Black Bean & Butternut Balti
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Protein, fiber, and pungent polyphenols abound in this tasty dish that’s good for your gut, heart, brain, and more:
You will need
- 2 cans (each 14 oz or thereabouts) black beans, drained and rinsed (or: 2 cups black beans, cooked, drained, and rinsed)
- 1 butternut squash, peeled and cut into ½” cubes
- 1 cauliflower, cut into florets
- 1 red onion, finely chopped
- 1 can (14 oz or thereabouts) chopped tomatoes
- 1 cup coconut milk
- ½ bulb garlic, crushed
- 1″ piece of fresh ginger, peeled and finely chopped
- 1 fresh red chili (or multiply per your preference and the strength of your chilis), finely chopped
- 1 tbsp black pepper, coarse ground
- 1 tbsp garam masala
- 2 tsp cumin seeds
- 2 tsp ground coriander
- 1 tsp ground turmeric
- 1 tsp ground paprika
- ½ tsp MSG or 1 tsp low-sodium salt
- Juice of ½ lemon
- Extra virgin olive oil
Method
(we suggest you read everything at least once before doing anything)
1) Preheat the oven to 400℉ / 200℃.
2) Toss the squash and cauliflower in a little olive oil, to coat evenly. No need to worry about seasoning, because these are going into the curry later and will get plenty there.
3) Roast them on a baking tray lined with baking paper for about 25 minutes.
You can enjoy a 10-minute break for the first 10 minutes of that, before continuing, such that the timing will be perfect:
4) Heat a little oil in a sauté pan (or anything that’s suitable for both frying and adding volume; we’re going to be using the space later; everything is going in here!) and fry the onion on medium for about 5 minutes, stirring well.
5) Add the spices/seasonings, including the garlic, ginger, and chili, and stir well to combine.
6) Add the tomatoes, beans, and coconut milk, and simmer for 10 minutes. You can add a little water at any time if it seems to need it.
7) Stir in the roasted vegetables (they should be finished now), and heat through. Add the lemon juice and stir.
8) Serve as-is, or with your preferred carbohydrate (we recommend our Tasty Versatile Rice recipe), or if you have time, keep it warm for a while until you’re ready to use it (the flavors will benefit from this time, if available).
Enjoy!
Want to learn more?
For those interested in some of the science of what we have going on today:
- Chickpeas vs Black Beans – Which is Healthier?
- Butternut Squash vs Pumpkin – Which is Healthier?
- Our Top 5 Spices: How Much Is Enough For Benefits? ← 5/5 today!
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The Surprising Link Between Type 2 Diabetes & Alzheimer’s
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The Surprising Link Between Type 2 Diabetes & Alzheimer’s
This is Dr. Rhonda Patrick. She’s a biomedical scientist with expertise in the areas of aging, cancer, and nutrition. In the past five years she has expanded her research of aging to focus more on Alzheimer’s and Parkinson’s, as she has a genetic predisposition to both.
What does that genetic predisposition look like? People who (like her) have the APOE-ε4 allele have a twofold increased risk of Alzheimer’s disease—and if you have two copies (i.e., one from each of two parents), the risk can be up to tenfold. Globally, 13.7% of people have at least one copy of this allele.
So while getting Alzheimer’s or not is not, per se, hereditary… The predisposition to it can be passed on.
What’s on her mind?
Dr. Patrick has noted that, while we don’t know for sure the causes of Alzheimer’s disease, and can make educated guesses only from correlations, the majority of current science seems to be focusing on just one: amyloid plaques in the brain.
This is a worthy area of research, but ignores the fact that there are many potential Alzheimer’s disease mechanisms to explore, including (to count only mainstream scientific ideas):
- The amyloid hypothesis
- The tau hypothesis
- The inflammatory hypothesis
- The cholinergic hypothesis
- The cholesterol hypothesis
- The Reelin hypothesis
- The large gene instability hypothesis
…as well as other strongly correlated factors such as glucose hypometabolism, insulin signalling, and oxidative stress.
If you lost your keys and were looking for them, and knew at least half a dozen places they might be, how often would you check the same place without paying any attention to the others?
To this end, she notes about those latter-mentioned correlated factors:
❝50–80% of people with Alzheimer’s disease have type 2 diabetes; there is definitely something going on❞
There’s another “smoking gun” for this too, because dysfunction in the blood vessels and capillaries that line the blood-brain barrier seem to be a very early event that is common between all types of dementia (including Alzheimer’s) and between type 2 diabetes and APOE-ε4.
Research is ongoing, and Dr. Patrick is at the forefront of that. However, there’s a practical take-away here meanwhile…
What can we do about it?
Dr. Patrick hypothesizes that if we can reduce the risk of type 2 diabetes, we may reduce the risk of Alzheimer’s with it.
Obviously, avoiding diabetes if possible is a good thing to do anyway, but if we’re aware of an added risk factor for Alzheimer’s, it becomes yet more important.
Of course, all the usual advices apply here, including a Mediterranean diet and regular moderate exercise.
Three other things Dr. Patrick specifically recommends (to reduce both type 2 diabetes risk and to reduce Alzheimer’s risk) include:
(links are to her blog, with lots of relevant science for each)
You can also hear more from Dr. Patrick personally, as a guest on Dr. Peter Attia’s podcast recently. She discusses these topics in much greater detail than we have room for in our newsletter:
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What’s the difference between a psychopath and a sociopath? Less than you might think
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Articles about badly behaved people and how to spot them are common. You don’t have to Google or scroll too much to find headlines such as 7 signs your boss is a psychopath or How to avoid the sociopath next door.
You’ll often see the terms psychopath and sociopath used somewhat interchangeably. That applies to perhaps the most famous badly behaved fictional character of all – Hannibal Lecter, the cannibal serial killer from The Silence of the Lambs.
In the book on which the movie is based, Lecter is described as a “pure sociopath”. But in the movie, he’s described as a “pure psychopath”. Psychiatrists have diagnosed him with something else entirely.
So what’s the difference between a psychopath and a sociopath? As we’ll see, these terms have been used at different times in history, and relate to some overlapping concepts.
Benoit Daoust/Shutterstock What’s a psychopath?
Psychopathy has been mentioned in the psychiatric literature since the 1800s. But the latest edition of the Diagnostic Statistical Manual of Mental Disorders (known colloquially as the DSM) doesn’t list it as a recognised clinical disorder.
Since the 1950s, labels have changed and terms such as “sociopathic personality disturbance” have been replaced with antisocial personality disorder, which is what we have today.
Was Hannibal Lecter from The Silence of the Lambs a psychopath, a sociopath or something else entirely? Ralf Liebhold/Shutterstock Someone with antisocial personality disorder has a persistent disregard for the rights of others. This includes breaking the law, repeated lying, impulsive behaviour, getting into fights, disregarding safety, irresponsible behaviours, and indifference to the consequences of their actions.
To add to the confusion, the section in the DSM on antisocial personality disorder mentions psychopathy (and sociopathy) traits. In other words, according to the DSM the traits are part of antisocial personality disorder but are not mental disorders themselves.
US psychiatrist Hervey Cleckley provided the first formal description of psychopathy traits in his 1941 book The Mask of Sanity. He based his description on his clinical observations of nine male patients in a psychiatric hospital. He identified several key characteristics, including superficial charm, unreliability and a lack of remorse or shame.
Canadian psychologist Professor Robert Hare refined these characteristics by emphasising interpersonal, emotional and lifestyle characteristics, in addition to the antisocial behaviours listed in the DSM.
When we draw together all these strands of evidence, we can say a psychopath manipulates others, shows superficial charm, is grandiose and is persistently deceptive. Emotional traits include a lack of emotion and empathy, indifference to the suffering of others, and not accepting responsibility for how their behaviour impacts others.
Finally, a psychopath is easily bored, sponges off others, lacks goals, and is persistently irresponsible in their actions.
So how about a sociopath?
The term sociopath first appeared in the 1930s, and was attributed to US psychologist George Partridge. He emphasised the societal consequences of behaviour that habitually violates the rights of others.
Academics and clinicians often used the terms sociopath and psychopath interchangeably. But some preferred the term sociopath because they said the public sometimes confused the word psychopath with psychosis.
“Sociopathic personality disturbance” was the term used in the first edition of the DSM in 1952. This aligned with the prevailing views at the time that antisocial behaviours were largely the product of the social environment, and that behaviours were only judged as deviant if they broke social, legal, and/or cultural rules.
Some of these early descriptions of sociopathy are more aligned with what we now call antisocial personality disorder. Others relate to emotional characteristics similar to Cleckley’s 1941 definition of a psychopath.
In short, different people had different ideas about sociopathy and, even today, sociopathy is less-well defined than psychopathy. So there is no single definition of sociopathy we can give you, even today. But in general, its antisocial behaviours can be similar to ones we see with psychopathy.
Over the decades, the term sociopathy fell out of favour. From the late 60s, psychiatrists used the term antisocial personality disorder instead.
Born or made?
Both “sociopathy” (what we now call antisocial personality disorder) and psychopathy have been associated with a wide range of developmental, biological and psychological causes.
For example, people with psychopathic traits have certain brain differences especially in regions associated with emotions, inhibition of behaviour and problem solving. They also appear to have differences associated with their nervous system, including a reduced heart rate.
However, sociopathy and its antisocial behaviours are a product of someone’s social environment, and tends to run in families. These behaviours has been associated with physical abuse and parental conflict.
What are the consequences?
Despite their fictional portrayals – such as Hannibal Lecter in Silence of the Lambs or Villanelle in the TV series Killing Eve – not all people with psychopathy or sociopathy traits are serial killers or are physically violent.
But psychopathy predicts a wide range of harmful behaviours. In the criminal justice system, psychopathy is strongly linked with re-offending, particularly of a violent nature.
In the general population, psychopathy is associated with drug dependence, homelessness, and other personality disorders. Some research even showed psychopathy predicted failure to follow COVID restrictions.
But sociopathy is less established as a key risk factor in identifying people at heightened risk of harm to others. And sociopathy is not a reliable indicator of future antisocial behaviour.
In a nutshell
Neither psychopathy nor sociopathy are classed as mental disorders in formal psychiatric diagnostic manuals. They are both personality traits that relate to antisocial behaviours and are associated with certain interpersonal, emotional and lifestyle characteristics.
Psychopathy is thought to have genetic, biological and psychological bases that places someone at greater risk of violating other people’s rights. But sociopathy is less clearly defined and its antisocial behaviours are the product of someone’s social environment.
Of the two, psychopathy has the greatest use in identifying someone who is most likely to cause damage to others.
Bruce Watt, Associate Professor in Psychology, Bond University and Katarina Fritzon, Associate Professor of Psychology, Bond University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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HIIT, But Make It HIRT
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This May HIRT A Bit
This is Ingrid Clay. She’s a professional athlete, personal trainer, chef*, and science writer.
*A vegan bodybuilding chef, no less:
Click Here If The Embedded Video Doesn’t Load Automatically!
For those who prefer reading…
This writer does too 😉
We’ve previously reviewed her book, “Science of HIIT”, and we’re going to be talking a bit about High Intensity Interval Training today.
If you’d like to know a little more about the woman herself first, then…
Centr | Meet Ingrid: Your HIIT HIRT trainer
Yes, that is Centr, as in Chris Hemsworth’s personal training app, where Clay is the resident HIIT & HIRT expert & trainer.
What’s this HIIT & HIRT?
“HIIT” is High Intensity Interval Training, which we’ve written about before:
How To Do HIIT (Without Wrecking Your Body)
Basically, it’s a super-efficient way of working out, that gets better results than working out for longer with other methods, especially because of how it raises the metabolism for a couple of hours after training (this effect is called EPOC, by the way—Excessive Post-exercise Oxygen Consumption), and is a good thing.
You can read more about the science of it, in the above-linked main feature.
And HIRT?
“HIRT” is High Intensity Resistance Training, and is resistance training performed with HIIT principles.
See also: Chris Hemsworth’s Trainer Ingrid Clay Explains HIRT
An example is doing 10 reps of a resistance exercise (e.g., a dumbbell press) every minute on odd-numbered minutes, and 10 reps of a different resistance exercise (e.g. dumbbell squats) on even-numbered minutes.
If dumbbells aren’t your thing, it could be resistance bands, or even the floor (press-ups are a resistance exercise!)
For HIRT that’s not also a cardio exercise, gaps between different exercises can be quite minimal, as we only need to confuse the muscles, not the heart. So, effectively, it becomes a specially focused kind of circuit training!
If doing planks though, you might want to check out Clay’s troubleshooting guide:
Want more from Clay?
Here she gives a full 20-minute full-body HIIT HIRT workout:
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Enjoy!
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Move over, COVID and Flu! We Have “Hybrid Viruses” To Contend With Now
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Move over, COVID and Flu! We have “hybrid viruses” to contend with now
COVID and influenza viruses can be serious, of course, so let’s be clear up front that we’re not being dismissive of those. But, most people are hearing a lot about them, whereas respiratory syncytial virus (RSV) has flown under a lot of radars.
Simply put, until recently it hasn’t been considered much of a threat except to the young, the old, or people with other respiratory illnesses. Only these days, the prevalence of “other respiratory illnesses” is a lot higher than it used to be!
It’s not just a comorbidity
It’s easy to think “well of course if you have more than one illness at once, especially similar ones, that’s going to suck” but it’s a bit more than that; it produces newer, more interesting, hybrid viruses. Here’s a research paper from last year’s “flu season”:
Coinfection by influenza A virus and respiratory syncytial virus produces hybrid virus particles
Best to be aware of this if you’re in the “older” age-range
It’s not just that the older we are, the more likely we are to get it. Critically, the older we are, the more likely we are to be hospitalized by it.
And..the older we are, the less likely we are to come back from hospital if hospitalized by it.
Some years back, the intensive care and mortality rates for people over the age of 65 were 8% and 7%, respectively:
Respiratory syncytial virus infection in elderly and high-risk adults
…but a new study this year has found the rates like to be 2.2x that, i.e. 15% intensive care rate and 18% mortality, respectively:
Want to know more?
Here are some hot-off-the-press news articles on the topic:
- Better awareness of RSV in older adults is needed to reduce hospitalizations
- Is there also a connection between RSV and asthma?
- Respiratory syncytial virus coinfections conspire to worsen disease
And as for what to do…
Same general advice as for COVID and Flu, just, ever-more important:
- Try to keep to well-ventilated places as much as possible
- Get any worrying symptoms checked out quickly
- Mask up when appropriate
- Get your shots as appropriate
See also:
Harvard Health Review | Fall shots: Who’s most vulnerable to RSV, COVID, and the flu, and which shots are the right choice for you to help protect against serious illness and hospitalization?
Stay safe!
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Hair-Loss Remedies, By Science
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10almonds Gets Hairy
Hair loss is a thing that at some point affects most men and a large minority of women. It can be a source of considerable dysphoria for both, as it’s often seen as a loss of virility/femininity respectively, and is societally stigmatized in various ways.
Today we’re going to focus on the most common kind: androgenic alopecia, which is called “male pattern baldness” in men and “female pattern baldness” in women, despite being the same thing.
We won’t spend a lot of time on the science of why this happens (we’re going to focus on the remedies instead), but suffice it to say that genes and hormones both play a role, with dihydrogen testosterone (DHT) being the primary villain in this case.
We’ve talked before about the science of 5α-reductase inhibitors to block the conversion of regular testosterone* to DHT, its more potent form:
One Man’s Saw Palmetto Is Another Woman’s Serenoa Repens…
*We all make this to a greater or lesser degree, unless we have had our ovaries/testes removed.
Finasteride
Finasteride is a 5α-reductase inhibitor that performs similarly to saw palmetto, but comes in tiny pills instead of needing to take a much higher dose of supplement (5mg of finasteride is comparable in efficacy to a little over 300mg of saw palmetto).
Does it work? Yes!
Any drawbacks? A few:
- It’ll take 3–6 months to start seeing effects. This is because of the hormonal life-cycle of human hairs.
- Common side-effects include ED.
- It is popularly labelled/prescribed as “only for men”
On that latter point: the warnings about this are severe, detailing how women must not take it, must not even touch it if it has been cut up or crushed.
However… That’s because it can carry a big risk to our unborn fetuses. So, if we are confident we definitely don’t have one of those, it’s not actually applicable to us.
That said, finasteride’s results in women aren’t nearly so clear-cut as in men (though also, there has been less research, largely because of the above). Here’s an interesting breakdown in more words than we have room for here:
Finasteride for Women: Everything You Need to Know
Spironolactone
This one’s generally prescribed to women, not men, largely because it’s the drug sometimes popularly known as a “chemical castration” drug, which isn’t typically great marketing for men (although it can be applied topically, which will have less of an effect on the rest of the body). For women, this risk is simply not an issue.
We’ll be brief on this one, but we’ll just drop this, so that you know it’s an option that works:
❝Spironolactone is an effective and safe treatment of androgenic alopecia which can enhance the efficacy when combined with other conventional treatments such as minoxidil.
Topical spironolactone is safer than oral administration and is suitable for both male and female patients, and is expected to become a common drug for those who do not have a good response to minoxidil❞
Minoxidil
This one is available (to men and women) without prescription. It’s applied topically, and works by shortcutting the hair’s hormonal growth cycle, to reduce the resting phase and kick it into a growth phase.
Does it work? Yes!
Any drawbacks? A few:
- Whereas you’ll remember finasteride takes 3–6 months to see any effect, this one will have an effect very quickly
- Specifically, the immediate effect is: your rate of hair loss will appear to dramatically speed up
- This happens because when hairs are kicked into their growth phase if they were in a resting phase, the first part of that growth phase is to shed each old hair to make room for the new one
- You’ll then need the same 3–6 months as with finasteride, to see the regrowth effects
- If you stop using it, you will immediately shed whatever hair you gained by this method
Why do people choose this over finasteride? For one of three reasons, mainly:
- They are women, and not offered finasteride
- They are men, and do not want the side effects of finasteride
- They just saw an ad and tried it
As to how it works:
Some final notes:
There are some other contraindications and warnings with each of these drugs by the way, so do speak with your doctor/pharmacist. For example:
- Finasteride can tax the liver a little
- Spironolactone can reduce bone turnover
- Minoxidil is a hypotensive; this shouldn’t be an issue for most people, but for some people it could be a problem
There are other hair loss remedies and practices, but the above three are the heavy-hitters, so that’s what we spent our time/space on today. We’ll perhaps cover the less powerful (but less risky) options one of these days.
Meanwhile, take care!
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Microplastics are in our brains. How worried should I be?
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Plastic is in our clothes, cars, mobile phones, water bottles and food containers. But recent research adds to growing concerns about the impact of tiny plastic fragments on our health.
A study from the United States has, for the first time, found microplastics in human brains. The study, which has yet to be independently verified by other scientists, has been described in the media as scary, shocking and alarming.
But what exactly are microplastics? What do they mean for our health? Should we be concerned?
Daniel Megias/Shutterstock What are microplastics? Can you see them?
We often consider plastic items to be indestructible. But plastic breaks down into smaller particles. Definitions vary but generally microplastics are smaller than five millimetres.
This makes some too small to be seen with the naked eye. So, many of the images the media uses to illustrate articles about microplastics are misleading, as some show much larger, clearly visible pieces.
Microplastics have been reported in many sources of drinking water and everyday food items. This means we are constantly exposed to them in our diet.
Such widespread, chronic (long-term) exposure makes this a serious concern for human health. While research investigating the potential risk microplastics pose to our health is limited, it is growing.
How about this latest study?
The study looked at concentrations of microplastics in 51 samples from men and women set aside from routine autopsies in Albuquerque, New Mexico. Samples were from the liver, kidney and brain.
These tiny particles are difficult to study due to their size, even with a high-powered microscope. So rather than trying to see them, researchers are beginning to use complex instruments that identify the chemical composition of microplastics in a sample. This is the technique used in this study.
The researchers were surprised to find up to 30 times more microplastics in brain samples than in the liver and kidney.
They hypothesised this could be due to high blood flow to the brain (carrying plastic particles with it). Alternatively, the liver and kidneys might be better suited to dealing with external toxins and particles. We also know the brain does not undergo the same amount of cellular renewal as other organs in the body, which could make the plastics linger here.
The researchers also found the amount of plastics in brain samples increased by about 50% between 2016 and 2024. This may reflect the rise in environmental plastic pollution and increased human exposure.
The microplastics found in this study were mostly composed of polyethylene. This is the most commonly produced plastic in the world and is used for many everyday products, such as bottle caps and plastic bags.
This is the first time microplastics have been found in human brains, which is important. However, this study is a “pre-print”, so other independent microplastics researchers haven’t yet reviewed or validated the study.
The most common plastic found was polyethylene, which is used to make plastic bags and bottle caps. Maciej Bledowski/Shutterstock How do microplastics end up in the brain?
Microplastics typically enter the body through contaminated food and water. This can disrupt the gut microbiome (the community of microbes in your gut) and cause inflammation. This leads to effects in the whole body via the immune system and the complex, two-way communication system between the gut and the brain. This so-called gut-brain axis is implicated in many aspects of health and disease.
We can also breathe in airborne microplastics. Once these particles are in the gut or lungs, they can move into the bloodstream and then travel around the body into various organs.
Studies have found microplastics in human faeces, joints, livers, reproductive organs, blood, vessels and hearts.
Microplastics also migrate to the brains of wild fish. In mouse studies, ingested microplastics are absorbed from the gut into the blood and can enter the brain, becoming lodged in other organs along the way.
To get into brain tissue, microplastics must cross the blood-brain-barrier, an intricate layer of cells that is supposed to keep things in the blood from entering the brain.
Although concerning, this is not surprising, as microplastics must cross similar cell barriers to enter the urine, testes and placenta, where they have already been found in humans.
Is this a health concern?
We don’t yet know the effects of microplastics in the human brain. Some laboratory experiments suggest microplastics increase brain inflammation and cell damage, alter gene expression and change brain structure.
Aside from the effects of the microplastic particles themselves, microplastics might also pose risks if they carry environmental toxins or bacteria into and around the body.
Various plastic chemicals could also leach out of the microplastics into the body. These include the famous hormone-disrupting chemicals known as BPAs.
But microplastics and their effects are difficult to study. In addition to their small size, there are so many different types of plastics in the environment. More than 13,000 different chemicals have been identified in plastic products, with more being developed every year.
Microplastics are also weathered by the environment and digestive processes, and this is hard to reproduce in the lab.
A goal of our research is to understand how these factors change the way microplastics behave in the body. We plan to investigate if improving the integrity of the gut barrier through diet or probiotics can prevent the uptake of microplastics from the gut into the bloodstream. This may effectively stop the particles from circulating around the body and lodging into organs.
How do I minimise my exposure?
Microplastics are widespread in the environment, and it’s difficult to avoid exposure. We are just beginning to understand how microplastics can affect our health.
Until we have more scientific evidence, the best thing we can do is reduce our exposure to plastics where we can and produce less plastic waste, so less ends up in the environment.
An easy place to start is to avoid foods and drinks packaged in single-use plastic or reheated in plastic containers. We can also minimise exposure to synthetic fibres in our home and clothing.
Sarah Hellewell, Senior Research Fellow, The Perron Institute for Neurological and Translational Science, and Research Fellow, Faculty of Health Sciences, Curtin University; Anastazja Gorecki, Teaching & Research Scholar, School of Health Sciences, University of Notre Dame Australia, and Charlotte Sofield, PhD Candidate, studying microplastics and gut/brain health, University of Notre Dame Australia
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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