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And now it's time for this week’s unbelievably nerdy proclamation: Orexin deserves the non-existent honor of “neurotransmitter of the year.” I’ll wait for your applause to stop.

Only discovered 15 years ago, young orexin (also called hypocretin) is a wakefulness-promoting brain chemical. Its discovery came out of narcolepsy research; scientists figured out that those suffering the sleep disorder pass out like flies because they lack the neurotransmitter. This year has seen the first orexin-inhibiting sleep drug hit the market. And now, new research links it and heart function, opening up new avenues for cardiac-failure treatment research.

Here’s what went down. In February 2015, Merck released the first orexin-based sleep drug, Belsomra. Also known by its generic name, suvorexant, Belsomra is an orexin antagonist, which means it induces sleep by blocking the release of the neurotransmitter. In “turning down” wakefulness, Belsomra works differently than other popular prescription sleep aids. Ambien and Xanax, for example, both bring on the yawns by activating GABA, which (in contrast to orexin) has a sedating impact when it floods the brain.

The jury’s still out on Belsomra — studies and consumer reviews depict the drug as having fewer side effects than GABA-drugs, but also as being a less effective sleep aid. Still, experts have hailed the introduction of an orexin-based downer as a windfall for sleep medicine. See, orexin is a localized neurotransmitter. Its receptors are confined to one area of the brain, which means orexin-based drugs are highly specific. Translation? Fewer side effects. In this way, orexin once again stands in contrast to GABA, whose receptors are scattered throughout the brain.

The difference between causing sleepiness through orexin and GABA is comparable to exterminating vermin by placing mousetraps in select rooms of the house versus fumigating the whole house. The first method may not eliminate your rodent problem in one fell swoop, but it won’t blast mouse-free rooms with chemicals, either.

Even if Belsomra doesn’t go down in history as a pharmaceutical godsend, it is nonetheless a precedent-setting drug. And it’s a safe bet that more orexin-based sleep meds are on their way.

Orexin, however, doesn’t only help control wakefulness. It’s also involved in appetite regulation, for example. And, according to a new study published in the Journal of the American College of Cardiology, it appears to play an important role in cardiac health. Researchers at Stanford University believe there’s a connection between a gene that regulates production of the neurotransmitter receptors and healthy heart function.

Orexin: Neurotransmitter of the Year

The research is complicated. But, in a nutshell, the Stanford team genotyped heart failure patients who either responded unusually well or very poorly to treatment. With help from publicly available genetic data sets, they were able to pinpoint what they believed to be a heart-function gene. The gene also happens to regulate the amount of orexin receptor made by a cell. They then found increased expression of the gene in diseased human heart tissue. They surmised the increased expression to mean that orexin and its receptor serve a protective function in the heart.

They didn’t stop there. Next, the research team used biologically modified mice to evaluate the impact of orexin on heart failure. When they gave orexin to mice with failing hearts, the mice showed better systolic heart function (systolic refers to heartbeat contractions) compared to rodents who didn’t get the chemical.

The researchers also performed ultrasounds on another group of mice who, through modification, lacked the orexin receptor, and found heightened diastolic heart dysfunction (diastolic refers to relaxation phase of heartbeat). So, the neurotransmitter seemed to improve function in the event of heart failure. And, the absence of orexin corresponded to greater dysfunction. Collectively, the research positions orexin and healthy hearts as a couple worth ‘shipping.

“The exciting thing is that this gene is in a completely different neurohormonal axis — a completely different pathway than what has been looked at previously,” said lead study author Marco Perez in a press release. “Nobody had ever studied heart function in relation to this gene.”

Give it up for orexin, everyone.