How (And Why) To Train Your Pre-Frontal Cortex
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Dr. Chapman’s Keys For Mental Focus
This is Dr. Sandra Chapman; she’s a cognitive neuroscientist, on a mission to, in her words, further our understanding of:
- what makes the brain stronger, faster and last longer
- what enhances human cognitive capacity, and
- what enhances the underlying brain systems across the lifespan.
To this end, she’s also the founder and Chief Director of the Center For Brain Health, where she has worked on her mission for the past 25 years (clocking up hundreds of peer-reviewed publications to her name), as well as being a professor of Behavioral and Brain Sciences at UT Dallas.
What does she want us to know?
Get your brain into gear
When it comes to your brainpower, it is “use it or lose it”, but it is also perfectly possible to use it and lose it.
Why?
Very often, what we are using our brains for is high-strain, low-yield stuff, such as multitasking, overthinking, or overthinking while multitasking. And to make it worse, we often do it without sufficient rest.
This is the equivalent of owning a Ferrari but trying to drive it in second and third gear at once by switching between the two as rapidly as possible. And doing that for 18 hours each day.
Suffice it to say, you’ll be going nowhere quickly.
An alternative “use” of brainpower is low-strain, low-yield stuff, such as having to pay close attention to a boring conversation. It’s enough to stop your mind from doing anything else, but not enough to actually stimulate you.
This is the equivalent of owning a Ferrari but keeping it idling. The wear and tear is minimal this time, but you’re not actually going anywhere either.
Better, of course, are the other two quadrants:
- low-strain, high-yield: consistently using our brain in relatively non-taxing ways that encourage its development
- high-strain, high-yield: here the Ferrari metaphor definitely fails, because unlike cars, our bodies (including our brains) are machines that benefit from judicious regular progressive overloading (but just by a bit, and with adequate recovery time between overloads).
See also: 12 Weeks To Measurably Boost Your Brain
How to do the “low-strain, low-yield” part
When it comes to “what’s the most important part of the brain to help in the face of cognitive decline?” the usual answer is either to focus on memory (hippocampi) or language (various parts, but for example Wernicke’s area and Broca’s area), since people most fear losing memory, and language is very important both socially and practically.
Those are indeed critical, and we at 10almonds stand by them, but Dr. Chapman (herself having originally trained as speech and language pathologist!) makes a strong case for adding a third brain part to the list.
Specifically, she advocates for strengthening the pre-frontal cortex, which is responsible for inhibition, task-switching, working memory, and cognitive flexibility. If that seems like a lot, do remember it’s a whole cortex and not one of the assorted important-but-small brain bits we mentioned above.
How? She has developed training programs for this, based on what she calls Strategic Memory Advanced Reasoning Tactics (SMART), to support support attention, planning, judgment and emotional management.
You can read more about those programs here:
Center For Brain Health | Our Programs
Participation in those is mostly not free, however, if you join their…
Center For Brain Health | BrainHealth Project
…then they will periodically invite you to join pilot programs, research programs, and the like, which will either be free or they-pay-you affairs—because this is how science is done, and you can read about yourself (anonymized, of course) later in peer-reviewed papers of the kind we often cite here.
If you’re not interested in any of that though, we will say that according to Dr. Chapman, the keys are:
Inhibition: be conscious of this function of your brain, and develop it. This is the function of your brain that stops you from making mistakes—or put differently: stops you from saying/doing something stupid.
Switching: do this consciously; per “I am now doing this task, now I am switching to this other task”, rather than doing the gear-grinding thing we discussed earlier
Working memory: this is effectively your brain’s RAM. Unlike the RAM of a computer (can be enhanced by adding another chip or replacing with a bigger chip), our brain’s RAM can be increased by frequent use, and especially by judicious use of progressive overloading (with rests between!) which we’ll discuss in the high-strain, high-yield section.
Flexibility: this is about creative problem-solving, openness to new ideas, and curiosity
See also: Curiosity Kills The Neurodegeneration
How to do the “high-strain, high-yield” part
Delighting this chess-playing writer, Dr. Chapman recommends chess. Although, similar games such as go (a Chinese game that looks simpler than chess but actually requires more calculation) work equally well too.
Why?
Games like chess and go cause structural changes that are particularly helpful, in terms of engaging in such foundational tasks as learning, abstract reasoning, problem-solving and self-control:
Chess Practice as a Protective Factor in Dementia
Basically, it checks (so to speak) a lot of boxes, especially for the pre-frontal cortex. Some notes:
- Focusing on the game is required for brain improvement; simply pushing wood casually will not do it. Ideally, calculating several moves ahead will allow for strong working memory use (because to calculate several moves ahead, one will have to hold increasingly many possible positions in the mind while doing so).
- The speed of play must be sufficiently slow as to allow not only for thinking, but also for what in chess is called “blunder-checking”, in other words, having decided on one’s move, pausing to consider whether it is a mistake, and actively trying to find evidence that it is. This is the crucial “inhibition habit”, and when one does it reflexively, one will make fewer mistakes. Tying this to dementia, see for example how one of the common symptoms of dementia is falling for scams that one wouldn’t have previously. How did cognitive decline make someone naïve? It didn’t, per se; it just took away their ability to, having decided what to do, pause to consider whether it was a mistake, and actively trying to find evidence that it is.
- That “conscious switching” that we talked about, rather than multitasking? In chess, there is a difference between strategy and tactics. Don’t worry about what that difference is for now (learn it if you want to take up chess), but know that strong players will only strategize while it is their opponent’s turn, and only calculate (tactics) while it is their own turn. It’s very tempting to flit constantly between one and the other, but chess requires players to have the mental discipline be able to focus on one task or the other and stick with that task until it’s the appointed time to switch.
If you feel like taking up chess, this site (and related app, if you want it) is free (it’s been funded by voluntary donations for a long time now) and good and even comes with free tuition and training tools: LiChess.org
Here’s another site that this writer (hi, it’s me) personally uses—it has great features too, but many are paywalled (I’m mostly there just because I’ve been there nearly since its inception, so I’m baked into the community now): Chess.com
Want to know more?
You might like this book by Dr. Chapman, which we haven’t reviewed yet but it did inform large parts of today’s article:
Make Your Brain Smarter: Increase Your Brain’s Creativity, Energy, and Focus – by Dr. Sandra Chapman
Enjoy!
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What’s So Special About Alpha-Lipoic Acid?
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The Access-All-Areas Antioxidant
Alpha-Lipoic Acid (ALA) is one of the most bioavailable antioxidants in existence. A bold claim, but most antioxidants are only water-soluble or fat-soluble, whereas ALA is both. This has far-reaching implications—and we mean that literally, because its “go everywhere” status means that it can access (and operate in) all living cells of the human body.
We make it inside our body, and we can also get it in our diet, or take it as a supplement.
What foods contain it?
The richest food sources are:
- For the meat-eaters: organ meats
- For everyone: broccoli, tomatoes, & spinach
However, supplements are more efficient at delivering it, by several orders of magnitude:
Read more: Lipoic acid – biological activity and therapeutic potential
What are its benefits?
Most of its benefits are the usual benefits you would expect from any antioxidant, just, more of it. In particular, reduced inflammation and slowed skin aging are common reasons that people take ALA as a supplement.
Does it really reduce inflammation?
Yes, it does. This one’s not at all controversial, as this systematic review of studies shows:
(C-reactive protein is a marker of inflammation)
Does it really reduce skin aging?
Again yes—which again is not surprising for such a potent antioxidant; remember that oxidative stress is one of the main agonists of cellular aging:
As a special feature, ALA shows particular strength against sun-related skin aging, because of how it protects against UV radiation and increases levels of gluthianone, which also helps:
- Photochemical stability of lipoic acid and its impact on skin ageing
- Modern approach to topical treatment of aging skin
Where can I get some?
We don’t sell it, but here for your convenience is an example product on Amazon
Enjoy!
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Sweet Potato & Black Bean Tacos
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Fiber, protein, and polyphenols! What more could one ask for? Well, great taste and warm healthy goodness, which these deliver:
You will need
For the sweet potatoes:
- 2 medium sweet potatoes, cubed (we recommend leaving the skin on, but you can peel them if you really want to)
- 1 tbsp extra virgin olive oil
- 2 tsp garlic powder
- 2 tsp smoked paprika
- 1 tsp chili powder
- 1 tsp black pepper
- 1 tsp ground cumin
- 1 tsp ground turmeric
- ½ tsp MSG or 1 tsp low-sodium salt
For the black beans:
- 2 cans black beans, drained and rinsed (or 2 cups black beans that you cooked yourself)
- ¼ bulb garlic, minced
- 1 fresh jalapeño finely chopped (or ¼ cup jalapeños from a jar, finely chopped) ← adjust quantities per your preference and per the quality of the pepper(s) you’re using; we can’t judge that from here without tasting them, so we give a good basic starting suggestion.
- 2 tsp black pepper
- 1 tsp red chili flakes
- ½ tsp MSG or 1 tsp low-sodium salt
For serving:
- 8 small corn tortillas, or your preference if substituting
- 1 avocado, pitted, peeled, cubed, and tossed in lime juice ← we’re mentioning this here because you want to do this as soon as you cut it, to avoid oxidation
- Any other salad you’d like to include; fresh parsley is also a good option when it comes to greenery, or cilantro if you don’t have the soap gene
- Tomato salsa (quantity and spice level per your preference)
Method
(we suggest you read everything at least once before doing anything)
1) Preheat the oven to 400°F / 200°C.
2) Toss the sweet potato cubes in a large bowl with the rest of the ingredients from the sweet potato section above, ensuring they are evenly coated.
3) Bake them in the oven, on a baking tray lined with baking paper, for about 30 minutes or until tender inside and crispy at the edges. Turn them over halfway through.
4) While that’s happening, mix the black beans in a bowl with the other ingredients from the black bean section above, and heat them gently. You could do this in a saucepan, but honestly, while it’s not glamorous, the microwave is actually better for this. Note: many people find the microwave cooks food unevenly, but there are two reasons for this and they’re both easily fixable:
- instead of using high power for x minutes, use medium power for 2x minutes; this will produce better results
- instead of putting the food just in a bowl, jug, or similar, use a wide bowl or similar container, and then inside that, place a small empty microwave-safe glass jar or similar upturned in the middle, and then add the food around it, so that the food is arranged in a donut shape rather than a wide cylinder shape. This means there is no “middle bit” to go underheated while the edges are heated excessively; instead, it will heat through evenly.
If you really don’t want to do that though, use a saucepan on a very low heat, add a small amount of liquid (or tomato salsa), and stir constantly.
5) Heat the tortillas in a dry skillet for about 30 seconds each on each side, when ready to serve.
6) Assemble the tacos; you can do this how you like but a good order of operations is: tortilla, leafy salad (if using), potato, beans, non-leafy salad including avocado, salsa or other topping per your preference.
Enjoy!
Want to learn more?
For those interested in some of the science of what we have going on today:
- White Potato vs Sweet Potato – Which is Healthier?
- Kidney Beans or Black Beans – Which is Healthier?
- Coconut vs Avocado – Which is Healthier?
- Glutathione: More Than An Antioxidant
- Our Top 5 Spices: How Much Is Enough For Benefits? ← we hit 4/5 today!
Take care!
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Come As You Are – by Dr. Emily Nagoski
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We’ve all heard the jokes, things like: Q: “Why is the clitoris like Antarctica?” A: “Most men know it’s there; most don’t give a damn”
But… How much do people, in general, really know about the anatomy and physiology of sexual function? Usually very little, but often without knowing how little we know.
This book looks to change that. Geared to a female audience, but almost everyone will gain useful knowledge from this.
The writing style is very easy-to-read, and there are “tl;dr” summaries for those who prefer to skim for relevant information in this rather sizeable (400 pages) tome.
Yes, that’s “what most people don’t know”. Four. Hundred. Pages.
We recommend reading it. You can thank us later!
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Greek Yogurt vs Cottage Cheese – Which is Healthier?
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Our Verdict
When comparing Greek yogurt to cottage cheese, we picked the yogurt.
Why?
These are both dairy products popularly considered healthy, mostly for their high-protein, low-carb, low-fat profile. We’re going to assume that both were made without added sugars. Thus, their macro profiles are close to identical, and nothing between them there.
In the category of vitamins, both are a good source of some B vitamins, and neither are good source of much else. The B-vitamins they have most of, B2 and B12, Greek yogurt has more.
We’ll call this a small win for Greek yogurt.
As they are dairy products, you might have expected them to contain vitamin D—however (unless they have been artificially fortified, as is usually done with plant-based equivalents) they contain none or trace amounts only.
When it comes to minerals, both are reasonable sources of calcium, selenium, and phosphorus. Of these, they’re equal on the selenium, while cottage cheese has more phosphorus and Greek yogurt has more calcium.
Since it’s also a mineral (even if it’s usually one we’re more likely to be trying to get less of), it’s also worth noting here that cottage cheese is quite high in sodium, while Greek yogurt is not.
Another win for Greek yogurt.
Beyond those things, we’d be remiss not to mention that Greek yogurt contains plenty of probiotic bacteria, while cottage cheese does not.
Want to learn more?
You might like to read:
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An Accessible New Development Against Alzheimer’s
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Dopamine vs Alzheimer’s
One of the key hallmarks of Alzheimer’s disease is the formation of hardened beta-amyloid plaques around neurons. The beta-amyloid peptides themselves are supposed to be in the brain, but the hardened pieces of them that form the plaques are not.
While the full nature of the relationship between those plaques and Alzheimer’s disease is not known for sure (there are likely other factors involved, and “the amyloid hypothesis” is at this stage nominally just that, a hypothesis), one thing that has been observed is that increasing or reducing the plaques increases or reduces (respectively) Alzheimer’s symptoms such as memory loss.
Neprilysin
There is an enzyme, neprilysin, that can break down those plaques.
Neprilysin is made naturally in the brain, and/but we cannot take it as a supplement or medication, because it’s too big to pass through the blood-brain barrier.
A team of researchers led by Dr. Takaomi Saido genetically manipulated mice to produce more neprilysin, and those mice resultantly experienced fewer beta-amyloid plaques and better memory in their old age.
However wonderful for the mice (and a great proof of principle) the above approach is not useful as a treatment for humans whose genomes weren’t modified at our conception in a lab.
Since (as mentioned before) we also can’t take it as a medication/supplement, that leaves one remaining option: find a way to make our already-existing brains produce more of it.
The team’s previous research allowed them to narrow this down to “there is probably a hormone made in the hypothalamus that modulates this”, so they began experimenting with making the mice produce more hormones there.
The DREADD switch
DREADDs, or Designer Receptors Exclusively Activated by Designer Drugs, were the next tool in the toolbox. The scientists attached these designer receptors to dopamine-producing neurons in the mice, so that they could be activated by the appropriate designer drugs—basically, allowing for a “make more dopamine” button, without having to literally wire up the brains with electrodes. The “button” gets triggered instead by a chemical trigger, the designer drug. You can read more about them here:
DREADDs for Neuroscientists: A Primer
The result was positive; when the mice made more dopamine, the result was that they also made more neprilysin. So far, the hypothesis is that the presence of dopamine upregulates the production of neprilysin. In other words, the increased neprilysin levels were caused by the increased dopamine levels (the alternatives would have been: they were both caused by the same thing—in this case that’d be the DREADD activation—or the increase was caused by something else entirely that hadn’t been controlled for).
As to how the causal relationship was determined…
“But I don’t have (or want) a DREADD switch in my head”
Happily for us (and probably happily for the mice too, because dopamine causes feelings of happiness), the experiments continued.
This time, instead of using the DREADD system, they tried simply supplementing the mouse food with l-dopa, a dopamine precursor. L-dopa is often used in the treatment of Parkinson’s disease, because the molecules are small enough to pass through the blood-brain barrier, and can be converted to full dopamine inside the brain itself. So, taking l-dopa normally raises dopamine levels.
The results? The mice who were given l-dopa enjoyed:
- higher dopamine levels
- higher neprilysin levels
- lower beta-amyloid plaque levels
- better memory in tests
The next step for the researchers is to investigate how exactly dopamine regulates neprilysin in the brain, but for now, the relationship between l-dopa consumption and the reduction of Alzheimer’s symptoms seems clear.
You can read about the study here:
The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain
Is there a catch?
L-dopa has common side effects that are not pleasant; the list begins with nausea and vomiting, and continues with things that one might expect from having “too much of a good thing” when it comes to dopamine, such as dyskinesia (extra movements) and hallucinations.
You can read about it more here at the Parkinson’s Foundation:
Parkinson’s Foundation | Levodopa
However! All is not lost. Rather than reaching for the heavy guns by taking l-dopa unnecessarily, there are other dopamine precursors that don’t have those side effects (and are consequently less restricted, to the point they can be purchased as supplements, or indeed, enjoyed where they occur naturally in some foods).
Top of the list of such safe* and readily-available dopamine precursors is…
N-Acetyl L-Tyrosine (NALT): The Dopamine Precursor & More
If you’d like to try that, here’s an example product on Amazon… Or you could eat fish, white beans, tofu, natto, or pumpkin seeds 😉
*Quick note on safety: “safe” is a relative term and may vary from person to person. Please speak with your own doctor to be sure, check with your pharmacist in case of any meds interactions, and be especially careful taking anything that increases dopamine levels if you have bipolar disorder or are otherwise prone to psychosis of any kind. For most people, this shouldn’t be an issue as our brains have a built-in mechanism for scrubbing excess dopamine and ensuring we don’t end up with too much, but for some people whose dopamine regulation is not so good in that regard, it can cause problems. So again, speak with your doctor to be sure, because we are not doctors, let alone your doctor.
Lastly…
If you’d like an entirely drug-free approach, that’s skipping even the “nutraceuticals”, you might enjoy:
Short On Dopamine? Science Has The Answer
Take care!
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What pathogen might spark the next pandemic? How scientists are preparing for ‘disease X’
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Before the COVID pandemic, the World Health Organization (WHO) had made a list of priority infectious diseases. These were felt to pose a threat to international public health, but where research was still needed to improve their surveillance and diagnosis. In 2018, “disease X” was included, which signified that a pathogen previously not on our radar could cause a pandemic.
While it’s one thing to acknowledge the limits to our knowledge of the microbial soup we live in, more recent attention has focused on how we might systematically approach future pandemic risks.
Former US Secretary of Defense Donald Rumsfeld famously talked about “known knowns” (things we know we know), “known unknowns” (things we know we don’t know), and “unknown unknowns” (the things we don’t know we don’t know).
Although this may have been controversial in its original context of weapons of mass destruction, it provides a way to think about how we might approach future pandemic threats.
Anna Shvets/Pexels Influenza: a ‘known known’
Influenza is largely a known entity; we essentially have a minor pandemic every winter with small changes in the virus each year. But more major changes can also occur, resulting in spread through populations with little pre-existing immunity. We saw this most recently in 2009 with the swine flu pandemic.
However, there’s a lot we don’t understand about what drives influenza mutations, how these interact with population-level immunity, and how best to make predictions about transmission, severity and impact each year.
The current H5N1 subtype of avian influenza (“bird flu”) has spread widely around the world. It has led to the deaths of many millions of birds and spread to several mammalian species including cows in the United States and marine mammals in South America.
Human cases have been reported in people who have had close contact with infected animals, but fortunately there’s currently no sustained spread between people.
While detecting influenza in animals is a huge task in a large country such as Australia, there are systems in place to detect and respond to bird flu in wildlife and production animals.
Scientists are continually monitoring a range of pathogens with pandemic potential. Edward Jenner/Pexels It’s inevitable there will be more influenza pandemics in the future. But it isn’t always the one we are worried about.
Attention had been focused on avian influenza since 1997, when an outbreak in birds in Hong Kong caused severe disease in humans. But the subsequent pandemic in 2009 originated in pigs in central Mexico.
Coronaviruses: an ‘unknown known’
Although Rumsfeld didn’t talk about “unknown knowns”, coronaviruses would be appropriate for this category. We knew more about coronaviruses than most people might have thought before the COVID pandemic.
We’d had experience with severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) causing large outbreaks. Both are caused by viruses closely related to SARS-CoV-2, the coronavirus that causes COVID. While these might have faded from public consciousness before COVID, coronaviruses were listed in the 2015 WHO list of diseases with pandemic potential.
Previous research into the earlier coronaviruses proved vital in allowing COVID vaccines to be developed rapidly. For example, the Oxford group’s initial work on a MERS vaccine was key to the development of AstraZeneca’s COVID vaccine.
Similarly, previous research into the structure of the spike protein – a protein on the surface of coronaviruses that allows it to attach to our cells – was helpful in developing mRNA vaccines for COVID.
It would seem likely there will be further coronavirus pandemics in the future. And even if they don’t occur at the scale of COVID, the impacts can be significant. For example, when MERS spread to South Korea in 2015, it only caused 186 cases over two months, but the cost of controlling it was estimated at US$8 billion (A$11.6 billion).
COVID could be regarded as an ‘unknown known’. Markus Spiske/Pexels The 25 viral families: an approach to ‘known unknowns’
Attention has now turned to the known unknowns. There are about 120 viruses from 25 families that are known to cause human disease. Members of each viral family share common properties and our immune systems respond to them in similar ways.
An example is the flavivirus family, of which the best-known members are yellow fever virus and dengue fever virus. This family also includes several other important viruses, such as Zika virus (which can cause birth defects when pregnant women are infected) and West Nile virus (which causes encephalitis, or inflammation of the brain).
The WHO’s blueprint for epidemics aims to consider threats from different classes of viruses and bacteria. It looks at individual pathogens as examples from each category to expand our understanding systematically.
The US National Institute of Allergy and Infectious Diseases has taken this a step further, preparing vaccines and therapies for a list of prototype pathogens from key virus families. The goal is to be able to adapt this knowledge to new vaccines and treatments if a pandemic were to arise from a closely related virus.
Pathogen X, the ‘unknown unknown’
There are also the unknown unknowns, or “disease X” – an unknown pathogen with the potential to trigger a severe global epidemic. To prepare for this, we need to adopt new forms of surveillance specifically looking at where new pathogens could emerge.
In recent years, there’s been an increasing recognition that we need to take a broader view of health beyond only thinking about human health, but also animals and the environment. This concept is known as “One Health” and considers issues such as climate change, intensive agricultural practices, trade in exotic animals, increased human encroachment into wildlife habitats, changing international travel, and urbanisation.
This has implications not only for where to look for new infectious diseases, but also how we can reduce the risk of “spillover” from animals to humans. This might include targeted testing of animals and people who work closely with animals. Currently, testing is mainly directed towards known viruses, but new technologies can look for as yet unknown viruses in patients with symptoms consistent with new infections.
We live in a vast world of potential microbiological threats. While influenza and coronaviruses have a track record of causing past pandemics, a longer list of new pathogens could still cause outbreaks with significant consequences.
Continued surveillance for new pathogens, improving our understanding of important virus families, and developing policies to reduce the risk of spillover will all be important for reducing the risk of future pandemics.
This article is part of a series on the next pandemic.
Allen Cheng, Professor of Infectious Diseases, Monash University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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