With Medical Debt Burdening Millions, a Financial Regulator Steps In to Help
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When President Barack Obama signed legislation in 2010 to create the Consumer Financial Protection Bureau, he said the new agency had one priority: “looking out for people, not big banks, not lenders, not investment houses.”
Since then, the CFPB has done its share of policing mortgage brokers, student loan companies, and banks. But as the U.S. health care system turns tens of millions of Americans into debtors, this financial watchdog is increasingly working to protect beleaguered patients, adding hospitals, nursing homes, and patient financing companies to the list of institutions that regulators are probing.
In the past two years, the CFPB has penalized medical debt collectors, issued stern warnings to health care providers and lenders that target patients, and published reams of reports on how the health care system is undermining the financial security of Americans.
In its most ambitious move to date, the agency is developing rules to bar medical debt from consumer credit reports, a sweeping change that could make it easier for Americans burdened by medical debt to rent a home, buy a car, even get a job. Those rules are expected to be unveiled later this year.
“Everywhere we travel, we hear about individuals who are just trying to get by when it comes to medical bills,” said Rohit Chopra, the director of the CFPB whom President Joe Biden tapped to head the watchdog agency in 2021.
“American families should not have their financial lives ruined by medical bills,” Chopra continued.
The CFPB’s turn toward medical debt has stirred opposition from collection industry officials, who say the agency’s efforts are misguided. “There’s some concern with a financial regulator coming in and saying, ‘Oh, we’re going to sweep this problem under the rug so that people can’t see that there’s this medical debt out there,’” said Jack Brown III, a longtime collector and member of the industry trade group ACA International.
Brown and others question whether the agency has gone too far on medical billing. ACA International has suggested collectors could go to court to fight any rules barring medical debt from credit reports.
At the same time, the U.S. Supreme Court is considering a broader legal challenge to the agency’s funding that some conservative critics and financial industry officials hope will lead to the dissolution of the agency.
But CFPB’s defenders say its move to address medical debt simply reflects the scale of a crisis that now touches some 100 million Americans and that a divided Congress seems unlikely to address soon.
“The fact that the CFPB is involved in what seems like a health care issue is because our system is so dysfunctional that when people get sick and they can’t afford all their medical bills, even with insurance, it ends up affecting every aspect of their financial lives,” said Chi Chi Wu, a senior attorney at the National Consumer Law Center.
CFPB researchers documented that unpaid medical bills were historically the most common form of debt on consumers’ credit reports, representing more than half of all debts on these reports. But the agency found that medical debt is typically a poor predictor of whether someone is likely to pay off other bills and loans.
Medical debts on credit reports are also frequently riddled with errors, according to CFPB analyses of consumer complaints, which the agency found most often cite issues with bills that are the wrong amount, have already been paid, or should be billed to someone else.
“There really is such high levels of inaccuracy,” Chopra said in an interview with KFF Health News. “We do not want to see the credit reporting system being weaponized to get people to pay bills they may not even owe.”
The aggressive posture reflects Chopra, who cut his teeth helping to stand up the CFPB almost 15 years ago and made a name for himself going after the student loan industry.
Targeting for-profit colleges and lenders, Chopra said he was troubled by an increasingly corporate higher-education system that was turning millions of students into debtors. Now, he said, he sees the health care system doing the same thing, shuttling patients into loans and credit cards and reporting them to credit bureaus. “If we were to rewind decades ago,” Chopra said, “we saw a lot less reliance on tools that banks used to get people to pay.”
The push to remove medical bills from consumer credit reports culminates two years of intensive work by the CFPB on the medical debt issue.
The agency warned nursing homes against forcing residents’ friends and family to assume responsibility for residents’ debts. An investigation by KFF Health News and NPR documented widespread use of lawsuits by nursing homes in communities to pursue friends and relatives of nursing home residents.
The CFPB also has highlighted problems with how hospitals provide financial assistance to low-income patients. Regulators last year flagged the dangers of loans and credit cards that health care providers push on patients, often saddling them with more debt.
And regulators have gone after medical debt collectors. In December, the CFPB shut down a Pennsylvania company for pursuing patients without ensuring the debts were accurate.
A few months before that, the agency fined an Indiana company working with medical debt for violating collection laws. Regulators said the company had “risked harming consumers by pressuring or inducing them to pay debts they did not owe.”
With their business in the crosshairs, debt collectors are warning that cracking down on credit reporting and other collection tools may prompt more hospitals and doctors to demand patients pay upfront for care.
There are some indications this is happening already, as hospitals and clinics push patients to enroll in loans or credit cards to pay their medical bills.
Scott Purcell, CEO of ACA International, said it would be wiser for the federal government to focus on making medical care more affordable. “Here we’re coming up with a solution that only takes money away from providers,” Purcell said. “If Congress was involved, there could be more robust solutions.”
Chopra doesn’t dispute the need for bigger efforts to tackle health care costs.
“Of course, there are broader things that we would probably want to fix about our health care system,” he said, “but this is having a direct financial impact on so many Americans.”
The CFPB can’t do much about the price of a prescription or a hospital bill, Chopra continued. What the federal agency can do, he said, is protect patients if they can’t pay their bills.
KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.
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Osteoarthritis Of The Knee
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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
❝Very informative thank you. And made me think. I am a 72 yr old whitewoman, have never used ( or even been offered) HRT since menopause ~15 yrs ago. Now I’m wondering if it would have delayed the onset of osteoarthritis ( knee) and give me more energy in general. And is it wise to start taking hrt after being without those hormones for so long?❞
(this was in response to our article about menopausal HRT)
Thanks for writing! To answer your first question, obviously we can never know for sure now, but it certainly is possible, per for example a large-ish (n=1003) study of women aged 45–64, in which:
- Those with HRT were significantly less likely to have knee arthritis than those without
- However, to enjoy this benefit depended on continued use (those who used it for a bit and then stopped did not enjoy the same results)
- While it made a big difference to knee arthritis, it made only a small (but still beneficial) difference to wrist/hand arthritis.
We could hypothesize that this is because the mechanism of action is more about strengthening the bones (proofing against osteoporosis is one of the main reasons many people take HRT) and cartilage than it is against inflammation directly.
Since the knee is load-bearing and the hand/wrist joints usually are not, this would mean the HRT strengthening the bones makes a big difference to the “wear and tear” aspect of potential osteoarthritis of the knee, but not the same level of benefit for the hand/wrist, which is less about wear and tear and more about inflammatory factors. But that latter, about it being load-bearing, is just this writer’s hypothesis as to why the big difference.
The researchers do mention:
❝In OA the mechanisms by which HRT might act are highly speculative, but could entail changes in cartilage repair or bone turnover, perhaps with cytokines such as interleukin 6, for example.❞
What is clear though, is that it does indeed appear to have a protective effect against osteoarthritis of the knee.
With regard to the timing, the researchers do note:
❝Why as little as three years of HRT should have a demonstrable effect is unclear. Given the difficulty in ascertaining when the disease starts, it is hard to be sure of the importance of the timing of HRT, and whether early or subclinical disease was present.
These results taken together suggest that HRT has a metabolic action that is only effective if given continuously, perhaps by preventing disease initiation; once HRT is stopped there might be a ‘rebound’ effect, explaining the rapid return to normal risk❞
~ Ibid.
You can read the study here:
On whether it is worth it now…
Again, do speak with an endocrinologist because your situation may vary, but:
- hormones are simply messengers, and your body categorically will respond to those messages regardless of age, or time elapsed without having received such a message. Whether it will repair all damage done is another matter entirely, but it would take a biological miracle for it to have no effect at all.
- anecdotally, many women do enjoy life-changing benefits upon starting HRT at your age and older!
(We don’t like to rely on “anecdotally”, but we couldn’t find studies isolating according to “length of time since menopause”—we’ll keep an eye out and if we find something in the future, we’ll mention it!)
Meanwhile, take care!
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7 Days Of Celery Juice: What’s The Verdict?
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Laura “Try” tries many popular trends, and reports on the benefits (or problems, or both). In this case, it’s 7 days of celery juice… Not as a fast, though, i.e. she doesn’t just have celery juice for 7 days, but rather, it’s how she kicks off each morning, with half a liter (16oz) on an empty stomach.
What she found
First, she bought a masticating juicer and organic celery. So, those are expenses to consider, especially the one-off expense of the juicer, and the ongoing expense of organic celery—estimated $90/month).
In terms of taste, she was surprised it wasn’t as bitter as expected, but from the second day onwards, she did use the juicer’s filter to remove the frothy sludge, and she also switched to juicing only the stalks, not the leaves—which are more bitter.
10almonds note: the leaves are more bitter because that’s where the polyphenols are more densely concentrated. The leaves are better for you than the stalks. Enjoy the leaves. Really: if you chop them finely you can use them as herbs in your cooking, and if you’re making a salad, just chop them into that too.
The reason she picked the quantity of half a liter is because this is what she found recommended to coat the stomach lining—on the promise of increased stomach acid production, reduced bacteria overgrowth, as well as antiviral, antifungal, and anti-inflammatory properties. As she’s just one woman without a personal lab, she couldn’t test and thus verify any of these though—but she did still have benefits to report:
She did experience clearer skin, more energy, and better sleep after a few days.
Ultimately, she decided to continue to do it just at the weekends, due to its positive effects, despite the cost and time consumption.
For more personal insights, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like to read:
Enjoy Bitter Foods For Your Heart & Brain
Take care!
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The Diabetes Drugs That Can Cut Asthma Attacks By 70%
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Asthma, obesity, and type 2 diabetes are closely linked, with the latter two greatly increasing asthma attack risk.
While bronchodilators / corticosteroids can have immediate adverse effects due to sympathetic nervous system activation, and lasting adverse effects due to the damage it does to metabolic health, diabetes drugs, on the other hand, can improve things with (for most people) fewer unwanted side effects.
Great! Which drugs?
Metformin, and glucagon-like peptide-1 receptor agonists (GLP-1RAs).
Specifically, researchers have found:
- Metformin is associated with a 30% reduction in asthma attacks
- GLP-1RAs are associated with a 40% reduction in asthma attacks
…and yes, they stack, making for a 70% reduction in the case of people taking both. Furthermore, the results are independent of weight, glycemic control, or asthma phenotype.
In terms of what was counted, the primary outcome was asthma attacks at 12-month follow-up, defined by oral corticosteroid use, emergency visits, hospitalizations, or death.
The effect of metformin on asthma attacks was not affected by BMI, HbA1c levels, eosinophil count, asthma severity, or sex.
Of the various extra antidiabetic drugs trialled in this study, only GLP-1 receptor agonists showed a further and sustained reduction in asthma attacks.
Here’s the study itself, hot off the press, published on Monday:
JAMA Int. Med. | Antidiabetic Medication and Asthma Attacks
“But what if I’m not diabetic?”
Good news:
More than half of all US adults are eligible for semaglutide therapy ← this is because they’ve expanded the things that semaglutide (the widely-used GLP-1 receptor agonist drug) can be prescribed for, now going beyond just diabetes and/or weight loss 😎
And metformin, of course, is more readily available than semaglutide, so by all means speak with your doctor/pharmacist about that, if it’s of interest to you.
Take care!
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We looked at genetic clues to depression in more than 14,000 people. What we found may surprise you
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The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.
Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.
But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.
Reactive vs endogenous depression
One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.
Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.
Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.
Many people working clinically in mental health accept this sub-typing. You might have read about this online.
But we think this approach is way too simple.
While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.
What we did and what we found
Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.
In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.
Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?
We looked at the genetic risk of mental illness to see how that was linked to stressful life events, such as childhood abuse and neglect. Kamira/Shutterstock You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.
We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.
If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.
But after studying more than 14,000 people with depression we found the opposite.
We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.
Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.
These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.
How do genes play a role?
Genetic risk for mental disorders changes people’s sensitivity to the environment.
Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.
Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.
If two people lose their jobs, one with a high genetic risk of depression the other at low risk, both will experience and remember the event differently. Inside Creative House/Shutterstock What does our study mean for depression?
First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.
Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.
Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.
So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.
If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.
Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Reading As A Cognitive Exercise
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Reading, Better
It is relatively uncontroversial to say that reading is good for cognitive health, but we don’t like to make claims without science if we can help it, so let’s get started:
There was a 2021 study, which found that even when controlling for many other factors, including highest level of education, socioeconomic status, and generalized pre-morbid intelligence:
❝high reading activity, as defined by almost daily reading, was associated with lower odds of cognitive decline, compared to low reading activity❞
Source: Can reading increase cognitive reserve?
However, not all reading is the same. And this isn’t just about complexity or size of vocabulary, either. It’s about engagement.
And that level of engagement remains the key factor, no matter how quickly or slowly someone reads, as the brain tends to automatically adjust reading speed per complexity, because the brain’s “processing speed” remains the same:
Read more: Cognitive coupling during reading
Everyone’s “processing speed” is different (and is associated with generalized intelligence and executive functions), though as a general rule of thumb, the more we practice it, the faster our processing speed gets. So if you balked at the notion of “generalized intelligence” being a factor, be reassured that this association goes both ways.
So is the key to just read more?
That’s a great first step! But…
The key factor still remains: engagement.
So what does that mean?
It is not just the text that engages you. You must also engage the text!
This is akin to the difference between learning to drive by watching someone else do it, and learning by getting behind the wheel and having a go.
When it comes to reading, it should not be a purely passive thing. Sure, if you are reading a fiction book at bedtime, get lost in it, by all means. But when it comes to non-fiction reading, engage with it actively!
For example, I (your writer here, hi), when reading non-fiction:
- Read at what is generally considered an unusually fast pace, but
- Write so many notes in the margins of physical books, and
- Write so many notes using the “Notes” function on my Kindle
And this isn’t just like a studious student taking notes. Half the time I am…
- objecting to content (disagreeing with the author), or
- at least questioning it, or which is especially important, or
- noting down questions that came to my mind as a result of what I am reading.
This latter is a bit like:
- when you are reading 10almonds, sometimes you will follow our links and go off down a research rabbit-hole of your own, and that’s great!
- sometimes you will disagree with something and write to tell us, and that’s great too (when this happens, one or the other or all of us will learn something, and yes, we have published corrections before now)!
- sometimes what you read here will prompt a further question, and you’ll send that to us, and guess what, also great! We love questions.
Now, if your enjoyment of 10almonds is entirely passive, don’t let us stop you (we know our readers like quick-and-easy knowledge, and that’s good too), it’s just, the more you actively engage with it, the more you’ll get out of it.
This, by the way, was also a lifelong habit of Leonardo da Vinci, which you can read about here:
How to Think Like Leonardo da Vinci: Seven Steps to Genius Every Day – by Michael J. Gelb
a very good book that we reviewed last year
How you read (i.e. what medium) matters too!
Are you reading this on a desktop/laptop, or a mobile device? That difference could matter more than the difference between paper and digital, according to this study from 2020 that found…
❝The cumulation of evidence from this and previous studies suggests that reading on a tablet affords different interactions between the reader and the text than reading on a computer screen.
Reading on a tablet might be more similar to reading on paper, and this may impact the attentional processes during reading❞
What if my mind wanders easily?
You can either go with it, or train to improve focus.
Going with it: just make sure you have more engaging reading to get distracted by. It’s all good.
Training focus: this is trickier, but worthwhile, as executive function (you will remember from earlier) was an important factor too, and training focus is training executive function.
As for one way to do that…
If you’d like a primer for getting going with that, then you may enjoy our previous main feature:
No-Frills, Evidence-Based Mindfulness
Enjoy!
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The Brain As A Work-In-Progress
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And The Brain Goes Marching On!
In Tuesday’s newsletter, we asked you “when does the human brain stop developing?” and got the above-depicted, below-described, set of responses:
- About 64% of people said “Never”
- About 16% of people said “25 years”
- About 9% of people said “65 years”
- About 5% of people said “13 years”
- About 3% of people said “18 years”
- About 3% of people said “45 years”
Some thoughts, before we get into the science:
An alternative wording for the original question was “when does the human brain finish developing”; the meaning is the same but the feeling is slightly different:
- “When does the human brain stop developing?” focuses attention on the idea of cessation, and will skew responses to later ages
- When does the human brain finish developing?” focuses on attention on a kind of “is it done yet?” and will skew responses to earlier ages
Ultimately, since we had to chose one word or another, we picked the shortest one, but it would have been interesting if we could have done an A/B test, and asked half one way, and half the other way!
Why we picked those ages
We picked those ages as poll options for reasons people might be drawn to them:
- 13 years: in English-speaking cultures, an important milestone of entering adolescence (note that the concept of a “teenager” is not precisely universal as most languages do not have “-teen” numbers in the same way; the concept of “adolescent” may thus be tied to other milestones)
- 18 years: age of legal majority in N. America and many other places
- 25 years: age popularly believed to be when the brain is finished developing, due to a study that we’ll talk about shortly (we guess that’s why there’s a spike in our results for this, too!)
- 45 years: age where many midlife hormonal changes occur, and many professionals are considered to have peaked in competence and start looking towards retirement
- 65 years: age considered “senior” in much of N. America and many other places, as well as the cut-off and/or starting point for a lot of medical research
Notice, therefore, how a lot of things are coming from places they really shouldn’t. For example, because there are many studies saying “n% of people over 65 get Alzheimer’s” or “n% of people over 65 get age-related cognitive decline”, etc, 65 becomes the age where we start expecting this—because of an arbitrary human choice of where to draw the cut-off for the study enrollment!
Similarly, we may look at common ages of legal majority, or retirement pensions, and assume “well it must be for a good reason”, and dear reader, those reasons are more often economically motivated than they are biologically reasoned.
So, what does the science say?
Our brains are never finished developing: True or False?
True! If we define “finished developing” as “we cease doing neurogenesis and neuroplasticity is no longer in effect”.
Glossary:
- Neurogenesis: the process of creating new brain cells
- Neuroplasticity: the process of the brain adapting to changes by essentially rebuilding itself to suit our perceived current needs
We say “perceived” because sometimes neuroplasticity can do very unhelpful things to us (e.g: psychological trauma, or even just bad habits), but on a biological level, it is always doing its best to serve our overall success as an organism.
For a long time it was thought that we don’t do neurogenesis at all as adults, but this was found to be untrue:
How To Grow New Brain Cells (At Any Age)
Summary of conclusions of the above: we’re all growing new brain cells at every age, even if we be in our 80s and with Alzheimer’s disease, but there are things we can do to enhance our neurogenic potential along the way.
Neuroplasticity will always be somewhat enhanced by neurogenesis (after all, new neurons get given jobs to do), and we reviewed a great book about the marvels of neuroplasticity including in older age:
Our brains are still developing up to the age of 25: True or False?
True! And then it keeps on developing after that, too. Now this is abundantly obvious considering what we just talked about, but see what a difference the phrasing makes? Now it makes it sound like it stops at 25, which this statement doesn’t claim at all—it only speaks for the time up to that age.
A lot of the popular press about “the brain isn’t fully mature until the age of 25” stems from a 2006 study that found:
❝For instance, frontal gray matter volume peaks at about age 11.0 years in girls and 12.1 years in boys, whereas temporal gray matter volume peaks at about age at 16.7 years in girls and 16.2 years in boys. The dorsal lateral prefrontal cortex, important for controlling impulses, is among the latest brain regions to mature without reaching adult dimensions until the early 20s.❞
Source: Structural Magnetic Resonance Imaging of the Adolescent Brain
There are several things to note here:
- The above statement is talking about the physical size of the brain growing
- Nowhere does he say “and stops developing at 25”
However… The study only looked at brains up to the age of 25. After that, they stopped looking, because the study was about “the adolescent brain” so there has to be a cut-off somewhere, and that was the cut-off they chose.
This is the equivalent of saying “it didn’t stop raining until four o’clock” when the reality is that four o’clock is simply when you gave up on checking.
The study didn’t misrepresent this, by the way, but the popular press did!
Another 2012 study looked at various metrics of brain development, and found:
- Synapse overproduction into the teens
- Cortex pruning into the late 20s
- Prefrontal pruning into middle age at least (they stopped looking)
- Myelination beyond middle age (they stopped looking)
Source: Experience and the developing prefrontal cortex ← check out figure 1, and make sure you’re looking at the human data not the rat data
So how’s the most recent research looking?
Here’s a 2022 study that looked at 123,984 brain scans spanning the age range from mid-gestation to 100 postnatal years, and as you can see from its own figure 1… Most (if not all) brain-things keep growing for life, even though most slow down at some point, they don’t stop:
Brain charts for the human lifespan ← check out figure 1; don’t get too excited about the ventricular volume column as that is basically “brain that isn’t being a brain”. Do get excited about the rest, though!
Want to know how not to get caught out by science being misrepresented by the popular press? Check out:
How Science News Outlets Can Lie To You (Yes, Even If They Cite Studies!)
Take care!
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