I have extreme delayed sleep phase disorder (DSPD), a circadian rhythm disorder (CRD). I fall asleep at dawn and wake up early afternoon. My dim light melatonin onset (DLMO) is at 5:30 am. A normal person’s DLMO may be at 9 pm, for example.

CRD treatment—prolonged bright light after temperature nadir, dark restriction/melatonin starting several hours before natural bedtime, darkness till temperature nadir—does not work... more »

There is evidence of a higher prevalence of sleep and circadian disorders in different ethnic groups. This is true for both adult and pediatric subjects. There is also evidence that minority populations in lower socioeconomic groups do not seek evaluation for sleep disorders as frequently as other segments of our population. There is also evidence that they are less adherent to treatments such as nasal CPAP for obstructive... more »

We need to understand sleep and circadian disorders at a more mechanistic level. This applies to both the pathogenesis of these disorders and to their impact on health. New neurobiological and molecular tools facilitate this research. The focus needs to be not only in brain but also the impact of these disorders on future of peripheral organs. The elucidation of the fundamental functions of sleep and the impact of... more »

Much of the current clinical research on sleep and circadian research depends on cohorts designed for other purposes. While this has been helpful, such studies have limitations. These limitations are related to availability of in-depth phenotyping data and questions as to whether individuals identified in population studies are equivalent to those who present clinically with specific disorders. These concerns could... more »

Sleep and circadian disorders are relatively new areas of medicine. Most universities currently lack a critical mass of investigators to develop institutional T32 grants. Thus, there are, unfortunately, few such programs nationally. The Sleep Research Society has recognized this and is taking active steps to facilitate development of other T32 institutional training grants.

This will not, however, help the majority... more »

There is an urgent need to develop quantifiable biomarkers for acute sleep loss, chronic sleep insufficiency, circadian disruption and sleep disorders such as obstructive sleep apnea. These problems are highly prevalent but currently we do not have biomarkers to use for case identification, prognosis, or assessing response to therapy. There are currently small studies that indicate the feasibility. A recent workshop... more »

There are developing data from clinical studies that sleep deficiency and circadian disruption have multiple adverse consequences for health. The clinical data provide the base for mechanistic studies. Studies in animal models indicate that both circadian disruption and insufficient sleep later gene expression in peripheral tissues. Moreover, the effect of sleep loss in molecular changes in brain changes with age.... more »

Studies in different subjects have shown that there are major individual differences in response to sleep loss and circadian disruption. Twin studies have shown that this is heritable. There needs to be an intensive effort to assess basis of these individual differences. This could include in-depth phenotyping studies, e.g., neuroimaging, genetic studies, “-omic” studies, epigenetic changes, etc.

Self-report data indicate that insufficient sleep is more common in minority populations. This seems to be related to socioeconomic status. There is a need to move this beyond self-report and obtain objective measures in the relevant populations. Moreover, the basis of this difference needs to be established. What aspect of the environment leads to these differences, e.g., noise, stress related to sense of vulnerability,... more »

Data indicate the association between short sleep and circadian disruption on a number of adverse outcomes such as cardiovascular disease, metabolic disorders, hypertension, etc. There is a need to move beyond association to interventions that can be shown to improve sleep duration and circadian disruption.

There is developing evidence of major individual differences in pathways to different common sleep disorders such as obstructive sleep apnea. Moreover, there is evidence of different clinical presentations of disease and different outcomes. For example, some subjects with obstructive sleep apnea who get excessive sleepiness while others do not. The latter are still at risk for other consequences of the disorder such... more »

There are several possible physiological causes of Circadian Rhythm Sleep-Wake Disorders (CRSWDs), including lack of sensitivity to light, over-sensitivity to light, deficiencies in the ipRGC cells of the retina, lack of melatonin production, long elimination time of melatonin, long intrinsic circadian period, differences in timing of sleep relative to internal circadian rhythms, differences in tolerance to phase mismatch,... more »

What circadian-based strategies (e.g. timing of medication) can be applied to improve the efficacy of treatments for heart, lung, and blood diseases (e.g. hypertension, nocturnal asthma, thrombosis, obesity/diabetes)?

Does the homeostasis and health of the lung depend on circadian-coupled genomic function?

Does circadian regulation modify the effects of environmental exposures (e.g., cigarette smoke, particulates, virus/bacteria, temperature, humidity, microbiome) on airway/lung remodeling and the intensity of associated epigenetic modifications?