Certain people with sleep disorders continually have to battle a powerful urge to sleep through the day, even after sleeping more than 10 hours a night. Caffeine doesn’t solve their problem, and more potent prescription stimulants don’t help much either. A new study has shown that this condition could have a naturally-occurring source that works on the brain like the key ingredients in Xanax and Valium.
The scientists published their findings in the journal Science Translational Medicine. This condition is known as hypersomnia, and it’s different from narcolepsy since patients have more persistent daytime sleepiness instead of sudden sleep attacks. David Rye, a neurologist at Emory University in Atlanta, and his colleagues began a new study after getting a hunch about what was really happening.
Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye thought that hypersomnia patients might have a compound in their brains that does something similar. The scientists performed spinal taps on 32 hypersomnia patients and collected the cerebrospinal fluid (CSF). This was added to cells genetically engineered to produce GABAA receptors. They looked for tiny currents that would indicate that the receptors had been activated.
The results suggested that the patients’ CSF doesn’t activate GABAA receptors directly, but it does make the receptors twice as sensitive to GABA. This is similar to the class of drugs called benzodiazepines, which form the active ingredients in anti-anxiety drugs like Valium.
The scientists discovered that the soporific compound is a peptide or a small protein, made by the brain. Using these results, Rye and his colleagues started a pilot study with seven patients using flumazenil, which counteracts benzodiazepines and is used to treat people who overdose on those drugs. The patients responded favorably, and improved to near-normal levels on measures of alertness and vigilance. These effects lasted up to a couple of hours.
The findings are interesting, but need to be replicated in a larger, double-blind trial to be truly convincing.
Reference: “Modulation of Vigilance in the Primary Hypersomnias by Endogenous Enhancement of GABAA Receptors” by David B. Rye, Donald L. Bliwise, Kathy Parker, Lynn Marie Trotti, Prabhjyot Saini, Jacqueline Fairley, Amanda Freeman, Paul S. Garcia, Michael J. Owens, James C. Ritchie and Andrew Jenkins, 21 November 2012, Science Translational Medicine.
DOI: 10.1126/scitranslmed.3004685
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