Light and Sleep Cycles

Introduction

We know that sleep cycles are governed by our body’s internal circadian rhythm(s), and that numerous studies have shown that blue light can disrupt these patterns – or conversely, promote alertness [1]. The proof of this is almost self-evident: imagine trying to drift off to sleep in a room flooded with (conventional) florescent lighting. Now, imagine trying to go to sleep in a room lit – perhaps even a little unevenly – with moderately bright incandescent fixtures. It’s easy to see that both could be disruptive to getting sleep. Still, we could further imagine that if we were to present this choice to a group, a few – more so than not – might subjectively prefer the warmer glow of incandescent lighting. Is it possible that there are underlying biological reasons for such a bias?

This week, I took a closer look at a few key parameters and systems governing light, sleep, alertness, and the some of the bodies’ underlying regulatory systems in-between.

 

What specific types of light promote alertness (or disrupt sleep)?

Let’s envision a curve representing the relationship between light wavelength (color) and the relative response strength of the body’s various neuroendocrine/neurobehavioral responses (here, we will use “non-visual responses” for short).

 

 

The optimum wavelengths of light for inducing mental alertness occur in the blue part of the spectrum (~450-480 nm) [2]. The optimal wavelength of light for circadian rhythm regulation occurs in the green part of the spectrum (~555 nm) [2].

White light works, too. This should intuitively make sense, since pure white light is merely a combination of all the wavelengths – including blue and green. Of course, the more bluish- or greenish-white the light may be, the more robust the neuroendocrine/neurobehavioral response. This also explains why there is such a strong correlation between natural daylight (which is typically bluish-white for the better portion of daylight hours) and non-visual responses.

Concerning the intensity of this light, studies [2] have found that light must illuminate the cornea at a strength at least ~300 lux to achieve the maximum strength of non-visual responses.

 

Short-wavelength light and the retina

Depending on the length and intensity of exposure, different parts of the retina are involved in the various non-visual responses to short-wavelength light.

 

 

Rod and cone cells have a greater role in response during low-intensity and short-duration exposures [1]. For longer durations, however, these cells cannot sustain their input strength for inducing the various non-visual responses.

Retinal ganglion cells – which are not involved with vision — have a greater role in response during high-intensity and long-duration exposures [1].

An interesting consequence of the dominance of retinal ganglion cells in non-visual responses is that even people who are completely visually blind can still respond to exposure to blue light, depending on the condition of the retinal ganglion cells [1]. One experiment [3] in mice involved inducing simulated glaucoma – a leading cause of blindness which is associated with retinal ganglion cell degeneration and optic nerve damage – and found that that some non-visual responses to light were reduced, but not entirely eliminated.

The dominance of retinal ganglion cells, however, does not preclude fact the in the absence (or reduced sensitivity) of cone cells sensitive to blue or green light, non-visual response time becomes larger [4].

 

Circadian response systems

The suprachiasmatic nuclei (SCN) in the brain constitute the main circadian “clock” in mammals, receiving light information exclusively from the eyes. In turn, the SCN regulates other circadian “clocks” throughout the brain, including those associated with sleep-wake cycles, alertness, melatonin, cortisol and core body temperature [2].

Melatonin, a hormone produced by the body’s pineal gland, is directly associated with the onset and regression of sleep [1]. When more melatonin is being produced, sleep occurs. Conversely, mental alertness is at its peak when melatonin is at virtually undetectable levels.

 

The role of melanopsin in non-visual responses

The photosensitivity of the ganglion cells in the retina is linked to the expression of the melanopsin gene [3]. Melanopsin-expressing retinal ganglion cells are called ipRGCs.

Melanopsin is a key determinant in photosensitivity to short-wavelength (blue) light [3]. It provides a sustained input for non-visual responses during continued blue light exposure.

In individuals suffering from seasonal affective disorder (SAD), melanopsin gene expression in the retinal ganglion cells is often abnormally low [3]. If there is a deficiency in melanopsin gene expression, then there will be reduced photosensitivity of the ganglion cells to blue light. This under-stimulation of the non-visual systems is compounded in the fall and winter months, when natural daylight hours are reduced.

Thus, the various neuroendocrine systems of an individual with SAD will have difficulty maintaining circadian rhythm (explaining symptoms of excessive/irregular sleep) and alertness (“sluggishness”, increased performance times), among other challenges.

 

How can we use this information toward designing health-promoting systems?

Some [2] [5] have begun to argue that information about light and neuroendocrine/neurobehavioral responses can be incorporated into the way we design the built environment.

 

 

We could analyze arbitrary points in space – particularly indoors – in terms of their “circadian potential.” Here, circadian potential would be defined as robustness of “circadian entrainment” achieved from that point, which in turn is largely governed by access to natural daylight. Key points of circadian potential could guide choices in the design process about things such as the programmatic function of a space, or when conditions are optimal (in terms of well-being) for occupying such a space.

Bright-light intervention therapy has had some success in treating seasonal affective disorder, as well as remedying “jet lag” in international travelers [6]. Still, there is research that would suggest caution with regard to drastic changes to light exposure cycles. One study [7] involved altering the light exposure cycles for mice. Despite the fact that no changes in structure were made to the sleep cycle architecture or circadian for this new exposure cycle, the animals presented “increased depression-like behaviours and impaired hippocampal long-term potentiation and learning.” Still, the study also concedes that the exact nature of the relationship between “aberrant” light exposure cycles, mood and cognitive performance remains unclear.

Finally, using the knowledge we have discussed, we might be able to test for the onset of ocular conditions such as glaucoma or seasonal affective disorder using relatively inexpensive equipment. One potential scheme could be as follows: First, we could infer some data about the photosensitivity of an individual user’s retinal ganglion cells by routinely (weekly?) measuring the non-visual response time for exposure to blue light. Or a non-invasive, inexpensive device could be deployed to collect data on group populations. Next, this data (either from individual users or groups) could be analyzed to arrive at a model for retinal ganglion cell photo-sensitivity. Finally, if non-visual response times for a user begin deviate from those predicted by the model, this could be a marker for closer examination by a medical professional. If detected early enough using such a system, perhaps the onset of some ocular or neuroendocrine pathologies could be slowed or even reversed.

 

Summary

-         Short-wavelength light (blue, and to a lesser extent, green) can promote alertness.

-         Different parts of the retina respond to short-wavelength light, depending on the light source’s intensity and duration.

-         There is a threshold corneal illumination value (~300 lux) for generating optimum non-visual responses.

-         Suprachiasmatic nuclei (SCN) constitute the body’s main circadian “clock”, which in turn regulates the body’s other circadian clocks.

-         Melatonin is the “sleep” hormone. More of it means sleep; less of it means alertness.

-         The expression of the melanopsin gene determines retinal ganglion cell photosensitivity.

-         Seasonal affective disorder (SAD) is associated with abnormally low melanopsin gene expression in retinal ganglion cells.

 

Bibliography

[1] Rahman SA, Flynn-Evans E, Aeschbach D, Brainard GC, Czeisler CA, Lockley SW. Diurnal spectral sensitivity of the acute alerting effects of light. Sleep. 2014;37(2):271-281.

[2] Andersen M, Mardaljevic J, Lockley SW. A framework for predicting the non-visual effects of daylight – part I: Photobiology- based model. Light Research & Technology. 2012;44(1):37-53.

[3] de Zavalía N, Plano SA, Fernandez DC, et al. Effect of experimental glaucoma on the non-image forming visual system. Journal of Neurochemistry. 2011;117(5):904-914.

[4] Dollet A, Albrecht U, Cooper HM, Dkhissi-Benyahya O. Cones are required for normal temporal responses to light of phase shifts and clock gene expression. Chronobiology International: The Journal of Biological & Medical Rhythm Research. 2010;27(4):768-781.

[5] Andersen M, Gochenour SJ, Lockley SW. Modelling ‘non-visual’ effects of daylighting in a residential environment. Building & Environment. 2013;70:138-149.

[6] Fisher PM, Madsen MK, Mc Mahon B, et al. Three-week bright-light intervention has dose-related effects on threat-related corticolimbic reactivity and functional coupling. Biol Psychiatry. 2013.

[7] LeGates TA, Altimus CM, Wang H, et al. Aberrant light directly impairs mood and learning through melanopsin-expressing neurons. Nature. 2012;491(7425):594-598.

Other useful references

Grote V, Kelz C, Goswami N, Stossier H, Tafeit E, Moser M. Cardio-autonomic control and wellbeing due to oscillating color light exposure. Physiology & Behavior. 2013;114:55-64.

Tsai JW, Hannibal J, Hagiwara G, et al. Melanopsin as a sleep modulator: Circadian gating of the direct effects of light on sleep and altered sleep homeostasis in Opn4(-/-) mice. PLoS Biology. 2009;7(6):e1000125-e1000125.