No one snorts a line to fall asleep. After all, the promise of cocaine is immediate energy, a direct line of jet fuel that makes it easy to party all night. Of course, the drug is incredibly dangerous and addictive. And in addition to increasing users’ likelihood of stroke, heart disease and general destitution (not to mention the desire to wriggle their jaws an uncomfortable amount of times), cocaine also causes your brain cells to devour one another — and seriously screws with sleep. In fact, long term use of the white powder seems to permanently damage circadian rhythms.
Let’s back up. Cocaine’s stimulant nature is Recreational Drugs 101: It blocks the brain’s ability to reabsorb dopamine, which leads to a buildup of that feel good neurotransmitter in the reward pathway, which causes intense pleasurable sensations (and manic energy), which vanish when the drug wears off, which induces a desperate lust for more cocaine. It also binds to glial cells — which help maintain stability in the nervous system — and causes an inflammatory reaction that produces even more dopamine. The immediate (pleasurable) effects are typically short-lived; many of the more devastating consequences are not.
Obviously nobody is dappling in the drug to woo sleep, but research suggests that even small doses disrupt circadian rhythms and suppress crucial REM sleep in the long term. A 2015 study published in Therapeutic Targets for Neurological Diseases revealed that cocaine seems to block the “photo phase-resetting response” of the suprachiasmatic nucleus — the brain’s “master clock” believed to govern circadian rhythms, keeping them in line with the earth’s natural light-dark cycle.
Working with mice and rats, the study authors found that cocaine taken at midday actually resets the circadian clock, a function typically performed by morning light. They also found that chronic cocaine use leads to lengthened circadian rhythms, which might permanently disrupt patients’ sleep cycles. It’s inconclusive what other physiological effects might stem from these circadian disturbances, though possibilities include everything from increased risk of heart disease to obesity and cancer.
For addicts and other long-term users, cocaine’s sleep-depriving effects can persist even after they quit. The Therapeutic Targets study also found that circadian disturbance persisted for months after cocaine access was withdrawn. An earlier study published in Society for Neuroscience corroborated similar findings, but featured a curious twist: Although EEG recordings of former users demonstrated the same sleep deficiencies as current users, the abstinent patients “reported that their sleep had improved.”
The study authors were unsure what caused this misperception, though they suspect it’s associated with the brain’s “reward and arousal circuits” — both of which cocaine acts upon. Researchers writing in Sleep Medicine Reviews in 2008 noted that this disconnect is the opposite of one common to insomniacs, who often report difficulty sleeping even after a night of uninterrupted shuteye. Cocaine’s effect, the authors concluded, “is unique in sleep medicine.”
Another recent study, published in January in the Proceedings of the National Academy of Sciences (PNAS), offers a more sinister reason to be skittish about that Bolivian marching powder. According to a group of Johns Hopkins researchers working with mice, high doses of cocaine trigger a process in which brain cells “literally digest their own insides.” Known as autophagy, it’s natural way for cells to destroy unnecessary waste. But overactive autophagy — the kind induced by cocaine — risks destroying essential cellular structures as well.
“A cell is like a household that is constantly generating trash,” lead author Prasun Guha said in a release. “Autophagy is the housekeeper that takes out the trash — it’s usually a good thing. But cocaine makes the housekeeper throw away really important things, like mitochondria, which produce energy for the cell.”
The results weren’t all grim. Guha and his team had previously learned that autophagy is associated with an interaction between nitric oxide — which brain cells use to communicate — and an enzyme known as GAPDH. They also knew that a compound called CGP3466B blocks that interaction. The compound has previously failed in clinical trials of treatments for Parkinson’s disease and ALS, but the Hopkins team discovered it successfully protects brain cells from autophagy — in mice, at least. They hope it may someday lead to effective therapies for cocaine abusers.
“If we can pinpoint the exact mechanism of autophagy, then the development of small molecules which efficiently can go through blood-brain barrier can be promising,” Dr. Guha told Van Winkle’s, cautioning that the development process will be a lengthy one and that “There are multiple steps” involved in reaching human trials. “We are far too early to start any of them now,” he added.
Fortunately, studies indicate that cocaine use is on the downswing in the US. According to the National Institute of Health, in 2013 there were 1.5 million users aged 12 or older; that’s down from 2-2.4 million between 2002 and 2007. It may not seem like a lot of people, but it’s a hell of a lot of brain cells — not to mention hours of lost sleep.