the way the cycle
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  Speaker 1: happens for sleep. Some of the neurotransmitters and hormones involved
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  Speaker 1: are serotonin, melotonin identity, and or rexin. They regulate sleep onset,
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  Speaker 1: depth and timing. Insomnia has the most common sleep disorder.
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  Speaker 1: Narcolepsy involves orxen deficiencies were you just fall asleep Everywhere
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  Speaker 1: sleep disturbances worsen and maintain conditions like depression, anxiety, PTSD,
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  Speaker 1: and bipolar disorder. I'll tell you sleep is one of
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  Speaker 1: the biggest things that can help replying quite a bit.
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  Speaker 1: They've even shown it drops one hour of extra sleep
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  Speaker 1: can drop six to seven points on the Hamilton Depression Inventory.
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  Speaker 1: It's pretty powerful stuff. Treating sleep problems biologically and behaviorally
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  Speaker 1: improves the psychological outcomes of these people, of the people
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  Speaker 1: with psychiatric issues, and for everybody. Really, it repairs tissues,
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  Speaker 1: consolidates memory. When we get to memory soon, you'll see
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  Speaker 1: how that operates. It recalibrates emotion and supports executive function
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  Speaker 1: back there in the pre final cortex. So let's look
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  Speaker 1: at some of a little bit more deep dive into
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  Speaker 1: the ends. So each night, sleep repeats, as we mentioned,
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  Speaker 1: a ninety minute cycle through non rapid eye movement. That's
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  Speaker 1: what n RAM stands for, and RM is rapid eye movement.
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  Speaker 1: So they just kind of abbreviate it to end one
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  Speaker 1: and one is light sleep. But stage number one and
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  Speaker 1: you transition kind of between wake and sleep. You got
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  Speaker 1: different brain waves, and you're going to be in here
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  Speaker 1: in the theta wave, so you have gamma and beta,
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  Speaker 1: which usually your alert alpha, Theta and delta deltas are
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  Speaker 1: completely out, so it's easily disrupted in the theta wave
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  Speaker 1: and accounts for about five percent of total sleep. Is
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  Speaker 1: a light sleep, the deeper light sleep stage n two.
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  Speaker 1: You'll see on the EGS sleep spindles and k complexes
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  Speaker 1: and temperature drops, heart rate slows. It makes up about
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  Speaker 1: forty five to fifty five percent of your total sleep.
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  Speaker 1: So I threw a couple of words in there. Sleep spindles,
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  Speaker 1: which are brief bursts of high frequency brain activity. The
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  Speaker 1: last about a half a second to two seconds. Again,
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  Speaker 1: they're in stage two and they're linked to memory consolidation,
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  Speaker 1: so sensory processing suppression as well and maintaining sleep stability
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  Speaker 1: by blocking out external stimuli. The K complex is. These
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  Speaker 1: are a sudden, sharp, high amplitude waves, often followed by
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  Speaker 1: a slow wave lasting about a half half a second
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  Speaker 1: to a second. They occur spontaneously in response to external
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  Speaker 1: stimuli like noise. Their job is to protect sleep by
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  Speaker 1: suppressing arousal while while assessing whether it's stimulus requires waking up,
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  Speaker 1: but it's almost like your personal security. Both are hardmarks of
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  Speaker 1: light sleep, aiding and transitioning to deeper sleep stages and
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  Speaker 1: supporting cognitive functions like memory and learning. Now we go
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  Speaker 1: to stage three, which is and three and this was
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  Speaker 1: when you didn't get into the delta wave, so you're
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  Speaker 1: pretty hard. You're knocked out. This is hard to wake from.
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  Speaker 1: The stage is physically restorative. It supports immune function, growth,
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  Speaker 1: hormone release, and memory consolidation. Unfortunately, it does decline with age,
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  Speaker 1: so immune function here is why a lot of times
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  Speaker 1: if you're not getting enough sleep, you're more susceptible to
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  Speaker 1: getting sick. The fourth and final stage is what everybody
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  Speaker 1: hears about rem sleep right. This is where you dream fast,
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  Speaker 1: low voltage brainwaigh, but with muscle paralysis, which they call atonia.
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  Speaker 1: Ato Nia is muscle paralysis. This stage is emotionally and
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  Speaker 1: cognitively restorative, associated processing emotional memories, problem solving, and creativity.
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  Speaker 1: We're not necessarily going to get into analyzing dreams here.
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  Speaker 1: We will be doing that and some other podcasts that
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  Speaker 1: I have. You can check those out at Circle of
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  Speaker 1: Insight podcast or Psychology Tidbits. I have done some dream
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  Speaker 1: analysis work over there. Now look at the newer chemistry
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  Speaker 1: of the sleep wake cycles. They're regulated by homeostatic and
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  Speaker 1: circadian processes. Think of them as pressure and timing. A
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  Speaker 1: dentistine builds up during wakefulness. It's the body's sleep debt signal.
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  Speaker 1: It promotes drowsiness and gets cleared during sleep, and then
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  Speaker 1: it starts building back up. Cause Caffeine blocks the dentistine receptors,
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  Speaker 1: which is why it keeps you alert. On a side note,
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  Speaker 1: a lot of paramedics will use a dentistine to calm
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  Speaker 1: down the patient at the time Melatonin is released by
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  Speaker 1: the pineal gland, the pineal p I N E A
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  Speaker 1: L and its response to diminishing light levels, So you
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  Speaker 1: get both of these working together, a dentisine and melatonin
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  Speaker 1: in a way. So when the light levels starts decreasing,
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  Speaker 1: melatonin starts increasing in the pineal gland. At the same time.
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  Speaker 1: Throughout the day, you're a dentisine is building up to
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  Speaker 1: a certain level till you fall asleep, So both of
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  Speaker 1: these are setting up your circadian timing. Note that exposure
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  Speaker 1: to blue light from screens in the evening can suppress
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  Speaker 1: melatonin release and disrupt sleep timing. Serotonin plays dual roles.
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  Speaker 1: It helps initiate sleep and supports RAM regulation. SSRIs can
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  Speaker 1: alter rem sleep patterns, often reducing RAM density. Orexin or
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  Speaker 1: hypocretin orexin is ori E xi N producing the hypothalmus
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  Speaker 1: keeps you awake and alert, and narcoleps orexin producing neurons
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  Speaker 1: are deficient or absent, leading to sudden, uncontrollable sleep attacks.
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  Speaker 1: Let's hurry over to your body's internal clock, which they
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  Speaker 1: call the circadian rhythm. They're roughly twenty four hour cycles
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  Speaker 1: regulated by the super chiasmatic nucleus the SCN in the hypothalmus.
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  Speaker 1: The SCN responds to light input from the retina, sinking
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  Speaker 1: the body clock to environmental cues like light meals social interaction.
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  Speaker 1: When circadian rhythms are misaligned, think about overnight midnight shifts.
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  Speaker 1: Things of that nature are jet lag, Sleep becomes fragmented,
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  Speaker 1: and hormonal rhythms shift and mood regulation weakens. So look
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  Speaker 1: now at some of the disorders associated with sleep. Will
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  Speaker 1: also look at some treatment strategies. So insomnia disorder difficulty
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  Speaker 1: falling asleep or staying asleep. Another one is early awakening
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  Speaker 1: must last at least more than three nights per week
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  Speaker 1: for three months and cause daytime impairment. The neurobiology associated
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  Speaker 1: with it as heightened cortisol levels due to hyper arousal.
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  Speaker 1: You also have an elevated metabolic rate and increase sympathetic activity.
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  Speaker 1: Remember the fight or flight system kicks in here. First
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  Speaker 1: line of treatment make sure you know this for the
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  Speaker 1: exam is CBT. Also sleep hygiene, melotonin, short term sedative hypnotics,
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  Speaker 1: and load dose trazodone. I've seen trousodon being prescribed a lot.
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  Speaker 1: Also zopidim so. Again, first line of treatment is CBT
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  Speaker 1: number two. It was obstructive sleep apney I repeated airway
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  Speaker 1: collapse during sleep, causing brief arousals and oxygen desaturation. Often
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  Speaker 1: missed unless the bed partner reports snoring or gasping. It
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  Speaker 1: can lead to daytime fatigue, increase srutability that's also linked
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  Speaker 1: to depression and hypertension. Treatment the most common is SEAPAP
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  Speaker 1: weight loss, avoiding alcohol sedatives. By the way, SEAPAP is
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  Speaker 1: the continuous positive airway pressure. It's a medical device that
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  Speaker 1: they use to treat sleep. APNA delivers a steady stream
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  Speaker 1: of air pressure through a mask worn over the nose
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  Speaker 1: or mouth, keeping the airway open to prevent breathing in eruptions.
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  Speaker 1: So what it does with the therapy can improve sleep architecture,
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  Speaker 1: potentially increasing the frequency or quality of Stage two. This
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  Speaker 1: is where we talked about sleep spindles and k complexes.
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  Speaker 1: Better airway pagency reduces arousals, allowing more consistent sleep cycles.
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  Speaker 1: We move on now to narcolepsy, which we've mentioned a
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  Speaker 1: little bit earlier. Narcolepsy is characterized by sleep attacks, cataplexy,
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  Speaker 1: sleep paralysis, and hypnagogic hallucinations. So you're hallucinating just before
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  Speaker 1: you go to sleep. Cause is usually a resin deficiency
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  Speaker 1: in the hypothalmus. Treatment is medophinol sodium oxybate structured naps.
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  Speaker 1: Stimulants can work as well for alertness and SSRIs for
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  Speaker 1: cattle AMPLEXI in cataplexy if you're wondering, is a sudden
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  Speaker 1: brief loss of muscle tone triggered by strong emotions, either laughter, surprise,
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  Speaker 1: or anger, often associated with narcolepsy. Episodes can range from
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  Speaker 1: mild droopy eyelids to head nodding to severe full body
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  Speaker 1: collapse lasting minutes I mean seconds to minutes, but preserved consciousness.
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  Speaker 1: So again, sudden brief loss of muscle tone triggered by
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  Speaker 1: strong emotions, and it is a symptom of narcolepsy. Sleep
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  Speaker 1: in psychological disorder is depression, which we talked about earlier.
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  Speaker 1: Shortened RIM latency, increased RIM density, poor sleep predicts onset
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  Speaker 1: and relapse. Sleep disturbances are both a symptom and a
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  Speaker 1: risk factor for depression. Unfortunately, antidepressants can suppress rem initially,
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  Speaker 1: which may be therapeutic in the beginning. So I'm going
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  Speaker 1: to take away that Unfortunately I mislooked at my notes.
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  Speaker 1: Anxiety disorders difficulty initiating or maintaining sleep due to hyper arousal.
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  Speaker 1: You got worry loops and elevated europe An effort to
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  Speaker 1: disrupt pre sleep relaxation. Sleep deprivation increases a migular reactivity,
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  Speaker 1: reducing emotional regulation as well. The increase in the megular reactivity,
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  Speaker 1: of course, makes you hypervigilant. Third is PTSD also having
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  Speaker 1: fragmented ram intrusive nightmares. REM rebound after trauma. Rem rebound
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  Speaker 1: is a phenomenon where rapid eye movements sleep increases in
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  Speaker 1: duration intensity following a period of rim deprivation or suppression,
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  Speaker 1: such as from certain medications, stress, things of that nature.
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  Speaker 1: It reflects the body's attempt to recover lost rem critical
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  Speaker 1: for memory consolidation as we remember in cognitive function, so
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  Speaker 1: rebound underscores the the brain's prioritization of rem sleep. In
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  Speaker 1: addition to get nightmares maintain hypervigilance. For PTSD, prazosis in
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  Speaker 1: an alpha one blocker can reduce trauma related nightmares, prosis
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  Speaker 1: and p R A Z O s I N bipolar disorder.
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  Speaker 1: Sleep deprivation can trigger manic episodes. Many of features decreased
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  Speaker 1: need for sleep without fatigue sleep regularity is essential to
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  Speaker 1: stabilizing mood cycles, so mood stabilizers often normalized sleep like valparate, depicoat,
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  Speaker 1: or lithium. Lastly, it's a treatment strategy, so CBT is
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  Speaker 1: your first line most effective long term treatment targets maladapted
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  Speaker 1: beliefs and condition to arousal stimulus controls, sleep restriction, relaxation, training,
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  Speaker 1: and cognitive restruction are some of the components. Pharmacological treatments
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  Speaker 1: short term hypnotics so zopiderm, s zola, piclon, zopiclon which
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  Speaker 1: is e z O p I c l O n
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  Speaker 1: E which bind gabba, melatonin agonists like raalmaton which is
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  Speaker 1: non sedating circadian regulators, ramaton is r ame te o
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  Speaker 1: n E. Rexin antagonists like superoxytin that's s u v
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  Speaker 1: O r e x A n T promotes sleep onset
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  Speaker 1: without suppressing rem Antidepressants low dose trazodone common for insomnia
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  Speaker 1: with comorbid depression or anxiety. And last is sleep hygiene.
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  Speaker 1: Consistent schedule even on weekends, no screens or stimulating activities
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  Speaker 1: sixty minutes before bed. I always recommend reading. I think
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  Speaker 1: that helps a lot of tends to put people's kind
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  Speaker 1: of get them drowsy just using out benergy in your
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  Speaker 1: brain right soon much glucose, cool, dark, quiet environment and
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  Speaker 1: no caffeine after two. Also avoid naff throughout the day
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  Speaker 1: that are longer than twenty minutes. You don't want to
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  Speaker 1: get into that mess for sure. We'll go back over
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  Speaker 1: the importance of REM sleep, memory consolidation and learning, emotional regulation,
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  Speaker 1: brain development, cognitive function, and neuronal restoration, so really important.
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  Speaker 1: Also you'll see sleep there too. Remember REM rebound highlights
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  Speaker 1: REM's importance. After deprivation, the brain prioritizes REM to recover
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  Speaker 1: its benefits, often at the expense of other sleep stages.
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  Speaker 1: This could alter into spindle and k complex frequency, but
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  Speaker 1: underscores REM's role in the cognitive and emotional health of
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  Speaker 1: an individual. So that's different. Now next time when we
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  Speaker 1: come back, we move away from sleep and we're heading
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  Speaker 1: into some of the foundations of human development across the
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  Speaker 1: last span and how biology plays a role in human development.