Webinar Q&A follow-up: How chronic stress experienced during early development epigenetically programs adult disease risk
Neuro Central recently hosted a free live webinar, ‘How chronic stress experienced during early development epigenetically programs adult disease risk’, featuring speaker James Coffman, Associate Professor at MDI Biological Laboratory (ME, USA). Following a fascinating presentation of his work, James took questions from our live audience – here, James responds to those questions that we didn’t have time for during the live webinar. Do let us know your thoughts on this topic or any of the questions posed by commenting below this feature!
Did you miss the webinar? You can watch it here.
Is anything known about the effect of acute stress?
Yes, and the effects of acute stress are very different. In fact, acute stress (in moderate doses) is healthy – a good example is exercise. More generally, we need occasional acute stress to become motivated.
I’m curious as to whether you’ve been able to identify a genetic pathway that is a master regulator of survival genes/mechanisms in the human body. What implications would natural re-activation of that pathway do for prevention/resolution of disease states caused by chronic stress/inflammation?
We have not, but such pathways are known to exist. There are known stress-activated pathways, often under the control of key transcriptional regulatory proteins that upregulate survival genes/mechanisms. FoxO is one such transcription factor. It is also known that activation of pathways under the control of hormones such as melatonin and oxytocin tend to counteract the unhealthy effects of stress.
Can you talk about the connection between circadian perturbations and immune health?
The immune system, like most systems of the body, is regulated by circadian rhythms. This occurs in part through circadian regulation of hematopoiesis – blood cell production is controlled by the circadian clock. In addition, the clock controls the types of signaling molecules (cytokines) produced by immune cells, with different sets of genes being expressed during the day and night. The disruption of circadian rhythms can increase susceptibility to disease, as shown by what happens in people with jet lag or who do shift work.
Could you revisit the advantages of using the zebrafish as a model for regenerative studies?
Zebrafish has very high regenerative capacity, and is able to regenerate most of its body parts when they are lost or surgically removed. This allows us to study the biological mechanisms underlying regeneration, which is not possible in animals (such as mice) that have much lower capacity for regeneration.
Would promoting health sleep be helpful?
Don’t forget, you can watch the full webinar On Demand here.