Session 3: Accessing Subjectivity

Overview

In the previous sessions, we explored how expectations shape perception and how individuals differ in their baseline subjective experiences. Now we ask: What can we learn about normal consciousness by studying abnormal or altered states? This session examines what happens when we perturb consciousness through psychedelic compounds, meditation, brain stimulation, dissociative states, and sleep. Each approach offers a unique window into the mechanisms underlying subjective experience. We'll see how pharmacological manipulations reveal the role of specific neurotransmitter systems, how meditation demonstrates voluntary control over conscious states, how brain stimulation tests causal relationships between brain regions and experience, and how dissociation illuminates the constructed nature of self and reality. Throughout, we grapple with fundamental questions: Can we ever truly access another person's altered state? What do these perturbations reveal about the "normal" waking consciousness we take for granted?

Finishing Up: Non-Visual Perception from Last Week

Neural Mechanisms of Time Perception

Unlike your eyes or ears, you don't have a specific "time organ" in your body. Instead, your brain uses several different regions working together to keep track of time:

  • Striatum (with dopamine): Coull et al. (2011) showed that this part of your brain acts like your internal clock's speed dial. When dopamine levels go up (like from certain drugs), your internal clock runs faster—so the outside world seems to move in slow motion. When dopamine goes down, your clock runs slower, making the world seem to speed up.
  • Cerebellum: This handles super-precise timing—think split-second coordination like catching a ball or speaking clearly.
  • Prefrontal cortex: This helps you pay attention to how long things take and remember durations.
  • Parietal cortex: This connects your sense of time with your sense of space (where things are).
The Clock in Your Head:

Think of your brain's timing system like this:

  • The Ticker: Imagine a metronome or heart beating steadily—tick, tick, tick. This is your internal "pacemaker" generating pulses.
  • The Counter: Your brain counts these ticks, like counting seconds.
  • The Speed Control: When you're excited or stressed, the ticker speeds up → more ticks per second → time feels like it's passing slowly (because you're counting MORE ticks for the same amount of real time).
  • The Gate: Your attention acts like a door. When you're focused on something interesting, the gate closes and you stop counting ticks—time flies by. When you're bored and watching the clock, the gate is wide open and you count every single tick—time drags.
Real-Life Examples:
  • Why a watched pot never boils: You're paying full attention to time passing (gate open), so you count every tick, making it feel longer.
  • Why fun activities feel short: You're absorbed in what you're doing (gate closed), so you stop counting ticks, and suddenly an hour has passed.
  • Why scary moments feel slow: Your arousal is high (ticker speeds up), so you're experiencing more "ticks" per second, making everything feel like it's happening in slow motion.

Individual and Cultural Differences

Wittmann (2013) reviewed factors affecting time perception:

  • Age: Older adults report time passing faster—possibly because each year is a smaller proportion of total life
  • Culture: "Clock time" cultures (Western industrial) vs. "event time" cultures (many traditional societies)
  • Personality: Impulsivity correlates with overestimating short durations; patience with underestimating
  • Body temperature: Fever makes subjective time pass faster (external world seems slower)

Wittmann, M. (2013). The inner sense of time: how the brain creates a representation of duration. Nature Reviews Neuroscience, 14(3), 217-223.

Taste Perception: Genetic Variation Creates Different Gustatory Worlds

The Discovery of Supertasters

In the 1930s, a chemist accidentally discovered that people perceive the bitter compound PTC (phenylthiocarbamide) very differently—some found it intensely bitter, others tasteless. This led to decades of research on genetic variation in taste.

The Genetics of Bitter Taste

Kim et al. (2003) identified the genetic basis:

  • The TAS2R38 gene encodes a bitter taste receptor
  • Two main variants: PAV (taster) and AVI (non-taster)
  • Three groups:
    • PAV/PAV homozygotes: Supertasters (~25%)
    • PAV/AVI heterozygotes: Medium tasters (~50%)
    • AVI/AVI homozygotes: Non-tasters (~25%)

Beyond Genetics: Taste Bud Density

Supertasters also tend to have more fungiform papillae (taste bud structures) on their tongues. This physical difference amplifies genetic variation:

  • Supertasters: ~425 taste buds per cm² of tongue
  • Medium tasters: ~180 taste buds per cm²
  • Non-tasters: ~96 taste buds per cm²

Real-World Consequences

Food Preferences and Health:
  • Supertasters often avoid bitter vegetables (broccoli, brussels sprouts)
  • They may consume less alcohol (tastes more bitter)
  • Non-tasters more likely to enjoy strong flavors, spicy foods
  • Potential dietary impacts: supertasters may miss out on healthy bitter vegetables
Discussion Point: If we gave everyone the PAV variant, would they all experience the same bitterness? Or would early food exposure and learning still create different taste preferences?

Kim, U. K., et al. (2003). Positional cloning of the human quantitative trait locus underlying taste sensitivity to phenylthiocarbamide. Science, 299(5610), 1221-1225.

The Default Mode Network: Your Brain's "Not-so-Idle" State

Discovery of the DMN

For decades, neuroscientists focused on what the brain does during tasks—reading, calculating, paying attention to stimuli. But in the early 2000s, researchers noticed something curious: certain brain regions were consistently more active when people were doing nothing than when they were engaged in cognitive tasks. This seemed backwards. Why would the brain work harder during rest?

The answer revealed a fundamental insight: the brain is never truly at rest. When we're not focused on external tasks, our minds naturally engage in internal mentation—thinking about ourselves, remembering the past, imagining the future, considering what others might be thinking. The network of regions supporting this internal focus came to be called the Default Mode Network.

Key Regions of the DMN

Refer to video at 2:37-5:07 for visual illustration of these regions:

  • Posterior Cingulate Cortex (PCC) / Precuneus: Located in the midline of the brain, toward the back. Central hub of the DMN, involved in self-referential processing and consciousness
  • Medial Prefrontal Cortex (mPFC): Front and center of the brain. Critical for thinking about yourself, your traits, your preferences—the narrative self
  • Angular Gyrus: Lateral parietal regions. Involved in memory retrieval and mental scene construction
  • Hippocampus: Deep structure critical for memory. Helps reconstruct past experiences and imagine future scenarios
  • Temporal Poles: Front of temporal lobes. Integrate semantic knowledge with personal experiences
The DMN as the "Narrative Self" Network:

The DMN maintains your sense of being a continuous self across time—the "you" that existed yesterday, exists now, and will exist tomorrow. It's the network that:

  • Constructs and maintains your autobiographical narrative
  • Thinks about your personality traits and preferences
  • Imagines what you'll do in the future
  • Considers what others think of you
  • Mind-wanders and daydreams

DMN Activity Patterns

The DMN shows a characteristic pattern of activity:

  • Active during rest: When you're sitting quietly, waiting in line, or taking a shower—times when your mind wanders
  • Deactivates during tasks: When you focus attention on external stimuli or demanding cognitive tasks, DMN activity decreases
  • Anti-correlated with attention networks: As attention networks ramp up, DMN ramps down, and vice versa
  • The "task-negative" network: Original researchers called it this because it seemed to work against task performance

Individual Differences in DMN Activity

Importantly, the DMN doesn't function identically in all people or situations. In my own research (Sava-Segal et al., 2023, 2025), we've shown that DMN activity varies both:

  • Between individuals: People with different interpretations of the same ambiguous stimuli show different patterns of DMN activity
  • Within individuals: When the same person shifts their interpretation of an ambiguous stimulus, their DMN activity changes correspondingly

This suggests the DMN isn't just a static "resting state" network—it dynamically reflects how we're currently making sense of the world and our place in it. Your subjective interpretation shapes your DMN activity, and vice versa.

When the DMN Goes Wrong

While the DMN is essential for self-reflection and planning, problems arise when it becomes overactive or stuck:

DMN Dysfunction in Mental Health:
  • Depression: Overactive DMN linked to rumination—repetitive negative thoughts about oneself
  • Anxiety: Excessive DMN activity associated with worry about future and self-focused anxiety
  • ADHD: Difficulty suppressing DMN when trying to focus on tasks
  • Alzheimer's disease: DMN shows abnormal patterns and is particularly vulnerable to degeneration

Why the DMN Matters for Understanding Altered States

The DMN has become a crucial target for understanding how various interventions alter consciousness. As we'll see throughout this session, psychedelics, meditation, and dissociative states all affect DMN functioning—though in different ways. This convergence suggests the DMN plays a fundamental role in maintaining normal waking consciousness, particularly the sense of being a bounded, continuous self.

The DMN Across Altered States:
  • Psychedelics: Dramatically decrease DMN activity and connectivity
  • Meditation: Trained reduction in DMN activity during practice
  • Stimulation-induced dissociation: Disrupting DMN regions produces feelings of unreality
  • Sleep: DMN activity changes across sleep stages

The common thread: altering the DMN alters the sense of self.

Default Mode Network regions

Image showing the key regions of the Default Mode Network

Psychedelics: Disrupting the Default Mode

What Are Psychedelics?

Psychedelics are substances that produce profound alterations in perception, mood, and thought. The "classic" psychedelics—psilocybin (magic mushrooms), LSD, and DMT—all act primarily on serotonin 2A receptors. They've been used in spiritual and therapeutic contexts for millennia, and after decades of legal restrictions, are experiencing a research renaissance.

Subjective Effects: What's It Like?

Common Phenomenology:
  • Perceptual: Enhanced colors, geometric patterns, synesthesia, distortion of space and time
  • Cognitive: Loosening of conceptual boundaries, novel associations, feeling of insight
  • Emotional: Intensified emotions, awe, mystical experiences
  • Sense of self: "Ego dissolution"—boundaries between self and world blur or disappear

Visualizing DMN Changes on Psilocybin

This video segment (starting at 6:24) provides a helpful visualization of how psilocybin affects the Default Mode Network. Notice how the normally highly active and interconnected DMN regions show reduced activity under the influence of psilocybin. This decrease in DMN function corresponds to:

  • Reduced self-referential thinking ("less thinking about myself")
  • Dissolution of the boundary between self and environment
  • Decreased rumination and stuck thought patterns
  • The characteristic "ego dissolution" experience
  • Feelings of unity and connection with surroundings

The visual representation makes clear why disrupting the DMN might have therapeutic potential—if the DMN is the network maintaining rigid patterns of self-focused negative thinking in depression, temporarily "turning down the volume" on this network might allow new patterns to form.

The Default Mode Network Discovery

Carhart-Harris et al. (2012) used fMRI to study psilocybin's effects on brain activity:

  • Contrary to expectations, found decreased activity in key brain regions
  • Strongest decreases in posterior cingulate cortex (PCC) and medial prefrontal cortex (mPFC)
  • These regions are core nodes of the Default Mode Network (DMN)
  • Amount of deactivation correlated with intensity of subjective effects, especially ego dissolution
The DMN Hypothesis of Ego Dissolution:

When psychedelics decrease DMN activity, the normally tight constraints on thought and self-concept loosen. The rigid boundaries of "self" vs. "other" relax. This may explain:

  • Feeling of unity with surroundings
  • Dissolution of normal identity
  • Novel thought patterns (increased "cognitive flexibility")
  • Mystical experiences of "oneness"

Increased Brain Network Integration

Tagliazucchi et al. (2016) showed psychedelics also increase connectivity:

  • Brain regions that normally don't communicate much show increased coordination
  • "Entropic brain" hypothesis: psychedelics increase the disorder and flexibility of neural dynamics
  • May allow novel combinations of thoughts and percepts that are normally kept separate
  • Could explain creative insights, synesthesia, and unusual associations during trips

Therapeutic Potential

Recent clinical trials suggest psychedelics may help treat depression, anxiety, PTSD, and addiction:

  • Depression: Davis et al. (2021) found two doses of psilocybin produced rapid antidepressant effects
  • Mechanism: May "reset" overactive DMN patterns in depression (rumination, negative self-focus)
  • End-of-life anxiety: Studies show mystical experiences can reduce death anxiety in terminal patients
  • Set and setting: Context matters enormously—clinical trials use careful preparation and guided sessions
Important Considerations:
  • These are still experimental treatments requiring medical supervision
  • Psychedelics can trigger anxiety, paranoia, or traumatic experiences in vulnerable individuals
  • Long-term effects and optimal protocols still being researched
  • Not a magic cure—therapeutic benefit seems to come from the psychological experience, not just the drug

Carhart-Harris, R. L., et al. (2012). Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. PNAS, 109(6), 2138-2143.

Meditation: Voluntary Control Over Consciousness

Why Study Meditation?

Meditation provides a complementary approach to psychedelics: rather than chemically disrupting normal consciousness, practitioners develop voluntary control over their mental states. Long-term meditators can reliably enter specific states of consciousness, making them ideal subjects for neuroscience research. Unlike most altered states which happen to you, meditative states are something you learn to do.

Types of Meditation and Their Neural Signatures

Brewer et al. (2011) compared three meditation styles in experienced practitioners:

  • Focused attention: Concentrating on a single object (like breath). Increased activity in attention networks.
  • Open monitoring: Non-reactive awareness of whatever arises. Increased sensory processing, decreased evaluation.
  • Loving-kindness: Generating feelings of compassion. Increased activity in emotion and empathy networks.

Meditation and the Default Mode Network

Across all three meditation types, experienced meditators showed a striking pattern:

  • Reduced DMN activity during all practices
  • Even during rest between practices, meditators had lower DMN activation
  • This corresponds to reduced mind-wandering and self-referential thought
  • Interesting parallel to psychedelics: both reduce DMN, but through opposite mechanisms (pharmacological disruption vs. trained control)
DMN deactivation in meditation

Image showing Default Mode Network regions with reduced activity during meditation

Understanding Subjective States Through First-Person Reports

One of the biggest challenges in consciousness research is connecting what people report experiencing with what we can measure in their brains. Meditation research uses a clever approach:

  • The basic idea: Combine detailed descriptions of what people experience (first-person reports) with brain measurements (third-person data)
  • Why meditators help: They've spent years training to pay attention to their inner experiences and can enter specific mental states on command
  • How it works: During brain scans, meditators press buttons when their mental state changes, then give detailed interviews afterward describing what they experienced
  • The goal: Find patterns in brain activity that reliably predict which mental state someone is in
Practical Example: A meditator might press a button when shifting from focused concentration to mind-wandering. By comparing brain activity before and after the button press across many sessions, researchers can identify the neural signature of that transition—even learning to predict state changes before the meditator consciously notices them.

Tang, Y. Y., Hölzel, B. K., & Posner, M. I. (2015). The neuroscience of mindfulness meditation. Nature Reviews Neuroscience, 16(4), 213-225.

Brain Stimulation: Testing Causal Relationships

Why Brain Stimulation Matters for Consciousness Research

Neuroimaging (fMRI, EEG) shows correlations between brain activity and experience. But correlation doesn't prove causation. Brain stimulation allows us to test: If we temporarily disrupt region X, does experience Y change? This provides causal evidence about which brain regions are necessary for specific aspects of consciousness.

Transcranial Magnetic Stimulation (TMS)

TMS uses magnetic pulses to temporarily activate or disrupt specific cortical regions:

How TMS Works:
  • A coil placed on the scalp generates brief magnetic pulses
  • These induce electrical currents in underlying cortical neurons
  • Single-pulse TMS: Disrupts processing for milliseconds
  • Repetitive TMS (rTMS): Multiple pulses produce effects lasting minutes to hours
  • Non-invasive, temporary, relatively targeted (though not perfectly localized)

TMS and Visual Awareness

Silvanto et al. (2005) used TMS to identify critical timing for visual consciousness:

  • Applied TMS to early visual cortex (V1) at different times after presenting a visual stimulus
  • Critical window: TMS at 80-140ms after stimulus eliminated conscious perception
  • Earlier or later TMS had less effect
  • Implication: Activity in V1 during this window is necessary for conscious visual experience
  • Some unconscious processing survived the disruption, helping dissociate neural correlates of consciousness from earlier sensory processing

Direct Brain Stimulation: The Fusiform Face Area

Last week we watched the remarkable video of intracranial stimulation affecting face perception. Let's discuss what this reveals:

Watch: Electrical Stimulation of Fusiform Face Area

In this video, neurosurgeon Dr. Josef Parvizi stimulates the fusiform face area (FFA) in an epilepsy patient during surgery. The patient is awake and reports what she experiences.

Key Observations:
  • Selective distortion: When stimulated, the patient reports the faces of people she's looking at appear distorted—stretched, morphed, or changed
  • Specificity: Only faces are affected, not other objects in her visual field
  • Immediate and reversible: Distortion appears when stimulation begins and disappears when it stops
  • Conscious experience: The patient remains fully aware and can describe the changes in real-time
What This Tells Us:
  • The FFA is not just correlated with face processing—it's causally necessary for normal face perception
  • Our experience of seeing a face is actively constructed by specific brain regions
  • Disrupting a specialized area produces highly specific perceptual changes, not general confusion
  • The constructed nature of perception: what we "see" depends on which neural circuits are active

This work comes from Dr. Josef Parvizi's lab at Stanford, which uses intracranial recordings and stimulation to study the neural basis of cognition and consciousness in epilepsy patients.

Dissociation: When Experience Fragments

What Is Dissociation?

Dissociation refers to disruption in the normally integrated functions of consciousness, memory, identity, and perception. It exists on a spectrum from common experiences (highway hypnosis, absorption in a book) to clinical disorders where the disconnection becomes distressing and impairing.

Depersonalization-Derealization Disorder (DDD)

DDD involves persistent feelings of detachment from one's self (depersonalization) or surroundings (derealization):

Patient Description: "I feel like I'm watching myself from outside my body, like I'm in a movie. Everything seems unreal, dreamlike, behind glass. Intellectually I know it's me and this is real, but I don't feel it emotionally. There's no sense of connection to anything."

Key Features:
  • Intact reality testing (they know it's a feeling, not actually detached)
  • Emotional numbing or blunting
  • Feeling like an outside observer of one's thoughts, body, or actions
  • World seems foggy, flat, colorless, or two-dimensional
  • Often triggered by stress, trauma, or anxiety, but can be persistent

Stimulation-Induced Dissociation: Parvizi's Findings

Parvizi et al. (2021) discovered they could induce dissociative experiences through brain stimulation. (Note: This is work I was involved in during my time at Stanford!)

Watch: Movie S1 - Patient experiencing stimulation-induced dissociation

  • Location: Stimulation of the posteromedial cortex (precuneus/posterior cingulate)
  • Patient reports: "Everything just feels weird," "I don't feel like I'm here," "Like watching myself from above"
  • Reproducible: Same experience occurred each time that specific location was stimulated
  • Implication: The sense of being present and connected to experience depends on specific brain regions functioning normally
  • Note: This is the same region (part of DMN) affected by psychedelics and meditation!
The Precuneus and Self-Awareness:

The precuneus/posterior cingulate region appears critical for:

  • First-person perspective
  • Sense of being present in one's body and experience
  • Integration of self-referential information
  • The feeling that experience is "mine"

Disrupting this region (through stimulation, drugs, or meditation) can uncouple awareness from the normal sense of self.

Ketamine: Pharmacologically Induced Dissociation

Ketamine, an NMDA receptor antagonist, produces dose-dependent dissociative effects and is increasingly used to study dissociation in controlled settings:

Ketamine Effects at Sub-Anesthetic Doses:
  • Feelings of detachment from body and environment
  • Out-of-body experiences
  • Altered time perception (time speeding up or slowing down)
  • Sense that things aren't real
  • Difficulty forming coherent thoughts
  • Research utility: Can induce controlled dissociative states while measuring neural correlates, helping identify mechanisms
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    Out-of-Body Experiences (OBEs)

    OBEs represent an extreme form of dissociation where people report perceiving from a location outside their physical body (like in the video above!):

    • Can occur spontaneously, during near-death experiences, or under extreme stress
    • Blanke et al. (2002): Electrical stimulation of temporo-parietal junction (TPJ) induced OBE-like experiences
    • TPJ integrates visual, vestibular, and somatosensory information to create sense of body location in space
    • Disrupting this integration can cause experienced location to dissociate from physical location
    • Implication: The sense of being "located" in your body is actively constructed, not a given

    What Dissociation Reveals About Consciousness

    Lessons from Dissociation:
    • The sense of self is not unitary but composed of multiple processes (agency, ownership, location, continuity) that can separate
    • Emotional connection to experience is dissociable from cognitive awareness
    • The feeling of "realness" is constructed—the same perceptual input can feel real or unreal
    • Body ownership and sense of location involve distinct neural mechanisms
    • The boundary between self and world is actively maintained and can be disrupted

    Closing Thoughts: What Have We Learned?

    Today we've seen how perturbing normal consciousness—whether through chemicals, practice, stimulation, or naturally occurring conditions—reveals the hidden architecture of subjective experience. Several key themes emerge:

    Common Threads:
    • The Default Mode Network appears central to self-experience: Psychedelics, meditation, dissociation, and stimulation all implicate DMN regions in maintaining our sense of self and presence
    • Consciousness is constructed, not given: Our experience depends on active neural processes that can be disrupted, revealing how fragile and fabricated "normal" consciousness is
    • Multiple methods converge: Different approaches (pharmacology, training, stimulation) point to the same brain regions and mechanisms
    • Experience is dissociable: What seems like unified consciousness can fragment into components—showing that integration itself is an achievement
    • Individual differences matter: As my own research shows, the same brain networks can produce different subjective experiences depending on how we interpret the world
    • The challenge of access remains: Even with all these tools, we still face the hard problem: we can correlate brain states with reported experiences, but we can't directly access what it's like to be someone else

    Thank You!

    As always, feel free to reach out with questions, reflections, or if you'd like to discuss any of these topics further!