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Can Humans Suffer from Light Deficiency? (Part 2)

In Part 2, I explore the relationships between retinal light exposure and Alzheimer’s disease, and in particular, sundowning in Alzheimer’s disease. I also explore the association between light exposure and longevity.

In Part 1, I suggested that there is sufficient scientific evidence that one could credibly speculate that humans can suffer from retinal light deficiency. I explored the relationships between retinal light exposure and melatonin secretion, slow-wave sleep, growth hormone secretion, daytime alertness, and the duration of a person’s waking day. In Part 2, I focus more specifically on the relationships between retinal light exposure and cognitive function with a special focus on Alzheimer’s disease.

Let’s get started with a quote from Part 1 from the National Sleep Foundation’s explanation of the relationship between melatonin and sleep, which will remind us of some physiological relationships between the biological structures and responses relevant to what I’ll discuss in this article (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 (2013) estimate that people with Alzheimer’s disease typically spend about 40% of their nighttime 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. (2016) might 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 whether one factor is the clear cause of the other.

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. (2016)). 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 (2010) 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. (2016) 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. (2016) 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. (2016) 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.

(Canevelli et al. (2016) presented a convenient summary of these studies in Table 2, which I invite readers to review.)

Regarding light exposure, Canevelli et al. (2016) 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 (2013) 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. (2018) 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;

In Part 1 of this series, I explored the observation that daytime bright light exposure enhances nighttime melatonin secretion. Given this relationship between light exposure and melatonin secretion, it might make sense to test the administration of melatonin in people with Alzheimer’s to see if it helps improve sundowning symptoms, if not Alzheimer’s disease more generally. And indeed, there have been some studies testing the use of melatonin for sundowning in Alzheimer’s.

Melatonin supplementation for sundowning and Alzheimer’s disease

Regarding the studies on melatonin supplementation for sundowning, Canevelli et al. (2016) 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. (2010) 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.

This is speculation, but I wonder if, once the brain atrophy occurs during Alzheimer’s disease (and human aging more generally (Peters (2006)), 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 structures controlling the responses to bright light might no longer function properly. If the reports of brain tissue destruction during Alzheimer’s are accurate, then one might doubt that any amount of retinal bright light exposure is going to stimulate brain rejuvenation sufficiently to replace the estimated 20-40% decline in brain weight between ages 20 and 100 (Svennerholm et al., 1997). At that point, perhaps the brain needs replacement and rejuvenation of cells and myelin much more than it needs retinal light exposure.

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 over the lifespan might help prevent the less severe age-associated brain atrophy in people without Alzheimer’s disease.

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 reasonably intuitive concerns about sun exposure increasing the risk of skin cancer, one would think that avoiding sun exposure would be good for longevity. But Lindqvist et al. (2016)  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 article series 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.

Further regarding this potential relationship between retinal light exposure and mortality is the connection between retinal light exposure and sleep quality. That is, perhaps insufficient light exposure contributes to the development of insomnia, and it is the associated insomnia that might reduce lifespan. Multiple studies referenced above report that retinal light exposure is associated with an improvement in sleep quality or treatment of insomnia. And there is an association between Alzheimer’s disease (a significant cause of death) and sleep disturbances, as well as a reported association between sleep disturbances and early mortality. For example, Sivertsen et al. (2014) 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 by way of its impairment of the circadian rhythm and reduction in sleep quality and duration.

Conclusion of Part 2

This concludes Part 2 in this article series exploring the possibility that humans might be capable of suffering from retinal light deficiency.

In Part 3, I provide a concise summary and synthesis of my findings on this topic for convenient review and consideration. In this detailed summary, I will also include some research findings on retinal light exposure, the hormone BDNF, and the potential for enhanced indoor lighting to reduce the incidence or intensity of depression and its associated medication use.

You can find Part 3 here.

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.

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