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0.  前言

年齡有兩種:時間年齡和生機年齡。後者可以經由DNA測試來估計。

影響一個人壽命的長短在「基因」這個因素外,絕大部分由「運氣」以及「生活習慣」決定;前者如投對了胎、碰巧遇到酒駕、或搭上死亡列車/航班等等。後兩者其實都在我們能力控制範圍之內;前者如不要在颱風天去爬山或海釣;後者則是該文主題(本攔下一篇貼文)

1.  測量「生機年齡」的四個方法:

1)  
照鏡子

數數臉上皺紋,跟其他大多數同年齡的朋友比較、比較。看起來年輕的人「生機年齡」也相對的低;做過拉皮、去眼袋、注射玻尿酸等醫美手術者自然不在被比較之列。

2) 
步行速度(10公尺距離)

a.  50
歲以下:每秒1.4公尺。
b.  80
歲以上:每秒1公尺。

3) 
金雞獨立

a.  40
歲以下:45(睜開眼睛)15 (閉上眼睛)
b.  60–69歲:32(睜開眼睛)4(閉上眼睛)

4) 
皮膚彈性(見「秘訣」6)

2. 
長壽九大秘訣

1)  
鍛鍊肌肉
2)  
不要迷信食療
3)  
正確的刷牙(次數和方式)
4) 
保持充分但不過多的睡眠時間
5)  
常戴太陽眼鏡
6) 
勤擦防曬霜
7)  
別在補品上花大把鈔票(可能適得其反)
8) 
多洗手
9) 
多讀通俗學新知(長壽科學進展神速多利用現有的長壽秘訣」,可能有希望活到「長生不老仙丹」問世)

此處僅僅翻譯出各節的子標題;在以上各節中,該文作者對各「秘訣」內容和它們何以能幫助長壽有詳細說明。請自行閱讀本攔下一篇貼文。

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為什麼越來越多的年輕人罹患癌症 -- Dylan Scott
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癌症患者年齡層降低是一個值得警惕的世界性問題下文從多方面角度來了解它作者也引用了本欄上一篇文章中所報導Cao教授的研究結果


Why are so many young people getting cancer?

Cancer used to be a disease of the old. Not anymore.



Dylan Scott is a senior correspondent and editor for Vox's Future Perfect, covering global health. He has reported on health policy for more than 10 years, writing for Governing magazine, Talking Points Memo, and STAT before joining Vox in 2017.

This story is part of a group of stories called “Future Perfect” -- Finding the best ways to do good.

When Princess Catherine, formerly Kate Middleton, revealed her cancer diagnosis in a surprise social media video last month, it answered one mystery that had been consuming the media: why the Princess of Wales had largely disappeared from view.

But Catherine’s story connects to another mystery, one that has been disturbing doctors for the past decade. Like the 42-year-old princess, people all over the world are developing cancer at younger ages.

Adults in the prime of their lives, often otherwise outwardly healthy, are dying of aggressive cancers that
appear to develop more quickly and be more deadly than in the past, for reasons that scientists cannot adequately explain.

Clinicians have especially been noticing a rise in cancers in the gastrointestinal (GI) system — including colorectal, kidney, and pancreatic cancers — in adults younger than 50, the cutoff for what is usually considered early-onset cancer.

Scientific authorities around the world see this as one of the most pressing questions for modern medicine and are now funding an ambitious, globe-spanning research project to provide some desperately needed answers.

Researchers in the US, Europe, and Asia are teaming up on a $25 million project jointly funded by the US National Cancer Institute, Cancer Research UK, Bowelbabe Fund for Cancer Research UK, and the French National Cancer Institute to investigate the leading lifestyle and environmental risk factors — from toxins to diets high in ultra-processed foods — believed to be contributing to the spike in early cancers. Over the next five years, the team will be gathering evidence on the ground in the US, Mexico, UK, France, Italy, and India.

“We want to do this from an international perspective because it’s an international problem,” Andrew Chan, a cancer epidemiologist and clinical gastroenterologist at Harvard Medical School and Mass General Hospital who is co-leading the project, told me. “That helps us to get insight into what’s common across these different parts of the world and what’s unique.”

Combining large population surveys, animal studies, and public health awareness campaigns, the team hopes to not only identify factors that play a role in early-onset cancers but also to establish the biological mechanisms that drive them. That could help lay the groundwork for better screenings and treatments and could ultimately have far-reaching implications for the foods we eat, the consumer goods we produce, and the very fabric of everyday life.

Cancers among young adults have become a global health crisis

One in five new colorectal cancer patients in the United States is under 55, according to a recent Wall Street Journal
analysis of data from the National Cancer Institute. That’s nearly twice the rate in 1995.

While deaths for colorectal cancer patients over 65 are going down, deaths among younger patients are increasing, a reflection of the higher mortality rates often observed in early-onset cancers. Scientists
say these cancers can be more deadly because they are not caught early enough for successful interventions. (Colonoscopies are not recommended until age 45.)

A decade ago, the known risk factors were largely limited to
diet and exercise, as obesity was associated with a higher chance of developing colorectal and GI cancers. But we now know that it’s a lot more complicated than how much a person weighs.

While the increase in global obesity rates since the mid-1990s likely plays a significant role in the uptick, scientists have found that specific diets, such as those rich in so-called
ultra-processed foods, have been associated with a higher risk of GI cancers, regardless of a person’s body-mass index.

Exposures to
toxins in the environment and in everyday goods, including phthalates found in makeup and hair products and formaldehyde in building materials, are now also suspected to increase cancer risk in younger patients — particularly if the exposure occurred at pivotal points in a person’s life. Getting less sleep or interrupted sleep may also be a factor.

“We know, for example, sleep and circadian rhythm is an important component of health,” Chan told me. “People are probably
getting less sleep or having more disrupted sleep for a variety of reasons. Is that potentially changing our biology in a way that is detrimental?”

Much of today’s cancer research is also focusing on the microbiome, the ecosystem — or rainforest, as one researcher put it — of bacteria that is concentrated in the gut. Certain kinds of microbiome bacteria
are associated with the development of GI cancers, but researchers are still puzzling out whether those changes are a cause or a consequence of cancer.

Finding solutions is crucial not only for wealthy nations, where increases in early cancer cases and deaths are most pronounced, but also for the rest of the world. Developing countries are contending with some of the same environmental contaminants as affluent countries, from
microplastics to air pollution, and they are already seeing rising death rates from other obesity-related diseases. As poorer countries become more economically developed, they are also expected to see more “first world” health problems — including cancer.

“This is going to be a problem that is going to be facing us as our economy gets stronger,” said Bhawna Sirohi, medical oncology director at the Balco Medical Center in Raipur, India, who is leading the project’s work in that country. It’s “facing us, the West, everywhere.”

What we know — and what we don’t — about early-onset cancers

The increase in early-onset cancers has become undeniable, replicated in study after study.
A BMJ article published last year found that the early onset of 29 different cancers, including breast, stomach, and colorectal, had risen nearly 80 percent between 1990 and 2019 worldwide. Another study published in JAMA Network Open last August found that the occurrence of a wide range of cancers among people under 50 had increased between 2010 to 2019 among American adults, particularly among women.

While colon and rectal cancers are driving much of that increase, cancers up and down the GI tract, including the bladder and kidneys, are on the rise among adults younger than 50.
A 2019 Lancet paper documented an uptick in cancers among US adults 25 to 49 years old, driven by higher rates of colorectal, uterine, gallbladder, kidney, and pancreatic cancers between 1995 and 2014. Gastrointestinal cancer incidence was up 15 percent overall from 2010 to 2019, according to the JAMA study. Bile duct cancers in the passage between the liver and gallbladder (up 142 percent over the past decade) and uterine cancers (up 76 percent) have seen some of the largest increases in prevalence, the same study found, though they still occur overall less often than colon cancers.

John Marshall, director of the Ruesch Center for the Cure of Gastrointestinal Cancers at Georgetown University, has been treating patients for 30 years. Early in his career, he says, he would never have a patient under the age of 50. Today, half of his patients are in that younger cohort, many of them otherwise healthy and fit. He first started to notice the trend with colorectal cancers, but later found an increase in other cancers as well, mirroring the research literature.

“We’ve been observing this for more than 10 years,” Marshall told me. “The trend is continuing and increasing and being observed now in other cancers beyond colorectal.”

When the spike in early cancers was first detected, scientists already knew obesity was a significant risk factor for developing cancers in the digestive tract. Groups such as the American Cancer Society targeted 
their recommendations around diet and exercise.

Systematic reviews of the available research, though, such as
one published in Frontiers in Nutrition in 2022, have identified dietary factors that are associated with a higher incidence of early-onset colorectal cancer, regardless of body weight. These include consumption of a lot of deep-fried foods, processed foods, foods high in fat, and sugary drinks and desserts, as well as low folate and fiber consumption.

Marathon runners with cardboard diets, Marshall said, can be more prone to GI cancers than their physical fitness might suggest. Higher alcohol consumption is
likewise associated with a higher risk of developing cancer early.

Scientists also hypothesize that changes in our environment, such as the proliferation of
microplastics, could be a contributing factor. From food containers to synthetic clothing, we are exposed to these tiny particles every day. They find their way into the environment and, when we inadvertently eat or drink them, into our bodies and our GI tracts.

According to a
paper published last year by a New Zealand research team, the upticks in cancers among young adults matched the timeline that we would expect from the multiplication of microplastics in the environment. Research on cellular and rodent models has suggested that microplastics could promote tumor growth. Though more research is needed, we already know these materials contain chemicals that can disrupt hormones and pose a risk to our health.

These findings also point to another revelation: “We have, each of us, different risk depending on when we are born,” Shuji Ogino, a molecular pathological epidemiologist at Harvard Medical School, told me.

People born in the first half of the 20th century had a lower risk of developing cancer by age 50 than people born in the second half, Ogino said. That would support the idea that environmental changes and society-wide alterations to our diet and food production may be contributing to the increase in early-onset cancers.

In the same vein, scientists increasingly suspect that exposures to risk factors at certain ages — whether in utero, early childhood, or early adulthood. — could be playing an important role in a person’s risk of developing cancer at a young age. Preliminary findings, such as
a study that found consuming more sugary drinks while in adolescence was associated with a higher risk of developing colorectal cancer early in women, lend support to those theories.

The next frontiers in understanding the increase in early-onset cancers

A definitive explanation for these increases in cancer rates among younger adults continues to elude scientists. They have a lot of theories and some evidence to support them, but scientific progress moves slowly. We know more than we did a decade ago, but we are still a long way from a clear answer.

“The reality is, we don’t know,” Marshall said.

The new research project led by Chan and Yin Cao of Washington University in St. Louis, the recipient of the $25 million Cancer Grand Challenges award, represents one of the most comprehensive attempts to find clearer answers.

“Are the things that we’re seeing truly causes or are they just bystanders of some of these associations?” Chan said. “We need to really understand what the true causes are. That will be difficult just relying on observational data in humans. We have the opportunity to experimentally model between the human and animal studies.”

Some of the researchers will collect population cohort data in the US, UK, Europe, and Mexico and ask participants about known cancer risk factors, such as their diet and lifestyle, as well as novel factors, such as environmental exposures and demographic characteristics. They will also collect stool samples to analyze the participants’ microbiomes to identify any links between changes in gut bacteria and cancer growth.

The information gathered from those studies will be used to generate hypotheses for animal and in vitro experiments. Scientists will test different potential carcinogens in different combinations and simulate exposure at different stages of the life cycle (including in utero and in adolescence).

With this multifaceted approach, the team will be able to test many of the leading hypotheses for the increase in early-onset cancers that need stronger evidence. The data on the carcinogenic potential of microplastics, for example, has been so far limited mostly to short-term studies on mice.

The researchers acknowledge their project won’t definitively answer every question about early-onset cancer. But their wide-ranging approach to an extraordinarily complex subject could start to bring more clarity.

“Even if we may not get 100 percent or even if we only answer 20 percent of the picture, we hope this mechanism, the paradigm in terms of integrating human and animal studies, is going to be the one that will lead to more and more future investigations,” Cao told me. “I think that would be a huge impact on the field.”

The trial will also compare cancer prevention and treatment interventions in diverse settings, from urban London to rural villages in India. As part of Sirohi’s contribution to the project, researchers will take a randomized approach to educating Indian villagers on colorectal cancer risk (she says many of her patients don’t know the symptoms to look for), encouraging them to submit a stool sample, and follow up with a colonoscopy if there are signs of bleeding.

Wherever these inquiries lead may eventually force us to rethink many dimensions of modern life.

“What does a truly balanced diet look like? How do you feed your microbiome and culture your rainforest?” Marshall said. “The hope is we will learn a lot from this.”

The answers may beget more questions. How do we feed a world of 8 billion people a diet that lowers the risk of more people dying too young?

Few scientific questions are more urgent right now.


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年輕人癌症風險增高與老化加速有關 -- Brenda Goodman
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我即將跨過80大關長壽對我來說,跟美女一樣,吸引力雖不能說幾等於零,但大大的、大大的不如以前。本欄完全是為了年輕網友而開。

今天讀到這篇報導,本欄前兩篇文章的相關性和重要性陡然提高了幾個層級。畢竟,相較於抽煙和喝酒,許多癌症可是二話不說見血封喉的殺手

時間年齡」(或稱「實際年齡」)與「生機年齡」兩個概念請見本欄前兩篇文章。根據以下這篇研究報導

1965
或之後出生的人,比1950 1954之間出生的人在老化程度上加快了17%。大概來說,就生機年齡而言1965 或之後出生的人1950年代前後出生的人老得快1/5實際年齡相同的兩組人前者的生機年齡比後者每10年要大個2歲左右。

如開欄文所說,當下長壽科學進展神速,大家應該多利用現有的科學「長壽秘訣」,來延遲自己生機年齡的增加60歲以下的朋友們,很可能有機會活到「長生不老仙丹」問世。如果你在這個年齡層,恭喜你但請仔細讀讀本欄這三篇文章。


Accelerated aging linked to cancer risk in younger adults, research shows

04/08/24

CNN
Researchers looking for clues about why some types of cancer are on the rise in younger adults say they’ve found an interesting lead: a connection to accelerated biological aging.

Aging is the major risk for many types of cancer, meaning the older you get, the more likely you are to be diagnosed. And increasingly, experts recognize that age is more than just the number of candles on a birthday cake. It’s also the wear and tear on the body, caused by lifestyle, stress and genetics, which is sometimes referred to as a person’s biological age.

“We all know cancer is an aging disease. However, it is really coming to a younger population. So whether we can use the well-developed concept of biological aging to apply that to the younger generation is a really untouched area,” said Dr. Yin Cao, an associate professor of surgery at the Washington University School of Medicine in St. Louis and senior author of the new research, which was presented Sunday at the American Association of Cancer Research’s annual conference in San Diego.

Factors of biological aging

Cao and her team looked at the medical records of 148,724 people ages 37 to 54 who are participants in a large data registry called the UK Biobank.

They homed in on nine blood-based markers that have been shown to correlate with biological age:

*  albumin: a protein made by the liver that declines with age
*  creatinine: a waste product in blood produced by protein digestion and the breakdown of muscle tissue; a
measure of kidney function. Lower levels correlate with better longevity.
*  glucose: With age, blood sugar stays higher for longer after meals.
*  c-reactive protein: made by the liver in response to inflammation; relatively
higher levels correspond to faster aging
*  lymphocyte percent: The concentration of these white blood cells related to immune function tends to
decrease with age.
*  mean cell volume: a measure of the average size of red blood cells, which
increases with age
*  red cell distribution width: the difference between the size of a person’s smallest and largest red blood cells, which tends to
increase with age
*  alkaline phosphatase: an enzyme produced mainly by the liver and bones that tends to
increase with age
*  white blood cell counts: Numbers of white cells in the
high end of the normal range in the blood may correspond with greater aging.

These nine values were then plugged into an
algorithm called PhenoAge that was used to calculate each person’s biological age. The researchers determined accelerated aging by comparing people’s biological ages with their chronological ages.

They then checked cancer registries to see how many in the group had been diagnosed with early cancers, which the researchers defined as cancers appearing before age 55. There were nearly such 3,200 cancers diagnosed.

The researchers found that people born in 1965 or later were 17% more likely to show accelerated aging than those born from 1950 through 1954.

What faster aging could tell us about cancer risk

After adjusting the data for factors they thought might bias their results, the researchers found that accelerated aging was associated with increased risk for cancer. The strongest associations were seen with lung, stomach and intestinal, and uterine cancers.

Compared with people who had the smallest amount of faster aging in the biobank sample, those who scored highest had twice the risk of early-onset lung cancer, more than 60% higher risk of a gastrointestinal tumor and more than 80% higher risk of uterine cancer.

The study wasn’t designed to answer questions about why these cancer types seemed to have the strongest ties to accelerated aging, but Ruiyi Tian, the graduate student who led the research, has some theories.

Tian said it’s possible that lungs are more vulnerable to aging than other types of tissues because the lung has a limited ability to regenerate. Stomach and intestinal cancers, she says, have been linked to inflammation, which increases with aging.

Cao said the strength of the research is that the researchers saw these signals in such a large number of people, but she acknowledges that the study has limitations, too.

For example, people in the study weren’t followed over time. The blood test results were from a single test, so they gave only a snapshot of risk, which may change. Ideally, she said, researchers would be able to follow the same group for years, taking blood samples along the way to get a more accurate trajectory of their risk.

“The ideal scenario is that we would have multiple blood collections throughout the life course, which is not feasible even in biobanks like UK Biobank,” Cao said.

She said the association should also be tested in more diverse populations, since the effects of social factors tied to racial discrimination need to be better illuminated, as well.

Dr. Anne Blaes, who studies the impact of biological aging in cancer survivors at the University of Minnesota, said the study results are exciting because they could point to a better way to find people who are at higher risk of getting cancer when they’re young. Right now, young adults who don’t have a family history or other risk factor aren’t regularly screened for most kind of cancer.

“We’re seeing more and more cancers, especially GI cancers and breast cancers, in younger individuals. And if we had a way of identifying who’s at higher risk for those, then really, you can imagine we’d be recommending screening at a different time,” said Blaes, a professor and director of the Division of Hematology and Oncology at UM medical school. She was not involved in the new research.

Blaes said that if you can find people who are at higher risk because their cells are aging faster, you can target lifestyle interventions too: things like nutrition, exercise and sleep.

“There are medications that also look like they can slow down accelerated aging,” said Blaes, who is testing two of them in cancer survivors. Cancer survivors often show greater biological aging, perhaps because of the after effects of therapies like chemotherapy and radiation.

The medications belong to a class called senolytics, drugs thought to target and get rid of damaged and aging cells.

Right now, it’s not clear who might benefit from these drugs, but assessments of accelerated aging like PhenoAge could one day help point doctors to the people who most need them.

“It’s super interesting. It’s not quite prime time, where we would go out and prescribe those medications for people, but this is really, really important work,” Blaes said.

For more CNN news and newsletters create an account at
CNN.com



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9 simple, science-backed changes that can reverse your biological age

Science says it’s time to rethink – and take control – of our body's age. Here’s how to slow, halt and potentially turn back your biological clock.


Andrew Steele, 03/31/24

Being asked ‘how old are you?’ used to be a simple question to answer. If you weren't sure, you could always just count the candles on your birthday cake. The candles may no longer tell you the whole story, however.

That’s according to a growing group of scientists who claim that you don’t just have a traditional chronological age, but also a potentially more fluid ‘biological age’. And that biological age could even be wound back… if you know how.

The excitement about this idea began around 2013,
with the first DNA tests that could estimate your age to within a few years. The fact that a person’s DNA and chronological ages were usually slightly different raised a question: if the test deemed that you were older than your age in years, was that an error, or could it indicate something about how fast you’re ageing on a biological level?

A decade of intervening research has shown us that people with an older DNA age, known more correctly as an ‘epigenetic age’, do indeed seem to be older biologically, and so they
tend to get ill and die sooner than others.

It’s a scientific discovery that demonstrates what many of us have believed all along: people age at different rates. But what does this actually mean, both biologically and practically speaking?

Biologically, we now understand many of the underlying cellular and molecular processes that drive ageing, from damage to the proteins that keep our bodies working, to the ageing of cells themselves. It’s these changes – known collectively as the ‘
hallmarks’ of ageing – that are behind wrinkles, grey hair, frailty, memory loss and diseases like cancer, heart disease and dementia, all of which become radically more likely as we get older.

Practically, therefore, if we could slow these hallmarks down – whether through healthy lifestyle choices or, hopefully soon, medical treatments for the ageing process – we could reduce the risk of many or even all of the problems of old age at the same time.

For now, you might want to start by measuring your biological age to find out what you’re working with. Don’t rely on an epigenetic age test – although available from a number of providers, they’re not cheap and results are too inconsistent. Instead, there are quite a few completely free measurements to try in the comfort of your own home to get a rough idea.

The first is just to gaze in the mirror and check how old you look. One study of Danish twins found those rated as looking older than their chronological age
were at greater risk of getting ill or dying than participants who appeared more youthful.

There are physical measurements that can be tested too. Seeing
how fast you can walk 10m (32ft) provides a gauge (with speed dropping from 1.4m/second – or 4.6ft/second – in those below 50 to less than 1m/second or 3.2ft/second in the over-80s); or you can try standing on one leg (under-40s can typically manage 45 seconds with their eyes open or 15 with their eyes closed, but that drops to 32 and 4 seconds respectively in 60–69-year-olds).

If these tests ring any alarm bells for you, there’s some good news: science tells us that our rate of ageing isn’t simply determined by genes. Studies ranging from comparisons of
lifespan in identical twins, to massive number-crunching exercises on gigantic databases of family trees suggest somewhere between 75 and 95 per cent of lifespan is down to lifestyle and luck, a huge chunk of which we can control.

So, where should you start on your journey to delay – and possibly reverse – age-related decline? Science furnishes us with a range of suggestions, from the obvious to the obscure.

Maintain your muscle

Doctors joke that if exercise were a drug everyone would be queuing up to take it. Alas, getting fit is harder than simply popping a pill and many of us don’t get enough of this miracle treatment – even though it seems to be able to slow the ageing process.

Most of us know that we should be getting 150 minutes of moderate activity (such as brisk walking), or 75 minutes of vigorous exercise, per week. What’s often overlooked is strength training. Resistance exercise can help preserve both bone density and muscle mass, which are really important as we age, for a variety of reasons. Muscle even helps to regulate your blood sugar levels after meals, which our bodies often get worse at as we age.

We lose roughly 5 per cent of our muscle and 10 per cent of our strength every decade after the age of 30. But resistance exercise can delay or even reverse this decline. This doesn’t need to be pumping iron at the gym: plenty of exercises can be done at home using your bodyweight, from press-ups to squats. It’s never too late to start, either. One particularly inspiring study gave 90-somethings a two-month resistance training programme and nearly doubled their muscle strength in the process.

Ignore the fad diets

You could spend a lifespan just trying every diet put forward as the best way to increase health and longevity. Fortunately, the big picture is fairly straightforward: most of us would benefit from
less meat and more vegetables, fruit, legumes, nuts and whole grains.

Exactly how much this could roll back your biological clock isn’t clear, though. Diet studies are challenging, considering that the biggest ones are ‘observational’ – you can’t enforce a diet on thousands of people over decades, so scientists make do with watching what people eat and observing what happens to their health.

The aforementioned recommendations do have the backing of
shorter-term studies that closely prescribe a diet to participants and then use the likes of blood tests to monitor their key health markers. But what about when to eat? And how much? While there’s solid evidence that maintaining a healthy weight is important for longevity, it’s far less clear whether practices like fasting or long-term calorie restriction will be of benefit.

Calorie restriction works well in many organisms, like single-celled yeast, worms, flies and mice, but results in monkeys (the closest animals to humans we’ve yet tried it in)
are more ambiguous. The evidence is thinner when it comes to fasting. Some human studies suggest it may result in weight loss, but disproportionately by loss of muscle rather than fat, which, given the importance of muscle at older ages, may well be a net negative for your biological age.

Brush your teeth

One of the most surprising connections in ageing biology is that between good oral hygiene and living longer. The first hints of this came with studies noting that
people with less tooth decay and gum disease seemed to have fewer heart attacks than those with worse oral health.

The exact link was unclear – there could have been an unrelated factor behind this correlation, or it might be that more health-conscious people spend more time brushing their teeth and engaging in other behaviours like eating well – but
further studies have solidified the link. What's more, they suggested what the connection could be: chronic inflammation.

Inflammation, a normal immune response to an infection or injury, is usually short-lived. As we get older, however, our immune systems become a little paranoid, entering a state of constant low alert inflammation that’s chronic – and scientists think this can accelerate the ageing process.

A neverending battle with bacteria on your teeth or gums provides a source of exactly this kind of low-grade and long-lasting inflammation, providing a mechanism by which the cleanliness of your teeth is connected to general health.

Get enough sleep. But not too much

You’ve heard it before: studies suggest that the sweet spot for sleep is around 7-8 hours per night on average. But what you may not have heard as much is that having too much sleep can have a detrimental effect on your health. Regularly getting over nine hours of shuteye a night is associated with a higher risk of death than getting as little as four hours.

There are a variety of possible causes here: it could be that people who are unwell in other ways are more tired and so sleep for longer. Or it may be down to more complex biology, like more time in bed changing immune system behaviour for the worse. Currently, scientists aren’t sure.

Though sleep remains one of the most mysterious aspects of our physiology, longevity science is uncovering mechanisms to explain how a good slumber can lengthen your lifespan. For example, while we sleep, our brains do a spring-clean, literally flushing out toxins, like the amyloid deposits associated with Alzheimer’s disease, via a recently discovered network of pipes in our skulls, known as the glymphatic system.

Given that the accumulation of toxic proteins is one of the hallmarks of ageing, this could slow down
brain ageing – hopefully making the well-worn advice to get enough shut-eye a bit more compelling.

Wear sunglasses more

It’s not only your skin that you need to keep safe from the Sun: looking after your
eyes is just as important – and the effects of shielding them could include preventing dementia. That’s because the damage that can be done by ultraviolet light has consequences that stretch beyond vision loss.

For example, the proteins in the lenses of your eyes are normally transparent, but UV damage may cause clouding and yellowing, which, if it gets severe enough, is known as a cataract.

UV light can also do damage to the light-sensitive cells on the back of the eye, accelerating the disease,
age-related macular degeneration (AMD), which can blur your vision. Both cataracts and AMD seem to increase the risk of dementia. One theory to explain this is that by cloudiness or blurriness reducing the amount of visual stimulation received by the brain, cognitive decline with ageing accelerates, so protecting your eyes from UV light can slow down these processes and, in turn, could well reduce dementia risk.

 The good news for those of you who wear glasses or contact lenses is that the majority of these come with built-in UV protection. For the rest of us, sunglasses – especially those that wrap around to prevent UV light from sneaking in at the sides – and a wide-brimmed hat are worth considering. These will not only help to maintain sight as you go into older age, but also brain function too.

Always wear sunscreen

For all the potions making promises in the beauty aisle, by far the most effective anti-ageing cream is the humble sunscreen. As well as causing skin cancer, ultraviolet (UV)
light emitted by the Sun accelerates the ageing of skin through a few different mechanisms.

Firstly, it damages the collagen and other structural proteins that make our skin strong yet supple in youth, leading to wrinkles and the skin being slower to return to position when pinched. (Incidentally, that's another at-home test of biological age.)

Secondly, the damage to our DNA caused by UV light means that almost all our skin cells are mutated by the time we reach our 50s. We don’t yet know exactly how this contributes to ageing, but these mutations aren’t present in young skin. Slapping on some sunscreen will help you maintain a more youthful mutational profile.

You need to seek out creams with factor 15 or higher and four or five stars for UV-A protection. It’s worth applying sunscreen every morning since UV rays can be strong enough to damage skin on overcast days or through a window. With this regime, it’s probably also worth supplementing vitamin D (10 micrograms a day), which is normally produced when UV light hits our skin.

Don’t waste your savings

Perhaps the most talked-about story in ageing biology of late has been the tale of American entrepreneur Bryan Johnson, who is burning $2 million (£1.6m) of his reported $400m (£326m) fortune every year on dozens of tests, hundreds of daily pills and supplements, and an extreme diet, exercise and sleep regime in the hope of stopping his biological ageing.

For the rest of us, the good news is that there’s no need to spend anywhere near that much. Almost all the bang for that considerable buck is probably coming from eating more vegetables, nuts and legumes; getting plenty of exercise; and consistent sleep patterns.

By contrast, scientific studies show that many common supplements
have no effect on life expectancy, or sometimes a slightly negative one. If you’re taking over 100 different pills, it’s likely to reduce life expectancy overall: while some anti-ageing interventions add together, other combinations don’t play nicely.

Biology is complicated and changing dozens of things at once doesn’t make for a safe, controlled experiment, whether or not you’re ultra-wealthy.

Wash your hands

If you heard it once during the pandemic then you heard it 1,000 times: wash your hands for 20 seconds, and be sure to scrub between your fingers and under your nails. We were told it would save lives by reducing the risk of infection, but washing your hands can boost your life expectancy too.

How? Firstly, we know that certain infectious diseases have a direct link to non-infectious ones later in life – from human papillomavirus (HPV) being the leading cause of cervical cancer, to a virus called cytomegalovirus (CMV) that seems to accelerate the ageing of the immune system.

After an initial infection that’s usually comparable to a mild cold, CMV hides away in your cells for the rest of your life. Because it can never quite get shot of CMV, ever more of your immune system ends up s
pecialising in fighting it, leaving less ‘immune memory’ for other threats as we age.

There’s even more general evidence suggesting that infections lead to problems in later life. As hygiene, vaccines and  
antibiotics gradually reduced the burden of infectious disease in childhood, people who got fewer bugs as kids have been shown to age better as adults. This is probably due to the same chronic inflammatory mechanisms as keeping your teeth clean.

It means that doing everything you can to avoid infections might have a positive impact beyond the short-term desire to avoid the misery of being ill.

Prepare for future super drugs

Perhaps the most important health tip for all of us in the medium term is to learn a bit more about the biology of ageing. That’s because there are drugs on the horizon that could slow down the ageing process and keep more of us healthier for longer.

Some could be drugs already available today, like metformin (a diabetes drug) or rapamycin (given to help transplant patients), which seem to have a broad anti-ageing effect.

Other new treatments could target one or more of the hallmarks of ageing, such as so-called ‘senolytic’ drugs designed to remove certain misbehaving cells, known as ‘senescent’ cells, that accumulate in our bodies as we get older.

The science of longevity offers the promise of treatments far more powerful than the lifestyle tips currently at our disposal.

That’s just another reason to stay as healthy as possible with the tools of today: in order to still be around to be able to benefit from the game-changing therapies of tomorrow.


Andrew Steele is a London-based scientist, writer and presenter. He is the author of Ageless: The New Science of Getting Older Without Getting Old (£20, Bloomsbury). After completing a PhD in Physics, Steele decided to make the unusual leap to biology as he saw understanding ageing as the greatest humanitarian mission of our time. A recent Research Fellow at the Francis Crick Institute in London, he has used computers to decode our DNA and unravel the secrets hidden in some of modern biology’s biggest data base.

Read more:

The end of ageing? A new AI is developing drugs to fight your biological clock
Forever young: Senescent cells and secret to stopping ageing
Why it's harder to stand up as you age: The science behind your stiff joints and tight muscles
Anti-ageing pills are real, and some of us are taking them without knowing it
The race to stop ageing: 10 breakthroughs that will help us grow old healthily
Why does time speed up when you get older?
What happens in my body as I age?

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