Alpha-Lipoic Acid
Mitochondrial redox cofactor that boosts GSH/Nrf2 and downregulates HIF-1α/AKT/NF-κB → angiogenesis & glycolysis ↓; human data skew to metabolic/QoL benefits.
Forms: Alpha-lipoic acid (racemic) capsules/tablets · R-alpha-lipoic acid (stabilized) capsules
Simple Summary
ALA recharges the body’s own antioxidants and turns down cancer growth switches (AKT, NF-κB, HIF-1α). That can reduce blood-vessel growth and glycolysis and help tumor cells self-destruct. Human studies mostly show symptom/metabolic benefits; direct tumor-control evidence is still early.
Evidence at a glance
Multiple human studies (metabolic/neuropathy/biomarker) and animal/mechanistic oncology data; definitive tumor-control trials are limited.
How it may work
Alpha-lipoic acid (ALA) is a mitochondrial coenzyme and redox regulator that restores glutathione, vitamin C, and vitamin E. It inhibits tumor-promoting pathways such as AKT, NF-κB, and HIF-1α, suppressing angiogenesis and glycolysis in cancer cells. ALA has been shown to induce apoptosis, arrest the cell cycle, and reduce oxidative stress in various cancer types including ovarian, lung, and breast cancer models.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
- Oxidative stress↓Restores cellular antioxidant network
- GSH↑Supports glutathione recycling
- Nrf2 signaling↑Transcriptional antioxidant response
- HIF-1α↓
- AKT↓
- NF-κB↓
- Glycolysis↓Via HIF-1α/AKT modulation
- Angiogenesis↓
- Apoptosis↑
- Cell cycle progression↓
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- Metformin: Complementary effects on glycolysis/insulin signaling.
- Curcumin: Convergent NF-κB/HIF-1α suppression.
Overlapping mechanisms
- Redox: If stacking antioxidants, schedule away from ROS-dependent therapy days; watch for reduced pro-oxidant intent.
Safety & interactions
Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.
- antidiabeticsDose AdjustMildTheoreticalMay lower glucose requirements; monitor and titrate.
- ROS-dependent chemotherapy/radiationSeparateModerateTheoreticalAntioxidant/redox-restorative effects could blunt intended ROS waves.
- minerals (iron, magnesium, zinc)SeparateMinorTheoreticalChelation can reduce mineral/ALA absorption—separate dosing.
Timing
- With-meal: Improves GI tolerance; separate from minerals by 2h.
- AM
- PM
References
- Nature 2024
- PMID 39696984
- PMID 34211631
- PMID 32090494
- PMID 37453954
- PMID 38069431
- PMID 32344912
- PMID 30991918
- PMID 28993193
- PMID 18237244
- PMID 40327992
- PMID 38578399
Research
No published studies for Alpha-Lipoic Acid yet
New studies appear here once they’ve been reviewed. Browse all studies.
Dose: as studied, not a recommendation
Ranges seen in adjunct / practice use: 300–1800 mg (oral) Commonly 600 mg/day (300 BID) to 1800 mg/day (600 TID) in oncology/neuropathy trials; R-ALA may require lower dose for equivalent effect, Often taken with meals for GI tolerance; some protocols prefer empty stomach for absorption—prioritize tolerance. Bioavailability ~30-40%; divide doses..
Trials studying Alpha-Lipoic Acid
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