Oxidative stress in biochemical terms indicates a state of imbalance between oxygen and nitrogen. It’s best understood as describing an apple when it’s cut, it begins to brown.  Oxidizing is just this, the aging/damaging of cells.    Oxidative stress results in systemic disease as well as neurological and even neuro-developmental problems.   There are dozens of medical journals that support that, in individuals prone to seizures, oxidative stress is present.

The brain is particularly vulnerable to oxidative stress because it requires more oxygen than any other organ in the body.  Oxidative stress is regarded as a possible mechanism in the pathogenesis of epilepsy. Furthermore, persistent seizures have been demonstrated to cause cell damage through increases in oxidative stress. Several animal models of epilepsy have consistently found significant increases of oxidative stress after seizures, and important alterations in the antioxidant system have been found in seizing animals and epileptic patients.

Several studies have demonstrated that antiepileptic drugs (AEDs) may impair the antioxidant defense system and induce or exacerbate oxidative injury in epileptic patients. Several first-choice AEDs for epileptic syndromes, such as valproic acid, carbamazepine, phenytoin, and phenobarbital, increases oxidative stress. AED treatment has also been associated with cognitive decline , and high doses increase the risk of cognitive side effects.

The presence of antioxidants are essential in reducing cellular damage.   The body’s major antioxidant, glutathione, is among other nutrients, Vitamins A, C and E that are often found deficient in individuals experiencing seizures. The ketogenic diet, utilizing fats as fuel for the brain, is known to boost glutathione levels.  And curcumin has been demonstrated to offer neuroprotective properties and reduce neurotoxicity.

Adequate levels of antioxidants can reduce the levels of oxidative stress and restore balance in the cells and in the central nervous system.

A word of caution.  Please do not run out and purchase glutathione or curcumin without testing your loved one first.  Curcumin is also a polyphenol and for those individuals that have phenol sensitivities, may experience adverse effects.  Likewise , glutathione is a sulfur compound and for those that have blockages in their transsulfuration pathways, glutathione may exacerbate symptoms.

It’s always important to test rather than “guess”.

  1. Szot, “Common factors among Alzheimer’s disease, Parkinson’s disease, and epilepsy: possible role of the noradrenergic nervous system,”Epilepsia, vol. 53, no. 1, pp. 61–66, 2012.
  2. Dringen, “Metabolism and functions of glutathione in brain,”Progress in Neurobiology, vol. 62, no. 6, pp. 649–671, 2000.Brain glutathione levels in patients with epilepsy measured by in vivo (1)H-MRS.https://www.ncbi.nlm.nih.gov/pubmed/11673583

    The possible role of endogenous glutathione as an anticonvulsant in mice.https://www.ncbi.nlm.nih.gov/pubmed/10784128

    Relevance of the Glutathione System in Temporal Lobe Epilepsy: Evidence in Human and Experimental Modelshttps://www.hindawi.com/journals/omcl/2014/759293/