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    Adderall Stats & Data

    aderal aderall adderal d-amphetamine d-amph
    PubChem
    MW135.21
    FormulaC9H13N
    LogP1.8
    IUPAC1-phenylpropan-2-amine
    InChIKeyKWTSXDURSIMDCE-UHFFFAOYSA-N
    Chemical Class Preparation/mixture
    Psychoactive Class Stimulant

    Toxicity

    PsychonautWiki

    As of March 2014, there is no evidence that amphetamine is directly neurotoxic in humans. However, high-dose amphetamine can cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine. In rodents and primates, sufficiently high doses of amphetamine causes damage to dopamine neurons, characterized as reduced transporter and receptor function. Animal models of neurotoxicity from high-dose amphetamine exposure indicate that the occurrence of hyperpyrexia (i.e., core body temperature ≥ 40 °C) is necessary for the development of amphetamine-induced neurotoxicity. Melatonin has been shown to prevent (if used 30min+ before dosing) and reverse amphetamine induced neurotoxicity of TH-pSer40 and calpastatin levels in the Substantia Nigra of rats.

    Addiction & dependence

    Amphetamine has high abuse potential and can cause psychological dependence with chronic use. When dependence has developed, cravings and withdrawal effects may occur if use is suddenly discontinued. Withdrawal symptoms include paranoia, depression, dream potentiation, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more amphetamine or other stimulants.

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Adults: d‑amphetamine ~9–11 h; l‑amphetamine ~11–14 h; urinary pH can shift apparent half‑life to ~7 h (acidic) or up to ~34 h (alkaline).
    Addiction Potential
    Moderate to high: frequent redosing can develop quickly into compulsive use; tolerance and psychological dependence escalate with consecutive days of use.

    Tolerance Decay

    Half tolerance 7d Baseline ~14d

    Acute tachyphylaxis to euphoric effects is common with short‑interval redosing; binge‑pattern multi‑day use rapidly escalates tolerance and markedly increases risk of stimulant psychosis. Allow multiple weeks off after heavy use.

    Experience Report Analysis

    Erowid
    19 Reports
    7 Single-substance
    2000–2012 Date Range
    4 With Age Data
    6 Effects Detected

    Demographics

    Gender Distribution

    Too few reports for a chart: gender is known from 19 reports, and a split is drawn only from 20 reports or more. Counts are shown instead. Why 20?

    • Male 13 of 19
    • Female 6 of 19

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 7 experience reports (7 single-substance Erowid)

    7 Reports
    6 Effects Detected
    4 Positive
    2 Adverse
    0 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Each bar is the share of reports mentioning the effect; its whisker, and the band on the rows below, is the 95% interval: where the share could plausibly be with other reports of the same kind.

    Too few reports for bars: these effects come from 7 single-substance Erowid reports, and a bar is drawn only from 20 reports or more. With fewer, a percentage cannot tell a common effect from a rare one. Counts are shown instead. Why 20?

    Positive Effects 4

    Stimulation 5 of 7 70%
    Empathy 4 of 7 70%
    Focus Enhancement 3 of 7 70%
    Music Enhancement 3 of 7 70%

    Adverse Effects 2

    Anxiety 4 of 7 70%
    Confusion 3 of 7 70%

    Also reported in combinations. In the 12 Adderall reports where another drug was taken too, 0 mention hospital, emergency services or an overdose, 1 a seizure and 0 psychosis (too few reports for percentages). In the 7 single-substance reports: 1, 0 and 0. These are not in the figures above: they cannot be put down to Adderall alone, and a mention is not always something that happened to the writer.

    Common Combinations

    Most co-occurring substances, as a share of all 19 reports filed under Adderall

    Too few reports for bars: these combinations come from 19 reports, and a bar is drawn only from 20 reports or more. With fewer, a percentage cannot tell a common effect from a rare one. Counts are shown instead. Why 20?

    • Amphetamine 11 of 19
    • THC 4 of 19
    • Alcohol 3 of 19

    Harm Reduction

    drugs.wiki

    1) Urinary pH strongly alters amphetamine clearance: alkaline urine markedly prolongs half-life (reports up to ~34 h) while acidic urine increases excretion. Intentionally alkalinizing (e.g., baking soda/antacids) can amplify and prolong effects unpredictably and raises cardiovascular and insomnia risks. Do not attempt; if taken inadvertently with antacids, lower redose plans and extend spacing. 2) Combining with MAOIs is contraindicated (hypertensive crisis/serotonin toxicity). A strict 14‑day washout from MAOIs is standard. 3) Serotonergic co‑use (SSRIs/SNRIs/TCAs, tramadol, DXM, some psychedelics) increases serotonin syndrome risk; warn, avoid, or use only with medical oversight if prescribed agents are involved. 4) Other stimulants (cocaine, methamphetamine, cathinones) additively increase heart rate, BP, and hyperthermia risks; such combos are a common context for rhabdomyolysis and acute complications—avoid. 5) Heat/exertion: plan active cooling and hydration. For hot venues or dancing, sip 250–500 mL/h fluid, preferably isotonic; take cooling breaks. Avoid overhydration by using electrolytes; aim for steady light sweating and clear, not excessive, urine. 6) Insufflation of tablets: binders/dyes and talc irritate nasal mucosa and may reach lungs; if one insists, use micro‑lines, alternate nostrils, and rinse with sterile saline before/after. Persistent bleeding, congestion, foul smell, or septal pain warrant cessation and medical assessment. XR beads are especially harsh intranasally and are best swallowed; crushing XR defeats time‑release and tends to cause a sharp, short peak with more comedown. 7) CYP2D6 inhibitors (e.g., fluoxetine, paroxetine, bupropion, quinidine, dronedarone) can raise levels and adverse effects; dose conservatively and avoid stacking with other stimulants. 8) Cardiovascular screening is prudent if history suggests risk (syncope, chest pain, arrhythmia, structural disease, family history). Avoid self‑treating stimulant‑induced hypertension with nonselective beta‑blockers; in emergencies, benzodiazepines and external cooling are first‑line while antihypertensives (e.g., nicardipine/labetalol) are clinician‑directed. 9) Redosing within a few hours produces diminishing euphoria and more side‑effects; set a cap and spacing window before starting. Multi‑day runs dramatically increase psychosis, sleep deprivation, and mood crash risk—plan ≥4 weeks off between binges. 10) Warning signs needing urgent care include severe chest pain, confusion/psychosis, hyperthermia (>40.5°C), muscle rigidity, dark urine (possible rhabdomyolysis), or uncontrollable agitation; early sedation and rapid cooling by professionals are standard in life‑threatening presentations. 11) Nutrition/dentition: stimulants suppress appetite and cause bruxism; plan small calorie‑dense meals/shakes and chew gum to reduce jaw clenching; refeed and sleep after use. 12) Prefer oral route over snorting or injection for pharmaceutical tablets to minimize tissue injury and excipient harms; never inject crushed tablets without appropriate filtration (high risk of emboli/infection).

    References

    Cited references

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