Nutraceuticals: 

Opioid Tapering with Nutraceutical Support – A Physician Guide

This document provides a comprehensive physician-facing review of  nutraceuticals and their mechanistic roles in opioid tapering, as well as their role in OAT and OIH prevention and reduction.

 

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Definitions and Terms Related to Pain

 

Nutraceutical Support for Opioid Tapering

INTRODUCTION

Opioid analgesic tolerance (OAT) and opioid-induced hyperalgesia (OIH) are neuroplastic phenomena that share a common molecular substrate: activation of NMDA receptors — particularly GluN2B-containing subtypes — in the spinal cord dorsal horn, with downstream engagement of nitric oxide synthase (NOS), neuroinflammatory cascades, and mitochondrial dysfunction.[1][2][3]

Mechanistic Profiles of:

Agmatine, Magnesium L-Threonate, Melatonin, and PEA

These four nutraceuticals target this shared pathophysiology of OAT and OIH through complementary, non-overlapping mechanisms, providing a multi-level pharmacological strategy for facilitating opioid tapering while maintaining analgesia and minimizing withdrawal.

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1. AGMATINE

Mechanisms:

  • GluN2B-Selective NMDA Receptor Antagonism (Primary Mechanism)
  • NOS Inhibition
  • Imidazoline Receptor Agonism

Facilitation of Opioid Tapering and Analgesia Enhancement

Agmatine potentiates opioid analgesia through at least two receptor systems. Via α₂-adrenoceptor and imidazoline I₂ receptor mechanisms, agmatine produces a 5- to 9-fold leftward shift in the morphine dose-response curve at the spinal level, meaning the same analgesic effect can be achieved at a fraction of the opioid dose.[4]

This potentiation is blocked by idazoxan (imidazoline antagonist) and yohimbine (α₂ antagonist), confirming receptor specificity.[4] The spinal potentiation (9-fold) substantially exceeds the supraspinal effect (2-fold), indicating the dorsal horn as the primary site of action — the same location where agmatine’s GluN2B antagonism operates.[1]

Critically, chronic opioid exposure depletes endogenous agmatine. Chronic morphine significantly decreases arginine decarboxylase (ADC) activity and agmatine levels in brain, liver, kidney, and other tissues, and naloxone-precipitated withdrawal further decreases these levels.[5]

This means chronic opioid patients are likely in an endogenous agmatine-depleted state, making supplementation restorative rather than merely additive.

Prevention of OAT

Agmatine prevents opioid tolerance through at least four independent mechanisms:

   1. GluN2B-selective NMDA antagonism (Primary Mechanism):

Agmatine preferentially antagonizes GluN2B-containing NMDARs in lamina II dorsal horn neurons, abbreviating the amplitude, duration, and decay constant of NMDA receptor-mediated EPSCs identically to the selective GluN2B antagonist ifenprodil. Both lose efficacy in GluN2B-knockdown mice. This is mechanistically critical because chronic morphine specifically upregulates GluN2B-containing NMDA receptors in primary sensory neurons.[1][6][7]

   2. NOS inhibition via the NMDAr-PSD95-nNOS pathway:

Agmatine requires an intact PSD95-nNOS tethering complex for its calcium transient inhibition and antihyperalgesic effects. Disruption of this pathway with IC87201 reverses agmatine’s effects both ex vivo and in vivo.[2]

   3. Prevention of µ-opioid receptor downregulation:

Agmatine inhibits DAMGO-induced µ-opioid receptor internalization and downregulation via imidazoline I₁ receptor activation (IRAS), preserving receptor availability during chronic opioid exposure.[8]

   4. Anti-neuroinflammatory BBB protection:

Agmatine ameliorates morphine-induced behavioral sensitization by protecting blood-brain barrier integrity and reducing neuroinflammation (TNF-α, IL-6, IL-1β) and microglial activation in the nucleus accumbens.[9]

The endogenous role of agmatine in moderating tolerance is confirmed by immunoneutralization studies: when endogenous spinal agmatine is sequestered using anti-agmatine antibodies, mice become sensitized to opioid tolerance — a sub-threshold opioid dose that normally produces no tolerance becomes tolerance-inducing.[3]

AAV-mediated gene transfer of arginine decarboxylase to the spinal cord prevented tolerance to both morphine and endomorphin-2, providing the strongest preclinical proof-of-concept for sustained agmatine elevation as a tolerance prevention strategy.[10]

Prevention/Reduction of OIH

Agmatine is mechanistically precisely targeted at OIH because GluN2B is the specific NMDA receptor subunit upregulated by chronic morphine in primary sensory neurons.[7] Co-administration of a selective GluN2B antagonist (Ro 25-6981) with morphine prevents OIH and increases morphine analgesia.[7][11]

Agmatine replicates this pharmacological profile as a GluN2B-selective antagonist that reverses chronic pain from inflammation, neuropathy, and spinal cord injury while having no effect on acute pain tests — the hallmark of an anti-plasticity agent targeting maladaptive neuroplasticity rather than normal nociception.[8]

Withdrawal Symptom Reduction

Agmatine reverses morphine tolerance and dependence in multiple species. In beagle dogs and rhesus monkeys, intragastric agmatine suppressed morphine-induced physiological dependence.[4] The mechanism involves suppression of the NMDA/NOS cascade that drives withdrawal-associated neuroplasticity, combined with α₂-adrenoceptor agonism that parallels the mechanism of clonidine (the standard pharmacological agent for opioid withdrawal).[12]

Evidence Level: 20+ preclinical studies across 4 species; 1 human RCT (pain, not opioid-specific); no human trials for opioid tapering.

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2. MAGNESIUM L-THREONATE

   Mechanisms:

  • Voltage-Dependent NMDA Channel Block (Primary Mechanism)
  • µ-Opioid Receptor Positive Allosteric Modulation
  • CNS-Preferential Bioavailability

   Rationale for L-Threonate Over Other Magnesium Salts

The critical limitation of conventional magnesium salts (glycinate, citrate, oxide) for CNS applications is poor blood-brain barrier penetration. Magnesium L-threonate (L-TAMS) was specifically developed to address this limitation. The L-threonate anion is naturally present in cerebrospinal fluid and, when administered orally, elevates CSF threonate levels. Threonate directly increases intraneuronal Mg²⁺ concentration through glucose transporter (GLUT)-mediated mechanisms — an effect unique to threonate that other common Mg²⁺ anions fail to replicate.[13] This results in significantly greater brain magnesium elevation compared to other magnesium salts at equivalent elemental magnesium doses.[14]

A 2025 comparative study of organic magnesium salts (citrate, glycinate, malate) found formulation-dependent tissue distribution: magnesium glycinate exhibited anxiolytic properties but did not preferentially elevate brain magnesium, while magnesium malate increased whole-brain tissue levels.[15] Magnesium L-threonate was specifically designed and validated for CNS bioavailability, making it the preferred formulation for targeting spinal cord and brain NMDA receptors relevant to OAT and OIH.[14][16]

   Facilitation of Opioid Tapering and Analgesia Enhancement

      Magnesium enhances opioid analgesia through a dual mechanism:

1. NMDA receptor antagonism: Mg²⁺ blocks the NMDA receptor ion channel pore in a voltage-dependent manner at the selectivity filter, where an asparagine ring forms coordination bonds with Mg²⁺. A 2025 cryo-EM structural study identified three distinct Mg²⁺-binding pockets on GluN1-N2B receptors: Site I (selectivity filter, voltage-dependent block), Site II (GluN2B NTD, allosteric potentiation), and Site III (GluN2B NTD, overlapping with Zn²⁺ pocket, allosteric inhibition). This is complementary to agmatine’s GluN2B subunit-selective antagonism — magnesium blocks the channel pore while agmatine targets the GluN2B subunit itself.[17]

2. µ-Opioid receptor positive allosteric modulation: Molecular dynamics simulations revealed that Mg²⁺ acts as a positive allosteric modulator of the µ-opioid receptor, increasing agonist binding affinity. In the presence of GDP-bound G-proteins, Mg²⁺ shifts µ-opioid receptors from a low-affinity to a high-affinity state for agonists, enhancing opioid signaling without directly activating the receptor. This dual action — NMDA antagonism plus µ-opioid receptor potentiation — makes magnesium uniquely positioned among NMDA antagonists.[18][19]

In clinical settings, multiple meta-analyses confirm that perioperative IV magnesium significantly reduces postoperative opioid consumption (SMD -1.51; 95% CI -2.15 to -0.87) and pain scores (SMD -0.61; 95% CI -0.90 to -0.32), with benefits persisting up to 48 hours.[20][21]

   Prevention of OAT

Intrathecal co-infusion of magnesium sulfate with morphine prevents the development of spinal morphine tolerance in rats.[12] The mechanism involves voltage-dependent NMDA channel block that reduces the glutamatergic neuroplasticity underlying tolerance development. Combined application of magnesium with MK-801 produces additive enhancement of morphine analgesia, confirming that magnesium’s NMDA blockade operates through a mechanism partially distinct from non-selective channel blockers.[22]

   Prevention/Reduction of OIH

Magnesium L-threonate specifically attenuates OIH through neuroinflammation-dependent central sensitization pathways. In a radicular pain model, oral L-TAMS inhibited spinal microglial activation, reduced pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), decreased C-fiber evoked field potentials, and reduced NR2B protein levels in the spinal cord. Critically, the NR2B reduction was rescued by intrathecal delivery of individual pro-inflammatory cytokines, establishing that L-TAMS acts upstream by suppressing neuroinflammation, which in turn normalizes NR2B expression.[23]

In remifentanil-induced hyperalgesia models, intrathecal MgSO₄ dose-dependently reduced both thermal and mechanical hyperalgesia and suppressed the upregulation of phosphorylated NR2B (pNR2B) in the spinal cord.[24] A 2025 meta-analysis of 22 RCTs (n=1,362) confirmed that IV magnesium significantly attenuates remifentanil-induced postoperative hyperalgesia.[20]

Magnesium L-threonate also attenuates vincristine-induced neuropathic pain by normalizing TNF-α/NF-κB signaling, preventing NR2B upregulation, and blocking C-fiber long-term potentiation in the spinal dorsal horn — all pathological plasticity mechanisms shared with OIH.[25]

   Withdrawal Symptom Reduction

While direct evidence for magnesium in opioid withdrawal is limited, magnesium deficiency is common in chronic opioid users and contributes to neuronal hyperexcitability, anxiety, and muscle cramping — all prominent withdrawal symptoms. Magnesium’s NMDA antagonism, anxiolytic properties (particularly magnesium glycinate), and muscle relaxant effects provide mechanistic rationale for symptom mitigation during tapering.[16][15][26]

Evidence Level: Multiple meta-analyses for perioperative opioid-sparing; strong preclinical evidence for L-threonate in central sensitization and NR2B modulation; no human trials specifically for chronic opioid tapering.

3. MELATON:IN

Mechanisms

  • Mitochondrial Protection (Primary Mechanism)
  • Anti-Neuroinflammation
  • NOS Inhibition
  • TLR2/NLRP3 Inflammasome Suppression

   Facilitation of Opioid Tapering and Analgesia Enhancement

Melatonin enhances opioid analgesia and has intrinsic analgesic properties mediated through multiple receptor systems (MT1/MT2 melatonin receptors, peripheral benzodiazepine receptors, and opioid receptor interactions). Co-administration of melatonin with morphine leads to reversal of multiple pathways affected by chronic opioid use, including mitochondrial dysfunction, excessive oxidative stress, and neuroinflammation.[27][28]

Melatonin’s role in opioid tapering extends beyond analgesia to include sleep optimization — a critical and often under-appreciated component of successful tapering. Sleep disruption is both a consequence of chronic opioid use and a major driver of pain amplification and withdrawal symptom severity.

In a randomized clinical trial of men with opioid addiction under methadone maintenance therapy, melatonin (vs. zolpidem vs. placebo) significantly improved both mental health scores and sexual function over 30 days, with the highest improvement in depression scores.[29]

   Prevention of OAT

      Melatonin reverses morphine tolerance through several well-characterized mechanisms:

1. Mitochondrial protection: Chronic morphine causes significant mitochondrial damage, including reduced mtDNA copy number in the hippocampus and peripheral blood, mediated by excessive autophagy. Co-administration of melatonin with morphine restored mtDNA content, prevented autophagy-mediated mitochondrial loss, and ameliorated morphine-induced behavioral sensitization and analgesic tolerance.[30]

2. Antioxidant enzyme activation: Intrathecal melatonin co-infusion attenuated morphine tolerance in both neuropathic and naïve rats through a mechanism independent of melatonin receptors (MT1/MT2 antagonists did not block the effect). Melatonin increased antioxidative enzymes SOD2, HO-1, and GPx1 in the spinal cord of morphine-tolerant rats while abolishing the upregulation of proinflammatory and pain-related receptor genes.[31]

3. TLR2/NLRP3 inflammasome suppression: Morphine tolerance is accompanied by increased TLR2 expression and NLRP3 inflammasome activation in the spinal cord, with concurrent downregulation of endogenous melatonin levels. Chronic melatonin administration reduced TLR2 expression and NLRP3 inflammasome activation, partially restoring morphine’s analgesic effect. A TLR2-melatonin negative feedback loop regulates microglial and NLRP3 inflammasome activation during tolerance development.[32]

4. Microglial inhibition and HSP27 modulation: Melatonin reversed morphine-induced microglial activation and HSP27 upregulation in the spinal dorsal horn, partially restoring morphine’s antinociceptive effect in tolerant rats.[33]

5. NOS inhibition: Melatonin’s reversal of morphine tolerance involves suppression of NOS activity. Co-administration of melatonin or L-NAME (NOS inhibitor) with morphine during the induction phase delayed tolerance development, while L-arginine (NOS substrate) enhanced tolerance. Melatonin antagonized L-arginine’s pro-tolerance effects.[34]

   Prevention/Reduction of OIH

Melatonin’s anti-OIH effects are primarily indirect, operating through suppression of the neuroinflammatory and oxidative stress cascades that drive OIH rather than through direct NMDA receptor antagonism.

The TLR2/NLRP3 inflammasome pathway suppression, microglial deactivation, and antioxidant enzyme upregulation collectively reduce the neuroinflammatory milieu that sustains OIH.[31][32][28] Constant light exposure (which suppresses endogenous melatonin) significantly aggravates morphine tolerance in neuropathic rats, while exogenous melatonin reverses this effect, suggesting that circadian melatonin rhythm disruption — common in chronic pain patients — may exacerbate OIH.[31]

   Withdrawal Symptom Reduction

     Melatonin has the most direct evidence for withdrawal symptom reduction among the four nutraceuticals:

  • Co-administration of melatonin (1–10 mg/kg) with morphine during the induction phase reversed the development of both tolerance and physical dependence. Acute melatonin administration during the expression phase reduced naloxone-precipitated withdrawal jumping.[34][35]
  • Melatonin blocks morphine-induced conditioned place preference (reward) and reduces c-Fos expression in the nucleus accumbens, suggesting modulation of the reward circuitry that drives psychological dependence.[36][37]
  • In the human RCT of men under methadone maintenance, melatonin significantly improved mental health (depression, anxiety) and sexual function — both major quality-of-life concerns during opioid tapering.[29]
  • During drug withdrawal in opioid-addicted patients, serum melatonin levels increase during improvement of protracted abstinence syndrome, suggesting an endogenous protective role.[30]

The mechanism of withdrawal reduction involves NOS inhibition (paralleling the mechanism of clonidine) and peripheral benzodiazepine receptor agonism (PK11195, a peripheral BZ receptor antagonist, partially blocked melatonin’s anti-withdrawal effect).[34][35]

Evidence Level: Multiple preclinical studies; 1 human RCT in methadone maintenance (mental health/sexual function outcomes); strong mechanistic rationale across multiple pathways.

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4. PALMITOYLETHANOLAMIDE (PEA)

   Mechanisms:

  • Mast Cell-Astrocyte Crosstalk Modulation (Primary Mechanism)
  • PPARα Agonism
  • Glial Deactivation
  • VEGF-A Downregulation

   Facilitation of Opioid Tapering and Analgesia Enhancement

PEA enhances opioid analgesia and delays tolerance through a mechanism entirely distinct from the NMDA-targeting agents (agmatine and magnesium). PEA is an endogenous lipid neuromodulator that acts primarily through PPARα activation and mast cell stabilization, modulating the neuroimmune environment that influences opioid efficacy.

In the chronic constriction injury (CCI) model of neuropathic pain, preemptive and concomitant administration of ultramicronized PEA (um-PEA) significantly decreased the effective dose of morphine required for analgesia and delayed the onset of morphine tolerance.[38] The effect extends beyond morphine: um-PEA delayed tolerance to both oxycodone and tramadol. In oxycodone-treated rats, the dose needed to be increased from 0.3 mg/kg to 1 mg/kg over 31 days in the vehicle group, while acute co-treatment with PEA (120 mg/kg) achieved equivalent analgesia without dose escalation.[39]

A meta-analysis of 18 RCTs (n=1,196) confirmed PEA’s independent analgesic efficacy across nociceptive (SMD -0.74), neuropathic (SMD -0.97), and nociplastic (SMD -0.59) pain types, with significant benefits observed within 4–6 weeks.[40]

   Prevention of OAT

      PEA delays morphine tolerance through at least three identified mechanisms:

1. Mast cell-astrocyte crosstalk modulation: Morphine treatment significantly increases mast cell degranulation. PEA pre-treatment prevents this degranulation (confirmed by β-hexosaminidase assay and histamine quantification). The secretome from morphine-treated mast cells activates astrocytes, upregulating CCL2, IL-1β, IL-6, Serpina3n, EAAT2, and GFAP. PEA pre-treatment of mast cells prevents this astrocyte activation, suggesting PEA delays tolerance by interrupting the mast cell → astrocyte inflammatory cascade.[41]

2. Glial deactivation: PEA prevents both microglia and astrocyte cell number increases induced by morphine in the spinal dorsal horn. While morphine-dependent increases in spinal TNF-α levels were not directly modified by PEA, immunohistochemistry revealed higher TNF-α immunoreactivity retained within astrocytes of PEA-treated rats, suggesting PEA decreases cytokine release from astrocytes rather than production.[42]

3. VEGF-A downregulation: A 2024 study identified a novel mechanism: PEA counteracts morphine-induced increases in VEGF-A expression in the nervous system (DRG and spinal cord). Bevacizumab (anti-VEGF-A antibody) replicated PEA’s effects on tolerance delay, confirming VEGF-A as a mediator. PEA also counteracted morphine-induced upregulation of pain-related genes Serpina3n and Eaat2.[43]

4. Endogenous PEA augmentation: Inhibition of N-acylethanolamine acid amidase (NAAA), the enzyme that degrades endogenous PEA, dose-dependently enhanced morphine’s antinociceptive effects and delayed tolerance development, confirming that the endogenous PEA system actively modulates opioid efficacy.[44]

   Prevention/Reduction of OIH

PEA’s anti-OIH effects are indirect, operating through suppression of the glial activation and neuroinflammatory cascades that sustain OIH rather than through direct NMDA receptor modulation. The mast cell stabilization, astrocyte deactivation, and VEGF-A suppression collectively reduce the neuroimmune environment that amplifies pain processing during chronic opioid exposure.[41][38][43] PEA’s independent analgesic efficacy across all pain types (nociceptive, neuropathic, nociplastic) provides additional pain relief that can compensate for any residual OIH during tapering.[40]

   Withdrawal Symptom Reduction

A 2024 study demonstrated that PEA attenuates negative emotions (anxiety and depression) induced by morphine withdrawal in mice, accompanied by reduction in monoamine neurotransmitter levels (5-HT, noradrenaline, dopamine) in the hippocampus and prefrontal cortex.[45] This suggests PEA may address the affective/psychological components of withdrawal that are often the most challenging aspect of opioid tapering.

Evidence Level: 6+ preclinical studies specifically on opioid tolerance; 18 RCTs for independent analgesic efficacy (meta-analysis); 1 preclinical study on withdrawal-related negative emotions; no human trials specifically for opioid tapering.

MECHANISTIC COMPLEMENTARITY: WHY ALL FOUR TOGETHER

The rationale for combining these four agents rests on their non-overlapping mechanisms targeting the shared pathophysiology of OAT and OIH:

  • Agmatine provides GluN2B subunit-selective NMDA antagonism (voltage-independent) + NOS inhibition + imidazoline receptor-mediated µ-opioid receptor preservation + endogenous depletion restoration
  • Magnesium L-threonate provides voltage-dependent NMDA channel pore block (complementary to agmatine’s subunit-selective block) + µ-opioid receptor positive allosteric modulation + neuroinflammation-dependent NR2B normalization
  • Melatonin provides mitochondrial protection against morphine-induced damage + TLR2/NLRP3 inflammasome suppression + antioxidant enzyme upregulation + sleep optimization + direct withdrawal symptom reduction
  • PEA provides mast cell-astrocyte crosstalk interruption + glial deactivation + VEGF-A downregulation + independent multimodal analgesia + withdrawal-related mood support

No single agent addresses all four domains (NMDA neuroplasticity, µ-opioid receptor preservation, neuroinflammation/oxidative stress, and neuroimmune modulation). The combination creates a pharmacological strategy that targets OAT and OIH at every identified mechanistic level — from receptor-level events (NMDA antagonism, µ-opioid receptor allosteric modulation) through intracellular signaling (NOS, NF-κB, NLRP3) to cellular-level responses (microglial polarization, mast cell stabilization, astrocyte deactivation) to organelle-level protection (mitochondrial preservation).

EVIDENCE LIMITATIONS

The evidence limitations section is emphasized:  transparent communication about the preclinical-to-clinical translation gap is essential for informed clinical decision-making.[7][40]

It must be emphasized that while the preclinical evidence for each agent is substantial and mechanistically well-characterized, no human clinical trials have tested any of these nutraceuticals specifically for opioid tapering support in chronic pain patients.

   The clinical evidence base consists of:

  • Agmatine: 1 RCT for lumbar radiculopathy pain (not opioid-specific)[46]
  • Magnesium: Multiple meta-analyses for perioperative opioid-sparing (acute, not chronic opioid tapering)[20][21]
  • Melatonin: 1 RCT in methadone maintenance (mental health/sexual function, not tapering per se)[29]
  • PEA: 18 RCTs for independent analgesic efficacy (not opioid-specific)[40]

 

The recommendation to use these agents in combination for opioid tapering support is therefore evidence-informed (strong mechanistic rationale + consistent preclinical data + favorable safety profiles) rather than evidence-proven by clinical trials.

This document synthesizes the mechanistic evidence for all four nutraceuticals in the context of opioid tapering, OAT, and OIH.

   Several key points merit emphasis:

The magnesium L-threonate section addresses the specific rationale for choosing this formulation over magnesium glycinate (which was listed in the original patient guide). The L-threonate anion uniquely elevates intraneuronal Mg²⁺ via GLUT-mediated transport — an effect not replicated by other magnesium anions — making it the preferred formulation for CNS targets.[13][14] The 2025 cryo-EM structural study identifying three distinct Mg²⁺-binding pockets on GluN1-N2B receptors provides the first atomic-level understanding of how magnesium modulates NMDA receptors relevant to OAT/OIH.[17]

The PEA evidence is particularly notable for the 2024 VEGF-A mechanism discovery, which identified an entirely new pathway by which PEA delays morphine tolerance — one that was confirmed by replication with bevacizumab.[43] This adds to the mast cell-astrocyte crosstalk mechanism identified in 2023.[41]

The melatonin section highlights the TLR2-melatonin negative feedback loop as a recently characterized mechanism: chronic morphine upregulates TLR2 while downregulating endogenous melatonin, creating a self-reinforcing neuroinflammatory cycle that exogenous melatonin can interrupt.[32]

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  31. The Circadian Hormone Melatonin Inhibits Morphine-Induced Tolerance and Inflammation via the Activation of Antioxidative Enzymes. Chen IJ, Yang CP, Lin SH, Lai CM, Wong CS. Antioxidants (Basel, Switzerland). 2020;9(9):E780. doi:10.3390/antiox9090780.
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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.

 

 

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