It's probably more accurate to say that it's more difficult to fall asleep in the light because the circadian rhythm is directly regulated by ambient light. Our retinas contain a small amount of cells specialized for detecting ambient light levels, and these are directly connected to the brain center which controls the circadian rhythm. As our eyelids don't completely block out ambient light, and the light which passes through and hits these specialized cells begins tampering with our circadian rhythm, it becomes more difficult to fall asleep.
The Suprachiasmatic Nucleus
The reason is a small nucleus above the optic chiasm in the hypothalamus called the suprachiasmatic nucleus (SCN), found across many different species. Comprising only approximately 20,000 neurons, the human SCN is nonetheless responsible for regulating a vast number of circadian functions over the entire body. The SCN is, for all intents and purposes, the pacemaker of the brain, and it runs on light: if ambient light is detected, then it must be because it is time to be awake, and the circadian rhythm is slowly adjusted accordingly.
(Suprachiasmatic nucleus. Source: Wikimedia Commons)
The Retinohypothalamic Tract
In mammals, the SCN receives input through the retinohypothalamic tract, which originates at a set of special photosensitive ganglion cells on the retina. They contribute to regulating the circadian rhythm by expressing melanopsin (Berson, Dunn and Takao, 2002). These highly specialized, sensitive and non-image-forming retinal neurons evolved to detect an environment's ambient light levels. They are most sensitive to blue light wavelengths of 488 nanometers (al Enazi et al., 2011), which may in part explain why users of electronic monitors sometimes report difficulties falling asleep.
(Effects of light exposure on the mammalian retinohypothalamic tract. Source: Wikimedia Commons)
A critical note
These fairly recent discoveries, while published in top-tier journals and widely hailed, have generated some controversy. Due to the ethical difficulties in deploying a methodology consisting mostly of disabling cones and rods in human samples, most of the evidence has come from animal models. At least one study, however, managed to discover patients naturally lacking cones and rods due to a rare illness, and they did report support for the SCN account in humans (Zaidi et al., 2007):
We examined the spectral sensitivity of non-image-forming responses in two profoundly blind subjects lacking functional rods and cones (one male, 56 yr old; one female, 87 yr old). In the male subject, we found that short-wavelength light preferentially suppressed melatonin, reset the circadian pacemaker, and directly enhanced alertness compared to 555 nm exposure, which is the peak sensitivity of the photopic visual system. In an action spectrum for pupillary constriction, the female subject exhibited a peak spectral sensitivity (λmax) of 480 nm, matching that of the pRGCs but not that of the rods and cones. This subject was also able to correctly report a threshold short-wavelength stimulus (∼480 nm) but not other wavelengths. Collectively these data show that pRGCs contribute to both circadian physiology and rudimentary visual awareness in humans and challenge the assumption that rod- and cone-based photoreception mediate all “visual” responses to light.
- al Enezi, J., Revell, V., Brown, T., Wynne, J., Schlangen, L., & Lucas, R. (2011). A “melanopic” spectral efficiency function predicts the sensitivity of melanopsin photoreceptors to polychromatic lights. Journal of biological rhythms, 26(4), 314-323.
- Berson, D. M., Dunn, F. A., & Takao, M. (2002). Phototransduction by retinal ganglion cells that set the circadian clock. Science, 295(5557), 1070-1073.
- Zaidi, F. H., Hull, J. T., Peirson, S. N., Wulff, K., Aeschbach, D., Gooley, J. J., ... & Lockley, S. W. (2007). Short-wavelength light sensitivity of circadian, pupillary, and visual awareness in humans lacking an outer retina. Current Biology, 17(24), 2122-2128.