Magnesium:  

Magnesium L-Threonate

Treatment guidelines for the use of magnesium supplements is complicated and commercial formulations come in a variety of magnesium salts, and each of these magnesium formulations in turn have their own unique characteristics  that affect the choice of formulations for treatment. The unique property of magnesium L-threonate is its ability to raise magnesium levels in the central nervous system (brain and spinal cord), which other formulations cannot achieve. This makes magnesium L-threonate a particularly important  choice in the management of chronic pain, especially in the presence of Central Sensitization (SI).

Caveat:

There is a lack of adequate data to establish human safety for magnesium L-threonate in migraine, headache, or trigeminal neuralgia—but no evidence suggesting it is less safe than other magnesium formulations.

 

See:  

Key to Links:

  • Grey text – handout
  • Red text – another page on this website
  • Blue text – Journal publication

Definitions and Terms Related to Pain

 

Magnesium L-Threonate

A review of different magnesium salt formulations

Treatment guidelines for the use of magnesium supplements can be difficult to understand. Guidelines generally guide dosing in terms of elemental magnesium doses, whereas commercial formulations come in a variety of magnesium salts, each of which has a different percentage content of elemental magnesium. This can make dosing recommendations difficult to follow, especially since there are multiple magnesium salt formulations commonly available. Each of these magnesium formulations in turn have their own unique characteristics  that affect the choice of formulations for treatment.

Elemental Magnesium Content by Formulation

Formulation

Elemental Mg Content

Notes

References

Magnesium Oxide

~60%

Highest elemental content but lowest bioavailability

[1], [2]

Magnesium Glycinate (Bisglycinate)

~14%

Excellent absorption, well tolerated

[1], [3]

Magnesium L-Threonate

~8%

Unique CNS penetration

[4], [5]

Magnesium Malate

~15%

Highest AUC in bioavailability studies

[2], [6]

Magnesium Citrate

~16-17%

Good absorption, mild laxative effect

[7]

 

Magnesium L-Threonate

L-threonate has the strongest evidence for increasing cerebrospinal fluid (CSF) and brain magnesium levels after oral administration. In animal models of radicular pain from lumbar disc herniation, oral L-threonate (604 mg/kg/day) prevented the decrease in CSF magnesium and attenuated mechanical allodynia and thermal hyperalgesia by inhibiting spinal microglial activation, suppressing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and reducing NR2B subunit expression of the NMDA receptor.[1] Similar findings were demonstrated in vincristine-induced neuropathic pain, where L-threonate normalized magnesium deficiency in CSF and dorsal root ganglion neurons, attenuating TNF-α/NF-κB signaling and preventing C-fiber sprouting in the spinal dorsal horn.[2]

The key mechanistic advantage is that L-threonate appears to cross the blood-brain barrier more effectively than other formulations. A comprehensive review found that “organic salts, threonate forms” have been specifically developed to improve BBB permeability, though human studies confirming this are still underway.[3] Importantly, standard IV magnesium sulfate produces only marginal 15% increases in CSF magnesium even with sustained hypermagnesemia, highlighting the challenge of CNS delivery that L-threonate may overcome.[4]

 

The unique property of magnesium L-threonate is its ability to elevate cerebrospinal fluid magnesium levels, which other formulations—including intravenous magnesium sulfate—fail to accomplish.[17][15] Clinical trials used 2,000 mg/day of the L-threonate compound (providing ~144-190 mg elemental magnesium) and demonstrated significant improvements in cognitive function within 30 days.[4]

 

Magnesium L-Threonate Dosing Conversions

Condition

Elemental Mg Dose

Magnesium L-Threonate Salt Dose

Dosing Frequency

References

Cognitive function/memory

140-190 mg/day

1,500-2,000 mg/day

Divided BID or TID

[1], [2]

Neuropathic pain (CIPN)

~144 mg/day

~1,800 mg/day

Divided doses

[3]

Central Sensitization

140-190 mg/day

1,500-2,000 mg/day

Divided BID or TID

[3], [4]

Sleep improvement

~96 mg/day

~1,000 mg/day

500 mg BID

[1]

Radicular pain

~145 mg/day (human equivalent)

~1,800 mg/day

Divided doses

[4]

 

References

  1. Magnesium Disorders. Touyz RM, de Baaij JHF, Hoenderop JGJ. The New England Journal of Medicine. 2024;390(21):1998-2009. doi:10.1056/NEJMra1510603.
  2. Timeline (Bioavailability) of Magnesium Compounds in Hours: Which Magnesium Compound Works Best?. Uysal N, Kizildag S, Yuce Z, et al. Biological Trace Element Research. 2019;187(1):128-136. doi:10.1007/s12011-018-1351-9.
  3. Dose-Dependent Absorption Profile of Different Magnesium Compounds. Ates M, Kizildag S, Yuksel O, et al. Biological Trace Element Research. 2019;192(2):244-251. doi:10.1007/s12011-019-01663-0.
  4. Short-Term Magnesium Therapy Alleviates Moderate Stress in Patients With Fibromyalgia: A Randomized Double-Blind Clinical Trial. Macian N, Dualé C, Voute M, et al. Nutrients. 2022;14(10):2088. doi:10.3390/nu14102088.
  5. Magnesium for Skeletal Muscle Cramps. Garrison SR, Korownyk CS, Kolber MR, et al. The Cochrane Database of Systematic Reviews. 2020;9:CD009402. doi:10.1002/14651858.CD009402.pub3.
  6. Evaluation of Di-Magnesium Malate, Used as a Novel Food Ingredient and as a Source of Magnesium in Foods for the General Population, Food Supplements, Total Diet Replacement for Weight Control and Food for Special Medical Purposes. Younes M, Aggett P, Aguilar F, et al. EFSA Journal. European Food Safety Authority. 2018;16(6):e05292. doi:10.2903/j.efsa.2018.5292.
  7. Magnesium Citrate Malate as a Source of Magnesium Added for Nutritional Purposes to Food Supplements. Turck D, Castenmiller J, De Henauw S, et al. EFSA Journal. European Food Safety Authority. 2018;16(12):e05484. doi:10.2903/j.efsa.2018.5484.
  8. Management of Headache (2023). Jane Abanes PhD DNP MSN/Ed PMHCNS PMHNP-BC RN, Natasha M. Antonovich PharmD BCPS, Andrew C. Buelt DO, et al. Department of Veterans Affairs.
  9. Magnesium in Migraine Prophylaxis-Is There an Evidence-Based Rationale? A Systematic Review. von Luckner A, Riederer F. Headache. 2018;58(2):199-209. doi:10.1111/head.13217.
  10. The Effects of Magnesium, L-Carnitine, and Concurrent Magnesium-L-Carnitine Supplementation in Migraine Prophylaxis. Tarighat Esfanjani A, Mahdavi R, Ebrahimi Mameghani M, et al. Biological Trace Element Research. 2012;150(1-3):42-8. doi:10.1007/s12011-012-9487-5.
  11. Oral Magnesium Oxide Prophylaxis of Frequent Migrainous Headache in Children: A Randomized, Double-Blind, Placebo-Controlled Trial. Wang F, Van Den Eeden SK, Ackerson LM, et al. Headache. 2003;43(6):601-10. doi:10.1046/j.1526-4610.2003.03102.x.
  12. Magnesium and Pain. Shin HJ, Na HS, Do SH. Nutrients. 2020;12(8):E2184. doi:10.3390/nu12082184.
  13. Bioavailability of Magnesium Food Supplements: A Systematic Review. Pardo MR, Garicano Vilar E, San Mauro Martín I, Camina Martín MA. Nutrition (Burbank, Los Angeles County, Calif.). 2021;89:111294. doi:10.1016/j.nut.2021.111294.
  14. Effects of Short-Term Magnesium Supplementation on Ionized, Total Magnesium and Other Relevant Electrolytes Levels. Ivanovic ND, Radosavljevic B, Zekovic M, et al. Biometals : An International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine. 2022;35(2):267-283. doi:10.1007/s10534-022-00363-y.
  15. Efficacy and Safety of Magnesium for the Management of Chronic Pain in Adults: A Systematic Review. Park R, Ho AM, Pickering G, et al. Anesthesia and Analgesia. 2020;131(3):764-775. doi:10.1213/ANE.0000000000004673.
  16. Magnesium for Pain Treatment in 2021? State of the Art. Morel V, Pickering ME, Goubayon J, et al. Nutrients. 2021;13(5):1397. doi:10.3390/nu13051397.
  17. Regulation of Structural and Functional Synapse Density by L-Threonate Through Modulation of Intraneuronal Magnesium Concentration. Sun Q, Weinger JG, Mao F, Liu G. Neuropharmacology. 2016;108:426-39. doi:10.1016/j.neuropharm.2016.05.006.
  18. Scottsdale Magnesium Study: Absorption, Cellular Uptake, and Clinical Effectiveness of a Timed-Release Magnesium Supplement in a Standard Adult Clinical Population. Weiss D, Brunk DK, Goodman DA. Journal of the American College of Nutrition. 2018 May-Jun;37(4):316-327. doi:10.1080/07315724.2017.1398686.

 

Magnesium L-Threonate and Central Sensitization

The Core Mechanism: NMDA Receptor Blockade

All magnesium formulations share a fundamental mechanism—voltage-dependent blockade of the NMDA receptor ion channel, which is the primary driver of central sensitization.[1][2] Under normal conditions, magnesium ions sit within the NMDA receptor pore and block calcium influx. When neurons become depolarized during pain signaling, this magnesium block is relieved, allowing calcium entry and subsequent amplification of pain signals. In magnesium-deficient states, this protective blockade is weakened, leading to excessive NMDA receptor activation, long-term potentiation at pain synapses, and the development of central sensitization.[3]

 

Why Magnesium L-Threonate Is Mechanistically Superior for Central Pain

The critical distinction of magnesium L-threonate lies in its unique ability to elevate cerebrospinal fluid (CSF) and brain magnesium levels, which other magnesium formulations—including intravenous magnesium sulfate—fail to accomplish.[4][5]  This is essential because central sensitization occurs within the spinal cord dorsal horn and brain pain-processing regions, where local magnesium concentrations directly determine NMDA receptor blockade efficacy.

Research demonstrates that magnesium L-threonate exerts its anti-nociceptive effects through a neuroinflammation-dependent pathway:[4][6]

1. Inhibition of microglial activation: L-threonate suppresses spinal cord microglia activation, which is a key driver of neuroinflammation in chronic pain states.[4][7]

2. Reduction of pro-inflammatory cytokines: It decreases TNF-α, IL-1β, and IL-6 expression in the spinal dorsal horn and brain regions like the anterior cingulate cortex.[4][7][6]

3. Normalization of NR2B subunit expression: Magnesium deficiency leads to upregulation of the NR2B-containing NMDA receptors, which are particularly implicated in pain hypersensitivity. L-threonate normalizes NR2B protein levels, restoring appropriate NMDA receptor function.[4][5]

4. Suppression of TNF-α/NF-κB signaling: This inflammatory cascade is activated by magnesium deficiency and drives pathological synaptic plasticity. L-threonate blocks this pathway.[5][6]

5. Reduction of C-fiber evoked potentials: L-threonate decreases the efficiency of pain synaptic transmission at the spinal level, directly reducing central sensitization.[4]

Importantly, when researchers administered intrathecal TNF-α, IL-6, or IL-1β to rats receiving L-threonate, the protective effects were reversed—demonstrating that the anti-nociceptive mechanism is dependent on neuroinflammation suppression.[4]

 

Comparative Limitations of Other Magnesium Formulations

Standard magnesium formulations (glycinate, citrate, oxide) increase serum magnesium levels but have limited ability to raise CSF magnesium concentrations. Studies show that even intravenous magnesium sulfate, which achieves high serum levels, does not significantly inhibit trigeminocervical complex activation when administered systemically—likely because adequate concentrations are not achieved in the central nervous system.[8]

For diabetic neuropathic pain, oral magnesium supplementation (non-threonate) has been shown to abolish thermal and tactile allodynia and prevent increased phosphorylation of the NMDA receptor NR1 subunit in the spinal dorsal horn.[3] However, this effect appears to require adequate peripheral-to-central magnesium transfer, which may be more efficient with L-threonate.

Summary of Mechanistic Differences

Mechanism

Magnesium L-Threonate

Standard Mg Formulations

References

Raises CSF magnesium levels

Yes (demonstrated)

Limited/minimal

[1], [2]

NMDA receptor blockade (spinal)

Strong (direct CNS access)

Moderate (indirect)

[3], [4]

Inhibits microglial activation

Yes

Not demonstrated

[1], [5]

Reduces TNF-α/IL-1β/IL-6 in CNS

Yes

Limited data

[1], [6]

Normalizes NR2B expression

Yes

Not demonstrated

[1], [2]

Blocks TNF-α/NF-κB pathway

Yes

Not demonstrated

[2], [6]

Reduces C-fiber evoked potentials

Yes

Not demonstrated

[1]

Addresses emotional comorbidities

Yes (ACC effects)

Limited data

[5], [6]

Clinical Implications

For patients with central sensitization, neuropathic pain, or chronic pain with cognitive/emotional comorbidities, magnesium L-threonate offers mechanistic advantages due to its ability to directly modulate CNS magnesium levels and suppress neuroinflammation-dependent central sensitization.[4][5][7] However, it is more expensive and provides less elemental magnesium per dose.

 

Alternatives

For patients primarily needing peripheral magnesium repletion or those with budget constraints, magnesium glycinate or citrate remain reasonable alternatives with good tolerability and established efficacy for conditions like migraine and fibromyalgia when there are few findings of cognitive impairment (brain fog) or central sensitization.

 

References

  1. Magnesium and Pain. Shin HJ, Na HS, Do SH. Nutrients. 2020;12(8):E2184. doi:10.3390/nu12082184.
  2. Magnesium in Pain Research: State of the Art. Srebro D, Vuckovic S, Milovanovic A, et al. Current Medicinal Chemistry. 2017;24(4):424-434. doi:10.2174/0929867323666161213101744.
  3. Magnesium Attenuates Chronic Hypersensitivity and Spinal Cord NMDA Receptor Phosphorylation in a Rat Model of Diabetic Neuropathic Pain. Rondón LJ, Privat AM, Daulhac L, et al. The Journal of Physiology. 2010;588(Pt 21):4205-15. doi:10.1113/jphysiol.2010.197004.
  4. Oral Application of Magnesium-L-Threonate Alleviates Radicular Pain by Inhibiting Neuro-Inflammation Dependent Central Sensitization of Rats. Li S, Yi H, Yuan F, et al. Brain Research. 2024;1839:148910. doi:10.1016/j.brainres.2024.148910.
  5. Oral Application of Magnesium-L-Threonate Attenuates Vincristine-Induced Allodynia and Hyperalgesia by Normalization of Tumor Necrosis Factor-Α/Nuclear Factor-κB Signaling. Xu T, Li D, Zhou X, et al. Anesthesiology. 2017;126(6):1151-1168. doi:10.1097/ALN.0000000000001601.
  6. Normalization of Magnesium Deficiency Attenuated Mechanical Allodynia, Depressive-Like Behaviors, and Memory Deficits Associated With Cyclophosphamide-Induced Cystitis by Inhibiting TNF-α/NF-κB Signaling in Female Rats. Chen JL, Zhou X, Liu BL, et al. Journal of Neuroinflammation. 2020;17(1):99. doi:10.1186/s12974-020-01786-5.
  7. Role of Magnesium-L-Threonate in Alleviating Skin/Muscle Incision and Retraction Induced Mechanical Allodynia and Anxiodepressive-Like Behaviors in Male Rats. Chen Y, Zhang Y, Lin W, et al. Brain Research. 2023;1817:148476. doi:10.1016/j.brainres.2023.148476.
  8. N-Methyl-D-Aspartate Receptor Open-Channel Blockers Memantine and Magnesium Modulate Nociceptive Trigeminovascular Neurotransmission in Rats. Hoffmann J, Storer RJ, Park JW, Goadsby PJ. The European Journal of Neuroscience. 2019;50(5):2847-2859. doi:10.1111/ejn.14423.

Magnesium L-Threonate for Migraines and Trigeminal Neuralgia

There is no clinical trial evidence demonstrating that magnesium L-threonate is superior to other magnesium formulations for migraine, headache, or trigeminal neuralgia. However…

Magnesium for Migraines

While magnesium L-threonate has theoretical advantages for brain penetration, all published clinical trials for migraine prevention have used other formulations, primarily magnesium oxide, magnesium citrate, and magnesium dicitrate.[1][2]

The clinical evidence for migraine prevention comes exclusively from trials using magnesium oxide (400-600 mg daily), magnesium citrate (500-600 mg daily), magnesium sulfate, and magnesium dicitrate (600 mg daily).[1][2] These formulations have demonstrated Grade C (possibly effective) evidence for migraine prophylaxis, with systematic reviews showing a mean reduction of 2.6 migraine headaches per month after 12 weeks of treatment.[1][2] No randomized controlled trials have evaluated magnesium L-threonate specifically for migraine or any headache disorder.

Magnesium L-threonate’s theoretical advantage relates to blood-brain barrier penetration. Preclinical research indicates that the L-threonate anion uniquely enhances intraneuronal magnesium concentration through glucose transporters (GLUTs), which other magnesium salts do not accomplish.[3][4] This property has generated interest for neurological applications requiring central nervous system magnesium elevation. Animal studies show that oral magnesium L-threonate increases cerebrospinal fluid magnesium levels and has demonstrated efficacy in models of neuropathic pain, including chemotherapy-induced peripheral neuropathy and radicular pain.[5][6][7]

Because magnesium L-Threonate Is mechanistically superior for central pain (See above), the critical distinction of magnesium L-threonate lies in its unique ability to elevate cerebrospinal fluid (CSF) and brain magnesium levels, which other magnesium formulations fail to accomplish.[4][5]  Research demonstrates that magnesium L-threonate exerts its anti-nociceptive effects through a neuroinflammation-dependent pathway: Thiese points are essential because central sensitization occurs within the spinal cord dorsal horn and brain pain-processing regions, where local magnesium concentrations directly determine NMDA receptor blockade efficacy. Central sensitization is a common complication of migraine headaches, making this argument alone sufficient to consider L-threonate as the first choice in magnesium supplements for migraine management. One treatment option would be to start with an alternate magnesium salt such as magnesium citrate and rotate to magnesium L-threonate if results are not satisfactory.

However, Magnesium L-threonate’s superior blood-brain barrier permeability remains unvalidated in human migraine studies. While preclinical research demonstrates enhanced brain delivery and potential benefits for neurological conditions, these findings have not been translated into clinical trials for headache disorders.[3] The theoretical mechanistic advantages for central sensitization and neuroplasticity, though compelling, cannot substitute for clinical evidence of efficacy and safety in migraine patients.

Is there any evidence to suggest that magnesium L-threonate is less safe than other formulations or is there just a lack of adequate data to establish human safety for magnesium L-threonate?

There is simply a lack of adequate data to establish human safety for magnesium L-threonate in migraine, headache, or trigeminal neuralgia—not evidence suggesting it is less safe than other magnesium formulations.

The safety profile of conventional magnesium formulations (oxide, citrate, dicitrate, sulfate) is well-established from clinical trials. These formulations demonstrate that adverse effects are largely limited to gastrointestinal intolerance (diarrhea, nausea) in patients with normal renal function.[1] Serious magnesium toxicity is associated with doses exceeding 5,000 mg daily and includes hypotension, ileus, muscle weakness, lethargy, and potentially cardiac arrest, with risk increased in patients with reduced renal function.[1] This safety data comes from decades of clinical use and multiple randomized controlled trials in migraine populations.[1][2][3]

In contrast, magnesium L-threonate lacks human safety data specifically in headache populations. While preclinical studies demonstrate its enhanced blood-brain barrier penetration and neurological effects, systematic reviews of magnesium for chronic pain note that “adverse events were inconsistently reported in the included studies,” making it difficult to draw conclusions about safety even for the studied formulations.[4][5] No published trials have evaluated magnesium L-threonate’s safety profile in migraine patients.

The theoretical concern with magnesium L-threonate relates to its unique pharmacokinetic properties. Enhanced CNS penetration could theoretically amplify both therapeutic and adverse central nervous system effects, though this remains speculative without clinical data. The compound’s ability to elevate cerebrospinal fluid magnesium levels and modulate NMDA receptors, synaptic density, and neurotransmitter systems suggests the potential for CNS-specific adverse effects that would not occur with poorly brain-penetrant formulations—but again, this is theoretical.[4]

From a regulatory and evidence-based perspective, the absence of safety data represents a meaningful limitation. Supplements are not FDA-regulated in the United States, and physicians should ensure patients understand these limitations.[6] The lack of standardized manufacturing, quality control, and pharmacovigilance data for magnesium L-threonate means that even basic safety parameters (optimal dosing, drug interactions, contraindications beyond renal impairment) remain undefined for headache populations.

The evidence gap is one of insufficient data rather than demonstrated harm, but this distinction matters for clinical decision-making and informed consent when choosing between formulations with established versus theoretical safety profiles.

References

  1. Management of Headache (2023). Jane Abanes PhD DNP MSN/Ed PMHCNS PMHNP-BC RN, Natasha M. Antonovich PharmD BCPS, Andrew C. Buelt DO, et al. Department of Veterans Affairs.
  2. Magnesium in Migraine Prophylaxis-Is There an Evidence-Based Rationale? A Systematic Review. von Luckner A, Riederer F. Headache. 2018;58(2):199-209. doi:10.1111/head.13217.
  3. An Evidence-Based Review of Oral Magnesium Supplementation in the Preventive Treatment of Migraine. Teigen L, Boes CJ. Cephalalgia : An International Journal of Headache. 2015;35(10):912-22. doi:10.1177/0333102414564891.
  4. A Mini Review on the Various Facets Effecting Brain Delivery of Magnesium and Its Role in Neurological Disorders. Mathew AA, Panonnummal R. Biological Trace Element Research. 2023;201(9):4238-4253. doi:10.1007/s12011-022-03517-8.
  5. Efficacy and Safety of Magnesium for the Management of Chronic Pain in Adults: A Systematic Review. Park R, Ho AM, Pickering G, et al. Anesthesia and Analgesia. 2020;131(3):764-775. doi:10.1213/ANE.0000000000004673.
  6. Migraine Headache Prophylaxis. Moreland P, Gaffney B, Lanham JS. American Family Physician. 2025;111(5):443-450.

In preclinical pain models, magnesium L-threonate (604 mg/kg/day in rats) attenuated mechanical allodynia and thermal hyperalgesia by inhibiting neuroinflammation and central sensitization.[5][6] These studies showed that magnesium L-threonate prevented activation of the TNF-α/NF-κB signaling pathway and reduced spinal microglial activation.[5][6][7] One study specifically examined trigeminovascular neurotransmission and found that local application of magnesium to the trigeminocervical complex inhibited NMDA receptor-mediated nociceptive activation, though systemic magnesium administration (100 mg/kg IV) did not significantly affect trigeminal activity.[8]

Magnesium for Trigeminal Neuralgia

For trigeminal neuralgia specifically, there is no clinical evidence supporting magnesium use in any formulation. The available literature on magnesium and pain focuses on migraine, neuropathic pain from chemotherapy, and chronic pain syndromes, but not trigeminal neuralgia.[5][8][9][6] The preclinical data on trigeminovascular modulation suggests a potential mechanism, but this has not been translated into clinical trials for trigeminal neuralgia.[8]

The lack of clinical trials with magnesium L-threonate for headache disorders represents a significant evidence gap. While the enhanced brain penetration is theoretically advantageous, this has not been validated in human studies for migraine or headache. The established formulations (oxide, citrate, dicitrate) have demonstrated clinical efficacy and remain the evidence-based choices for migraine prophylaxis.[1][2] Magnesium L-threonate may warrant investigation in future clinical trials, particularly given its superior CNS bioavailability demonstrated in preclinical models, but currently lacks the clinical evidence base to recommend it over established formulations.[3][4]

References

  1. Management of Headache (2023). Jane Abanes PhD DNP MSN/Ed PMHCNS PMHNP-BC RN, Natasha M. Antonovich PharmD BCPS, Andrew C. Buelt DO, et al. Department of Veterans Affairs.
  2. Magnesium in Migraine Prophylaxis-Is There an Evidence-Based Rationale? A Systematic Review. von Luckner A, Riederer F. Headache. 2018;58(2):199-209. doi:10.1111/head.13217.
  3. A Mini Review on the Various Facets Effecting Brain Delivery of Magnesium and Its Role in Neurological Disorders. Mathew AA, Panonnummal R. Biological Trace Element Research. 2023;201(9):4238-4253. doi:10.1007/s12011-022-03517-8.
  4. Regulation of Structural and Functional Synapse Density by L-Threonate Through Modulation of Intraneuronal Magnesium Concentration. Sun Q, Weinger JG, Mao F, Liu G. Neuropharmacology. 2016;108:426-39. doi:10.1016/j.neuropharm.2016.05.006.
  5. Oral Application of Magnesium-L-Threonate Alleviates Radicular Pain by Inhibiting Neuro-Inflammation Dependent Central Sensitization of Rats. Li S, Yi H, Yuan F, et al. Brain Research. 2024;1839:148910. doi:10.1016/j.brainres.2024.148910.
  6. Oral Application of Magnesium-L-Threonate Attenuates Vincristine-Induced Allodynia and Hyperalgesia by Normalization of Tumor Necrosis Factor-Α/Nuclear Factor-κB Signaling. Xu T, Li D, Zhou X, et al. Anesthesiology. 2017;126(6):1151-1168. doi:10.1097/ALN.0000000000001601.
  7. Role of Magnesium-L-Threonate in Alleviating Skin/Muscle Incision and Retraction Induced Mechanical Allodynia and Anxiodepressive-Like Behaviors in Male Rats. Chen Y, Zhang Y, Lin W, et al. Brain Research. 2023;1817:148476. doi:10.1016/j.brainres.2023.148476.
  8. N-Methyl-D-Aspartate Receptor Open-Channel Blockers Memantine and Magnesium Modulate Nociceptive Trigeminovascular Neurotransmission in Rats. Hoffmann J, Storer RJ, Park JW, Goadsby PJ. The European Journal of Neuroscience. 2019;50(5):2847-2859. doi:10.1111/ejn.14423.
  9. Efficacy and Safety of Magnesium for the Management of Chronic Pain in Adults: A Systematic Review. Park R, Ho AM, Pickering G, et al. Anesthesia and Analgesia. 2020;131(3):764-775. doi:10.1213/ANE.0000000000004673.

Emphasis on Education

 

Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.

 

For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.

 

Should you wish more information regarding any of the subjects listed – or not listed –  here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.

 

For more information, please contact Accurate Clinic.

 

Supplements recommended by Dr. Ehlenberger may be purchased commercially online

Please read about our statement regarding the sale of products recommended by Dr. Ehlenberger.

 

 

.