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Stress does turn hair gray (and it’s reversible)

And while it may seem intuitive that stress can accelerate graying, the researchers were surprised to discover that hair color can be restored when stress is eliminated, a finding that contrasts with a recent study in mice that suggested that stressed-induced gray hairs are permanent.

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Legend has it that Marie Antoinette’s hair turned gray overnight just before her beheading in 1791. Though the legend is inaccurate–hair that has already grown out of the follicle does not change color–a new study from researchers at Columbia University Vagelos College of Physicians and Surgeons is the first to offer quantitative evidence linking psychological stress to graying hair in people.

And while it may seem intuitive that stress can accelerate graying, the researchers were surprised to discover that hair color can be restored when stress is eliminated, a finding that contrasts with a recent study in mice that suggested that stressed-induced gray hairs are permanent.

The study, published June 22 in eLife, has broader significance than confirming age-old speculation about the effects of stress on hair color, says the study’s senior author Martin Picard, PhD(link is external and opens in a new window), associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.

“Understanding the mechanisms that allow ‘old’ gray hairs to return to their ‘young’ pigmented states could yield new clues about the malleability of human aging in general and how it is influenced by stress,” Picard says.

“Our data add to a growing body of evidence demonstrating that human aging is not a linear, fixed biological process but may, at least in part, be halted or even temporarily reversed.”

Studying hair as an avenue to investigate aging

“Just as the rings in a tree trunk hold information about past decades in the life of a tree, our hair contains information about our biological history,” Picard says. “When hairs are still under the skin as follicles, they are subject to the influence of stress hormones and other things happening in our mind and body. Once hairs grow out of the scalp, they harden and permanently crystallize these exposures into a stable form.”

Though people have long believed that psychological stress can accelerate gray hair, scientists have debated the connection due to the lack of sensitive methods that can precisely correlate times of stress with hair pigmentation at a single-follicle level.

Splitting hairs to document hair pigmentation Ayelet Rosenberg, first author on the study and a student in Picard’s laboratory, developed a new method for capturing highly detailed images of tiny slices of human hairs to quantify the extent of pigment loss (graying) in each of those slices. Each slice, about 1/20th of a millimeter wide, represents about an hour of hair growth.

“If you use your eyes to look at a hair, it will seem like it’s the same color throughout unless there is a major transition,” Picard says. “Under a high-resolution scanner, you see small, subtle variations in color, and that’s what we’re measuring.”

The researchers analyzed individual hairs from 14 volunteers. The results were compared with each volunteer’s stress diary, in which individuals were asked to review their calendars and rate each week’s level of stress.

The investigators immediately noticed that some gray hairs naturally regain their original color, which had never been quantitatively documented, Picard says.

When hairs were aligned with stress diaries by Shannon Rausser, second author on the paper and a student in Picard’s laboratory, striking associations between stress and hair graying were revealed and, in some cases, a reversal of graying with the lifting of stress.

“There was one individual who went on vacation, and five hairs on that person’s head reverted back to dark during the vacation, synchronized in time,” Picard says.

Blame the mind-mitochondria connection

To better understand how stress causes gray hair, the researchers also measured levels of thousands of proteins in the hairs and how protein levels changed over the length of each hair.

Changes in 300 proteins occurred when hair color changed, and the researchers developed a mathematical model that suggests stress-induced changes in mitochondria may explain how stress turns hair gray.

“We often hear that the mitochondria are the powerhouses of the cell, but that’s not the only role they play,” Picard says. “Mitochondria are actually like little antennas inside the cell that respond to a number of different signals, including psychological stress.”

The mitochondria connection between stress and hair color differs from that discovered in a recent study of mice, which found that stress-induced graying was caused by an irreversible loss of stem cells in the hair follicle.

“Our data show that graying is reversible in people, which implicates a different mechanism,” says co-author Ralf Paus, PhD, professor of dermatology at the University of Miami Miller School of Medicine. “Mice have very different hair follicle biology, and this may be an instance where findings in mice don’t translate well to people.”

Hair re-pigmentation only possible for some

Reducing stress in your life is a good goal, but it won’t necessarily turn your hair to a normal color.

“Based on our mathematical modeling, we think hair needs to reach a threshold before it turns gray,” Picard says. “In middle age, when the hair is near that threshold because of biological age and other factors, stress will push it over the threshold and it transitions to gray.

“But we don’t think that reducing stress in a 70-year-old who’s been gray for years will darken their hair or increasing stress in a 10-year-old will be enough to tip their hair over the gray threshold.”

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More sleep boosts teens’ ability to cope with pandemic

Changes to daily routines triggered by lockdowns allowed teenagers to follow their biological impulse to wake up and sleep later, reducing daytime sleepiness.

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While poor sleep was linked to higher levels of stress during the COVID-19 pandemic, more teens actually obtained the recommended amount of sleep compared to pre-pandemic sleep patterns, according to a new study from McGill University. Changes to daily routines triggered by lockdowns allowed teenagers to follow their biological impulse to wake up and sleep later, reducing daytime sleepiness.

The study, published in Child and Adolescent Psychiatry and Mental Health, explores pre‑pandemic sleep behavior and stress during the COVID-19 pandemic. According to the researchers, encouraging better sleeping habits could help reduce teens’ stress and improve their ability to cope in times of crisis.

“The pandemic has shown that delaying school start times could help and should be implemented by schools interested in supporting the mental health of their students,” says lead author Reut Gruber, a Full Professor in the Department of Psychiatry at McGill University.

Reducing stress by promoting more sleep

During the pandemic, the wake-up and sleep time of teens shifted by about two hours later. Many teens also slept longer and had less of a need to catch up on lost sleep during the weekend.

The elimination of the morning commute, a delayed school start time, and cancellation of extracurricular activities allowed teens to follow their ‘delayed biological rhythm’ – or natural tendency to wake up and go to bed later, the researchers explain.

These changes meant that teens had more ‘useable hours’ during the weekdays to complete their homework and didn’t have to sacrifice sleep to fulfill their obligations during the week. Similar findings have been reported in multiple countries around the world during the COVID-19 pandemic.

Less sleep linked to higher levels of stress

The researchers found a connection between the amount of sleep teenagers were getting before the pandemic and their level of perceived stress during the pandemic.

“Shorter sleep duration and higher level of arousal at bedtime were linked to higher levels of stress, whereas longer sleep and lower level of arousal at bedtime was linked to reduced stress,” says Gruber, who is also the Director of the Attention, Behavior and Sleep Laboratory at the Douglas Research Centre.

“The tendency of teens not getting enough sleep was already a global concern prior to the COVID-19 pandemic. Now more than ever it’s critical we tackle the problem,” says co-author Sujata Saha, a Principal at Heritage Regional High School of the Riverside School Board. “Across the world the pandemic has increased levels of uncertainty and psychological stress. It’s projected that today’s elevated mental health challenges will continue well beyond the pandemic itself.”

“Not sleeping enough and being overly stimulated before bedtime are poor habits that are modifiable. We can target these behaviors with preventative measures to reduce teens’ stress in the face of overwhelming situations like to COVID-19 pandemic,” says Gruber.

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Eye conditions linked to heightened risk of dementia

Vision impairment can be one of the first signs of dementia, and reduced stimulation of visual sensory pathways is believed to accelerate its progression.

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Age-related macular degeneration, cataract and diabetes-related eye disease are linked to an increased risk of dementia, suggests research published online in the British Journal of Ophthalmology.

Vision impairment can be one of the first signs of dementia, and reduced stimulation of visual sensory pathways is believed to accelerate its progression.

Some small studies have suggested there may be a link between ophthalmic conditions that cause vision impairment – age-related macular degeneration, cataract, diabetes-related eye disease and glaucoma – and cognitive impairment. The incidence of these ophthalmic conditions increases with age, as does the incidence of systematic conditions such as diabetes, high blood pressure, heart disease, depression and stroke, which are accepted risk factors for dementia.

It is therefore unclear whether these ophthalmic conditions are associated with a higher incidence of dementia independently of these systematic conditions, so to investigate, the authors analysed data on 12,364 adults aged 55-73 years enrolled in the UK Biobank study. 

The participants were assessed between 2006 and 2010 at baseline and followed up until early 2021. During the 1,263,513 person-years of follow-up 2,304 cases of dementia were recorded.

Analysis of these data showed that age-related macular degeneration, cataract and diabetes-related eye disease, but not glaucoma, were independently associated with increased risk of dementia from any cause.

Compared with people who did not have ophthalmic conditions at the start of the study, the risk of dementia was 26% higher in those with age-related macular degeneration, 11% higher in those with cataract, and 61% higher in those with diabetes-related eye disease.

While glaucoma was not associated with increased risk of Alzheimer’s disease, it was associated with a higher risk of vascular dementia.

At the start of the study, participants were asked whether they had ever experienced heart attack, angina, stroke, high blood pressure or diabetes, and were assessed for depression. Diabetes, heart disease, stroke and depression were all associated with increased risk of dementia.

Having one of these conditions (a systemic condition) as well as an ophthalmic condition increased the risk of dementia further, and the risk was greatest when diabetes-related eye disease occurred alongside a systemic condition. Larger relative risk for dementia was observed among individuals with more ophthalmic conditions.

This is an observational study, and as such, can’t establish cause, and the authors also highlight several potential limitations, mostly related to data capture. They point out that ophthalmic conditions were defined based on self-reported and inpatient record data which was likely to underestimate their prevalence, that medical records and death registers may not have captured all cases of dementia, and that some dementia documented during follow-up may have occurred before eye diseases.

Nevertheless, they conclude: “Age-related macular degeneration, cataract and diabetes-related eye disease but not glaucoma are associated with an increased risk of dementia. Individuals with both ophthalmic and systemic conditions are at higher risk of dementia compared with those with an ophthalmic or systemic condition only.”

They add: “Newly developed hypertension, diabetes, stroke, heart disease and depression mediated the association between cataract/ diabetes-related eye disease and dementia.”

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Exposure to traffic noise linked to higher dementia risk

Reducing noise is a public health priority, say experts.

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Exposure to noise from traffic on roads and railways over a long period is associated with a higher risk of developing dementia, especially Alzheimer’s disease, suggests a study from Denmark published in The BMJ

The researchers estimate that as many as 1,216 out of the 8,475 cases of dementia registered in Denmark in 2017 could be attributed to these noise exposures, indicating a great potential for dementia prevention through reduction in traffic related noise. 

Worldwide, the number of people with dementia is expected to exceed 130 million by 2050, making it a costly and growing global health crisis. Besides well established risk factors, such as cardiovascular diseases and unhealthy lifestyle, environmental exposures may also play a role in the development of dementia.

Transportation noise is considered the second worst environmental risk factor for public health in Europe after air pollution, and around a fifth of the European population is exposed to transportation noise above the recommended level of 55 dB (decibels).

Studies have consistently linked transportation noise to various diseases and health conditions, such as coronary heart disease, obesity, and diabetes. There is, however, little research on transportation noise and dementia and findings are inconsistent.

To address this, researchers investigated the association between long term residential exposure to road traffic and railway noise and risk of dementia among two million adults aged over 60 and living in Denmark between 2004 and 2017. 

The researchers estimated road traffic and railway noise at the most and least exposed sides (or façades) of all residential addresses in Denmark. 

They then analysed national health registers to identify cases of all-cause dementia and different types of dementia (Alzheimer’s disease, vascular dementia, and Parkinson’s disease related dementia) over an average of 8.5 years.

They found 103,500 new cases of dementia during the study period.

After taking account of potentially influential factors related to residents and their neighbourhoods, the researchers found that a 10-year average exposure to road traffic and railway noise at the most and least exposed sides of buildings was associated with a higher risk of all-cause dementia.

These associations showed a general pattern of higher risk with higher noise exposure, but with a levelling off or even small declines in risk at higher noise levels.

Further analysis by type of dementia showed both road traffic and railway noise were associated with a higher risk of Alzheimer’s disease – up to 27% higher for exposure to road traffic noise of 55 dB and up to 24% higher for exposure to railway noise of 50 dB compared with less than 40 dB.

However, only road traffic noise was associated with an increased risk of vascular dementia, and not railway noise.

Possible explanations for an effect of noise on health include release of stress hormones and sleep disturbance, leading to a type of coronary artery disease, changes in the immune system and inflammation – all of which are seen as early events in the onset of dementia and Alzheimer’s disease.

This is an observational study so can’t establish cause, and the authors point to some limitations such as a lack of information about lifestyle habits, which can play a part in a person’s risk of developing dementia, and a lack of information on factors such as sound insulation in homes that might affect personal exposure to noise.

However, the study’s strengths included its large size, long follow-up time, and high quality assessment of noise exposure from two different transportation sources.

As such, the authors conclude: “If these findings are confirmed in future studies, they might have a large effect on the estimation of the burden of disease and healthcare costs attributed to transportation noise. Expanding our knowledge on the harmful effects of noise on health is essential for setting priorities and implementing effective policies and public health strategies focused on the prevention and control of diseases, including dementia.”

This large and comprehensive study has substantial strengths, but does not present the full picture of possible harm to the ageing brain associated with long term exposure to noise, for example from airports, industrial activities, or occupational exposure, say US researchers in a linked editorial.

Noise might also affect the risk of other chronic disorders such as high blood pressure, through which noise contributes indirectly to dementia risk, they add. 

The widespread and substantial exposures to noise worldwide, the severity of associated health consequences, and the limited tools available for people to protect themselves, strongly support the WHO’s argument that “noise pollution is not only an environmental nuisance but also a threat to public health,” they write.

“Reducing noise through transportation and land use programs or building codes should become a public health priority,” they conclude.

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