Foods That Stop Circadian Rhythm From Slowing Down May Lead To Dietary Supplements That Treat Age-Related Diseases And Increase Lifespan
Imagine a dietary supplement that could slow down age-related diseases and possibly lengthen the life humans live. Well, polyamines, compounds found abundantly in nearly every living cell, may have the power to do this. They play an intrinsic role in the body’s internal clock and regulate cell growth and death. Researchers discovered that as mice aged, their levels of polyamines began to drop, slowing down the body clock’s natural cycle (roughly 24 hours), and increasing their susceptibility to disease. The findings, published in the journal Cell Metabolism, explain that by eating polyamines, we may be able to stave off disease and even increase longevity.
"This discovery demonstrates the tight intertwining between circadian clocks and metabolism, and opens new possibilities for nutritional interventions that modulate the clock's function," said the study’s senior author Gad Asher, a researcher from the Weizmann Institute of Science, in a press release. "Impaired circadian rhythmicity has been linked to a wide variety of age-related diseases, including cancer, Alzheimer's disease, Parkinson's disease, and inflammation."
For the study, researchers treated a group of young mice with a drug that stops the body from processing polyamines. This caused their circadian rhythms to slow down by roughly 11 minutes with each passing day when compared to young mice that were left to process polyamines as they normally would, without drugs. In order to see if the opposite was true, a separate set of adult mice was then given drinking water that contained spermidine, the edible form of polyamines typically found in foods, like soybeans, corn, green peas, and blue cheese. Their circadian rhythms subsequently sped up to about eight minutes faster than untreated adult mice, ultimately reversing it back to normal. An effect, researchers believe, could help curb age-related diseases.
"If they hold true in humans, they will have broad clinical implications," Asher said of the findings. "The ability to repair the clock simply through nutritional intervention, namely polyamine supplementation, is exciting and obviously of great clinical potential."
Internal clocks can be traced down to a neurological level inside the hypothalamus, a region in the brain that controls sleep and wakefulness on a roughly 24-hour cycle. The hypothalamus is also where the optic nerve connects and communicates with the brain about light levels, or lack thereof, depending on whether it’s day or night. Located directly above the optic nerve is the suprachiasmatic nucleus (SCN), a group of 20,000 neurons that are stimulated by the light passing through the eye. The message that there’s light travels along the optic nerve, ultimately regulating neural and hormonal activity, and thus creating our circadian rhythms.
Each individual, regardless of age, is born with a specific chronotype, or internal timer, that is designed to determine whether they’re a morning person or a night owl. As people age, their ticker starts slowing down, and diseases become more likely to develop. These rhythms are complex; they affect numerous activities in the brain, which is why researchers are only now discovering these processes. According to the researchers, even tiny changes in a person’s circadian rhythm can be linked to metabolic and age-related diseases.
They said future research would allow them to determine whether the same results ring true in humans. "I would not recommend that old people rush out for anything, especially not to buy polyamines, until this is tested and proven in humans," Asher said. "But I do envision testing polyamines in clinical trials as a tool against a wide variety of age-related diseases in humans. There is evidence in flies and mice that polyamines extend lifespan, and future studies might also support the use of polyamines in humans."
Source: Asher G and Zwighaft et al. Circadian Clock Control by Polyamine Levels through a Mechanism that Declines with Age. Cell Metabolism. 2015.