Much of the research on the consequences of sleep/circadian disorders has focused on their consequences or behavior. This type of research needs to be continued and there are new opportunities in this area. These behavioral studies need to be established in model systems to parallel studies in humans. In addition, new neurobiological approaches, including optogenetics and use of DREAD, provide new tools for this investigation. Moreover, we now have powerful molecular tools to evaluate effects of sleep/circadian disorders both in humans and animal models. These include microarrays, RNA seq, etc. Moreover, genetic studies, e.g., in restless legs syndrome, have identified gene variants conferring risk for the disorder. We do not know, however, how these particular genes are involved in the pathogenesis of the disorder or whether they represent potentially targets for drug intervention. There is a need for studies both in animal models and in humans to elucidate the function of these genes. Studies in other areas are obtaining stem cells from biopsies in patients and then turning these into relevant target cells such as neurons to elucidate gene function using in vitro approaches.
The impact of this effort will be the following:

a. Taking our understanding of pathogenesis of sleep and circadian disorders to a new level.
b. Understanding the consequences of sleep and circadian disorders on different end organs at a more in-depth molecular level.

The sleep and circadian field have access to all the major cells systems for these studies—C. elegans, aplysia, Drosophila, zebra-fish, mice, etc. Moreover, there are already gene variants identified in human studies which require follow-up functional studies. The field has the expertise in all of the techniques described above. Moreover, there are more validated animal models for many of the common sleep disorders. Thus, this new approach is very feasible. 

For example, we still do not have a comprehensive understanding of how depression increases incident CHD.

Alternative treatments for depression are needed that target disrupted pathways known to promote CVD (e.g. autonomic, inflammation).

What are the mechanisms through which PTSD doubles incident CHD within a decade?

What are the mechanisms through which exercise, sleep, and certain diet patterns mediate the effects of psychosocial stress on health?

Not all stressed people get CVD and some data suggests that coping style mediates stress effects on CVD risk. If so, perhaps we can teach coping styles. But to do so we need to know more about whether and how certain coping styles modulate stress effects on the CV system.

A major cause of psychosocial stress in modern America is social density. The higher the density, the less tolerance there is for deviance from the norm. How does increased social density effect CV physiology? Are there ways to intervene through spatial partitioning or interaction patterns that alter perceptions of crowdedness or lack of privacy?

We have all the tools to address this over-arching area and these specific questions. They just need to be made a priority.