Stop Checking Your Likes – by Susie Moore
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You might think this one’s advice is summed up sufficiently by the title, that there’s no need for a book! But…
There’s a lot more to this than “stop comparing the worst out-takes of your life to someone else’s highlight reel”, and there’s a lot more to this than “just unplug”.
Instead, Susie Moore discusses the serious underlying real emotional considerations of the need for approval (and even just acceptance) by our community, as well the fear of missing out.
It’s not just about how social media is designed to hijack various parts of our brain, or how The Alogorithm™ is out to personally drag your soul through Hell for a few more clicks; it’s also about the human element that would exist even without that. Who remembers MySpace? No algorithm in those days, but oh the drama potential for those “top 8 friends” places. And if you think that kind of problem is just for young people 20 years ago, you have mercifully missed the drama that older generations can get into on Facebook.
Along with the litany of evil, though, Moore also gives practical advice on how to overcome those things, how to “see the world through comedy-colored glasses”, how to ask “what’s missing, really?”, and how to make your social media experience work for you, rather than it merely using you as fuel. ← link is to our own related article!
Bottom line: if social media sucks a lot of your time, there may be more to it than just “social media sucks in general”, and there are ways to meet your emotional needs without playing by corporations’ rules to do so.
Click here to check out Stop Checking Your Likes, and breathe easy!
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Staying Healthy and Active After 60
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Questions and Answers at 10almonds
Have a question or a request? You can always hit “reply” to any of our emails, or use the feedback widget at the bottom!
This newsletter has been growing a lot lately, and so have the questions/requests, and we love that! 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
Q: How to be your best self after 60: Self motivation / Avoiding or limiting salt, sugar & alcohol: Alternatives / Ways to sneak in more movements/exercise
…and, from a different subscriber…
Q: Inflammation & over 60 weight loss. Thanks!
Here are some of our greatest hits on those topics:
- Where Nutrition Meets Habits ← focusing on food that’s all three of: healthy + easy + cheap
- How To Keep On Keeping On ← exercise tips for when the motivation wanes
- Keep Inflammation At Bay ← science-based tips and advice
Also, while we’ve recommended a couple of books on stopping (or reducing) drinking, we’ve not done a main feature on that, so we definitely will one of these days!
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How To Reduce Your Alzheimer’s Risk
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Reduce Your Alzheimer’s Risk
Alzheimer’s is just one cause of dementia, but it’s a very notable one, not least of all because it’s
- a) the most common cause of dementia, and
- b) a measurably terminal disease.
For that reason we’re focusing on Alzheimer’s today, although most of the advice will go for avoiding dementia in general.
First, some things not everyone knows about Alzheimer’s:
- Alzheimer’s is a terminal disease.
- People who get a diagnosis at age 60 are typically given 4–8 years to live.
- Some soldier on for as many as 20, but those are rare outliers.
- Alzheimer’s begins 20 years or more before other symptoms start to develop.
- This makes this information very relevant for younger people approaching 40, for example.
- Alzheimer’s accounts for 60–80% of dementia, and affects around 6% of people over 60.
- By the age of 65, that figure is 10%. By the age of 70, however, the percentage is still about the same—this is because of the mortality rate preventing the accumulation of Alzheimer’s patients over time.
Want to know more? Read: 2023 Alzheimer’s Disease Facts And Figures Special Report ← this is a very comprehensive downloadablereference, by the way, including a lot of information about diagnosis, treatmentpathways, and earlyinterventions.
Speaking of diagnosis…
Know what the symptoms are… and aren’t!
Forgetting your car keys can be frustrating. Forgetting them frequently can be worrying.
But: there’s a difference between forgetting your car keys, and forgetting what car keys are used for. The latter is the kind of memory loss that’s more of a red flag for Alzheimer’s.
Similarly: forgetting someone’s name can be embarrassing. Forgetting someone’s name, asking them, forgetting asking them, asking them again, forgetting again (lather rinse repeat) is more of a red flag for Alzheimer’s.
There are other symptoms too, some of them less commonly known:
❝Difficulty remembering recent conversations, names or events; apathy; and depression are often early symptoms. Communication problems, confusion, poor judgment and behavioral changes may occur next. Difficulty walking, speaking, and swallowing are common in the late stages of the disease❞
If you or a loved one are experiencing worrying symptoms: when it comes to diagnosis and intervention, sooner is a lot better than later, so do talk to your doctor.
As for reducing your risk? First, the obvious stuff:
The usual 5 things that go for almost everything:
- Have a good diet—the Mediterranean Diet is once again recommended (we expect this will not be a surprise to regular readers!)
- Get regular exercise—in the case of avoiding Alzheimer’s and other dementias, typically the most important thing here is heart health, so getting regular cardiovascular exercise, such walking, running, or dancing is great. Cycling too. Swimming, not so much. Not that swimming’s bad or anything, it’s just that when your body is horizontal, the heart has less work to do, especially in the upper part of the body, because it’s not defying gravity. Similarly, yoga is great for the health but won’t particularly help with this, nor will weight training.
- Get good sleep—as we get older, we tend to need less sleep, and tend more towards the lower end of the standard “7–9 hours” prescription, but getting at least those 7 hours makes a huge difference.
- Cut down (or eliminate) alcohol consumption—and especially avoid binge-drinking. While “binge-drinking” is typically associated with young people, that Christmas party where that one uncle gets very drunk is also binge-drinking, for example. Plus, heavy drinking in early life has also been correlated with higher risk of Alzheimer’s later.
- Don’t smoke. It’s bad for everything, and Alzheimer’s risk is no exception.
How much do lifestyle changes alone make a difference?
They make a big difference. This 2022 population-based cohort study (so: huge sample size) looked at people who had 4–5 of the healthy lifestyle factors being studied, vs people who had 0–1 of them. They found:
❝A healthy lifestyle was associated with a longer life expectancy among men and women, and they lived a larger proportion of their remaining years without Alzheimer’s dementia.❞
The numbers of years involved by the way ranged between 3 and 20 years, in terms of life expectancy and years without or with Alzheimer’s, with the average increase of healthy life years being approximately the same as the average increase in years. This is important, because:
A lot of people think “well if I’m going to go senile, I might as well [unhealthy choice that shortens lifespan]”, but they misunderstand a critical factor:
The unhealthy choices will reduce their healthy life years, and simply bring the unhealthy ones (and subsequent death) sooner. If you’re going to spend your last few years in ill-health, it’s better to do so at 90 than 50.
The other thing you may already know… And a thing about it that not everyone considers:
Keeping cognitively active is important. This much is broadly known by the general public, and to clinicians, this was the fourth “healthy factor” in the list of five (instead of the sleep that we put there, because we were listing the 5 things that go for most preventable health issues).
Everyone leaps to mention sudoku at this point, so if that’s your thing, great, enjoy it! (This writer personally enjoys chess, which isn’t everyone’s cup of tea; if it yours though, you can come join her on Chess.com and we’ll keep sharp together)
But the more parts of your mental faculties you keep active, the better. Remember, brainpower (as with many things in health and life) is a matter of “use it or lose it” and this is on a “per skill” basis!
What this means: doing sudoku (a number-based puzzle game) or chess (great as it may be) won’t help as much for keeping your language skills intact, for example. Given that language skills are one of the most impactful and key faculties to get lost to Alzheimer’s disease, neglecting such would be quite an oversight!
Some good ways to keep your language skills tip-top:
- Read—but read something challenging, if possible. It doesn’t have to be Thomas Scanlon’s What We Owe To Each Other, but it should be more challenging than a tabloid, for example. In fact, on the topic of examples:
- This newsletter is written to be easy to read, while not shying away from complex ideas or hard science. Our mission is literally to “make [well-sourced, science-based] health and productivity crazy simple”.
- But the academic papers that we link? Those aren’t written to be easy to read. Go read them, or at least the abstracts (in academia, an abstract is essentially an up-front summary, and is usually the first thing you’ll see when you click a link to a study or such). Challenge yourself!
- Write—compared to reading/listening, producing language is a (related, but) somewhat separate skill. Just ask any foreign language learner which is more challenging: reading or writing!
- Journaling is great, but writing for others is better (as then you’ll be forced to think more about it)
- Learn a foreign language—in this case, what matters it that you’re practicing and learning, so in the scale of easy to hard, or doesn’t matter if it’s Esperanto or Arabic. Duolingo is a great free resource that we recommend for this, and they have a wide range of extensive courses these days.
Now for the least obvious things…
Social contact is important.
Especially in older age, it’s easy to find oneself with fewer remaining friends and family, and getting out and about can be harder for everyone. Whatever our personal inclinations (some people being more introverted or less social than others), we are fundamentally a social species, and hundreds of thousands of years of evolution have built us around the idea that we will live our lives alongside others of our kind. And when we don’t, we don’t do as well.
See for example: Associations of Social Isolation and Loneliness With Later Dementia
If you can’t get out and about easily:
- Online socialising is still socializing.
- Online community is still community.
- Online conversations between friends are still conversations between friends.
If you don’t have much (or anyone) in the category of friends and family, join Facebook groups related to your interests, for example.
Berries are surprisingly good
^This may read like a headline from 200,000 BCE, but it’s relevant here!
Particularly recommended are:
- blueberries
- blackberries
- raspberries
- strawberries
- cranberries
We know that many of these berries seem to have a shelf-life of something like 30 minutes from time of purchase, but… Frozen and dried are perfectly good nutritionally, and in many cases, even better nutritionally than fresh.
Read: Effect of berry-based supplements and foods on cognitive function: a systematic review
Turmeric’s health benefits appear to include protecting against Alzheimer’s
Again, this is about risk reduction, and turmeric (also called curcumin, which is not the same as cumin) significantly reduces the build-up of amyloid plaques in the brain. Amyloid plaques are part of the progression of Alzheimer’s.
See for yourself: Protective Effects of Indian Spice Curcumin Against Amyloid Beta in Alzheimer’s Disease
If you don’t like it as a spice (and even if you do, you probably don’t want to put it in your food every day), you can easily get it as a supplement in capsule form.
Lower your homocysteine levels
Lower our what now? Homocysteine is an amino acid used for making certain proteins, and it’s a risk factor for Alzheimer’s.
Foods high in folate (and possible other B-vitamins) seem to lower homocysteine levels. Top choices include:
- Leafy greens
- Cruciferous vegetables
- Tomatoes
Get plenty of lutein
We did a main feature about specifically this a little while ago, so we’ll not repeat our work here, but lutein is found in, well, the same things we just listed above, and lower levels of lutein are associated with Alzheimer’s disease. It’s not a proven causative factor—we don’t know entirely what causes Alzheimer’s, just a lot of factors that have a high enough correlation that it’d be remiss to ignore them.
Catch up on our previous article: Brain Food? The Eyes Have It
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Total Recovery – by Dr. Gary Kaplan
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First, know: Dr. Kaplan is an osteopath, and as such, will be mostly approaching things from that angle. That said, he is also board certified in other things too, including family medicine, so he’s by no means a “one-trick pony”, nor are there “when your only tool is a hammer, everything starts to look like a nail” problems to be found here. Instead, the scope of the book is quite broad.
Dr. Kaplan talks us through the diagnostic process that a doctor goes through when presented with a patient, what questions need to be asked and answered—and by this we mean the deeper technical questions, e.g. “what do these symptoms have in common”, and “what mechanism was at work when the pain become chronic”, not the very basic questions asked in the initial debriefing with the patient.
He also asks such questions (and questions like these get chapters devoted to them) as “what if physical traumas build up”, and “what if physical and emotional pain influence each other”, and then examines how to interrupt the vicious cycles that lead to deterioration of one’s condition.
The style of the book is very pop-science and often narrative in its presentation, giving lots of anecdotes to illustrate the principles. It’s a “sit down and read it cover-to-cover” book—or a chapter a day, whatever your preferred pace; the point is, it’s not a “dip directly to the part that answers your immediate question” book; it’s not a textbook or manual.
Bottom line: a lot of this work is about prompting the reader to ask the right questions to get to where we need to be, but there are many illustrative possible conclusions and practical advices to be found and given too, making this a useful read if you and/or a loved one suffers from chronic pain.
Click here to check out Total Recovery, and solve your own mysteries!
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NADᐩ Against Aging
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.
Nicotinamide adenine dinucleotide, or “NAD” to its friends, is a coenzyme produced in the human body (amongst other places), and it is critical for cellular energy metabolism, but there’s more to it than that.
Today we’ll be looking mostly at NAD+, of which the + indicates the positive formal charge of one of its nitrogen atoms. We won’t get too much into the chemistry of this, but we will mention that it’s a cofactor with NADH—the former accepting electrons and the latter donating electrons.
Both NAD+ and NADH are critical to good health, but we’re going to focus on NAD+ for the simple reason that it gets depleted with aging.
Note: it gets depleted with aging.
Chronological age is not so important here, but there is a direct relationship between biological aging and NAD+ depletion.
For example, healthy centenarians tend not to have depleted NAD+ levels. Further, its depletion (in those in whom it is depleted) is then a causal factor for many age-related diseases:
❝Remarkably, ageing is accompanied by a gradual decline in tissue and cellular NAD+ levels in multiple model organisms, including rodents and humans.
This decline in NAD+ levels is linked causally to numerous ageing-associated diseases, including cognitive decline, cancer, metabolic disease, sarcopenia and frailty.
Many of these ageing-associated diseases can be slowed down and even reversed by restoring NAD+ levels.❞
~ Dr. Rosalba Perrone et al.
Read in full: NAD+ metabolism and its roles in cellular processes during ageing
As for restoring those NADᐩ levels, that does help in interventional trials, whether by supplementing directly, or with NAD precursors*:
❝NAD+ levels steadily decline with age, resulting in altered metabolism and increased disease susceptibility.
Restoration of NAD+ levels in old or diseased animals can promote health and extend lifespan, prompting a search for safe and efficacious NAD-boosting molecules that hold the promise of increasing the body’s resilience, not just to one disease, but to many, thereby extending healthy human lifespan.❞
~ Dr. David Sinclair et al.
Read more: Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence
*There are actually also other NAD-boosting molecules besides NAD itself and its precursors. For example, the liver will not produce NADᐩ unless it has aminocarboxymuconate-semialdehyde decarboxylase (or “ACMSD”, to its friends), which limits the production of NADᐩ. Why, you ask? The theory is that it is a kind of evolutionary conservativism, much like not lighting a fire without the ability to put it out. In any case, taking ACMSD-blockers will thus result in an increased endogenous production of NADᐩ.
You can read about this here:
De novo NAD+ synthesis enhances mitochondrial function and improves health
Nor is taking supplements or drugs the only way to get more of it; there’s an enzyme nicotinamide phosphoribosyltransferase (“NAMPT”, to its friends) involved in the synthesis of NADᐩ, and exercise boosts levels by 127% (i.e., it more than doubles the levels), based on a modest three-week exercise bike regimen:
Skeletal muscle NAMPT is induced by exercise in humans
And to underline that point, another study found that resistance training (so, a different kind of exercise from that of the previous study) boosts levels of NADᐩ itself by the same 127%:
One way to get more out of NADᐩ
We’ll get straight to the point: it works very well paired with a senolytic agent, i.e. something that kills aging cells so that they get recycled sooner:
NAD+, Senolytics, or Pyruvate for Healthy Aging?
To read more about senolytics, check out:
Fisetin: The Anti-Aging Assassin
Want to try some?
We don’t sell it, but here for your convenience is an example product on Amazon 😎
Enjoy!
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How To Eat To Lose Belly Fat (3 Stages)
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Belly fat is easier to gain than it is to lose, and it’s absolutely something that needs more attention in the kitchen than in the gym. Here’s one way of doing it:
By the numbers
First note: this video is by a man, and judging by the numbers mentioned, assumes that the viewer is also a man. An end goal of 10% body fat is a little on the low side for men, and would be dangerous for women. The magic 15% mark that he mentions as being a point where various metabolic things change, is more like 20% for women. All assuming normal hormones, of course, since it is hormones that direct this.
Healthy body fat percentages are (assuming normal hormones) in the range of 20–25% for women and 15–20% for men.
With that in mind…
The idea of this approach is to lose enough weight that your body gets rid of even the most awkward bits (e.g: visceral belly fat, which will often be the last to get used) before, if desired, then maintaining at a slightly higher body fat percentage.
- Stage 1: count calories (we don’t usually recommend this at 10almonds, but he does, so we’re reporting it here) and use your weight in pounds multiplied by 12 to give your daily calorie target. Make the majority of your diet foods that have a large volume:calorie ratio, such as fruits and vegetables, in order to feel full without overloading your metabolism. He has an interesting method of calculating a protein target; instead of the usual “1g/kg of body weight”, he says 1g per cm of height. Doing this consistently should get you to 15% body fat (so, 20%, for women).
- Stage 2: start counting fat intake too, and aim for 20–25% of your daily calories as fat. Continue, aside from that, with what you were doing in Stage 1. Doing this consistently should get you to 12% body fat (so, about 17%, for women). Being under the usual healthy level for a while should allow your body to start getting rid of visceral fat.
- Stage 3: track everything, levelling up your precision (no more “this little thing doesn’t count”), and planning ahead when it comes to social events etc. Doing this consistently should yet you to 10% body fat (so, about 15%, for women). This stage has a good chance of making most people miserable, so if that happens, consider the benefits of going back to the healthier 15% body fat (men) or 20% (women).
For more on all of this, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like to read:
Visceral Belly Fat & How To Lose It ← without calorie-counting! We prefer this 😉
Take care!
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The first pig kidney has been transplanted into a living person. But we’re still a long way from solving organ shortages
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In a world first, we heard last week that US surgeons had transplanted a kidney from a gene-edited pig into a living human. News reports said the procedure was a breakthrough in xenotransplantation – when an organ, cells or tissues are transplanted from one species to another. https://www.youtube.com/embed/cisOFfBPZk0?wmode=transparent&start=0 The world’s first transplant of a gene-edited pig kidney into a live human was announced last week.
Champions of xenotransplantation regard it as the solution to organ shortages across the world. In December 2023, 1,445 people in Australia were on the waiting list for donor kidneys. In the United States, more than 89,000 are waiting for kidneys.
One biotech CEO says gene-edited pigs promise “an unlimited supply of transplantable organs”.
Not, everyone, though, is convinced transplanting animal organs into humans is really the answer to organ shortages, or even if it’s right to use organs from other animals this way.
There are two critical barriers to the procedure’s success: organ rejection and the transmission of animal viruses to recipients.
But in the past decade, a new platform and technique known as CRISPR/Cas9 – often shortened to CRISPR – has promised to mitigate these issues.
What is CRISPR?
CRISPR gene editing takes advantage of a system already found in nature. CRISPR’s “genetic scissors” evolved in bacteria and other microbes to help them fend off viruses. Their cellular machinery allows them to integrate and ultimately destroy viral DNA by cutting it.
In 2012, two teams of scientists discovered how to harness this bacterial immune system. This is made up of repeating arrays of DNA and associated proteins, known as “Cas” (CRISPR-associated) proteins.
When they used a particular Cas protein (Cas9) with a “guide RNA” made up of a singular molecule, they found they could program the CRISPR/Cas9 complex to break and repair DNA at precise locations as they desired. The system could even “knock in” new genes at the repair site.
In 2020, the two scientists leading these teams were awarded a Nobel prize for their work.
In the case of the latest xenotransplantation, CRISPR technology was used to edit 69 genes in the donor pig to inactivate viral genes, “humanise” the pig with human genes, and knock out harmful pig genes. https://www.youtube.com/embed/UKbrwPL3wXE?wmode=transparent&start=0 How does CRISPR work?
A busy time for gene-edited xenotransplantation
While CRISPR editing has brought new hope to the possibility of xenotransplantation, even recent trials show great caution is still warranted.
In 2022 and 2023, two patients with terminal heart diseases, who were ineligible for traditional heart transplants, were granted regulatory permission to receive a gene-edited pig heart. These pig hearts had ten genome edits to make them more suitable for transplanting into humans. However, both patients died within several weeks of the procedures.
Earlier this month, we heard a team of surgeons in China transplanted a gene-edited pig liver into a clinically dead man (with family consent). The liver functioned well up until the ten-day limit of the trial.
How is this latest example different?
The gene-edited pig kidney was transplanted into a relatively young, living, legally competent and consenting adult.
The total number of gene edits edits made to the donor pig is very high. The researchers report making 69 edits to inactivate viral genes, “humanise” the pig with human genes, and to knockout harmful pig genes.
Clearly, the race to transform these organs into viable products for transplantation is ramping up.
From biotech dream to clinical reality
Only a few months ago, CRISPR gene editing made its debut in mainstream medicine.
In November, drug regulators in the United Kingdom and US approved the world’s first CRISPR-based genome-editing therapy for human use – a treatment for life-threatening forms of sickle-cell disease.
The treatment, known as Casgevy, uses CRISPR/Cas-9 to edit the patient’s own blood (bone-marrow) stem cells. By disrupting the unhealthy gene that gives red blood cells their “sickle” shape, the aim is to produce red blood cells with a healthy spherical shape.
Although the treatment uses the patient’s own cells, the same underlying principle applies to recent clinical xenotransplants: unsuitable cellular materials may be edited to make them therapeutically beneficial in the patient.
CRISPR technology is aiming to restore diseased red blood cells to their healthy round shape. Sebastian Kaulitzki/Shutterstock We’ll be talking more about gene-editing
Medicine and gene technology regulators are increasingly asked to approve new experimental trials using gene editing and CRISPR.
However, neither xenotransplantation nor the therapeutic applications of this technology lead to changes to the genome that can be inherited.
For this to occur, CRISPR edits would need to be applied to the cells at the earliest stages of their life, such as to early-stage embryonic cells in vitro (in the lab).
In Australia, intentionally creating heritable alterations to the human genome is a criminal offence carrying 15 years’ imprisonment.
No jurisdiction in the world has laws that expressly permits heritable human genome editing. However, some countries lack specific regulations about the procedure.
Is this the future?
Even without creating inheritable gene changes, however, xenotransplantation using CRISPR is in its infancy.
For all the promise of the headlines, there is not yet one example of a stable xenotransplantation in a living human lasting beyond seven months.
While authorisation for this recent US transplant has been granted under the so-called “compassionate use” exemption, conventional clinical trials of pig-human xenotransplantation have yet to commence.
But the prospect of such trials would likely require significant improvements in current outcomes to gain regulatory approval in the US or elsewhere.
By the same token, regulatory approval of any “off-the-shelf” xenotransplantation organs, including gene-edited kidneys, would seem some way off.
Christopher Rudge, Law lecturer, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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