MOJ ISSN: 2381-179X MOJCR

Clinical & Medical Case Reports
Case Report
Volume 5 Issue 1 - 2016
Acetylcholine Blockers Weakness and Exhaustion from the Epstein Barr Virus
Nadira T Pardo*
School of Behavioral Sciences, California Southern University, USA
Received: October 28, 2016 | Published: November 02, 2016
*Corresponding author: Nadira T Pardo, School of Behavioral Sciences, California Southern University, USA, Email:
Citation: Pardo NT (2016) Acetylcholine Blockers Weakness and Exhaustion from the Epstein Barr Virus. MOJ Clin Med Case Rep 5(1): 00118. DOI: 10.15406/mojcr.2016.05.00118

Abstract

Whether you refer to the Epstein-Barr virus as Mononucleosis or as Glandular Fever, cases of mild to severe muscular weakness have been documented in the literature as a result of this illness. However, what has not been fully explored is the how certain foods may trigger neurochemical reactions in the neuro-muscular interface in some cases of those previously infected with the Epstein-Barr virus, resulting in skeletal flaccidity on the one end or healthy muscular performance on the other. This article will explore the literature related to several cases in Australia in the hope of raising awareness in the wider community.

Keywords: Epstein barr; Skeletal flaccidity; Muscle weakness

Introduction

The research on how many of the entero viruses can live dormant in the receptor sites and can reactivate under certain conditions throughout the life of the human host is well known [1-3] however, the characteristics linked to certain foods and how these trigger the reactivation has not been examined Colovic et al. [4]. In addition, the symptoms of weakness and exhaustion have not been linked by medical practitioners to the previous viral infections due to the time delay of these symptoms and a pervading attitude of unwillingness by medical practitioners to examine the link between food sensitivities and those symptoms [3,5]. This paper will examine three aspects of the mechanism that result in the overall weakness and exhaustion of the human host. First, the foods that can block the acetylcholine uptake at the receptor site [4,5]. Second, the foods that can enhance acetylcholine production [6]. Third, the foods that can enhance the acetylcholine uptake [7]. The combination of these three areas can prevent the symptoms of the weakness and exhaustion otherwise experienced by those previously infected with the Epstein-Barr virus [1,3].

Chemical Mechanisms

Generally speaking, the chemical mechanisms in the body, being considered in this paper, begin with eating certain foods that are high in choline, which then converts to acetylcholine and then is used by the nervous system to communicate with the muscular system. Specifically insert chemical formulae and general knowledge from Funderluund & Eriksson et al. [3]. Acetylcholine Blockers Possibly specific proteins in cow milk products, capsicums or bell peppers, white flour, white potato, onion, Acetylcholine Production, Beef, cauliflower, eggs, Acetylcholine Enhancers and Caffeine [8].

Conclusion

In conclusion, the medical and public health communities need to be aware that the weakness and exhaustion experienced by many of their clients who have a history of infection from the Epstein-Barr virus could potentially be prevented or better managed by diet or food management regarding the limited intake of foods that are acetylcholine blockers, increasing the intake of foods high in choline, and adding an enhancer to improve the uptake of acetylcholine at the neuromuscular interface at the receptor sites that have dormant viruses. This may also help with those previously infected with Entroviruses although this case presented in this paper has focused on the Epstein-Barr but may be the same chemical reaction in the body that has in the past seen misdiagnosis or misunderstanding the phenomena, often being viewed as psychosomatic, hypochondriacal or other potential forms of mental health issues linked to victimology, PTSD reactions or chronic fatigue syndrome.

References

  1. Verschuuren J, Strijbos E, Vincent A (2016) neuromuscular junction disorders. Handbook of Clinical Neurology 133: 447-466.
  2. Taylor BV, Dyck JB (2004) Multifocal motor neuropathy: Pathologic alterations at the site of conduction block. Journal ofNeuropathology & Experimental Neurology 63(2): 129-137.
  3. Fagerlund MJ Eriksson LI (2009) Current concepts in neuromuscular transmission. British Journal of Anaesthesia 103(1): 108-104.
  4. ÄŒolović MB, Krstić DZ, Lazarević-Pašti TD, Bondžić AM, Vasić VM (2013) Acetylcholinesterase inhibitors: Pharmacology and toxicology. Curr Neuropharmacol 11(3): 315-335.
  5. Pahud G, Bontron S, Eder-Colli L (2001) Modulation of choline acetyltransferase synthesis by okadaic acid, a phosphatase inhibitor, and KN-62, a CaM kinase inhibitor, in NS-20Y neuroblastoma. Neurochem Int 38(1): 75-82.
  6. Zeisel SH, da Costa KA (2009) Choline: An essential nutrient for public health. Nut Rev67(11):615-623.
  7. Acquas E, Tanda G, Chiara D (2002) Differential effects of caffeine on dopamine and acetylcholine transmission in brain areas of drug-naive and caffeine-pretreated rats. Neuropsychopharmacology 27(2): 182-193.
  8. Smith CP, Brougham LR, Vargas HM (1993) Linopirdine (DuP 996) selectively enhances acetylcholine release induced by high potassium, but not electrical stimulation, in rat brain slices and guinea pig ileum. Drug Development Research 29(4): 262-270.
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