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Please Note: Adderall is a trade name for amphetamine. It can be highly addictive for some individuals. If you think someone you know may need help, please check out signs someone is addicted to Adderall.

Other names:

dextroamphetamine, Dexamphetamine, D-Amphetamine,  Dexamfetamine, (S)-Amphetamine, (+)-Amphetamine, (+)-Phenaminum, Desamfetamina, Amsustain, Dephadren,  Sympamin, (+)-(S)-Amphetamine, (S)-(+)-Amphetamine, D-(S)-Amphetamine, (S)-1-Phenyl-2-propylamine, (S)-1-Phenyl-2-aminopropane, (2S)-(+)-Amphetamine, (S)-alpha-Phenylethylamine, D-alpha-methylphenethylamine, (S)-(+)-beta-Phenylisopropylamine, (S)-alpha-Methylphenethylamine, (+)-alpha-Methylphenethylamine, (2S)-1-phenylpropan-2-amine, D-AM D-1-Phenyl-2-aminopropane, D-2-Amino-1-phenylpropane, Dexamfetaminum , D-(+)-Amphetamine [7]

Adderall’s Background:

Adderall is defined by the FDA to be a CNS stimulant with a single-entity amphetamine product combining the neutral salts of dextroamphetamine and amphetamine, with the dextro isomer of amphetamine saccharate and d, l-amphetamine aspartate monohydrate [3].

Adderall was originally produced by Shire Pharmaceuticals in 1996 as an instant release pill, initially advertised to eliminate the need for multiple administrations during the day [6]. Shire Pharmaceuticals sold Adderall to DuraMed, which later was acquired by Teva. Teva now owns Adderall, however Shire still produces the extended release (XR) version of the medication.

Adderall consists of four salts by equal weight: D-amphetamine saccharate, D,L-amphetamine aspartate, D-amphetamine sulfate, and D,L-amphetamine sulfate yielding ~75%/25% D-amphetamine/L-amphetamine, respectively [5].

Active ingredients:

Dextroamphetamine saccharate, amphetamine aspartate monohydrate, dextroamphetamine sulfate, USP, amphetamine sulfate, USP [3].

Inactive ingredients:

Lactitol, Microcrystalline cellulose, colloidal silicon dioxide, magnesium stearate, and other ingredients [3].

Adderall’s Mode of action:

The exact mechanism, by which adderall helps people afflicted with ADHD, is unknown. It is known that levels of the neurotransmitter dopamine (DA) and catecholamines are affected after dosing adderall. Unfortunately, the exact method of action remains elusive, however, it is thought that adderall acts to inhibit the reuptake of dopamine from the synaptic terminal by the inhibition of the dopamine transporter (DAT).

One theory separates the actions of Adderall in two different phases. In the figure below, a. represents normal physiologic function of the DAT, while b. shows the effects of Adderall on the inhibition of reuptake of dopamine from the synaptic cleft (phase I). In this model, it is thought that the DAT is also downregulated from the neuronal membrane a la the second phase, which is thought to be responsible for the prolonged duration of dopaminergic signal, seen with Adderall compared to other single agent amphetamines.

The D/L-amphetamine mixture of adderall has, so far, demonstrated a faster onset and longer duration of action as compared to D-amphetamine at the same total dose. In rat studies, it has been found that L-amphetamine is roughly three to six times less potent than D-amphetamine albeit the (DA) transporter currents produced by the isomers are identical. The release of DA by amphetamine displayed characteristics similar to the potassium-induced or electrically induced release of DA [6].


The efficacy of Adderall in combating symptoms of ADHD/ADD by augmenting one’s attention  is well known and is, currently, the reason for its primary indication for prescription. In children, over a period of a year, Adderral has been shown to increase IQ scores in 100% of the children that participated in the study compared to no change in IQ in children not taking any medication [4]. Its stimulant nature also makes it widely used for patients suffering from conditions of hypersomnolence (e.g. narcolepsy).

Depending on one’s goals, whether treating ADHD/ADD or some other indicated use for Adderall, there seems to be a real benefit to using Adderall over other amphetamines, in its quicker onset and longer duration of action. This effect seems to be directly related to the use of a racemic, rather than pure, mixture of amphetamines.

With respect to convergent creative thought, Adderall has been found to enhance one’s ability. This effect was found to be dependent on one’s baseline creative, providing the most benefit for people with already low levels. Alternatively and possibly quite counterintuitively, in people with very high baseline convergent creativity there was noticeable decrease in ability [2].

Common Side Effects:

poor appetite, insomnia, stomachache, headache, staring/daydreaming, sadness, changes in vision, increased muscle tension, euphoria and anxiety/irratability [1].

Adderall Tolerance

It’s important to define tolerance to Adderall in persons with ADHD/ADD and in persons with otherwise normal physiology who use Adderall for recreational, work or study purposes. Adderall is a prescription amphetamine medication and should not be used outside of medical supervision.

There’s been no research conducted specifically with Adderall tolerance for non ADD/ADHD sufferers. As adderall is a mixture of dextroamphetamine and levoamphetamine salts and is essentially amphetamine, the clinical research on amphetamine tolerance can likely be extended to gain a picture of how fast adderall tolerance may develop.  One study conducted with healthy volunteers suggests that slight tolerance to dextroamphetamine developed after two doses spread over 4 days, though the majority of the subjective effects were still noted by volunteers. (8). In animal models, tolerance to dextroamphetamine has been noted at as little as 4 days (9). Anecdotal evidence suggests tolerance to Adderall in persons without ADHD is rapid and onset appears within a matter of weeks with multiples of original doses being required to achieve the same effect.

In persons with ADHD/ADD tolerance has been noted (10) with striatal dopamine transporter density higher in patients who have previously been exposed to stimulants.

Maximising / Potentiating Your Adderall Dose

Amphetamine urinary excretion is decreased under alkaline conditions and increased under acidic conditions. (11)(12)(13). Taking urinary alkalising agents such as sodium bicarbonate will interfere with amphetamine excretion and increase the active duration of Adderall, while the opposite can be expected from urinary acidifying agents such as ammonium chloride.

One study of 65 healthy volunteers showed urinary PH to be significantly increased (more alkaline) following  consumption of 300mg/KG of sodium bicarbonate (14). This translates to roughly 21 grams for a 70KG adult male, or roughly 1 heaped tablespoon.

The use of Vitamin C (ascorbic acid) to acidify urine has been investigated and found ineffective. Two studies (15) (16) show ascorbic acid supplementation is an unreliable urine acidifier. The same can be said for cranberry juice which has been found to be ineffective with one review with researchers concluded that PH urine samples for those drinking cranberry vs placebo, were actually higher for the cranberry group, IE less acidic. (17)Practically speaking there appears to be no easily obtainable urine acidifiers.

Editors Note: Alkalising or acidifying urine could potentially used to boost or blunt the effectiveness of Adderall and be useful for maximising a dose or lowering effectiveness when over stimulated, such as near bedtime. We advise consulting with your doctor before taking any substances which can interfere with the effectiveness of your medication.

Supplements and Adderall

L-Tyrosine – L tyrosine is a naturally occurring amino acid that is a precursor to the catecholamine neurotransmitters dopamine and adrenaline. Adderall’s main effects stem from enhancing dopamine signalling via inhibition of DAT (18) , MAO (19) and via acting as a substrate for VMAT2 (18).  While there’s no evidence to support specific combination of tyrosine and amphetamine, tyrosine has been shown to prevent stressor associated memory deficits by preventing neurotransmitter depletion in both animals and humans. (20) (21)

Editors Note: Research on tyrosine appears to suggest it is more suited to attenuating stress related deficits caused by neurotransmitter depletion, rather than raising one above baseline. There’s no evidence to suggest it will enhance stimulant effectiveness. Though given the relatively low cost of tyrosine, it may be worth investigating.

Sulbutiamine – Sulbutiamine is a man made vitamin B1 (thiamine) derivative that is fat soluble and crosses the blood brain barrier. A nootropic in its own right, sulbutiamine has been shown to modulate dopaminergic transmission in one animal study (22) though oddly the effects resulted in a decrease of dopamine in the prefrontal cortex and a subsequent compensatory increase of D1 receptors.

Editors Note: Given the lack of research on sulbutiamine and there being no evidence for its interaction with stimulants, save for scant anecdotal reports, it’s currently nothing but speculation behind the idea that sulbutiamine enhances Adderall’s effects.

Other information:

In patients with ADHD and and generalized anxiety disorder (GAD) who were refractory to 8 week treatment of SSRIs, there was a trial to add Adderall as an adjunct in therapy. After 8 weeks it was shown that the patients displayed a vast reduction in symptoms as seen vis-a-vis all effectivements measures, including symptoms of anxiety [5].

such studies go to show that the field of study for Adderall and its potential to curb symptoms of mental health, both as a primary agent and as an adjunct in therapy, are still in their infancy.


1.     Ahmann PA, Theye FW, Berg R, Linquist AJ, Van Erem AJ, Campbell LR. Placebo-controlled evaluation of amphetamine mixture-dextroamphetamine salts and amphetamine salts (Adderall): efficacy rate and side effects. Pediatrics. 2001 Jan;107(1):E10. PubMed PMID: 11134474.

2.    Farah MJ, Haimm C, Sankoorikal G, Smith ME, Chatterjee A. When we enhance cognition with Adderall, do we sacrifice creativity? A preliminary study. Psychopharmacology (Berl). 2009 Jan;202(1-3):541-7. Epub 2008 Nov 15. Erratum in: Psychopharmacology (Berl). 2009 Apr;203(3):651. Smith, M Elizabeth [added]. PubMed PMID: 19011838.

3.    FEDERAL DRUG ADMINISTRATION. “ADDERALL (CII).” 2007. Federal Drug Administration. March 2007. <>.

4.    Gimpel GA, Collett BR, Veeder MA, Gifford JA, Sneddon P, Bushman B, Hughes K, Odell JD. Effects of stimulant medication on cognitive performance of children with ADHD. Clin Pediatr (Phila). 2005 Jun;44(5):405-11. PubMed PMID: 15965546.

5.    Glaser PE, Thomas TC, Joyce BM, Castellanos FX, Gerhardt GA. Differential effects of amphetamine isomers on dopamine release in the rat striatum and nucleus accumbens core. Psychopharmacology (Berl). 2005 Mar;178(2-3):250-8. Epub 2004 Sep 30. PubMed PMID:

6.    Joyce BM, Glaser PE, Gerhardt GA. Adderall produces increased striatal dopamine release and a prolonged time course compared to amphetamine isomers. Psychopharmacology (Berl). 2007 Apr;191(3):669-77. Epub 2006 Oct 10. PubMed PMID: 17031708.

7.    NATIONAL INSTITUTE OF HEALTH. “PubChem Compound: Dextroamphetamine – Compound Summary.” 2012. National Institute of Health. <>