Stress can lead to mental illness down the road
Researchers have long known that when people endure long periods of chronic stress, their risk for developing future mental health problems increases. Indeed, prior studies have shown abnormalities in the brains of people suffering from stress-related conditions, such as chronic anxiety and post-traumatic stress disorder (PTSD) – and a new study now tells us why.
Researchers from the University of California, Berkeley conducted the study, which found that too much “white matter” existed in certain areas of the brain of people who suffer from chronic stress.
Our brains consist of both “white matter” and “gray matter”, but the researchers found the people under chronic stress have an excessive amount of “white matter”, which gets its name from the white layer of myelin that forms around the nerves, serving to insulate them while increasing the transmission of signals between brain cells.
While the researchers were unable to determine conclusively why people under stress have more white matter than their less-stressed counterparts, the focus of their study was primarily on brain cells that produce myelin, as they noticed the experience of chronic stress appeared to generate more myelin-producing cells and less neurons than that which is considered normal.
And when too much myelin is generated in brain cells, it can disrupt the “delicate balance” of the brain, resulting in a lapse in communication between brain cells that causes them to malfunction.
To demonstrate how this delicate balancing act works, the researchers used adult rats for a series of experiments on the hippocampus regions of their brains. As a result, they discovered that the neural stem cells in the hippocampus regions of the rats’ brains performed in surprising and unpredictable ways.
It was previously believed that the neural stem cells only matured into a type of neuron called an astrocyte, but when the rats were undergoing chronic stress, such stem cells morphed into a different kind of cell called an oligodendrocyte, which creates myelin within “white matter” to aid the formation of structures known as synapses that enable nerve cells to communicate with one another.
Accordingly, the question that remained was whether a state of chronic stress could actually cause brain changes that disrupt and interfere with brain connectivity?
For example, if someone with PTSD exhibited a disruption in brain connectivity, it is possible that their hippocampus – the area of the brain that regulates emotions and memory – could end up forging a deeper connection to their amygdala, where the "fight or flight" response is controlled.
If such hypothesis is true, the research team suspects it could also mean that those with PTSD have a weaker connection between the hippocampus and the prefrontal cortex, which is the area of the brain that controls our responses.
Study author Professor Daniela Kaufer pointed out that when the amygdala and hippocampus regions of the brain are connected normally, a person’s fear reactions are much more rapid, which is often seen in people who have survived chronic stress experiences.
By the same token, she added that if the connection between the amygdala and hippocampus is not as well connected to the prefrontal cortex, it impairs the ability to inhibit or shut down one’s responses to certain situations.
Prof. Kaufer said that she and her research team are conducting additional research in order to test this hypothesis.
In the meantime, however, she believes that the effect of chronic stress on memory and learning ability in the rats “may be accounted for by the rat stem cells maturing into myelin-producing cells rather than the neurons that process and transmit the electrical information necessary for learning and memory skills.”
1. Molecular Psychiatry, Stress and glucocorticoids promote oligodendrogenesis in the adult hippocampus (published February 11, 2014) doi:10.1038/mp.2013.190.
2.University of California, Berkley, News Release: New evidence that chronic stress predisposes brain to mental illness (published February 11, 2014)