
Sleep & Exercise: A One-Way Relationship?
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It’s a long-held reasonable assumption that sleep and exercise benefit each other. After all, sleep is restorative ready for exercise, and exercise tires you out ready for sleep.
Indeed, this forms at least part of a lot of circadian rhythm-based approaches to healthy living, for example:
10 Tips for Better Sleep: Starting In The Morning ← note though that the exercise timing advice here is “Exercise regularly but avoid strenuous activity 2 hours before bed. Optimal exercise time is 4–6 hours before bedtime.”
And yet, it turns out that the relationship is a lot more one-sided than has been believed:
You snooze, you… Choose? Enthuse? Put on your running shoes?
Researchers (Dr. Hannah Scott et al.) looked at data from 70,963 people (using an under-mattress sleep sensor and a wrist-worn health tracker) for a little over three and a half years, and found some surprising things, including:
- only 12.9% regularly attained the recommended seven to nine hours of sleep and more than 8,000 steps per day
- on the other end of the scale, 16.5% slept less than seven hours and walked fewer than 5,000 steps—an association with higher risks of chronic disease, weight gain, and mental-health challenges
However, putting the data together in a way we haven’t seen done before, Dr. Scott and her team were able to establish that there was more to this than “healthy people tend to be healthy in multiple life areas; unhealthy people tend to be unhealthy in multiple life areas”.
Specifically, six to seven hours of sleep was linked to the highest next-day step counts, though sleep quality remained most important. In other words, high-quality, efficient sleep (less tossing and turning) reliably predicted higher step counts the next day.
On the other hand, and which is more surprising, doing more steps during the day did not meaningfully improve sleep that night.
Putting it in numbers, we’ll quote directly from the “results” section of the paper:
❝We show that only 12.9% of people achieve the recommended sleep duration of 7-9hrs/night and >8,000 steps/day, with 16.5% having short sleep (<7hrs/night) and sedentary lives (<5,000 steps/day). Approximately 6hrs sleep equates to the greatest next-day step count (e.g., +339 steps vs 8 hrs/night), and sleep efficiency positively predicts next-day step count in a dose-dependent manner (25th vs 75th percentile: +282 steps/day). Sleep appears largely unaffected by previous-day step count. Effects are similar across age groups but decline in magnitude when adjusted for awake duration.❞
You can read the paper in full, here: Bidirectional associations between sleep and physical activity investigated using large-scale objective monitoring data
Note: curiously, and which doesn’t really affect the science here but we should found it interesting:
- Josh Fitton is the corresponding (and thus first-listed) author of the study, although he is a student, and
- Dr. Hannah Scott is Senior Research Fellow, NHMRC Emerging Leadership Fellow, and co-Lead of the Clinical Sleep Health research group at the Flinders Health and Medical Research Institute (FHMRI): Sleep Health Flagship program, and also has getting on for a hundred peer-reviewed papers to her name. Oh, and she’s the Chair on the Board of the Australasian Sleep Association (ASA): Australia’s peak sleep advocacy body. Aside from that, she’s received multiple awards including the Flinders University Vice-Chancellor’s Early Career Researcher Award, the ASA New Investigator Award and ASA Helen Bearpark Award, and the Society of Behavioural Sleep Medicine Fellow Rising Star Award. In short, she’s pretty cool and she knows her stuff.
Given that Dr. Scott’s research specialty involves investigating the use of digital technologies to better assess and manage sleep health and sleep disorders, we infer that Mr. Fitton is one of her students.
About those technologies, Dr Scott is also one of the researchers responsible for THIM: the first wearable device specifically to track and treat chronic insomnia.
On which note, you might want to check out: What Your Fitness Tracker Is Best & Worst At
Want to learn more?
For a particular kind of exercise that can help you sleep, you might like this book that we reviewed a while back:
Yoga For Better Sleep – by Mark Stephens
Sweet dreams!
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Habits of a Happy Brain – by Dr. Loretta Graziano Breuning
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There are lots of books on “happy chemicals” and “how to retrain your brain”, so what makes this one different?
Firstly, it focuses on four “happy chemicals”, not just one:
- Serotonin
- Dopamine
- Oxytocin
- Endorphins
It also looks at the role of cortisol, and how it caps off each of those just a little bit, to keep us just a little malcontent.
Behavioral psychology tends to focus most on dopamine, while prescription pharmaceuticals for happiness (i.e., most antidepressants) tend to focus on serotonin. Here, Dr. Breuning helps us understand the complex interplay of all of the aforementioned chemicals.
She also clears up many misconceptions, since a lot of people misattribute the functions of each of these.
Common examples include “I’m doing this for the serotonin!” when the activity is dopaminergic not serotoninergic, or considering dopamine “the love molecule” when oxytocin, or even something else like phenylethylamine would be more appropriate.
The above may seem like academic quibbles and not something of practical use, but if we want to biohack our brains, we need to do better than the equivalent of a chef who doesn’t know the difference between salt and sugar.
Where things are of less practical use, she tends to skip over or at least streamline them. For example, she doesn’t really discuss the role of post-dopamine prolactin in men—but the discussion of post-happiness cortisol covers the same ground anyway, for practical purposes.
Dr. Breuning also looks at where our evolved neurochemical responses go wrong, and lays out guidelines for such challenges as overcoming addiction, or embracing delayed gratification.
Bottom line: this book is a great user-manual for the brain. If you’d like to be happier and more effective with fewer bad habits, this is the book for you.
Click here to check out Habits of a Happy Brain, and get biohacking yours!
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Spermine vs Alzheimer’s & Parkinson’s!
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Alzheimer’s and Parkinson’s are both neurodegenerative disorders that involve an accumulation of harmful proteins in the brain, including α-synuclein, β-amyloid (also called amyloid-β; it’s the exact same protein just written down differently), and tau protein*.
*…which just gets written like that instead of using a Greek letter τ, probably to avoid looking like the Greek letter τ that in mathematics denotes the ratio of the circumference to the radius of a circle (so in other words, 2π).
Back to biology
Because of the association of those harmful proteins with the development and progression of neurodegenerative disorders, a lot of attention has been given to how to get rid of them.
In a health brain, the glymphatic system (a portmanteau of glial cells doing the job of the lymphatic system, but in the brain, where there is no lymph) does this adequately.
We’ve written about this previously, for example:
How To Clean Your Brain (Glymphatic Health Primer)
Take Care Of Your Lymphatic System To Beat Cognitive Decline ← still relevant because once the waste products have been removed from the brain, they still need to be removed further, or else they would just pile up right outside the brain, as though a city’s sanitation workers went on strike.
On which note, because the glymphatic system is strongly affected by gravity, the brain’s ability to remove toxins is dependent on the orientation of the head. This is critical for the clearance of α-synuclein and β-amyloid proteins, amongst others, and so this has a consequence that we’ve done a main feature about before:
- sleeping sideways is far better than sleeping on one’s back.
- sleeping on one’s right side is better than sleeping on one’s left side.
For more details on that, see:
Goodnight, Glymphatic System: How Your Sleep Position Changes Dementia Risk
Now, about spermine!
Firstly, what is it? Spermine is a rather small polyamine (protein made of more than one amino acid) that occurs naturally in most living cells of the body that are capable of mitosis.
Next, why is called that? Spermine was first identified in seminal fluid about 150 years ago, as it’s present in relatively high concentrations there. Aside from that, there is no particular connection with sperm, and as we say, it’s made throughout the body.
Finally, why is there a chef’s hat on the brain in the image next to this article’s title? For this one, you can blame the lead researcher, Dr. Jinghui Lui, who explained spermine’s anti-Alzheimer’s and anti-Parkinson’s powers in the following way:
❝Autophagy is more effective at handling larger protein clumps. And spermine is, so to speak, the binding agent that brings the strands together. There are only weakly attractive electrical forces between the molecules, and these organize them but do not firmly bind them together.
The spermine is like cheese that connects the long, thin noodles without gluing them together, making them easier to digest.
If we better understand the underlying processes, we can cook tastier and more digestible dishes, so to speak, because then we’ll know exactly which spices, in which amounts, make the sauce especially tasty.❞
Lexical note: Autophagy = literally, “eating oneself”; it’s the name given to the cellular process of “eating” old cells, either for recycling or waste disposal, or a combination of the above.
Now, maybe she got carried away in the last bit there about making the sauce especially tasty, but her point is that the presence of spermine causes the harmful proteins to clump in ways that make them easier for the body to eliminate.
You might be wondering how it does that, and to use slightly more scientific words than Dr. Lui’s cooking metaphor, spermine promotes biomolecular condensation—gently drawing protein fibers together through weak electrical interactions (like how static charge makes things cling together)—so that the cell’s waste-removal system can degrade them more efficiently.
You might next be wondering what level testing is at, and it’s currently at the level of our dear old friend C. elegans (a nematode, a kind of tiny worm, used a lot in biological research). Now, that may not sound inspiring of confidence, but C. elegans is used a lot in medical research of this kind because:
- Despite being very small and very simple, C. elegans shares many fundamental biological pathways with humans, including those governing aging, metabolism, stress responses, autophagy, and cell death. This makes it a great choice for first-line experiments in things pertaining to those areas of biology.
- Of particular relevance to this study, it has 302 neurons with a complete, published connectome—the only animal with a fully mapped neural wiring diagram—making it awesome for studying neurobiology and degeneration.
- And, as a bonus, the worm’s entire body is transparent, allowing real-time imaging of cellular processes, protein aggregation (yes, exactly of the kinds we’ve been talking about today), and more (we’ll be here all day if we list the things) without invasive procedures (that would create a confounding observer bias by killing the worm and thus halting the process, or at the very least injuring the worm and thus interfering with the process).
So that’s why Dr. Liu and her team used that.
Of course, C. elegans is only the first step, and future experiments will need to scale things up—probably mice next, then humans. A full step-by-step progression would go something like C. elegans → D. melanogaster (fruit fly) → mouse → non-human primate of some kind → human, but realistically, the only stages probably needed for this are nematode → mouse → human.
In summary: spermine’s protein-clustering effect can now accelerate the development of new treatments for neurodegenerative diseases.
You can read the (fascinating) paper in full, here: Spermine modulation of Alzheimer’s Tau and Parkinson’s α-synuclein: implications for biomolecular condensation and neurodegeneration
So… Should I eat sperm?
Well, don’t let us stop you if you feel so inclined, but no, there’s no medical reason to do so that we’re aware of, including the above.
We hit a similar issue issue with: Spermidine For Longevity ← note that this is spermidine, not spermine; similar name and similar etymology; different molecule!
…in which we noted:
Does that mean that consuming semen is good for longevity?
Aside from the health benefits of a healthy sex life… No, not really. Semen does contain spermidine as well as some important minerals, but you’d need to consume approximately 1 cup of semen to get the equivalent spermidine you’d get from 1 tbsp of edamame (young soy) beans.
Unless your lifestyle is rather more exciting than this writer’s, it’s a lot easier to get 1 tbsp of edamame beans than 1 cup of semen.
Learn more: Frontiers in Nutrition | Polyamines in Food
Enjoy!
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Relationships: When To Stick It Out & When To Call It Quits
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Like A Ship Loves An Anchor?
Today’s article may seem a little bit of a downer to start with, but don’t worry, it picks up again too. Simply put, we’ve written before about many of the good parts of relationships, e.g:
Only One Kind Of Relationship Promotes Longevity This Much!
…but what if that’s not what we have?
Note: if you have a very happy, secure, fulfilling, joyous relationship, then, great! Or if you’re single and happy, then, also great! Hopefully you will still find today’s feature of use if you find yourself advising a friend or family member one day. So without further ado, let’s get to it…
You may be familiar with the “sunk cost fallacy”; if not: it’s what happens when a person or group has already invested into a given thing, such that even though the thing is not going at all the way they hoped, they now want to continue trying to make that thing work, lest their previous investment be lost. But the truth is: if it’s not going to work, then the initial investment is already lost, and pouring out extra won’t help—it’ll just lose more.
That “investment” in a given thing could be money, time, energy, or (often the case) a combination of the above.
In the field of romance, the “sunk cost fallacy” keeps a lot of bad relationships going for longer than perhaps they should, and looking back (perhaps after a short adjustment period), the newly-single person says “why did I let that go on?” and vows to not make the same mistake again.
But that prompts the question: how can we know when it’s right to “keep working on it, because relationships do involve work”, as perfectly reasonable relationship advice often goes, and when it’s right to call it quits?
Should I stay or should I go?
Some questions for you (or perhaps a friend you might find yourself advising) to consider:
- What qualities do you consider the most important for a partner to have—and does your partner have them?
- If you described the worst of your relationship to a close friend, would that friend feel bad for you?
- Do you miss your partner when they’re away, or are you glad of the break? When they return, are they still glad to see you?
- If you weren’t already in this relationship, would you seek to enter it now? (This takes away sunk cost and allows a more neutral assessment)
- Do you feel completely safe with your partner (emotionally as well as physically), or must you tread carefully to avoid conflict?
- If your partner decided tomorrow that they didn’t want to be with you anymore and left, would that be just a heartbreak, or an exciting beginning of a new chapter in your life?
- What things would you generally consider dealbreakers in a relationship—and has your partner done any of them?
The last one can be surprising, by the way. We often see or hear of other people’s adverse relationship situations and think “I would never allow…” yet when we are in a relationship and in love, there’s a good chance that we might indeed allow—or rather, excuse, overlook, and forgive.
And, patience and forgiveness certainly aren’t inherently bad traits to have—it’s just good to deploy them consciously, and not merely be a doormat.
Either way, reflect (or advise your friend/family member to reflect, as applicable) on the “score” from the above questions.
- If the score is good, then maybe it really is just a rough patch, and the tools we link at the top and bottom of this article might help.
- If the score is bad, the relationship is bad, and no amount of historic love or miles clocked up together will change that. Sometimes it’s not even anyone’s fault; sometimes a relationship just ran its course, and now it’s time to accept that and turn to a new chapter.
“At my age…”
As we get older, it’s easy for that sunk cost fallacy to loom large. Inertia is heavy, the mutual entanglement of lives is far-reaching, and we might not feel we have the same energy for dating that we did when we were younger.
And there may sometimes be a statistical argument for “sticking it out” at least for a while, depending on where we are in the relationship, per this study (with 165,039 participants aged 20–76), which found:
❝Results on mean levels indicated that relationship satisfaction decreased from age 20 to 40, reached a low point at age 40, then increased until age 65, and plateaued in late adulthood.
As regards the metric of relationship duration, relationship satisfaction decreased during the first 10 years of the relationship, reached a low point at 10 years, increased until 20 years, and then decreased again.❞
Source: Development of Relationship Satisfaction Across the Life Span: A Systematic Review and Meta-Analysis
And yet, when it comes to prospects for a new relationship…
- If our remaining life is growing shorter, then it’s definitely too short to spend in an unhappy relationship
- Maybe we really won’t find romance again… And maybe that’s ok, if w’re comfortable making our peace with that and finding joy in the rest of life (this widowed writer (hi, it’s me) plans to remain single now by preference, and her life is very full of purpose and beauty and joy and yes, even love—for family, friends, etc, plus the memory of my wonderful late beloved)
- Nevertheless, the simple fact is: many people do find what they go on to describe as their best relationship yet, late in life ← this study is with a small sample size, but in this case, even anecdotal evidence seems sufficient to make the claim reasonable; probably you personally know someone who has done so. If they can, so can you, if you so wish.
- Adding on to that last point… Later life relationships can also offer numerous significant advantages unique to such (albeit some different challenges too—but with the right person, those challenges are just a fun thing to tackle together). See for example:
An exploratory investigation into dating among later‐life women
And about those later-life relationships that do work? They look like this:
this one looks like the title says it all, but it really doesn’t, and it’s very much worth at least reading the abstract, if not the entire paper—because it talks a lot about the characteristics that make for happy or unhappy relationships, and the effect that those things have on people. It really is very good, and quite an easy read.
See again: Healthy Relationship, Healthy Life
Take care!
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Do We Need Sunscreen In Winter, Really?
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It’s Q&A Day at 10almonds!
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 😎
❝I keep seeing advice that we shoudl wear sunscreen out in winter even if it’s not hot or sunny, but is there actually any real benefit to this?❞
Short answer: yes (but it’s indeed not as critical as it is during summer’s hot/sunny days)
Longer answer: first, let’s examine the physics of summer vs winter when it comes to the sun…
In summer (assuming we live far enough from the equator to have this kind of seasonal variation), the part of the planet where we live is tilted more towards the sun. This makes it closer, and more importantly, it’s more directly overhead during the day. The difference in distance through space isn’t as big a deal as the difference in distance through the atmosphere. When the sun is more directly overhead, its rays have a shorter path through our atmosphere, and thus less chance of being blocked by cloud cover / refracted elsewhere / bounced back off into space before it even gets that far.
In winter, the opposite of all that is true.
Morning/evening also somewhat replicate this compared to midday, because the sun being lower in the sky has a similar effect to seasonal variation causing it to be less directly overhead.
For this reason, even though visually the sun may be just as bright on a winter morning as it is on a summer midday, the rays have been filtered very differently by the time they get to us.
This is one reason why you’re much less likely to get sunburned in the winter, compared to the summer (others include the actual temperature difference, your likely better hydration, and your likely more modest attire protecting you).
However…
The reason it is advisable to wear sunscreen in winter is not generally about sunburn, and is rather more about long-term cumulative skin damage (ranging from accelerated aging to cancer) caused by the UV rays—specifically, mostly UVA rays, since UVB rays (with their higher energy but shorter wavelength) have nearly all been blocked by the atmosphere.
Here’s a good explainer of that from the American Cancer Society:
UV (Ultraviolet) Radiation and Cancer Risk
👆 this may seem like a no-brainer, but there’s a lot explained here that demystifies a lot of things, covering ionizing vs non-ionizing radiation, x-rays and gamma-rays, the very different kinds of cancer caused by different things, and what things are dangerous vs which there’s no need to worry about (so far as best current science can say, at least).
Consequently: yes, if you value your skin health and avoidance of cancer, wearing sunscreen when out even in the winter is a good idea. Especially if your phone’s weather app says the UV index is “moderate” or above, but even if it’s “low”, it doesn’t hurt to include it as part of your skincare routine.
But what if sunscreens are dangerous?
Firstly, not all sunscreens are created equal:
Learn more: Who Screens The Sunscreens?
Secondly: consider putting on a protective layer of moisturizer first, and then the sunscreen on top. Bear in mind, this is winter we’re talking about, so you’re probably not going out in a bikini, so this is likely a face-neck-hands job and you’re done.
What about vitamin D?
Humans evolved to have more or less melanin in our skin depending on where we lived, and white people evolved to wring the most vitamin D possible out of the meagre sun far from the equator. Black people’s greater melanin, on the other hand, offers some initial protection against the sun (but any resultant skin cancer is then more dangerous than it would be for white people if it does occur, so please do use sunscreen whatever your skintone).
Nowadays many people live in many places which may or may not be the places we evolved for, and so we have to take that into account when it comes to sun exposure.
Here’s a deeper dive into that, for those who want to learn:
Take care!
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Vaccines and cancer: The myth that won’t die
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Two recent studies reported rising cancer rates among younger adults in the U.S. and worldwide. This prompted some online anti-vaccine accounts to link the studies’ findings to COVID-19 vaccines.
But, as with other myths, the data tells a very different story.
What you need to know
- Baseless claims that COVID-19 vaccines cause cancer have persisted online for several years and gained traction in late 2023.
- Two recent reports finding rising cancer rates among younger adults are based on pre-pandemic cancer incidence data. Cancer rates in the U.S. have been on the rise since the 1990s.
- There is no evidence of a link between COVID-19 vaccination and increased cancer risk.
False claims about COVID-19 vaccines began circulating months before the vaccines were available. Chief among these claims was misinformed speculation that vaccine mRNA could alter or integrate into vaccine recipients’ DNA.
It does not. But that didn’t prevent some on social media from spinning that claim into a persistent myth alleging that mRNA vaccines can cause or accelerate cancer growth. Anti-vaccine groups even coined the term “turbo cancer” to describe a fake phenomenon of abnormally aggressive cancers allegedly linked to COVID-19 vaccines.
They used the American Cancer Society’s 2024 cancer projection—based on incidence data through 2020—and a study of global cancer trends between 1999 and 2019 to bolster the false claims. This exposed the dishonesty at the heart of the anti-vaccine messaging, as data that predated the pandemic by decades was carelessly linked to COVID-19 vaccines in viral social media posts.
Some on social media cherry-pick data and use unfounded evidence because the claims that COVID-19 vaccines cause cancer are not true. According to the National Cancer Institute and American Cancer Society, there is no evidence of any link between COVID-19 vaccines and an increase in cancer diagnosis, progression, or remission.
Why does the vaccine cancer myth endure?
At the root of false cancer claims about COVID-19 vaccines is a long history of anti-vaccine figures falsely linking vaccines to cancer. Polio and HPV vaccines have both been the target of disproven cancer myths.
Not only do HPV vaccines not cause cancer, they are one of only two vaccines that prevent cancer.
In the case of polio vaccines, some early batches were contaminated with simian virus 40 (SV40), a virus that is known to cause cancer in some mammals but not humans. The contaminated batches were discovered, and no other vaccine has had SV40 contamination in over 60 years.
Follow-up studies found no increase in cancer rates in people who received the SV40-contaminated polio vaccine. Yet, vaccine opponents have for decades claimed that polio vaccines cause cancer.
Recycling of the SV40 myth
The SV40 myth resurfaced in 2023 when vaccine opponents claimed that COVID-19 vaccines contain the virus. In reality, a small, nonfunctional piece of the SV40 virus is used in the production of some COVID-19 vaccines. This DNA fragment, called the promoter, is commonly used in biomedical research and vaccine development and doesn’t remain in the finished product.
Crucially, the SV40 promoter used to produce COVID-19 vaccines doesn’t contain the part of the virus that enters the cell nucleus and is associated with cancer-causing properties in some animals. The promoter also lacks the ability to survive on its own inside the cell or interact with DNA. In other words, it poses no risk to humans.
Over 5.6 billion people worldwide have received COVID-19 vaccines since December 2020. At that scale, even the tiniest increase in cancer rates in vaccinated populations would equal hundreds of thousands of excess cancer diagnoses and deaths. The evidence for alleged vaccine-linked cancer would be observed in real incidence, treatment, and mortality data, not social media anecdotes or unverifiable reports.
This article first appeared on Public Good News and is republished here under a Creative Commons license.
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Guess How Much Lead Is Released By Disposable Vapes
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We’ll not bury the lead, so to speak:
❝To place the potential for Pb exposure in the context of traditional cigarettes, Figure 3B compares the mass of Pb in a pack of traditional cigarettes (20 cigarettes) to the mass of Pb of a comparable nicotine dose from the Esco Bar devices (details provided in SI Section S2.4).
In comparison to the highest Pb delivery measured for traditional cigarettes, on average Esco Bar devices (Flavored and Clear) emitted ∼4 to 13 times more Pb (4.9 and 15.4 μg, respectively) in the first 200 puffs than the highest reported for a pack of cigarettes (20 cigarettes; 1.2 μg) (42) (Figure 3B, Table S13.2).
For context, this level of Pb exposure is equivalent to smoking as many as 19 packs of cigarettes in a single day (Table S13.3).❞
Pb = lead, as in the heavy metal of that name
Read in full: Elevated Toxic Element Emissions from Popular Disposable E-Cigarettes: Sources, Life Cycle, and Health Risks
There are several things at hand here:
- This is of course only looking at lead, and not other considerations.
- You can read about some of the other considerations in the paper, by the way; they did look at other toxic elements too; we’re just focusing on lead here
- Vapes (of various kinds) contain many other unpleasantries, and/but so do cigarettes (partially overlapping; each method has its relative strengths and weaknesses)
- This is specifically about disposable vapes, and will not apply to refillable vapes in the same way (because those “first 200 puffs” aren’t being repeated every day with a new device bringing more lead; instead it’s the same device every day, delivering gradually less lead each day)
- That does not, however, mean that refillable vapes are safe or healthy, just that they will be relatively less unsafe and less unhealthy than disposable ones
You may be wondering: why is this only just now coming out?
And the answer is:
tobacco companies have a huge amount of influence on what research is (and isn’t) done/published with regard to tobaccoBesides any research/publication bias that may be occurring, there are more reasons too:
- Companies manufacturing these disposable vapes outright lied about what went into their construction (the paper discusses this “illicit use of leaded bronze”
- Unlike a lot of health risks, lead poisoning is cumulative and/but very slow to show ill effects (one of the reasons it took humanity until quite recent times to establish lead’s toxicity; it was hard to isolate the effects of a toxin that acts so very slowly and that everyone was getting from the ubiquity of lead plumbing)
- This problem is much more severe in the latest generation of e-cigarettes (the paper compared and contrasted them to older devices)
For reference, OSHA puts the Permissible Exposure Limit (PEL) for lead exposure in the workplace at 50 micrograms per cubic meter (of air) over 8 hours.
The paper cites finding 175 ppm of lead, which is approximately 1,533,540 micrograms per cubic meter.
Suffice it to say, neither you nor your loved ones should be inhaling a gram and half of lead.
Want to learn more?
You can learn more about vaping from our older article about this, which (obviously) doesn’t cover the heavy metal content that’s just been revealed, but examines the other considerations (including pros and cons vs smoking): Vaping: A Lot Of Hot Air?
Take care!
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