ADHD และ Dopamine

1. Overview — ADHD and Dopamine

ADHD is a neurodevelopmental condition that is directly related to the brain’s self-regulation system, in which one of the most important “main actors” is dopamine. But one thing that must be clearly understood first is this: ADHD is not a state of “low dopamine throughout the whole brain,” as many people oversimplify it. In reality, the abnormality lies in the pattern of dopamine signaling that is imbalanced, mistimed, and context-inappropriate in certain brain circuits, not in all of them.

More than 40 years of research have found that people with ADHD often have abnormalities in several components of the dopamine system, such as:

• The sensitivity of dopamine receptors (D1, D2 receptors)
• The density of dopamine transporters (dopamine transporter: DAT)
• The functioning of fronto-striatal and fronto-cerebellar networks

All of these directly affect the ability to focus, plan, decide, and control impulses.

Dopamine is also the neurotransmitter behind the human reward–motivation system. When this system is disrupted, an ADHD brain cannot easily “power on” or “light up” for tasks that are not engaging, have low stimulation, or lack emotional meaning. This explains why people with ADHD may perform very well on difficult tasks under high pressure or close to a deadline — because the brain has just received a “rapid dopamine boost.”

In terms of time perception, dopamine is also involved. People with ADHD often experience “time blindness”: they feel unable to track time accurately, do not realize how much time has passed, and do not feel the internal drive to start tasks until it is too late. All of this reflects abnormalities in the circuits that use dopamine to control timing and time prediction.

Moreover, dopamine does not work alone. The norepinephrine (NE) system works closely alongside it, especially in the prefrontal cortex, which is the command center for executive function, working memory, and impulse control. Therefore, ADHD is not merely a “dopamine disorder,” but rather a broader catecholamine dysregulation.

Ultimately, what should be remembered is this: dopamine abnormalities in ADHD are more about “circuit instability” than about the sheer quantity of the chemical itself. In some situations, dopamine may be too low for boring tasks, while in other moments it may spike at the wrong time in highly stimulating tasks, leading to hyperfocus. These patterns tell us that ADHD is a brain that responds to environmental conditions differently from the norm, not a “damaged” brain. It is a brain that requires different environmental structures and working processes in order for its dopamine system to function at its best.

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2. Core Symptoms — Key Symptoms Linked to Dopamine

This section is the heart of understanding ADHD from a “neuroscience” perspective, because every observable symptom — from being easily distracted to suddenly “warping” into scrolling the phone without realizing it — all traces back to unstable dopamine signaling (dopamine dysregulation).
It is not just “low dopamine,” but rather dopamine that does not respond appropriately to context — for example, tasks that require prolonged focus, tasks with no immediate reward, boring tasks, and tasks that must be initiated independently.

2.1 Inattention — Short Attention Span / Easily Distracted (Dopamine in Depth)

Inattention in ADHD is not a matter of “lack of discipline,” but a failure to properly activate the prefrontal–striatal networks.
These circuits rely on dopamine as a “goal selector switch” that allows the brain to choose what to focus on. When dopamine signaling is inconsistent, the brain will:

• Fail to switch into “focus mode” for tasks that lack stimulation
• Lose the ability to effectively filter out distractions
• Pay attention to whatever is more interesting, even if it’s not important
• Keep switching between tasks like having 20 browser tabs open at once

Most importantly, dopamine also plays a role in reward prediction, so an ADHD brain is reluctant to initiate tasks where the reward is “far away,” where there is “no feedback,” or where the task is simply “boring,” because the reward system does not help push it into action.

Behavioral outcomes:

• Easily forgets tasks
• Misses small details in work
• Severe procrastination
• Cannot initiate tasks even when they know they must be done
• Cannot sustain external focus, while the inside of the mind is full of noise and thoughts

What research has found:
Brain scans show that people with ADHD have reduced activation in the dorsolateral prefrontal cortex (DLPFC), which is responsible for working memory and sustained attention → this aligns with the clinical pattern of poor task sequencing and difficulty retaining details.

2.2 Hyperactivity — Restlessness / Inability to Stay Still (Dopamine in Depth)

Hyperactivity does not always mean “naughty hyperactive child.” Especially in adults, it often appears in a form called internal hyperactivity, or “inner restlessness.”

Biological explanation:
When dopamine circulation in the prefrontal cortex is unstable, the brain feels as though it is not receiving enough stimulation. As a result, it tries to “generate its own stimulation” through behaviors such as:

• Leg shaking
• Constant body movements
• Fidgeting with objects in hand
• Flipping pens, spinning the phone
• Constantly getting up from the chair

It is as if the body is saying:

“I have to move, or I can’t think.”

In adults, this may be suppressed at the physical level, but it reappears at the mental level instead, such as:

• Rapid, looping thoughts
• Mental restlessness / constant mind-chatter
• Feeling uncomfortable when having to stay still
• Being unable to engage in activities that require sitting quietly

An unstable dopamine system makes the brain “seek outlets” through movement throughout the day, often without the person even realizing it.

2.3 Impulsivity — Acting on Impulse (Dopamine in Depth)

Impulsivity reflects a conflict between two systems in the brain:

• The reward system → responds quickly to dopamine and acts fast
• The control system (executive control / PFC) → works more slowly and depends on inhibition

In ADHD, the reward system “fires strong dopamine signals” when it sees something immediately desirable — a pop-up notification, a message, something interesting on the desk, or the urge to speak during a meeting — but the prefrontal cortex “fails to inhibit it in time.”

Real-life outcomes:

• Blurting things out without intending to
• Making immediate purchases without thinking
• Making quick decisions in relationships
• Switching tasks every 2 minutes
• Grabbing what they want as soon as they see it

Impulsive behavior is therefore not “stubbornness,” but the result of a dopamine-driven reward circuitry that responds too quickly, combined with a PFC that is slower at applying the brakes.

2.4 Motivation & Reward — A Mis-Timed Motivation System (Dopamine in Depth)

This is one of the most misunderstood symptom clusters.
People often interpret ADHD as = laziness.
In reality, it is a dysfunction in the activation of dopaminergic circuits related to reward anticipation.

People with ADHD tend to:

• Fail to “start up” for tasks that “do not give immediate rewards”
• Prefer tasks with urgent deadlines because of the dopamine boost
• Slip into hyperfocus easily when the task is highly engaging
• Feel little internal drive even when they know they should do something

The dopamine system responds to stimuli that have emotional meaning, not equally to every task like in a neurotypical brain.
As a result, motivation in ADHD is context-dependent, not a lack of “discipline.” It is more accurate to say the brain chooses to invest energy in tasks that stimulate dopamine.

This is why they can focus for 10 hours straight on something they love, but cannot start a 10-minute task if it is boring.

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3. Diagnostic Criteria — DSM-5-TR

The DSM-5-TR does not explicitly mention dopamine, but its criteria strongly reflect the neurobiology of ADHD, especially dysfunction in the prefrontal cortex, fronto-striatal circuits, and dopamine-mediated reward processing.

3.1 Symptom Count

The DSM states that in order to diagnose ADHD, there must be a sufficient number of symptoms in either the inattention or the hyperactivity-impulsivity clusters:

• Children: ≥ 6 symptoms
• Adults (≥17 years): ≥ 5 symptoms

An important note is that the number of required symptoms decreases in adults because some symptoms “change their form” — for example, hyperactivity in children becomes internal restlessness in adults, but still disrupts dopamine-related circuits in the same way.

3.2 Duration ≥ 6 Months (Chronic Pattern)

ADHD is not a temporary state or a reaction to acute stress.
The 6-month duration criterion is meant to distinguish ADHD from:

• Short-term stress reactions
• Mood fluctuations
• Temporary attention problems due to illness
• Attention issues caused by sleep deprivation

If symptoms are chronic and form part of the person’s “habitual behavior pattern,” that is what the DSM aims to capture — and this reflects that dopamine circuits and prefrontal function are abnormal at a structural or developmental level.

3.3 Symptoms Must Occur in ≥ 2 Settings (Multiple Settings)

This is the golden rule of diagnosis.
If symptoms occur only in specific contexts, such as:

• Only at home
• Only with certain people
• Only in a particular type of relationship

then it may not be ADHD, but rather an issue related to emotions, stress, relationship dynamics, or environment.

True ADHD is a neurodevelopmental disorder → it must appear across multiple contexts, such as:

• Home
• Workplace
• School
• Social situations
• Various interpersonal settings

This criterion reflects that the core problem lies in the brain, not purely in external factors.

3.4 Onset Before Age 12

Because ADHD is a disorder of “brain development” (neurodevelopment), it must begin in childhood, even if some individuals are not diagnosed until adulthood.

In childhood, hyperactive symptoms are often obvious, but as the person grows, the symptoms transform:

• From “a child running around all day” → to “thoughts that never stop in the head”
• From “talking non-stop” → to “constantly wanting to speak in every meeting”

Identifying the age of onset helps distinguish ADHD from other conditions such as depression, anxiety, PTSD, or cognitive fatigue in adults, which can also reduce attention but arise from different causes.

3.5 Functional Impairment

ADHD symptoms must interfere with daily functioning, for example:

• Tasks not completed
• Falling behind in studies
• Relationships breaking down due to impulsivity
• Forgetting meetings
• Poor time management

From a dopamine perspective, this is where the picture becomes clearest, because functional impairment reflects dopamine circuits that cannot maintain goal-directed behavior in the real-world context.

3.6 The DSM Never Says “Dopamine” — But Dopamine Is in Every Criterion

If you examine every DSM-5-TR criterion closely, you’ll see that they almost all map onto dopamine’s roles:

• Inattention = low dopamine-related activity in PFC circuits
• Impulsivity = a reward system that reacts too quickly
• Poor time management = dysfunction in dopamine–cerebellar and time perception circuits
• Forgetfulness = working memory dependent on dopaminergic modulation
• Difficulty initiating tasks = a motivation system dependent on dopamine

In other words, even though the DSM doesn’t spell out the word “dopamine,” dopamine is essentially “the backbone of all the symptoms.”

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4. Subtypes or Specifiers

The DSM-5-TR uses the term “presentations” rather than “subtypes”:

• Predominantly Inattentive Presentation (ADHD-PI)
  Mainly characterized by distractibility, forgetfulness, and poor task management.
  Dopamine picture: the primary issues lie in attention and executive function circuits rather than in outward hyperactivity.
  
  
• Predominantly Hyperactive-Impulsive Presentation (ADHD-PHI)
  Characterized by impulsivity + restlessness.
  In children, this is often obvious: leaving seats, running, climbing, talking excessively.
  Dopamine picture: may relate to an overdriven reward-seeking system combined with weaker prefrontal inhibition.
  
  
• Combined Presentation (ADHD-C)
  Includes both inattentive and hyperactive-impulsive symptoms.
  This is the most commonly seen presentation in clinical practice.

Additional specifiers:

• Partial remission — previously met full diagnostic criteria but now only some symptoms remain.
• Severity — mild / moderate / severe, depending on the number and intensity of symptoms.

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5. Brain & Neurobiology

This section is the core of understanding “why the ADHD brain works the way it does.”
Every symptom — distractibility, restlessness, impulsivity, slow task initiation, time blindness — arises from brain structures and chemical signaling that differ from the general population, especially the dopamine and norepinephrine systems that govern attention circuits, memory, and impulse control.

5.1 Major Brain Circuits Involved in ADHD

1. Fronto-striatal Circuits (PFC ↔ Striatum)

This is the most frequently discussed circuit and is almost a signature of ADHD.
It consists of:

• Prefrontal Cortex (PFC) → the “executive manager,” responsible for planning, decision-making, and inhibiting impulses
  
  
• Striatum (Caudate, Putamen) → involved in task initiation, task switching, reward processing, and motor control

Problems identified in ADHD:

• Connectivity in this circuit is lower than normal (hypoconnectivity)
  
  
• Dopamine signaling within the circuit is weak or mistimed
  
  
• This leads to problems such as:
• Inability to initiate tasks
• Rapid task switching
• Immediate distraction by external stimuli
• Poor planning and sequencing
• Weak performance on tasks that require working memory

Simply put:

Fronto-striatal circuits = the brain’s system for “choosing goals – taking action – self-control.”

In ADHD, this system is flickering on and off, like a signal that keeps cutting out.

2. Fronto-striato-cerebellar Circuits (PFC ↔ Striatum ↔ Cerebellum)

Many people think the cerebellum is only for motor control, but in ADHD, the cerebellum is an MVP that is often overlooked. Research has shown that children and adults with ADHD often have slightly smaller cerebellar volume and abnormal connectivity.

Behavioral effects:

• Time blindness (distorted sense of time)
• Poor sequencing of task steps
• Slow work, delays, or skipping steps
• Inability to regulate “thinking tempo” (too fast / too slow / stacked thoughts)
• Poor motor rhythm, such as slow typing or messy handwriting

The cerebellum is the “metronome of the brain.”
In ADHD, when this metronome is off-beat, other systems start to fall apart too.

3. Default Mode Network (DMN) vs Task-Positive Networks (TPN)

DMN = the “mind-wandering mode” — internal thoughts, imagination, revisiting the past, projecting into the future.
TPN = the “task mode” — doing, goal-directed thinking, focusing on the task at hand.

In neurotypical people, the DMN shuts down when they begin focusing on a task.
But in ADHD:

• The DMN doesn’t fully shut off
• DMN and TPN switch in and out of phase irregularly
• This produces mind-wandering even when the person intends to focus

This explains why…

• They drift off after only a short while in a meeting
• They read but don’t know how many pages have gone by
• They suddenly start thinking of other things in the middle of work, without intending to
• They can only stay focused in tasks where dopamine is high

Stimulants such as methylphenidate and amphetamine will:

• Increase dopamine/NE in the PFC
• Suppress DMN activity
• Boost TPN activity

→ resulting in more stable focus.

5.2 Dopamine Transporter (DAT), Receptors, and Chemical-Level Abnormalities

1. Higher DAT Density Than the General Population

Research has found that ADHD, especially of the inattentive type, is associated with increased DAT density in the striatum.
Consequences:

• Dopamine is reabsorbed too quickly
• Dopamine levels in the synapse drop prematurely
• Dopamine signals become short and weak → tasks requiring sustained attention deteriorate

It’s like sending an important message, but the recipient only reads it for 1 second and immediately deletes it.

2. Abnormal Dopamine Receptors (D4, D5)

The DRD4 gene, especially the 7-repeat allele, has been linked to:

• Increased risk of ADHD
• Slower response to reward
• Higher distractibility
• Greater difficulty inhibiting impulses

Behaviorally, this results in:

• Needing stronger motivation than average
• Finding boring tasks especially hard to complete
• Seeking extra stimulation (novelty-seeking)

5.3 Catecholamines: Dopamine + Norepinephrine (The Brain’s Duo)

In the PFC, the core mechanism for focus does not rely on dopamine alone, but on a balanced combination of dopamine + norepinephrine.

• Dopamine helps “select what to focus on”
• Norepinephrine helps “stabilize the signal”

In ADHD, both signals are out of sync → the executive function system collapses.
This is also why non-stimulant medications such as atomoxetine, which primarily increases NE, can be very effective for some individuals.

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6. Causes & Risk Factors

ADHD emerges from the convergence of many factors rather than a single cause, and dopamine is the “central mechanism” of these combined influences. In truth, it is a neurodevelopmental disorder that starts while the brain is still forming in the womb, not a condition that suddenly appears in adulthood.

6.1 Genetic Factors

ADHD is one of the most highly heritable conditions in psychiatry.
Twin studies estimate heritability at around 70–80%.

The most studied genes include:

• DAT1 (dopamine transporter gene) → regulates dopamine reuptake
• DRD4 / DRD5 (dopamine receptors) → control how the brain responds to reward
• COMT → enzyme that breaks down dopamine in the PFC
• SNAP-25 → involved in neurotransmitter release

The combined effect of abnormalities in these genes includes:

• Unstable dopamine signaling
• Weak working memory
• Low impulse control
• Underperforming attention circuits

Genetics does not “determine that you will definitely have ADHD,” but it “increases the risk that brain structure and chemistry will develop differently.”

6.2 Neurodevelopmental Factors — Brain Development Influences

The period of brain development in the fetus is a golden window; if disrupted, the effects can be long-lasting.

Risk factors include:

• Premature birth
• Low birth weight
• Perinatal hypoxia (lack of oxygen)
• Maternal exposure to alcohol / nicotine / toxins
• Infections during pregnancy
• Complications during birth

All of these can disrupt the development of:

• The prefrontal cortex
• Dopaminergic pathways
• Cerebellar growth

The result is that self-regulation networks do not fully develop, and this effect can persist into adulthood.

6.3 Environmental & Psychosocial Factors

Environment does not “create ADHD,” but it amplifies or dampens symptoms.

Risk factors that intensify symptoms:

• Chaotic home environment with poor structure
• Chronic stress in childhood
• Neglect or inconsistent caregiving
• Educational systems that do not fit ADHD learning styles
• Childhood trauma

Chronic stress directly affects dopamine pathways,
causing the brain to use dopamine in a “survival” mode rather than a “goal-directed/focus” mode.

6.4 Comorbidity — Co-occurring Conditions Related to Dopamine

ADHD has a high rate of comorbidity with other conditions because they share overlapping brain circuits, such as dopamine–serotonin–glutamate networks.

Common comorbidities:

• Anxiety disorders (around 50%)
• Depression
• Bipolar spectrum disorders
• Substance use disorders (this group is at risk due to pre-existing dopamine dysregulation)
• Learning disorders such as dyslexia

When comorbidities are present, the dopamine system becomes even more imbalanced, requiring highly individualized treatment adjustments.

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7. Treatment & Management

This section provides knowledge-based information and is not a substitute for personal medical advice.
Any use or adjustment of medication must be done under the supervision of a physician.

7.1 Pharmacological Treatment (Medication)

1. Stimulants (e.g., methylphenidate, amphetamine derivatives)

Main mechanisms:

• Inhibit the reuptake of dopamine and norepinephrine via DAT and NET
  
  
• Some agents increase dopamine release in the synapse
  → This prolongs dopamine and NE presence in the prefrontal cortex → improves the ability to focus and control impulses
  Psychiatrist.com+2PubMed+2

Behavioral effects:

• Better focus on tasks that were previously unmanageable
• Less distractibility and less frequent task switching
• Decreased hyperactivity / impulsivity

However, there are side effects that must be monitored, such as loss of appetite, weight loss, insomnia, irritability; newer research and regulatory agencies such as the FDA have adjusted warnings in young children, for example, weight-related risks in extended-release stimulants in children under 6 years of age.
Cleveland Clinic+1

2. Non-stimulants

Such as atomoxetine (SNRI), guanfacine, clonidine, etc.

• Atomoxetine primarily increases norepinephrine but also has indirect effects on dopamine in the prefrontal cortex.
  
  
• Guanfacine / clonidine stimulate alpha-2 adrenergic receptors, helping to stabilize PFC functioning.

Used when:

• Stimulants are not tolerated
  
  
• Certain comorbid conditions are present
  
  
• Specific side effects from stimulants need to be avoided
  Cleveland Clinic+1

7.2 Psychosocial & Behavioral Interventions

These affect dopamine indirectly by “designing the environment” to fit an ADHD brain.

• Cognitive-Behavioral Therapy (CBT) for ADHD
  Helps manage time, planning, and emotion regulation.
  
  

• Coaching / Skills Training
  

  Teaches techniques for organizing the workspace, making to-do lists in ways that “reduce dopamine load” — for example, breaking tasks into smaller steps with mini-rewards.
  
  

• Parent Training / Psychoeducation
  

  In children: teaches parents to understand that their child’s brain uses dopamine differently from other children.
  
  Reduces interpretations such as “stubborn / lazy” and shifts toward more effective behavioral management strategies.

7.3 Lifestyle & Self-Management

These are areas where research shows moderate evidence of links to dopamine and attention:

• Aerobic exercise
  

  Increases dopamine and BDNF in the brain → improves short-term attention after exercise.
  
  
• Adequate sleep
  Sleep deprivation disrupts the dopamine system and worsens ADHD symptoms.
  
  
• Nutrition / Caffeine / Sugar
  These are not the root cause of ADHD, but they can enhance or undermine energy levels and attention.

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8. Notes — Key Points & Common Misunderstandings

• “ADHD = low dopamine” = oversimplification.
  

  In reality, it is “dopamine dysregulation” in specific circuits.
  
  In some areas dopamine may be too low; in others it may be too high, or fluctuate depending on the situation.

• Medications do not “fill the brain with as much dopamine as possible.”
  

  The goal is to “tune the signal to a functional balance”, not to boost it like an addictive drug.
  
  Dosage and release format (immediate vs extended-release) are designed so that the dopamine curve is as stable as possible during the hours when the brain needs to work.
  PMC+1

• ADHD = a differently developing brain, not a character flaw.
  

  Interpreting it as “lazy / undisciplined” makes the person feel guilty, even though the core problem lies in dopamine circuits and the prefrontal cortex.

• Treatment response varies.
  

  Two individuals with ADHD may have very different baseline dopamine profiles → they may respond differently to medication type and dosage.
  
  There are subgroups for which the dopamine hypothesis explains a great deal, and subgroups for which other circuits play a larger role.
  Frontiers+1

• Do not self-diagnose based solely on online content.
  

  Even though knowledge about dopamine can help you “understand yourself” better, proper diagnosis still requires comprehensive clinical evaluation.

READ ADHD

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📚 References — Academic & Clinical Sources

Compiled from research in neuroscience, psychiatry, neurobiology, dopamine pathways, DSM-5-TR, and clinical pharmacology

• American Psychiatric Association. (2022). Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR).
• Del Campo, N., Fryer, T. D., Hong, Y. T., & Rubia, K. (2011). A review of the role of the dopamine system in ADHD. Biological Psychiatry, 69(12), e145–e157.
• Faraone, S. V., Biederman, J., & Mick, E. (2006). The age-dependent decline of ADHD: A meta-analysis of follow-up studies. Psychological Medicine, 36(2), 159–165.
• Arnsten, A. F. T. (2009). The emerging neurobiology of ADHD and the role of catecholamines in prefrontal cortical function. Journal of Clinical Psychiatry, 70.
• Volkow, N. D., Wang, G. J., Newcorn, J., Fowler, J. S., et al. (2007). Brain dopamine transporter levels in treatment-naive ADHD adults. JAMA, 286(9), 1123–1131.
• MacDonald, H. J., et al. (2024). Evaluating the dopamine hypothesis of ADHD: A systematic review. Frontiers in Psychiatry, 15.
• Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., et al. (2007). Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. PNAS.
• Cortese, S. (2012). The neurobiology and genetics of ADHD: An update. Child and Adolescent Psychiatric Clinics of North America.
• Arnsten, A. F. T., & Li, B. M. (2005). Neurobiology of executive functions: Catecholamine influences on prefrontal cortical functions. Biological Psychiatry.
• Spencer, T., Biederman, J., Wilens, T., et al. (1998). Pharmacotherapy of ADHD across the life cycle. Journal of the American Academy of Child & Adolescent Psychiatry.
• Nigg, J. T. (2012). Future directions in ADHD neuropsychology: Understanding neural pathways and developmental trajectories. Developmental Psychology.
• Rubia, K. (2018). Cognitive neuroscience of attention deficit hyperactivity disorder (ADHD) and its clinical translation. Frontiers in Human Neuroscience.
• Sripada, C. S., et al. (2014). Disrupted network architecture of the resting brain in ADHD. Brain Connectivity.
• Castellanos, F. X., et al. (2002). Developmental trajectories of brain volume abnormalities in ADHD. JAMA.
• Faraone, S. V., & Larsson, H. (2019). Genetics of ADHD: State of the field. Current Psychiatry Reports.
• American Academy of Child & Adolescent Psychiatry (AACAP). ADHD Clinical Practice Guidelines.
• National Institute of Mental Health (NIMH). ADHD: Causes, Brain Circuits & Treatments.

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