By: Maximus Peto
Light exposure on the retina of the eye plays a critical role in entraining the circadian rhythm—the daily oscillation of tissue function, including the secretion of different hormones at different times. Humans evolved mostly outdoors, where light intensity is as much as 2,000 times greater than contemporary indoor lighting (100,000 lux vs. 50 lux). Many modern humans have very limited exposure to what might be considered “normal” intensities of light exposure, and this retinal light deficiency may have significant negative effects on human health. Here, I explore some of these possible negative health implications of what we might call “retinal light deficiency”, including reduced melatonin secretion, reduced growth hormone secretion, reduced slow-wave sleep, impaired morning awakening response, higher prevalence of fatigue, elevated risk of depression, and even an association with elevated incidence of death from any cause. I also describe some of my self-experimentation with indoor light exposure, and make some suggestions for how readers can achieve health-promoting light exposure with the proper intensities of light at the proper times of day. Studies of retinal light supplementation in humans have reported various promising effects, including restoration of 24-hour melatonin to the level of healthy young controls, alleviation of sleep disturbance and “sundowning” in Alzheimer’s disease patients, and enhancement of alertness and reduction of fatigue. From results of sleep studies in humans and animals, one might also reasonably expect restoration of growth hormone secretion in elderly humans with chronic bright light exposure to the retina. Synthesizing the literature explored herein, I speculate that neurodegenerative diseases such as Alzheimer’s may even be caused by decades-long retinal light deficiency, though I admit I found little direct evidence to support this hypothesis. To address insufficient indoor lighting intensity, light therapy glasses, combined with greatly enhanced indoor environmental lighting provided by LED bulbs and fixtures, may be effective methods of addressing chronic retinal light deficiency for chronically indoor-dwelling humans, if it indeed exists.
N-of-1 experiment: summary of benefits
1. Reversal of lethargy
2. Improved cognitive function
3. Better sleep: sleeping 7.0 to 8.5 hours in one session, rather than broken up sleep
4. Less sleep: sleeping 7.0 to 8.5 hours/day, instead of 8.5 to 10 hours
5. Reduced sleep latency (falling asleep faster)
6. Earlier waking time (6-8 AM instead of 8-9 AM)
7. Easier awakening (less grogginess)
8. Reduction of afternoon sleepiness
9. Increased rate of dreaming I can recall the next day (3-4 days/week instead of 0)
10. Improved mood (happier, more patient)
11. More regular bowel movements, now timed with waking time (7-8 AM), rather than food intake
12. I cannot think of any negative effects that might be associated with my retinal light exposure experimentation, except eye aches from blue light exposure
· A tripod stand to mount the above LED light on
· Three, 5000 K, 50 W LED shop lights
· Ayo blue light therapy glasses (not recommended)
· Dr. Meter LX1010B digital illuminance/light meter
· Android smartphone app Lux Meter by waldau-webdesign.de
Does retinal light deficiency degrade human health?
I have found several lines of evidence suggesting that a great many people may be exposed to insufficient retinal light to be optimal for their health. Retinal light exposure and its relative lack has been reported to have many different effects on human health. Types of effects include the cortisol awakening response and associated daytime alertness and fatigue, melatonin secretion, slow-wave sleep duration, mood and depression, behavioral dysfunctions in Alzheimer’s disease known as “sundowning”, and possibly the amount of growth hormone secreted during sleep. I explore each in-turn.
Effects on awakening response, alertness, and fatigue
The hormone cortisol is one important factor that influences when we wake up. A higher peak cortisol response is associated with less grogginess and greater alertness after awaking in the morning. Regular bright light exposure shortly after awakening has been shown to considerably enhance this cortisol response. Leproult et al. reported the following (bold emphasis mine):
The early morning transition from dim to bright light suppressed melatonin secretion, induced an immediate, greater than 50% elevation of cortisol levels, and limited the deterioration of alertness normally associated with overnight sleep deprivation…Afternoon exposure to bright light did not have any effect on either hormonal or behavioral parameters. The data unambiguously demonstrate an effect of light on the corticotropic axis that is dependent on time of day.
Also note that the suppression of melatonin secretion may have an additional energy- and alertness-enhancing effect. Numerous reports, such as this one, note that melatonin supplements can enhance sleepiness, even during the day. So bright light exposure not only raises cortisol, but also suppresses melatonin secretion.
A study by Wehr investigated the effects of the duration of daytime light (16 hours vs. 10 hours) on wakefulness. The longer light condition (16 hr/day) was associated with 7.7 hours of sleep per night, while the shorter light condition (mimicking winter) was associated with a dramatic lengthening of the sleep period to 11.0 hours/day (+3.3 hours/day, or +43%). Not telling our brains to stay awake with bright light appears to cause relative lethargy and sleepiness. Thus, bright light early in the morning, and continuing throughout the day, may improve alertness and productive capacity as well as reduce fatigue and possibly reduce sleep requirements. These effects appear to occur both by enhancing cortisol secretion, and inhibiting melatonin production.
Focusing on the specific wavelengths (colors) of light that might affect wakefulness, Figueiro and Rea studied the effect of blue light exposure for 80 minutes, shortly after awakening, on sleep-restricted adolescents. They found the cortisol awakening response to be considerably enhanced—by over 100%--with blue light exposure shortly after awakening.
This elevation in cortisol level in response to morning bright light exposure is important if one is interested in avoiding fatigue during the day. For example, Kumari et al. assessed cortisol levels and fatigue in 4,299 older adults. They reported that low waking cortisol was associated with a higher likelihood of experiencing fatigue. A meta-analysis by Powell et al. also reported that the cortisol awakening response is associated with fatigue.
This may relate to human aging because it has been observed that the amplitude of circadian rhythms is reduced with advanced age. That is, the waking and sleeping signals are blunted, leaving us more tired when we’re awake, more restless when we sleep, and less rejuvenated after we sleep. Arellanes-Licea et al. describe this observation:
In humans, the changes in circadian properties associated with aging are: 1) the amplitude of the circadian rhythms is reduced, 2) there is a phase advance in the circadian rhythms dependent on the [suprachiasmatic nucleus], and 3) there is a disruption of nocturnal sleep….Many pathological entities such as metabolic syndrome, cancer and cardiovascular events are strongly connected with a disruptive condition of the circadian cycle.
I suspect this age-related blunting of circadian rhythms might in fact be less than what has been reported in the scientific literature—or might even not exist at all—because these observations appear to be confounded by the endemic retinal light deficiency of modern indoor-dwelling humans. Studies I explore later will illustrate this point, such as the one by Mishima et al. reporting complete restoration of elderly insomniacs’ melatonin production to youthful control levels with only 4 hours of bright light exposure during the day.
Effects on slow-wave sleep and growth hormone secretion
The effects of light exposure on sleep function relate primarily to melatonin production (covered later), slow-wave sleep duration, and growth hormone secretion (the latter two reviewed in this section). Slow-wave sleep, in addition to affecting growth hormone secretion, may also affect memory and cognitive ability. Let’s first explore the relationship between slow-wave sleep and growth hormone secretion.
Slow-wave sleep and growth hormone secretion
Slow-wave sleep, also called “deep sleep”, is a phase of non-rapid eye movement (NREM) sleep during which EEG activity is synchronized, and the brain displays slow waves of activity between 0.5-2.0 Hz (Wikipedia).
Slow-wave sleep is particularly interesting because it is the phase of sleep during which a significant amount of growth hormone is secreted. For example, a research paper by Van Cauter and Plat reported:
…in men, approximately 70% of the growth hormone pulses occur during slow-wave sleep.
In a different paper, Van Cauter et al. assessed slow-wave sleep and growth hormone secretion in 149 healthy men aged 16 to 83. They reported that growth hormone secretion was associated with slow-wave sleep duration at all ages. They also found that both slow-wave sleep and growth hormone secretion declined together during aging.
Note that both slow-wave sleep and 24-hour growth hormone secretion decline dramatically during human aging. Van Cauter et al. reported that time during slow-wave sleep declined by approximately 82% between the ages of 16 to 50.
Growth hormone is a protein secreted by the pituitary gland in the brain. As its name suggests, it has important growth-promoting effects, particularly on muscle and bone. These effects are mainly caused by the protein IGF-1, the synthesis of which growth hormone stimulates.
Both growth hormone and IGF-1 decline during normal human aging. A study by Cauter and Plat cited earlier reported a substantial decline in 24-hour growth hormone secretion between the ages of 30 and 40: a reduction of 50-66%.
That slow-wave sleep has a strong association with growth hormone has important implications for the possibility of retinal light deficiency in humans. If growth hormone helps maintain tissue health during aging, we may want to promote endogenous growth hormone secretion to the extent possible. This may involve getting adequate retinal light exposure, as it appears to increase slow-wave sleep, which may enhance growth hormone secretion.
Effects of retinal light exposure on sleep architecture
Interestingly, one study by Wams et al. evaluated the associations of different parameters of light exposure on sleep architecture. They found that exposure to light sooner after awakening, and a higher maximal intensity of that light exposure, was associated with greater slow-wave sleep. In the discussion section of this paper, the authors asserted:
Through the sleep stage accumulation analysis, it can be observed that [slow-wave sleep] has a direct relationship with the timing and intensity of light.
I speculate that this increased slow-wave sleep associated with earlier and brighter light exposure after awakening is likely to also enhance growth hormone secretion during sleep, which may help delay global, age-associated tissue atrophy and dysfunction.
Effects on melatonin secretion
Melatonin is a hormone produced and secreted by the pineal gland in the brain that has a strong effect on sleepiness. The National Sleep Foundation has the following to say about melatonin:
Melatonin is a natural hormone made by your body's pineal (pih-knee-uhl) gland. This is a pea-sized gland located just above the middle of the brain. During the day the pineal is inactive. When the sun goes down and darkness occurs, the pineal is "turned on" by the SCN and begins to actively produce melatonin, which is released into the blood. Usually, this occurs around 9 pm. As a result, melatonin levels in the blood rise sharply and you begin to feel less alert. Sleep becomes more inviting. Melatonin levels in the blood stay elevated for about 12 hours - all through the night - before the light of a new day when they fall back to low daytime levels by about 9 am.
Many—but not all—studies have reported that melatonin secretion declines during human aging (reviewed by Touitou). The reported decline ranges from between 20% and 80%, depending on the study. However, there have been a few studies suggesting that other factors besides age may affect melatonin secretion. For example, the review by Touitou described a study by Zeitzer et al. in this way (bold emphases mine):
In a recent study, Zeitzer et al. (1999) analyzed the amplitude of plasma melatonin profiles during a constant routine in 34 healthy old subjects (20 women: 68 + 4.2 yr and 14 men: 67.7 + 3.3 yr) and compared them with those in 98 health young men (23.2 + 3.8 yr). Throughout the constant routine protocol, which lasted at least 30 h, subjects remained awake, in bed in a semi-recumbent position under constant dim ambient illumination of less than 15 lux and received equicaloric snacks and fluids hourly. The authors reported in these conditions that the endogenous circadian rhythm of melatonin among most of the elderly had an amplitude similar to that of young adults; the mean 24 h average melatonin concentration, duration, and the mean and integrated area of the nocturnal plasma melatonin peak were also similar. They concluded that their results did not support the hypothesis that decreased plasma melatonin concentrations are characteristic of healthy aging. They did, nonetheless, also find a small group of elderly subjects whose plasma melatonin cycle had a significantly lower amplitude.
To explain the difference between their results and those of other investigators, they suggested that the other studies might not have been controlled for the use of melatonin-suppressing drugs (β-blockers, non-steroidal anti-inflammatory agents, aspirin), for the lighting regimen or for medical conditions.
These results suggest that it may not be age-related dysfunction of the circadian system that causes the often-observed age-related decline in melatonin secretion. It may be caused insufficient retinal light exposure.
However, Touitou goes on to doubt this explanation, but one more intriguing study suggests to me that it may be correct. This next study also suggests to me that most of indoor-dwelling humanity may suffer from the negative health effects of decades of retinal light deficiency.
This noteworthy study was undertaken by Mishima et al. In this study, the research team studied retinal light exposure and its effects on melatonin concentration and sleep dynamics in three groups:
· 10 healthy young controls (mean age 20.9)
· 10 healthy elderly controls (mean age 72.7)
· 10 elderly insomniacs (mean age 74.2)
They noted that during their normal routines, the two elderly groups were exposed to significantly less daily light, especially so in the elderly insomniac group. Correspondingly, both elderly groups had considerably less 24-hour melatonin secretion, with elderly insomniacs having the lowest, being 42% lower than the healthy young controls (young = 359.2 pg/mL*hr; healthy elderly = 250.3; elderly insomniacs = 211.3).
The researchers then administered 4 hours of retinal light exposure at 2,500 lux, between 1000 and 1200 hours and between 1400 and 1600 hours, for 4 weeks, to the elderly insomniacs.
After this intervention, elderly insomniacs had substantial increases in 24-hour melatonin secretion, such that it was similar to the young control group. I found this remarkable; that the “age-related decline in melatonin secretion” could be eliminated with bright light exposure of sufficient duration. And 2,500 lux is not even particularly bright—outdoor light intensity on a sunny day can easily be over 80,000 lux. And nor is 4 hours per day particularly long; some studies suggest 12-16 hours would optimize the physiological responses to light. The elderly insomniacs in this study also reported significant improvement in their insomnia, improvement which tended to track increases in melatonin.
On the next page is Figure 1 from the full-text. Note the white squares are elderly insomniacs (EI), and the white circles are the same insomniacs after the light exposure protocol, with the grey shaded area the healthy young controls (YC). “EC” stand for “elderly controls”, and is represented by the black dashed line:
Mishima et al. go on to conclude (bold emphasis mine):
We demonstrate here that resident elderly persons can suffer from insufficient environmental light and that supplementation with bright light at levels similar to those in the young living at home can improve melatonin secretion and sleep quality, suggesting that the discrepancies in previously reported studies could be attributable, at least in part, to the exposure of the experimental subjects to varying degrees of environmental light.
Seeing in the scientific literature what I’ve presented to you so far, I can’t help but wonder how much systemic degeneration, and possibly especially neurodegeneration, might be caused by decades of retinal light deficiency, and not by aging-intrinsic processes per se.
Does melatonin enhance growth hormone secretion?
In addition to bright light exposure enhancing melatonin secretion, a second-order effect of this may again be the enhancement of growth hormone secretion. One study by Forsling et al. gave melatonin supplements to eight young (average age 21) men. They reported that the 0.5 mg and 5.0 mg doses of melatonin increased growth hormone secretion. Nagane et al. reported that 24-hour growth hormone and melatonin curves correlated very strongly in healthy young people with regular circadian rhythms.
However, not all evidence supports the hypothesis that melatonin enhances growth hormone secretion. For example, Morris et al. mention several observations suggesting that growth hormone secretion is dependent on sleep, particularly slow-wave sleep, and not on melatonin per se. For example, they cite studies reporting that growth hormone secretion increases rapidly after sleep onset, regardless of the time of day (this does not happen with melatonin), and studies reporting that when nocturnal sleep is interrupted, a growth hormone surge occurs soon after resumption of sleep. Based on the evidence I reviewed, I suspect the possibility that when peaks in melatonin and growth hormone occur together, the presence of melatonin may enhance the sleep-dependent increase in growth hormone secretion.
Unfortunately, I could not find studies reporting an association between light exposure and growth hormone secretion in humans. I could not find studies even attempting to answer this question. I did find a few interesting observations in animals. For example, Halevy et al. tested the effects of different colors of light on muscle stem cell counts and growth hormone receptor expression in broiler chickens. They found that blue and green light exposure was associated with higher muscle stem cell counts, and higher growth hormone receptor expression, compared to red or white light. A different study in chickens reported that melatonin concentration was nearly perfectly correlated with growth hormone concentrations. In this study, Zhang et al. tested the effect of blue, green, red, and white light on chickens, assessing their effects on melatonin, growth hormone-releasing hormone (GHRH), and growth hormone. Remarkably, the researchers reported an extremely strong association between melatonin concentrations and growth hormone-releasing hormone (r = 0.96) and growth hormone (r = 0.993). Interestingly, they found that green light exposure (it might be blue for humans) was associated with 5-35% higher GHRH mRNA, protein, and growth hormone concentrations, compared to red, blue, or white light.
Given the very high r-values reported in this last study, I’m very interested to see whether bright light exposure enhances growth hormone secretion in humans, in addition to the other potential benefits explained herein.
Effects on brain function
While doing research for this article and learning about the physiology of the eye and brain and their responses to light, I couldn’t help but think that light exposure into the eyes might serve as “exercise” for certain parts of the brain. Much like how active muscles are preserved or strengthened with strenuous muscle contraction, I wonder if bright light exposure intensely stimulates parts of the brain, and this intense stimulation enhances neurogenesis, neuronal survival, and possibly even whole-body function.
The National Sleep Foundation describes how light exposure in the eyes affects various parts of the brain (bold emphases mine):
A key factor in how human sleep is regulated is exposure to light or to darkness. Exposure to light stimulates a nerve pathway from the retina in the eye to an area in the brain called the hypothalamus. There, a special center called the suprachiasmatic nucleus (SCN) initiates signals to other parts of the brain that control hormones, body temperature and other functions that play a role in making us feel sleepy or wide awake.
The SCN works like a clock that sets off a regulated pattern of activities that affect the entire body. Once exposed to the first light each day, the clock in the SCN begins performing functions like raising body temperature and releasing stimulating hormones like cortisol. The SCN also delays the release of other hormones like melatonin, which is associated with sleep onset, until many hours later when darkness arrives.
All of this is affected by simple light exposure on the retina of the eye.
The hypothalamus has a critical role in sleep architecture, and sleep has an important role in memory. So it is not surprising that there have been some concerning associations between Alzheimer’s disease, sleep, and retinal light exposure.
Could retinal light deficiency contribute to Alzheimer’s disease development?
Alzheimer’s disease is a degenerative disease of the brain, where there is a considerable loss of brain tissue, associated with progressive cognitive dysfunction. I am interested in the possibility that long-term retinal light deficiency may contribute to—or even be a primary cause of—human Alzheimer’s disease. I have not found strong evidence supporting this theory, but there seems to be enough evidence that the possibility should be considered carefully and explored further. It may be that the links between light exposure and Alzheimer’s disease are distant enough that it is difficult to make the causative relationship clear.
One of the main pathways through which retinal light deficiency may contribute to the development of Alzheimer’s disease is by affecting sleep quality. Sleep disturbance is prevalent in Alzheimer’s disease. Hanford and Figueiro estimate that people with Alzheimer’s disease typically spend about 40% of their night time awake, and a large proportion of the solar daytime asleep, suggesting dysfunction of the circadian system. I explored earlier how light exposure can dramatically affect melatonin production, and melatonin has an important role in being tired and remaining asleep through the night.
But teasing out which factor causes the other—if there is a cause-effect relationship between them at all—is difficult. Does poor sleep quality cause Alzheimer’s, or does Alzheimer’s cause deterioration in sleep quality? A study by Branger et al. may suggest an answer. The research team assessed the relationship between sleep parameters and amyloid beta burden in healthy older adults. They found that impaired sleep parameters, such as taking a long time to get to sleep and the number of nighttime awakenings, was associated with increased amyloid beta burden and lower grey matter brain volume in some regions, but before an impairment in brain glucose metabolism. And these changes were observed before any these individuals could be diagnosed with Alzheimer’s disease or even the earlier “mild cognitive impairment” (MCI) condition. This suggests two possibilities: (1) poor sleep quality (and thus possibly retinal light deficiency) contributes to Alzheimer’s development, or (2) early changes in Alzheimer’s development, such as increased amyloid beta burden and grey matter atrophy, may damage important parts of the brain, and this damage impairs sleep quality. At this point in my research on this topic, it’s not clear to me which is the case.
Another interesting piece of evidence is that people with very low vitamin D level (< 10 ng/mL) develop Alzheimer’s disease at over twice the rate of those with higher vitamin D (> 20 ng/mL; Hoel et al.). Even having serum vitamin D between 10 and 20 ng/mL was associated with a 69% increased incidence of Alzheimer’s. Note that for most people, serum vitamin D level is indictive of sunlight exposure. Could it be that low vitamin D is a useful biomarker of chronic light deficiency, which itself contributes to cognitive degeneration?
And I also can’t help but wonder about the gender difference in the incidence of Alzheimer’s disease. Viña and Lloret note that after age 80, women are more likely to develop Alzheimer’s than men, with a difference of incidence as large as 50%. For example, 50% more women develop Alzheimer’s after age 90 than do men the same age. In other words, if 10 out of 100 men develop Alzheimer’s disease, 15 out of 100 women would develop it at the same age. Why? Could lifetime light exposure have something to do with it? I speculate that men are far more likely to work in outdoor jobs, or to get more outdoor time as they age, though I was unable to find data to support these speculations.
Alzheimer’s disease and sundowning
Given how much I’ve explored light exposure and its effect on the circadian rhythm, the concept of “sundowning” in Alzheimer’s is particularly interesting. If you haven’t heard of it, “sundowning” is a term for the behavioral changes people with Alzheimer’s display around the time of sunset. Canevelli et al. describe it:
…these behaviors may consist of a wide variety of symptoms such as anxiety, agitation, aggression, pacing, wandering, resistance, screaming, yelling, visual and auditory hallucinations, and so forth…Sundowning has been observed to represent the second most common type of disruptive behavior in institutionalized patients with dementia after wandering and has been frequently described as “endemic” in nursing homes hosting cognitively impaired older subjects (8, 16). At the same time, it has also been commonly described among community-dwelling individuals with dementing illnesses [e.g., in the 66% of patients with Alzheimer’s disease (AD) living at home (17)].
Canevelli et al. go on to describe several studies aimed at alleviating sundowning in dementia (including Alzheimer’s) patients, many of which focused on melatonin supplementation or retinal bright light exposure, which I’ll summarize next.
Light exposure for sundowning and Alzheimer’s disease
The studies reviewed by Canevelli et al. mostly consist of interventions of either retinal light exposure, or melatonin supplementation. I remind the reader that there is evidence that retinal light exposure causes elevated nocturnal melatonin. I suspect these two interventions may have their positive effects from the same mechanism: elevation of nocturnal melatonin. But retinal light exposure may have additional benefits—unassessed in these studies—that are not induced by oral melatonin supplementation.
Regarding light exposure, Canevelli et al. report (bold emphases mine):
…light therapy (i.e., the exposition to bright light during the afternoon/evening hours) has been observed to produce a significant reduction of sundowning episodes (41) and motor restless behaviors (42) in open-label studies conducted on patients with dementia, as well as to improve agitated behaviors in institutionalized elderly individuals (43). Nevertheless, no [randomized controlled trial] selectively investigating the efficacy of light therapy on sundowning has been yet conducted.
Hanford and Figueiro summarized many more studies of retinal light exposure for the treatment of sleep disorders in Alzheimer’s disease. I refer readers to Table 1 for a convenient summary of these studies.
Some of the findings of these studies are promising. Select quotes of the results reported in Table 1 include “significant improvement in circadian rhythms disturbances and in cognition” and “earlier onset sleep time and longer sleep duration”. The results are mixed, though so are the interventions, varying on parameters such as light intensity (200 lux to 10,000 lux), time of day, and duration (between 2 hours and the length of solar daytime). It appears that the optimal retinal light exposure parameters for Alzheimer’s patients has not been established yet.
Mitolo et al. conducted a systematic review of the literature on light treatment in Alzheimer’s, and offer a conclusion with which I agree:
Overall, the current literature suggests that the effects of light treatment in AD patients are mixed and may be influenced by several factors, but with a general trend toward a positive effect. Bright light seems to be a promising intervention treatment without significant adverse effects;
Melatonin supplementation for sundowning and Alzheimer’s disease
Regarding the studies on melatonin supplementation for sundowning, Canevelli et al. concluded:
Most of available evidences concerning the pharmacological management of sundowning have been focused on the clinical efficacy of melatonin supplementation…To date, only three [randomized controlled trials] have investigated the effectiveness of melatonin in reducing agitated behaviors in patients with dementia compared to placebo, also reporting inconclusive and conflicting results (45–47). Nevertheless, these studies were not specifically designed to assess sundowning, while more widely investigating changes in sleep quality, overall daytime functioning and behavior.
De Jonghe et al. reviewed all studies of melatonin for sundowning, and reported:
Nine papers, including four randomised controlled trials (RCTs) (n = 243), and five case series (n = 87) were reviewed. Two of the RCTs found a significant improvement on sundowning/agitated behaviour. All five case series found an improvement.
I wonder if, once the brain atrophy occurs during Alzheimer’s disease (and human aging more generally), the parts of the brain responsible for controlling behavior no longer respond as vigorously to light exposure and melatonin supplementation; the damage may have already been done, and the controlling structures may no longer function properly. If the reports of brain tissue destruction during Alzheimer’s are accurate, then I doubt that any amount of retinal bright light exposure is going to stimulate brain rejuvenation sufficiently to replace the estimated 20% decline in brain weight between ages 20 and 100. Perhaps the brain needs cell replacement and rejuvenation—more than retinal light exposure—at that point.
Above, I explored studies of the effects of retinal light exposure and melatonin supplementation on Alzheimer’s disease because this disease represents a remarkable example of brain atrophy and cognitive decline. If these interventions show promise in such a severe disease, I think it reasonable to suspect that consistent, retinal bright light exposure may help prevent the less severe age-associated brain atrophy, and cognitive dysfunction.
There is also some evidence that increased retinal light exposure is associated with greater longevity and protection against certain prevalent causes of death.
Light exposure and mortality
My colleague Dave Gobel found an interesting report of avoidance of sun exposure being associated with higher mortality. If one were to take seriously the concerns about sun exposure and skin cancer, one would think that avoiding sun exposure would be good for longevity. But Lindqvist et al. studied sun exposure habits (avoidance vs. actively seeking) in nearly 30,000 Swedes with a 20-year follow-up, and had some very interesting things to report (bold emphasis mine):
Nonsmokers who avoided sun exposure had a life expectancy similar to smokers in the highest sun exposure group, indicating that avoidance of sun exposure is a risk factor for death of a similar magnitude as smoking. Compared to the highest sun exposure group, life expectancy of avoiders of sun exposure was reduced by 0.6–2.1 years.
The report you are now reading is focused on the effects of retinal light exposure, while sunlight exposure or avoidance involves light (including UV) exposure on a much larger proportion of the body. Thus, the relative effects of retinal light exposure vs. whole-body sunlight exposure would be expected to be different (such as synthesis of vitamin D in the skin after UV-B exposure). So this report of sunlight exposure/avoidance is not perfectly relevant to the question of whether retinal light deficiency exists in humans, but it does seem to support the promising aspects of increased retinal light exposure for indoor-dwelling humans.
Another interesting connection to consider is that between retinal light exposure and sleep quality. Multiple studies referenced above report that retinal light exposure is associated with an improvement in sleep quality or treatment of insomnia. There is an association between Alzheimer’s disease (a significant cause of death) and sleep disturbances, and also a reported association between sleep disturbances and early mortality. For example, Sivertsen et al. reported that insomnia was associated with a nearly 5-times higher mortality in men, and 2-times higher mortality in women. Note that participants in this study lived in Norway, which has an especially high latitude, and thus, more dramatic range of day length. Given these correlations, it seems plausible that insufficient retinal light exposure may contribute to early death in some cases.
Putting it all together
Having now explored above, the many interesting observations I considered during this research dive, I’ll now summarize the full hypothesis I’ve developed during this work:
Consistent, long-term retinal bright light exposure while awake may have multiple positive effects on human health, ultimately resulting in enhanced maintenance of global tissue health and function during aging, and preservation of cognitive function in particular, with additional beneficial effects on heightened alertness, reduced fatigue, and a reduction in the risk of depression.
My reasoning about how retinal bright light exposure could have such remarkable benefits is as follows:
1. Retinal bright light exposure during the day suppresses melatonin production during the day. This enhances alertness and reduces fatigue.
2. Sleep that follows daytime bright light exposure involves considerably higher melatonin level, at least in some groups. (It has been reported to increase by nearly 50% in at least one study of elderly people.) Slow-wave sleep duration—a component of sleep that appears to decline dramatically during aging—also appears to be enhanced with retinal bright light exposure.
4. If retinal bright light exposure enhances nocturnal melatonin level, and melatonin enhances growth hormone, then retinal bright light exposure may also enhance growth hormone secreted at night, following a day of sufficient retinal bright light exposure.
5. The resulting elevated growth hormone should result in improved tissue maintenance and function during human aging.
6. I speculate that this may have particularly important tissue-maintenance effects on the brain. It appears that bright light exposure acts as a strong stimulatory factor for the brain, much like muscle contraction induces repair, maintenance, and growth of skeletal muscle.
7. For example, the protein called “brain-derived neurotrophic factor” (BDNF) is understood to have an important role in neuronal survival, memory consolidation, long-term memory storage, and even neurogenesis. For an example of the latter, Zigova et al. reported that administration of BDNF into adult rat brains doubled the rate of neurogenesis, and concluded, “These results demonstrate that the generation and/or survival of new neurons in the adult brain can be increased substantially by an exogenous factor.”
8. However, BDNF need not be an exogenous factor, because humans synthesize it endogenously, with an average level around 33 ng/mL with considerable variance (Naegelin et al.). For example, Molendijk et al. report that BDNF concentrations in humans vary significantly based on the season, with BDNF higher in the summer, and 5-10% lower in the winter, as well as declining concentrations in the fall, and ascending concentrations in the spring. The results of this study suggest that BDNF concentrations vary with retinal light exposure. Addressing whether 5-10% could make a significant difference in health outcomes, Molendijk et al. reported that BDNF level closely paralleled psychiatric diagnoses. They reported major depressive disorder being ~33% more common in winter and antidepressant medication use being 20% more common. Moreover, I think it reasonable to conclude that summer months do not ensure the participants sampled are exposed to melatonin-suppressing intensities of light for 12-16 hours per day, every day, a protocol which I suspect may increase BDNF levels further.
9. Involvement of BDNF in Alzheimer’s disease has been explored. In a review of the topic, Budni et al. state: “Evidence has suggested the involvement of BDNF with AD pathology. Studies have shown alterations in the levels of this neurotrophin in AD patients. Results show reduction (21-30%) in pro-BDNF in patients with MCI (mild cognitive impairment) and major reduction (40%) in terminal patients. These results suggest the involvement of BDNF with cognitive dysfunction in AD patients.”
10. Moreover, there has been some discussion in the scientific literature that makes me suspect that long-term lack of retinal bright light exposure may cause the suprachiasmatic nucleus (SCN) to atrophy or otherwise cease to function properly. The SCN has a critical role in sensing light from the retina and secreting melatonin in response to relative darkness. See Van Erum et al. for more on this topic.
11. Given the above, I conclude there is sufficient evidence to speculate that indoor-dwelling humans (including and especially the elderly) may be experiencing some degree of environmentally-induced (not age-related) neurodegeneration, a process which may even be a primary factor causing Alzheimer’s disease. I imagine this neurodegeneration process possibly being caused by failure to achieve adequate retinal light exposure to elevate nocturnal melatonin and growth hormone, and to keep BDNF concentrations sufficiently elevated to promote neuronal survival and neurogenesis throughout the lifespan.
12. I am eagerly curious to discover whether the health, well-being, and especially cognitive function of humans of all ages can be considerably preserved or enhanced by consistent, long-term, retinal bright light exposure (20,000 to 40,000 lux) for 12-16 hours during the waking period.
13. From my personal experimentation with indoor lighting fixtures to achieve the above retinal light exposure regimen, I report that this is very difficult to do. Accomplishing this efficiently may be best achieved by wearing a light visor, which sits very close to the surface of the eye and directs light into retina. This markedly reduces the energy needed to achieve 20,000+ lux at the eye, compared to commonly-used indoor lighting.
The above line of reasoning is partly predicated on my assumption that, during human evolution, humans spent the vast majority of their waking time outdoors, i.e. experiencing far higher light intensity than modern indoor-dwelling humans do. This assumption includes the idea that the human organism functions its best in the environment in which it evolved. Thus, if we want to prolong human physiological function, we may need to simulate—in our daily lives—the retinal light exposure environment in which our ancestors evolved.
If at least some of what I outline here is accurate, then the endemic retinal light deficiency seems analogous to the current “overnutrition” phenomenon, sometimes described as “diseases of affluence”. I understand (though I’m not well-read on this topic) that while humans evolved in a much brighter environment, they also evolved in relative calorie scarcity. This is not the environment in which wealthy modern humans find themselves, and our physiological biases toward sweet, fatty, and salty foods has played an important role in destroying many millions (billions?) of human life-years.
If there is any benefit to consistent retinal bright light exposure, it is important to know exactly what we mean by the terms “consistent” and “bright”.
In the next section, I summarize my findings on what types, intensities, and durations of light have been reported to be associated with some of the positive effects described above.
Taking action: type, intensity, timing, and duration of retinal light exposure
From my research for this working paper, I am convinced that humans have not made a concerted effort to determine the exact parameters of retinal light exposure with indoor lighting that will fully replicate the benefits of sunlight exposure on clear, sunny days outdoors. Much more research needs to be done on this topic, and thus for now, we must self-experiment to determine which parameters optimize our biomarkers, function, and sense of well-being. In this section, I present my recommendations for starting places for self-experimentation, focusing on four parameters of retinal light exposure:
1. Type (i.e. wavelength) of light
2. Intensity of light
3. Timing of light exposure
4. Duration of light exposure
Because the length of this working paper is becoming considerable, and this section is dedicated to actionable details, I will endeavor to present the upcoming practical information concisely.
Type of light (5000 K “daylight” temperature)
By “type”, I’m referring to the wavelength. Many different wavelengths of light have been explored in scientific studies of animals and humans. I recommend self-experimenting with only one type of light: “daylight” temperature, white light (light bulbs rated at 5000 K).
“K” values refer to color spectra (often called color “temperature”) emitted by lighting equipment, with lower numbers (e.g. 3000 K) being “warmer” (more red spectrum), and higher values (e.g. 6000 K) being “cooler” (more blue spectrum).
A caution about blue light
One remarkable observation is that blue light—at approximately 470 nanometers (nm)—appears to be the cause of at least some of the promising effects of retinal bright light exposure. As mentioned above, Figueiro and Rea reported that 80 minutes of exposure to 470 nm blue light increased the cortisol awakening response in sleep-deprived adolescents by about 60%. Cajochen et al. reported that blue light at 460 nm caused a greater suppression of melatonin, and a significantly increased alerting response, core body temperature, and heart rate, than did 550 nm (yellow) light, while vasodilation was enhanced by either wavelength light.
Personally, I experimented with 250 lux of blue light at 470 nm using the Ayo blue light therapy glasses. However, when using them daily for 40-80 minutes, my eyes would have a dull aching sensation around 6 AM the next day. This concerning experience takes a day of not using the device for it to go away.
I studied some concerning reports in the science literature about what has been called the “blue light hazard”. For example, Nakamura et al. reported some concerning effects of retinal blue light exposure in mice, though the light exposure lasted 3 days—quite extreme compared to the 40-80 minutes to which I was exposing my eyes. At first, I dismissed these concerns as not being relevant for humans. Most studies I found were in mice, usually albino mice, whose eyes are far less protected from light damage, and the studies often used extreme light exposure regimens, such as the 3 days of blue light used by Nakamura et al..
But with the occasional aching sensation I’ve experienced 24 hours after using the Ayo blue light therapy glasses, I’ve decided to stop using that device, and recommend against experimenting with it. It appears that sufficiently bright white light may achieve the same benefits without the risks of blue-only light.
I suspect that the discomfort I experienced from blue-only light might be due to brightness insufficient to constrict the pupil—a method for the eye to protect the retina from excessive light exposure. So the eye is exposed to the full effects of dim blue light with a relatively open pupil.
However, when exposed to bright white light, the pupil will close considerably, and perhaps this protects against the potential damage caused by the blue light component of white light. At any rate, I have never experienced this aching sensation from exposure of up to 40,000 lux for up to 8 hours per day.
But the above explanation about pupil dilation is speculation on my part. The dull ache of my eyes is sufficient for me to recommend against experimenting with this wavelength of light.
Intensity of light (20,000 to 40,000+ lux)
The intensity of light striking a surface is often measured in units called “lux”. This is how I compared intensities of light exposure during my self-experimentation, and is the most common unit of measure I observed in the science literature.
Remember that in addition to enhancing the cortisol awakening response, retinal light exposure should also suppress daytime melatonin, which is likely part of the reason why bright light enhances alertness and decreases fatigue. Fortunately, Hanford and Figueiro summarized some research literature on which colors of light suppress melatonin by 50%, and at what intensities those colors do so. These are summarized in Table 2 of their paper, presented below.
In short, 470 nm blue light is by far the most effective for suppressing melatonin levels, with only 50 lux needed to suppress melatonin by 50% after 1 hour. However, as described above, there may be risks associated with blue-only light, and it may be impractical to use only 470 nm blue light indoors. There may also be additional benefits from white light, given that it contains all colors of the visible spectrum.
For white light, 5000 K appears to be optimal for increasing retinal light exposure, as it requires the least intensity of light to suppress melatonin level (430 lux to suppress melatonin by 50% after 1 hour).
Besides suppressing melatonin and enhancing the cortisol waking response, it is not clear from the scientific literature what intensity is optimal for daytime retinal light exposure. I have the impression that researchers have not attempted to test for the optimal light intensity for human health. The only other clues I use to recommend 10,000 to 20,000 lux are:
1. Normal daytime light intensity on a clear day in the shade (approximately 20,000 lux, see Wikipedia)
2. The intensity of light reported to be effective in treating seasonal affective disorder (approximately 5,000+ lux for 30+ minutes; see Penders et al.)
I also caution readers to pay attention to how they feel if they experiment with brightness higher than approximately 40,000 lux. While this intensity is difficult to achieve with indoor lighting, I suspect that the eyes might possibly be damaged with retinal exposure to such high intensity levels for the duration I recommend self-experimenting with (12-16 hours/day; see below).
A very important aspect of light intensity to keep in mind is that it declines rapidly as you move away from the source. Therefore, a light visor placed in front of the eyes can provide far higher lux values than overhead lighting with much higher power; the distance between the light source and the eyes is dramatically different between these two methods. During my self-experimentation, I tested lux values using two methods, an Android smartphone app called Lux Meter, and a hand-held lux meter by Dr. Meter.
Another interesting point to keep in mind about light intensity (lux) is that outdoor sunshine on a sunny day can be as high as 100,000 lux, even without looking directly at the sun. Compare this to what I’ve observed for common indoor overhead fluorescent lighting at 10-50 lux.
Timing of light exposure (within minutes of awakening)
Earlier, I summarized one study reporting that light exposure around the normal waking time caused a substantial increase (> 50%) in the waking cortisol response, while being exposed to this light later resulted in no change in that response. So there may be something remarkable about retinal bright light exposure shortly after the normal waking time (to coincide with the cortisol awakening response).
However, other research has reported some improvements with retinal bright light exposure at different times of the day. For example, the study reporting restoration of nocturnal melatonin secretion in elderly insomniacs used bright light exposure between 10 AM and 12 PM, then again between 2 PM and 4 PM. And Hanford and Figueiro summarized in Table 1, studies utilizing many times throughout the day, usually 2-3 hours of exposure at a time, starting at 7 AM, 8 AM, 9 AM, 9:30 AM, 4 PM, 5 PM 5:30 PM, and 6 PM.
Given the above studies, combined with the assumption that humans evolved to function best under outdoor lighting conditions, it seems reasonable to begin light exposure shortly after normal waking time (within 15 minutes), and continuing with it throughout the day, stopping 4 hours or less before sleep time.
Duration of light exposure (continuous for 12-16 hours/day)
I did not perform exhaustive research on what duration of light exposure would be optimal, partly because very few studies tested continuous bright light exposure during their experiments, even when trying to help people with a terminal illness (such as Alzheimer’s disease). I presume that a more aggressive protocol would be tested (i.e. 12-16 hours of bright retinal light exposure per day) for people who are otherwise going to die of their condition. But I did not find these studies. In other words, there appears to be very little data to inform the optimal duration of retinal bright light exposure.
But I suspect one study presented earlier gives us an important clue. Earlier I summarized a study conducted by Wehr, in which he exposed 8 volunteers to either 10 hours of light per day, simulating winter, or 16 hours of light, simulating summer. He found that the 16-hour light period was associated with 7.7 hours of sleep per night, while the 10-hour light period was associated with a remarkable 11.0 hours of sleep per night—43% more than the summer simulation. This suggests that if we want to be awake, active, and alert, we want to suppress melatonin with bright light for as long as we want to be awake.
Given the above, and assuming that humans evolved to function optimally outdoors where light intensity was over 1,000 times higher than common indoor lighting, I recommend readers self-experiment with light exposure periods of 12-16 hours, starting within 15 minutes of awakening. I imagine that 16 hours of bright light may not allow for sufficient rest, while 12 hours may not keep a person stimulated and alert enough to make it through the day without a nap or going to sleep early. Additional research, (including and especially personal experimentation) should help us optimize this variable.
My personal retinal light exposure regimen
Over the past several months, I have been experimenting with all four of the above variables to optimize my levels of energy, alertness, emotional affect, and subjective sleep quality. After many personal experiments, my favorite daily protocol is as follows:
1. Within 15 minutes of waking, I expose my eyes to 20,000 to 40,000 lux of 5000 K light from a 240 watt LED stadium light mounted on a tripod stand. This must stay within approximately 5 feet of my face to achieve 20,000 to 40,000 lux.
2. Continue the light exposure from #1 for 14 hours per day, though this is very difficult to do, because dragging around a tripod with a stadium light mounted on it is highly inconvenient. I imagine a well-designed light visor or light therapy glasses might make this level of retinal light exposure much more convenient and energy-efficient.
I still occasionally use 5000 K, 50 W LED shop lights, as these are less expensive, and I can place them in my usual working places near my computers and on my treadmill desk. But I must be so close to them to achieve 20,000 lux that it is uncomfortable, so I essentially use these to supplement an otherwise relatively dim room, and this rarely achieves 20,000+ lux.
Unfortunately, due to the considerable inconvenience of the tripod-mounted stadium light, I have only been able to achieve 12-16 hours of exposure to 20,000 to 40,000 lux on about 33% of my days. Most days (~80%) have at least 2 hours of exposure, and about 50% of the days I have 4 hours of exposure. But even with my treadmill desk to keep me from sitting so long as to be uncomfortable, it is highly inconvenient to drag this big contraption around my house with me as I prepare and eat meals, go to the bathroom, exercise, socialize, etc.
One interesting observation about this inconvenience is that it may have helped me understand how important retinal bright light exposure is for alertness and energy level. The time of the day I most frequently feel tired is about 30 minutes after lunch. This seems like a common occurrence for many people. However, the very interesting part is that the 30 minutes before lunch is the most reliable period when I am not exposed to bright light. So, 30 minutes of meal preparation combined with 20 minutes of eating, adds up to nearly an hour in very dim lighting (< 25 lux).
With a colleague, I explored the possibility that the afternoon sleepiness that so commonly affects humans might be at least in part due to the reduced light exposure when preparing and eating the lunch meal (usually indoors). I have noticed that when I prepare a meal ahead of time, and eat the meal in front of the bright light, I rarely feel tired enough to take a nap.
Effects of my indoor lighting experiments
Since self-experimenting, I have associated multiple improvements in my quality of life with the above retinal light exposure regimen.
13. Reversal of lethargy
a. Before light experimentation, I would find it difficult to do more work than my paid work responsibilities for my clients. Once that work was done, I had little energy to do any additional work. Since using the above light exposure regimen, I find that I can work several hours longer each day, and the quality of my work—and the speed at which I work—have all increased. I suspect this is caused by the increased alertness and reduced fatigue associated with retinal bright light exposure.
14. Improved cognitive function (see improved work quality above)
15. Better sleep: sleeping 7.0 to 8.5 hours in one session, rather than broken up sleep
16. Less sleep: sleeping 7.0-8.5 hours/day, instead of 8.5 to 10 hours
a. I now notice that I feel better rested on less sleep each night. I now nap less frequently, but when I do nap, it’s for a shorter period of time (40 minutes instead of 90).
17. Reduced sleep latency (falling asleep faster)
a. I have also noticed that I am tired enough at bedtime that it takes me almost no time to fall asleep. It is almost satisfying to feel so tired when I go to sleep now.
18. Earlier waking time (6-8 AM instead of 8-9 AM)
19. Easier awakening (less grogginess).
a. Before light experimentation, on about 50% of my days, I would experience grogginess and lethargy for 1-3 hours after awakening. The incidence of this lethargy has been reduced to less than 25% of my days, and it is shorter when I do experience it.
20. Reduction of afternoon sleepiness
a. I still experience afternoon sleepiness about every third day, but both its frequency and intensity has been reduced.
21. Increased rate of dreaming I can recall the next day (3-4 days/week instead of 0)
a. For the past ~10 years, I am accustomed to experiencing dreams that I can recall, only very rarely. But over the past few months of bright light exposure, the frequency of recallable dreams has increased dramatically, to 3-4 nights per week. I suspect it may be higher, if only I could regularly achieve 12-16 hours of 20,000 to 40,000 lux of retinal light exposure every day (I still only achieve this on about 33% of my days, due to the inconvenience of transporting the light fixture I currently use).
22. Improved mood (happier, more patient)
a. I have always been a relatively happy, patient person. But the last few months of light exposure experimentation has been associated with a qualitative improvement in my mood. I feel better able to happily persist at an essentially infinite list of work projects and ambitions. I feel I am even more patient with the irrational behavior and emotional outbursts of other people. My life feels at least some degree happier and more satisfying.
23. More regular bowel movements timed with waking time (7-8 AM), rather than food intake
a. Before consistent bright retinal light exposure, my first and sometimes only bowel movement of the day used to be 1-2 hours after breakfast. Now, it happens within 1 hour of waking, before food intake. I suspect this may have to do with my waking cortisol response being elevated from retinal bright light exposure.
b. I also used to have only 1 bowel movement/day. I now have 2, within a few hours of one another, in the morning (I presume because this is when cortisol is highest: in the few hours after waking while being exposed to bright light). I occasionally have 3 bowel movements per day. I wonder what effects increased elimination might have on bowel health, colon cancer risk, etc.
24. I can not think of any negative effects that might be associated with my retinal light exposure experimentation, except eye aches from blue light exposure.
Given what I’ve observed in the scientific literature on this topic, combined with my months of self-experimentation, if we are to develop the optimal indoor retinal light exposure regimen for human health and longevity, I suspect the single most important factor is the development of a light therapy visor or glasses that can achieve a maximum of 40,000 lux and has a wireless power source that can last more than 16 hours at a time. Note that this intensity of light constricts the pupils sufficiently to make it difficult to see indoors without there also being bright ambient lighting.
If this hypothetical device were to allow the user to customize for different light intensities and exposure durations, its development and manufacture would be a terrific research tool for experimenting with retinal light exposure, both for personal experimenters such as myself, and for rigorous clinical and research settings, such as the Alzheimer’s studies summarized herein.
Origin of and support for this article
Interest in this article arose from a combination of my ongoing interest in this topic and conversations with Dave Gobel, CEO of Methuselah Foundation. My work on this article was sponsored by Methuselah Foundation.
I remind readers that the above report includes my personal research and self-experimentation, i.e. an “n-of-1” experiment. Your experience with the same parameters may give you very different results. Nothing here is to be taken as a recommendation in any particular person’s case. This report is intended to inspire a starting point for your own personal experimentation, or as a basis for designing clinical or experimental research.