The Official Website for The Nemechek Protocol™ Medical Recovery Program

CASE REPORT: Reversal of Combat PTSD with tVNS in Combination with an Anti-Neuroinflammatory Regimen

INTRODUCTION

Stressful life events lead to microdamage in the brain triggering an injury repair response.

The response consists of a neuroinflammatory and regeneration phases involving microglia, neurotrophins and neurogenesis (See figure 1).1,2

The risk of post-deployment post-traumatic stress disorder (PTSD) in soldiers is associated with markers of inflammation (elevated CRP and IL-6, and low HRV) 3,4,5

The chronicity of PTSD may be the result of a dysfunctional repair response from 2 major sources: excessive pro-inflammatory cytokines levels within the CNS and abnormal functioning of primed microglia.6

These proinflammatory cytokines can also impair the neuronal repair process (See figure 2).

Figure 1: Neuron Repair Process

Figure 2 Neuroinflamation and Dysfunction of Neuron Repair Process

We theorized that shifting microglia to the anti-inflammatory rejuvenating M2-phenotype and reducing pro-inflammatory cytokines levels would improve the brain’s injury repair response sufficiently to reverse longstanding PTSD.

Our protocol utilizes transcutaneous vagus nerve stimulation (tVNS)7,8 high concentration docosahexaenoic acid (DHA) fish oil 9, 10, olive oil 11 and 10-day course of rifaximin 12 to achieve these goals.

We are excited to report the clinical remission of 2 soldiers with chronic PTSD using such an approach.

METHODS

The subjects were two men (age: subject #1 – 78, subject #2 – 36) who had suffering from severe combat-induced PTSD for 60 and 11 years in duration, respectively.

The predominant symptoms for subject #1 were weekly violent war-related nightmares, severe depression and recurrent bouts of alcoholism. His symptoms had continued non-stop for 60 years since he served as a U.S. Marine in the Korean War.

The predominant symptoms for subject #2 were frequent fits of rage and anger that occurred several times per week. These episodes could become so intense that they resulted in the destruction of property, job loss and significant disruption of his family. These symptoms had persisted for 11 years since serving in the U.S. Army in Afghanistan.

Both subjects had been diagnosed with PTSD by psychiatrists within the U.S. Veteran Affairs health care system as well as private community-based mental health specialist.

Both subjects were started on the Nemechek Protocol, a regimen designed to normalize brain recovery mechanisms though shifting of microglia to the M2-phenotypes and suppression of systemic pro-inflammatory cytokines.

The protocol consists of:

  • tVNS (5 Hz, 250 uS, 1 mA, continuous), 2 hours (cumulative time
    on device), patient-administered via the tragus or concha)
  • Rifaximin, 550 mg BID x 10 days
  • Fish Oil containing 3,000 mg of DHA and 1,500 mg of EPA
  • 30 ml of EVOO containing an estimated 8 grams of oleic acid
  • 1/4 cup of nuts, 1 tbsp. of ground flax or 1,000 mg flax oil capsule.

Clinical and Autonomic Monitoring Every 2-3 Months:

  • Monitoring of PTSD and Depression was based on clinical assessment.
  • Autonomic assessment was performed via spectral analysis (ANSAR Inc., ANX 3.0).

RESULTS

After 8 and 5 months of treatment, respectively, both subjects experienced complete resolution of their PTSD- associated symptoms as well as normalization of their resting autonomic indices.

SUBJECT #1

REGIMEN TIME COURSE:

STARTS REGIMEN:

  • Daily tVNS, DHA, EVOO plus rifaximin x 10 days.
  • The patient is not taking any psychotropic medication.

AFTER 6 MONTHS:

  • Flashbacks reduced from 1 per week to 1 per month.
  • Depression is lessening.
  • Orthostasis, nocturia and headaches also resolve.

AFTER 8 MONTHS:

  • PTSD symptoms stop.
  • Flash backs and depression completely resolved after 60 years.

NEXT 2 ½ YEARS:

  • Patient remains in remission on maintenance tVNS, DHA and EVOO.

SUBJECT #1 BASELINE:

RESTING AUTONOMIC FUNCTION

SUBJECT #1 AFTER 27 MONTHS:

RECOVERY OF RESTING AUTONOMIC FUNCTION

SUBJECT #2

REGIMEN TIME COURSE:

STARTS REGIMEN:

  • Daily tVNS, DHA, EVOO plus rifaximin x 10 days.
  • The patient is not taking any psychotropic medication.

AFTER 2 MONTHS:

  • Clinical improvement in autonomic function (Improved cognition, energy, and resolution of headaches, thirst and nocturia).

AFTER 5 MONTHS:

  • PTSD symptoms, fits of rage and depression completely disappear after 11 years.

SUBJECT #2 BASELINE:

RESTING AUTONOMIC FUNCTION

SUBJECT #2 AFTER 5 MONTHS:

RECOVERY OF RESTING AUTONOMIC FUNCTION

CONCLUSION

Chronic PTSD and associated autonomic dysfunction are reversible with tVNS in combination with a multifaceted regimen targeted at reducing proinflammatory cytokines levels.

The dramatic recovery of chronic PTSD in 2 former soldiers supports our thesis that chronic PTSD is due to failure of the brain’s injury repair response because of excessive pro-inflammatory cytokines levels and abnormal functioning of primed microglia.

PTSD, chronic depression and the risk of suicide among military personnel are very high. This treatment regimen needs to urgently be tested in larger numbers of individuals to see if this unique finding is applicable to a broader array of soldiers.

FUTURE CONSIDERATIONS

The simplicity of a regimen that can safely reverse brain injury associated with PTSD andautonomic dysfunction could greatly enhance the readiness of military personnel while in the theater of combat.

The emotional and physical rigors of combat have been known throughout history to cause emotional trauma. Former diagnoses such as Shellshock, Combat Fatigue, Battle Neurosis are now understood be referring to PTSD.

The use of small portable tVNS devices, changes in cooking oils used in food preparation and daily supplement packets of fish oil could potentially allow soldiers to recover more quickly from and even prevent the physical and emotional traumas capable of causing brain injury.

Obviously, the use of the regimen could greatly benefit soldiers with pre-existing PTSD, chronic depression, generalized anxiety as well as chronic autonomic dysfunction from post-concussion syndrome.

REFERENCES

1. Wager-Smith, K and Markou A. “Depression: A Repair Response to Stress-Induced Neuronal Microdamage That Can Grade into a Chronic Neuroinflammatory Condition?” Neuroscience and biobehavioral reviews 35.3 (2011): 742–764.

2. Sun, Rao et al. “Hippocampal Activation of Microglia May Underlie the Shared Neurobiology of Comorbid Posttraumatic Stress Disorder and Chronic Pain.” Molecular Pain 12 (2016): 1744806916679166.

3. Eraly, Satish A. et al. “Assessment of Plasma C-Reactive Protein as a Biomarker of PTSD Risk.” JAMA psychiatry 71.4 (2014): 423–431. PMC. Web. 22 Apr. 2017.

4. Minassian A et al. “Association of Predeployment Heart Rate Variability With Risk of Postdeployment Posttraumatic Stress Disorder in Active-Duty Marines.” JAMA Psychiatry. 2015 Oct;72(10):979-86.

5. Cooper T et al. “Heart Rate Variability Predicts Levels of Inflammatory Markers: Evidence for the Vagal Anti-Inflammatory Pathway.” Brain Behav Immun. 2015 October; 49: 94–100. 6. McKee A and Robinson M. “Military-related traumatic brain injury and neurodegeneration.” Alzheimers Dement. 2014 June; 10(3 0): S242–S253.

7. Zhang Q et al. “Activation of the α7 nicotinic receptor promotes lipopolysaccharide-induced conversion of M1 microglia to M2.” Am J Transl Res 2017;9(3):971-985.

8. Meneses, G. et al. “Electric Stimulation of the Vagus Nerve Reduced Mouse Neuroinflammation Induced by Lipopolysaccharide.” Journal of Inflammation (London, England) 13 (2016): 33.

9. Chang, Philip K-Y et al. “Docosahexaenoic Acid (DHA): A Modulator of Microglia Activity and Dendritic Spine Morphology.” Journal of Neuroinflammation 12 (2015): 34.

10. Harvey, Lloyd D. et al. “Administration of DHA Reduces Endoplasmic Reticulum Stress-Associated Inflammation and Alters Microglial or Macrophage Activation in Traumatic Brain Injury.” ASN NEURO 7.6 (2015): 1759091415618969.

11. Liu, Joanne J. et al. “Pathways of Polyunsaturated Fatty Acid Utilization: Implications for Brain Function in Neuropsychiatric Health and Disease.” Brain research 0 (2015): 220–246.

12. Gao J et al. “Rifaximin, gut microbes and mucosal inflammation: unraveling a complex relationship.” Gut Microbes. 2014 Jul 1;5(4):571-5.

Send this to friend