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NEW TODAY: Huntsman study could help sleep disorder sufferers
Chris Lindsay knew he had a problem when he totaled his Taurus because he fell asleep behind the wheel - at noon.
Lindsay delivered newspapers for four years, and woke up at 3 a.m. to complete the job. Add the business he also ran, and his waking hours stretched from 3 a.m. to 10 or 11 p.m. As the years passed, he began falling asleep in the middle of the day, which led to the crash.
Lindsay recently stopped delivering newspapers and started attending the University of Utah's Sleep-Wake Center for sleep evaluations in the hopes he can get back on a normal rhythm soon.
New genetic research from the Huntsman Cancer Institute in Salt Lake City could lead to medications that will help people such as Lindsay to cope with late-night or early-morning shifts.
In a study published online today in the journal Proceedings of the National Academy of Sciences, cancer researcher David Virshup challenges previous research about circadian rhythms - the body's natural cycle of sleeping. He urges researchers and drug developers to change their approach to making medications that treat jet lag, depression and sleeping patterns.
He found that the "Tau mutation," which caused a hamster to have a 20-hour day instead of a 24-hour cycle, was caused by increased gene activity, not decreased activity as was previously believed. The gene processes a protein that causes sleep. When the protein disappears, sleep occurs. A more active gene causes the protein to disappear too quickly, meaning a shorter cycle and less sleep. This is especially problematic for people whose schedules are already interrupted because of nontraditional work hours.
He started his research thanks to mathematician Daniel Forger, assistant professor of mathematics at the University of Michigan. Forger created a mathematical model of the Tau mutation, but every time he entered decreased genetic activity, the day became longer instead of shorter. When he entered an increase in genetic activity, the model produced the correct 20-hour day.
"David Virshup, very much to his credit, was the first person in the genetics field who took my model seriously instead of discounting it."
That model quickly led to Virshup's lab, which experiments on protein synthesis, normally focused on cancer-fighting applications. His experiments proved that the sped-up gene made the protein responsible for the mammal body clock disappear more quickly, which shortened a mouse's day.
Andrew Loudon, a researcher focused on the Tau mutation at the University of Manchester in England, calls Virshup and Forger's research an "important breakthrough."
"There are major potential applications of this work as it offers new insight into how we may regulate the activity of key clock molecules and may lead to the development of novel pharmacological approaches for rhythm disorders in man," Loudon said.
That's good news for Lance Pearson, who worked from 7 p.m. to 7 a.m. for six years as a mainframe computer operator. He worked four days on and three days off until 2001 when he switched to a full-time day shift, but still has a problem sleeping.
"If I go to bed before 11 p.m., I'll be up at 2 a.m., and there's no going back to sleep after that," said Pearson, who tried the natural melatonin sleep aid, but it didn't help.
Virshup plans to do further experiments to provide enough research for drug companies to produce new pharmaceuticals to treat circadian rhythm disorders in humans.
"The gene is a good drug target because of where it's located," Virshup said. "We just need to work out the details of how it makes the proteins."
