Two months and twenty degrees change the face of Chicago. In March, doors and closed and heat is on; everyone is wrapped in coats and lips pressed together in a grumpy expression. Few people talk to each other, hurrying home to nestle beneath blankets in high apartments, angrily watching the snow come down as they drink weak coffee and urge the spring to hurry with sighs. They frequently check their email from notices from the doctor about their antidepressant medication and antibiotics.
In May, children are everywhere. White legs poke from beneath sundresses, laughter comes from the patios decorating every sidewalk and, it seems, fewer people are home sick. The city comes to life with music, festivals, drinking and active living. There is no empty sidewalk and there are few reasons to stay inside.
If it seems that everyone feels healthier, albeit sweatier, in the summer, it could be true. A new study from researcher at the University of Cambridge has linked increase immune system activity to higher temperatures, like those in the summer. Other diseases, such as chronic conditions like diabetes, rheumatoid arthritis or asthma, could be less severe in the warm months.
The study, published in the journal Nature Communications, explored disease genetic expression. Many chronic diseases are ruled by the expression of their genetics, and sets of those genes seem to suppress their function based on the seasons. More than 4,000 protein-coding mRNA sets have seasonal fluctuation, and the researchers knew that proving this correlation would show something significant about human evolution. They focused on one anti-inflammatory circadian transcription factor, which influences immune response.
We think of genes as a constant. However, genes are moderated by a number of outside pathways that change the expression over time. This study, called epigenetics, has suggested that genes may not be the single pilots in the course of how our bodies develop. Instead, they are moderated in their function.
The immune system is a unique place to study how genes express themselves. Fluid and adaptable, the network of T and B cells can react completely differently among individuals—one may completely ignore the presence of pollen while another may swell up as his or her white blood cells overreact. A study published in PLOS Computational Biology in November 2013 anchored the immune system reaction to a host of outside factors, making it more complicated to measure than the standard scratch-off test. It changes over time, and the study suggested using the new model of outside factors to engage in research of how genes express themselves over time.
The Nature Communications study riffs upon the base established by the earlier study, explaining that the “studies of the function, dynamics and variability of the immune system are undergoing a long-awaited renaissance partly owing to the development and application of new phenotyping technologies.” The authors did not pin down a particular function of how to manipulate these variations over time—obviously, summer doesn’t cure the chronic diseases or the symptoms individuals experience—but the research paves the way for what is to follow.
Genes are becoming increasingly important in medicine. Some medical professionals are calling it the introduction to the “golden age of medicine,” when we will be able to genotype an individual and forecast the risks to him or her. The reduction in cost of full-exome genotyping has enabled the quick identification of genetic factors in disease, but our knowledge of how genes really influence how our bodies work is still limited. Before we begin taking a count on all of our threads, we need to understand how they work together.
And if that leads us to be less sick for the summer, so much the better.