This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

Compact view
Research pass: thorough Compound SKIP-FOR-NOW HIGH

1,3-DMAA

Extended Research
High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

Extended Research

Our depth — beyond the mirror

Deeper analysis, verdict reasoning, and per-archetype recommendations from our research team.

Editor's verdict SKIP-FOR-NOW HIGH

Banned in supplements by FDA since 2013 because it caused multiple deaths (military service members on training runs in Afghanistan 2011, gym-going civilians 2011-2013, hemorrhagic stroke + MI + hypertensive crisis case reports). Not a "this is risky but might be worth it" compound — it is a "documented to kill people in pre-workout doses" compound, with no medical indication and no athletic advantage that ephedrine or caffeine + paraxanthine + phenylpiracetam cannot match more cleanly. WADA-banned (drug-tested fighters, never). For a 20yo MMA athlete + business owner this is one of the few hard NO compounds in the entire encyclopedia. Verdict will not flip without (a) a clean reformulation under medical supervision, which is not on the horizon, and (b) a clinical indication, which does not exist for DMAA. The cleaner positional isomer 1,4-DMAA (also banned 2017) and the post-DMAA replacement DMHA (warned by FDA 2019) both inherit the same problem.

Research pass: thorough
Decision matrix by user profile Per-archetype
  • 20yo MMA athlete + business owner (this user)
    HARD SKIP

    Drug-tested context (any reasonable competitive scenario flags him on standard urinalysis). Cardiovascular load incompatible with combat-athlete training schedule. No documented cognitive-enhancement benefit beyond what cleaner compounds provide. Multiple deaths in his demographic from this exact use case (young military service members during PT in Afghanistan). The "20yo who feels invincible" cohort is precisely the case-report demographic.

  • Drug-tested at any level
    SKIP

    WADA S6, standard urinalysis catches it for ~2-3 weeks post-dose.

  • Cardiovascular history (any)
    SKIP

    Hard contraindication.

  • Brain-priority / cognitive performance goal
    SKIP

    Modafinil + bromantane + phenylpiracetam dominate every metric DMAA could be argued to touch.

  • Fat loss / cutting
    SKIP

    Caffeine + green tea + L-carnitine + protocol adherence dominate. The DMAA "magic" was peripheral vasoconstriction + appetite suppression — both achievable without lethal BP spikes.

  • Pre-workout focus / aggression
    SKIP

    Caffeine + paraxanthine + creatine + beta-alanine deliver every actionable benefit at zero cardiovascular tail risk.

  • Endurance / time-to-exhaustion
    SKIP

    Caffeine 3-6 mg/kg has an enormous evidence base; DMAA does not improve on it.

  • Older user (40+) interested in "old-school" pre-workouts
    HARDER SKIP

    Cardiovascular risk compounds with age.

  • Pregnant / breastfeeding
    A

    contraindication. There is no archetype in which DMAA is the right tool.

Subjective experience (deep)

Onset: 20-40 minutes oral, peak 1-2 hr.

Peak (25-50 mg, no caffeine): Hard sympathetic surge — vasoconstriction (cold extremities, "tight" feeling), focus narrowing, mild euphoria, appetite suppression, increased respiratory rate, mild tremor. Less mood-lift than amphetamine, more peripheral edge. Vasoconstrictive "pump-prep" feel that pre-workout users often describe as superior to caffeine alone.

Peak (50-75 mg + 200-400 mg caffeine — typical Jack3d 2-scoop dose): Significantly more aggressive — racing heart, full-body sympathetic dominance, narrowed focus, sometimes anxiety/irritability, occasional chest tightness. This is the dose range where case-report fatalities occurred in young users.

Peak (>100 mg): Risk territory. BP can spike >180/110 in healthy users; HR >130 resting; chest pain reported; severe anxiety/agitation; documented MI and hemorrhagic stroke at this dose range.

Tail / comedown: 4-8 hr. Crash less pronounced than amphetamine but persistent fatigue, often accompanied by rebound hunger, headache, and disrupted sleep if dosed after noon. Multi-day-stacking users often report cumulative anxiety and elevated resting HR/BP.

Biomarkers to track (deep)

Pre-exposure (irrelevant — DMAA should not be used)

N/A.

During or after exposure (acute presentation)

  • BP — measure repeatedly in any user who has consumed DMAA + caffeine + exercise + heat. SBP >180 or DBP >120 = ER.
  • HR + ECG — rule out arrhythmia, look for ST changes, prolonged QT.
  • Troponin (high-sensitivity) — if any chest pain, dyspnea, or arrhythmia.
  • CMP / ALT / AST — hepatic check (case-report population).
  • Lipid panel — baseline if chronic exposure history.
  • CBC + CMP + UA + CK — if rhabdomyolysis suspected.
  • CT head — any neurological symptoms, especially with hypertension (rule out hemorrhagic stroke).
  • TSH / fT4 — rule out coexisting hyperthyroidism amplifying the sympathomimetic profile.

Post-exposure surveillance

  • BP + HR home monitoring 2-4 weeks
  • Repeat ECG if any abnormality on initial trace
  • Liver panel at 4-8 weeks if any baseline elevation
Controversies / open debates Live debate

1. "I used Jack3d for years and was fine." Survivor bias. DMAA has a real death count and a real serious-adverse-event count, and the case-report literature is consistent across multiple independent author groups, jurisdictions, and years. Individual non-events do not refute the population-level signal. The Sparling and Cola fatalities were in healthy 20-30yo military service members — this is not a "weak users only" pattern.

2. "DMAA is just like ephedrine, and ephedrine is fine." Ephedrine has a longer half-life advantage (shorter — ~6 hr vs DMAA ~9 hr), an established Rx history with defined dose-response, and decades of clinical pharmacology data. DMAA's three-decade Lilly Forthane history was at a low inhaled dose, not oral 25-100 mg in a stacked pre-workout. The "DMAA = natural ephedrine" framing was supplement-industry marketing, not pharmacology.

3. "The geranium-natural-source defense should give it dietary-ingredient legitimacy." Multiple analytical chemistry studies (Lisi 2011, Zhang 2012, Fleming 2012, Cohen 2014) failed to detect DMAA in geranium plants or oils at clinically meaningful levels. The natural-source claim was a regulatory cover story. Even if trace amounts existed, the doses sold in supplements were synthetic-sourced and required industrial synthesis.

4. "FDA bans things conservatively; the death count is small relative to caffeine." Caffeine has billions of person-years of exposure and a vast denominator. DMAA had a few hundred million doses at most over 5-7 years and accumulated >100 reported serious adverse events including multiple deaths in young healthy users at advertised doses. The risk-per-dose is in a different class.

5. "Modern reformulations / clean-label DMAA from premium brands are safer." There is no FDA-permitted clean-label DMAA. "Premium" gray-market suppliers have the same Cohen-2014 dose-variability problem and no regulatory oversight. The mechanism that caused the 2011-2013 deaths is intrinsic to the molecule, not the manufacturer.

6. "If I tested it carefully on myself I could titrate." The case-report deaths included healthy young men at 25-75 mg single dose during exercise. There is no titration window with a safety margin.

Verdict change log
  • 2026-05-10 — Initial verdict: SKIP-FOR-NOW / HIGH CONFIDENCE. For this user (20yo MMA, drug-tested context, brain-priority): banned by FDA in supplements (2013), WADA S6, multiple deaths documented including in his exact demographic (young athletic men during exercise/heat), no clinical indication, cleaner alternatives exist for every claimed benefit. This is one of the few entries in the encyclopedia with no plausible verdict-flip pathway.
Open questions / gaps Open
  1. Hepatic toxicity mechanism — the post-DMAA OxyElite Pro hepatitis cluster (2013) was attributed to aegeline, but sporadic DMAA-only hepatic events have been reported. Mechanism (idiosyncratic vs dose-dependent) is unclear.
  2. PK in stacked context — most PK data is single-dose clean DMAA; little human data on DMAA + caffeine + heat + exercise interaction PK, which is the actual fatality context.
  3. Sex / ethnicity / genotype risk modifiers — case-report demographics skew young-male-athletic, but this likely reflects the user demographic, not a true risk modifier. CYP2D6 polymorphism status and DMAA clearance has not been characterized in the published literature.
  4. DMHA clinical surveillance — DMHA has been on the market longer than DMAA had been by 2013. Whether DMHA case-report counts will catch up to DMAA's is an open empirical question; current trend suggests yes but slower per-dose given lower potency.
  5. 2024-2026 gray-market DMAA quality — most modern "DMAA" sold internationally is unverified; some product seizures in Europe 2023-2024 found 1,4-DMAA or DMHA mislabeled as 1,3-DMAA. Cohen-style analytical chemistry on the current gray market would be valuable.

References

Eliason, M.J., Eichner, A., Cancio, A., Bestervelt, L., Adams, B.D., Deuster, P.A. 2012 — Case reports: Death of active duty soldiers following ingestion of dietary supplements containing 1,3-dimethylamylamine (DMAA)

pubmed.ncbi.nlm.nih.gov · 2012

Military Medicine. Sparling/Cola context plus mechanistic discussion.

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Cohen, P.A., Travis, J.C., Venhuis, B.J. 2014 — A methamphetamine analog (N,α-diethyl-phenylethylamine) identified in a mainstream dietary supplement / DMAA analytical work

pubmed.ncbi.nlm.nih.gov · 2014

Drug Testing and Analysis. Cohen lab series on supplement analytical chemistry; 5-10x dose variability across DMAA products.

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Lardieri, A., Cheng, C., Jones, S.C., McCulley, L. 2015 — Effects of dietary supplements containing 1,3-dimethylamylamine (DMAA): Reports submitted to the U.S. Food and Drug Administration

pubmed.ncbi.nlm.nih.gov · 2015

Journal of Dietary Supplements. FDA case-series review, hemorrhagic stroke and MI cases.

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Foley, S., Butlin, E., Shields, W., Lacey, B. 2014 — Experience with OxyELITE Pro and acute liver injury in active duty service members

pubmed.ncbi.nlm.nih.gov · 2014

Drug Testing and Analysis. Case series including military fatalities.

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Bloomer, R.J., Harvey, I.C., Farney, T.M., Bell, Z.W., Canale, R.E. 2011 — Effects of 1,3-dimethylamylamine and caffeine alone or in combination on heart rate and blood pressure in healthy men and women

pubmed.ncbi.nlm.nih.gov · 2011

Phys Sportsmed. Industry-funded acute hemodynamic data; +10-20 mmHg SBP at 50 mg.

View Study

FDA Statement: DMAA in Dietary Supplements (April 2013 enforcement action)

fda.gov · 2013

formal "not a dietary ingredient" determination.

View Source

DoD Safety Review 2013 — DMAA-containing dietary supplements

health.mil · 2013

Department of Defense formal safety review post-Sparling/Cola.

View Source

Health Canada DMAA Advisory 2012

recalls-rappels.canada.ca · 2012

first major Western regulator ban.

View Source

TGA Australia DMAA Scheduling 2012

tga.gov.au · 2012

TGA scheduling decision.

View Source

WADA Prohibited List 2026 — S6 Stimulants

wada-ama.org · 2026

methylhexaneamine specified stimulant.

View Source

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Anonymous · one vote per session · results below at 5+ votes.

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