Personal light exposure patterns and incidence of type 2 diabetes: analysis of 13 million hours of light sensor data and 670,000 person-years of prospective observation
A study in The Lancet
https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(24)00110-8/fulltext#%20
found that people who were exposed to the most light between 12:30 AM and 6 AM were 1.5 times more likely to develop type 2 diabetes than those who remained in darkness during that timeframe.
The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.
"Those previous studies likely underestimated the effect," said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, "since they did not capture indoor light environments."
Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.
"This is really a phenomenal study," said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham's Diabetes Research Center, who was not involved in the study. "This is the first large-scale study we have looking at people's light exposure patterns and linking it to their long-term health."
What the Study Showed
The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.
"About half of the people that we looked at had very dim levels of light at night, so less than one lux — that basically means less than candlelight," said Phillips. "They were the people who were protected against type 2 diabetes."
Those exposed to more light at night — defined in the study as 12:30 AM-6 AM — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.
Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That's about the risk increase you'd get from having a family history of type 2 diabetes, the researchers said.
Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, "we still found there was this very strong relationship between light exposure and risk of type 2 diabetes," said Phillips.
How Light at Night May Increase Diabetes Risk
The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.
Light at night can disrupt the circadian rhythm, or your body's internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.
One's internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.
Phillips speculated that the sleep hormone melatonin also plays a role.
"Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses," Phillips said. "So if you're chronically getting light exposure at night, that's reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes."
Previous studies have explored melatonin supplementation to help manage diabetes. "However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far," Miedlich said.
Takeaways
Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.
That said, "there's no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes," said Phillips.
Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and metformin and GLP-1 agonists.
From www.medscape.com
ABSTRACT
Personal light exposure patterns and incidence of type 2 diabetes: analysis of 13 million hours of light sensor data and 670,000 person-years of prospective observation
Summary
Background
Methods
Findings
Interpretation
Funding
Evidence before this study
Added value of this study
Implications of all the available evidence
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https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(24)00110-8/fulltext#%20
FROM THE ARTICLE
Introduction
Circadian rhythms are disrupted by light exposure at night, which shifts the timing (phase-shift) and weakens the signal (amplitude suppression) of the central circadian pacemaker in the hypothalamus. This central pacemaker orchestrates the timing of metabolic processes required for glucose homeostasis, including circadian rhythms in insulin secretory capacity that peak during the day, and circadian rhythms in glucose secretion that peak at night. Mismatch of internal circadian rhythms with external environmental and behavioral rhythms can cause a pre-diabetic state in healthy humans. Prolonged exposure to internal-external mismatch is associated with higher risk of type 2 diabetes in shift workers and people with social jetlag.
Emerging research demonstrates that light at night is linked with cardiometabolic pathophysiology, including type 2 diabetes. Higher risks for type 2 diabetes, obesity, and hypertension have been observed in people with greater exposure to night light, measured with wrist-worn, and bedside light sensors in small cohort studies, and experimental exposure to light during sleep has been shown to increase next-day insulin resistance.
Experimental work in animal models supports night light exposure and circadian disruption as causal factors in diabetes pathophysiology. Reduced glucose tolerance, altered insulin secretion, and weight gain occur in mice exposed to light during the biological night, after controlling for physical activity and food intake, and circadian clock-mutant mice have altered insulin, glucose, and lipid profiles, and higher obesity, compared with wild type.
Large-scale cohort studies in humans have recently linked night light assessed from satellite data with the incidence and prevalence of type 2 diabetes. However, satellite data do not capture the personal indoor lighting environment, where most people spend over 80% of their time.
To our knowledge, no large-scale study has examined whether objective, personal light exposure is linked with risk of developing type 2 diabetes, or assessed the role of circadian disruption in this relationship. We assessed whether risk of incident type 2 diabetes was associated with exposure to light at night, and with modeled circadian amplitude and phase, in 84,790 UK Biobank participants using 13 million hours of data from wrist-worn light sensors, and type 2 diabetes diagnoses from hospital, primary-care, and death register records across 7.9 ± 1.2 years of follow-up.
Discussion
We confirm these findings in a much larger cohort after controlling for potential confounding factors, and using personal light sensors that capture more than the bedroom environment at night. Our findings are also consistent with studies of satellite-derived night light in larger cohorts.
These studies demonstrate significant but comparatively weaker relationships between night light and type 2 diabetes (e.g., 7% greater diabetes risk per quintile of brighter night light), possibly reflecting the fact that satellite data do not capture personal light exposure across 24 h.
We applied a validated computational model representing the response of the human central circadian clock to light, to identify participants with weekly light patterns that could suppress the amplitude or shift the phase of their central circadian clock.
Risk of incident diabetes was higher in people with light patterns that could suppress circadian amplitude (7% higher risk per standard deviation reduction in amplitude), and in people with light patterns that could advance circadian phase (18–39%) or delay phase (6–30%) compared to the group average. These results are in keeping with experimental and epidemiological work demonstrating that disrupted circadian rhythms, or exposure to zeitgebers capable of disrupting rhythms, are linked to type 2 diabetes and its associated pathophysiology.
Exposure to light that suppresses or shifts central circadian rhythms to an abnormal phase may alter circadian rhythms in insulin secretory capacity and glucose secretion, by either suppressing these rhythms, or shifting their timing relative to behavioral rhythms in nutritional intake, sleep, and physical activity. For example, disrupted circadian melatonin or glucocorticoid rhythms may exhibit elevated concentrations during waking hours, thereby reducing pancreatic insulin secretion and promoting hepatic glucose production at times that coincide with food intake. Persistent circadian misalignment may lead to persistently elevated postprandial glucose levels, initiating the development of type 2 diabetes by increasing the size and inflammation of adipocytes, thereby promoting insulin resistance and the secretion of inflammatory markers (e.g., interleukin-1β) that inhibit pancreatic beta-cell function.
Sleep likely plays an important role in the relationships between light exposure, circadian disruption, and diabetes risk. Sleep and light exposure patterns share a bidirectional relationship, and sleep disruption is an established risk factor for type 2 diabetes.
he relationship between light exposure and diabetes could therefore be partially explained by sleep disruption that co-occurs with night light exposure. Light exposure during the night could lead to disrupted sleep, but awakenings during the night could also lead to greater night light exposure, due to light usage during awakenings. Notably, in our analyses, night light exposure was an independent predictor of type 2 diabetes risk after adjustment for sleep duration. This finding supports night light as a predictor of diabetes risk, independent of sleep duration.
Night light exposure and genetic risk were found to be independent risk factors for developing type 2 diabetes. We derived polygenic risk scores for type 2 diabetes, and confirmed that they were robust predictors of type 2 diabetes diagnoses in the UK Biobank cohort. Higher polygenic scores were associated with 1.6, 2.3, and 4.2 times greater risk of incident diabetes in the second, third, and fourth polygenic risk quartiles, respectively, compared with the lowest-risk quartile. The difference between the 0–50% and 90–100% night light groups was similar to the difference between the 0–25% and 25–50% or the 25–50% and 50–75% polygenic risk categories. This indicates that, while polygenic risk score is a stronger predictor than night light exposure, reducing light exposure at night could attenuate an individual's susceptibility due to genetic risk of developing diabetes. A robust dose-dependent relationship between brighter light at night and higher diabetes risk was observed after adjustment for polygenic risk. This finding indicates that reduction of night light is a potential beneficial strategy for all individuals, including those with high genetic risk.
Estimated circadian phase and amplitude may therefore not reflect changes in the central circadian clock with age.
Seventh, covariates were collected several years prior to light recordings, and some of these covariates may change over time. Finally, relationships between light exposure patterns and diabetes risk in Models 2–3 may be attenuated by mediating pathways. Model 1 may therefore provide a closer approximation of the casual relationship between light exposure patterns and type 2 diabetes risk; however, large-scale intervention studies are required to establish the true causal relationship.
Our findings show that maintaining a dark environment during the night may mitigate risk of developing type 2 diabetes, likely due to the disruptive effects of light at night on circadian rhythms. Advising people to turn off their lights at night, or use lights that reduce the circadian impact (dim and “warm” light), is a simple, cost-effective, and easily-implementable recommendation that may promote cardiometabolic health and ease the growing global health burden of type 2 diabetes.
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