Pills could be the cure for addiction. Image via epSos/Flickr
A Japanese drug, used for over two decades to treat asthma, might find a new use in the treatment of amphetamine and opioid addiction. There is a desperate need for drugs that reduce cravings in drug addicts, drugs that might function in ways radically different from the current addiction treatment arsenal. And this drug, Ibudilast, might fit the bill.
It’s thought that Ibudilast works by acting on glial cells in the nervous system. These cells--once considered the “glue” connecting neurons and thought to play no role in neurotransmission--act to physically support and connect neurons. They deliver nutrients, fend off pathogens, and assist in the removal of dead neurons. Though they were not thought to have any direct effect on neurotransmission, they’re no longer considered passive cells.
Ibudilast is thought to affect the action of the glial cells in some way, preventing or attenuating their activation. But because we don’t really understand what they’re doing in the first place, it’s tough to understand how the drug works to help. Recent research has revealed glial cells do sometimes participate in synaptic transmission (helping to clear and regulate the neurotransmitters in the synaptic cleft).
Results are only preliminary, with positive outcomes on study performed on 11 meth addicts, but they were promising enough for the FDA to fast track the investigation. A larger-scale trial will be underway soon.
Though there are some pharmaceuticals used in the treatment of opioid addiction, there’s not been a true drug treatment therapy for amphetamine addiction.
The 11 meth addicts were housed in a lockdown facility for three weeks where they were intravenously treated with meth two to three times a week while simultaneously taking Ibudilast. Dr. Aimee Swanson, co-investigator on the trial and research director at the UCLA Center for Behavioral and Addiction Medicine, said, "very preliminary results would indicate that Ibudilast may dampen craving and improve cognitive functioning.”
Though there are some pharmaceuticals used in the treatment of opioid addiction—mostly replacement therapies like methadone and buprenorphine, or opioid blockers like naltrexone—there’s not been a true drug treatment therapy for amphetamine addiction.
An addiction to meth is sometimes thought to be a “mental” addiction, rather than a physical dependence like what heroin addicts experience. Regardless, both are obviously incredibly damaging, which makes these initial results around meth addiction exciting.
Ibudilast is also being investigated as an alternative to replacement and maintenance therapies in those with opioid addiction. It’s heralded as the first non-opioid treatment therapies for opioid addicts—though I might argue that Ibogaine does just that, despite falling outside of mainstream medicine—and it also has some novel effects on the strength of opioid effects.
Study participants who were given both oxycodone and Ibudilast had a higher pain threshold than those who took oxycodone alone. This has important implications not only for addicts, but also for individuals who hope to avoid the side effects and addiction potential of high-dose opioid medications, but who have chronic pain. Being able to hack drug effects could have a huge effect not only on the lives of current addicts, but also on reducing the number of future addicts.
It’s amazing to consider that an entire class of cells, once thought to simply function as the glue that held together the all-important neurons, could function in such important ways.
In a fantastic 2007 meta study on glial impact on pain and the effects of painkillers, researchers posit that we’ve been approaching pain management from a faulty and simplistic conception of how pain is conveyed in the brain: “Owing to the pain transmission capacity of neurons, these cells have been the primary intentional target of all pharmacotherapies developed to date.”
Sure, neurons physically conduct the pain transmission, but research into glial cells is showing their importance in mediating the signals. They conclude, “The pharmacological targeting of glia, rather than solely neurons, will be shown to be a novel and as yet clinically unexploited approach for potentially achieving both effective pain control and enhanced efficacy of opioids.” It’s a drastic shift in how we conceptualize the brain’s response to pain—integrating another layer in to the complexity of how neurons respond to pain stimuli—that is necessary to more fully describe what’s actually going on.
It’s amazing to consider that an entire class of cells, once thought to simply function as the glue that held together the all-important neurons, could function in such important ways. If attenuation of glial cells can have such an important effect on addiction response, craving, and pain management (and we’ve only really scratched the surface in terms of researching the role they play), then entire classes of drugs that act on these cells could be developed to treat a host of afflictions.
Neurobiology can be deceptively complex. It can seem like we know so much about the workings of the brain—the neurotransmitters and drugs commonly used to alter them—that we have a firm grasp on what is happening. But there's so much going on, so many interactions combining and building off of one another to produce our experience of the world, that we're just at the very beginning of understanding it all.