How much does your phone’s blue light really delay your sleep? Relax, it’s just 2.7 minutes

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It’s one of the most pervasive messages about technology and sleep. We’re told bright, blue light from screens prevents us falling asleep easily. We’re told to avoid scrolling on our phones before bedtime or while in bed. We’re sold glasses to help filter out blue light. We put our phones on “night mode” to minimise exposure to blue light.

But what does the science actually tell us about the impact of bright, blue light and sleep? When our group of sleep experts from Sweden, Australia and Israel compared scientific studies that directly tested this, we found the overall impact was close to meaningless. Sleep was disrupted, on average, by less than three minutes.

We showed the message that blue light from screens stops you from falling asleep is essentially a myth, albeit a very convincing one.

Instead, we found a more nuanced picture about technology and sleep.

Mangostar/Shutterstock

What we did

We gathered evidence from 73 independent studies with a total of 113,370 participants of all ages examining various factors that connect technology use and sleep.

We did indeed find a link between technology use and sleep, but not necessarily what you’d think.

We found that sometimes technology use can lead to poor sleep and sometimes poor sleep can lead to more technology use. In other words, the relationship between technology and sleep is complex and can go both ways.

How is technology supposed to harm sleep?

Technology is proposed to harm our sleep in a number of ways. But here’s what we found when we looked at the evidence:

  • bright screen light – across 11 experimental studies, people who used a bright screen emitting blue light before bedtime fell asleep an average of only 2.7 minutes later. In some studies, people slept better after using a bright screen. When we were invited to write about this evidence further, we showed there is still no meaningful impact of bright screen light on other sleep characteristics including the total amount or quality of sleep
  • arousal is a measure of whether people become more alert depending on what they’re doing on their device. Across seven studies, people who engaged in more alerting or “exciting” content (for example, video games) lost an average of only about 3.5 minutes of sleep compared to those who engaged in something less exciting (for example, TV). This tells us the content of technology alone doesn’t affect sleep as much as we think
  • we found sleep disruption at night (for example, being awoken by text messages) and sleep displacement (using technology past the time that we could be sleeping) can lead to sleep loss. So while technology use was linked to less sleep in these instances, this was unrelated to being exposed to bright, blue light from screens before bedtime.

Which factors encourage more technology use?

Research we reviewed suggests people tend to use more technology at bedtime for two main reasons:

There are also a few things that might make people more vulnerable to using technology late into the night and losing sleep.

We found people who are risk-takers or who lose track of time easily may turn off devices later and sacrifice sleep. Fear of missing out and social pressures can also encourage young people in particular to stay up later on technology.

What helps us use technology sensibly?

Last of all, we looked at protective factors, ones that can help people use technology more sensibly before bed.

The two main things we found that helped were self-control, which helps resist the short-term rewards of clicking and scrolling, and having a parent or loved one to help set bedtimes.

Mother looking over shoulder of teen daughter sitting on sofa using smartphone
We found having a parent or loved one to help set bedtimes encourages sensible use of technology. fast-stock/Shutterstock

Why do we blame blue light?

The blue light theory involves melatonin, a hormone that regulates sleep. During the day, we are exposed to bright, natural light that contains a high amount of blue light. This bright, blue light activates certain cells at the back of our eyes, which send signals to our brain that it’s time to be alert. But as light decreases at night, our brain starts to produce melatonin, making us feel sleepy.

It’s logical to think that artificial light from devices could interfere with the production of melatonin and so affect our sleep. But studies show it would require light levels of about 1,000-2,000 lux (a measure of the intensity of light) to have a significant impact.

Device screens emit only about 80-100 lux. At the other end of the scale, natural sunlight on a sunny day provides about 100,000 lux.

What’s the take-home message?

We know that bright light does affect sleep and alertness. However our research indicates the light from devices such as smartphones and laptops is nowhere near bright or blue enough to disrupt sleep.

There are many factors that can affect sleep, and bright, blue screen light likely isn’t one of them.

The take-home message is to understand your own sleep needs and how technology affects you. Maybe reading an e-book or scrolling on socials is fine for you, or maybe you’re too often putting the phone down way too late. Listen to your body and when you feel sleepy, turn off your device.

Chelsea Reynolds, Casual Academic/Clinical Educator and Clinical Psychologist, College of Education, Psychology and Social Work, Flinders University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • Why do some people’s hair and nails grow quicker than mine?

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    Throughout recorded history, our hair and nails played an important role in signifying who we are and our social status. You could say, they separate the caveman from businessman.

    It was no surprise then that many of us found a new level of appreciation for our hairdressers and nail artists during the COVID lockdowns. Even Taylor Swift reported she cut her own hair during lockdown.

    So, what would happen if all this hair and nail grooming got too much for us and we decided to give it all up. Would our hair and nails just keep on growing?

    The answer is yes. The hair on our head grows, on average, 1 centimeter per month, while our fingernails grow an average of just over 3 millimetres.

    When left unchecked, our hair and nails can grow to impressive lengths. Aliia Nasyrova, known as the Ukrainian Rapunzel, holds the world record for the longest locks on a living woman, which measure an impressive 257.33 cm.

    When it comes to record-breaking fingernails, Diana Armstrong from the United States holds that record at 1,306.58 cm.

    Most of us, however, get regular haircuts and trim our nails – some with greater frequency than others. So why do some people’s hair and nails grow more quickly?

    Jari Lobo/Pexels

    Remind me, what are they made out of?

    Hair and nails are made mostly from keratin. Both grow from matrix cells below the skin and grow through different patterns of cell division.

    Nails grow steadily from the matrix cells, which sit under the skin at the base of the nail. These cells divide, pushing the older cells forward. As they grow, the new cells slide along the nail bed – the flat area under the fingernail which looks pink because of its rich blood supply.

    Person plays guitar
    Nails, like hair, are made mostly of keratin. Scott Gruber/Unsplash

    A hair also starts growing from the matrix cells, eventually forming the visible part of the hair – the shaft. The hair shaft grows from a root that sits under the skin and is wrapped in a sac known as the hair follicle.

    This sac has a nerve supply (which is why it hurts to pull out a hair), oil-producing glands that lubricate the hair and a tiny muscle that makes your hair stand up when it’s cold.

    At the follicle’s base is the hair bulb, which contains the all-important hair papilla that supplies blood to the follicle.

    Matrix cells near the papilla divide to produce new hair cells, which then harden and form the hair shaft. As the new hair cells are made, the hair is pushed up above the skin and the hair grows.

    But the papilla also plays an integral part in regulating hair growth cycles, as it sends signals to the stem cells to move to the base of the follicle and form a hair matrix. Matrix cells then get signals to divide and start a new growth phase.

    Unlike nails, our hair grows in cycles

    Scientists have identified four phases of hair growth, the:

    1. anagen or growth phase, which lasts between two and eight years
    2. catagen or transition phase, when growth slows down, lasting around two weeks
    3. telogen or resting phase, when there is no growth at all. This usually lasts two to three months
    4. exogen or shedding phase, when the hair falls out and is replaced by the new hair growing from the same follicle. This starts the process all over again.
    Stages of hair growth graphic
    Hair follicles enter these phases at different times so we’re not left bald. Mosterpiece/Shutterstock

    Each follicle goes through this cycle 10–30 times in its lifespan.

    If all of our hair follicles grew at the same rate and entered the same phases simultaneously, there would be times when we would all be bald. That doesn’t usually happen: at any given time, only one in ten hairs is in the resting phase.

    While we lose about 100–150 hairs daily, the average person has 100,000 hairs on their head, so we barely notice this natural shedding.

    So what affects the speed of growth?

    Genetics is the most significant factor. While hair growth rates vary between individuals, they tend to be consistent among family members.

    Nails are also influenced by genetics, as siblings, especially identical twins, tend to have similar nail growth rates.

    Girls compare nailpolish
    Genetics have the biggest impact on growth speed. Cottonbro Studio/Pexels

    But there are also other influences.

    Age makes a difference to hair and nail growth, even in healthy people. Younger people generally have faster growth rates because of the slowing metabolism and cell division that comes with ageing.

    Hormonal changes can have an impact. Pregnancy often accelerates hair and nail growth rates, while menopause and high levels of the stress hormone cortisol can slow growth rates.

    Nutrition also changes hair and nail strength and growth rate. While hair and nails are made mostly of keratin, they also contain water, fats and various minerals. As hair and nails keep growing, these minerals need to be replaced.

    That’s why a balanced diet that includes sufficient nutrients to support your hair and nails is essential for maintaining their health.

    Two people lay on the end of a bed. One has much longer hair.
    Nutrition can impact hair and nail growth. Cottonbro Studio/Pexels

    Nutrient deficiencies may contribute to hair loss and nail breakage by disrupting their growth cycle or weakening their structure. Iron and zinc deficiencies, for example, have both been linked to hair loss and brittle nails.

    This may explain why thick hair and strong, well-groomed nails have long been associated with perception of good health and high status.

    However, not all perceptions are true.

    No, hair and nails don’t grow after death

    A persistent myth that may relate to the legends of vampires is that hair and nails continue to grow after we die.

    In reality, they only appear to do so. As the body dehydrates after death, the skin shrinks, making hair and nails seem longer.

    Morticians are well aware of this phenomenon and some inject tissue filler into the deceased’s fingertips to minimise this effect.

    So, it seems that living or dead, there is no escape from the never-ending task of caring for our hair and nails.

    Michelle Moscova, Adjunct Associate Professor, Anatomy, UNSW Sydney

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • Older Americans Say They Feel Trapped in Medicare Advantage Plans

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    In 2016, Richard Timmins went to a free informational seminar to learn more about Medicare coverage.

    “I listened to the insurance agent and, basically, he really promoted Medicare Advantage,” Timmins said. The agent described less expensive and broader coverage offered by the plans, which are funded largely by the government but administered by private insurance companies.

    For Timmins, who is now 76, it made economic sense then to sign up. And his decision was great, for a while.

    Then, three years ago, he noticed a lesion on his right earlobe.

    “I have a family history of melanoma. And so, I was kind of tuned in to that and thinking about that,” Timmins said of the growth, which doctors later diagnosed as malignant melanoma. “It started to grow and started to become rather painful.”

    Timmins, though, discovered that his enrollment in a Premera Blue Cross Medicare Advantage plan would mean a limited network of doctors and the potential need for preapproval, or prior authorization, from the insurer before getting care. The experience, he said, made getting care more difficult, and now he wants to switch back to traditional, government-administered Medicare.

    But he can’t. And he’s not alone.

    “I have very little control over my actual medical care,” he said, adding that he now advises friends not to sign up for the private plans. “I think that people are not understanding what Medicare Advantage is all about.”

    Enrollment in Medicare Advantage plans has grown substantially in the past few decades, enticing more than half of all eligible people, primarily those 65 or older, with low premium costs and perks like dental and vision insurance. And as the private plans’ share of the Medicare patient pie has ballooned to 30.8 million people, so too have concerns about the insurers’ aggressive sales tactics and misleading coverage claims.

    Enrollees, like Timmins, who sign on when they are healthy can find themselves trapped as they grow older and sicker.

    “It’s one of those things that people might like them on the front end because of their low to zero premiums and if they are getting a couple of these extra benefits — the vision, dental, that kind of thing,” said Christine Huberty, a lead benefit specialist supervising attorney for the Greater Wisconsin Agency on Aging Resources.

    “But it’s when they actually need to use it for these bigger issues,” Huberty said, “that’s when people realize, ‘Oh no, this isn’t going to help me at all.’”

    Medicare pays private insurers a fixed amount per Medicare Advantage enrollee and in many cases also pays out bonuses, which the insurers can use to provide supplemental benefits. Huberty said those extra benefits work as an incentive to “get people to join the plan” but that the plans then “restrict the access to so many services and coverage for the bigger stuff.”

    David Meyers, assistant professor of health services, policy, and practice at the Brown University School of Public Health, analyzed a decade of Medicare Advantage enrollment and found that about 50% of beneficiaries — rural and urban — left their contract by the end of five years. Most of those enrollees switched to another Medicare Advantage plan rather than traditional Medicare.

    In the study, Meyers and his co-authors muse that switching plans could be a positive sign of a free marketplace but that it could also signal “unmeasured discontent” with Medicare Advantage.

    “The problem is that once you get into Medicare Advantage, if you have a couple of chronic conditions and you want to leave Medicare Advantage, even if Medicare Advantage isn’t meeting your needs, you might not have any ability to switch back to traditional Medicare,” Meyers said.

    Traditional Medicare can be too expensive for beneficiaries switching back from Medicare Advantage, he said. In traditional Medicare, enrollees pay a monthly premium and, after reaching a deductible, in most cases are expected to pay 20% of the cost of each nonhospital service or item they use. And there is no limit on how much an enrollee may have to pay as part of that 20% coinsurance if they end up using a lot of care, Meyers said.

    To limit what they spend out-of-pocket, traditional Medicare enrollees typically sign up for supplemental insurance, such as employer coverage or a private Medigap policy. If they are low-income, Medicaid may provide that supplemental coverage.

    But, Meyers said, there’s a catch: While beneficiaries who enrolled first in traditional Medicare are guaranteed to qualify for a Medigap policy without pricing based on their medical history, Medigap insurers can deny coverage to beneficiaries transferring from Medicare Advantage plans or base their prices on medical underwriting.

    Only four states — Connecticut, Maine, Massachusetts, and New York — prohibit insurers from denying a Medigap policy if the enrollee has preexisting conditions such as diabetes or heart disease.

    Paul Ginsburg is a former commissioner on the Medicare Payment Advisory Commission, also known as MedPAC. It’s a legislative branch agency that advises Congress on the Medicare program. He said the inability of enrollees to easily switch between Medicare Advantage and traditional Medicare during open enrollment periods is “a real concern in our system; it shouldn’t be that way.”

    The federal government offers specific enrollment periods every year for switching plans. During Medicare’s open enrollment period, from Oct. 15 to Dec. 7, enrollees can switch out of their private plans to traditional, government-administered Medicare.

    Medicare Advantage enrollees can also switch plans or transfer to traditional Medicare during another open enrollment period, from Jan. 1 to March 31.

    “There are a lot of people that say, ‘Hey, I’d love to come back, but I can’t get Medigap anymore, or I’ll have to just pay a lot more,’” said Ginsburg, who is now a professor of health policy at the University of Southern California.

    Timmins is one of those people. The retired veterinarian lives in a rural community on Whidbey Island just north of Seattle. It’s a rugged, idyllic landscape and a popular place for second homes, hiking, and the arts. But it’s also a bit remote.

    While it’s typically harder to find doctors in rural areas, Timmins said he believes his Premera Blue Cross plan made it more challenging to get care for a variety of reasons, including the difficulty of finding and getting in to see specialists.

    Nearly half of Medicare Advantage plan directories contained inaccurate information on what providers were available, according to the most recent federal review. Beginning in 2024, new or expanding Medicare Advantage plans must demonstrate compliance with federal network expectations or their applications could be denied.

    Amanda Lansford, a Premera Blue Cross spokesperson, declined to comment on Timmins’ case. She said the plan meets federal network adequacy requirements as well as travel time and distance standards “to ensure members are not experiencing undue burdens when seeking care.”

    Traditional Medicare allows beneficiaries to go to nearly any doctor or hospital in the U.S., and in most cases enrollees do not need approval to get services.

    Timmins, who recently finished immunotherapy, said he doesn’t think he would be approved for a Medigap policy, “because of my health issue.” And if he were to get into one, Timmins said, it would likely be too expensive.

    For now, Timmins said, he is staying with his Medicare Advantage plan.

    “I’m getting older. More stuff is going to happen.”

    There is also a chance, Timmins said, that his cancer could resurface: “I’m very aware of my mortality.”

    KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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  • Can You Get Addicted To MSG, Like With Sugar?

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    Have a question or a request? We love to hear from you!

    In cases where we’ve already covered something, we might link to what we wrote before, but will always be happy to revisit any of our topics again in the future too—there’s always more to say!

    As ever: if the question/request can be answered briefly, we’ll do it here in our Q&A Thursday edition. If not, we’ll make a main feature of it shortly afterwards!

    So, no question/request too big or small 😎

    ❝Hello, I love your newsletter 🙂 Can I have a question? While browsing through your recepies, I realised many contained MSG. As someone based in Europe, I am not used to using MSG while cooking (of course I know that processed food bought in supermarket containes MSG). There is a stigma, that MSG is not particulary healthy, but rather it should be really bad and cause negative effects like headaches. Is this true? Also, can you get addicted to MSG, just like you get addicted to sugar? Thank you :)❞

    Thank you for the kind words, and the interesting questions!

    Short answer: no and no 🙂

    Longer answer: most of the negative reputation about MSG comes from a single piece of satire written in the US in the 1960s, which the popular press then misrepresented as a genuine concern, and the public then ran with, mostly due to racism/xenophobia/sinophobia specifically, given the US’s historically not fabulous relations with China, and the moniker of “Chinese restaurant syndrome”, notwithstanding that MSG was first isolated in Japan, not China, more than 100 years ago.

    The silver lining that comes out of this is that because of the above, MSG has been one of the most-studied food additives in recent decades, with many teams of scientists in many countries trying to determine its risks and not finding any (except insofar as anything in extreme quantities can kill you, including water or oxygen).

    You can read more about this and other* myths about MSG, here:

    Monosodium Glutamate: Sinless Flavor-Enhancer Or Terrible Health Risk?

    *such as pertaining to gluten sensitivity, which in reality MSG has no bearing on whatsoever as it does not contain gluten and is not even made of the same basic stuff; gluten being a protein made of (amongst other things) the amino acid glutamine, not a glutamate salt. Glutamate is as closely related to gluten as cyanocobalamin (vitamin B12) is to cyanide (the famous poison).

    PS: if you didn’t click the above link to read that article, then 1) we really do recommend it 2) we did some LD50 calculations there and looked at available research, and found that for someone of this writer’s (very medium) size, eating 1kg of MSG at once is sufficient to cause toxicity, and injecting >250g of MSG may cause heart problems. So we don’t recommend doing that.

    However, ½ tsp in a recipe that gives multiple portions is not going to get you anywhere close to the danger zone, unless you consume that entire meal by yourself hundreds of times per day. And if you do, the MSG is probably the least of your concerns.

    (2 tsp of cassia cinnamon, however, is enough to cause coumarin toxicity; for this reason we recommend Ceylon (or “True” or “Sweet”) cinnamon in our recipes, as it has almost undetectable levels of coumarin)

    With regard to your interesting question about addiction, first of all let’s speak briefly about sugar addiction:

    Sugar addiction is, by broad scientific consensus, agreed-upon as an extant thing that does exist, and contemporary research is more looking into the “hows” and “whys” and “whats” rather than the “whether”. It is a somewhat complicated topic, because it’s halfway between what science would usually consider a chemical addiction, and what science would usually consider a behavioral addiction:

    The Not-So-Sweet Science Of Sugar Addiction

    The reasonable prevailing hypothesis, therefore, is that sugar simply has two moderate mechanisms of addiction, rather than one strong one.

    The biochemical side of sugar addiction comes from the body’s metabolism of sugar, so this cannot be a thing for MSG, because there is nothing to metabolize in the same sense of the word (MSG being an inorganic compound with zero calories).

    People can crave salt, especially when deficient in it, and MSG does contain sodium (it’s what the “S” stands for), but it contains a little under ⅓ of the sodium that table salt does (sodium chloride in whatever form, be it sea salt, rock salt, or such):

    MSG vs. Salt: Sodium Comparison ← we do molecular calculations here!

    Sea Salt vs MSG – Which is Healthier? ← this one for a head-to-head

    However, even craving salt does not constitute an addiction; nobody is shamefully hiding their rock salt crystals under their bed and getting a fix when they feel low, and nor does withdrawal cause adverse side effects, except insofar as (once again) a person deficient in salt will crave salt.

    Finally, the only other way we know of that one might wonder if MSG could be addictive, is about glutamate and glutamate receptors. The glutamate in MSG is the same glutamate (down to the atoms) as the glutamate formed if one consumes tomatoes in the presence of salt, and triggers the same glutamate receptors in the same way. We have the same number of receptors either way, and uptake is exactly the same (because again, it’s exactly the same chemical) so there is a maximum to how strong this effect can be, and that maximum is the same whatever the source of the glutamate was.

    In this respect, if MSG is addictive, then so is a tomato salad with a pinch of salt: it’s not—it’s just tasty.

    We haven’t cited papers in today’s article, but it’s just because we cited them already in the articles we linked, and so we avoided doubling up. Most of them are in that first link we gave 🙂

    One final note

    Technically anyone can develop a sensitivity to anything, so in theory someone could develop a sensitivity to MSG, just like they could for any other ingredient. Our usual legal/medical disclaimer applies.

    However, it’s certainly not a common trigger, putting it well below common allergens like nuts (or less common allergens like, say, bananas), not even in the same league as common intolerances such as gluten, and less worthy of health risk warnings than, say, spinach (high in oxalates; fine for most people but best avoided if you have kidney problems).

    The reason we use it in the recipes we use it in, is simply because it’s a lower-sodium alternative to salt, and while it contains a (very) tiny bit less sodium than low-sodium salt (which itself has about ⅓ the sodium of regular salt), it has more of a flavor-enhancing effect, such that one can use half as much, for a more than sixfold total sodium reduction. Which for most of us in the industrialized world, is beneficial.

    Want to try some?

    If today’s article has inspired you to give MSG a try, here’s an example product on Amazon 😎

    Enjoy!

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  • When Bad Joints Stop You From Exercising (5 Things To Change)

    10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.

    The first trick to exercising with bad joints is to have better joints.

    Now, this doesn’t necessarily mean you can take a supplement and magically your joint problems will be cured, but there are adjustable lifestyle factors that can and will make things relatively better or worse.

    We say “and will”, because you don’t get a choice in that part. Everything we do, every little choice in our day, makes our health a little better or a little worse in some aspect(s). But we do get a choice between “relatively better” and “relatively worse”.

    With that in mind, do check out:

    Ok, you have bad joints though; what next?

    Let’s assume you’re doing your best with the above, and/or have simply decided not to, which is your call. You know your circumstances best. Either way, your joints are still not in sufficiently good condition to be able to exercise the way you’d like.

    First, the obvious: enjoy low-impact exercises

    For example:

    • Swimming
    • Yoga (much more appropriate here than the commonly-paired “and tai chi”)*
    • Isometric exercises (i.e. exercise without movement, e.g. squeezing things, or stationary stability exercises)

    *This is not to say that tai chi is bad. But if your problem is specifically your knees, there are many movements in most forms of tai chi that require putting the majority of one’s weight on one bent leg, which means the knee of that leg is going to suffer. If your knees are fine, then this won’t be an issue and it will simply continue strengthening your knees without discomfort. But they have to be fine first.

    See also: Exercising With Osteoporosis

    Second: support your joints through a full range of motion

    If you have bad joints, you probably know that there’s an unfortunate paradox whereby you get to choose between:

    1. Exercise, and inflame your joints
    2. Rest, and your joints seize up

    This is the way to get around that damaging dilemma.

    Moving your joints through a full range of motion regularly is critical for their maintenance, so do that in a way that isn’t straining them:

    If it’s your shoulders, for example, you can do (slow, gentle!) backstroke or front-crawl or butterfly motions while standing in the comfort of your living room.

    If it’s your knees, then supported squats can do you a world of good. That means, squat in front of a table or other stable object, with your fingertips (or as much of your hands as you need) on it, to take a portion of your weight (it can be a large portion; that’s fine too!) while you go through the full range of motion of the squat. Repeat.

    And so forth for other joints.

    See also: The Most Underrated Hip Mobility Exercise (Not Stretching)

    Third: work up slowly, and stop early

    You can do exercises that involve impact, and if you live a fairly normal life, you’ll probably have to (walking is an impact exercise). You can also enjoy cycling (low-impact, but not so low-impact as we discussed in the last section) and work up to running if you want to.

    However…

    While building up your joints’ mobility and strength, it is generally a good idea to stop before you think you need to.

    This means that it’s important to do those exercises in a way that you can stop early. For example, an exercise bike or a treadmill can be a lot of use here, so that you don’t find you need to stop for the day while miles from your house.

    If you get such a device, it doesn’t even have to be fancy and/or expensive. This writer got herself an inexpensive exercise bike like this one, and it’s perfectly adequate.

    Fourth: prioritize recovery, even if it doesn’t feel like you need it

    Everyone should do this anyway, but if your joints are bad, it goes double:

    Overdone It? How To Speed Up Recovery After Exercise (According To Actual Science)

    Fifth: get professional help

    Physiotherapists are great for this. Find one, and take their advice for your specific body and your specific circumstances and goals.

    Take care!

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  • How Healers Heal – by Dr. Shilpi Pradhan

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    First note: the listed author here is in fact the compiler, with the authors being a collection of no fewer than 33 board-certified lifestyle medicine physicians. So, we’re not getting just a single person’s opinions/bias here!

    But what is lifestyle medicine? This book holds the six pillars of lifestyle medicine to be:

    1. Nutrition
    2. Physical activity
    3. Stress management
    4. Restorative sleep
    5. Social connections
    6. Avoidance of risky substances

    …and those things are what we read about throughout the book, both in highly educational mini-lecture form, and sometimes highly personal storytelling.

    It’s not just a “do these things” book, though yes, there’s a large part of that. It also covers wide topics, from COVID to alopecia, burnout to grief, immune disorders to mysterious chest pains (and how such mysteries are unravelled, when taken seriously).

    One of the greatest strengths of this book is that it’s very much “medicine, as it should be”, so that the reader knows how to recognize the difference.

    Bottom line: this book doesn’t fit into a very neat category, but it’s a very worthwhile book to read, and one that could help inform a decision that changes the entire path of your life or that of a loved one.

    Click here to check out How Healers Heal, and learn to recognize the healthcare you deserve!

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  • What pathogen might spark the next pandemic? How scientists are preparing for ‘disease X’

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    Before the COVID pandemic, the World Health Organization (WHO) had made a list of priority infectious diseases. These were felt to pose a threat to international public health, but where research was still needed to improve their surveillance and diagnosis. In 2018, “disease X” was included, which signified that a pathogen previously not on our radar could cause a pandemic.

    While it’s one thing to acknowledge the limits to our knowledge of the microbial soup we live in, more recent attention has focused on how we might systematically approach future pandemic risks.

    Former US Secretary of Defense Donald Rumsfeld famously talked about “known knowns” (things we know we know), “known unknowns” (things we know we don’t know), and “unknown unknowns” (the things we don’t know we don’t know).

    Although this may have been controversial in its original context of weapons of mass destruction, it provides a way to think about how we might approach future pandemic threats.

    Anna Shvets/Pexels

    Influenza: a ‘known known’

    Influenza is largely a known entity; we essentially have a minor pandemic every winter with small changes in the virus each year. But more major changes can also occur, resulting in spread through populations with little pre-existing immunity. We saw this most recently in 2009 with the swine flu pandemic.

    However, there’s a lot we don’t understand about what drives influenza mutations, how these interact with population-level immunity, and how best to make predictions about transmission, severity and impact each year.

    The current H5N1 subtype of avian influenza (“bird flu”) has spread widely around the world. It has led to the deaths of many millions of birds and spread to several mammalian species including cows in the United States and marine mammals in South America.

    Human cases have been reported in people who have had close contact with infected animals, but fortunately there’s currently no sustained spread between people.

    While detecting influenza in animals is a huge task in a large country such as Australia, there are systems in place to detect and respond to bird flu in wildlife and production animals.

    Scientists in a lab.
    Scientists are continually monitoring a range of pathogens with pandemic potential. Edward Jenner/Pexels

    It’s inevitable there will be more influenza pandemics in the future. But it isn’t always the one we are worried about.

    Attention had been focused on avian influenza since 1997, when an outbreak in birds in Hong Kong caused severe disease in humans. But the subsequent pandemic in 2009 originated in pigs in central Mexico.

    Coronaviruses: an ‘unknown known’

    Although Rumsfeld didn’t talk about “unknown knowns”, coronaviruses would be appropriate for this category. We knew more about coronaviruses than most people might have thought before the COVID pandemic.

    We’d had experience with severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) causing large outbreaks. Both are caused by viruses closely related to SARS-CoV-2, the coronavirus that causes COVID. While these might have faded from public consciousness before COVID, coronaviruses were listed in the 2015 WHO list of diseases with pandemic potential.

    Previous research into the earlier coronaviruses proved vital in allowing COVID vaccines to be developed rapidly. For example, the Oxford group’s initial work on a MERS vaccine was key to the development of AstraZeneca’s COVID vaccine.

    Similarly, previous research into the structure of the spike protein – a protein on the surface of coronaviruses that allows it to attach to our cells – was helpful in developing mRNA vaccines for COVID.

    It would seem likely there will be further coronavirus pandemics in the future. And even if they don’t occur at the scale of COVID, the impacts can be significant. For example, when MERS spread to South Korea in 2015, it only caused 186 cases over two months, but the cost of controlling it was estimated at US$8 billion (A$11.6 billion).

    Coronavirus statistics on a screen.
    COVID could be regarded as an ‘unknown known’. Markus Spiske/Pexels

    The 25 viral families: an approach to ‘known unknowns’

    Attention has now turned to the known unknowns. There are about 120 viruses from 25 families that are known to cause human disease. Members of each viral family share common properties and our immune systems respond to them in similar ways.

    An example is the flavivirus family, of which the best-known members are yellow fever virus and dengue fever virus. This family also includes several other important viruses, such as Zika virus (which can cause birth defects when pregnant women are infected) and West Nile virus (which causes encephalitis, or inflammation of the brain).

    The WHO’s blueprint for epidemics aims to consider threats from different classes of viruses and bacteria. It looks at individual pathogens as examples from each category to expand our understanding systematically.

    The US National Institute of Allergy and Infectious Diseases has taken this a step further, preparing vaccines and therapies for a list of prototype pathogens from key virus families. The goal is to be able to adapt this knowledge to new vaccines and treatments if a pandemic were to arise from a closely related virus.

    Pathogen X, the ‘unknown unknown’

    There are also the unknown unknowns, or “disease X” – an unknown pathogen with the potential to trigger a severe global epidemic. To prepare for this, we need to adopt new forms of surveillance specifically looking at where new pathogens could emerge.

    In recent years, there’s been an increasing recognition that we need to take a broader view of health beyond only thinking about human health, but also animals and the environment. This concept is known as “One Health” and considers issues such as climate change, intensive agricultural practices, trade in exotic animals, increased human encroachment into wildlife habitats, changing international travel, and urbanisation.

    This has implications not only for where to look for new infectious diseases, but also how we can reduce the risk of “spillover” from animals to humans. This might include targeted testing of animals and people who work closely with animals. Currently, testing is mainly directed towards known viruses, but new technologies can look for as yet unknown viruses in patients with symptoms consistent with new infections.

    We live in a vast world of potential microbiological threats. While influenza and coronaviruses have a track record of causing past pandemics, a longer list of new pathogens could still cause outbreaks with significant consequences.

    Continued surveillance for new pathogens, improving our understanding of important virus families, and developing policies to reduce the risk of spillover will all be important for reducing the risk of future pandemics.

    This article is part of a series on the next pandemic.

    Allen Cheng, Professor of Infectious Diseases, Monash University

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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