Journal of Addiction and Therapies (ISSN: 2577-1507)

research article

The Prevalence and Role of MTHFR Polymorphisms in Opiate Dependency

Andrew Farah*, Tara McKenzie, Sydney T. Smith

Chief of Psychiatry, High Point Division of the University of North Carolina Healthcare System, USA

*Corresponding author: Andrew Farah MD DFAPA, Chief of Psychiatry, High Point Division of the University of North Carolina Healthcare System, USA. Tel: +13368786226; Email: brian.farah@unchealth.unc.edu

Tara McKenzie PAC, Department of Internal Medicine, Wake Forest University, USA.

Sydney T. Smith, Department of Psychology, University of North Carolina at Greensboro, USA.

Received Date:  31 January, 2018; Accepted Date: 16 February, 2018; Published Date: 23 February, 2018

1.       Abstract

Studies of genetic polymorphisms associated with the diseases of opiate dependency and abuse have focused primarily on genes related to dopamine and opioid receptors, neurotrophic factors, or the catechol-o-methyltransferase (COMT) gene [1,2]. Despite the high prevalence of methylene tetrahydrofolate reductase (MTHFR) polymorphisms in numerous neuropsychiatric and neurodegenerative diseases, only one prior study examined the prevalence of MTHFR C677T variants in opiate dependency [3].

We screened consecutively admitted patients who were dependent on heroin and/or other opiates, for C677T and A1298C polymorphisms. Over a six-month period, 86 of 96, or 90% of subjects, were positive for at least one of these MTHFR variants.

The mean age of all qualifying patients was 31.6 years, and majority of subjects, 68%, were female. The MTHFR distribution was fairly even; of the 86 patients who were MTHFR positive, 28% were heterozygous for only C677T (CT:AA), 11% were homozygous for only C677T (TT:AA), 22% were heterozygous for only A1298C (CC:AC), 13% were homozygous for only A1298C (CC:CC), while 26% were heterozygous for both mutations (CT:AC). 

We theorize that impaired methylation, and the inadequate monoamine synthesis that result from MTHFR variants, likely contribute to the illness of opiate use disorder. These vulnerable individuals are incapable of adequate monoamine balance, and may seek opiates as compensation. These findings may further imply a new treatment option, in the form of fully metabolized folate. This therapy would circumvent the less functional MTHFR enzymes expressed by the C677T and A1298C mutations, and therefore allow for more optimal monoamine synthesis.


Copyright and Licensing: This is an Open Access Journal Article Published Under Attribution-Share Alike CC BY-SA: Creative Commons Attribution-Share Alike 4.0 International License. With this license readers can share, distribute, download, even commercially, as long as the original source is properly cited. Read More.