3 Life-Changing Mobility Movements To Train
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If you’ve ever momentarily struggled to stand up straight after sitting for too long, or had to take a moment to get up off the floor, this one’s for you.
And if you’ve never done those things? Well, this one’s still for you—prevention is better than cure, after all!
From the hips
Most movements that we need to do in life depend on our hips. They support our spine, on which almost everything else depends, and on the flipside, they’re where our legs are plugged in, so they’re pretty critical for lower body mobility too.
So, with that in mind, here are the three exercise promised—or five, depending on how you want to count them:
- For hip mobility most directly: start with a combination of donkey kicks and fire hydrants. From a tabletop position, lift one leg behind you as if putting a footprint on the ceiling, keeping your tailbone tucked in and your core engaged to avoid using your lower back. Then, bring your leg back and lift it sideways like a dog peeing on a hydrant, keeping your torso level and pelvis stable. Alternate between the two movements for 20 total reps (i.e. 10 each), then switch legs.
- For hip, spinal, and upper body mobility: now we get to thread the needle. From all fours, inhale and reach one arm up (as far as comfortable), then exhale and thread it under your body to the opposite side. Lower your shoulder close to the mat but without touching it, using your core to twist. Follow your breath rhythm—inhale to lift, exhale to thread—and do 10 reps on each side.
- For hip and ankle mobility: use a split lunge with two parts. From an upright lunge, put your hands on your front thigh and tuck your tailbone in to engage the back glute. Lunge forwards while keeping your front heel flat on the floor, while your knee moves past the toes. Then, without changing pelvis position, lift your back knee and try to straighten your leg, pushing your heel backwards without raising your hips. Return to start and repeat 10 times per side.
For more on all of this plus visual demonstrations, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like:
How Tight Are Your Hips? Test (And Fix!) With This
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Intuitive Eating Might Not Be What You Think
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In our recent Expert Insights main features, we’ve looked at two fairly opposing schools of thought when it comes to managing what we eat.
First we looked at:
What Flexible Dieting Really Means
…and the notion of doing things imperfectly for greater sustainability, and reducing the cognitive load of dieting by measuring only the things that are necessary.
And then in opposition to that,
What Are The “Bright Lines” Of Bright Line Eating?
…and the notion of doing things perfectly so as to not go astray, and reducing the cognitive load of dieting by having hard-and-fast rules that one does not second-guess or reconsider later when hungry.
Today we’re going to look at Intuitive Eating, and what it does and doesn’t mean.
Intuitive Eating does mean paying attention to hunger signals (each way)
Intuitive Eating means listening to one’s body, and responding to hunger signals, whether those signals are saying “time to eat” or “time to stop”.
A common recommendation is to “check in” with one’s body several times per meal, reflecting on such questions as:
- Do I have hunger pangs? Would I seek food now if I weren’t already at the table?
- If I hadn’t made more food than I’ve already eaten so far, would that have been enough, or would I have to look for something else to eat?
- Am I craving any of the foods that are still before me? Which one(s)?
- How much “room” do I feel I still have, really? Am I still in the comfort zone, and/or am I about to pass into having overeaten?
- Am I eating for pleasure only at this point? (This is not inherently bad, by the way—it’s ok to have a little more just for pleasure! But it is good to note that this is the reason we’re eating, and take it as a cue to slow down and remember to eat mindfully, and enjoy every bite)
- Have I, in fact, passed the point of pleasure, and I’m just eating because it’s in front of me, or so as to “not be wasteful”?
See also: Interoception: Improving Our Awareness Of Body Cues
And for that matter: Mindful Eating: How To Get More Out Of What’s On Your Plate
Intuitive Eating is not “80:20”
When it comes to food, the 80:20 rule is the idea of having 80% of one’s diet healthy, and the other 20% “free”, not necessarily unhealthy, but certainly not moderated either.
Do you know what else the 80:20 food rule is?
A food rule.
Intuitive Eating doesn’t do those.
The problem with food rules is that they can get us into the sorts of problems described in the studies showing how flexible dieting generally works better than rigid dieting.
Suddenly, what should have been our free-eating 20% becomes “wait, is this still 20%, or have I now eaten so much compared to the healthy food, that I’m at 110% for my overall food consumption today?”
Then one gets into “Well, I’ve already failed to do 80:20 today, so I’ll try again tomorrow [and binge meanwhile, since today is already written off]”
See also: Eating Disorders: More Varied (And Prevalent) Than People Think
It’s not “eat anything, anytime”, either
Intuitive Eating is about listening to your body, and your brain is also part of your body.
- If your body is saying “give me sugar”, your brain might add the information “fruit is healthier than candy”.
- If your body is saying “give me fat”, your brain might add the information “nuts are healthier than fried food”
- If your body is saying “give me salt”, your brain might add the information “kimchi is healthier than potato chips”
That doesn’t mean you have to swear off candy, fried food, or potato chips.
But it does mean that you might try satisfying your craving with the healthier option first, giving yourself permission to have the less healthy option afterwards if you still want it (you probably won’t).
See also:
I want to eat healthily. So why do I crave sugar, salt and carbs?
Want to know more about Intuitive Eating?
You might like this book that we reviewed previously:
Intuitive Eating – by Evelyn Tribole and Elyse Resch
Enjoy!
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Rethinking Diabetes – by Gary Taubes
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We’ve previously reviewed this author’s “The Case Against Sugar” and “Why We Get Fat And What To Do About It“. There’s an obvious theme, and this book caps it off nicely:
By looking at the history of diabetes treatment (types 1 and 2) in the past hundred years, and analysing the patterns over time, we can see how:
- diabetics have been misled a lot over time by healthcare providers
- we can learn from those mistakes going forwards
Happily, he does this without crystal-balling the future or expecting diet to fix, for example, a pancreas that can’t produce insulin. But what he does do is focus on the “can” items rather than the “can’t” items.
In the category of criticism, one of the strategies he argues for is basically the keto diet, which is indeed just fine for diabetes but often not great for the heart in the long-term (it depends on various factors, including genes). However, even if you choose not to implement that, there is plenty more to try out in this book.
Bottom line: whether you have diabetes, love someone who does, or just plain like to be on top of your glycemic health, this book is full of important insights and opportunities to improve things progressively along the way.
Click here to check out Rethinking Diabetes, and rethink diabetes!
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New Eye Drops vs Age-Related Macular Degeneration
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We’ve written previously on preventative interventions against age-related macular degeneration (AMD):
How To Avoid Age-Related Macular Degeneration
…and then supplemented that, to to speak, with:
Fatty Acids For The Eyes & Brain: The Good And The Bad
However, what if ADM happens anyway?
Not a dry eye in the house
Age-related macular degeneration comes in two forms, wet and dry, of which, dry is by far the most common (being 9 out of 10 of all cases of AMD).
It sounds like the sort of thing that eye drops should be in order for, but in fact, the wetness vs dryness is about what’s going on inside the macula, not what’s happening on the surface of the eye. Up until now, the only treatments available (aside from supplement regimes, which we linked just above) have been injectable drugs, which:
- are not fun (yes, the injection goes into the eyeball)
- don’t actually work very well (modest improvements in vision; significantly better than nothing though)
…and even those won’t help in the late stages.
However, a Korean research team has developed eye drops with peptides that inhibit the interactions between Toll-like receptors (TLRs) and TLR-signalling proteins, in a way that addresses part of the pathogenesis of AMD:
That’s quite a dense read though, so here’s a pop-science article that explains it more simply, but in more detail than we can here:
New eye drop treatment offers hope for dry AMD patients
This is a big improvement from the state of affairs previously, in which eye drops really couldn’t help at all:
What eye drops can treat macular degeneration? ← pop-science article from January 2023
No AMD, and/but want your eye health to be better?
Check out these:
10 Great Exercises to Improve Your Eyesight ← you can quickly see the results for yourself
Take care!
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How Fish Oil Can Harm Your Brain
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Omega-3 fatty acids have many benefits for the health, including for the brain!
We wrote about some of them, here: What Omega-3 Fatty Acids Really Do For Us
There are even some less well-known benefits, such as: Why Healthy Teeth May Depend On Omega-3 & Exercise
Now, the press has not been all positive, for example: Fish Oil Can Backfire Without This Enzyme
But what’s this about omega-3s harming the brain?
Brain recovery impediment
Researchers (Dr. Eda Karakaya et al.) examined how omega-3 fatty acids from fish oil affect brain recovery, and the results were not happy ones.
In few words: the fish-derived omega-3 fatty acid EPA (eicosapentaenoic acid) accumulated in the brain and was linked to reduced recovery capacity after injury.
Further, EPA altered cortical gene programs by suppressing pathways involved in vascular repair* and extracellular matrix organization while increasing lipid metabolism activity.
*And this is critical. Regular 10almonds readers will remember that we often say “what’s good for your heart is good for your brain”, and it’s because the former feeds the latter, with nutrients, oxygen, etc, and also ultimately takes away detritus (yes, it’s the glymphatic system that does it directly, but without good blood flow, there’s nowhere for it to usefully drain to). So all this means that if cerebrovascular repair is impaired, then ultimately, brain maintenance will be impaired too.
More than just that, in human brain microvascular endothelial cells, EPA reduced the ability to form repair networks under conditions promoting fatty acid use.
And while no ethics board would let the researchers take brain slices from living human volunteers to look at under the microscope, postmortem brain samples from humans with chronic traumatic encephalopathy showed disrupted fatty acid balance and vascular-related gene changes consistent with EPA-linked effects.
In other words: a further smoking gun that strongly suggests (albeit does not outright prove, in this case) “EPA did this”.
There is one thing that’s not completely bad news for fish oil here, which is that DHA (docosahexaenoic acid), another omega-3 fatty acid, did not show the same negative effects and remains associated with normal brain structure.
But since fish oil contains both EPA and DHA in generous amounts, there’s a limit to how helpful this is:
❝Fish oil supplements are everywhere, and people take them for a range of reasons, often without a clear understanding of their long-term effects
But in terms of neuroscience, we still don’t know whether the brain has resilience or resistance to this supplement. That’s why ours is the first such study in the field.❞
~ Dr. Onder Albaryam, a colleague of Dr. Karakaya, and part of the “et al.” in this study
You can read the paper in full, here: Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy
Want to do better for your brain?
You do have other options!
For example, as well as the difference between EPA and DHA that we talked about above, there are also plant-based omega-3s that just have ALA (and not EPA or DHA) which the body can convert to whatever omega-3 form it needs (just like the fish did, for we too are animals that can do that, and for this reason our liver fats would, if healthy, also be a good source of EPA/DHA if something were to predate on us).
For more on that, check out: Omega-3s: Different Sources, Different Benefits?
Enjoy!
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Reverse Stroke Damage (Within A 6-Hour Window)
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❝Each year in the US, over half a million people have a first stroke; however, up to 80% of strokes may be preventable.❞
~ American Stroke Association
Source: New guideline: Preventing a first stroke may be possible with screening, lifestyle changes
If you’re reading this and thinking that it happens to other people, older people perhaps… There is a first time for everything, and most people are caught off guard by their first stroke.
Which means our health plan in this regard needs to be in two parts:
- let’s try to not have a stroke in the first place (which involves not assuming we are invulnerable right now)
- let’s try to minimize any damage done, and hasten recovery, if stroke strikes.
With regard to the first part, we’ve written about that before, including: Don’t Get Caught Out By These “Nontraditional” Stroke Risk Factors
And our most comprehensive article on the topic of stroke avoidance: Reduce Your Stroke Risk
To be truly well-prepared, you can also bear in mind: 6 Signs Of Stroke (One Month In Advance)
But what if stroke strikes?
Firstly, know this:
What To Do If Having A Stroke Alone? ← with the caveat that, if you have a stroke, there’s a good chance you’ll forget all this. However, this is good to know anyway, in case someone else is having a stroke (and if you don’t live alone, it can be good for whoever is with you to know this too).
And now there’s a new recourse: a Japanese team of researchers (Dr. Masanori Itakura et al.) have developed a drug that (per preliminary testing*, in any case) prevents the usual kind of harm done by stroke, if administered up to 6 hours after the stroke in question.
*So far, it’s completed the animal testing stage. Next is human models, and then actual humans.
How does it work, you ask?
In human blood there’s a protein (an enzyme, in fact) called glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and it has a lot of important jobs to do, including DNA repair, tRNA export, transcription membrane trafficking, heme metabolism, regulation of kinases, as well as cellular apoptosis and necrosis—which latter may sound bad, but individual cell death is an important part of the overall organism’s ongoing life. And by “the overall organism”, we mean you.
However, in stroke, this causes problems when this protein aggregates (clumps together), and starts killing everything it touches. You can probably imagine how that’s a bad thing to have happening inside your brain.
To combat this, the researchers developed a peptide to inhibit the aggregation of GAPDH, and gave this the catchy name of GAPDH aggregation inhibitor peptide-17, or GAI-17 to its friends.
In mice, GAI-17 significantly mitigated brain cell death and paralysis even when given up to six hours* after a stroke. The drug showed no significant side effects, including no harm to the heart or blood vessels.
*It was tested at 3, 6, and 9 hours. In the first two cases (at 3hrs and 6hrs) it was very effective; in the latter case (at 9 hours), it performed only marginally better than control.
You can see the paper itself, and graphs of the results, here: Inhibition of GAPDH aggregation as a potential treatment for acute ischemic stroke
And a pop-science article with some additional speculation, here: Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s
Want to learn more?
Here’s a good way to get started, by asking the right questions:
12 Questions For Better Brain Health
Take care!
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What’s The Difference Between Minoxidil For Men vs For Women?
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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’m confused, does minoxidil work the same for women and for men? The label on the minoxidil I was looking at says it is only for men❞
Great question!
Simple answer: yes, it works (or not, as the case may be for some people, more on that later) exactly the same for men and women.
You may be wondering: what, then, is the difference between minoxidil for men and minoxidil for women?
And the answer is: the packaging/marketing. That’s literally it.
It’s like with razors, there are razors marketed to men and razors marketed to women, and both come with advertising/marketing promising to be enhance your masculine/feminine appearance (as applicable), but at the end of the day, in both cases it’s just sharp steel blades that cut through hairs as closely as possible to the skin. The sharp steel neither knows nor cares about your gender.
When it comes to minoxidil, in both cases the active ingredient is indeed minoxidil, usually at 2% or 5% strength (though other options exist, and all these get marketed to men and women), and in both cases it works in the same ways, by:
- dilating the blood vessels that feed the hair follicles and thus allowing them to perform better
- kicking the follicles into anagen (growth phase) and keeping them there for longer
Note: this is why we mentioned that it won’t work for all people, and it’s because (regardless of sex/gender), it cannot do those things for your hair follicles if you do not have hair follicles to treat. In the case of someone who has had hair loss for a long time, sometimes there will not be enough living follicles remaining to do anything useful with. As a general rule of thumb, provided you have some hairs there (even if they are little downy baby hairs), they can usually be coaxed back to full life.
In both cases, it’s for treating “pattern hair loss”, the pattern being “male pattern” or “female pattern”, respectively, but in both cases it’s androgenetic alopecia, and in both cases it’s caused by the corresponding genetic factors and hormone-mediated gene expression (the physical pattern therefore is usually a little different for men and women; that’s because of the “hormone-mediated gene expression”, or to put it into lay terms “the hormones tell the body which genes to turn on and off”.
Fun fact: it’s the same resultant phenotype as for PCOS, though usually occurring at different stages in life; PCOS earlier and AGA later—sometimes people (including people with both ovaries and hair) can get one without the other, though, as there may be other considerations going on besides the genetic and hormonal.
Limitation: if the hair loss is for reasons other than androgenetic alopecia, it’s unlikely to work. In fact, it is usually flat-out stated that it won’t work, but since one of the common listed side effects of minoxidil is “hair growth in other places”, it seems fair to say that the scalp is not really the only place it can cause hair to grow.
Want to know more?
You can read about the science of various pharmaceutical options (including minoxidil) here:
Hair-Loss Remedies, By Science ← this also goes more into the pros and cons of minoxidil than we have today, so if you’re considering minoxidil, you might want to read this first, to make the most informed decision.
And if you want to be a bit less pharmaceutical about it:
Take care!
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