It’s Not Fantastic To Be Plastic

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We Are Such Stuff As Bottles Are Made Of

We’ve written before about PFAS, often found in non-stick coatings and the like:

PFAS Exposure & Cancer: The Numbers Are High

Today we’re going to be talking about microplastics & nanoplastics!

What are microplastics and nanoplastics?

Firstly, they’renot just the now-banned plastic microbeads that have seen some use is toiletries (although those are classified as microplastics too).

Many are much smaller than that, and if they get smaller than a thousandth of a millimeter, then they get the additional classification of “nanoplastic”.

In other words: not something that can be filtered even if you were to use a single-micron filter. The microplastics would still get through, for example:

Scientists find about a quarter million invisible nanoplastic particles in a liter of bottled water

And unfortunately, that’s bad:

❝What’s disturbing is that small particles can appear in different organs and may cross membranes that they aren’t meant to cross, such as the blood-brain barrier❞

~ Dr. Zoie Diana

Note: they’re crossing the same blood-brain barrier that many of our nutrients and neurochemicals are too big to cross.

These microplastics are also being found in arterial plaque

What makes arterial plaque bad for the health is precisely its plasticity (the arterial walls themselves are elastic), so you most certainly do not want actual plastic being used as part of the cement that shouldn’t even be lining your arteries in the first place:

Microplastics found in artery plaque linked with higher risk of heart attack, stroke and death

❝In this study, patients with carotid artery plaque in which MNPs were detected had a higher risk of a composite of myocardial infarction, stroke, or death from any cause at 34 months of follow-up than those in whom MNPs were not detected❞

~ Dr. Raffaele Marfella et al.

(MNP = Micro/Nanoplastics)

Source: Microplastics and Nanoplastics in Atheromas and Cardiovascular Events

We don’t know how bad this is yet

There are various ways this might not be as bad as it looks (the results may not be repeated, the samples could have been compromised, etc), but also, perhaps cynically but nevertheless honestly, it could also be worse than we know yet—only more experiments being done will tell us which.

In the meantime, here’s a rundown of what we do and don’t know:

Study links microplastics with human health problems—but there’s still a lot we don’t know

Take care!

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  • The Brain Alarm Signs That Warn Of Dementia

    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.

    When it comes to predicting age-related cognitive impairment:

    First there are genetic factors to take into account (such as the APOE4 gene for Alzheimer’s), as well as things such as age and sex.

    When it comes to sex, by the way, what matters here is hormones, which is why [it seems; this as technically as yet unproven with full rigor, but the hypothesis is sound and there is a body of evidence gradually being accumulated to support it] postmenopausal women with untreated menopause get Alzheimer’s at a higher rate and deteriorate more quickly:

    Alzheimer’s Sex Differences May Not Be What They Appear

    Next, there are obviously modifiable lifestyle factors to take into account, things that will reduce your risk such as getting good sleep, good diet, good exercise, and abstaining from alcohol and smoking, as well as oft-forgotten things such as keeping cognitively active and, equally importantly, socially active:

    How To Reduce Your Alzheimer’s Risk

    (the article outlines what matters the most in each of the above areas, by the way, so that you can get the most bang-for-buck in terms of lifestyle adjustments)

    Lastly (in the category of risk factors), there are things to watch out for in the blood such as hypertension and high cholesterol.

    Nipping it in the blood

    In new research (so new it is still ongoing, but being at year 2 of a 4-year prospective study, they have published a paper with their results so far), researchers have:

    1. started with the premise “dementia is preceded by mild cognitive impairment”
    2. then, asked the question “what are the biometric signs of mild cognitive impairment?”

    Using such tools as functional near-infrared spectroscopy (fNIRS) while the participants performed cognitive tasks, they were able to record changes in plasma levels of extracellular vesicles, assessing them with small-particle flow cytometry.

    Translating from sciencese: they gave the participants mental tasks, and while they completed them, the researchers scanned their brains and monitored blood flow and the brain’s ability to compensate for any lack of it.

    What they found:

    • in young adults, blood flow increased, facilitating neurovascular coupling (this is good)
    • in older adults, blood flow did not increase as much, but they engaged other areas of the brain to compensate, by what’s called functional connectivity (this is next best)
    • in those with mild cognitive impairment, blood flow was reduced, and they did not have the ability to compensate by functional connectivity (this is not good)

    They also performed a liquid biopsy, which sounds alarming but it just means they took some blood, and tested this for density of cerebrovascular endothelial extracellular vesicles (CEEVs), which—in more prosaic words—are bits from the cells lining the blood vessels in the brain.

    People with mild cognitive impairment had more of these brain bits in their blood than those without.

    You can read the paper itself here:

    Neurovascular coupling, functional connectivity, and cerebrovascular endothelial extracellular vesicles as biomarkers of mild cognitive impairment

    What this means

    The science here is obviously still young (being as it is still in progress), but this will likely contribute greatly to early warning signs of dementia, by catching mild cognitive impairment in its early stages, by means of a simple blood test, instead of years of wondering before getting a dementia diagnosis.

    And of course, forewarned is forearmed, so if this is something that could be done as a matter of routine upon hitting the age of, say, 65 and then periodically thereafter, it would catch a lot of cases while there’s still more time to turn things around.

    As for how to turn things around, well, we imagine you have now read our “How To Reduce Your Alzheimer’s Risk” article linked up top (if not, we recommend checking it out), and there is also…

    Do Try This At Home: The 12-Week Brain Fitness Program To Measurably Boost Your Brain

    Take care!

    When it comes to predicting age-related cognitive impairment:

    First there are genetic factors to take into account (such as the APOE4 gene for Alzheimer’s), as well as things such as age and sex.

    When it comes to sex, by the way, what matters here is hormones, which is why [it seems; this as technically as yet unproven with full rigor, but the hypothesis is sound and there is a body of evidence gradually being accumulated to support it] postmenopausal women with untreated menopause get Alzheimer’s at a higher rate and deteriorate more quickly:

    Alzheimer’s Sex Differences May Not Be What They Appear

    Next, there are obviously modifiable lifestyle factors to take into account, things that will reduce your risk such as getting good sleep, good diet, good exercise, and abstaining from alcohol and smoking, as well as oft-forgotten things such as keeping cognitively active and, equally importantly, socially active:

    How To Reduce Your Alzheimer’s Risk

    (the article outlines what matters the most in each of the above areas, by the way, so that you can get the most bang-for-buck in terms of lifestyle adjustments)

    Lastly (in the category of risk factors), there are things to watch out for in the blood such as hypertension and high cholesterol.

    Nipping it in the blood

    In new research (so new it is still ongoing, but being at year 2 of a 4-year prospective study, they have published a paper with their results so far), researchers have:

    1. started with the premise “dementia is preceded by mild cognitive impairment”
    2. then, asked the question “what are the biometric signs of mild cognitive impairment?”

    Using such tools as functional near-infrared spectroscopy (fNIRS) while the participants performed cognitive tasks, they were able to record changes in plasma levels of extracellular vesicles, assessing them with small-particle flow cytometry.

    Translating from sciencese: they gave the participants mental tasks, and while they completed them, the researchers scanned their brains and monitored blood flow and the brain’s ability to compensate for any lack of it.

    What they found:

    • in young adults, blood flow increased, facilitating neurovascular coupling (this is good)
    • in older adults, blood flow did not increase as much, but they engaged other areas of the brain to compensate, by what’s called functional connectivity (this is next best)
    • in those with mild cognitive impairment, blood flow was reduced, and they did not have the ability to compensate by functional connectivity (this is not good)

    They also performed a liquid biopsy, which sounds alarming but it just means they took some blood, and tested this for density of cerebrovascular endothelial extracellular vesicles (CEEVs), which—in more prosaic words—are bits from the cells lining the blood vessels in the brain.

    People with mild cognitive impairment had more of these brain bits in their blood than those without.

    You can read the paper itself here:

    Neurovascular coupling, functional connectivity, and cerebrovascular endothelial extracellular vesicles as biomarkers of mild cognitive impairment

    What this means

    The science here is obviously still young (being as it is still in progress), but this will likely contribute greatly to early warning signs of dementia, by catching mild cognitive impairment in its early stages, by means of a simple blood test, instead of years of wondering before getting a dementia diagnosis.

    And of course, forewarned is forearmed, so if this is something that could be done as a matter of routine upon hitting the age of, say, 65 and then periodically thereafter, it would catch a lot of cases while there’s still more time to turn things around.

    As for how to turn things around, well, we imagine you have now read our “How To Reduce Your Alzheimer’s Risk” article linked up top (if not, we recommend checking it out), and there is also…

    Do Try This At Home: The 12-Week Brain Fitness Program To Measurably Boost Your Brain

    Take care!

    Share This Post

  • Feel Great, Lose Weight – by Dr. Rangan Chatterjee

    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.

    We all know that losing weight sustainably tends to be harder than simply losing weight. We know that weight loss needs to come with lifestyle change. But how to get there?

    One of the biggest problems that we might face while trying to lose weight is that our “metabolic thermostat” has got stuck at the wrong place. Trying to move it just makes our bodies think we are starving, and everything gets even worse. We can’t even “mind over matter” our way through it with willpower, because our bodies will do impressive things on a cellular level in an attempt to save us… Things that are as extraordinary as they are extraordinarily unhelpful.

    Dr. Rangan Chatterjee is here to help us cut through that.

    In this book, he covers how our metabolic thermostat got stuck in the wrong place, and how to gently tease it back into a better position.

    Some advices won’t be big surprises—go for a whole foods diet, avoiding processed food, for example. Probably not a shocker.

    Others are counterintuitive, but he explains how they work—exercising less while moving more, for instance. Sounds crazy, but we assure you there’s a metabolic explanation for it that’s beyond the scope of this review. And there’s plenty more where that came from, too.

    Bottom line: if your weight has been either slowly rising, or else very stable but at a higher point than you’d like, Dr. Chatterjee can help you move the bar back to where you want it—and keep it there.

    Click here to check out “Feel Great, Lose Weight” and reset your metabolic thermostat to its healthiest point!

    Share This Post

  • Chair Stretch Workout Guide

    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.

    It’s Q&A Day 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!

    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

    ❝The 3 most important exercises don’t work if you can’t get on the floor. I’m 78, and have knee replacements. What about 3 best chair yoga stretches? Love your articles!❞

    Here are six!

    Share This Post

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  • Why are my muscles sore after exercise? Hint: it’s nothing to do with lactic acid

    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.

    As many of us hit the gym or go for a run to recover from the silly season, you might notice a bit of extra muscle soreness.

    This is especially true if it has been a while between workouts.

    A common misunderstanding is that such soreness is due to lactic acid build-up in the muscles.

    Research, however, shows lactic acid has nothing to do with it. The truth is far more interesting, but also a bit more complex.

    It’s not lactic acid

    We’ve known for decades that lactic acid has nothing to do with muscle soreness after exercise.

    In fact, as one of us (Robert Andrew Robergs) has long argued, cells produce lactate, not lactic acid. This process actually opposes not causes the build-up of acid in the muscles and bloodstream.

    Unfortunately, historical inertia means people still use the term “lactic acid” in relation to exercise.

    Lactate doesn’t cause major problems for the muscles you use when you exercise. You’d probably be worse off without it due to other benefits to your working muscles.

    Lactate isn’t the reason you’re sore a few days after upping your weights or exercising after a long break.

    So, if it’s not lactic acid and it’s not lactate, what is causing all that muscle soreness?

    Muscle pain during and after exercise

    When you exercise, a lot of chemical reactions occur in your muscle cells. All these chemical reactions accumulate products and by-products which cause water to enter into the cells.

    That causes the pressure inside and between muscle cells to increase.

    This pressure, combined with the movement of molecules from the muscle cells can stimulate nerve endings and cause discomfort during exercise.

    The pain and discomfort you sometimes feel hours to days after an unfamiliar type or amount of exercise has a different list of causes.

    If you exercise beyond your usual level or routine, you can cause microscopic damage to your muscles and their connections to tendons.

    Such damage causes the release of ions and other molecules from the muscles, causing localised swelling and stimulation of nerve endings.

    This is sometimes known as “delayed onset muscle soreness” or DOMS.

    While the damage occurs during the exercise, the resulting response to the injury builds over the next one to two days (longer if the damage is severe). This can sometimes cause pain and difficulty with normal movement.

    The upshot

    Research is clear; the discomfort from delayed onset muscle soreness has nothing to do with lactate or lactic acid.

    The good news, though, is that your muscles adapt rapidly to the activity that would initially cause delayed onset muscle soreness.

    So, assuming you don’t wait too long (more than roughly two weeks) before being active again, the next time you do the same activity there will be much less damage and discomfort.

    If you have an exercise goal (such as doing a particular hike or completing a half-marathon), ensure it is realistic and that you can work up to it by training over several months.

    Such training will gradually build the muscle adaptations necessary to prevent delayed onset muscle soreness. And being less wrecked by exercise makes it more enjoyable and more easy to stick to a routine or habit.

    Finally, remove “lactic acid” from your exercise vocabulary. Its supposed role in muscle soreness is a myth that’s hung around far too long already.The Conversation

    Robert Andrew Robergs, Associate Professor – Exercise Physiology, Queensland University of Technology and Samuel L. Torrens, PhD Candidate, Queensland University of Technology

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

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  • Is alcohol good or bad for you? Yes.

    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.

    This article originally appeared in Harvard Public Health magazine.

    It’s hard to escape the message these days that every sip of wine, every swig of beer is bad for your health. The truth, however, is far more nuanced.

    We have been researching the health effects of alcohol for a combined 60 years. Our work, and that of others, has shown that even modest alcohol consumption likely raises the risk for certain diseases, such as breast and esophageal cancer. And heavy drinking is unequivocally harmful to health. But after countless studies, the data do not justify sweeping statements about the effects of moderate alcohol consumption on human health.

    Yet we continue to see reductive narratives, in the media and even in science journals, that alcohol in any amount is dangerous. Earlier this month, for instance, the media reported on a new study that found even small amounts of alcohol might be harmful. But the stories failed to give enough context or probe deeply enough to understand the study’s limitations—including that it cherry-picked subgroups of a larger study previously used by researchers, including one of us, who concluded that limited drinking in a recommended pattern correlated with lower mortality risk.

    “We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.”

    Those who try to correct this simplistic view are disparaged as pawns of the industry, even when no financial conflicts of interest exist. Meanwhile, some authors of studies suggesting alcohol is unhealthy have received money from anti-alcohol organizations.

    We believe it’s worth trying, again, to set the record straight. We need more high-quality evidence to assess the health impacts of moderate alcohol consumption. And we need the media to treat the subject with the nuance it requires. Newer studies are not necessarily better than older research.

    It’s important to keep in mind that alcohol affects many body systems—not just the liver and the brain, as many people imagine. That means how alcohol affects health is not a single question but the sum of many individual questions: How does it affect the heart? The immune system? The gut? The bones?

    As an example, a highly cited study of one million women in the United Kingdom found that moderate alcohol consumption—calculated as no more than one drink a day for a woman—increased overall cancer rates. That was an important finding. But the increase was driven nearly entirely by breast cancer. The same study showed that greater alcohol consumption was associated with lower rates of thyroid cancer, non-Hodgkin lymphoma, and renal cell carcinoma. That doesn’t mean drinking a lot of alcohol is good for you—but it does suggest that the science around alcohol and health is complex.

    One major challenge in this field is the lack of large, long-term, high-quality studies. Moderate alcohol consumption has been studied in dozens of randomized controlled trials, but those trials have never tracked more than about 200 people for more than two years. Longer and larger experimental trials have been used to test full diets, like the Mediterranean diet, and are routinely conducted to test new pharmaceuticals (or new uses for existing medications), but they’ve never been done to analyze alcohol consumption. 

    Instead, much alcohol research is observational, meaning it follows large groups of drinkers and abstainers over time. But observational studies cannot prove cause-and-effect because moderate drinkers differ in many ways from non-drinkers and heavy drinkers—in diet, exercise, and smoking habits, for instance. Observational studies can still yield useful information, but they also require researchers to gather data about when and how the alcohol is consumed, since alcohol’s effect on health depends heavily on drinking patterns.  

    For example, in an analysis of over 300,000 drinkers in the U.K., one of us found that the same total amount of alcohol appeared to increase the chances of dying prematurely if consumed on fewer occasions during the week and outside of meals, but to decrease mortality if spaced out across the week and consumed with meals. Such nuance is rarely captured in broader conversations about alcohol research—or even in observational studies, as researchers don’t always ask about drinking patterns, focusing instead on total consumption. To get a clearer picture of the health effects of alcohol, researchers and journalists must be far more attuned to the nuances of this highly complex issue. 

    One way to improve our collective understanding of the issue is to look at both observational and experimental data together whenever possible. When the data from both types of studies point in the same direction, we can have more confidence in the conclusion. For example, randomized controlled trials show that alcohol consumption raises levels of sex steroid hormones in the blood. Observational trials suggest that alcohol consumption also raises the risk of specific subtypes of breast cancer that respond to these hormones. Together, that evidence is highly persuasive that alcohol increases the chances of breast cancer.    

    Similarly, in randomized trials, alcohol consumption lowers average blood sugar levels. In observational trials, it also appears to lower the risk of diabetes. Again, that evidence is persuasive in combination. 

    As these examples illustrate, drinking alcohol may raise the risk of some conditions but not others. What does that mean for individuals? Patients should work with their clinicians to understand their personal risks and make informed decisions about drinking. 

    Medicine and public health would benefit greatly if better data were available to offer more conclusive guidance about alcohol. But that would require a major investment. Large, long-term, gold-standard studies are expensive. To date, federal agencies like the National Institutes of Health have shown no interest in exclusively funding these studies on alcohol.

    Alcohol manufacturers have previously expressed some willingness to finance the studies—similar to the way pharmaceutical companies finance most drug testing—but that has often led to criticism. This happened to us, even though external experts found our proposal scientifically sound. In 2018, the National Institutes of Health ended our trial to study the health effects of alcohol. The NIH found that officials at one of its institutes had solicited funding from alcohol manufacturers, violating federal policy.

    It’s tempting to assume that because heavy alcohol consumption is very bad, lesser amounts must be at least a little bad. But the science isn’t there, in part because critics of the alcohol industry have deliberately engineered a state of ignorance. They have preemptively discredited any research, even indirectly, by the alcohol industry—even though medicine relies on industry financing to support the large, gold-standard studies that provide conclusive data about drugs and devices that hundreds of millions of Americans take or use daily.

    Scientific evidence about drinking alcohol goes back nearly 100 years—and includes plenty of variability in alcohol’s health effects. In the 1980s and 1990s, for instance, alcohol in moderation, and especially red wine, was touted as healthful. Now the pendulum has swung so far in the opposite direction that contemporary narratives suggest every ounce of alcohol is dangerous. Until gold-standard experiments are performed, we won’t truly know. In the meantime, we must acknowledge the complexity of existing evidence—and take care not to reduce it to a single, misleading conclusion.

    This article first appeared on The Journalist’s Resource and is republished here under a Creative Commons license.

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  • Beetroot vs Sweet Potato – Which is Healthier?

    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.

    Our Verdict

    When comparing beetroot to sweet potato, we picked the sweet potato.

    Why?

    Quite a straightforward one today!

    In terms of macros, sweet potato has more protein, carbs, and fiber. The glycemic index of both of these root vegetables is similar (and in each case varies similarly depending on how it is cooked), so we’ll call the winner the one that’s more nutritionally dense—the sweet potato.

    Looking at vitamins next, beetroot has more vitamin B9 (and is in fact a very good source of that, unlike sweet potato), and/but sweet potato is a lot higher in vitamins A, B1, B2, B3, B5, B6, B7, C, E, K, and choline. And we’re talking for example more than 582x more vitamin A, more than 17x more vitamin E, more than a 10x more vitamin K, and at least multiples more of the other vitamins mentioned. So this category’s not a difficult one to call for sweet potato.

    When it comes to minerals, beetroot has more selenium, while sweet potato has more calcium, copper, magnesium, manganese, phosphorus, and potassium. They’re approximately equal in iron and zinc. Another win for sweet potato.

    Of course, enjoy both. But if you’re looking for the root vegetable that’ll bring the most nutrients, it’s the sweet potato.

    Want to learn more?

    You might like to read:

    No, beetroot isn’t vegetable Viagra. But here’s what else it can do

    Take care!

    Don’t Forget…

    Did you arrive here from our newsletter? Don’t forget to return to the email to continue learning!

    Learn to Age Gracefully

    Join the 98k+ American women taking control of their health & aging with our 100% free (and fun!) daily emails: