Mental illness, psychiatric disorder or psychological problem. What should we call mental distress?
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We talk about mental health more than ever, but the language we should use remains a vexed issue.
Should we call people who seek help patients, clients or consumers? Should we use “person-first” expressions such as person with autism or “identity-first” expressions like autistic person? Should we apply or avoid diagnostic labels?
These questions often stir up strong feelings. Some people feel that patient implies being passive and subordinate. Others think consumer is too transactional, as if seeking help is like buying a new refrigerator.
Advocates of person-first language argue people shouldn’t be defined by their conditions. Proponents of identity-first language counter that these conditions can be sources of meaning and belonging.
Avid users of diagnostic terms see them as useful descriptors. Critics worry that diagnostic labels can box people in and misrepresent their problems as pathologies.
Underlying many of these disagreements are concerns about stigma and the medicalisation of suffering. Ideally the language we use should not cast people who experience distress as defective or shameful, or frame everyday problems of living in psychiatric terms.
Our new research, published in the journal PLOS Mental Health, examines how the language of distress has evolved over nearly 80 years. Here’s what we found.
Generic terms for the class of conditions
Generic terms – such as mental illness, psychiatric disorder or psychological problem – have largely escaped attention in debates about the language of mental ill health. These terms refer to mental health conditions as a class.
Many terms are currently in circulation, each an adjective followed by a noun. Popular adjectives include mental, mental health, psychiatric and psychological, and common nouns include condition, disease, disorder, disturbance, illness, and problem. Readers can encounter every combination.
These terms and their components differ in their connotations. Disease and illness sound the most medical, whereas condition, disturbance and problem need not relate to health. Mental implies a direct contrast with physical, whereas psychiatric implicates a medical specialty.
Mental health problem, a recently emerging term, is arguably the least pathologising. It implies that something is to be solved rather than treated, makes no direct reference to medicine, and carries the positive connotations of health rather than the negative connotation of illness or disease.
Arguably, this development points to what cognitive scientist Steven Pinker calls the “euphemism treadmill”, the tendency for language to evolve new terms to escape (at least temporarily) the offensive connotations of those they replace.
English linguist Hazel Price argues that mental health has increasingly come to replace mental illness to avoid the stigma associated with that term.
How has usage changed over time?
In the PLOS Mental Health paper, we examine historical changes in the popularity of 24 generic terms: every combination of the nouns and adjectives listed above.
We explore the frequency with which each term appears from 1940 to 2019 in two massive text data sets representing books in English and diverse American English sources, respectively. The findings are very similar in both data sets.
The figure presents the relative popularity of the top ten terms in the larger data set (Google Books). The 14 least popular terms are combined into the remainder.
Several trends appear. Mental has consistently been the most popular adjective component of the generic terms. Mental health has become more popular in recent years but is still rarely used.
Among nouns, disease has become less widely used while illness has become dominant. Although disorder is the official term in psychiatric classifications, it has not been broadly adopted in public discourse.
Since 1940, mental illness has clearly become the preferred generic term. Although an assortment of alternatives have emerged, it has steadily risen in popularity.
Does it matter?
Our study documents striking shifts in the popularity of generic terms, but do these changes matter? The answer may be: not much.
One study found people think mental disorder, mental illness and mental health problem refer to essentially identical phenomena.
Other studies indicate that labelling a person as having a mental disease, mental disorder, mental health problem, mental illness or psychological disorder makes no difference to people’s attitudes toward them.
We don’t yet know if there are other implications of using different generic terms, but the evidence to date suggests they are minimal.
Is ‘distress’ any better?
Recently, some writers have promoted distress as an alternative to traditional generic terms. It lacks medical connotations and emphasises the person’s subjective experience rather than whether they fit an official diagnosis.
Distress appears 65 times in the 2022 Victorian Mental Health and Wellbeing Act, usually in the expression “mental illness or psychological distress”. By implication, distress is a broad concept akin to but not synonymous with mental ill health.
But is distress destigmatising, as it was intended to be? Apparently not. According to one study, it was more stigmatising than its alternatives. The term may turn us away from other people’s suffering by amplifying it.
So what should we call it?
Mental illness is easily the most popular generic term and its popularity has been rising. Research indicates different terms have little or no effect on stigma and some terms intended to destigmatise may backfire.
We suggest that mental illness should be embraced and the proliferation of alternative terms such as mental health problem, which breed confusion, should end.
Critics might argue mental illness imposes a medical frame. Philosopher Zsuzsanna Chappell disagrees. Illness, she argues, refers to subjective first-person experience, not to an objective, third-person pathology, like disease.
Properly understood, the concept of illness centres the individual and their connections. “When I identify my suffering as illness-like,” Chappell writes, “I wish to lay claim to a caring interpersonal relationship.”
As generic terms go, mental illness is a healthy option.
Nick Haslam, Professor of Psychology, The University of Melbourne and Naomi Baes, Researcher – Social Psychology/ Natural Language Processing, The University of Melbourne
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Self-Care for Tough Times – by Suzy Reading
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A note on the author: while not “Dr. Reading”, she is a “CPsychol, B Psych (Hons), M Psych”; a Chartered Psychologist specializing in wellbeing, stress management and facilitation of healthy lifestyle change. So this is coming from a place of research and evidence!
The kinds of “tough times” she has in mind are so numerous that listing them takes two pages in the book, so we won’t try here. But suffice it to say, there are a lot of things that can go wrong for us as humans, and this book addresses how to take care of ourselves mindfully in light of them.
The author takes a “self-care is health care” approach, and goes about things with a clinical mindset and/but a light tone, offering both background information, and hands-on practical advice.
Bottom line: there may be troubles ahead (and maybe you’re in the middle of troubles right now), but there’s always room for a little sunshine too.
Click here to check out Self-Care For Tough Times, and care for yourself in tough times!
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Why We Get Fat: And What to Do About It – by Gary Taubes
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We’ve previously reviewed Taubes’ “The Case Against Sugar“. What does this one bring differently?
Mostly, it’s a different focus. Unsurprisingly, Taubes’ underlying argument is the same: sugar is the biggest dietary health hazard we face. However, this book looks at it specifically through the lens of weight loss, or avoiding weight gain.
Taubes argues for low-carb in general; he doesn’t frame it specifically as the ketogenic diet here, but that is what he is advocating. However, he also acknowledges that not all carbs are created equal, and looks at several categories that are relatively better or worse for our insulin response, and thus, fat management.
If the book has a fault it’s that it does argue a bit too much for eating large quantities of meat, based on Weston Price’s outdated and poorly-conducted research. However, if one chooses to disregard that, the arguments for a low-carb diet for weight management remain strong.
Bottom line: if you’d like to cut some fat without eating less (or exercising more), this book offers a good, well-explained guide for doing so.
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Rapamycin Can Slow Aging By 20% (But Watch Out)
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Rapamycin’s Pros & Cons
Rapamycin is generally heralded as a wonderdrug that (according to best evidence so far) can slow down aging, potentially adding decades to human lifespan—and yes, healthspan.
It comes from a kind of soil bacteria, which in turn comes from the island of Rapa Nui (a Chilean territory best known for its monumental moai statues), hence the name rapamycin.
Does it work?
Yes! Probably! With catches!
Like most drugs that are tested for longevity-inducing properties, research in humans is very slow. Of course for drugs in general, they must go through in vitro and in vivo animal testing first before they can progress to human randomized clinical trials, but for longevity-inducing drugs, it’s tricky to even test in humans, without waiting entire human lifetimes for the results.
Nevertheless, mouse studies are promising:
Rapamycin: An InhibiTOR of Aging Emerges From the Soil of Easter Island
(“Easter Island” is another name given to the island of Rapa Nui)
That’s not a keysmash in the middle there, it’s a reference to rapamycin’s inhibitory effect on the kinase mechanistic target of rapamycin, sometimes called the mammalian target of rapamycin, and either way generally abbreviated to “mTOR”—also known as “FK506-binding protein 12-rapamycin-associated protein 1” or “FRAP1“ to its friends, but we’re going to stick with “mTOR”.
What’s relevant about this is that mTOR regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, autophagy, and transcription.
Don’t those words usually get associated with cancer?
They do indeed! Rapamycin and its analogs have well-demonstrated anti-cancer potential:
❝Rapamycin, the naturally occurring inhibitor of mTOR, along with a number of recently developed rapamycin analogs (rapalogs) consisting of synthetically derived compounds containing minor chemical modifications to the parent structure, inhibit the growth of cell lines derived from multiple tumor types in vitro, and tumor models in vivo.
Results from clinical trials indicate that the rapalogs may be useful for the treatment of subsets of certain types of cancer.❞
…and as such, gets used sometimes as an anticancer drug—especially against renal cancer. See also:
Research perspective: Cancer prevention with rapamycin
What’s the catch?
Aside from the fact that its longevity-inducing effects are not yet proven in humans, the mouse models find its longevity effects to be sex-specific, extending the life of male mice but not female ones:
Rapamycin‐mediated mouse lifespan extension: Late‐life dosage regimes with sex‐specific effects
One hypothesis about this is that it may have at least partially to do with rapamycin’s immunomodulatory effect, bearing in mind that estrogen is immune-enhancing and testosterone is immunosuppressant.
And rapamycin? That’s another catch: it is an immunosuppressant.
This goes in rapamycin’s favor for its use to avoiding rejection when it comes to some transplants (most notably including for kidneys), though the very same immunosuppressant effect is a reason it is contraindicated for certain other transplants (such as in liver or lung transplants), where it can lead to an unacceptable increase in risk of lymphoma and other malignancies:
Prescribing Information: Rapamune, Sirolimus Solution / Sirolimus Tablet
(Sirolimus is another name for rapamycin, and Rapamune is a brand name)
What does this mean for the future?
Researchers think that rapamycin may be able to extend human lifespan to a more comfortable 120–125 years, but acknowledge there’s quite a jump to get there from the current mouse studies, and given the current drawbacks of sex-specificity and immunosuppression:
Advances in anti-aging: Rapamycin shows potential to extend lifespan and improve health
Noteworthily, rapamycin has also shown promise in simultaneously staving off certain diseases associated most strongly with aging, including Alzheimer’s and cardiac disease—or even, starting earlier, to delay menopause, in turn kicking back everything else that has an uptick in risk peri- or post-menopause:
Effect of Rapamycin in Ovarian Aging (Rapamycin)
👆 an upcoming study whose results are thus not yet published, but this is to give an idea of where research is currently at. See also:
Pilot Study Evaluates Weekly Pill to Slow Ovarian Aging, Delay Menopause
Where can I try it?
Not from Amazon, that’s for sure!
It’s still tightly regulated, but you can speak with your physician, especially if you are at risk of cancer, especially if kidney cancer, about potentially being prescribed it as a preventative—they will be able to advise about safety and applicability in your personal case.
Alternatively, you can try getting your name on the list for upcoming studies, like the one above. ClinicalTrials.gov is a great place to watch out for those.
Meanwhile, take care!
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New research suggests intermittent fasting increases the risk of dying from heart disease. But the evidence is mixed
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Kaitlin Day, RMIT University and Sharayah Carter, RMIT University
Intermittent fasting has gained popularity in recent years as a dietary approach with potential health benefits. So you might have been surprised to see headlines last week suggesting the practice could increase a person’s risk of death from heart disease.
The news stories were based on recent research which found a link between time-restricted eating, a form of intermittent fasting, and an increased risk of death from cardiovascular disease, or heart disease.
So what can we make of these findings? And how do they measure up with what else we know about intermittent fasting and heart disease?
The study in question
The research was presented as a scientific poster at an American Heart Association conference last week. The full study hasn’t yet been published in a peer-reviewed journal.
The researchers used data from the National Health and Nutrition Examination Survey (NHANES), a long-running survey that collects information from a large number of people in the United States.
This type of research, known as observational research, involves analysing large groups of people to identify relationships between lifestyle factors and disease. The study covered a 15-year period.
It showed people who ate their meals within an eight-hour window faced a 91% increased risk of dying from heart disease compared to those spreading their meals over 12 to 16 hours. When we look more closely at the data, it suggests 7.5% of those who ate within eight hours died from heart disease during the study, compared to 3.6% of those who ate across 12 to 16 hours.
We don’t know if the authors controlled for other factors that can influence health, such as body weight, medication use or diet quality. It’s likely some of these questions will be answered once the full details of the study are published.
It’s also worth noting that participants may have eaten during a shorter window for a range of reasons – not necessarily because they were intentionally following a time-restricted diet. For example, they may have had a poor appetite due to illness, which could have also influenced the results.
Other research
Although this research may have a number of limitations, its findings aren’t entirely unique. They align with several other published studies using the NHANES data set.
For example, one study showed eating over a longer period of time reduced the risk of death from heart disease by 64% in people with heart failure.
Another study in people with diabetes showed those who ate more frequently had a lower risk of death from heart disease.
A recent study found an overnight fast shorter than ten hours and longer than 14 hours increased the risk dying from of heart disease. This suggests too short a fast could also be a problem.
But I thought intermittent fasting was healthy?
There are conflicting results about intermittent fasting in the scientific literature, partly due to the different types of intermittent fasting.
There’s time restricted eating, which limits eating to a period of time each day, and which the current study looks at. There are also different patterns of fast and feed days, such as the well-known 5:2 diet, where on fast days people generally consume about 25% of their energy needs, while on feed days there is no restriction on food intake.
Despite these different fasting patterns, systematic reviews of randomised controlled trials (RCTs) consistently demonstrate benefits for intermittent fasting in terms of weight loss and heart disease risk factors (for example, blood pressure and cholesterol levels).
RCTs indicate intermittent fasting yields comparable improvements in these areas to other dietary interventions, such as daily moderate energy restriction.
There are a variety of intermittent fasting diets. Fauxels/Pexels So why do we see such different results?
RCTs directly compare two conditions, such as intermittent fasting versus daily energy restriction, and control for a range of factors that could affect outcomes. So they offer insights into causal relationships we can’t get through observational studies alone.
However, they often focus on specific groups and short-term outcomes. On average, these studies follow participants for around 12 months, leaving long-term effects unknown.
While observational research provides valuable insights into population-level trends over longer periods, it relies on self-reporting and cannot demonstrate cause and effect.
Relying on people to accurately report their own eating habits is tricky, as they may have difficulty remembering what and when they ate. This is a long-standing issue in observational studies and makes relying only on these types of studies to help us understand the relationship between diet and disease challenging.
It’s likely the relationship between eating timing and health is more complex than simply eating more or less regularly. Our bodies are controlled by a group of internal clocks (our circadian rhythm), and when our behaviour doesn’t align with these clocks, such as when we eat at unusual times, our bodies can have trouble managing this.
So, is intermittent fasting safe?
There’s no simple answer to this question. RCTs have shown it appears a safe option for weight loss in the short term.
However, people in the NHANES dataset who eat within a limited period of the day appear to be at higher risk of dying from heart disease. Of course, many other factors could be causing them to eat in this way, and influence the results.
When faced with conflicting data, it’s generally agreed among scientists that RCTs provide a higher level of evidence. There are too many unknowns to accept the conclusions of an epidemiological study like this one without asking questions. Unsurprisingly, it has been subject to criticism.
That said, to gain a better understanding of the long-term safety of intermittent fasting, we need to be able follow up individuals in these RCTs over five or ten years.
In the meantime, if you’re interested in trying intermittent fasting, you should speak to a health professional first.
Kaitlin Day, Lecturer in Human Nutrition, RMIT University and Sharayah Carter, Lecturer Nutrition and Dietetics, RMIT University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Somatic Exercises For Nervous System Regulation – by Rose Kilian
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We’ve written before about the vagus nerve, its importance, and how to make use of it, but it’s easy to let it slip from one’s mind when it comes to exercises. This book fixes that!
The promised 35 exercises are quite a range, and are organized into sections:
- Revitalizing through breath
- Stress and tension release
- Spinal and postural health
- Mindfulness and grounding
- Movements for flexibility
- Graceful balance and focus
While it’s not necessary to do all 35 exercises, it’s recommended to do at least some from each section, to “cover one’s bases”, and enjoy the best of all worlds.
The exercises are drawn from many sources, but tai chi and yoga are certainly the most well-represented. Others, meanwhile, are straight from physiotherapy or are things one might expect to be advised at a neurology consultation.
Bottom line: if you’d like to take better care of your vagus nerve, the better for it to take care of you, this book can certainly help with that.
Click here to check out Somatic Exercises For Nervous System Regulation, and take care of yourself!
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How Much Does A Vegan Diet Affect Biological Aging?
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Slow Your Aging, One Meal At A Time
This one’s a straightforward one today, and the ““life hack” can be summed up:
Enjoy a vegan diet to enjoy younger biological age.
First, what is biological age?
Biological age is not one number, but a collection of numbers, as per different biomarkers of aging, including:
- Visual markers of aging (e.g. wrinkles, graying hair)
- Performative markers of aging (e.g. mobility tests)
- Internal functional markers of aging (e.g. tests for cognitive decline, eyesight, hearing, etc)
- Cellular markers of aging (e.g. telomere length)
We wrote more about this here:
Age & Aging: What Can (And Can’t) We Do About It?
A vegan diet may well impact multiple of those categories of aging, but today we’re highlighting a study (hot off the press; published only a few days ago!) that looks at its effect on that last category: cellular markers of aging.
There’s an interesting paradox here, because this category is:
- the most easily ignorable; because we all feel it if our knees are giving out or our skin is losing elasticity, but who notices if telomeres’ T/S ratio changed by 0.0407? ← the researchers, that’s who, as this difference is very significant
- the most far-reaching in its impact, because cellular aging in turn has an effect on all the other markers of aging
Second, how much difference does it make, and how do we know?
The study was an eight-week interventional identical twin study. This means several things, to start with:
- Eight weeks is a rather short period of time to accumulate cellular aging, let alone for an intervention to accumulate a significant difference in cellular aging—but it did. So, just imagine what difference it might make in a year or ten!
- Doing an interventional study with identical twin pairs already controlled for a lot of factors, that are usually confounding variables in population / cohort / longitudinal / observational studies.
Factors that weren’t controlled for by default by using identical twins, were controlled for in the experiment design. For example, twin pairs were rejected if one or more twin in a given pair already had medical conditions that could affect the outcome:
❝Inclusion criteria involved participants aged ≥18, part of a willing twin pair, with BMI <40, and LDL-C <190 mg/dL. Exclusions included uncontrolled hypertension, metabolic disease, diabetes, cancer, heart/renal/liver disease, pregnancy, lactation, and medication use affecting body weight or energy.
Eligibility was determined via online screening, followed by an orientation meeting and in-person clinic visit. Randomization occurred only after completing baseline visits, dietary recalls, and questionnaires for both twins❞
~ Dr. Varun Dwaraka et al. ← there’s a lot of “et al.” to this one; the paper had 16 collaborating authors!
As to the difference it made over the course of the 8 weeks…
❝Various measures of epigenetic age acceleration (PC GrimAge, PC PhenoAge, DunedinPACE) were assessed, along with system-specific effects (Inflammation, Heart, Hormone, Liver, and Metabolic).
Distinct responses were observed, with the vegan cohort exhibiting significant decreases in overall epigenetic age acceleration, aligning with anti-aging effects of plant-based diets. Diet-specific shifts were noted in the analysis of methylation surrogates, demonstrating the influence of diet on complex trait prediction through DNA methylation markers.❞
~ Ibid.
You can read the whole paper here (it goes into a lot more detail than we have room to here, and also gives infographics, charts, numbers, the works):
Were they just eating more healthily, though?
Well, arguably yes, as the results show, but to be clear:
The omnivorous diet compared to the vegan diet in this study was also controlled; both groups were given a healthy meal plan for their respective diet. So this wasn’t a case of “any omnivorous diet vs healthy vegan diet”, but rather “healthy omnivorous diet vs healthy vegan diet”.
Again, the paper itself has the full details—a short version is that it involved a healthy meal kit delivery service, followed by ongoing dietician involvement in an equal and carefully-controlled fashion.
So, aside from that one group had an omnivorous meal plan and the other vegan, both groups received the same level of “healthy eating” support, guidance, and oversight.
But isn’t [insert your preferred animal product here] healthy?
Quite possibly! For general health, general scientific consensus is that eating at least mostly plants is best, red meat is bad, poultry is neutral in moderation, fish is good in moderation, dairy is good in moderation if fermented, eggs are good in moderation if not fried.
This study looked at the various biomarkers of aging that we listed, and not every possible aspect of health—there’s more science yet to be done, and the researchers themselves are calling for it.
It also bears mentioning that for some (relatively few, but not insignificantly few) people, extant health conditions may make a vegan diet unhealthy or otherwise untenable. Do speak with your own doctor and/or dietician if unsure.
See also: Do We Need Animal Products To Be Healthy?
We would hypothesize, by the way, that the anti-aging benefits of a vegan diet are probably proportional to abstention from animal products—meaning that even if you simply have some “vegan days”, while still consuming animal products other days, you’ll still get benefit for the days you abstained. That’s just our hypothesis though.
Take care!
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