Taking The Gamble Out Of Antidepressants
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…and other items from this week’s health news:
Melancholy, blood, and signs
Sounds like it could be a headline for our Halloween edition, but no!
The problem: as it stands, major depressive disorder often requires a prolonged trial-and-error process with selective serotonin reuptake inhibitors (SSRIs) and potentially other kinds of antidepressants, meaning many patients spend many weeks or months on medications that don’t improve their symptoms.
The solution: researchers (Dr. Eleni Tzavara et al.) have found that a blood-based circular RNA marker known to its friends as “CDR1as” can predict how people with major depressive disorder respond to sertraline (most doctor’s go-to first-try antidepressant, despite it having a famously high hit to miss ratio).
- How it works: CDR1as is an RNA enriched in the brain that is stable in blood, crosses the blood–brain barrier, and is sensitive to synaptic activity and neuronal receptor signaling.
- What they did: Dr. Tzavara and her team measured baseline CDR1as levels in whole blood from two independent cohorts in the EMBARC and ANTARES studies before treatment with sertraline, and compared future responders with non-responders.
- What they found: baseline CDR1as levels differed between people who later responded to sertraline and those who didn’t, and changes in CDR1as after treatment were linked to long-term remission. Further, CDR1as predicted response and remission with SSRI treatment, but not with placebo or bupropion, suggesting the marker may be specific to serotonin-based therapies.
So, this may mean a lot of people will no longer have to suffer for longer while potentially getting adverse side effects for a medication that won’t work for them specifically!
Read in full: A blood marker could predict how people respond to antidepressants
Related: Antidepressants: Personalization Is Key!
Soon, more American women will have cardiovascular disease than not
A newly-released statement from the American Heart Association warns that by 2050, nearly 60% of women in the US are projected to have high blood pressure, more than 60% obesity, and over 25% diabetes, all key contributors to heart disease, heart failure, atrial fibrillation, and stroke.
Not only that, but it isn’t just tied to the nature of an aging population (as the US population is), but rather, nearly one in three women aged 22–44 are expected to have some form of CVD, diabetes in this group is projected to rise from 6% to nearly 16%, and more than one third are expected to have high blood pressure.
❝One in every three women will die from cardiovascular disease—maybe it’s your grandmother, or your mother or your daughter❞
~ Dr. Stacey E. Rosen, President of the American Heart Association & Executive Director of the Katz Institute for Women’s Health
Read in full: American Heart Association warns 60% of US women will have cardiovascular disease by 2050
Related: Heart Health vs Systemic Stress
“Not addicted, but”
In the category of “I could quit anytime” beliefs, you would think that something that results in episodes of abdominal pain paired with screaming and vomiting would be something quickly desisted. Of course, we might still choose to take it if it were somehow necessary for life, or perhaps if it bestowed us with particularly impressive superpowers.
But for a mostly recreational drug whose main medical uses are primarily against pain and against anxiety, those benefits seem moot when the result is pain and screaming and vomiting.
But according to research, analyzing 188 million US emergency visits found Cannabinoid Hyperemesis Syndrome cases rose from 4.4 per 100,000 visits in 2016 to 33.1 per 100,000 in just 4 years.
The reason for the rise: while cause and effect hasn’t been proven, scientists believe it is due to the much higher potency of THC available these days, compared to the much lower-strength cannabis products available previously.
The cure is simple: stop taking cannabis.
The outcome, however? Well, mostly people don’t do that.
Read in full: Screaming, vomiting, and daily weed: The rise of “scromiting” among chronic cannabis users
Related: How Much THC Is Safe?
Take care!
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Carbonated Water: For Weight Loss, Satiety, Or Just Gas?
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There are two main mechanisms of action by which sparkling water is considered to help satiety and/or weight loss; they are:
- It “fills us up” such that we feel fuller sooner, and thus eat less, and thus (all other things being equal) perhaps lose weight
- The carbon dioxide is absorbed into the bloodstream, where (as a matter of chemistry) it improves glucose metabolism, thus lowering blood sugars and indirectly leading (potentially) to weight loss, but even if not, lowered blood sugars are good for most people most of the time, right?
However, there are just a few problems:
Full of gas?
Many people self-report enjoying sparkling water as a way to feel fuller while fasting (or even while eating). However, the plural of “anecdote” is not “data”, so, here be data… Ish:
❝In order to determine whether such satiating effects occur through oral carbonic stimulation alone, we conducted modified sham-feeding (SF) tests (carbonated water ingestion (CW), water ingestion (W), carbonated water sham-feeding (CW-SF), and water sham-feeding (W-SF)), employing an equivalent volume and standardized temperature of carbonated and plain water, in a randomized crossover design.
Thirteen young women began fasting at 10 p.m. on the previous night and were loaded with each sample (15ºC, 250 mL) at 9 a.m. on separate days. Electrogastrography (EGG) recordings were obtained from 20 min before to 45 min after the loading to determine the power and frequency of the gastric myoelectrical activity. Appetite was assessed using visual analog scales. After ingestion, significantly increased fullness and decreased hunger ratings were observed in the CW group. After the load, transiently but significantly increased fullness as well as decreased hunger ratings were observed in the CW-SF group. The powers of normogastria (2-4 cpm) and tachygastria (4-9 cpm) showed significant increases in the CW and W groups, but not in the CW-SF and W-SF groups. The peak frequency of normogastria tended to shift toward a higher band in the CW group, whereas it shifted toward a lower band in the CW-SF group, indicating a different EGG rhythm.
Our results suggest that CO2-induced oral stimulation is solely responsible for the feeling of satiety.❞
~ Dr. Maki Suzuki et al.
Now, that’s self-reported, and a sample size of 13, so it’s not the most airtight science ever, but it is at least science. Here’s the paper, by the way:
Oral Carbonation Attenuates Feeling of Hunger and Gastric Myoelectrical Activity in Young Women
Here’s another small study with 8 people, which found that still and sparkling water had the exact same effect:
Effect of carbonated water on gastric emptying and intragastric meal distribution
However, drinking water (still or sparkling) with a meal will not have anywhere near the same effect for satiety as consuming food that has a high water-content.
See also: Some Surprising Truths About Hunger And Satiety ← our main feature in which we examine the science of volumetrics, including a study that shows how water incorporated into a food (but not served with a food) decreases caloric intake.
As an aside, one difference that carbonation can make is to increase ghrelin levels—that’s the hunger hormone (the satiety hormone is leptin, by the way). This one’s a rat study, but it seems reasonable that the same will be true of humans:
…which is worth bearing in mind even if you yourself are not, in fact, a male rat.
The glucose guzzler?
This one has simply been the case of a study being misrepresented, for example here:
Fizzy water might aid weight loss by providing a small boost to glucose uptake and metabolism
The idea is that higher levels of carbon dioxide in the blood mean faster glucose metabolism, which is technically true. Now, often “technically true” is the best kind of true, but not here, because it’s simply not useful.
In short, we produce so much carbon dioxide as part of our normal respiratory processes, that any carbon dioxide we might consume in a carbonated water is barely a blip in the graph.
Oh, and that article we just linked? Even within the article, despite running with that headline, the actual scientists quoted are saying such things as:
❝While there is a hypothetical link between carbonated water and glucose metabolism, this has yet to be tested in well-designed human intervention studies❞
~ Professor Sumantra Ray
Note: the word “hypothetical” means “one level lower than theoretical”. This is very far from being a conclusion.
And the study itself? Wasn’t even about carbonated water, it was about kidney dialysis and how the carbon dioxide content can result in hypoglycemia:
The mechanism of hypoglycemia caused by hemodialysis
…which got referenced in this paper (not a study):
Can carbonated water support weight loss?
…and even that concluded:
❝CO2 in carbonated water may promote weight loss by enhancing glucose uptake and metabolism in red blood cells.
However, the amount is so small that it is difficult to expect weight loss effects solely from the CO2 in carbonated water.
Drinking carbonated water may also affect blood glucose measurements.❞
Note: the word “may”, when used by a scientist and in the absence of any stronger claims, means “we haven’t ruled out the possibility”.
What breaking news that is.
Stop the press! No, really, stop it!
So… What does work?
There are various ways of going about actually hacking hunger (and they stack; i.e. you can use multiple methods and get cumulative results), and we wrote about them here:
Enjoy!
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Can High-Volume Exercise Be Bad For Your Heart? It Depends On Your Sex
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Endurance exercise has often been questioned for its potential to increase heart attack risk, a large (n=61,150) comprehensive (a meta-analysis of studies) research has shown, in a nutshell:
- In men, high-volume endurance exercise is associated with higher coronary artery calcium (CAC) scores (that’s bad) and higher calcified plaque volume (also bad) compared to non-athlete men.
- In women, however, no such increase was found (for CAC or plaque) regardless of exercise volume.
In fact, high-volume female athletes* had less calcified plaque than non-athlete women.
*as in, the exercise was high volume; the volume of the athletes themselves was not mentioned!
You may be wondering: does this mean that men should skip the exercise?
And the answer is: no, because moderate exercise was linked to lower calcified plaque volume in men and women.
As to what “high-volume”, “moderate”, and “non-athletes” mean, for the purposes of the study:
- High: >3,000 MET-minutes/week
- Moderate: 1,500–3,000 MET-minutes/week
- Non-athletes: <1,500 MET-minutes/week
MET = Metabolic Equivalent of Task, i.e. the number your phone exercise tracker app shows, whereby if you exercise for 1 minute with your heart above a certain percentage of its maximum, the tracker records it as 2 minutes, because it is the metabolic equivalent of 2 minutes at the lower heart rate.
Thus, in terms of practical advice: the researchers make clear that they don’t want to discourage exercise ,but to support comprehensive risk assessment, especially in men doing high-volume exercise.
You can read the paper in full here: Sex Differences in the Impact of Exercise Volume on Subclinical Coronary Atherosclerosis: A Meta-Analysis
“I’m a woman without a man in my life, so is this irrelevant to me?”
It might be, or it might not be! The question the researchers didn’t ask is: what’s the current state of your hormones?
Because, in this paper…
Let’s do a quick tally of how many times certain words are mentioned (bearing in mind that the paper is about sex differences, and is 8,301 words long):
- Hormone: 1
- Testosterone: 1
- Estrogen: 0
- Menopause: 0
- HRT: 0
Do you see the problem? An entire paper about sex differences, and we’re still getting medically sidelined.
And, this is likely important, because hormones make a huge difference to heart health; see for example:
- What Menopause Does To The Heart
- Hormones & Health, Beyond The Obvious
- His & Hers? The Hidden Complexities of Statins and Cardiovascular Disease (CVD)
What this means: it is likely, but not known for sure, that sex hormone differences are what affect the coronary artery calcium and calcified plaque scores so drastically as seen in the study.
In practical terms: if you are a woman who is post-menopause and not on hormone replacement therapy (HRT), you could well have higher risk factors in this case.
Want to learn more?
If you’re curious about the current state of your arteries, then please do book a professional test, but meanwhile:
Try This At Home: ABI Test For Clogged Arteries
Take care!
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Ozempic and other weight-loss drugs linked to rare but serious eye conditions
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Drugs such as Ozempic, Wegovy and Mounjaro (known as semaglutide and tirzepatide) have changed the way clinicians manage diabetes and obesity around the world.
Collectively known as GLP-1 agonists, these drugs mimic the hormone GLP-1. This limits both hunger and interest in food, helping users lose weight, and helps control blood sugar levels.
But two new studies published today show that people taking these drugs may have a small increased risk of serious eye conditions and vision loss.
Here’s what you need to know if you’re taking or considering these medications.
What damage can occur?
Non-arteritic anterior ischaemic optic neuropathy, or NAION, is a rare but devastating eye condition that occurs when blood flow to the optic nerve is suddenly reduced or blocked. It’s also called an “eye stroke”.
The exact cause of NAION remains unclear and there are no current treatments available. People with diabetes are at increased risk of developing NAION.
Unlike other eye conditions that develop gradually, NAION causes a sudden, painless loss of vision. Patients typically notice the condition when they wake up and discover they’ve lost vision in one eye.
Vision tends to worsen over a couple of weeks and slowly stabilises. Recovery of vision is variable, but around 70% of people do not experience improvement in their vision.
What has previous research shown?
A previous study from 2024 found participants prescribed semaglutide for diabetes were four times more likely to develop NAION. For those taking it for weight loss, the risk was almost eight times higher.
In June, the European Medicines Agency concluded NAION represented a “very rare” side effect of semaglutide medications: a one in 10,000 chance. In a first for medicines regulators, the agency now requires product labels to include NAION as a documented risk.
However the recent studies suggest the risks may be lower than we first thought.
In addition to NAION, there is also evidence to suggest GLP-1 drugs can worsen diabetic eye disease, also known as diabetic retinopathy. This occurs when high blood sugar levels damage the small blood vessels in the retina, which can lead to vision loss.
It may sound counter-intuitive, but rapid blood sugar reductions can also destabilise the fragile blood vessels in the retina and lead to bleeding.
What do the new studies say?
Two newly published studies investigated people with type 2 diabetes living in the United States over two years. The studies looked at the medical records of 159,000 to 185,000 people.
One study found semaglutide or tirzepatide was associated with a more modest risk of developing NAION than previously thought. Of 159,000 people with type 2 diabetes who were taking these drugs, 35 people (0.04%) developed NAION, compared with 19 patients (0.02%) in the comparison group.
The researchers also found an increased risk of developing “other optic nerve disorders”. However, it’s unclear what kind of optic nerve disorders this includes, as the medical record codes used didn’t specify.
Counter to this, the second study did not find an increased risk of NAION among those taking GLP-1 drugs.
However, the researchers found a small increase in the number of people developing diabetic retinopathy in those prescribed GLP-1 drugs.
But overall, participants on GLP-1 drugs experienced fewer sight-threatening complications related to their diabetic retinopathy and required less invasive eye treatments compared to the group taking other diabetes medications.
Further studies are still needed to understand how GLP-1 drugs can lead to eye complications. A current, five-year clinical trial is studying the long-term effects of semaglutides and diabetic eye disease in 1,500 people, which should tell us more about the ocular risks in the future.
What does this mean for people taking GLP-1 drugs?
NAION is a serious condition. But we need to strike a balance between these (and other) risks and the benefits of GLP-1 medications in diabetes care, obesity treatment, reducing heart attack risks and extending lives.
The key lies in informed decision-making and identifying different levels of risk.
People with multiple NAION risk factors – such as sleep apnoea, high blood pressure and diabetes – should undergo careful consideration with their treating doctor before starting these medications.
“Crowded” optic nerve heads are also a risk factor for NAION. This is an anatomical feature where blood vessels at the optic nerve head are tightly packed together. People with crowded optic nerve heads should also undergo careful consideration before starting GLP-1 medications.
Although NAION can strike without warning, regular comprehensive eye examinations with your optometrist or ophthalmologist still serve important purposes. They can detect other drug-related eye problems, including worsening diabetic retinopathy, and can identify patients with crowded optic nerve heads. It’s also important to tell them if you are taking GLP-1 medications so they can keep a close watch on your eye health.
Emerging research also suggests that improving your heart health might help reduce risks of developing NAION. This includes proper management of high blood pressure, diabetes and cholesterol – all conditions that compromise the small blood vessels feeding the optic nerve.
Studies also show patients with heart conditions who better adhere to their medication prescriptions have lower risks of NAION than those who don’t.
Doctors should discuss NAION risks during prescribing decisions and work with eye care providers to monitor regularly for diabetic eye disease. Patients need clear instructions to seek immediate medical attention for sudden vision loss and the need for regular eye examinations.
Aggressive treatment of sleep apnoea and other heart conditions may also help reduce NAION risks. But for now, there remains an ongoing need for more research to understand how GLP-1 medications can affect the eye.
Flora Hui, Research Fellow, Centre for Eye Research Australia and Honorary Fellow, Department of Surgery (Ophthalmology), The University of Melbourne and Pete A Williams, Ulla and Ingemar Dahlberg Professor in Vision Science, Research Group Leader, Karolinska Institutet
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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What is type 1.5 diabetes? It’s a bit like type 1 and a bit like type 2 – but it’s often misdiagnosed
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While you’re likely familiar with type 1 and type 2 diabetes, you’ve probably heard less about type 1.5 diabetes.
Also known as latent autoimmune diabetes in adults (LADA), type 1.5 diabetes has features of both type 1 and type 2 diabetes.
More people became aware of this condition after Lance Bass, best known for his role in the iconic American pop band NSYNC, recently revealed he has it.
So, what is type 1.5 diabetes? And how is it diagnosed and treated?
Pixel-Shot/Shutterstock There are several types of diabetes
Diabetes mellitus is a group of conditions that arise when the levels of glucose (sugar) in our blood are higher than normal. There are actually more than ten types of diabetes, but the most common are type 1 and type 2.
Type 1 diabetes is an autoimmune condition where the body’s immune system attacks and destroys the cells in the pancreas that make the hormone insulin. This leads to very little or no insulin production.
Insulin is important for moving glucose from the blood into our cells to be used for energy, which is why people with type 1 diabetes need insulin medication daily. Type 1 diabetes usually appears in children or young adults.
Type 2 diabetes is not an autoimmune condition. Rather, it happens when the body’s cells become resistant to insulin over time, and the pancreas is no longer able to make enough insulin to overcome this resistance. Unlike type 1 diabetes, people with type 2 diabetes still produce some insulin.
Type 2 is more common in adults but is increasingly seen in children and young people. Management can include behavioural changes such as nutrition and physical activity, as well as oral medications and insulin therapy.
People with diabetes may need to regularly monitor their blood sugar levels. Dragana Gordic/Shutterstock How does type 1.5 diabetes differ from types 1 and 2?
Like type 1 diabetes, type 1.5 occurs when the immune system attacks the pancreas cells that make insulin. But people with type 1.5 often don’t need insulin immediately because their condition develops more slowly. Most people with type 1.5 diabetes will need to use insulin within five years of diagnosis, while those with type 1 typically require it from diagnosis.
Type 1.5 diabetes is usually diagnosed in people over 30, likely due to the slow progressing nature of the condition. This is older than the typical age for type 1 diabetes but younger than the usual diagnosis age for type 2.
Type 1.5 diabetes shares genetic and autoimmune risk factors with type 1 diabetes such as specific gene variants. However, evidence has also shown it may be influenced by lifestyle factors such as obesity and physical inactivity which are more commonly associated with type 2 diabetes.
What are the symptoms, and how is it treated?
The symptoms of type 1.5 diabetes are highly variable between people. Some have no symptoms at all. But generally, people may experience the following symptoms:
- increased thirst
- frequent urination
- fatigue
- blurred vision
- unintentional weight loss.
Typically, type 1.5 diabetes is initially treated with oral medications to keep blood glucose levels in normal range. Depending on their glucose control and the medication they are using, people with type 1.5 diabetes may need to monitor their blood glucose levels regularly throughout the day.
When average blood glucose levels increase beyond normal range even with oral medications, treatment may progress to insulin. However, there are no universally accepted management or treatment strategies for type 1.5 diabetes.
Type 1.5 diabetes might be managed with oral medications, at least initially. Dragana Gordic/Shutterstock Type 1.5 diabetes is often misdiagnosed
Lance Bass said he was initially diagnosed with type 2 diabetes, but later learned he actually has type 1.5 diabetes. This is not entirely uncommon. Estimates suggest type 1.5 diabetes is misdiagnosed as type 2 diabetes 5–10% of the time.
There are a few possible reasons for this.
First, accurately diagnosing type 1.5 diabetes, and distinguishing it from other types of diabetes, requires special antibody tests (a type of blood test) to detect autoimmune markers. Not all health-care professionals necessarily order these tests routinely, either due to cost concerns or because they may not consider them.
Second, type 1.5 diabetes is commonly found in adults, so doctors might wrongly assume a person has developed type 2 diabetes, which is more common in this age group (whereas type 1 diabetes usually affects children and young adults).
Third, people with type 1.5 diabetes often initially make enough insulin in the body to manage their blood glucose levels without needing to start insulin medication. This can make their condition appear like type 2 diabetes, where people also produce some insulin.
Finally, because type 1.5 diabetes has symptoms that are similar to type 2 diabetes, it may initially be treated as type 2.
We’re still learning about type 1.5
Compared with type 1 and type 2 diabetes, there has been much less research on how common type 1.5 diabetes is, especially in non-European populations. In 2023, it was estimated type 1.5 diabetes represented 8.9% of all diabetes cases, which is similar to type 1. However, we need more research to get accurate numbers.
Overall, there has been a limited awareness of type 1.5 diabetes and unclear diagnostic criteria which have slowed down our understanding of this condition.
A misdiagnosis can be stressful and confusing. For people with type 1.5 diabetes, being misdiagnosed with type 2 diabetes might mean they don’t get the insulin they need in a timely manner. This can lead to worsening health and a greater likelihood of complications down the road.
Getting the right diagnosis helps people receive the most appropriate treatment, save money, and reduce diabetes distress. If you’re experiencing symptoms you think may indicate diabetes, or feel unsure about a diagnosis you’ve already received, monitor your symptoms and chat with your doctor.
Emily Burch, Accredited Practising Dietitian and Lecturer, Southern Cross University and Lauren Ball, Professor of Community Health and Wellbeing, The University of Queensland
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Why Is Sitting So Bad For Us?
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Dr. Murat Dalkilinç walks us through it:
Don’t take it sitting down
The human body has evolved for movement, and prolonged sitting—a very recent innovation on the evolutionary timescale—places physical stresses on multiple body systems that can affect both short-term function and long-term health.
In fact, with over 360 joints, about 700 skeletal muscles, an upright posture, circulation that benefits from movement, responsive nerve cells, and elastic skin, we’re build of almost nothing but features that reflect a body well adapted for frequent motion.
So, what happens if we sit too much?
- Effects on the spine: sitting with a curved back and slumped shoulders places uneven pressure on the spinal discs, overworks certain ligaments and joints, and strains muscles that then must try (and generally fail) to adapt to the hunched position.
- Effects on nerves: compressed nerves can impair nerve signaling and cause numbness, while restricted blood flow through compressed vessels can contribute to swelling in the limbs.
- Effects on breathing: a hunched posture reduces the size of the chest cavity, giving the lungs less room to expand, and reducing the amount of oxygen entering the blood.
- Effects on fat metabolism: prolonged sitting reduces the activity of lipoprotein lipase, an enzyme that helps break down fats in the bloodstream, making fat metabolism less efficient.
- Effects on the brain: reduced movement can decrease blood flow and oxygen delivery, which can lower alertness, concentration, and cognitive performance.
No surprise, then, that extended periods of sitting have been associated with increased risks of various cancers, heart disease, diabetes, kidney disease, liver disease, and more.
Indeed, research cited in the video estimates that this kind of physical inactivity contributes to about 9% of premature deaths worldwide, representing more than 5 million deaths annually.
For more on all of this plus visual illustrations, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like:
Stand Up For Your Health (Or Don’t) ← this is about reducing the damage done by sitting, including if for whatever reason you have to spend a lot of time sitting, including if you physically cannot stand and/or cannot walk.
Take care!
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Is It Dementia?
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Spot The Signs (Because None Of Us Are Immune)
Dementia affects increasingly many people, and unlike a lot of diseases, it disproportionately affects people in wealthy industrialized nations.
There are two main reasons for this:
- Longevity (in poorer countries, more people die of other things sooner; can’t get age-related cognitive decline if you don’t age)
- Lifestyle (in the age of convenience, it has never been easier to live an unhealthy lifestyle)
The former is obviously no bad thing for those of us lucky enough to be in wealthier countries (though even in such places, good healthcare access is of course sadly not a given for all).
The latter, however, is less systemic and more epidemic. But it does cut both ways:
- An unhealthy lifestyle is much easier here, yes
- A healthier lifestyle is much easier here, too!
This then comes down to two factors in turn:
- Information: knowing about dementia, what things lead to it, what to look out for, what to do
- Motivation: priorities, and how much attention we choose to give this matter
So, let’s get some information, and then give it our attention!
More than just memory
It’s easy to focus on memory loss, but the four key disabilities directly caused by dementia (each person may not get all four), can be remembered by the mnemonic: “AAAA!”
No, somebody didn’t just murder your writer. It’s:
- Amnesia: memory loss, in one or more of its many forms
- e.g. short term memory loss, and/or inability to make new memories
- Aphasia: loss of ability to express oneself, and/or understand what is expressed
- e.g. “More people have been to Berlin than I have”
- Or even less communication-friendly, Broca’s (Expressive) Aphasia and Wernicke’s (Receptive) Aphasia
- Apraxia: loss of ability to do things, through no obvious physical disability
- e.g. staring at the bathroom mirror wondering how to brush one’s teeth
- Agnosia: loss of ability to recognize things
- e.g. prosopagnosia, also called face-blindness.
If any of those seem worryingly familiar, be aware that while yes, it could be a red flag, what’s most important is patterns of these things.
Another difference between having a momentary brainlapse and having dementia might be, for example, the difference between forgetting your keys, and forgetting what keys do or how to use one.
That said, some are neurological deficits that may show up quite unrelated to dementia, including most of those given as examples above. So if you have just one, then that’s probably worthy of note, but probably not dementia.
Writer’s anecdote: I have had prosopagnosia all my life. To give an example of what that is like and how it’s rather more than just “bad with faces”…
Recently I saw my neighbor, and I could tell something was wrong with her face, but I couldn’t put my finger on what it was. Then some moments later, I realized I had mistaken her hat for her face. It was a large beanie with a panda design on it, and that was facelike enough for me to find myself looking at the wrong face.
Subjective memory matters as much as objective
Objective memory tests are great indicators of potential cognitive decline (or improvement!), but even a subjective idea of having memory problems, that one’s memory is “not as good as it used to be”, can be an important indicator too:
Subjective memory may be marker for cognitive decline
And more recently:
If your memory feels like it’s not what it once was, it could point to a future dementia risk
If you’d like an objective test of memory and other cognitive impairments, here’s the industry’s gold standard test (it’s free):
SAGE: A Test to Detect Signs of Alzheimer’s and Dementia
(The Self-Administered Gerocognitive Exam (SAGE) is designed to detect early signs of cognitive, memory or thinking impairments)
There are things that can look like dementia that aren’t
A person with dementia may be unable to recognize their partner, but hey, this writer knows that feeling very well too. So what sets things apart?
More than we have room for today, but here’s a good overview:
What are the early signs of dementia, and how does it differ from normal aging?
Want to read more?
You might like our previous article more specifically about reducing Alzheimer’s risk:
Reducing Alzheimer’s Risk Early!
Take care!
Don’t Forget…
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