Though ASD (Autism spectrum disorder) is mentioned a lot in this piece, the information it presents relates to all neuro-immune disorders, including ME/CFS.
Unstable at the Core? New Study Looks at ‘Genomic Instability’
via Phoenix Rising
The new National CFIDS Foundation study will determine if something called ‘genomic instability’ contributes to chronic fatigue syndrome. Dr. Henry Heng found surprisingly high levels of significant chromosome alterations in a set of Gulf War Syndrome patients and now he’ll be looking in ME/CFS patients. Get the scoop on this intriguing research in this Phoenix Rising blog.
Most people who have ME/CFS also have genetic mutations in their genes involved in methylation, namely MTRR, MTR and perhaps MTHFR. For these people, just going by lab diagnostics for B12 is useless at best, and misleading at worst. Their B12 needs are extremely high.
Vol. 128 No. 12, December 1993
Neurologic Degeneration Associated With Nitrous Oxide Anesthesia in Patients With Vitamin B12 Deficiency
Teresa S. Flippo, MD; Walter D. Holder, Jr, MD
Arch Surg. 1993;128(12):1391-1395.
Vitamin B12 [cobalamin] is an integral component of two biochemical reactions in man: the conversion of L-methylmalonylcoenzyme A into succinyl coenzyme A and the formation of methionine by methylation of homocysteine. The transmethylation reactionis essential to DNA synthesis and to the maintenance of the myelin sheath by the methylation of myelin basic protein. Active vitamin B12 contains cobalt in its reduced form (Co+). Nitrous oxide produces irreversible oxidation to the Co++ and Co+++ forms that renders vitamin B12 inactive. Five cases (four from the literature and one new case) are presented in which patients unsuspected of having vitamin B12 deficiency developed subacute combined degeneration of the spinal cord following nitrous oxide anesthesia. Patients with vitamin B12 deficiency are exceedingly sensitive to neurologic deterioration following nitrous oxide anesthesia. If unrecognized, the neurologic deterioration becomes irreversible and may result in death.
(Arch Surg. 1993;128:1391-1395)
"This paper summarizes research on genes that may be linked to increased susceptibility in developing and maintaining these disorders, and research on resting and stressor-evoked changes in leukocyte gene expression, highlighting physiological pathways linked to stress and distress. These include the adrenergic nervous system, the hypothalamic-pituitary-adrenal axis and serotonergic pathways, and exercise responsive metabolite-detecting ion channels. The findings to date provide some support for both inherited susceptibility and/or physiological dysregulation in all three systems, particularly for catechol-O-methyl transferase (COMT) genes, the glucocorticoid and the related mineralocorticoid receptors (NR3C1, NR3C2), and the purinergic 2X4 (P2X4) ion channel involved as a sensory receptor for muscle pain and fatigue and also in upregulation of spinal microglia in chronic pain models. Methodological concerns for future research, including potential influences of comorbid clinical depression and antidepressants and other medications, on gene expression are also addressed."