Alpha-Lipoic Acid (ALA)
“The Universal Antioxidant & Mitochondrial Recharger.” A targeted tool for mitochondrial energy + oxidative stress—especially when nerves and glucose control are under strain.
The Naturopathic Perspective
“The Universal Antioxidant.”
Alpha-lipoic acid (ALA) is one of the few nutrients we reach for when the *root cause pattern* is metabolic oxidative stress + mitochondrial slowdown—especially when nerves, blood sugar regulation, and inflammatory signalling all start to “fray” at once. Clinically, it sits at the intersection of energy chemistry and redox chemistry: it supports mitochondrial enzyme complexes that turn fuel into ATP, and it also participates in antioxidant recycling (helping restore redox balance).
We also think of ALA as a *therapeutic lever* when a patient’s symptom picture points to glycation + inflammation + microvascular compromise (common in insulin resistance and diabetes). The nervous system is particularly vulnerable because peripheral nerves are long, energy-hungry, and sensitive to oxidative injury. ALA’s clinical “feel” is often: less burning/paresthesia, steadier glucose swings, and improved tolerance of metabolic stress.
💡 Clinical Insight: The Depletion Gap
Why not just get this from food?
1. Protein-Bound: In foods, lipoic acid is covalently bound to proteins (lipoyllysine). Supplement doses (50–600 mg) are likely up to ~1,000× higher than typical food intake.
2. Low Bioavailability: Consumption of foods containing it does not meaningfully increase “free” lipoic acid in the blood, whereas supplements reach measurable peaks.
“We prescribe this to bridge the gap between biological necessity and modern depletion.”
Naturopathic Use Cases
How we use this in clinical practice, validated by evidence.
1. Diabetic Peripheral Neuropathy
Clinical Goal: Nerve Resilience
The Clinical Logic:
We use ALA when neuropathy looks driven by oxidative stress + mitochondrial dysfunction + microvascular compromise—a pattern common in diabetes. Mechanistically, ALA supports mitochondrial enzyme systems and redox recycling, which can reduce oxidative injury and improve nerve metabolic resilience.
Clinically, this often translates into improved symptom scores (burning pain, paresthesia) over weeks.
Very High
Grade A
Verdict: Multiple RCTs show oral ALA can improve symptomatic diabetic polyneuropathy, particularly at doses of 600 mg/day. Long-term safety at this dose has been demonstrated.
2. Type 2 Diabetes Support
Clinical Goal: Glycaemic Control
The Clinical Logic:
ALA is often chosen when the clinical goal is to lower oxidative stress that worsens insulin signalling and to support mitochondrial handling of glucose/fat substrates. It is most relevant when a patient has post-meal crashes, metabolic inflammation, and early neuropathic “noise.”
Moderate
Grade B
Verdict: Meta-analytic data of RCTs suggest oral ALA supplementation is associated with modest improvements in HbA1c and fasting plasma glucose. Best used as an adjunct.
3. Biological Function: Energy & Redox
Clinical Goal: ATP Generation
The Clinical Logic:
R-lipoic acid is a required cofactor bound to mitochondrial multi-enzyme complexes (e.g., pyruvate dehydrogenase) central to converting fuel into acetyl-CoA. In its reduced form (DHLA), it also participates in antioxidant regeneration (vitamin E/C/glutathione systems).
Incontestable
Grade A
Verdict: Established biological fact. Cofactor role is essential for life.
Form Matters: Quality Comparison
Why we prescribe Stabilised R-ALA over other forms.
The “Hero” Form
We prioritize Stabilised R-alpha-lipoic acid (e.g., sodium R-lipoate). The R-isomer is the biologically native form; stabilisation matters because ALA is sensitive to degradation and rapid absorption is key. Taking it away from meals significantly improves bioavailability.
Food Sources (Approximate)
Food sources provide minute amounts compared to supplementation.
Spinach (Cooked)
~0.01–0.03 mg
(Per Serving)
Broccoli (Cooked)
~0.01 mg
(Per Serving)
Liver (Beef/Chicken)
~0.03–0.09 mg
(Per 100g)
Brussels/Peas
~0.005–0.02 mg
(Per Serving)
📚 Clinical References & Evidence
-
Mechanisms & Overview:
Lipoic Acid | Linus Pauling Institute. Oregon State University.
[Read Source] -
Neuropathy Trial (SYDNEY 2):
Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy. PubMed.
[Read Source] -
Diabetes Meta-Analysis:
Efficacy and safety of oral alpha-lipoic acid supplementation for type 2 diabetes management. PMC.
[Read Source] -
Thyroid Interaction:
Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine. PubMed.
[Read Source] -
Autoimmune Hypoglycaemia:
Insulin Autoimmune Syndrome Induced by α–Lipoic Acid. PMC.
[Read Source] -
Long-Term Safety (NATHAN 1):
Efficacy and safety of antioxidant treatment with α-lipoic acid over 4 years in diabetic polyneuropathy. PubMed.
[Read Source] -
Food Sources Analysis:
α-Lipoic Acid: Cell Regulatory Function and Potential. ScienceDirect.
[Read Source]
*Disclaimer: Links connect to third-party scientific repositories. Access may require institutional login for some journals.
📋 Dosage & Safety Guidelines
600 mg
Typically for neuropathy. Maintenance: 100-300mg.
- Benfotiamine (B1): Supports nerve/metabolic pathways.
- Acetyl-L-carnitine: Complementary mitochondrial support.
- Note: Take away from meals for absorption.
Unsure if this is right for you?
Supplements work best when tailored to your individual biochemistry.