Ever wonder why you catch a cold from every nearby sneeze and sniffle while your best friend sails through unscathed? According to Sheldon Cohen, Carnegie Mellon University psychology professor, you can blame it on your telomeres.
Cohen and his research team recently discovered that — starting in young adulthood — this biological marker can predict our susceptibility to the common cold.
Telomeres are protein complexes that act like protective caps on the ends of chromosomes. Each time the cells replicate, the complexes shorten slightly. Unfortunately, as cell telomeres shorten, cells lose their ability to function appropriately, and eventually die.
Research had previously shown that older adults with shorter telomeres are at greater risk for immune-related illness, such as cardio-vascular disease, cancer and infectious diseases, as well as increased mortality risk. What drew the attention of Cohen, the Robert E. Doherty Professor of Psychology, were studies showing that factors other than aging, such as chronic stress, are associated with shorter telomeres in this population.
He wondered — what role could varied telomere length play in the health of younger people? He and his team decided to investigate.
The team gathered 152 volunteers, aged 18–55, and measured the telomere length of their white blood cells. They then exposed them to a rhinovirus, the germ responsible for the common cold. They were monitored throughout five days of quarantine for signs of infection.
"We found that the shorter their telomeres, the more likely they were to develop a cold," said Cohen of the study, published in the Journal of the American Medical Association. "Even more interesting was when we broke the sample up by age."
For the youngest — those between 18 and 21 — there was no relationship between telomere length and infection. Beginning at age 22, however, telomere length became a predictor, and the relationship strengthened with age.
"This suggests the possibility that telomere length is a relatively consistent marker across life span and can start predicting disease susceptibility as early as our mid-20's," said Cohen. "It may actually start being a risk very early on in young adulthood."
Cohen speculates that the apparent lack of predictive ability in the youngest participants is due to their having fewer short telomeres, or because their young immune systems were capable of compensating. While Cohen notes that these are "preliminary" findings, he looks forward to further research that can "clarify its implications."