The childhood is a crucial period in the life of anyone, but for many it seems those early experiences could change our body even at the genetic level. A team of scientists from Northwestern University (USA) has analyzed more than a hundred genes associated with inflammation, looking for evidence of epigenetic changes. They discovered that a handful of genes responsible for the regulation of inflammation are altered by key events of childhood, suggesting that the diseases we suffer in later life could be the result of the events suffered in our years formative
The experts started from the hypothesis that the link between the child’s environment and the differences in the inflammation processes of the body could also reach the genes themselves.
Although the DNA sequence of our genome is more or less focused on conception, we have learned over time that individual genes can continue to be modified through processes that we refer to as epigenetic.
One of the most prominent forms of these epigenetic processes is methylation, which implies that a methyl group (-CH3) is added to the DNA structure in such a way that it interferes with its function.
Thanks to methylation and other epigenetic changes, we have come to understand that even subtle environmental phenomena can have an impact on our genetic plan.
“We could have genes in our body that could lead to some adverse health outcomes, but if those genes are silenced, if they are turned off due to epigenetic processes, it’s interesting,” says Thom McDade, leader of the work.
Although it is relatively early to understand the full range of epigenetic changes we can experience, childhood is clearly an important part of life that can establish biological processes that can affect our health and well-being in the following years.
The latter study included a sample of some 500 participants from the Philippines, and included a series of data from the early 1980s.
Blood tests revealed that methylation of 9 of the 114 genes associated with immune processes that regulate inflammation had a close relationship with several childhood variables, including socioeconomic status, prolonged absence of a father in childhood and even if the person was born in hot months.
In other words, by identifying certain childhood experiences , researchers could predict if one or more of those 9 genes of inflammation would be ‘on’ or ‘off’.
This study could help explain the prevalence of cardiovascular diseases and certain inflammatory diseases in specific communities. It also adds to the growing body of evidence that highlights the various ways in which changes in our immune system can affect the way our adult bodies deal with diseases.
While we await new results in this field, we now have more evidence to reinforce that what happens to us at the beginning of our lives can affect us during the rest of it.