With summer nearly a month away, there's a reason everyone is anticipating its arrival. The sun is always shining, school's out, you lay on the beach and tan, and you just feel better. Well, the latter may be because people are generally healthier in the summer.
At least, that's according to a new study published in the journal Nature Communications, which shows that our immune systems vary with the seasons. Specifically, nearly 25 percent of our genes (5,136 out of 22,822 genes tested) differ in activity level according to the time of year, with some more active in winter and others more active in summer. This seasonality also affects our immune cells and the composition of our blood and adipose tissue (fat).
Scientists have long known that incidents of various diseases - including cardiovascular disease, autoimmune diseases such as type 1 diabetes and multiple sclerosis, and psychiatric disorders - vary with the seasons. But this study is the first to suggest that this is to blame on seasonal changes in how our immune systems function.
"This is a really surprising - and serendipitous - discovery as it relates to how we identify and characterize the effects of the susceptibility genes for type 1 diabetes," Professor John Todd, with the University of Cambridge, said in a statement. "In some ways, it's obvious - it helps explain why so many diseases, from heart disease to mental illness, are much worse in the winter months - but no one had appreciated the extent to which this actually occurred. The implications for how we treat disease like type 1 diabetes, and even how we plan our research studies, could be profound."
To better understand the role the seasons play in aggravating certain conditions, an international team of scientists led by the University of Cambridge examined both blood and adipose tissue samples from over 16,000 people living all over the world - including the United Kingdom, United States, Iceland and Australia.
By looking at the samples the researchers were able to measure the level of expression of the individuals' genes - a gene is said to be "expressed" when it is active in a particular cell or tissue, usually involving the generation of proteins.
They found that the activity of thousands of genes in the samples differed from winter to summer. Similarly, they identified seasonal differences in the types of cells found in the blood.
One gene in particular, called ARNTL, which has been shown to suppress inflammation in mice, interested researchers because it was more active in the summer and less active in the winter. If the gene functions the same way in humans, then levels of inflammation will be higher during winter (at least in the Northern Hemisphere).
Inflammation is a risk factor for a range of diseases, therefore, these diseases will likely be aggravated in winter months.
"We know that humans adapt to changing environments," said Dr. Chris Wallace, one of the researchers. "Our paper suggests that human immune systems adapt to show different seasonal variation in equatorial regions with fewer distinct seasons compared to regions at higher and lower latitudes with more pronounced differences between winter and season."
Though the underlying mechanism behind the immune system's seasonal variation remains unclear, the new findings may help scientists better treat various conditions.
For example, drugs that target the mechanisms behind inflammation could offer a way of helping treat these diseases more effectively during the winter periods. Also, vaccination programs might be more effective if carried out during winter months, when the immune system is already "primed" to respond.
"While we all love winter sun, flying south for the whole of each winter isn't something anyone can practically recommend as a way of preventing type 1 diabetes," concluded researcher Karen Addington. "But this new insight does open new avenues of research that could help untangle the complex web of genetic and environmental factors behind a diagnosis."
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