The Bare-Bones Truth About Osteoporosis

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In yesterday’s issue of 10almonds, we asked you “at what age do you think it’s important to start worrying about osteoporosis?”, and here’s the spread of answers you gave us:

The Bare-bones Truth About Osteoporosis

In yesterday’s issue of 10almonds, we asked you “at what age do you think it’s important to start worrying about osteoporosis?”, and here’s the spread of answers you gave us:

At first glance it may seem shocking that a majority of respondents to a poll in a health-focused newsletter think it’ll never be an issue worth worrying about, but in fact this is partly a statistical quirk, because the vote of the strongest “early prevention” crowd was divided between “as a child” and “as a young adult”.

This poll also gave you the option to add a comment with your vote. Many subscribers chose to do so, explaining your choices… But, interestingly, not one single person who voted for “never” had any additional thoughts to add.

We loved reading your replies, by the way, and wish we had room to include them here, because they were very interesting and thought-provoking.

Let’s get to the myths and facts:

Top myth: “you will never need to worry about it; drink a glass of milk and you’ll be fine!”

The body is constantly repairing itself. Its ability to do that declines with age. Until about 35 on average, we can replace bone mineral as quickly as it is lost. After that, we lose it by up to 1% per year, and that rate climbs after 50, and climbs even more steeply for those who go through (untreated) menopause.

Losing 1% per year might not seem like a lot, but if you want to live to 100, there are some unfortunate implications!

About that menopause, by the way… Because declining estrogen levels late in life contribute significantly to osteoporosis, hormone replacement therapy (HRT) may be of value to many for the sake of bone health, never mind the more obvious and commonly-sought benefits.

Learn more: Management of osteoporosis in postmenopausal women: the 2021 position statement of The North American Menopause Society

On the topic of that glass of milk…

  • Milk is a great source of calcium, which is useless to the body if you don’t also have good levels of vitamin D and magnesium.
  • People’s vitamin D levels tend to directly correlate to the level of sun where they live, if supplementation isn’t undertaken.
  • Plant-based milks are usually fortified with vitamin D (and calcium), by the way.
  • Most people are deficient in magnesium, because green leafy things don’t form as big a part of most people’s diets as they should.

See also: An update on magnesium and bone health

Next most common myth: “bone health is all about calcium”

We spoke a little above about the importance of vitamin D and magnesium for being able to properly use that. But potassium is also critical:

Read more: The effects of potassium on bone health

While we’re on the topic…

People think of collagen as being for skin health. And it is important for that, but collagen’s benefits (and the negative effects of its absence) go much deeper, to include bone health. We’ve written about this before, so rather than take more space today, we’ll just drop the link:

We Are Such Stuff As Fish Are Made Of

Want to really maximize your bone health?

You might want to check out this well-sourced LiveStrong article:

Bone Health: Best and Worst Foods

(Teaser: leafy greens are in 2nd place, topped by sardines at #1—where do you think milk ranks?)

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  • What Is Earwax & Should You Get Rid Of It?

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    Earwax (cerumen) forms in the outer ear canal when dead skin cells mix with oily sweat (a specialty of the apocrine glands) and sebum, a fatty substance mostly associated with facial oiliness. But, does it have a purpose, or is it just a waste product?

    Nature is (mostly) best in this case

    Earwax plays an important role in ear health, acting as a natural lubricant that prevents dryness and itchiness, trapping debris and microbes, and forming a protective barrier for the ear canal. It even contains proteins that help fight bacterial infections.

    As for removal: the body has a natural mechanism for removing excess earwax: as skin cells grow, they migrate outward, carrying earwax with them.

    In contrast, manual removal of earwax can do more harm than good. Using swabs or other items often pushes wax deeper, risks damaging the ear canal, and disrupts its protective barrier, potentially leading to infection.

    Ear candling, which claims to extract earwax, not only does not work (its main premise has been actively disproven and clinical evidence shows unequivocally that it doesn’t work by any mysterious method either; it just plain doesn’t work), but also can cause injuries and will tend to leave more harmful debris behind than was there originally.

    For those prone to earwax buildup, over-the-counter eardrops can help soften wax for natural removal, and medical professionals have safe methods to clear blockages if necessary.

    To maintain ear health, it’s best to clean only the outer ear with a damp cloth, limit the use of earplugs or earbuds, and generally leave earwax alone unless it causes discomfort or hearing issues.

    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:

    Ear Candling: Is It Safe & Does It Work? ← the answer is “no and no”, but the science may interest you

    Take care!

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  • Huperzine A: A Natural Nootropic

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    Huperzine A: A Natural Nootropic

    Huperzine A is a compound, specifically a naturally occurring sesquiterpene alkaloid, that functions as an acetylcholinesterase inhibitor. If that seems like a bunch of big words, don’t worry, we’ll translate in a moment.

    First, a nod to its origins: it is found in certain kinds of firmoss, especially the “toothed clubmoss”, Huperzia serrata, which grows in many Asian countries.

    What’s an acetylcholinesterase inhibitor?

    Let’s do this step-by-step:

    • An acetylcholinesterase inhibitor is a compound that inhibits acetylcholinesterase.
    • Acetylcholinesterase is an enzyme that catalyzes (speeds up) the breakdown of acetylcholine.
    • Acetylcholine is a neurotransmitter; it’s an ester of acetic acid and choline.
      • This is the main neurotransmitter of the parasympathetic nervous system, and is also heavily involved in cognitive functions including memory and creative thinking.

    What this means: if you take an acetylcholinesterase inhibitor like huperzine A, it will inhibit acetylcholinesterase, meaning you will have more acetylcholine to work with. That’s good.

    What can I expect from it?

    Huperzine A has been well-studied for a while, mostly for the prevention and treatment of Alzheimer’s disease:

    However, research has suggested that huperzine A is much better as a prevention than a treatment:

    ❝A central event in the pathogenesis of Alzheimer’s disease (AD) is the accumulation of senile plaques composed of aggregated amyloid-β (Aβ) peptides.

    Ex vivo electrophysiological experiments showed that 10 μM of Aβ1-40 significantly decreased the effect of the AChE inhibitor huperzine A on the synaptic potential parameters. ❞

    ~ Dr. Irina Zueva

    Source: Can Activation of Acetylcholinesterase by β-Amyloid Peptide Decrease the Effectiveness of Cholinesterase Inhibitors?

    In other words: the answer to the titular question is “Yes, yes it can”

    And, to translate Dr. Zueva’s words into simple English:

    • People with Alzheimer’s have amyloid-β plaque in their brains
    • That plaque reduces the effectiveness of huperzine A

    So, what if we take it in advance? That works much better:

    ❝Pre-treatment with [huperzine A] at concentrations of 50, 100, and 150 µg/mL completely inhibited the secretion of PGE2, TNF-α, IL-6, and IL-1β compared to post-treatment with [huperzine A].

    This suggests that prophylactic treatment is better than post-inflammation treatment. ❞

    ~ Dr. Thu Kim Dang

    Source: Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata

    As you may know, neuroinflammation is a big part of Alzheimer’s pathology, so we want to keep that down. The above research suggests we should do that sooner rather than later.

    Aside from holding off dementia, can it improve memory now, too?

    There’s been a lot less research done into this (medicine is generally more concerned with preventing/treating disease, than improving the health of healthy people), but there is some:

    Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students

    ^This is a small (n=68) old (1999) study for which the full paper has mysteriously disappeared and we only get to see the abstract. It gave favorable results, though.

    The effects of huperzine A and IDRA 21 on visual recognition memory in young macaques

    ^This, like most non-dementia research into HupA, is an animal study. But we chose to spotlight this one because, unlike most of the studies, it did not chemically lobotomize the animals first; they were and remained healthy. That said, huperzine A improved the memory scores most for the monkeys that performed worst without it initially.

    Where can I get it?

    As ever, we don’t sell it, but here’s an example product on Amazon for your convenience

    Enjoy!

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  • Gut-Healthy Sunset Soup

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    So-called for its gut-healthy ingredients, and its flavor profile being from the Maghreb (“Sunset”) region, the western half of the N. African coast.

    You will need

    • 1 can chickpeas (do not drain)
    • 1 cup low-sodium vegetable stock
    • 1 small onion, finely chopped
    • 1 carrot, finely chopped
    • 2 tbsp sauerkraut, drained and chopped (yes, it is already chopped, but we want it chopped smaller so it can disperse evenly in the soup)
    • 2 tbsp tomato paste
    • 1 tbsp harissa paste (adjust per your heat preference)
    • 1 tbsp ras el-hanout
    • ¼ bulb garlic, crushed
    • Juice of ½ lemon
    • ¼ tsp MSG or ½ tsp low-sodium salt
    • Extra virgin olive oil
    • Optional: herb garnish; we recommend cilantro or flat-leaf parsley

    Method

    (we suggest you read everything at least once before doing anything)

    1) Heat a little oil in a sauté pan or similar (something suitable for combination cooking, as we’ll be frying first and then adding liquids), and fry the onion and carrot until the onion is soft and translucent; about 5 minutes.

    2) Stir in the garlic, tomato paste, harissa paste, and ras el-hanout, and fry for a further 1 minute.

    3) Add the remaining ingredients* except the lemon juice. Bring to the boil and then simmer for 5 minutes.

    *So yes, this includes adding the “chickpea water” also called “aquafaba”; it adds flavor and also gut-healthy fiber in the form of oligosaccharides and resistant starches, which your gut microbiota can use to make short-chain fatty acids, which improve immune function and benefit the health in more ways than we can reasonably mention as a by-the-way in a recipe.

    4) Stir in the lemon juice, and serve, adding a herb garnish if you wish.

    Enjoy!

    Want to learn more?

    For those interested in some of the science of what we have going on today:

    Take care!

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  • One in twenty people has no sense of smell – here’s how they might get it back

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    During the pandemic, a lost sense of smell was quickly identified as one of the key symptoms of COVID. Nearly four years later, one in five people in the UK is living with a decreased or distorted sense of smell, and one in twenty have anosmia – the total loss of the ability to perceive any odours at all. Smell training is one of the few treatment options for recovering a lost sense of smell – but can we make it more effective?

    Smell training is a therapy that is recommended by experts for recovering a lost sense of smell. It is a simple process that involves sniffing a set of different odours – usually essential oils, or herbs and spices – every day.

    The olfactory system has a unique ability to regenerate sensory neurons (nerve cells). So, just like physiotherapy where exercise helps to restore movement and function following an injury, repeated exposure to odours helps to recover the sense of smell following an infection, or other cause of smell loss (for example, traumatic head injury).

    Several studies have demonstrated the effectiveness of smell training under laboratory conditions. But recent findings have suggested that the real-world results might be disappointing.

    One reason for this is that smell training is a long-term therapy. It can take months before patients detect anything, and some people may not get any benefit at all.

    In one study, researchers found that after three months of smell training, participation dropped to 88%, and further declined to 56% after six months. The reason given was that these people did not feel as though they noticed any improvement in their ability to smell.

    Cross-modal associations

    To remedy this, researchers are now investigating how smell training can be improved. One interesting idea is that information from our other senses, or “cross-modal associations”, can be applied to smell training to promote odour perception and improve the results.

    Cross-modal associations are described as the tendency for sensory cues from different sensory systems to be matched. For example, brightness tends to be associated with loudness. Pitch is related to size. Colours are linked to temperature, and softness is matched with round shapes, while spiky shapes feel more rough. In previous studies, these associations have been shown to have a considerable influence on how sensory information is processed. Especially when it comes to olfaction.

    Recent research has shown that the sense of smell is influenced by a combination of different sensory inputs – not just odours. Sensory cues such as colour, shape, and pitch are believed to play a role in the ability to correctly identify and name odours, and can influence perceptions of odour pleasantness and intensity.

    In one study, participants were asked to complete a test that measured their ability to discriminate between different odours while they were presented with the colour red or yellow, an outline drawing of a strawberry or a lemon, or a combination of these colours and shapes. The results suggested that corresponding odour and colour associations (for example, the colour red and strawberry) were linked to increased olfactory performance compared with odours and colours that were not associated (for example, the colour yellow and strawberry).

    Strawberries
    People who associated strawberries with the colour red performed better on smell tests. GCapture/Shutterstock

    While projects focusing on harnessing these cross-modal associations to improve treatments for smell loss are underway, research has already started to deliver some promising results.

    In a recent study that aimed to investigate whether the effects of smell training could be improved with the addition of cross-modal associations, participants watched a guidance video containing sounds that matched the odours that they were training with. The results suggest that cross-modal interactions plus smell training improved olfactory function compared to smell training alone.

    The results reported in recent studies have been promising and offer new insights into the field of olfactory science. It is hoped that this will soon lead to the development of more effective treatment options for smell recovery.

    In the meantime, smell training is one of the best things you can do for a lost sense of smell, so patients are encouraged to stick with it so that they give themselves the best chance at recovery.

    Emily Spencer, PhD Candidate, Olfaction, Edinburgh Napier University

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

    The Conversation

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  • Why 7 Hours Sleep Is Not Enough

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    How Sleep-Deprived Are You, Really?

    This is Dr. Matthew Walker. He’s a neuroscientist and sleep specialist, and is the Director of the Center for Human Sleep Science at UC Berkeley’s Department of Psychology. He’s also the author of the international bestseller “Why We Sleep”.

    What does he want us to know?

    Sleep deprivation is more serious than many people think it is. After about 16 hours without sleep, the brain begins to fail, and needs more than 7 hours of sleep to “reset” cognitive performance.

    Note: note “seven or more”, but “more than seven”.

    After ten days with only 7 hours sleep (per day), Dr. Walker points out, the brain is as dysfunctional as it would be after going without sleep for 24 hours.

    Here’s the study that sparked a lot of Dr. Walker’s work:

    The Cumulative Cost of Additional Wakefulness: Dose-Response Effects on Neurobehavioral Functions and Sleep Physiology From Chronic Sleep Restriction and Total Sleep Deprivation

    Importantly, in Dr. Walker’s own words:

    Three full nights of recovery sleep (i.e., more nights than a weekend) are insufficient to restore performance back to normal levels after a week of short sleeping❞

    ~ Dr. Matthew Walker

    See also: Why You Probably Need More Sleep

    Furthermore: the sleep-deprived mind is unaware of how sleep-deprived it is.

    You know how a drunk person thinks they can drive safely? It’s like that.

    You do not know how sleep-deprived you are, when you are sleep-deprived!

    For example:

    ❝(60.7%) did not signal sleepiness before a sleep fragment occurred in at least one of the four MWT trials❞

    Source: Sleepiness is not always perceived before falling asleep in healthy, sleep-deprived subjects

    Sleep efficiency matters

    With regard to the 7–9 hours band for optimal health, Dr. Walker points out that the sleep we’re getting is not always the sleep we think we’re getting:

    ❝Assuming you have a healthy sleep efficiency (85%), to sleep 9 hours in terms of duration (i.e. to be a long-sleeper), you would need to be consistently in bed for 10 hours and 36 minutes a night. ❞

    ~ Dr. Matthew Walker

    At the bottom end of that, by the way, doing the same math: to get only the insufficient 7 hours sleep discussed earlier, a with a healthy 85% sleep efficiency, you’d need to be in bed for 8 hours and 14 minutes per night.

    The unfortunate implication of this: if you are consistently in bed for 8 hours and 14 minutes (or under) per night, you are not getting enough sleep.

    “But what if my sleep efficiency is higher than 85%?”

    It shouldn’t be.If your sleep efficiency is higher than 85%, you are sleep-deprived and your body is having to enforce things.

    Want to know what your sleep efficiency is?

    We recommend knowing this, by the way, so you might want to check out:

    Head-To-Head Comparison of Google and Apple’s Top Sleep-Monitoring Apps

    (they will monitor your sleep and tell you your sleep efficiency, amongst other things)

    Want to know more?

    You might like his book:

    Why We Sleep: Unlocking the Power of Sleep and Dreams

    …and/or his podcast:

    The Matt Walker Podcast

    …and for those who like videos, here’s his (very informative) TED talk:

    !

    Prefer text? Click here to read the transcript

    Want to watch it, but not right now? Bookmark it for later

    Enjoy!

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  • Shedding Some Obesity Myths

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    Let’s shed some obesity myths!

    There are a lot of myths and misconceptions surrounding obesity… And then there are also reactive opposite myths and misconceptions, which can sometimes be just as harmful!

    To tackle them all would take a book, but in classic 10almonds style, we’re going to put a spotlight on some of the ones that might make the biggest difference:

    True or False: Obesity is genetically pre-determined

    False… With caveats.

    Some interesting results have been found from twin studies and adoption studies, showing that genes definitely play some role, but lifestyle is—for most people—the biggest factor:

    In short: genes predispose; they don’t predetermine. But that predisposition alone can make quite a big difference, if it in turn leads to different lifestyle factors.

    But upon seeing those papers centering BMI, let’s consider…

    True or False: BMI is a good, accurate measure of health in the context of bodyweight

    False… Unless you’re a very large group of thin white men of moderate height, which was the demographic the system was built around.

    Bonus information: it was never intended to be used to measure the weight-related health of any individual (not even an individual thin white man of moderate height), but rather, as a tool to look at large-scale demographic trends.

    Basically, as a system, it’s being used in a way it was never made for, and the results of that misappropriation of an epidemiological tool for individual health are predictably unhelpful.

    To do a deep-dive into all the flaws of the BMI system, which are many, we’d need to devote a whole main feature just to that.

    Update: we have now done so!

    Here it is: When BMI Doesn’t Measure Up

    True or False: Obesity does not meaningfully impact more general health

    False… In more ways than one (but there are caveats)

    Obesity is highly correlated with increased risk of all-cause mortality, and weight loss, correspondingly, correlates with a reduced risk. See for example:

    Effects of weight loss interventions for adults who are obese on mortality, cardiovascular disease, and cancer: systematic review and meta-analysis

    So what are the caveats?

    Let’s put it this way: owning a horse is highly correlated with increased healthy longevity. And while owning a horse may come with some exercise and relaxation (both of which are good for the health), it’s probably mostly not the horse itself that conveys the health benefits… it’s that someone who has the resources to look after a horse, probably has the resources to look after their own health too.

    So sometimes there can be a reason for a correlation (it’s not a coincidence!) but the causative factor is partially (or in some cases, entirely) something else.

    So how could this play out with obesity?

    There’s a lot of discrimination in healthcare settings, unfortunately! In this case, it often happens that a thin person goes in with a medical problem and gets treated for that, while a fat person can go in with the same medical problem and be told “you should try losing some weight”.

    Top tip if this happens to you… Ask: “what would you advise/prescribe to a thin person with my same symptoms?”

    Other things may be more systemic, for example:

    When a thin person goes to get their blood pressure taken, and that goes smoothly, while a fat person goes to get their blood pressure taken, and there’s not a blood pressure cuff to fit them, is the problem the size of the person or the size of the cuff? It all depends on perspective, in a world built around thin people.

    That’s a trivial-seeming example, but the same principle has far-reaching (and harmful) implications in healthcare in general, e.g:

    • Surgeons being untrained (and/or unwilling) to operate on fat people
    • Getting a one-size-fits-all dose that was calculated using average weight, and now doesn’t work
    • MRI machines are famously claustrophobia-inducing for thin people; now try not fitting in it in the first place

    …and so forth. So oftentimes, obesity will be correlated with a poor healthcare outcome, where the problem is not actually the obesity itself, but rather the system having been set up with thin people in mind.

    It would be like saying “Having O- blood type results in higher risks when receiving blood transfusions”, while omitting to add “…because we didn’t stock O- blood”.

    True or False: to reduce obesity, just eat less and move more!

    False… Mostly.

    Moving more is almost always good for most people. When it comes to diet, quality is much more important than quantity. But these factors alone are only part of the picture!

    But beyond diet and exercise, there are many other implicated factors in weight gain, weight maintenance, and weight loss, including but not limited to:

    • Disrupted sleep
    • Chronic stress
    • Chronic pain
    • Hormonal imbalances
    • Physical disabilities that preclude a lot of exercise
    • Mental health issues that add (and compound) extra levels of challenge
    • Medications that throw all kinds of spanners into the works with their side effects

    …and even just those first two things, diet and exercise, are not always so correlated to weight as one might think—studies have found that the difference for exercise especially is often marginal:

    Read: Widespread misconceptions about obesity ← academic article in the Journal of the College of Family Physicians of Canada

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