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Can Humans Suffer from Light Deficiency? (Part 3)

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.

Putting it all together

Having now explored the many interesting observations I considered during this research investigation, I’ll now concisely summarize the hypothesis I’ve developed in this article series:

Chronic retinal light deficiency might be a condition that humans can suffer from. It is associated with relatively lower nighttime melatonin secretion, insomnia, increased fatigue, reduced daytime alertness, and a higher incidence of depression. It might also be a causative factor in the development or progression of Alzheimer’s disease. Moreover, some of the “age-related” brain atrophy observed in humans might be, to some extent, in fact an environmentally induced condition and not age-related per se. Inversely, consistent, long-term retinal bright light exposure might have multiple positive effects on human health, ultimately resulting in enhanced maintenance of global tissue health and function during aging including the preservation of normal sleep patterns in particular, with additional beneficial effects on heightened alertness, reduced fatigue, and a reduction in the risks of insomnia and depression. 

The following is my reasoning about why the avoidance of chronic retinal light deficiency might have remarkable benefits for human health:

  1. Retinal bright light exposure during the day suppresses melatonin production during the day. This is associated with enhanced daytime alertness, reduced fatigue, and a longer waking day.
  2. Sleep that follows hours-long daytime bright light exposure involves considerably higher melatonin level during sleep, at least in some groups. It has been reported to increase by nearly 50% in at least one study of elderly people (Mishima et al., 2001). 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.
  3. Melatonin has been observed in multiple studies to enhance growth hormone secretion (e.g. see Valcavi et al. (1993) for this observation in humans, and Zhang et al. (2016) for this observation in chickens).
  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 might result in improved tissue maintenance and function during human aging.
  6. I speculate that retinal bright light exposure might 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” (abbreviated 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. (1998) 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. (2018)). And there is some evidence that BDNF is affected by retinal light exposure. For example, Molendijk et al. (2012) 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. (2012) 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. (2015) 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.” Based on this evidence, it is reasonable to suspect that chronic deficiency of retinal bright light exposure might cause a chronic reduction in circulating BDNF level, which in turn might induce or accelerate brain atrophy.
  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. (2018) 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 might 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 (2,000 to 20,000 lux) for 8-14 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 intensity and duration of retinal light exposure is difficult to achieve. 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 higher-intensity light at the eye, compared to commonly used indoor lighting (overhead bulbs). However, I could find no device currently on the market that has the color spectrum, intensity, and battery capacity to achieve the goal of simulating natural outdoor light intensity on the human retina while indoors.

The above explanation 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 (8,000+ lux) than modern indoor-dwelling humans do (< 50 lux). 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 possibly played an important role in deteriorating the quality of or outright destroying many millions (billions?) of human life-years.

If one is going to change one’s personal ambient lighting environment, it is important to know exactly what I mean by the terms “color spectrum, “timing”, “intensity”, “duration” so one can choose the proper equipment and time of the day to expose oneself to the light. In Part 4, I summarize the lighting equipment I have experimented with in my efforts to expose my eyes to the color spectrum, intensity, timing, and duration of light that has been reported in scientific studies to enhance nighttime melatonin secretion, growth hormone secretion, slow-wave sleep, the waking cortisol response, and mood as described in Parts 1-3. I’ll also tell you how these experiments made me feel and make some equipment recommendations in the case readers want to experiment on enhancing their personal ambient lighting environment.

You can find Part 4 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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