sabato, Luglio 24, 2021
HomeHealthCareExtended exposure to light during nighttime can have negative consequences for human...

Extended exposure to light during nighttime can have negative consequences for human health

Extended exposure to light during nighttime can have negative consequences for human health. But now, researchers from Japan have identified a new type of light with reduced consequences for physiological changes during sleep.

In a study published this month in Scientific Reports, researchers from University of Tsukuba compared the effects of light-emitting diodes (LEDs), which have been widely adopted for their energy-saving properties, with organic light-emitting diodes (OLEDs) on physical processes that occur during sleep.

Polychromatic white LEDs emit a large amount of blue light, which has been linked with many negative health effects, including metabolic health.

In contrast, OLEDs emit polychromatic white light that contains less blue light. However, the impact of LED and OLED exposure at night has not been compared in terms of changes in energy metabolism during sleep, something the researchers at University of Tsukuba aimed to address.

“Energy metabolism is an important physiological process that is altered by light exposure,” says senior author of the study Professor Kumpei Tokuyama. “We hypothesized that compared with LEDs, OLED exposure would have a reduced effect on sleep architecture and energy metabolism, similar to that of dim light.”

To test this hypothesis, the researchers exposed 10 male participants to LED, OLED, or dim light for four hours before they slept in a metabolic chamber. The researchers then measured energy expenditure, core body temperature, fat oxidation, and 6-sulfatoxymelatonin – which is a measure of melatonin levels – during sleep. The participants had not recently traveled or participated in shift work.

“The results confirmed part of our hypothesis,” explains Professor Tokuyama. “Although no effect on sleep architecture was observed, energy expenditure and core body temperature during sleep were significantly decreased after OLED exposure. Furthermore, fat oxidation during sleep was significantly lower after exposure to LED compared with OLED.”

In addition, fat oxidation during sleep was positively correlated with 6-sulfatoxymelatonin levels following exposure to OLED, suggesting that the effect of melatonin activity on energy metabolism varies depending on the type of light exposure.

“Thus, light exposure at night is related to fat oxidation and body temperature during sleep. Our findings suggest that specific types of light exposure may influence weight gain, along with other physiological changes,” says Professor Tokuyama.

Many occupations and activities involve exposure to artificial light before sleep. New information about the effects of different kinds of light on physical processes may facilitate the selection of alternative light sources to mitigate the negative consequences of light exposure at night. Furthermore, these findings advance our knowledge regarding the role of light in energy metabolism during sleep.


In 2016, nearly 40% of adults worldwide were reported to have overweight and 13% were reported to have obesity (1). Overweight and obesity are associated with type 2 diabetes and cardiovascular disease. As the development of these diseases can in large part be ascribed to lifestyle, it is important to look at societal changes.

Over the past century, we have gotten used to abundant food often rich in fat and refined carbohydrates. Cars, public transportation, and office jobs have reduced the need for physical activity. Moreover, we have shifted away from nature’s 24‐hour day/night rhythm toward a society in which people work around the clock, stay out late, and have their screens on until the early hours.

Most organisms, including mammals, have developed an endogenous circadian timing system under the earth’s natural 24‐hour rhythm that is adapted to the regular alternation of light and dark phases. Thus, it seems likely that changing these conditions will impact physiology. The aim of this review is to summarize the current evidence on the impact of exposure to light at night (LAN) on metabolic parameters and present an anatomical framework through which this may happen.

Our modern society exposes us to various types of artificial LAN. Outdoor artificial LAN caused by street lighting is usually low in intensity and chronically present. Shift work, on the contrary, exposes us to single nights of bright light. The usage of screens exposes us to light of shorter wavelengths and might thus impact metabolism differently.

The aim of this review is to summarize the current evidence of the impact of exposure to LAN on metabolic parameters as well as an anatomical framework through which this may happen. To properly map the effects of different exposures of LAN, a distinction will be made between chronic and acute LAN exposures and the impact of different wavelengths.

Light’s Connection to Metabolism: An Anatomical Framework

Both rodents and humans have, apart from rods and cones, a third type of ocular photoreceptor, the so‐called intrinsically photosensitive retinal ganglion cells (ipRGCs). These ipRGCs contain the photopigment melanopsin, which is optimally sensitive to light at a wavelength of 484 nm in rodents (2). Human ipRGC subtypes have shown peak activity in response to 457, 459, and 470 nm light with a maximal sensitivity at 480 nm (2, 3).

Rods and cones, with peak sensitivities varying within a range of 440 to 580 nm (4), provide input to the ipRGCs as well, lowering ipRGC response thresholds and increasing their action potential discharge rates (2). Several brain areas are responsible for coordinating energy homeostasis by regulating locomotor activity, food intake, energy expenditure, hormone levels, and activity in metabolic tissues. Some of these areas receive direct input from the ipRGCs, which contain the photopigment melanopsin (5, 6).

One of the areas receiving input from the ipRGCs is the suprachiasmatic nucleus of the hypothalamus (SCN) (6) or master biological clock (7). The molecular mechanism of this biological clock consists of negative transcription and translation feedback loops, causing oscillations in gene and protein expression with a period close to 24 hours (i.e., a circadian rhythm) (8).

Daily alternations of light and dark synchronize the circadian clock in the SCN neurons to the exact 24‐hour cycle in our environment. Light information reaching the SCN via ipRGCs is the most important synchronizer or “Zeitgeber” for the SCN neurons. Depending on the timing, light exposure will enhance or dampen the expression of certain clock genes. Light exposure at the end of the night will advance the clock’s phase, whereas light at the beginning of the night will delay it (9).

The SCN has reciprocal interactions with the arcuate nucleus of the hypothalamus, which regulates daily rhythms in food intake (10) and locomotor activity (11). The dorsomedial nucleus of the hypothalamus receives projections from the SCN and is involved in coordinating daily rhythms of food intake and locomotor activity with the sleep‐wake cycle (12).

Furthermore, the SCN interacts with the intergeniculate leaflet, which receives a direct input from the ipRGCs and further helps coordinate circadian rhythms (6). Moreover, the SCN projects to the lateral habenula, a structure involved in several brain functions, including reward, memory, learning, mood, and sleep (13). The lateral habenula also receives projections from the lateral hypothalamic area that regulates feeding and reward (14).

The SCN, the dorsomedial nucleus of the hypothalamus, and ipRGCs also project to the paraventricular nucleus of the hypothalamus (PVN) and via this connection transmit the time‐of‐day signal to other brain areas and periphery. The PVN projects to the intermediolateral column of the spinal cord, regulating the secretion of melatonin from the pineal gland (15).

It also has sympathetic projections to the adrenal gland, via which it modulates the sensitivity of the adrenal cortex to ACTH (adrenocorticotropic hormone). (16), and sympathetic and parasympathetic projections to the thyroid gland (17), the pancreas (18), the liver (19), and white adipose tissue (WAT) (20).

Furthermore, the PVN controls the activity of the hypothalamo‐pituitary‐thyroid and hypothalamo‐pituitary‐adrenal axis via the release of thyrotropin‐releasing hormone (21) and corticotrophin‐releasing hormone (22). Thus, by means of its influence on the autonomic and neuroendocrine output of the hypothalamus, the SCN’s circadian rhythm is transmitted to other brain areas, endocrine glands, and peripheral tissues (20).

Likewise, peripheral tissues themselves also show a circadian rhythm in clock gene expression. Thus, the molecular clock mechanism is present not just in SCN neurons but also in virtually every cell. As peripheral cells cannot be entrained by light directly, they depend on the SCN to keep their clock synchronized with the environment (23).

Additionally, peripheral clocks have been shown to respond to other Zeitgebers, including glucocorticoids (24), glucose (25), body temperature (26), melatonin (27), activity rhythms (28), food intake (29), and the microbiome (30). Altogether, the SCN has a vast reach, and therefore, through its impact on the SCN, the effects of light are likely to be widespread too (Figure ​(Figure11).

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Figure 1
Sagittal view of a mouse brain providing a schematic overview of brain areas involved in the control of energy metabolism that receive input from the master clock located in the SCN or direct light input via the ipRGCs. RHT, retinohypothalamic tract; SCN, suprachiasmatic nucleus; VLPO, ventrolateral preoptic nucleus; MPO, medial preoptic area; ARH, arcuate nucleus of the hypothalamus; VMH, ventromedial nucleus of the hypothalamus; DMH, dorsomedial nucleus of the hypothalamus; LHA, lateral hypothalamic area; PVN, paraventricular nucleus of the hypothalamus; IGL, intergeniculate leaflet; PHb, perihabenular complex; IML, intermediolateral column of the spinal cord; DMX, dorsal motor nucleus of the vagus.

Moreover, the ipRGCs also project directly to many of the SCN target areas mentioned above. Hence, light exposure could also affect energy metabolism, feeding behavior, and reward directly (i.e., independent) from the SCN.

The Effects of Chronic Exposure to LAN on Human Metabolism

It has been established that 99% of the population of the European Union and the United States lives in areas where nighttime illumination is above the threshold for light pollution (59). It is therefore essential to determine the extent to which LAN is a health hazard and how it affects metabolic parameters in humans. Cross‐sectional studies have found that high outdoor LAN was associated with disturbances in the daily sleep/wake cycles and in sleep duration (60, 61).

Obayashi et al. (62) performed a cross‐sectional study in elderly individuals and measured LAN intensity in people’s bedrooms. They found that exposure to LAN correlated with elevated plasma triglycerides and LDL and lowered high‐density lipoprotein, although urinary melatonin levels were not affected. In another study, this same group found LAN to be associated with subclinical atherosclerosis (63).

Park et al. (64) analyzed data of 43,722 women and found that those who slept in light rooms had higher body weight compared with women sleeping in dark rooms. Similarly, a cross‐sectional analysis of over 100,000 women in the Breakthrough Generations Study showed that the odds of having overweight and obesity were higher when sleeping in a light room (65).

The odds of having an increased waist circumference, waist‐hip ratio, and waist‐height ratio were also higher in people who slept in light rooms (62, 64, 65). When satellite data of outdoor LAN were matched with data on body weight, it was observed that LAN was a strong positive predictor for overweight and obesity in both men and women (60, 66, 67).

Several experiments conducted in men living on Antarctica found that in December, when outdoor light exposure is continuous, plasma levels of glucose, insulin, and thyroid‐stimulating hormone were altered compared with other months (68, 69, 70, 71). Unfortunately, in these experiments, the indoor lighting regiment was not specified. In addition, variations in temperature, physical activity, and food intake between months likely will also have impacted the changes in physiology mentioned above.

Overall, ample evidence has suggested that high LAN levels, either outdoor or in the bedroom, correlate with increased body weight and obesity in humans. Furthermore, increased incidence in dyslipidemia, subclinical atherosclerosis, and central obesity suggest LAN might be an important risk factor for the development and deterioration of cardiovascular disease.

Acute Effects of Exposure to light at night (LAN) on Human Metabolism

In an experiment in which 48 participants were exposed to a night of dim light, sleep duration was decreased without affecting salivary melatonin levels (86). In another study in 14 men, salivary cortisol levels were acutely increased by a light pulse in the morning but not in the evening (87). Similarly, in an experiment involving 17 men, exposure to light acutely increased heart rate in the morning and middle of the night but not in the evening.

Furthermore, the increase in heart rate was intensity dependent in the morning but not in the evening (88). Increased heart rate during morning light exposure has been shown to likely rely on an increase in sympathetic activity (89, 90). Interestingly, morning light has also been shown to cause elevated plasma triglycerides levels in healthy men and elevated plasma glucose levels and plasma TAG levels in men with type 2 diabetes, indicating exposure to light in the morning increases energy availability (89).

A study in 17 participants found that salivary melatonin levels as well as evening preprandial plasma free‐fatty acid levels were decreased in individuals exposed to a night of bright light compared with a night of dim light. Evening postprandial plasma glucose and insulin levels were elevated in individuals exposed to a night of bright light. Basal TAG levels and basal plasma glucose and insulin levels were similar between lighting conditions (91).

Another study in eight male participants also found that LAN elevated postprandial plasma insulin levels in the evening. Interestingly, plasma insulin and glucagon‐like peptide 1 levels were also elevated after a meal in the morning following LAN exposure. Postprandial glucose levels were not affected at any time point in this study. Plasma glucocorticoid levels were briefly elevated by LAN in the middle of the night. Plasma melatonin levels were decreased (92).

Results of experiments using LAN and light in the morning indicate light has an arousing effect on humans at the onset of the activity period, which is most likely mediated by the autonomic nervous system. Results of LAN exposure on plasma cortisol levels and heart rate at the beginning of the subjective night differed from results found in the morning, indicating the arousing effects of LAN are circadian‐phase dependent.

Contrarily, effects of LAN on postprandial plasma glucose and insulin levels at the beginning of the subjective night and the following morning were similar, suggesting acute effects of LAN on glucose metabolism are more constant. Impairment of glucose metabolism indicates LAN might especially propose a risk to individuals that are prone to or suffer from type 2 diabetes.

Conclusion

The metabolic implications of exposure to chronic and acute LAN and LAN of different wavelengths are summarized in Figure ​Figure2.2. It seems that chronic LAN exposure gives rise to metabolic inefficiency, especially by disturbing daily behavioral rhythms, through its impact on the SCN. However, other more acute experiments have shown that LAN also directly impacts peripheral tissues, independent of circadian rhythm disturbance, probably via the ventral region of the SCN or via non‐SCN pathways.

In the majority of cases, the metabolic consequences of acute LAN most likely will be limited, as homeostasis is very well able to cope with such challenges. On the contrary, it is not clear what the consequences are of prolonged and repeated exposures to acute LAN. However, in the real‐life situation, most organisms (including humans) will be exposed to chronic LAN and experience the metabolic consequences of both the acute and chronic effects of light.

The metabolic consequences of chronic LAN are mainly caused by its disruptive effects on the SCN. On the contrary, for the acute effects of LAN, it is not clear whether they involve the SCN or not. In fact, a combination of SCN‐mediated and non‐SCN–mediated effects is also possible. In addition, for now, it is also not clear whether there are fundamental differences between the metabolic consequences of acute and chronic LAN, but it seems reasonable to assume that, if anything, the effects of acute LAN will enhance those of chronic LAN.

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Figure 2
Summary of the metabolic implications of exposure to light at night. TSH, thyroid‐stimulating hormone; FFA, free fatty acids; TG, triglycerides; LDL, low‐density lipoprotein; HDL, high‐density lipoprotein; RER, respiratory exchange ratio.

Moreover, the effects of LAN are wavelength dependent and differ within and among peripheral tissues, raising the questions of to what extent the effects of light are modulated by the SCN and whether light also affects metabolism via non‐SCN pathways (Figure ​(Figure1).1). In this regard, several recent observations are interesting.

First, using mice with a genetic ablation of all ipRGCs except those that project to the SCN, acute non‐SCN–dependent effects of light were shown on physiology and behavior (13, 108). Second, Koronowsky et al. (45) showed that the autonomous oscillations of the liver clock are independent from all other clocks (including the SCN clock) yet depends on the presence of an LD cycle.

Third, subcutaneous WAT adipocytes in both mice and humans have been reported to be directly sensitive to light, as these cells also express melanopsin (and encephalopsin, another photopigment) (109, 110). However, for now, it is not clear whether these photopigments in WAT have any physiological relevance.

Further research using LAN of different wavelengths will be necessary in answering these questions but will also help to determine what type of light has the most harmful consequences on health. As it has been shown that both acute and chronic LAN exposure impact glucose metabolism and are associated with the development of overweight, obesity, and cardiovascular disease in humans, it is of great importance that research on this topic continues.

reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7497102/


More information: Asuka Ishihara et al, Metabolic responses to polychromatic LED and OLED light at night, Scientific Reports (2021). DOI: 10.1038/s41598-021-91828-6

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