Connect with us

Wellness

Shift work disrupts biological ‘clocks’, profoundly impacting ageing and muscle decline

Published

on

Stanford Muscke ageing research

Muscle cells contain their own circadian clocks and disrupting them with shift work can have a profound impact on ageing, according to new research.

The research team from King’s College London has team revealed how muscle cells have an intrinsic timekeeping mechanism that regulates protein turnover, modulating muscle growth and function. At night, the muscle clock activates the breakdown of defective proteins, replenishing muscles while the body rests.

Altering this intrinsic muscle clock was associated with muscle decline seen with age, known as sarcopenia. This implies that disrupting circadian rhythms, as with shift work, accelerates the ageing process.

The scientists used zebrafish in the research – which are often used in biological studies. Zebrafish share up to 70 per cent of genes with humans, which are easy to modify in the laboratory, and are transparent, so their muscles are easily observed under a microscope.

Lead Author Jeffrey Kelu, research associate at King’s College London, said: “To investigate the impact of circadian disruption on muscle cells, we impaired the muscle clock function in zebrafish by over-expressing a malfunctioning clock protein. We then monitored the fish for two years, comparing them to healthy controls.

“While no significant differences in muscle size were observed at younger ages – six months and one year – fish lacking a functional muscle clock showed clear signs of premature ageing at two years. They were shorter, weighed less, swam less frequently and at slower speeds. These are hallmarks of sarcopenia and overall decline in mobility, which has been reported in shift workers.”

To understand the underlying mechanism, the researchers investigated protein turnover, a process essential for maintaining muscle mass, often impaired with ageing. They showed that during rest at night, the muscle clock regulates the degradation of defective muscle proteins, which accumulate throughout the day due to usage.

The study showed that this ‘nocturnal clearance’ is essential for preserving muscle function. So, the accumulation of defective proteins may drive the accelerated muscle decline observed in aged fish with a dysfunctional muscle clock and in shift workers.

Dr Kelu said: “In the UK, approximately four million shift workers play a vital role in keeping businesses and emergency services operational around the clock. Our study provides further evidence that the disruption of circadian rhythms in shift workers compromises multiple aspects of health.

“Understanding how circadian disruption contributes to sarcopenia is essential for developing strategies to improve the health and wellbeing of shift workers.

“Our findings highlight the possibility of using circadian biology to develop treatments aimed at preventing muscle decline in shift workers. Preclinical studies using drugs to modulate specific clock proteins are currently underway. This paves the way for future therapies that could improve ageing in shift workers.”

Co-author Professor Simon Hughes, expert in developmental cell biology, said: “This work shows how studying something as complicated as muscle growth in a simple system, like little fish larva, can really teach us something. Of course, someone then has to check if it’s also true in people – but at least the fish show us where to look.”

News

ATW’s research round-up: new Alzheimer trigger identified, UK university targets longevity. fibre not protein?…and more

Published

on

A UK university will become one of the first in the country to make improving the health and well-being of the elderly one of its six ‘mission-led’ research priorities.

Bournemouth University’s choice to focus on pensioners is partly the result of the Labour Government’s wish for universities to specialise, whilst also reflecting the area’s demographics – the south-coast city has one of the one of the oldest populations in the world.

“Our demographics are much older than other places – about 10 years older on average compared to the rest of the UK,” explained Tom Wainwright, professor of orthopaedics at Bournemouth.

Vary your exercise

The university’s Orthopaedic Research Institute is already heavily involved in work with the surrounding area and its recently published study, in The Lancet, showed that over-65s with osteoarthritis who undertook group-based cycle classes enjoyed much better outcomes than those receiving one-to-one physiotherapy.

Research published in leading British doctors’ publication the BMJ Journal, which tracked 100,000 people over the last 30 years, has shown that mixed exercise routines can have a significant impact on overall health and longevity.

The study tracked the cohorts exercise habits over three decades and found that participants who engaged in the highest variety of exercises had a 19% lower risk of death, compared to those who engaged in the lowest variety.

Benefits were even bigger when looking at specific causes like heart disease, cancer, and respiratory illness, with risk reductions ranging from 13 to 41 percent.

“People naturally choose different activities over time based on their preferences and health conditions,” says Yang Hu, corresponding author and research scientist in the Harvard TH Chan Department of Nutrition.

“When deciding how to exercise, keep in mind that there may be extra health benefits to engaging in multiple types of physical activity, rather than relying on a single type alone.”

US researchers have identified over five dozen new potential blood-based metabolites which could predict a Type 2 diabetes risk, years in advance.

Key Alzheimer trigger identified

Scientists at Mass General Brigham and Albert Einstein College of Medicine, followed 23,634 participants for up to 26 years and over that time analysed 469 metabolites in blood samples, alongside additional genetic, diet and lifestyle data.

In doing so they identified 235 metabolites associated with higher or lower diabetes risk, including 67 new molecules previously unreported.

The researchers say their work supports a shift toward precision prevention strategies which are more reliable than current indicators such as BMI or family history.

Further research into the Alzheimer’s predicting APOE (apolipoprotein E) gene has left UK researchers with renewed conviction of their ability to develop preventive measures, earlier in life.

Researchers at University College London analysed nearly 470,000 people across four major studies, focusing on participants aged 60 and older with confirmed Alzheimer’s diagnoses and genetic data.

Whilst previous studies had identified the ε4 allele of APOE as the one most predictive of Alzheimer’s development the UCL researchers also highlighted how allele ε3 may also carry a significant risk

Dr Dylan Williams, the study’s lead author, explained that the APOE gene’s contribution to the prevalence of Alzheimer’s has been significantly underestimated for a long time, and that the ε3 allele has historically been misunderstood as having a neutral effect on risk.

He said: “Intervening on the APOE gene, or the molecular pathway between the gene and Alzheimer’s, could have huge potential for preventing or treating a large majority of cases.”

Fibre first

Researchers say that fibre – found in beans, lentils, chia seeds, oats, bran, and certain fruits – is emerging as the ‘new hero’ of nutrition science.

Longevity expert Dr Vassily Eliopoulos, MD, who trained at Cornell, highlights how protein has ruled diet trends for years, but says fibre is now stepping into the spotlight.

“Everyone’s chasing protein, but the next big longevity macro is fibre. And fibre might be the most under-appreciated longevity nutrient that you’re missing daily.”

Explaining why fibre plays such a crucial role, he highlights the connection between gut health and overall well-being.

“Here’s the secret, your gut microbes eat what you don’t digest. These microbes convert fibre into powerful compounds that protect the body. They turn fibre into short-chain fatty acids, which act as your body’s natural anti-inflammatory molecules,”

Dr Eliopoulos highlights how chronic inflammation is closely linked to ageing and disease and he recommends aiming for 30 to 40 grams of fibre a day.

Continue Reading

News

Assisted dying should be ‘gradually’ extended to dementia, author Ian McEwan says

Published

on

Author Ian McEwan said legalised assisted dying should be gradually extended to people with dementia.

Speaking at a public book event in London on 28 January, he criticised attempts to block the UK’s assisted dying bill, citing more than 1,000 amendments.

Supporters believe it is near impossible for it to pass the House of Lords before the end of the session in May due to alleged filibustering.

If passed, the bill would legalise assisted dying in England and Wales for adults with less than six months to live.

“I like it when some bishop says on the radio: ‘It’s the thin end of the wedge,’ and I think yes, it is the thin end of the wedge,” said McEwan, who is a patron of Dignity in Dying.

“Certain groups are missing from it, such as those with dementia. It has to be physical pain.

“My guess is that if we pushed it through with all the protections around it – of doctors and dispassionate people making judgements – we’ll look back on this and think, ‘Why did we ever let people die in agony?'”

Asked if he would add an amendment to extend assisted dying to dementia sufferers, McEwan said: “Gradually, yeah, I would. But I think it does require a lot more thought and the idea of living wills.”

“My mother used to say to me: ‘If I ever become really terrible, I’d like you to finish me off.’ But of course, that’s to commit murder as things stand. Imagine standing up in court and saying: ‘Well, she did say when we were on the beach 20 years ago…'”

McEwan spoke about dementia’s impact on his family.

His mother Rose had dementia, as well as his brother-in-law and another close family member.

“By the time my mother was well advanced and could not recognise anyone, she was dead. She was alive and dead all at once.

“It was a terrible thing. And the burden on those closest is also part of the radioactive damage of it all.”

McEwan was speaking at St Martin-in-the-Fields church in central London, as part of its Conversation series, discussing his latest book, What We Can Know, in which dementia is a major theme.

He has also written about dementia in previous novels, Lessons and Saturday.

Continue Reading

News

Study confirms gut inflammation link to Alzheimer’s

Published

on

New research links gut inflammation to Alzheimer’s, with higher levels associated with more amyloid plaque in the brain.

Animal studies have shown Alzheimer’s can be passed to young mice through gut microbe transfer, strengthening the link between the gut and the brain.

A 2023 study adds support to inflammation as a possible mechanism.

Barbara Bendlin, psychologist at the University of Wisconsin, said: “We showed people with Alzheimer’s disease have more gut inflammation, and among people with Alzheimer’s, when we looked at brain imaging, those with higher gut inflammation had higher levels of amyloid plaque accumulation in their brains.”

Margo Heston, pathologist at the University of Wisconsin, and an international team tested faecal calprotectin, a marker of gut inflammation, in stool samples from 125 individuals in two Alzheimer’s prevention cohorts.

Participants completed cognitive tests at enrolment, family history interviews and testing for a high-risk Alzheimer’s gene. Amyloid plaques are abnormal protein clumps in the brain that signal disease processes.

A subset of participants took clinical tests for signs of amyloid protein clumps.

Whilst calprotectin levels were generally higher in older participants, they were even more pronounced in those with Alzheimer’s-characteristic amyloid plaques.

Levels of other Alzheimer’s biomarkers also rose with inflammation, and memory scores fell as calprotectin increased. Even participants without an Alzheimer’s diagnosis recorded poorer memory with higher calprotectin.

Heston said: “We can’t infer causality from this study; for that, we need to do animal studies.”

Laboratory analyses have shown gut-bacteria chemicals can stimulate inflammatory signals in the brain. Other studies have reported increased gut inflammation in patients with Alzheimer’s compared with controls.

The researchers suspect microbiome shifts trigger gut changes that lead to mild but chronic, system-wide inflammation, gradually weakening the body’s protective barriers.

Federico Rey, bacteriologist at the University of Wisconsin, said: “Increased gut permeability could result in higher blood levels of inflammatory molecules and toxins derived from gut lumen, leading to systemic inflammation, which in turn may impair the blood-brain barrier and may promote neuroinflammation, and potentially neural injury and neurodegeneration.”

The team is now testing whether diet-induced inflammation in mice can trigger the rodent version of Alzheimer’s.

Continue Reading

Trending

Agetech World