Hydrogen Therapy Shows Promise for Treating Methamphetamine Addiction

Authors
Journal
Progress in Neuropsychopharmacology and Biological Psychiatry
Year
DOI
10.1016/j.pnpbp.2019.109781
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Methamphetamine Addiction
Body System
Nervous System

TL;DR

Molecular hydrogen treatments can reduce the effects of methamphetamine addiction in mice by decreasing abnormal behaviors and brain changes associated with drug exposure.

Key Finding

Hydrogen-rich saline reduced methamphetamine-induced behavioral sensitization and decreased associated brain signaling changes in mice, potentially through its antioxidant effects.

Summary

Researchers gave mice methamphetamine (a stimulant drug) repeatedly to study how the brain changes with drug exposure and addiction-like behavior. They tested whether hydrogen-rich saline (a salt solution containing dissolved hydrogen gas) could reduce these changes. The hydrogen treatment reduced the mice's increased movement response to methamphetamine and lowered markers of brain activity associated with drug sensitization, possibly by reducing harmful molecules called free radicals in a brain region linked to reward and addiction.

Practical Takeaway

This is early-stage animal research showing hydrogen may have theoretical value in addressing methamphetamine-related brain changes, but it is far too preliminary to draw any conclusions about human use. The study was conducted only in mice, and much more research—including human trials—would be needed before any therapeutic claims could be considered.

Abstract

Methamphetamine (METH) is one of the most prevalently used illegal psychostimulants in many countries. Continuous exposure to METH leads to behavioral sensitization in animals, which can be used as a behavioral model with many mechanisms in common with relapse in humans. Molecular hydrogen has recently gained attention for its potential as a novel healthcare product with preventive and therapeutic applicability to a wide range of pathological conditions. However, it remains unclear whether and, if so, how hydrogen regulates METH-induced behavioral abnormalities. In the present study, we investigated the roles of molecular hydrogen on the acquisition and transfer of METH-induced behavioral sensitization and the accompanying changes in ERK phosphorylation and ΔFosB activation in the nucleus accumbens (NAc) of mice. To this end, male C57BL/6 mice received METH (0.1, 0.5 and 1.0 mg/kg, i.p.) injections for 7 days followed by a METH challenge (0.1, 0.5 and 1.0 mg/kg, i.p.) after a 7-day transfer period. Molecular hydrogen, delivered through a hydrogen-rich saline (HRS) injection (10 mL/kg, i.p., 3-h interval), was administered during the acquisition and transfer periods. We found that HRS administration was able to inhibit the acquisition and transfer of 0.1 and 0.5 mg/kg METH-induced behavioral sensitization to a certain extent, thereby attenuating the expression of behavioral sensitization. The HRS injections alone did not induce any obvious changes in locomotor activity in mice. Intriguingly, the increases in pERK and ΔFosB in the NAc, which accompanied the METH-induced behavioral sensitization, were also attenuated by the HRS treatments. Due to the anti-oxidative function of molecular hydrogen, the HRS injections reduced METH-induced reactive oxygen species and malondialdehyde generation in the NAc. These results suggest that molecular hydrogen serves as an anti-oxidative agent with potentially therapeutic applicability to the treatment of METH addicts.