Supplements for Amyotrophic Lateralsclerosis

Current list 2025

This list does not contain any remedies for potential co-triggers of disease: dental foci, Lyme disease or other brain infections, heavy metals (= NMBI or Irminix), aluminum, etc. – we only have an orthomolecular supplementation list here.

If anyone has an even better idea, please write (e.g., as a comment). Any causal therapy against prions would be fantastic!

1. Promotion of neuroplasticity

• Magnesium L-threonate: 1.5-2 g/day
• Citicoline (CDP-choline): 500-1000 mg/day
• Uridine monophosphate: 250-500 mg/day

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2. Antioxidant and mitochondrial protection

• Coenzyme Q10 (ubiquinol): 200-400 mg/day
• Alpha lipoic acid (R-ALA): 600-1200 mg/day
• N-Acetylcysteine (NAC): 600-1800 mg/day
• Vitamin E: 400-800 IU/day (new)
• Selenium: 100-200 µg/day (new, with caution)
• Vitamin C: 500-1000 mg/day (new)
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3. Neuroinflammation & Cell Protection

• Omega-3 fatty acids (DHA/EPA): 1000–2000 mg/day
• Melatonin: 10–60 mg at night  –> High-dose capsules must be prescribed by a doctor; we now have a relatively inexpensive source (German pharmacy)
• Lithium orotate: 5–10 mg elemental lithium/day (experimental)
• Vitamin D3: 5000 IU/day (with blood level monitoring)
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4. Energy metabolism and cellular resilience

• Acetyl-L-carnitine: 1–2 g/day
• Creatine monohydrate: 3–5 g/day
• B vitamins (B6, B12, folic acid): B complex, dosage as needed (new)
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5. Other possible add-ons (experimental)

• PQQ: 10–20 mg/day
• Resveratrol: 100–250 mg/day
• Nicotinamide riboside / NMN: 250–500 mg/day
• TUDCA: 500–1000 mg/day
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6. Conventional medical therapy

• Riluzole: 100 mg/day
• Edaravone: As indicated by a doctor

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More details on this list

1. Neuroplasticity promotion

• Magnesium L-threonate (1.5–2 g/day)
  Evaluation: Magnesium L-threonate is valued for its high bioavailability and ability to cross the blood-brain barrier. It promotes synaptic plasticity and may support cognitive functions, which may be relevant in ALS, as cognitive impairment can occur. Studies show that magnesium influences glutamate metabolism, which is important in ALS because excess glutamate damages nerve cells. However, there are no specific studies directly investigating magnesium L-threonate in ALS. The dosage of 1.5–2 g/day is plausible, as it provides approximately 120–160 mg of elemental magnesium, which is safe and well-tolerated.
  Conclusion: Plausible addition, but the evidence is indirect.
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• Citicoline (CDP-Choline, 500–1000 mg/day)
  Evaluation: Citicoline supports cholinergic transmission and may have neuroprotective effects, particularly by promoting membrane repair and synaptogenesis. There are no specific studies on citicoline in ALS, but its role in neurodegenerative diseases (e.g., stroke, dementia) is well documented. Synergy with transcranial stimulation (tDCS) is speculative but theoretically plausible, as citicoline may promote neuronal plasticity. The dosage is within the usual range.
  Conclusion: Useful supplementation with theoretical benefit, but direct evidence for ALS is lacking. 
• Uridine monophosphate (UMP, 250–500 mg/day)
  Evaluation: UMP promotes phospholipid synthesis and synapse formation, particularly in combination with choline and DHA. There is preclinical data showing neuroprotective effects in neurodegenerative models, but no specific studies on ALS. The combination with citicoline and omega-3 is theoretically useful, as they may act synergistically. The dosage is appropriate.
  Conclusion: Experimental but plausible supplementation. Direct evidence is lacking, but the combination remains useful..

2. Antioxidant and mitochondrial protection

• Coenzyme Q10 (Ubiquinol, 200–400 mg/day)
  Evaluation: Coenzyme Q10 is an antioxidant and supports mitochondrial energy production. It has been studied in ALS because of mitochondrial dysfunction.ction plays a role. However, one study showed no significant benefit in ALS patients. Preclinical data (e.g., mouse models) suggest a potential benefit, but clinical evidence is weak. Ubiquinol is the most bioavailable form and is preferable. The dosage is appropriate, but interactions with medications (e.g., anticoagulants) should be considered.
  Conclusion: Plausible addition, but limited evidence. No change is necessary, but expectations should be realistic.
• Alpha-lipoic acid (R-ALA, 600–1200 mg/day)
  Evaluation: Alpha-lipoic acid (ALA) is a potent antioxidant that regenerates other antioxidants (e.g., vitamins C, E, glutathione) and chelates heavy metals. There are no specific studies on ALA in ALS, but its neuroprotective properties have been documented in other neurodegenerative diseases (e.g., multiple sclerosis). The dosage is safe, but high doses can cause digestive upset or skin reactions. Combining it with NAC and glutathione may have a synergistic effect.
  Conclusion: Useful supplement with theoretical benefit, but direct evidence is lacking.
• N-Acetylcysteine ​​(NAC, 600–1800 mg/day)
  Evaluation: NAC is a precursor to glutathione and reduces oxidative stress, which plays a key role in ALS. It also loosens mucus in the airways, which may be helpful for ALS patients with breathing problems. Preclinical studies (e.g., animal models) show neuroprotective effects, but clinical studies are largely lacking. The dosage is safe, but interactions with nitroglycerin should be noted.
  Conclusion: Very plausible supplementation with indirect evidence.
• Vitamin E (400–800 IU/day)
  Evaluation: Cohort studies show that higher vitamin E levels are associated with a lower risk of ALS. Vitamin E is a fat-soluble antioxidant that may protect nerve cells from oxidative stress. It is often recommended in combination with other antioxidants. The dosage is safe, but interactions with anticoagulants should be considered.
• Selenium (100–200 µg/day)
  Evaluation: Selenium is an essential trace element with antioxidant properties. It supports glutathione peroxidase and may reduce oxidative stress. However, cohort studies show conflicting results, and high doses may be toxic. Low doses are safe and could be useful in an antioxidant combination.

• Vitamin C (500–1000 mg/day)
  Rationale: Vitamin C is a powerful antioxidant and regenerates other antioxidants such as vitamin E. There are no specific studies on vitamin C in ALS, but its role in reducing oxidative stress is well established. The dosage is safe and cost-effective..

3. Neuroinflammation & Cell Protection

• Omega-3 Fatty Acids (DHA/EPA, 1000–2000 mg/day)
  Evaluation: Omega-3 fatty acids are anti-inflammatory and stabilize cell membranes. There are no specific studies on omega-3 in ALS, but their general neuroprotective effect is well documented. Cohort studies suggest that a diet rich in antioxidants and omega-3 could have a positive impact on disease progression. The dosage is appropriate.
  Conclusion: Useful supplementation with indirect evidence. No change necessary.
• Melatonin (10–60 mg at night)
  Evaluation: Melatonin is a potent antioxidant and reduces neuroinflammation. Studies in ALS (e.g., animal models and smaller human studies) show positive effects, including prolonged survival and reduced oxidative damage. High-dose melatonin (up to 60 mg) is safe but may cause drowsiness or gastrointestinal disturbances. The dosage is within the experimental range but plausible.
  Conclusion: Strong evidence for ALS, especially at higher doses.
• Lithium orotate (5–10 mg elemental lithium/day)Evaluation: Lithium inhibits GSK-3β, promotes autophagy, and may have neuroprotective effects. A small study (2008) showed promising results in ALS, but subsequent studies were disappointing. The evidence is conflicting, and lithium orotate has not been well studied compared to lithium carbonate. The dosage is low and presumably safe, but the benefits are unclear.
  Conclusion: Controversial evidence. Can remain as an experimental supplement, but caution should be exercised.
• Vitamin D3 (5000 IU/day)
  Evaluation: Vitamin D3 has neuroimmunomodulatory effects and may reduce inflammation.Vitamin D deficiency is common in ALS patients and should be corrected. Studies show that adequate vitamin D intake can improve quality of life, but direct effects on disease progression are unclear. A dosage of 5000 IU is safe but should be combined with blood level monitoring (25-OH vitamin D).
  Conclusion: Important supplementation, especially in cases of deficiency..

4. Energy metabolism and cellular resilience

• Acetyl-L-carnitine (1–2 g/day)
  Evaluation: Acetyl-L-carnitine supports mitochondrial energy metabolism and is neuroprotective. One study showed that ALS patients taking riluzole plus 3 g of L-carnitine had better independence than the placebo group. The evidence is limited but positive. Acetyl-L-carnitine is more readily penetrant than L-carnitine, making it preferable. The dosage is appropriate.
  Conclusion: Good evidence for ALS.
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  Creatine monohydrate (3–5 g/day)
  Evaluation: Creatine buffers ATP and may support motor function. Preclinical studies (mouse models) showed prolonged survival, but clinical studies (e.g., 10 g/day) were disappointing and showed no clear benefit. The dosage of 3–5 g/day is safe, but the benefit is questionable.
  Conclusion: Weak evidence. Can be maintained, but expectations should be low.’
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• B vitamins (especially B6, B12, folic acid)
  Rationale: B vitamins support energy metabolism and the breakdown of homocysteine, which can have neurotoxic effects. Vitamin B6 is important for the conversion of glutamine to GABA, which could dampen glutamate metabolism. Low levels of B12 and folic acid are common in neurodegenerative diseases. Supplementation (e.g., B complex) is safe and could be supportive..

5. Other possible add-ons

• PQQ (pyrroloquinoline quinone, 10–20 mg/day)
  Rating: PQQ promotes mitochondrial regeneration and has antioxidant effects. There are no studies on PQQ in ALS, but preclinical data suggest neuroprotective effects. The dosage is safe and plausible.
  Conclusion: Experimental, but theoretically reasonable.
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• Resveratrol (100–250 mg/day)
  Evaluation: Resveratrol activates sirtuins and may have neuroprotective effects. There are no specific studies on resveratrol in ALS, but its antioxidant properties are well documented. The dosage is safe.
  Conclusion: Experimental, but plausible.
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• Nicotinamide riboside / NMN (250–500 mg/day)
  Evaluation: Nicotinamide riboside and NMN increase NAD+ levels, which supports mitochondrial function. There are no studies on NAD+ boosters in ALS, but their role in neurodegenerative diseases is promising. The dosage is safe.
  Conclusion: Experimental, but theoretically reasonable.
• TUDCA (tauroursodeoxycholic acid, 500–1000 mg/day)
  Evaluation: TUDCA protects cell membranes and reduces ER stress. Clinical studies (e.g., in combination with edaravone) show promising results, including a slowing of disease progression. The dosage is safe and well-studied.
  Conclusion: Strong evidence, especially in combination with edaravone.
• Riluzole and edaravoneRiluzole (100 mg/day) is the standard treatment for ALS and slows the progression of the disease by several months, especially in early stages. Edaravone (intravenous) shows benefits in certain ALS patients but is not universally effective. Both are established in conventional medicine.
  Conclusion: Indispensable in ALS therapy.”

Critical Comments

… This makes them experimental, but not ineffective.

• Interactions: Supplements such as coenzyme Q10, ALA, and NAC can interact with medications (e.g., anticoagulants, nitroglycerin). Medical evaluation is essential.
• Individualization: The effectiveness of supplements depends on the individual status (e.g., vitamin D deficiency, oxidative stress). Blood level checks (e.g., vitamin D, selenium) are recommended.
• Placebo effect: In ALS, the psychological component is important. Supplements can improve quality of life, even if the objective benefit is limited.

Conclusion

The list considers the most important pathophysiological mechanisms in ALS (oxidative stress, mitochondrial dysfunction, neuroinflammation, glutamate excitotoxicity). Supplements (vitamin E, selenium, vitamin C, B vitamins) enhance antioxidant and metabolic support based on indirect evidence.

The strongest evidence is for melatonin, TUDCA, acetyl-L-carnitine, riluzole, and edaravone.

Many other supplements are experimental but safe and theoretically useful. Medical supervision is crucial to consider interactions and individual needs.

References / Studies

I still need to add!