The Profound Impact of Light on Human Health and Metabolism

Light has played a crucial role in shaping the behavior and physiology of most species on Earth. For diurnal animals, including humans, natural daylight has been a key regulator of wakefulness, while the onset of darkness signals the time for sleep. This light–dark cycle has been a constant throughout most of our evolutionary history. However, the advent of artificial light has dramatically altered these natural patterns, extending human activity into the night and giving us control over when and how we engage with our environment. While these advancements have brought about numerous benefits, they have also introduced significant challenges to our health.
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One of the most critical issues arising from the use of artificial light is its impact on sleep and circadian rhythms. The human circadian rhythm, which regulates our sleep-wake cycle, is highly sensitive to light. Disruptions in this rhythm due to irregular light exposure have been linked to various health problems, including sleep disturbances and an increased risk for obesity and metabolic disorders. These conditions have been on the rise globally, partly due to our altered light exposure patterns.

Light is detected by specialized photoreceptors in the retina, including rods, cones, and intrinsically photosensitive retinal ganglion cells (ipRGCs). While rods and cones are primarily responsible for image formation, ipRGCs play a crucial role in non-visual responses to light, such as circadian entrainment and sleep regulation. These cells are particularly sensitive to light at around 480 nm (blue light), which is known to have strong effects on circadian rhythms. The ipRGCs transmit light information to the brain's central circadian pacemaker, the suprachiasmatic nucleus (SCN), which regulates the release of melatonin from the pineal gland. Melatonin is a key hormone that promotes sleep and helps maintain the circadian rhythm by signaling the body when it’s time to sleep.

Beyond sleep regulation, light exposure also influences energy metabolism. During the deepest stage of non-rapid eye movement (NREM) sleep, known as slow-wave sleep (SWS), energy expenditure is at its lowest, indicating that sleep serves as a period of energy conservation. The SCN also drives daily rhythms in the concentrations of various hormones linked to metabolism, such as insulin, glucagon, and corticosterone, which in turn influence energy balance and substrate utilization in the body.
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The disruption of natural light cycles, particularly through exposure to artificial light at night, can therefore have wide-ranging effects on both sleep and metabolic health. Understanding these mechanisms is critical as we navigate the modern world, where artificial light is ubiquitous and often unavoidable. Balancing our exposure to natural and artificial light may be key to maintaining optimal health and well-being.

Light Intensity on Sleep and Metabolism

The central circadian clock in the SCN is highly sensitive to external light cues, with characteristics such as intensity, duration, timing, and wavelength playing critical roles in regulating sleep and circadian rhythms. Each of these light properties has specific effects on human physiology, with varying degrees of influence depending on their combination and context.

Natural light intensities can range dramatically, from the intense midday sunlight of 20,000 to 100,000 lux to the much dimmer artificial indoor light, which typically ranges between 14 and 430 lux. Human exposure to these varying light levels can significantly influence physiological processes, especially when these exposures occur at night.

Studies have shown that increased light intensity at night can disrupt sleep and shift circadian rhythms. For example, continuous illumination during the dark phase in mice has been linked to increased body mass and reduced glucose processing, even without changes in food intake or activity levels. Similarly, in humans, increasing light intensity at night can lead to melatonin suppression and increased alertness, indicating a phase shift in the circadian rhythm. Epidemiological studies have also documented a relationship between light intensity at night and metabolic health. For instance, brighter bedroom environments have been associated with a higher risk of obesity and metabolic disorders, such as diabetes.

Moreover, even low levels of light at night (as low as 5 lux) can disrupt sleep architecture, leading to changes in sleep stages and a decrease in total sleep time. This disruption in sleep has secondary effects on metabolism, potentially increasing the risk for insulin resistance and other metabolic issues.

In addition to intensity, the duration and timing of light exposure are crucial. Prolonged exposure to artificial light at night can exacerbate its disruptive effects on sleep and circadian rhythms. The timing of light exposure is equally important, with evening exposure being particularly detrimental. Late-day light exposure can delay the onset of melatonin secretion, shifting the circadian rhythm and leading to difficulties in falling asleep and maintaining sleep.

Furthermore, light exposure in the evening has been shown to increase the risk of metabolic disorders. For instance, studies have found that individuals exposed to light in the evening are more likely to develop insulin resistance, which can lead to type 2 diabetes. This effect is partly mediated by the impact of light on the sympathetic nervous system, which regulates glucose metabolism.

While intensity and duration are significant, the wavelength or spectral composition of light also plays a critical role. Blue light, with a wavelength around 480 nm, is particularly effective at suppressing melatonin and disrupting sleep. This has implications for the use of screens and devices that emit blue light, especially in the hours leading up to bedtime.
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Other characteristics, such as the color temperature of light, flickering, and the type of light source (e.g., LED vs. OLED), also influence physiological responses. For instance, light-emitting diodes (LEDs) often have higher blue light content compared to organic light-emitting diodes (OLEDs), making them more likely to disrupt sleep and circadian rhythms.

Duration and timing of Light Exposure

The duration of light exposure significantly affects sleep and circadian rhythms in a dose-dependent manner. Research has shown that even a single session of high-intensity light exposure can have profound effects. In a study involving 39 healthy young adults, exposure to 10,000 lux light for varying durations (ranging from 0.2 to 4.0 hours) led to dose-dependent suppression of melatonin and shifts in circadian rhythm. This finding underscores the sensitivity of the circadian system to prolonged light exposure, particularly at high intensities.

The effects of light exposure duration extend beyond circadian disruption and impact metabolic health as well. For instance, in a study of 48 young children, prolonged exposure to light above 200 lux was associated with increased body mass index (BMI), even when controlling for sleep duration, timing, and activity levels. Additionally, observational studies have linked extended screen time, a form of prolonged light exposure, to an increased risk of overweight and obesity in children and adolescents. A meta-analysis further supported this association, highlighting the metabolic consequences of extended exposure to light from electronic devices.

The nature of light exposure, however, is complex. Circadian phase shifts can occur even with brief, intermittent light exposure. In one study, as little as 60 minutes of 2-millisecond light pulses in the evening led to significant phase delays in the circadian rhythm of participants. This finding suggests that not only continuous light exposure but also intermittent light patterns can disrupt circadian timing and potentially affect metabolism.

The timing of light exposure plays a crucial role in determining its impact on the circadian system. Depending on whether light exposure occurs in the early or late evening, the circadian rhythm may either advance or delay. This has important implications for sleep quality and metabolic regulation. For example, exposure to light in the late evening is more likely to phase delay the circadian system, leading to difficulties in falling asleep and potential metabolic disruptions.
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In summary, both the duration and timing of light exposure are critical determinants of their effects on sleep and metabolism. Prolonged and mistimed light exposure, whether continuous or intermittent, can lead to circadian misalignment and adverse metabolic outcomes. Understanding these dynamics is essential for mitigating the potential negative health effects of artificial light in modern environments.

Morning light exposure

​Morning bright light exposure is widely recognized as an effective treatment for individuals with Seasonal Affective Disorder (SAD) and winter depression, helping to shift the circadian rhythm and potentially improve metabolic states. Research has shown that such exposure can lower the resting metabolic rate (RMR) in SAD patients and may lead to reductions in body weight and depressive symptoms. Studies also indicate a potential influence on glycemic control, as observed in diabetic patients with winter depression, though the effects on metabolism in individuals without depression are less consistent. The combination of morning light therapy and exercise has shown promise in reducing body fat among overweight individuals. Additionally, morning bright light is effective in improving sleep, making it a viable non-invasive treatment for circadian rhythm and metabolic disorders. Further research is needed to explore these benefits across different populations.

daytime light exposure

Daytime light exposure in animals is often considered a “dead zone” in the circadian phase-response curve, where light does not significantly reset the circadian rhythm. The presence of this "dead zone" in humans remains uncertain due to differences in activity patterns between diurnal and nocturnal species. Few studies have explored how daytime light exposure impacts human metabolism.

Research shows mixed results: 14 hours of daytime light exposure did not significantly affect 24-hour energy expenditure or fat and carbohydrate oxidation in healthy individuals. However, dim daytime light combined with bright evening light reduced the usual rise in postprandial glucose in insulin-resistant older adults. Additionally, daytime light treatment in individuals with SAD led to weight loss and increased oxygen consumption. Dim light during the day also affected digestion, leading to signs of carbohydrate malabsorption and reduced gastric activity.
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Daytime light exposure can also influence metabolism during sleep, with studies indicating that dim daytime light and bright evening light may decrease the sleeping metabolic rate. These findings highlight the significant role of daytime light conditions in sleep and overall energy metabolism, warranting further investigation into their long-term health implications.

evening light exposure

Extended light exposure during the dark phase can significantly disrupt metabolism. In animals, constant light exposure reduces the amplitude of the circadian rhythm in the suprachiasmatic nucleus (SCN), increases food intake, decreases energy expenditure, and leads to weight gain and reduced insulin sensitivity. This exposure disrupts the regular circadian rhythm and peripheral clocks, contributing to metabolic imbalances.
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In humans, evening and prolonged light exposure are linked to higher body weight, increased BMI, and a greater risk of obesity. Actigraphy studies have shown a positive correlation between mean light exposure timing, BMI, and sleep midpoint, indicating the role of light in metabolic regulation.
Shift workers, who are exposed to light during atypical hours, consistently show higher risks of metabolic disorders, including overweight, obesity, diabetes, and metabolic syndrome. This population often faces circadian disruption, sleep deprivation, and irregular eating patterns due to their work schedules, further complicating metabolic health.

Evening light exposure also affects energy metabolism during sleep. Studies have shown that exposure to bright light before sleep increases respiratory quotient and decreases fat oxidation, suggesting a shift towards carbohydrate metabolism. This is accompanied by a suppression of melatonin, a hormone crucial for regulating sleep and metabolic processes.

Furthermore, evening light exposure can impair carbohydrate digestion and increase glucose intolerance and insulin insensitivity, especially when combined with disrupted sleep and circadian misalignment. Shift workers and individuals with night eating syndrome are particularly vulnerable to these metabolic disturbances, often showing a preference for high-fat foods and altered dietary intake patterns.

Understanding the timing and intensity of light exposure, along with dietary habits, is essential for minimizing metabolic consequences, particularly in populations with atypical light exposure, such as shift workers. Proper management of light exposure and food intake timing can help maintain circadian rhythm and support healthier metabolic outcomes.

Role of melatonin

In humans, the activity of the suprachiasmatic nucleus (SCN) is often gauged through endogenous melatonin levels, with nighttime production typically ranging from 10 to 80 μg in young adults. Peak melatonin concentrations vary widely, with one study reporting levels between 2 and 84 pg/mL among a group of 170 individuals. Although melatonin secretion is primarily driven by photic input, its receptors are distributed throughout the body in areas beyond the pineal gland, such as the retina, gastrointestinal tract, bone marrow, skin, and lymphocytes. This widespread distribution means that melatonin’s influence extends beyond regulating sleep and circadian rhythms, playing significant roles in thermoregulation and energy metabolism.
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Research has demonstrated the critical role of melatonin in metabolic processes. Animal studies involving pinealectomy, which removes the source of melatonin, have shown that the absence of melatonin leads to metabolic abnormalities, including diminished glucose tolerance, reduced glycogen storage in the liver and muscles, and insulin resistance—conditions that mirror those found in diabetogenic syndrome. In humans, similar findings have been observed, with reduced melatonin amplitude and blunted rhythms reported in individuals with type 2 diabetes. Additionally, melatonin interacts with insulin, particularly in individuals with metabolic syndrome, highlighting its vital role in maintaining energy balance and metabolic health.

Melatonin Supplementation

Exogenous melatonin has been widely studied for its effectiveness in managing sleep disorders and circadian rhythm disruptions, particularly in individuals experiencing jet lag, shift work, or visual impairments. Earlier research has established its role in improving sleep quality and aligning circadian rhythms in these populations. Beyond its influence on sleep, melatonin has garnered attention for its potential effects on human metabolism, particularly in the regulation of lipid and glucose metabolism.

In women with obesity, studies have highlighted a negative correlation between melatonin supplementation and BMI, suggesting potential benefits for weight management. For instance, a three-week randomized crossover trial involving individuals with type 2 diabetes and insomnia revealed that melatonin treatment improved sleep efficiency and reduced wakefulness after sleep onset, though it did not significantly impact glucose or lipid metabolism. Another study focusing on normolipidemic postmenopausal women found that a two-week course of melatonin (6 mg nightly) led to an increase in plasma triglyceride and VLDL cholesterol levels, underscoring the hormone's complex metabolic effects.

The benefits of melatonin extend to the shift-working population, where its administration has been shown to alleviate circadian misalignment and enhance sleep quality, alertness, and energy intake. Notably, a randomized crossover trial demonstrated that melatonin (3 mg) reduced body weight, BMI, waist circumference, and hip circumference in shift workers without altering caloric intake, alongside a significant reduction in circadian misalignment. Another trial over 12 weeks in female shift workers with elevated BMI reported that melatonin administration did not significantly affect energy intake or food choices, indicating that melatonin's effects on weight may be independent of dietary factors.

Interestingly, the interaction between melatonin and light exposure has also been explored, revealing varying effects on metabolism. For example, in a study involving healthy males, nighttime melatonin administration under bright light conditions increased leptin levels and reduced hunger, along with improvements in glucose tolerance and insulin sensitivity. However, contrasting findings were observed in healthy females, where melatonin impaired glucose tolerance, suggesting a potential decrease in insulin sensitivity. These mixed results, likely influenced by differing light conditions across studies, highlight the need for future research to clarify the interplay between melatonin and environmental light.

In summary, while exogenous melatonin shows promise in improving sleep and potentially influencing metabolic outcomes, its effects are nuanced and may vary based on individual factors such as light exposure and underlying metabolic conditions.

Natural sources of melatonin

Melatonin, a hormone that follows a daily rhythm in vertebrates, also exists in various non-animal sources, such as unicellular algae, food plants, and medicinal herbs. This naturally occurring melatonin can be found in fruits, vegetables, grains, and beverages like coffee, tea, beer, and wine. Some foods, particularly cranberries, coffee, and certain herbs, are known to contain high levels of melatonin. Additionally, melatonin is present in meats like lamb, beef, pork, chicken, and fish. However, the impact of melatonin from these food sources on human physiology, particularly sleep, remains an area of ongoing research, as the concentration of melatonin in foods can vary significantly.

Fruits such as sour cherry, also known as Montmorency cherry, are particularly noted for their high melatonin and tryptophan content, both of which are linked to improved sleep. In studies involving healthy adults, consuming tart cherry juice for a week significantly increased melatonin levels and improved sleep parameters, including total sleep time and sleep efficiency. The sleep-promoting effects of cherry-based products have been further explored in older adults and individuals with insomnia, where improvements in sleep duration, sleep quality, and reduced wakefulness after sleep onset were observed. Moreover, studies on fruits like pineapple, oranges, and bananas have demonstrated elevated serum melatonin concentrations following their consumption, suggesting a potential role in sleep enhancement.

Milk, which naturally contains both tryptophan and melatonin, has also been investigated for its potential to improve sleep. However, the melatonin content in milk can vary widely, making it challenging to measure its exact impact on sleep. Research involving melatonin-enriched milk has shown promising results, particularly in young adults, where significant improvements in sleep satisfaction and reductions in daytime sleepiness were noted. In children, while milk-based evening drinks did not significantly affect overall sleep time, they did reduce nocturnal awakenings and improved memory recall, indicating some benefits. The use of fermented milk with probiotics, such as Lactobacillus casei strain Shirota (LcS), has also shown to improve subjective sleep quality and reduce sleep latency under stressful conditions.

​Grains, including rice, corn, barley, and whole grains, have been identified as high in melatonin, and their consumption has been associated with better sleep quality. For example, a study on cereal enriched with tryptophan demonstrated improvements in sleep efficiency and total sleep time in older adults. The potential hypnotic effects of food-derived tryptophan have also been explored, with evidence suggesting that tryptophan-rich foods, such as de-oiled gourd seeds, can improve insomnia when combined with carbohydrates. Additionally, tryptophan supplementation, particularly when paired with daytime light exposure, has been shown to promote evening melatonin secretion and enhance sleep.

In summary, while melatonin is present in a wide variety of foods, its effectiveness in improving sleep and metabolism requires further investigation. The interaction between melatonin and other nutrients within these foods, as well as the role of environmental factors like light exposure, is complex and necessitates well-controlled studies to fully understand its impact on human health.

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References

Ishihara, Asuka, et al. “The Complex Effects of Light on Metabolism in Humans.” Nutrients, vol. 15, no. 6, 14 Mar. 2023, pp. 1391–1391, https://doi.org/10.3390/nu15061391.