As strange as it sounds, upon examining the scientific data on the relationships between bright light exposure and things like growth hormone secretion, nighttime melatonin level, and neurodegeneration, I think there is a credible case to be made that many modern people could be suffering from negative effects of chronic light deficiency. In this article series, I report on my thorough exploration of the scientific literature related to the topics of retinal light exposure and its effects on and relationships with nighttime melatonin secretion, nighttime growth hormone secretion, the morning waking (cortisol) response, fatigue, daytime alertness, and Alzheimer’s disease. I also report on my self-experimentation with bright light therapy and give some equipment and light exposure protocol recommendations based on my experiences.

Introduction to this article series

Light exposure on the retina of the eye has 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; note that “lux” is a unit of measure of illuminance, and is equivalent to one lumen per square meter).

Even though humans presumably spent most of their time outdoors throughout much of their evolutionary history, many modern humans have very limited exposure to what might be considered “normal” intensities and durations of light exposure, and this retinal light deficiency might have significant negative effects on human health.

Note that I mention the term “retinal” which refers to the retina in the back of the eye which sends light signals to the brain via the optic nerve. I will use this term throughout this article series to distinguish retinal light exposure from light exposure on the skin, such as may be desirable for enhancing vitamin D synthesis and/or possibly reducing serum cholesterol (Patwardhan et al., 2017).

In this article series, I explore some of these possible negative health implications of what we might call “retinal light deficiency”. These  include reduced nighttime melatonin secretion, reduced slow-wave sleep, reduced growth hormone secretion, impaired morning awakening response, higher prevalence of fatigue, elevated risk of depression, a possible causative factor in Alzheimer’s disease, and even an association with elevated incidence of death from any cause. I also describe some of my self-experimentation with enhancement of indoor light exposure and make some suggestions for how readers can achieve potentially 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 scientific literature explored herein, I speculate that neurodegenerative diseases such as Alzheimer’s might even be caused by decades-long retinal light deficiency, though I admit I found little direct evidence to support this hypothesis.

To address insufficient modern 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 light deficiency indeed exists). At the end of this article series, I give specific equipment recommendations based on my personal experiences and measurements of the illuminance (lux) of the equipment I tested and used.

Let’s start with some basic information about the eye and how light exposure in the eye affects the brain and body.

Light Exposure, the Eye, and the Brain

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, if only through the actions of hormones.

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.

 

 

Next, let’s explore the relationship that many readers will already know about: the relationship between retinal light exposure and nighttime melatonin secretion.

Retinal Light Exposure and Melatonin

From my perspective, it appears as though the relationship between melatonin production and retinal light exposure has been popular over the past 10 years. More specifically, many bloggers have made mention of the observation that retinal light exposure (and especially blue light exposure) can impair the nighttime secretion of melatonin. Because an elevation in melatonin is associated with higher-quality sleep, this could be relevant to optimizing one’s evening and nighttime light habits to reduce light exposure and consequently (hopefully) enhance nighttime melatonin secretion and improve sleep quality. For example, knowing that bright light and/or blue light can reduce melatonin secretion before and during sleep might motivate a person to install software on phones and computers that will selectively reduce blue hues in the evening hours or even wear “blue-blocking” eyeglasses in the evenings.

Indeed, some scientific studies have reported that light exposure is associated with reduced melatonin secretion. For example, Hanford and Figueiro (2013) reported the color and illuminance required by different light bulbs to achieve a 50% melatonin suppression after one hour of exposure (see Table 2 in their manuscript). They reported that the “warmer” (more red/orange) the color spectrum of the bulb, the greater the illuminance required to achieve 50% melatonin suppression. The warm color spectrum of 2,700-4,000 K required approximately 1,000 lux to achieve 50% melatonin suppression in one hour, while daylight bulbs of 5,000-6,000 lux required 500 lux, and blue-only LED bulbs required only 50 lux.

You can see Table 2 below:

However, there is an observation about retinal light exposure and melatonin that I’ve never heard discussed in the popular science media or by popular health websites, and that is the relationship between bright light exposure and enhanced melatonin secretion. Yes, you read that correctly. Prolonged bright light exposure early in the day has been shown to enhance melatonin secretion at nighttime. This observation has me concerned that many people who suspect nighttime light exposure as the cause of their poor sleep quality might be mistaken about the cause of their sleeplessness. It might not be nighttime light exposure. It might be daytime light deficiency.

This observation was reported in a remarkable way in a study by Mishima et al. (2001). In that study, Mishima and colleagues convinced 10 elderly insomniacs to agree to bright light exposure each day.  The researchers measured melatonin secretion every hour for 24 hours before and after this period of bright light exposure. The insomniacs were found to have significantly lower melatonin secretion than non-insomniac healthy control people.

For 4 weeks, the elderly insomniacs were exposed to 4 hours of bright light (~2,400 lux)—for two hours between 10 AM and 12 PM, then again between 2 PM and 4 PM. At the end of the study, these elderly insomniacs were found to have melatonin secretion that was no different than healthy young control participants. You can see this effect in the image I adapted from Figure 1 in Mishima et al. (2001), shown below.

These results are remarkable because they suggest (1) that low nighttime melatonin secretion can be restored to normal with prolonged daytime bright light exposure, and (2) that the sometimes-reported observation of lower melatonin secretion in elderly people might be caused by inadequate bright light exposure during the day and might not be an inevitable consequence of degenerative aging.

Touitou (2001) reviewed the scientific literature about the possibility of an age-related decline in melatonin secretion. In their report, Touitou described a relevant study by Zeitzer et al. (1999) 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 lighting regimen…

The findings of these two studies (Mishima et al. (2001) and Zeitzer et al. (1999)) suggest that older people might have difficulty sleeping not because they experience an age-related reduction in melatonin secretion, but because they get less bright light exposure. One might presume this could be caused by less time outdoors.

If these findings are representative of what happens during human aging, they might have very important implications for how we think about age-related degeneration as well as our choices about our personal lighting environments. The point about one’s lighting environment seems obvious, but the point about age-related degeneration might be less obvious. These studies have implications for how we think about age-related degeneration because of the associations between bright light exposure and factors such as sleep quality, growth hormone secretion, alertness, and fatigue, with sleep quality alertness, and fatigue being related to cognitive performance and growth hormone being associated with body composition and maintenance of lean mass with aging. Next, let’s explore the association between retinal light exposure and these factors.

Retinal light exposure and sleep quality, growth hormone, alertness, and fatigue

When analyzed in a certain way, sleep can be characterized by distinct phases. Each phase can be characterized by the frequency of electrical activity in the brain. You have might have heard of “REM sleep” or “slow-wave sleep” or “deep sleep”, which are examples of distinct phases of brain activity during sleep. There is a significant amount of scientific research that associates retinal light exposure to the phase of sleep called “slow-wave sleep”—also called “deep sleep” or NREM sleep (an acronym meaning “non-REM “). This relationship between retinal light exposure and slow-wave sleep is interesting because of the strong link between slow-wave sleep and growth hormone secretion. So, let’s first discuss the association between retinal light exposure and slow-wave sleep.

According to Wikipedia:

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.

Interestingly, one study by Wams et al. (2017) 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 their research report, 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.

A research paper by Van Cauter and Plat (1996) reported:

…in men, approximately 70% of the growth hormone pulses occur during slow-wave sleep.

In a different paper, Van Cauter et al. (2000) 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.

These relationship are interesting because if the intensity and duration of bright light exposure strongly influences slow-wave sleep, and slow-wave sleep strongly influences growth hormone secretion, then we might be able to enhance growth hormone secretion by enhancing our lighting environments. Growth hormone has many important effects in the body (Wikipedia), including a mobilization of body fat for use as energy and as a stimulus for the liver to manufacture the anabolic hormone called IGF-1. IGF-1 can have important systemic effects on the body because IGF-1 can enhance the growth of bones, muscles, and organs—effects which might benefit older people suffering from conditions like osteoporosis and sarcopenia (characterized by bone and muscle loss, respectively).

Unfortunately, I could not find studies reporting a direct association between retinal 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. (1998) 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 that study, Zhang et al.(2016) 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

Retinal light exposure, the awakening response, daytime alertness, and fatigue

Personally, I found the relationships between retinal light exposure and the secretion of melatonin and growth hormone to be remarkable, in part because it suggests that the often-observed decline in both hormones with age might actually be in large part caused by insufficient retinal light exposure and not by age-related processes. Some scientific reports about the relationship between retinal light exposure and daytime alertness and fatigue make light exposure seem even more important than I had initially understood when I first investigated this topic in great detail.

The hormone cortisol is one important factor that influences when we wake up (Steptoe and Serwinski, 2016). A higher peak cortisol response is associated with less grogginess and greater alertness after waking in the morning. Regular bright light exposure shortly after awakening has been shown by Leproult et al. (2001) to considerably enhance this cortisol response. In that study, the authors 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.

I want to emphasize that this effect was only found with bright light exposure shortly after waking and wasn’t observed if the first instance of bright light exposure occurred in the afternoon. These effects were observed in the group of study participants that were exposed to bright light continuously between 5 AM and 8 AM in an escalating manner from between 2,000 lux and 4,000 lux, then back to 2,000 lux. Frankly, this strikes me as a protocol that isn’t very practical for someone not participating in a controlled scientific study, but it suggests that 2,000-4,000 lux shortly after waking might have these benefits on daytime alertness.

Also note that the suppression of melatonin secretion may have an additional energy- and alertness-enhancing effect. I found numerous reports, such one by Arendt (2009), noting that melatonin supplements can induce sleepiness, even during the day. So bright light exposure shortly after waking not only raises cortisol (which enhances alertness), but also suppresses melatonin secretion, which might be an additional mechanism by which it reduces fatigue and enhances alertness.

Focusing on the specific wavelengths (colors) of light that might affect wakefulness, Figueiro and Rea (2012) studied the effect of blue light exposure (470 nm at 40 lux) for 80 minutes, shortly after awakening, on sleep-restricted adolescents. They found the cortisol awakening response to be considerably enhanced—by over 100%—with this blue light exposure protocol 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. (2009) 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. (2013) also reported that the cortisol awakening response is associated with fatigue.

For readers who would like to get more done during the day, one study by Wehr (1991) might interest you. In this study, the researcher exposed study participants to light for either 16 hours or 11 hours per day. He found that those people exposed to the long, summer-like, 16-hour daily light period slept an average of 7.7 hours per night, while those exposed to only 11 hours of light per day slept for a remarkable 11 hours per night. Consistent with this, the researcher also found that when participants were exposed to a shorter daily duration of light, they had a longer period of daily melatonin secretion. This might be part of what kept the short-light group relatively tired and sleeping such long hours. In summary, the shorter light period the study participants were exposed to, the longer they secreted melatonin and the longer they slept at night. The results of this small study suggest that retinal light exposure may have profound effects on our length of sleep and how much time we have to accomplish things during the day before we get tired. In other words, longer periods of bright light may give us the energy to have a longer, more active waking day.

Conclusion of Part 1

This is a good point to conclude Part 1 of this article series on the potential for humans to suffer from retinal light deficiency. In Part 2 of this series, I explore the relationships between retinal light exposure and cognitive function, Alzheimer’s disease, and its association with longevity.

You can read Part 2 here.

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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. This article series is based on research that was sponsored by Methuselah Foundation.