One thing that has annoyed me more than anything since starting Nootropics Expert. The ignorant bloggers, so-called professional journalists and “science writers” who equate nootropics with smart drugs.
I see headlines like this every week:
“Not So Smart: The Dangers behind Nootropics, aka ‘Smart Drugs’”
“Potential Dangers Of Nootropics: What To Consider Before Using Smart Drugs”
“The Dark Side of Smart Drugs – The dangers, risks, and side effects of nootropics.”
Let’s be clear.
Smart drugs can kill you. And
nootropics can heal your brain.
Smart drugs and nootropics are completely different compounds used to optimize the brain. In this post we’re going to briefly explore the difference between the two.
We’ll dig into the pros and cons of smart drugs. The negative effects of smart drugs. And why they can be so dangerous for the young and aging brain.
We’ll also briefly look at some safe and natural nootropic alternatives to smart drugs that can achieve similar brain optimization goals for most people.
And if you need to use smart drugs to manage ADHD, we’ll look at some nootropics that can help mitigate the damage caused by these drugs.
Table of Contents
Cognitive Enhancement by Any Means Necessary
In 2013, Alan Schwarz of the New York Times wrote an article entitled, “Drowned in a Stream of Prescriptions”.[i] It’s a story about a young college class president named Richard Fee.
Richard did not have ADHD. This 24-year old college graduate lied to doctor after doctor. And for years, received a quick diagnosis and got a prescription for Adderall.
Young Mr. Fee became violently delusional and spent a week in a psychiatric hospital in 2011. He met with his doctor and got a prescription for another 90 days of Adderall. Two weeks after the prescription ran out, young Richard hanged himself in his bedroom closet.
Richard Fee is just one of an estimated one in four American teens who has misused or abused a prescription drug at least once their short lifetime.[ii]
The same study found that one in eight teens have taken a stimulant like Ritalin or Adderall. Without a prescription.
The researchers also pointed out the lax attitude of parents regarding the misuse of prescription stimulants by their kids.
If you are using or considering using prescription stimulants to help with your school work. Or to get ahead in business. It is certainly not my intention to insult your intelligence. Or to dismiss your desire to optimize your brain for whatever reason.
It is my intention however, to explore the danger involved in using prescription medications for cognitive enhancement. And to suggest safer alternatives using nootropic supplements to achieve the same goals.
The Dark Side of Smart Drugs
In January 2008, the science journal Nature conducted an informal poll of 1,400 readers from 60 countries. The journal specifically asked about three drugs: methylphenidate (Ritalin), modafinil (Provigil) and beta blockers.
One in five respondents said they had used drugs for non-medical reasons to stimulate their focus, concentration or memory. For those who did use, 62% reported using methylphenidate, 44% reported taking modafinil, and 15% said they had taken beta blockers like propranolol. A few survey respondents said they were using Adderall.[iii]
We’re going to dig into each of these smart drugs. What they are, how they work in your brain, and potential problems caused by these drugs.
Let’s start with…
Methylphenidate (Ritalin®;MPH) was originally developed to treat ADHD and narcolepsy. And is currently the most prescribed medication for the treatment of ADHD.[iv]
MPH is a stimulant that blocks the transporters that reuptake dopamine and norepinephrine into the presynaptic neuron following their release. This action prolongs the availability of these neurotransmitters in synapses to exert effects on postsynaptic neurons.[v]
MPH also affects glutamate transmission which we’ll deal with in a minute.
Studies found that reduced hyperactivity and impulsivity in MPH-treated ADHD patients also occurred in healthy people given the same dose.[vi] And this is the reason that methylphenidate is considered a cognitive enhancer.
But MPH is dose dependent. For example, doses higher than what is used to treat ADHD increases hyperactivity. And impairs attention and performance on cognition that is dependent on the prefrontal cortex.
But lower doses reduce hyperactivity and improve cognition even in healthy people.[vii]
Lower methylphenidate doses result in slight increases in dopamine and norepinephrine in the prefrontal cortex. While not affecting other brain regions. Allowing for improvements in executive function and working memory. Without increasing hyperactivity.
The Dark Side of Methylphenidate
The problem with cognitive enhancers like methylphenidate is directly related to their effects on regulation of dopamine and norepinephrine in your brain.
At optimal doses, dopamine binds to D1 receptors. And norepinephrine binds to α2 receptors. This action leads to an increase in prefrontal cortex signal-to-noise ratio. Which enhances the flow of information and strengthens communication between neurons.[viii] Helping executive function and working memory.
When dopamine and norepinephrine go beyond optimal levels, you have a problem. They activate dopamine D2 receptors and noradrenergic α1 and β receptors. This weakens the signal-to-noise ratio by activating neurons that are not supposed to be involved in the current task.
This activation of neurons that are not supposed to be involved results in hyperactivity, distractibility and poor impulse control.
But to further complicate things. Levels of dopamine and norepinephrine in a normal, healthy brain are not constant. They vary slightly even within the same person based on seasons, time of day, or the activity you are involved in.
And to be honest, there’s no way to measure optimal levels of these neurotransmitters. So dosing methylphenidate (or any other stimulant) is mostly guess work.
Methylphenidate and the Developing Brain
Methylphenidate is particularly popular in high schools and college campuses right around exam time. MPH helps you stay awake. And even helps with cognition and memory.[ix]
But there is growing evidence that methylphenidate plays havoc with the developing young brain.
Your prefrontal cortex is the region in your brain at the center for judgement control, behavior inhibition and control, emotion, logical thinking, working memory and decision making.
And continues to develop through to your late 20’s and early 30’s.[x]
Dopamine and norepinephrine levels rise and fall to allow for the maturation of executive control and reward pathways in your brain. And using MPH during this maturation process can disrupt this natural ebb and flow. Resulting in lasting behavior problems.
Studies show that using MPH early in life can alter circadian rhythms, increase anxiety that persists into adulthood, and even cause problems with object-recognition memory.[xi]
Methylphenidate and Ion Channels
Methylphenidate works differently in young brains compared to adult brains.
Researchers have recently found that methylphenidate depresses neuron activity and synaptic transmission in the prefrontal cortex of young brains. But the same dose in adult brains produces the opposite effect.[xii]
The researchers then discovered why neuronal activity was depressed in young brains. Because of activation of a channel called the hyperpolarization-activated non-specific cation channel (HCN).
The HCN channel allows for flow of positively-charged ions (like potassium), out of a neuron. Lowering its voltage potential and making it harder for the neuron to fire action potentials.
This HCN channel is activated by a hyper-dopaminergic state (too much dopamine). Which suggests that in the young brain, excess dopamine and norepinephrine caused by MPH depresses neuron activity and synaptic transmission.
But wait. There’s more…
Methylphenidate and Neuroplasticity
One important and unique property of the prefrontal cortex is its high level of neuroplasticity. Allowing for executive functions like working memory and decision-making. Neuroscientists believe this neuroplasticity may be due to the slow maturation of this part of the brain.[xiii]
Neuroplasticity is controlled by levels of AMPA receptors and NMDA receptors. Both are glutamate receptors.
NMDA receptors contain two NR1 subunits with a combination of either NR2A or NR2B subunits. NR2B conveys a slower biochemical reaction to the channel. Allowing it to remain partially open during multiple stimulations.[xiv]
This property results in continuation of neuron activity briefly after input has stopped. Which is thought by neuroscientists to be part of how working memory works.
I’ll not go into detail with the molecular biology here. Except to say that the ratio of NR2A to NR2B receptors is hypersensitive to dopamine levels.
Your prefrontal cortex has high levels of this NR2B subunit throughout life. And it’s involved in working memory formation. When this ratio is knocked out of whack from dopamine boosted by methylphenidate, you have problems with working memory.
Researchers have found that while methylphenidate can impair working memory. They also found that long-term potentiation needed to form long-term memory and sustained attention is strengthened.
And this could by why young people using methylphenidate who are not ADHD, seem to pay more attention in the classroom, and are less hyperactive. Which means learning might improve.
But what does this mean out in the ‘real world’? Take someone out of a classroom setting and put them behind the wheel of a car. And you’ve got problems.
Behavioral flexibility is needed for driving a car. You need to be able to quickly shift attention from the road, to road signs, other vehicles, and back to the road.
Rigid attention and lack of flexibility could potentially lead to inattentive or distracted driving. I’m Adult ADD and use Ritalin daily. And my wife can certainly verify her level of anxiety when I’m behind the wheel. Now I know why.
Behavioral flexibility is also part of interpersonal skills. We must be able to adapt to different people. And when at work, be able to shift plans and roles within a group to meet team goals.
A change or reduction in this behavioral flexibility caused by methylphenidate can lead to problems at work. Resulting in lower wages, unemployment or even disciplinary action.
Methylphenidate in Summary
Methylphenidate has been around for a long time. It’s safety has been proven through countless clinical trials.[xv] And treatment by 10’s of thousands with ADD, ADHD and narcolepsy has been a life-changer for many.
But recent research shows that methylphenidate is bad news for the developing brain. Anyone aged 5 – 35 years ago should take pause before dosing with this drug. Because it negatively affects the developing brain. The results of using methylphenidate could stay with you for life. Long after you stop using it.
Modafinil (Provigil®) was originally developed in France in the 1970’s for the treatment of narcolepsy. It is currently approved by the US FDA for the treatment of narcolepsy, shift-work disorder and obstructive sleep apnea.
Modafinil elevates histamine levels in the hypothalamus region of your brain.[xvi] Histamine neurons increase wakefulness and prevent sleep.[xvii] (This is why ‘antihistamines’ produce drowsiness).
Modafinil also binds to the dopamine transporter. And acts as a dopamine reuptake inhibitor (similar to methylphenidate).[xviii] Which increases dopamine, norepinephrine, and serotonin in the prefrontal cortex.
Modafinil produces a unique response in the brain compared to other stimulant drugs. It enhances the efficiency of prefrontal cortex information processing which affects executive function and working memory. While reducing reactivity to fear stimuli in the amygdala (the brain region involved in anxiety).[xix]
Modafinil and the Developing Brain
Since Modafinil affects dopamine reuptake transporters. It could induce similar effects on the brain as methylphenidate.[xx] In fact, it was shown to be as effective as methylphenidate in ADHD.[xxi]
If this is true, then it’s a cause for concern when used as a cognitive enhancer in adolescent and developing young adult brains.
As I mentioned earlier in this post, the prefrontal cortex is the center for attention and executive function. And this brain area does not finish development until the late 20’s and early 30’s.
So use of modafinil by healthy young adults under 30 years old are at risk of disruptions in brain development. Similar to young adult use of methylphenidate.[xxii]
This means that modafinil could cause changes in neuroplasticity and behavioral problems. Affecting working memory and decision making.
Modafinil and IQ
Some research shows that modafinil may only be effective in improving cognition for those with a lower IQ.
Researchers at Kings College in London analyzed two previous studies on the effects of modafinil with healthy university students. Modafinil (100 and 200 mg) significantly improved target sensitivity in a test. But only in the group of lower IQ students. And not students with a higher IQ.
In other tests using modafinil, researchers found the same results. A significant improvement in test scores. But only in students with a lower IQ.
The researchers concluded that “the results indicate that high IQ may limit modafinil’s positive effects”.[xxiii]
So if you try modafinil, are not happy with the result. It may be because you’re too smart for the drug.
Modafinil in Summary
Research indicates that modafinil is the ‘safer’ smart drug compared to the others in this post.[xxiv] And of all the stimulants used for cognitive improvement, there seems to be less addictive potential with modafinil.
Similar to methylphenidate, modafinil shows improvements in working memory in healthy adults and sleep-deprived neurohackers.
Both MPH and modafinil affect dopamine levels through blockade of dopamine reuptake transporters. And changes in glutamate signaling.
But modafinil at certain doses can cause a reduction in NMDA receptor levels which impairs working memory. While at the same time, promoting long-term potentiation and long-term memory.
Smart Drugs alter the developing brain. So anyone aged 5 – 35 years should think twice before dosing with this drug. Because it could negatively affect neuroplasticity of your developing brain. The results of using modafinil could stay with you for life. Long after you stop using it.
And finally, research shows that if you try modafinil. And are not happy with its effects. It could be because you’re too smart. Modafinil benefits seem to be limited to those with a lower IQ.
Amphetamine was first synthesized in Berlin in 1887 as 1-methyl-2-phenethylamine. It was the first of several chemicals which include methamphetamine and methylenedioxymethamphetamine.
Current prescription versions of amphetamine include names you likely recognize. They include salts of d-amphetamine (DextroStat, Dexedrine), mixed d- and l-amphetamine (Adderall™), d-methamphetamine (Desoxyn), and an amphetamine pro-drug compound, lisdexamfetamine dimesylate (Vyvanse™).
Ecstasy (methylenedioxymethamphetamine) also belongs to the amphetamine family. But is not currently contained in any prescription drug.
Amphetamine is one of the most potent central nervous system stimulants. And commonly used for treating ADHD, narcolepsy and obesity.
Amphetamine works primarily by increasing the neurotransmitters dopamine and norepinephrine in the brain. It also triggers the release of other hormones and neurotransmitters including epinephrine, histamine and serotonin.
Adderall Mechanism of Action
In your brain (not on drugs), vesicular monoamine transporter 2 (VMAT2) moves monoamines (dopamine, histamine, norepinephrine and serotonin) from inside the neuron, into its synaptic vesicles. These vesicles are like the neuron’s chemical storage units.[xxv]
When you take an amphetamine like Adderall, and it enters a neuron. It interacts with VMAT2. And the transporter reverses direction of transport. Which releases stored neurotransmitters from inside synaptic vesicles back into the neuron.
Amphetamine also activates the protein trace amine-associated receptor 1 (TAAR1) which is located in the presynaptic neuron.[xxvi]
When TAAR1 is activated, the receptor causes the neurons monoamine transporters (dopamine transporter, norepinephrine transporter, serotonin transporter) to either stop transporting those neurotransmitter molecules altogether. Or like VMAT2, transport them in reverse.
In plain English; the reversed neurotransmitter transporter pushes dopamine, norepinephrine and serotonin out of the neuron and back into the synaptic cleft.
Amphetamines like Adderall help those with ADHD and narcolepsy by increasing the activity of dopamine and norepinephrine in the brain.
The Dark Side of Amphetamines
The problem with continued or chronic use of amphetamines like Adderall is brain damage.
Amphetamines have been shown to be toxic to dopamine neurons. This “neurotoxicity” shows up as damage to dopamine dendrites and axons. Resembling the brain alterations in patients with schizophrenia. And this damage to dopamine neurons continues for years. Long after stopping use of amphetamines.[xxvii]
Long-term use of amphetamines are associated with disruption of a neuron’s vesicular storage. Leading to an accumulation of reactive oxygen species and severe oxidative stress which damage dopamine neurons.[xxviii]
It’s interesting to note that researchers have found no evidence that this neurotoxicity happens with long-term use of methylphenidate (Ritalin). Likely because MPH only blocks dopamine reuptake without disrupting the vesicular storage pool.[xxix]
Another important reason to consider avoiding amphetamines. It’s hard to stop. And I’m not talking about their addiction potential here. Which is a major concern for anyone with addictive tendencies.
If you’re using amphetamines to help cram for an exam, keep you awake on a long-haul drive, improve athletic performance, or simply enhance your experience at a party. For whatever reason, regular use of these smart drugs motivates many to continue use. Simply because it’s a bitch to stop. The withdrawal symptoms from use of any stimulant are uncomfortable to say the least.
And research shows that stimulant use during the years of brain development (ages 5 – early 30’s) can be a major problem.
The young brain in constantly in flux as it develops. Pruning of frontal cortex synapses. Decreases in receptors of different neurotransmitter systems. And substantial reorganization of dopamine neuron circuits.[xxx]
Rather than repeating what we already covered about stimulant use and neuroplasticity. I’m going to refer you back to the section on “Methylphenidate and Neuroplasticity” on why stimulant use during brain development from 5 – 35 years of age has real-life consequences.
Amphetamines and Psychosis
High doses (55 – 75 mg) of amphetamines can produce psychotic behavior that looks just like schizophrenia in healthy adults. Even a single dose.[xxxi]
One clinical study of healthy adults used repeated administrations of 5 – 10 mg of dextroamphetamine. Which produced paranoid delusions in all subjects at cumulative dosages between 55 and 75 mg.[xxxii]
And it’s not difficult to meet the criteria for amphetamine psychosis. About 30 – 40% of amphetamines are excreted unchanged after you take it. The rest of the drug is converted to metabolites. And the portion of amphetamine that is metabolized is strongly affected by urinary pH.
Eating anything acidic (peanuts, walnuts, sunflower seeds, blueberries, corn oil, sugar, etc.) causes faster elimination of amphetamine. But eating anything alkaline (i.e. antacids) can dramatically increase both retention and absorption of amphetamines. Sometimes to dangerously high levels.
Studies suggest that the accumulation of metabolites may contribute to the generation of psychotic symptoms.[xxxiii] And neurotoxicity.
One case study concluded that a daily dose of 10 mg of Adderall taken over five weeks for ADHD induced classic psychosis symptoms in a 12 year old girl. The study reported that…
“She had flight of ideas, tangential thought, a flat affect, psychomotor retardation, loss of short-term memory, and extremely poor hygiene. She also displayed magical thought, describing a personal acquaintance with characters from Greek mythology, and described visual hallucinations: disembowelment of her baby brother and bugs crawling on the walls. She had command auditory hallucinations instructing her to “stab holes in [her] brother. And bugs crawling under her skin”.[xxxiv]
Chances are you’ll not experience psychotic episodes while taking an amphetamine like Adderall. Just consider this when deciding whether amphetamines are worth the risk.
Amphetamines in Summary
Amphetamines have been around since 1887. Their safety has been in debate since. But if you have been diagnosed ADD or ADHD and prescribed Adderall or its equivalent, I’m certainly not suggesting you avoid taking your medication. Just be aware of what amphetamines could be doing to your brain. And take whatever protective measures you can.
There is little doubt that amphetamines are bad news for the developing brain. Anyone aged 5 – 35 years should take pause before dosing with these smart drugs. Because they negatively affect the developing brain. The results of using amphetamines could stay with you for life. Long after you stop using it.
And the chances of experiencing psychotic episodes while taking amphetamines are low. But certainly worth considering.
Preventing Brain Damage Caused by Amphetamines with Nootropics
In a relevant animal model, researchers looked at amphetamine use in baboons and squirrel monkeys. The animals matched human ADHD patients after clinical treatment with Adderall.
The animals showed a 30 – 50% reduction in dopamine, its major metabolite, its rate-limiting enzyme, its membrane transporter, and its vesicular transporter.[xxxv]
Parkinson’s Disease typically requires about 80 – 90% reductions in dopamine resulting in symptoms. So we’re not equating amphetamine use to Parkinson’s.
But aging itself produces declines in dopamine neurons, dopamine metabolites and dopamine receptor binding. Similar to the losses seen from amphetamine use. Which leads to cognition problems.[xxxvi]
So if you are using Adderall or a similar medication for treating ADHD. I’m not suggesting you stop taking your meds. I am suggesting that you take precautionary measures to protect your brain. Here’s how…
If you have bipolar disorder and are taking stimulant meds. One study showed that using lithium helps protect against dextroamphetamine-induced alterations of brain choline concentrations.[xxxvii]
Recent animal studies have produced evidence for neuroprotection against amphetamine-caused toxicity by supplementing with:
Prescription Ampakine Alzheimer’s Drugs
The last class of smart drug we’ll look at in this post are prescription ampakines.
Ampakines are a class of smart drugs that bind to the glutamate AMPA receptor. Which enhances the receptor’s activity by slowing deactivation. And reduces desensitization of AMPA receptor currents. Which increases synaptic response and long-term potentiation.
These are the same reasons we use ampakine nootropics for boosting cognition and long-term memory. Nootropics like Aniracetam, Coluracetam, Noopept, Oxiracetam, Piracetam, and Resveratrol.
All nootropic ampakines are considered non-toxic and safe when dosed correctly. But if you are using any of these natural or synthetic nootropics, and are under the age of 35, this section on prescription ampakines also applies to you.
AMPA receptors are critical to regulating prefrontal cortex neuroplasticity. Which leads to long-term potentiation.[xlii] And the development of working memory and long-term memory.
But AMPA receptors do not work solo. Another glutamate receptor called NMDA receptors actually trigger the induction of long-term potentiation. But these receptors are normally blocked by magnesium at resting membrane potentials.
Activation of AMPA receptors induces Excitatory Post-Synaptic Currents (EPSCs), which polarize the neuron. And remove the magnesium block of NMDA. Which allows long-term potentiation.
Activated NMDA receptors then increase trafficking of more AMPA receptors to the synapse. And this is how long-term potentiation is maintained. For the encoding of long-term memory.
No ampakines are currently FDA-approved. But are being investigated by several drug companies for Alzheimer’s, Parkinson’s, ADHD, Rhett syndrome, schizophrenia, depression, autism, and other cognitive problems.
Drugs like CX516 and CX546 are structurally derived from the nootropic Aniracetam. And are currently undergoing clinical trials.[xliii]
Some of these ampakine drugs have shown effectiveness for improving memory and cognition in healthy adults.[xliv] And the reason why there is significant interest in nootropic communities like reddit and Longecity for these drugs.
Several studies by DARPA (Defense Advanced Research Projects Agency) have been done using ampakines with the US Military. To give them the edge on the battlefield.
Ampakines are being studied for use as cognitive enhancers and alertness promoters for soldiers in high-stress combat situations.[xlv]
Ampakines are some of the most low-risk cognitive enhancers we have available. But they do present a danger for the young, developing brain (ages 5 – 35).
Ampakines and Glutamate Toxicity
Glutamate toxicity typically occurs when excess glutamate attacks AMPA and NMDA receptors in your brain. Causing a massive influx of calcium. This excess calcium activates enzymes like proteases and phospholipases. Which damage the brain cell membrane and DNA.[xlvi]
Using prescription ampakines has the potential to cause a similar mass influx of cations (positive ions) that could also cause excitotoxicity.
One example is an ampakine called CX929 that has been tested on Angelman syndrome (AS) in animals. AS is mostly caused by an abnormal expression of the UBE3A gene leading to the deletion of E6-associated protein.
The result is severe intellectual and developmental disability, sleep disturbance, seizures, jerky movements and usually a happy demeanor. And there is no cure.
Researchers at the University of Southern California found that in mice, the ampakine CX929 reduced dendritic spine abnormality and learning impairments. And significantly enhanced long-term potentiation.
The team suggested the drug CX929 held promise for treating the currently untreatable Angelman Syndrome.[xlvii]
But this type of ampakine drug bought on the gray market. And used as a cognitive enhancer by someone with a developing brain (ages 5 – 30 years) could cause serious problems in the young brain.
It’s not difficult to imagine that CX929 would have a similar effect on synaptic transmission and neuron communication in a normal brain. And enhancing neuroplasticity in brain regions associated with emotions and other functions.
This would likely lead to the inability to control emotions and other behaviors. Especially if neuroplasticity is excessive and unregulated.
One of the critical mechanisms involved in brain connections – they are maintained and tuned through synaptic pruning. Where highly active synapses are strengthened. And less active synapses are removed (pruning).
We use ampakine nootropics to provide faster learning and improved cognition. But excessive neuroplasticity could lead to high activity in all synapses. And as a result, reduce synaptic pruning. Impairments in synaptic pruning have been associated with autism.[xlviii]
This is a classic example of how ampakines can strengthen synapses, increase neuroplasticity by promoting dendritic spine growth. But could lead to autism-like syndrome.
Ampakines in Summary
Both natural nootropic compounds, and ampakines under development by drug companies have the potential to boost neuroplasticity. Leading to long-term potentiation that can improve the main aspects of learning and cognition.
We know how nootropic ampakines work through personal use. And feedback from thousands of our neurohacking peers. But experimental drugs bought on the gray market could lead unsuspecting people to take far more than safe doses. And suffer neuronal damage from glutamate toxicity.
And since the action of ampakines is to promote neuroplasticity. We know we can lower the threshold for inducing long-term potentiation and increase the magnitude of LTP.
While this alteration in neuroplasticity can help boost learning and cognition. It also comes with a decrease in long-term depression (LTD). LTD is vital for formation of spatial memory. And likely plays a role in motor learning as well.
This shifting in favor of neuroplasticity to raise long-term potentiation could lead to problems with spatial memory and possibly even motor function. Particularly in younger brains.
Smart Drugs Not So ‘Smart’
In 1972, Romanian psychologist and chemist Dr. Corneliu Giurgea coined the term “nootropic”. It is derived from the Greek words nous (mind) and trepein (to bend).[xlix]
Dr. Giurgea described a nootropic as having the characteristics of enhancing learning and memory. It should protect the brain while increasing natural cognitive processes. And should not be toxic, nor stimulate or depress the brain.
By this definition, smart drugs are not nootropics.
And anyone who writes about, or refers to prescription stimulants and beta blockers as “nootropics”, either don’t know what they’re talking about. Or are intentionally attempting to categorize these prescription meds as nootropics for marketing purposes. And corporate profits.
If you are dealing with clinically-diagnosed ADD or ADHD. And using prescription stimulants like Ritalin, Adderall, Modafinil or their cousins to manage your symptoms. I am NOT suggesting you stop taking your medication.
But after contemplating what you read in this post. You may want to consider asking your doctor to switch you to relatively safer methylphenidate (Ritalin), or modafinil (Provigil).
Both of these drugs work primarily by boosting dopamine and norepinephrine in your brain. They are not messing with your neuron’s vesicles or synapses for the most part.
You may also want to consider supplementing with nootropics to safeguard your brain from potential damage. And possibly even boost the efficacy of the prescription meds you are taking.
You can read more about managing ADHD and ADD symptoms in this post Best Nootropics for ADHD & ADD.
If you are currently using, or plan to use, amphetamines (i.e. Adderall) or beta blockers to boost learning and memory. I encourage you to consider safer alternatives that can help you achieve the same or similar goals. Check out this post for Best Nootropics for Learning and Memory.
And one final thing… Studies show that Smart Drugs alter the developing brain.[l]
So if you are 5 – 35 years old and using prescription stimulants to help cram for an exam or finish a paper. Or using smart drugs to keep you awake on long-haul drives. Or for whatever reason. I ask you the please, please reconsider.
You are messing with the natural neuroplasticity that the developing brain is designed to go through. So you can enjoy a happy, healthy rest of your life. As tempting as smart drugs may sound, spend some time on NootropicsExpert.com and find safer alternatives.
[i] Schwarz A. “Drowned in a Stream of Prescriptions” The New York Times February 3, 2013 nytimes.com Retrieved January 29, 2017 (source)
[ii] Goldberg C. “Full Report and Key Findings: The 2012 Partnership Attitude Tracking Study, Sponsored by MetLife Foundation” Partnership for Drug-Free Kids April 22, 2013 drugfree.org (source)
[iii] Maher B. “Poll results: look who's doping” Nature 9 April 2008 (source)
[iv] Challman T.D., Lipsky J.J. “Methylphenidate: its pharmacology and uses.” Mayo Clinic Proceedings. 2000 Jul;75(7):711-21. (source)
[v] Kuczenski, R., and Segal, D. S. (2005). “Stimulant actions in rodents: implications for attention-deficit/hyperactivity disorder treatment and potential substance abuse”. Biological Psychiatry 57, 1391–1396. (source)
[vi] Rapoport, J. L. B., Buchsbaum, M. S., Weingartner, H., Zahn, T. P., Ludlow, C., and Mikkelsen, E. J. (1980). “Dextroamphetamine- its cognitive and behavioral effects in normal and hyperactive boys and normal men”. Archives of General Psychiatry 37, 933–943. (source)
[vii] Mehta, M. A., Sahakian, B. J., Mavaddat, N., Pickard, J. D., and Robbins, T. W. (2001). “Comparative psychopharmacology of methylpyhenidate and related drugs in human volunteers, patients with ADHD and experimental animals,” Stimulant Drugs and ADHD: Basic and Clinical Neuroscience (New York: Oxford University Press), 303–331. (source)
[viii] Arnsten, A. F., and Li, B. M. (2005). “Neurobiology of executive functions: catecholamine influences on prefrontal cortical functions.” Biological Psychiatry 57, 1377–1384. (source)
[ix] Franke A.G., Bonertz C., Christmann M., Huss M., Fellgiebel A., Hildt E., Lieb K. “Non-medical use of prescription stimulants and illicit use of stimulants for cognitive enhancement in pupils and students in Germany.” Pharmacopsychiatry. 2011 Mar;44(2):60-6. (source)
[x] Casey, B. J., Jones, R. M., and Hare, T. A. (2008). “The adolescent brain”. Annals of the New York Academy of Sciences. 1124, 111–126. (source)
[xi] Lee, M. J., Yang, P. B., Wilcox, V. T., Burau, K. D., Swann, A. C., and Dafny, N. (2009). “Does repetitive Ritalin injection produce long-term effects on SD female adolescent rats?” Neuropharmacology 57, 201–207. (source)
[xii] Urban, K. R., and Gao, W. J. (2012). “Evolution of the study of methylphenidate and its actions on the adult versus juvenile brain.” Journal of Attention Deficit Disorders. 24, 65–74. (source)
[xiii] Jernigan, T. L., Trauner, D. A., Hesselink, J. R., and Tallal, P. A. (1991). “Maturation of human cerebrum observed in vivo during adolescence”. Brain 114 (Pt. 5), 2037–2049. (source)
[xiv] Cull-Candy, S., Brickley, S., and Farrant, M. (2001). “NMDA receptor subunits: diversity, development and disease”. Current Opinion in Neurobiology. 11, 327–335. (source)
[xv] Yuan J., McCann U., Ricaurte G. “Methylphenidate and brain dopamine neurotoxicity.” Brain Research. 1997 Aug 29;767(1):172-5. (source)
[xvi] Ishizuka, T., Sakamoto, Y., Sakurai, T., and Yamatodani, A. (2003). “Modafinil increases histamine release in the anterior hypothalamus of rats.” Neuroscience Letters. 339, 143–146. (source)
[xvii] Brown R.E., Stevens D.R., Haas H.L. “The physiology of brain histamine.” Progress in Neurobiology. 2001 Apr;63(6):637-72. (source)
[xviii] Zolkowska, D., Jain, R., Rothman, R. B., Partilla, J. S., Roth, B. L., Setola, V., Prisinzano TE, Baumann MH. (2009). “Evidence for the involvement of dopamine transporters in behavioral stimulant effects of modafinil”. Journal of Pharmacology and Experimental Therapeutics 329, 738–746. (source)
[xix] Rasetti, R., Mattay, V. S., Stankevich, B., Skjei, K., Blasi, G., Sambataro, F., et al. (2010). “Modulatory effects of modafinil on neural circuits regulating emotion and cognition”. Neuropsychopharmacology 35, 2101–2109 (source)
[xx] Bobak M.J., Weber M.W., Doellman M.A., Schuweiler D.R., Athens J.M., Juliano S.A., Garris P.A. “Modafinil Activates Phasic Dopamine Signaling in Dorsal and Ventral Striata” Journal of Pharmacology and Experimental Therapeutics. 2016 Dec;359(3):460-470. (source)
[xxi] Goez H.R., Scott O., Nevo N., Bennett-Back O., Zelnik N. “Using the test of variables of attention to determine the effectiveness of modafinil in children with attention-deficit hyperactivity disorder (ADHD): a prospective methylphenidate-controlled trial.” Journal of Child Neurology. 2012 Dec;27(12):1547-52 (source)
[xxii] Urban, K. R., Waterhouse, B. D., and Gao, W. J. (2012). “Distinct age-dependent effects of methylphenidate on developing and adult prefrontal neurons.” Biological Psychiatry 72, 880–888. (source)
[xxiii] Randall D.C., Shneerson J.M., File S.E. “Cognitive effects of modafinil in student volunteers may depend on IQ.” Pharmacology, Biochemistry and Behavior. 2005 Sep;82(1):133-9 (source)
[xxiv] Müller U., Steffenhagen N, Regenthal R, Bublak P. “Effects of modafinil on working memory processes in humans.” Psychopharmacology (Berlin). 2004 Dec;177(1-2):161-9 (source)
[xxv] Eiden L.E., Weihe E. “VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse” Annals of the New York Academy of Sciences. 2011 Jan; 1216: 86–98. (source)
[xxvi] Miller G.M. “The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity” Journal of Neurochemistry 2011 Jan; 116(2): 164–176. (source)
[xxvii] Selemon L.D., Begović A., Goldman-Rakic P.S., Castner S.A. “Amphetamine sensitization alters dendritic morphology in prefrontal cortical pyramidal neurons in the non-human primate.” Neuropsychopharmacology. 2007 Apr;32(4):919-31 (source)
[xxviii] Tata D.A., Yamamoto B.K. “Interactions between methamphetamine and environmental stress: role of oxidative stress, glutamate and mitochondrial dysfunction.” Addiction. 2007 Apr;102 Suppl 1:49-60. (source)
[xxix] Yuan J., McCann U., Ricaurte G. “Methylphenidate and brain dopamine neurotoxicity.” Brain Research. 1997 Aug 29;767(1):172-5. (source)
[xxx] Spear L.P. “The adolescent brain and age-related behavioral manifestations.” Neuroscience and Behavioral Reviews 2000 Jun;24(4):417-63. (source)
[xxxi] Curran C., Byrappa N., McBride A. “Stimulant psychosis: systematic review.” British Journal of Psychiatry. 2004 Sep;185:196-204. (source)
[xxxii] Griffith J. “A study of illicit amphetamine drug traffic in Oklahoma City.” American Journal of Psychiatry. 1966 Nov; 123(5):560-9 (source)
[xxxiii] Anggård E., Jönsson L.E., Hogmark A.L., Gunne L.M. “Amphetamine metabolism in amphetamine psychosis.” Clinical Pharmacology and Therapeutics. 1973 Sep-Oct;14(5):870-80. (source)
[xxxiv] Surles L.K., May H.J., Garry J.P. “Adderall-induced psychosis in an adolescent.” Journal of the American Board of Family Practice. 2002 Nov-Dec;15(6):498-500. (source)
[xxxv] Ricaurte G.A., Mechan A.O., Yuan J., Hatzidimitriou G., Xie T., Mayne A.H., McCann U.D. “Amphetamine treatment similar to that used in the treatment of adult attention-deficit/hyperactivity disorder damages dopaminergic nerve endings in the striatum of adult nonhuman primates” Journal of Pharmacology and Experimental Therapeutics. 2005 Oct; 315(1):91-8. (source)
[xxxvi] Volkow N.D., Gur R.C., Wang G.J., Fowler J.S., Moberg P.J., Ding Y.S., Hitzemann R., Smith G., Logan J. “Association between decline in brain dopamine activity with age and cognitive and motor impairment in healthy individuals.” American Journal of Psychiatry. 1998 Mar; 155(3):344-9. (source)
[xxxvii] Silverstone P.H., Asghar S.J., O'Donnell T., Ulrich M., Hanstock C.C. “Lithium and valproate protect against dextro-amphetamine induced brain choline concentration changes in bipolar disorder patients.” World Journal of Biological Psychiatry. 2004 Jan; 5(1):38-44. (source)
[xxxviii] Klongpanichapak S., Govitrapong P., Sharma S.K., Ebadi M. “Attenuation of cocaine and methamphetamine neurotoxicity by coenzyme Q10.” Neurochemical Research. 2006 Mar;31(3):303-11. (source)
[xxxix] Wu P.H., Shen Y.C., Wang Y.H., Chi C.W., Yen J.C. “Baicalein attenuates methamphetamine-induced loss of dopamine transporter in mouse striatum.” Toxicology. 2006 Sep 21;226(2-3):238-45 (source)
[xl] Klongpanichapak S., Phansuwan-Pujito P., Ebadi M., Govitrapong P. “Melatonin protects SK-N-SH neuroblastoma cells from amphetamine-induced neurotoxicity.” Journal of Pineal Research. 2007 Aug; 43(1):65-73. (source)
[xli] Achat-Mendes C., Anderson K.L., Itzhak Y. “Impairment in consolidation of learned place preference following dopaminergic neurotoxicity in mice is ameliorated by N-acetylcysteine but not D1 and D2 dopamine receptor agonists.” Neuropsychopharmacology. 2007 Mar; 32(3):531-41. (source)
[xlii] Malinow R., Malenka R.C. “AMPA receptor trafficking and synaptic plasticity.” Annual Review of Neuroscience. 2002;25:103-26. (source)
[xliii] Arai A.C., Kessler M. " Pharmacology of ampakine modulators: from AMPA receptors to synapses and behavior.” Current Drug Targets. 2007 May;8(5):583-602. (source)
[xliv] Ingvar M., Ambros-Ingerson J., Davis M., Granger R., Kessler M., Rogers G.A., Schehr R.S., Lynch G. “Enhancement by an ampakine of memory encoding in humans.” Experimental Neurology. 1997 Aug;146(2):553-9. (source)
[xlv] Saletan, W. (2008). “Night of the living meds: the US military’s sleep-reduction program”, Slate magazine. The Slate Group. Retrieved February 1, 2017 (source)
[xlvi] Manev H., Favaron M., Guidotti A., Costa E. “Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death.” Molecular Pharmacology. 1989 Jul;36(1):106-12. (source)
[xlvii] Baudry M., Kramar E., Xu X., Zadran H., Moreno S., Lynch G., Gall C., Bi X.
“Ampakines promote spine actin polymerization, long-term potentiation, and learning in a mouse model of Angelman syndrome.” Neurobiology of Disease. 2012 Aug;47(2):210-5. (source)
[xlviii] Belmonte, M. (2000). “Abnormal attention in autism shown by steady-state visual evoked potentials”. Autism 4, 269–285. (source)
[xlix] Giurgea C. “Pharmacology of integrative activity of the brain. Attempt at nootropic concept in psychopharmacology” [in French] Actualités Pharmacologiques (Paris). 1972;25:115-56. (source)
[l] Urban K.R., Gao W.J. “Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain” Frontiers in Systems Neuroscience 2014; 8: 38. (source)
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I know you for quite some time now
and appreciate your work
regarding getting off stimulating medications Vyvanse70mg and
I’m on a path of tapering them off
what your thoughts of restoring / recover/ normalize
the brain in general
and I guess the dopamine system as whole
I’m talking about when I reach
the zero mark of ceasing them all together and to avoid severe withdrawal symptoms
to take this nootropics Temporarily
I’m asking if they help recovery
if what they will do is heal / recover/ upregulates/ normalize/
the brain in a permanent way
and if they are not tolerance developing agents also and a cuse
of problems exactly like the medications
using them temporarily to progress the healing and the normalization,
and then cease taking them for good and relaying on true health
lifestyle which I know a lot about today
David Tomen says
Dani, you can use NAC to restore dysfunctional dopamine receptors. And any supplement that increases BDNF should help as well: https://nootropicsexpert.com/13-nootropics-to-boost-bdnf/
Hello David! I hope you have a great week 🙂
Is IDRA-21 Nootropic or Smart Drug?
Ooops sorry. I just readed the article again. Yes this is smart drug.
Michelle Guerrein says
Mr. Tomen, I recently learned about the “MTHFR” genetic mutation. The experts on this say 1 in 5 people cannot break down “folate or “folic acid. Because of this they suffer from severe anxiety with 1 genetic mutation and depression with the other mutation. The first reports of this came from Australia in 2015, from a patient’s experience and her doctor who determined he would find the problem. Much research has been done on this and though there are scientists who deny this genetic mutation, more than 179,000 articles come up regarding this mutation.
Your product “Nutrigenesis” contains “Folate'” not the broken down version. Please research this topic so you can change the Folate to a an L-5 methyltetrahyhrofolate in this product. You also need to change the B12 to a methylated B12.
David Tomen says
Michelle, the Performance Lab NutriGenesis uses methylfolate and not synthetic folic acid which is what you should be concerned with. Especially if you are dealing with a mutation of the MTHFR gene. Same thing with Vitamin B12 in that Multi which is methylcobalamin.
Would you have a safe recommendation to take for depression while on Vyvanse?
David Tomen says
Angie, it all depends on the cause of the depression. Most MAOIs are contraindicated with Vyvanse.
This is a comprehensive list of drugs and a few natural supplements that are contraindicated with Vyvanse: https://www.drugs.com/drug-interactions/lisdexamfetamine-index.html
Hey David, what is your opinion on Bromantane(Ladasten)?
David Tomen says
Scott, it’s a Smart Drug developed in Russia for treating neurasthenia which is defined as muscle weakness amongst other neurological issues. I don’t have an ‘opinion’ on it other than it’s another Russian Smart Drug.
I have tried it. It is an interesting compound. For me, it seems to have less of energy effect than ADHD stimulants, more creativity than Modafinil, and seems to have adaptogen like qualities.
I still prefer herbal nootropics most days.
Thank you so much for help. Your blog changed my life. I have severe ADHD which made me unable to even remember about my life goals. I bought many calendars and planners and forgot about them next day…
1. I follow your ADHD protocol and made my life more productive. I need to work on my own, this protocol helped me to work 4h/day where before working 2h was a nightmare for me.
2. For 3 days I was prescribed Medikinet (Ritalin) custom release. 20 or 30mg in the morning allowed me to work 7h on my project which is my personal record.
My question to you would be about other stimulants for increasing decision making/organising. Do you know something else I could add to my stack?
I thought about Oroxylin A (Sabroxy) it’s fairly new.
Or maybe modafinil to stack with my ritalin? Due to it’s unique mechanism it could be good compliment to ritalin in terms of decision making?
Thank you Master
David Tomen says
I have not done the research on Sabroxy yet so cannot offer an intelligent answer.
But I would not recommend combining two stimulants unless your doctor is supervising it. More is never better in my experience.
Some of the supplements in my ADHD protocol are meant to be used 2 or 3-times per day because of a short half-life. For example, 500 mg L-Tyrosine 3-times per day. The last dose is meant to prevent the stimulant crash later in the afternoon.
Sabroxy is way more helpful than I expected, however you have to figure out your dosage, I have a very high tolerance to stimulants, but I’m finding I need 300-500mg probably twice a day. I have ADD and excessive daytime sleepiness EDS and I normally take 70mg of vyvanse a day, Adderral doesn’t work for me, hasn’t in 10 years, but I used too take way too much of it for 3 years. Still trying fix my brain but at least vyvanse has given me my life back and sabroxy really helps me on mornings I don’t take my vyvanse.
David Tomen says
Thanks Cassy. Sabroxy is on my “to do” list to review when I have the time.
Can you advise when you will be reviewing Sabroxy? Sounds like it be promising but would like to be sure of safety concerns if taking with Vyvanse.
David Tomen says
Angie, I have Sabroxy on my to-do list but cannot tell you when I’ll get around to researching it. I’m swamped right now and looks like it’ll be like this for the rest of the year. Hopefully I’ll be able to hire more help by then which will free up some of my time.
Does agmatine reduce tolerance to Ritalin?
David Tomen says
Maia, I have not seen any evidence that it can. The only thing I’ve found to prevent Ritalin tolerance is consistent daily use of L-Tyrosine, a B-Complex and NAC to restore dysfunctional dopamine receptors.
I’m 21 and use Aniracetam daily. Before 35 am putting myself into danger of developing autism like symptoms?
David Tomen says
Michael, I don’t see how you could. Aniracetam like the other racetams are considered very safe.
Started off as a genius and promising child with untreated ADHD. A fork in the road let me to abusing methamphetamine, then cocaine daily for years in my 20s.
It has been years since I quit – however the damage seems to be permanent. It feels like dopamine signaling has been permanently altered.
The anhedonia was somehow reduced after a handful of trips with a certain psychoactive fungus, but cognitively I have trouble focusing and caring about things I should care about. My priorities are all out of whack and I suffer from some form of executive dysfunction.
Recently a psychiatrist insisted I had ADHD-C and prescribed me Adderall XR. This worked for a month or so until I decided the side effects were not worth it as I have become a hyper-responder to stimulants (possibly from reduction in dopamine receptor density)
Aside from Lion’s mane, which you seem to recommend, are there any nootropics that could heal this damage to an extent?
David Tomen says
Pascal, NAC has been shown to reactivate dysfunctional dopamine receptors. And any nootropic that increases BDNF should also help long-term: https://nootropicsexpert.com/13-nootropics-to-boost-bdnf/
I know Adderal is under the black spectrum with it’s dangerous mechanism of action. But I was prescribed with it. And I would like to know if MInd lab pro would fix the issues that Adderall may cause. I’m already taking NAC & DHA.
TY in advance
David Tomen says
Robert, Mind Lab Pro is my first line of defense against possible brain damage from using simulants. I suggest adding another 500 – 1,000 mg Lion’s Mane extract, another 100 mg PS twice per day after your first MLP dose, and make sure your daily DHA dose is 1,000 mg.
What do you think of Wellbutrin XL as an alternative to Ritalin? I have severe ADHD but I cannot handle the crash of vyvanse anymore. I was thinking of taking Wellbutrin XL and Concerta as a combo. What do you think of it?
David Tomen says
Josh, don’t write off Ritalin until you try using my ADHD stack to support it. Which includes a small stack around 4 PM of L-Tyrosine, ALCAR and Alpha GPC that should prevent the crash. It does for me and many others as well.
Wellbutrin is not a direct alternative to Ritalin because they have different mechanisms of action. Try Wellbutrin and see if it works for you. But do not be surprised if it doesn’t work as well as Ritalin. It may or may not depending on your unique brain chemistry.
I don’t like the extended release forms of these stimulants because I no longer have control over when it works or how much is getting into my system. If the only reason you are considering Wellbutrin with Concerta is to avoid the crash please consider trying my protocol first and see if it works for you.
Hi David, first I wanted to thank you for saving my life and that of my family with this page. I would like you to please help me understand something. You mention that anyone aged 5 – 35 years should think twice before dosing with Modafinil. Because it could negatively affect neuroplasticity of the developing brain. But I am 37 years old, is it safe for me to take it or is it still dangerous? And if you recommend it, how many days a week should I take it at most and how many milligrams?
David Tomen says
Mabel, of all the stimulants available Modafinil seems to be the gentlest on the brain. At 37 your brain is no longer developing like it was up until your early 20’s. So you do not need to worry about it messing with that type of plasticity.
But you do need to be concerned about damaging neurons and its appendages like axons, dendrites and synapses. Modafinil has not been recorded as far as I know for having any detrimental effect on those brain elements.
Thanks David for answering, in other countries Modafinil could be marketed under other names? In my country it is only available under the name “Activigil”, do you think it is just as effective?
And finally at my age,
– how many days a week should I take it ?,
– at what time ?,
– I need to cycle it ?,
– and how many milligrams ?, that’s all thanks
David Tomen says
Mabel, I’m the wrong person to ask because that type of information needs to come from a doctor of which I am not. My area of expertise is in natural supplements that any one can buy without a prescription in most countries around the world.
Modafinil is marketed under several brand names. The chemical formula should be exactly the same. As long as it was manufactured by a pharmaceutical company and not made by some guy in his garage.
So if you are 35 years or younger one should not take any Racetams?
David Tomen says
Rob, I’m not talking about racetams in this article. This article is about prescription stimulants normally used to treat ADD/ADHD. You’ll notice I’ve also included links to clinical studies showing how the human brain continues to develop during your 20’s and early 30’s. And what happens when these stimulants are used in developing brains.
The racetams are nothing like prescription stimulants. The racetams are powerful compounds and although they are synthetics, they are all based on a pyrrolidine core which is a cyclic derivative of GABA. They do not assault receptors, transporters and other neurons components like stimulants do.
Last note, the racetams are not “smart drugs”. They are classed as “nootropics” and given that name by the doctor who invented Piracetam.
Thank you for clarifying this!!!
This is great information and I have stopped taking Amphetamines because of it. I have been on Amphetamines for the past 3 years almost daily. I take roughly 20 mg to 30 mg a day. I noticed that I started to have issues with my heart and the drug stopped having an effect on me. I am 31 years old. Other than nootropics what else can I take to repair the damage I have done to my brain? I keep seeing people post about BPC 157 and that it can repair the damage to my brain. What nootropics do you recommend the most for brain repair? Also, not to get off topic with this, but I knew something was really wrong when I took MDMA. I rarely do the drug and when I took a high dose with friends at a rave I had almost no feeling of the drug while my friends rolled their brains off. I concluded that it was certainly the high amount of Adderal that caused this. Will my brain ever be normal again? If so how long? Really could use some help thank you so much
David Tomen says
Robert, amphetamines are not friendly to neurons, receptors, or synapses. But your brain has an amazing ability to heal itself given the right tools.
Neurogenesis is the mechanism behind brain repair. And we support neurogenesis by boosting Nerve Growth Factor and BDNF. Lion’s Mane Mushroom is the most potent supplement I know of for boosting Nerve Growth Factor.
And here’s an article detailing 13 nootropic supplements for boosting BDNF: https://nootropicsexpert.com/13-nootropics-to-boost-bdnf/. You are likely already familiar with at least a couple of supplements on that list. I suggest adding 3 or 4 to your stack following dosage recommendations and use them until you start feeling the difference. And keep on using them.
One pre-made stack I’ve found to be helpful in supporting 13 years of daily Ritalin use is Mind Lab Pro. One of its many benefits is supporting brain repair: https://bit.ly/3lh3w8a. I use it as my ‘base’ and build the rest of my stack from there.
Thank you so much for your help!!!!! I think I need to set up a consultation with you soon I have so many questions. I was hit by an IED in Afghanistan and I suffered from a TBI along with many health problems because of it. I am running out of options as doctors keep wanting to prescribe me more and more meds. Thank you again and god bless
David Tomen says
Great idea Robert. And I look forward to working with you.
You mentioned n-acetyl l-cysteine. How is this important here? I use probably a variety of nootropics / smart drugs. Probably about 40. I rotate them. Pertinent to this discussion or possibly related are some in my arsenal: modafinil, adrafanil, bromantane, and tienaptine sulfate. My experience (I’m 54) of 4 – 5 months has shown a most positive response and life-changing to these and other dopaminergics such as tyrosine and phenylalanine. I value your research and postive approach to nootropics not only because of the thoroughness but because of your supporting life experience and encouragement for humankind!
David Tomen says
Ray, the science shows that amphetamine abuse causes damage to dopamine receptors and cognitive deficit. This was prevented in animal studies by dosing the animals with N-Acetyl L-Cysteine (NAC): https://www.ncbi.nlm.nih.gov/pubmed/16760923/
Is NAC a good idea with other dopaminergics, and does it inhibit the effect?
David Tomen says
Dor, studies show that NAC has the ability to help restore dopamine receptors so that they work as intended.
We have a 10 year old who has been diagnosed with ADHD (combined type) after a thorough, multi-day comprehensive psychoeducational evaluation. We first tried Strattera, which worked well for 8-12 weeks, but then symptoms of impulsivity and hyperactivity returned and over time anxiety developed. At the one-year mark, we took him off it and took him to an integrative pediatrician who ran a bunch of tests, treated him for yeast overgrowth and a chronic immune response to strep, and gave several supplements (multi-vitamin, probiotic, PharmaGABA, L-Glutamine, transdermal glutathione, magnesium, melatonin). He is calmer now and the anxiety is gone, but impulsivity and lack of focus are still causing him a great deal of trouble at school and at home. We’re debating whether we should give stimulant meds a try, but I have many reservations including worrying about any potential long-term effects. I’ve read this article and am not clear whether you are saying that stimulant meds are potentially dangerous to all young minds (both healthy and ADHD kids), or when you say they are dangerous are you only referring to those who have healthy minds and are just taking them for a concentration boost on exams and things like that?
David Tomen says
Sally, great question and I realize it can be confusing with all the conflicting information out there.
My research shows that methylphenidate (Ritalin) and stimulants based off of it are safest to use long-term. And have the longest track record. Clinical studies also show that the right stimulants meds actually benefit someone with a truly ADHD brain. But can be detrimental to someone with a health, ‘normal’ brain.
It’s fairly easy to grow ‘tolerant’ to a stimulant because the brain can’t keep up with the neurotransmitters and receptor repair/sensitivity for them to work after awhile. And tolerance builds and varies depending on the individual brain.
But I’ve found that the nootropic stack I describe in this post helps eliminate that tolerance. And helps prescription stimulants work better: https://nootropicsexpert.com/best-nootropics-for-adhd-add/
David Tomen…. thank you so much for your excellent videos too !! Myself and many others would like you to report on
Methylene Blue… I’ve been taking it for months and I believe that it’s a true Nootropic.
David Tomen says
Thomas, thanks about the YouTube videos. And Methylene Blue is on my list. Watch for it in the next couple of weeks.
I would like to ask about modafinil and piracetam.
In a few months I will take a Japanese test and require a great concentration and focus since the listening part of the exam is very difficult.
I was thinking of using modafinil for focus and piracetam for cerebral blood flow.
What is your opinion on this stack? Thank you.
P.S. I would only use them for my test.
David Tomen says
Suna, that combo would likely work. But I’d suggest checking Oxiracetam out first > https://nootropicsexpert.com/oxiracetam/. Combine Oxiracetam with 250 – 500 mg of Alpha GPC. But I’d try either combo before your test to see how they work for you. Experimenting the day of the test is a very bad idea.
Thanks for the reply.
I would like to try oxiracetam first, but unfortunately in my country it does not exist in pharma-grade, here i can find piracetam and I can get it without a prescription like modafinilo.
Can I combine Piracetam with 250 – 500 mg of Alpha GPC?
At what dose do you suggest me?
Alpha GPC 250-500 mg
And of course I’ll try them first to see how I feel.
David Tomen says
Suna, when using any of the racetams including Piracetam you need to include an acetylcholine precursor like Alpha GPC. How much Alpha GPC you use depends on how much Piracetam you use. It’s best to split your dose throughout the day as detailed in this review > https://nootropicsexpert.com/piracetam/. I’d try 250 mg of Alpha GPC every time you dose Piracetam. If you get a ‘racetam-headache’ it means you need to increase your dose of Alpha GPC. But using too much Alpha GPC is not good either. Please review the side effects in this review so you know how to recognize them > https://nootropicsexpert.com/alpha-gpc/
Thanks for your reply, i wasn’t able to send a message because an anti-spam blocker on this page did not allow to me.
I will try piracetam with CDP-Choline, creatine, omega 3, caffeine and Vitamin B.
The other day i tried Modafinil and was amazing y could study for 7 hours with a concentration that i had never felt.