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Alpha Lipoic Acid

Metabolic & Weight Loss

Last reviewed: May 26, 2026

Also Known As: ALA, thioctic acid, lipoic acid, R-ALA (the bioactive stereoisomer), Na-R-ALA / sodium R-lipoate (a stabilized R-ALA form)

Supplement Class: Organosulfur compound / universal antioxidant (fat + water soluble) / AMPK activator / mitochondrial enzyme cofactor (pyruvate dehydrogenase, α-ketoglutarate dehydrogenase)

Evidence Tier: Strong — the ALADIN study (Ziegler et al. 1995, n=328) and Mijnhout et al. 2012's meta-analysis for diabetic peripheral neuropathy (an approved medical treatment in Germany, largely via IV administration); Jacob et al. 1995 and Zhang et al. 2011 for IV-protocol insulin sensitization; Namazi et al. 2018's meta-analysis for modest oral-dose weight reduction.

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What is alpha lipoic acid?

Alpha lipoic acid (ALA) is a naturally occurring organosulfur compound produced in small amounts by the body and found in trace amounts in red meat, spinach, and broccoli. Its supplement profile rests on a combination of reported mechanisms: it is a universal antioxidant active in both fat-soluble and water-soluble environments, it activates AMPK (the same metabolic pathway metformin and berberine target), it is a mitochondrial enzyme cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, and it regenerates other antioxidants (vitamins C and E, glutathione, CoQ10) back to their active forms. The most clinically validated application is diabetic peripheral neuropathy — ALA is approved as a medical treatment in Germany, based on the ALADIN study (Ziegler et al. 1995) and confirmed by Mijnhout et al. 2012's meta-analysis, with the strongest reported effects from intravenous administration. Secondary evidence, also largely from IV protocols, supports insulin sensitization (Jacob et al. 1995 reports roughly 50% greater glucose clearance in a clamp study; Zhang et al. 2011 reports a 41% insulin-sensitivity-index improvement alongside significant lipid and inflammatory-marker reductions). Namazi et al. 2018's meta-analysis reports a modest oral-dose weight-reduction effect. The practical considerations reported in the literature are stereoisomer choice (R-ALA is reported as more bioavailable than the S-ALA half of racemic ALA) and empty-stomach timing (food is reported to reduce absorption). ALA is discussed alongside mitochondrial peptides like MOTS-c and NAD+ peptide via overlapping AMPK and cofactor mechanisms at different signaling layers.

Reported benefits:

  • Significant diabetic peripheral neuropathy symptom reduction, largely via IV administration (the ALADIN study, Mijnhout et al. 2012's meta-analysis — a German medical approval)
  • Insulin sensitization — roughly 50% greater glucose clearance rate (Jacob et al. 1995, glucose-clamp methodology) and a 41% insulin-sensitivity-index improvement (Zhang et al. 2011), both via IV protocols
  • Modest oral-dose weight reduction (Namazi et al. 2018's meta-analysis)
  • Reduced lipid and inflammatory markers (Zhang et al. 2011)
  • Universal antioxidant activity across fat-soluble and water-soluble cellular compartments
  • Regeneration of oxidized vitamin C, vitamin E, glutathione, and CoQ10 back to active forms
  • AMPK activation (the same mechanism class as metformin and berberine)

Common dose: 300–600 mg/day stabilized R-ALA, or 600–1,200 mg/day racemic ALA, for general/metabolic use, per commonly labeled ranges. For diabetic neuropathy, oral doses in the 600–1,800 mg/day range appear in the meta-analyses reviewed (clinician coordination standard); the clinical trials with the strongest reported effects used IV administration (600 mg/day for 2–3 weeks) rather than oral dosing.

Reported safety considerations: Hypoglycemia when combined with metformin, sulfonylureas, insulin, or GLP peptides — glucose monitoring is standard guidance. A theoretical biotin-competition interaction over chronic long-term use (6+ months at 600+ mg/day) — a standard B-complex is a commonly discussed buffer.

On this page
  1. 1.How does alpha lipoic acid work?
  2. 2.What does the evidence say alpha lipoic acid does?
  3. 3.How is alpha lipoic acid dosed in trials and on labels?
  4. 4.How alpha lipoic acid is taken
  5. 5.What does alpha lipoic acid stack with?
  6. 6.Side effects and interactions
  7. 7.What isn't established about alpha lipoic acid
  8. 8.Product-quality considerations
  9. 9.Alpha Lipoic Acid FAQ
  10. 10.References
  11. 11.Published Studies

How does alpha lipoic acid work?

Alpha lipoic acid is reported to work through multiple parallel mechanisms — universal antioxidant activity (fat and water soluble, regenerating other antioxidants), AMPK activation (overlapping with metformin and berberine), mitochondrial cofactor activity, and nerve-tissue protection.

  1. Universal antioxidant — fat AND water soluble. ALA's small molecular size and disulfide bond structure are reported to make it active in both lipid membranes and aqueous cellular compartments, unusual among antioxidants. It is reported to directly scavenge hydroxyl radicals, hypochlorous acid, singlet oxygen, and peroxynitrite.
  2. Antioxidant regeneration network. ALA is reported to regenerate oxidized forms of vitamin C, vitamin E, glutathione, and CoQ10 back to their active reduced forms, amplifying the effective capacity of the broader antioxidant network.
  3. AMPK activation. ALA is reported to activate AMP-activated protein kinase, improving insulin sensitivity and glucose uptake and reducing hepatic gluconeogenesis — the same mechanism class as metformin and berberine, discussed as the basis for ALA's metabolic and weight-related effects.
  4. Mitochondrial enzyme cofactor. ALA is an essential cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, two key citric-acid-cycle enzymes connecting glycolysis to mitochondrial energy production.
  5. Nerve tissue protection. In diabetic peripheral neuropathy, ALA is reported to reduce oxidative stress in nerve tissue and improve nerve conduction velocity — the mechanism underlying the ALADIN study and Mijnhout et al. 2012's meta-analysis cited above.
  6. Anti-inflammatory effects. ALA is reported to reduce NF-κB activation and downstream inflammatory cytokines (TNF-α, IL-6), per Zhang et al. 2011's findings, discussed as secondary to the antioxidant mechanism.

What does the evidence say alpha lipoic acid does?

ALA has a substantial European medical-supplement evidence base. The strongest evidence reviewed is for diabetic peripheral neuropathy, largely from intravenous protocols; moderate evidence supports insulin sensitivity and modest weight reduction.

  1. Diabetic peripheral neuropathy (Strong). The ALADIN study (Ziegler et al. 1995, n=328) reports IV ALA at 600 mg/day or 1,200 mg/day for 3 weeks significantly reduces Total Symptom Score versus placebo. Mijnhout et al. 2012's meta-analysis confirms this for IV ALA specifically, with oral ALA producing a more moderate effect — the basis for ALA's medical approval in Germany.
  2. Insulin sensitivity (Moderate — largely IV-protocol evidence). Jacob et al. 1995 reports a roughly 50% increase in glucose metabolic clearance rate with a single IV ALA dose in a glucose-clamp study (n=13). Zhang et al. 2011 reports a 41% improvement in insulin sensitivity index after 2 weeks of IV ALA in obese patients with impaired glucose tolerance (n=22). Both trials used intravenous administration; oral-dose insulin-sensitivity evidence in the sources reviewed for this page is thinner.
  3. Body weight reduction (Moderate). Namazi et al. 2018's meta-analysis reports a statistically significant but modest weight reduction with ALA supplementation versus placebo, with a larger reported effect at higher doses.
  4. Lipid and inflammatory marker improvement (Moderate). Zhang et al. 2011 reports significant reductions in free fatty acids, triglycerides, total and LDL cholesterol, and inflammatory markers (TNF-α, IL-6), alongside increased adiponectin, in the same IV-protocol trial cited above.
  5. Cardiac autonomic neuropathy (Moderate). Some trials in the broader literature report symptomatic improvement in diabetic cardiac autonomic neuropathy with ALA supplementation.
  6. Cognitive and neurodegenerative applications (Emerging). Preclinical evidence is discussed as encouraging for various neurodegenerative contexts; human RCT outcomes in the broader literature are described as mixed.
  7. Liver disease (Emerging). Some trials in the broader literature report a hepatoprotective signal in NAFLD/metabolic-associated liver disease contexts; this evidence is described as preliminary.

How is alpha lipoic acid dosed in trials and on labels?

Dosing in the literature reviewed varies substantially by route and goal. The major clinical trials cited on this page used intravenous administration; oral dosing patterns are drawn from labels and the oral arm of the Mijnhout et al. 2012 meta-analysis.

Prof. Peptide reports what trials established and what research communities practice, labelled separately. Neither is a recommendation.

  1. General/metabolic use (R-ALA). 300–600 mg/day of stabilized R-ALA (Na-R-ALA) is a commonly labeled range, split AM/PM, dosed on an empty stomach.
  2. General/metabolic use (racemic ALA). 600–1,200 mg/day is a commonly labeled range for racemic ALA, reflecting its lower reported per-mg bioavailability relative to R-ALA.
  3. Diabetic neuropathy (oral). Mijnhout et al. 2012's meta-analysis reports oral doses in the 600–1,800 mg/day range across the trials reviewed, producing a more moderate effect than the IV protocol; clinician coordination is standard guidance for this indication.
  4. Weight-related use. Namazi et al. 2018's meta-analysis reports a larger effect at higher doses within the trials pooled.
  5. IV ALA (clinical setting only). 600 mg/day for 3 weeks is the ALADIN protocol for neuropathy; 600 mg/day for 2 weeks is the Zhang et al. 2011 protocol for insulin sensitivity. Both are clinically administered, not self-administered.

Reported timeline: the ALADIN trial measured neuropathy symptom improvement at 3 weeks with IV dosing; oral protocols in the meta-analyses reviewed generally ran longer. Zhang et al. 2011 measured insulin-sensitivity and lipid changes at 2 weeks with IV dosing.

Label math. A label reading "alpha lipoic acid 600 mg" commonly means racemic ALA (roughly 300 mg R-ALA plus 300 mg of the less-active S-ALA). "R-ALA 300 mg" or "Na-R-ALA / sodium R-lipoate 300 mg" refers to 300 mg of the active stereoisomer specifically.

How alpha lipoic acid is taken

Oral ALA is taken as capsules or tablets; the clinical trials with the strongest evidence used intravenous administration. The table below reports what labels and the oral literature describe.

AspectReported
FrequencyTwice daily for general oral use; up to three times daily for higher-dose oral neuropathy protocols per the meta-analyses reviewed.
Time of day30–60 minutes before meals is a commonly labeled pattern, since food is reported to reduce absorption via competition with dietary amino acids for gut transport.
FoodAn empty stomach is commonly recommended for absorption reasons; a small low-protein snack is a common accommodation for GI discomfort.
FormR-ALA or stabilized Na-R-ALA is marketed as the more bioavailable stereoisomer form; racemic ALA (50/50 R+S) is the form used in the major clinical trials cited on this page and is available at lower cost per gram.
Standardization markerLabels vary in whether "R-ALA," "R-alpha lipoic acid," or "Na-R-ALA / sodium R-lipoate" is explicitly disclosed versus an undifferentiated "alpha lipoic acid" listing, which is typically racemic.
B-vitamin pairingFor chronic long-term use, a standard B-complex or modest biotin supplementation is a commonly discussed mitigation for the theoretical biotin-competition interaction described above.

What does alpha lipoic acid stack with?

ALA is discussed alongside the broader mitochondrial bioenergetics and metabolic supplement toolkit, given its antioxidant, AMPK-activation, and mitochondrial-cofactor mechanisms.

With peptides

ALA is discussed alongside the mitochondrial peptide cluster. MOTS-c is reported to activate AMPK and support mitochondrial biogenesis at the genetic/regulatory level — a mechanism overlap with ALA's AMPK arm, but at a different layer (peptide-level signaling versus a small-molecule modulator). NAD+ peptide delivers NAD+, the cofactor for sirtuins and Complex I of the electron transport chain. ALA is discussed as operating at multiple layers — AMPK activation, mitochondrial enzyme cofactor activity, antioxidant protection, and regeneration of CoQ10, glutathione, and vitamins C and E — converging on mitochondrial bioenergetics from a different angle than either peptide. No negative interaction is documented in the sources reviewed for this page. For users on GLP-1 peptides ( semaglutide, tirzepatide ), ALA is discussed as a compatible metabolic adjunct via AMPK-mediated insulin sensitization.

With supplements

  1. CoQ10 — ALA is reported to regenerate oxidized CoQ10 back to its active form, a mechanistically direct pairing.
  2. Berberine — an additional AMPK activator with metformin-comparable glycemic effects.
  3. Chromium — reported insulin-receptor support via a different mechanism than ALA's AMPK activation.
  4. Magnesium — a cofactor for glucose metabolism enzymes.
  5. Vitamin C — ALA is reported to regenerate oxidized vitamin C, a complementary antioxidant pairing.
  6. Biotin — a commonly discussed mitigation for the theoretical competitive-uptake interaction over chronic ALA use.

With lifestyle factors

  1. Meal timing. Dosing 30 minutes before meals is reported to support absorption.
  2. Glucose monitoring. Relevant when combining ALA with metformin, sulfonylureas, insulin, berberine, or GLP peptides, given the reported additive glucose-lowering effect.
  3. B-vitamin supplementation for chronic use. A standard mitigation discussed for the theoretical biotin-competition interaction.
  4. Exercise. Exercise is reported to independently activate AMPK, discussed as additive with ALA's mitochondrial effects.

Side effects and interactions

ALA shows a favorable safety profile at standard supplemental doses across the trials cited on this page. The main considerations reported are GI effects, hypoglycemia risk when combined with diabetes medications, a theoretical biotin-competition interaction over chronic use, and rare skin/allergic reactions.

Common (mostly transient)

  1. Mild GI discomfort — nausea or abdominal pain, reported particularly on an empty stomach.
  2. Garlic or sulfur-like body odor — ALA is an organosulfur compound; some users report a mild distinctive odor.
  3. Headache — reported occasionally, generally mild and dose-related.
  4. No serious adverse events are documented at standard supplemental doses across the human trial base cited above.

Less common (watch-list)

  1. Hypoglycemia — a reported risk when combined with insulin, sulfonylureas, metformin, or GLP peptides; glucose monitoring is standard guidance during titration.
  2. Biotin competition — a theoretical interaction over chronic, high-dose use (6+ months at 600+ mg/day); a standard B-complex is a commonly discussed buffer.
  3. Thiamine considerations — ALA's mitochondrial enzyme cofactor activity is discussed as competing with thiamine, a theoretical consideration relevant primarily in malnourished populations.
  4. Skin rash or allergic reactions — reported rarely; discontinuation is standard guidance if persistent.
  5. Insulin autoimmune syndrome — a very rare finding reported primarily in populations with specific HLA genotypes.

Drug and supplement interactions

  1. Diabetes medications (metformin, sulfonylureas, insulin). An additive glucose-lowering effect is reported; glucose monitoring and possible medication dose adjustment by the prescribing clinician is standard guidance.
  2. GLP-1 peptides (semaglutide, tirzepatide). Reported as compatible, with a mechanistically additive effect on insulin sensitivity; hypoglycemia monitoring is relevant if also combined with sulfonylureas or insulin.
  3. Thyroid medication (levothyroxine). ALA may modestly affect thyroid hormone metabolism at high doses; clinician coordination is standard guidance.
  4. Chemotherapy — ALA's antioxidant activity could theoretically interfere with treatment-induced oxidative mechanisms in some regimens; oncologist coordination is standard guidance.
  5. Heavy metal chelation therapy — ALA has mild chelation activity reported; specialist guidance is standard before combining with active chelation therapy.
  6. Pregnancy and breastfeeding — supplemental-dose data is insufficient; clinician guidance is standard.

What isn't established about alpha lipoic acid

ALA has solid European medical-supplement evidence in diabetic neuropathy, largely from intravenous protocols, but several open questions affect how confidently it can be recommended for broader oral use cases.

IV-to-oral translation. The strongest clinical trials cited on this page (the ALADIN study, Jacob et al. 1995, Zhang et al. 2011) used intravenous administration. Oral ALA is reported to produce more modest effects in the meta-analyses reviewed; the precise oral-dose equivalence to the IV protocols' reported effects is not established.

R-ALA vs racemic head-to-head outcomes. R-ALA is reported as more bioavailable per gram, but the major clinical trials reviewed used racemic or IV ALA. Whether R-ALA at lower oral doses produces clinically equivalent outcomes to the racemic-ALA trial evidence is not directly head-to-head tested in the sources reviewed.

Healthy young-adult metabolic transfer. The strongest evidence reviewed is in type 2 diabetes, diabetic neuropathy, and impaired-glucose-tolerance populations. Whether ALA produces meaningful benefit in metabolically healthy adults is less directly supported by the trial data reviewed.

Long-term high-dose safety. Most trial data reviewed extends to 2–8 weeks. Multi-year continuous use at higher oral doses has not been characterized in controlled trials reviewed for this page.

Biotin competition clinical significance. The mechanism is discussed in the pharmacology literature; clinical relevance over multi-year oral use is not well-quantified in the sources reviewed.

Cognitive and neurodegenerative applications. Preclinical evidence is described as encouraging; human RCT outcomes in the broader literature have been mixed.

Weight-loss clinical significance. Namazi et al. 2018's meta-analytic effect is statistically significant but small in absolute terms. Whether ALA adds meaningfully to weight-management protocols already employing GLP peptides or other established interventions is not established in the sources reviewed.

Product-quality considerations

Alpha lipoic acid is widely available over-the-counter. Quality is reported to vary, particularly around stereoisomer disclosure (R-ALA vs racemic vs S-ALA), stabilization, and source authentication.

Quality markers reported in the category

  • Stabilized R-ALA (Na-R-ALA / sodium R-lipoate) — a shelf-stable form of the more bioavailable stereoisomer.
  • Racemic ALA as a lower-cost alternative — the form used in the major clinical trials cited on this page, at higher labeled doses to account for lower per-mg bioavailability.
  • Stereoisomer explicitly disclosed — "R-ALA," "R-alpha lipoic acid," "Na-R-ALA," or "sodium R-lipoate." An undifferentiated "alpha lipoic acid" listing is typically racemic.
  • Third-party testing — USP, NSF, or ConsumerLab certification; HPLC verification of stereoisomer purity is the relevant additional check.
  • cGMP-certified manufacturing facility.
  • Proprietary blends that obscure the actual ALA dose or stereoisomer composition don't allow independent evaluation.
  • Fresh manufacture date — unstabilized R-ALA is reported to degrade with heat and humidity; Na-R-ALA is more stable.
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Alpha Lipoic Acid FAQ

How do R-ALA and racemic ALA compare?

R-ALA (R-alpha lipoic acid) is the naturally occurring stereoisomer, reported in the pharmacology literature as substantially more bioavailable than the S-ALA enantiomer. Standard racemic ALA is a 50/50 mixture of R-ALA and S-ALA, with the S-ALA half described as largely inert. Stabilized R-ALA (Na-R-ALA / sodium R-lipoate) products are marketed at lower mg doses (commonly 300–600 mg/day) than racemic ALA products (commonly 600–1,200 mg/day) to account for this bioavailability difference; the major clinical trials cited on this page (the ALADIN study, Jacob et al. 1995, Zhang et al. 2011) all used racemic or intravenous ALA rather than isolated R-ALA.

Why do labels recommend taking alpha lipoic acid on an empty stomach?

ALA is reported in the pharmacology literature to compete with dietary amino acids for transporter-mediated gut absorption, with food reducing oral absorption. Labels commonly recommend dosing 30–60 minutes before meals, split across two daily doses.

What does the evidence say about ALA and diabetic neuropathy?

This is the most clinically established application, with regulatory approval as a medical treatment in Germany. The ALADIN study (Ziegler et al. 1995), a 3-week multicenter RCT of intravenous ALA (600 mg or 1,200 mg daily) in 328 patients with diabetic peripheral neuropathy, reports both doses significantly improved Total Symptom Score versus placebo. Mijnhout et al. 2012's meta-analysis of RCTs reports IV ALA (600 mg/day for 3 weeks) significantly reduced neuropathy symptoms, with oral ALA producing a more moderate symptom reduction. IV administration for this indication is a clinical, not self-administered, protocol.

What does the evidence show for ALA and weight?

A modest effect. Namazi et al. 2018's meta-analysis of RCTs reports ALA produced a statistically significant weight reduction versus placebo, with the effect described as small in absolute terms and greater at higher doses. The proposed mechanism involves AMPK activation, a pathway shared with berberine and metformin.

Does ALA stack with MOTS-c or NAD+ peptide?

The mechanisms are reported as complementary rather than overlapping. MOTS-c is a mitochondrial-derived peptide reported to activate AMPK and support mitochondrial biogenesis at the genetic/regulatory level. NAD+ peptide delivers the cofactor for sirtuins and the electron transport chain. ALA is discussed as operating at multiple layers: AMPK activation, mitochondrial enzyme cofactor activity (pyruvate dehydrogenase and α-ketoglutarate dehydrogenase), antioxidant protection of mitochondrial membranes, and regeneration of CoQ10, glutathione, and vitamins C and E. No negative interaction is documented in the sources reviewed for this page.

Is combining ALA with metformin or other diabetes medications discussed as safe?

The literature discusses ALA's AMPK activation as overlapping with metformin's primary mechanism, with the combination reported to produce an additive glucose-lowering effect. Glucose monitoring and clinician coordination for potential diabetes-medication dose adjustment are standard guidance when starting ALA alongside metformin, sulfonylureas, insulin, berberine, or GLP peptides.

Does ALA interact with biotin?

A theoretical competitive-uptake interaction is discussed in the literature: ALA and biotin are reported to compete for cellular transport at high doses over chronic use, with long-term high-dose ALA (months to years) potentially reducing biotin status. A standard B-complex or modest biotin supplementation alongside chronic ALA use is a commonly discussed mitigation; the interaction is not described as clinically significant for shorter courses.

How long do ALA's reported effects take to appear?

For neuropathy, the ALADIN trial measured effects at 3 weeks with IV administration; oral protocols are commonly discussed as taking longer. For insulin sensitivity, Zhang et al. 2011 measured effects after a 2-week IV protocol. For weight loss, Namazi et al. 2018's meta-analysis pooled trials of varying duration, with effect reported to build over weeks of consistent use.

References

  1. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week multicentre randomized controlled trial (ALADIN Study). Diabetologia. 1995;38(12):1425-1433. https://pubmed.ncbi.nlm.nih.gov/8786016/
  2. Mijnhout GS, Kollen BJ, Alkhalaf A, Kleefstra N, Bilo HJ. Alpha lipoic acid for symptomatic peripheral neuropathy in patients with diabetes: a meta-analysis of randomized controlled trials. Int J Endocrinol. 2012;2012:456279. https://pubmed.ncbi.nlm.nih.gov/22331979/
  3. Namazi N, Larijani B, Azadbakht L. Alpha-lipoic acid supplement in obesity treatment: a systematic review and meta-analysis of clinical trials. Clin Nutr. 2018;37(2):419-428. https://pubmed.ncbi.nlm.nih.gov/28629898/
  4. Zhang Y, Han P, Wu N, et al. Amelioration of lipid abnormalities by α-lipoic acid through antioxidative and anti-inflammatory effects. Obesity (Silver Spring). 2011;19(8):1647-1653. https://pubmed.ncbi.nlm.nih.gov/21593803/
  5. Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung. 1995;45(8):872-874. https://pubmed.ncbi.nlm.nih.gov/7575750/
  6. Golbidi S, Badran M, Laher I. Diabetes and alpha lipoic acid. Front Pharmacol. 2011;2:69. https://pubmed.ncbi.nlm.nih.gov/22125537/

Published Studies

Plain-English summaries of the peer-reviewed studies behind the claims above. Click any title to read the source paper.

Diabetologia · 1995Paywalled
Treatment of Symptomatic Diabetic Peripheral Neuropathy with the Anti-Oxidant Alpha-Lipoic Acid: A 3-Week Multicentre Randomized Controlled Trial (ALADIN Study) →

Ziegler D, Hanefeld M, Ruhnau KJ, Meissner HP, Lobisch M, Schütte K, Gries FA

A multicenter randomized double-blind placebo-controlled trial of intravenous alpha-lipoic acid (600 mg or 1,200 mg daily for 3 weeks) in 328 patients with diabetic peripheral neuropathy. Reports both ALA doses significantly improved Total Symptom Score (pain, burning, paresthesia, numbness) versus placebo — the foundational trial behind ALA's medical approval in Germany for this indication.

International Journal of Endocrinology · 2012Open Access
Alpha Lipoic Acid for Symptomatic Peripheral Neuropathy in Patients with Diabetes: A Meta-Analysis of Randomized Controlled Trials →

Mijnhout GS, Kollen BJ, Alkhalaf A, Kleefstra N, Bilo HJ

A systematic review and meta-analysis of RCTs of ALA in diabetic peripheral neuropathy, reporting IV ALA (600 mg/day for 3 weeks) significantly reduced neuropathy symptoms, with oral ALA producing a more moderate symptom reduction.

Clinical Nutrition · 2018Paywalled
Alpha-Lipoic Acid Supplement in Obesity Treatment: A Systematic Review and Meta-Analysis of Clinical Trials →

Namazi N, Larijani B, Azadbakht L

A meta-analysis of RCTs of ALA supplementation on body weight, reporting a statistically significant but modest weight reduction versus placebo, with greater effects at higher doses and longer durations.

Obesity · 2011Open Access
Amelioration of Lipid Abnormalities by α-Lipoic Acid Through Antioxidative and Anti-Inflammatory Effects →

Zhang Y, Han P, Wu N, et al.

A 2-week trial of intravenous ALA (600 mg once daily) in 22 obese patients with impaired glucose tolerance (13 treated). Reports insulin sensitivity index improved by 41%, with significant reductions in free fatty acids, triglycerides, total and LDL cholesterol, and inflammatory markers (TNF-α, IL-6), and a significant increase in adiponectin.

Arzneimittelforschung · 1995Paywalled
Enhancement of Glucose Disposal in Patients with Type 2 Diabetes by Alpha-Lipoic Acid →

Jacob S, Henriksen EJ, Schiemann AL, et al.

A glucose-clamp study in 13 patients with type 2 diabetes (7 given intravenous ALA 1,000 mg, 6 given vehicle only). Reports the metabolic clearance rate for glucose rose by roughly 50% with acute IV ALA administration versus no significant change in the control group.

Frontiers in Pharmacology · 2011Open Access
Diabetes and Alpha Lipoic Acid →

Golbidi S, Badran M, Laher I

A review of ALA's biology and clinical evidence in diabetes and its complications, covering antioxidant mechanisms, insulin sensitization, and the neuropathy evidence base.

Universal AntioxidantDiabetic NeuropathyAMPK ActivatorMitochondrial CofactorR-ALAInsulin Sensitization

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