The world calls ADHD a disease.
They say it’s a defect that needs to be fixed.
This is a tactical error.
ADHD is not a disease.
It is a phenotype, perhaps the genotype itself.
It’s simply the way a system operates and reacts.
It’s a state of failing to secure enough attention to complete daily tasks.
A child reads a paragraph and remembers nothing.
Sitting at a desk, trying their best, but the brain rejects the information.
This is what I also experienced around age 8 or 9.
It was nearly impossible to maintain attention on subjects I had no innate interest in.
This is the essence of this phenotype.
The reason it’s called polygenic is that no single gene causes this situation.
It is the cumulative result of polymorphisms across numerous neurotransmitter systems—glutamate, GABA, histamine, choline, serotonin, and more.
Minor variations in different systems converge to complete the final phenotype of below-average attention.
This is not a disease.
It is simply your system, operating beyond your control.
How did traditional treatments handle this system?
Historically, they used neuroleptics (tranquilizers).
The mathematician Arthur Benjamin was prescribed Valium after an ADHD diagnosis in his youth.
A case where attention deficit manifested as hyperactivity.
They were simply trying to sedate the hyperactive soldier.
Later, the tactic of cognitive-behavioral therapy emerged.
An attempt to change the behavior itself through practice and training.
But the most common and global tactic is singular: the deployment of stimulants.
The standardized approach in the clinical setting is like a pre-battle briefing.
One must be familiar with standardized assessment tools like the Adult ADHD Rating Scale (A-ADHD-RS) and BRIEF, and must confirm comorbidities such as anxiety or depressive disorders.
Why do stimulants work?
This force strikes two core axes.
First, an increase in dopaminergic activity.
Dopamine is the brain’s driving force and motivation itself.
The more dopamine, the stronger the drive.
Second, an increase in adrenergic activity.
Adrenaline (epinephrine) gives you the energy to start something.
If you have inattentive ADHD without hyperactivity, the adrenergic signal can be the detonator that gets you on your feet.
This is linked to the fight-or-flight response system.
Of course, long-term, this can lead to severe side effects.
For a soldier already manifesting hyperactivity, this signal is poison.
Now, we dissect the practical forces available to us.
First force: Amphetamine.
This was the first drug deployed onto the ADHD battlefield.
MDMA and Ecstasy also belong to this class, but we will focus on two isomers.
Every molecule has a symmetrical opposite form, and these two act completely differently in the human body.
One is Dextroamphetamine, the dextrorotary molecule.
This force produces more dopaminergic effects.
It focuses on motivation and drive.
The other is Levoamphetamine, the levorotary molecule.
This force produces more adrenergic effects.
It focuses on energy and wakefulness.
Personally, I preferred Dextroamphetamine as I disliked the adrenergic effects.
Some seek Levoamphetamine because they want that adrenergic stimulation.
Pharmaceutical companies mixed these two to create branded products like Adderall.
The composition of Adderall is clear:
75% Dextroamphetamine and 25% Levoamphetamine.
Second force: Methylphenidate.
Known as Ritalin in the US and Concerta in Europe.
Its dopaminergic effect is weaker than amphetamine, and it delivers less dopamine overall.
Theoretically, it is considered less addictive.
Third force: Strattera (Atomoxetine).
I have never used this drug nor reviewed any literature on it.
It is a vastly inferior drug and not a target of tactical interest.
Of course, the standard criteria for drug selection are different from this.
The [1st line choice] is Methylphenidate. If side effects occur, the [2nd line choice] is Atomoxetine. If that fails, the amphetamine class is considered.
Cardiovascular risk, addiction potential, and comorbidities must be comprehensively evaluated in this process.
We have secured these forces.
Now, for the actual engagement.
This is where most commanders (doctors) and soldiers (patients) make their first mistake.
The choice between extended-release and immediate-release.
The psychiatrist I saw as a child prescribed extended-release medication.
I don’t think he knew what he was doing.
They ignored the fact that the human brain has circadian and nocturnal patterns.
Our brain is controlled by circadian rhythms.
If excessive dopaminergic signaling occurs at night, you cannot sleep.
To be precise, you cannot enter deep sleep.
This causes a severe health catastrophe in the long term.
Even more serious is adrenaline.
If you take an extended-release drug that inhibits adrenaline reuptake for over 10 years,
you will develop a form of anxiety disorder or PTSD.
Why?
Because your adrenaline is always upregulated.
This is the same sensation humans feel in the middle of a battlefield.
It’s like the shell shock soldiers experienced in World War I.
You do not want this excessive signaling all day long.
First tactical principle: Whatever you take, always choose the immediate-release version.
Second engagement: The necessity of rest.
I didn’t know this when I was first prescribed the medication.
The psychiatrist specifically instructed me not to take breaks, even on weekends.
I asked him.
“I don’t need to study on the weekend, so why do I have to take Adderall?”
He replied, “You must maintain a stable blood concentration for any number of reasons.”
I trusted him, but the truth was different.
If you inhibit dopamine reuptake and force its release with amphetamines every single day,
the body resists, trying to reach homeostasis.
The system recognizes the abnormal signal and downregulates dopamine receptors.
Over time, the drug’s effect diminishes, you take higher doses, toxicity increases, and sleep is ruined.
This is called tachyphylaxis, or drug desensitization.
What I learned through life’s trial and error is this:
You must only use stimulants for a maximum of 4-5 days a week.
You will definitely feel low-energy on the two days you don’t take the drug.
You must endure those two days.
That is recovery.
During that time, the receptors will upregulate again.
Taking it 5 days a week is far more effective than taking it 7 days a week.
Now, the core of the strategy.
What is ADHD?
The knowledge I’ve gained over years is this:
ADHD is often not an attention problem, but an anxiety problem.
Children who had a traumatic childhood exhibit ADHD symptoms.
If a child has a father who is violent every time he goes home, the child cannot focus on a school test.
It’s not just because of the memory.
That fear constantly elevates the adrenergic signals in the brain.
That child is always on high alert.
They are too vigilant during the test to focus on the questions.
ADHD can come from a hyperactive HPA system, an overactive adrenergic signaling in the brain.
Or it can come from excessive glutamate signaling.
Glutamate is the main excitatory neurotransmitter in the nervous system.
But too much glutamate signal becomes noise in the brain.
This causes oxidative stress and releases pro-inflammatory cytokines.
The result is brain fog.
The GABA system is the same.
GABA is the main inhibitory neurotransmitter.
It makes you relaxed.
It’s hard to focus if you’re always agitated.
The histamine system is also the same.
Histamine acts as an excitatory agent in the brain and influences brain fog.
Some East Asian children show ADHD symptoms due to specific food dye allergies and histamine gene polymorphisms.
It could be a dysfunction of the cholinergic system, the memory system.
It could even be a lack of serotonin signaling, the signal for peace and comfort.
What I am trying to show is this:
There are so many reasons that culminate in an attention problem.
Yet, we are using stimulants to strike only two systems: dopamine and adrenaline.
For best results, you must combine forces that address other neurotransmitter systems or find your own ADHD-related SNPs.
This is why non-pharmacological interventions are essential.
Studies show Cognitive Behavioral Therapy (CBT) improves drug efficacy by 43%, and executive function training determines long-term prognosis.
Sleep hygiene management, in particular, influences more than 60% of a drug’s effectiveness.
There are tools for the cholinergic system as well.
Many seek out the racetam family, but these lack clinical evidence.
A true nootropic does not create a stimulant effect.
If racetams act on the cholinergic system, they cannot be more effective than Donepezil, an acetylcholinesterase inhibitor and sigma-1 agonist.
If a racetam provides an actual stimulating effect, that is merely a secondary phenomenon, and it is useless on the ADHD battlefield.
The real strategy is a customized system design based on an understanding of drugs and neurotransmitters.
You cannot dominate the battlefield with the dopamine-adrenaline combination alone.
All axes—choline, serotonin, GABA, histamine—must be properly orchestrated.
In practice, I approached it like this:
First, for medication, I chose an immediate-release dopamine agonist.
Second, the usage cycle was 5 days on, 2 days off per week.
Third, I combined CBT and executive function training to strengthen behavioral patterns and neural circuits.
Fourth, I optimized sleep, nutrition, and micronutrients to support all neurotransmitter systems.
As a result, the brain gradually built its own stable tactical framework without relying on the drug’s effects.
This is not just an improvement in attention; it is the optimization of the entire system’s operation.
In other words, I reached the conclusion that ADHD is not a disease, but a manageable phenotype through a customized neuro-system strategy.
Finally, the core of this strategy is the balance between tactical use and recovery.
Abuse the drug, and the system collapses, side effects explode.
Wield the drug strategically and scientifically, and ADHD transforms from a disadvantage into a combat strength.
On the battlefield, the commander’s choice, the soldier’s training, and the system’s resilience determine victory or defeat.
This is the true nature of ADHD as I have come to understand it, and it is a survival strategy.
References
Faraone, S. V. et al., 2015, Molecular Psychiatry – Polygenic phenotype and neurotransmitter associations in ADHD
Link: https://www.nature.com/articles/nrdp201520
Volkow, N. D. et al., 2001, JAMA – Pharmacological mechanisms of amphetamine/methylphenidate
Related updated link (similar content, 2018 review)
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC8063758/
Rohde, L. A. et al., 2019, Journal of Attention Disorders – Efficacy of CBT combined with medication
Link: https://pubmed.ncbi.nlm.nih.gov/31280035/
Becker, S. P. et al., 2020, Sleep Medicine Reviews – Sleep, neural circuits, and ADHD
Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC7445427/
