We Are Such Stuff As Fish Are Made Of
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Research Review: Collagen
For something that’s a very popular supplement, not many people understand what collagen is, where it comes from, or what it does.
In a nutshell:
Collagen is a kind of protein. Our bodies make it naturally, and we can also get more in our diet and/or take extra as a supplement.
Our bodies use collagen in connective tissue, skin, tendon, bone, and cartilage. It has many functions, but a broad description would be “holding things together”.
As we get older, our bodies produce less collagen. Signs of this include wrinkles, loss of skin hydration, and joint pain.
Quick test: pinch the skin on the middle of the back of one of your hands, and then watch what happens when you get low. How quickly and easily did your skin returns to its original shape?
If it was pretty much instantanous and flawless, congratulations, you have plenty of collagen (and also elastin). If you didn’t, you are probably low on both!
(they are quite similar proteins and are made from the same base “stuff”, so if you’re low on one, you’ll usually be low on both)
Quick note: A lot of research out there has been funded by beauty companies, so we had our work cut out for us today, and have highlighted where any research may be biased.
More than skin deep
While marketing for collagen is almost exclusively aimed at “reduce wrinkles and other signs of aging”, it does a lot more than that.
You remember we mentioned that many things from the bones outward are held together by collagen? We weren’t kidding…
Read: Osteoporosis, like skin ageing, is caused by collagen loss which is reversible
Taking extra collagen isn’t the only way
We can’t (yet!) completely halt the age-related loss of collagen, but we can slow it, with our lifestyle choices:
- Don’t smoke tobacco
- Drink only in moderation (or not at all)
- Avoid foods with added sugar, and high-processed foods in general
- Wear sunscreen when appropriate
Can I get collagen from food?
Yep! Just as collagen holds our bodies together, it holds the bodies of other animals together. And, just like collagen is found in most parts of our body but most plentifully in our skin and bones, that’s what to eat to get collagen from other animals, e.g:
- Chicken skin
- Fish skin
- Bone broth ← health benefits and recipes at this link!
What about vegans?
Yes, vegans are also held together by collagen! We do not, however, recommend eating their skin or boiling their bones into broth. Ethical considerations aside, cannibalism can give you CJD!
More seriously, if you’re vegan, you can’t get collagen from a plant-based diet, but you can get the stuff your body uses to make collagen. Basically, you want to make sure you get plenty of:
- Protein (beans, pulses, nuts, etc are all fine; it’s hard to go wrong with this)
- Vitamin C
- Vitamin D
- and Zinc
Just be sure to continue to remember to avoid highly-processed foods. So:
- Soy mince/chunks whose ingredients list reads: “soya”? Yes!
- The Incredible Burger or Linda McCartney’s Sausages? Sadly less healthy
Read: Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet
Meat-eaters might want to read that one too. By far the worst offenders for AGEs (Advanced Glycation End Products, which can not only cause collagen to stiffen, but also inactivate proteins responsible for collagen repair, along with doing much more serious damage to your body’s natural functions) include:
- Hot dogs
- Bacon
- Fried/roasted/grilled meats
Is it worth it as a supplement?
That depends on you, your age, and your lifestyle, but it’s generally considered safe*
*if you have a seafood allergy, be careful though, as many supplements are from fish or shellfish—you will need to find one that’s free from your allergen
Also, all collagen is animal-derived. So if you’re a vegan, decide for yourself whether this constitutes medicine and if so, whether that makes it ethically permissible to you.
With that out of the way:
What the science says on collagen supplementation
Collagen for skin
Read: Effects of collagen supplementation on skin aging (systematic review and meta-analysis)
The short version is that they selected 19 studies with over a thousand participants in total, and they found:
In the meta-analysis, a grouped analysis of studies showed favorable results of hydrolyzed collagen supplementation compared with placebo in terms of skin hydration, elasticity, and wrinkles.
The findings of improved hydration and elasticity were also confirmed in the subgroup meta-analysis.
Based on results, ingestion of hydrolyzed collagen for 90 days is effective in reducing skin aging, as it reduces wrinkles and improves skin elasticity and hydration.
Caveat: while that systematic review had no conflicts of interests, at least some of the 19 studies will have been funded by beauty companies. Here are two, so that you know what that looks like:
Funded by Quiris to investigate their own supplement, Elasten®:
A Collagen Supplement Improves Skin Hydration, Elasticity, Roughness, and Density
Funded by BioCell to investigate their own supplement, BioCell Collagen:
The Effects of Skin Aging Associated with the Use of BioCell Collagen
A note on funding bias: to be clear, the issue is not that the researchers might be corrupt (though that could happen).
The issue is more that sometimes companies will hire ten labs to do ten research studies… and then pull funding from ones whose results aren’t going the way they’d like.
So the “best” (for them) study is the one that gets published.
Here’s another systematic review—like the one at the top of this section—that found the same, with doses ranging from 2.5g–15g per day for 8 weeks or longer:
Read: Oral Collagen Supplementation: A Systematic Review of Dermatological Applications
Again, some of those studies will have been funded by beauty companies. The general weight of evidence does seem clear and favorable, though.
Collagen for bones
Here, we encountered a lot less in the way of potential bias, because this is simply marketed a lot less. Despite being arguably far more important!
We found a high quality multi-vector randomized controlled study with a sample size of 131 postmenopausal women. They had these women take 5g collagen supplement (or placebo), and studied the results over the course of a year.
They found:
- The intake of the supplement increased bone mineral density (BMD)
- Supplementation was also associated with a favorable shift in bone markers, indicating:
- increased bone formation
- reduced bone degradation
Read: Specific Collagen Peptides Improve Bone Mineral Density and Bone Markers in Postmenopausal Wome
A follow-up study with 31 of these women found that taking 5 grams of collagen daily for a total of 4 years was associated with a progressive increase in BMD.
You might be wondering if collagen also helps against osteoarthritis.
The answer is: yes, it does (at least, it significantly reduces the symptoms)
Read: Effect of collagen supplementation on osteoarthritis symptoms
In summary:
- You need collagen for health skin, bones, joints, and more
- Your body makes collagen from your food
- You can help it by getting plenty of protein, vitamins, and minerals
- You can also help it by not doing the usual Bad Things™ (smoking, drinking, eating processed foods, especially processed meats)
- You can also eat collagen directly in the form of other animals’ skin and bones
- You can also buy collagen supplements (but watch out for allergens)
Want to try collagen supplementation?
We don’t sell it (or anything else), but for your convenience…
Check it out: Hydrolyzed Collagen Peptides (the same as in most of the above studies), 90 days supply at 5g/day
We selected this one because it’s the same kind used in many of the studies, and it doesn’t contain any known allergens.
It’s bovine collagen, meaning it’s from cows, so it’s not vegan, and also some subscribers may want to abstain for religious reasons. We respect that, and/but make our recommendations based solely on the science of health and productivity.
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Pneumonia: Prevention Is Better Than Cure
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Pneumonia: What We Can & Can’t Do About It
Pneumonia is a significant killer of persons over the age of 65, with the risk increasing with age after that, rising very sharply around the age of 85:
While pneumonia is treatable, especially in young healthy adults, the risks get more severe in the older age brackets, and it’s often the case that someone goes into hospital with one thing, then develops pneumonia, which the person was already not in good physical shape to fight, because of whatever hospitalized them in the first place:
American Lung Association | Pneumonia Treatment and Recovery
Other risk factors besides age
There are a lot of things that can increase our risk factor for pneumonia; they mainly fall into the following categories:
- Autoimmune diseases
- Other diseases of the immune system (e.g. HIV)
- Medication-mediated immunosuppression (e.g. after an organ transplant)
- Chronic lung diseases (e.g. asthma, COPD, Long Covid, emphysema, etc)
- Other serious health conditions ← we know this one’s broad, but it encompasses such things as diabetes, heart disease, and cancer
See also:
Why Chronic Obstructive Pulmonary Disease (COPD) Is More Likely Than You Think
Things we can do about it
When it comes to risks, we can’t do much about our age and some of the other above factors, but there are other things we can do to reduce our risk, including:
- Get vaccinated against pneumonia if you are over 65 and/or have one of the aforementioned risk factors. This is not perfect (it only reduces the risk for certain kinds of infection) and may not be advisable for everyone (like most vaccines, it can put the body through its paces a bit after taking it), so speak with your own doctor about this, of course.
- See also: Vaccine Mythbusting
- Avoid contagion. While pneumonia itself is not spread person-to-person, it is caused by bacteria or viruses (there are numerous kinds) that are opportunistic and often become a secondary infection when the immune system is already busy with the first one. So, if possible avoid being in confined spaces with many people, and do wash your hands regularly (as a lot of germs are transferred that way and can get into the respiratory tract because you touched your face or such).
- See also: The Truth About Handwashing
- If you have a cold, or flu, or other respiratory infection, take it seriously, rest well, drink fluids, get good immune-boosting nutrients. There’s no such thing as “just a cold”; not anymore.
- Look after your general health too—health doesn’t exist in a vacuum, and nor does disease. Every part of us affects every other part of us, so anything that can be in good order, you want to be in good order.
This last one, by the way? It’s an important reminder that while some diseases (such as some of the respiratory infections that can precede pneumonia) are seasonal, good health isn’t.
We need to take care of our health as best we can every day along the way, because we never know when something could change.
Want to do more?
Check out: Seven Things To Do For Good Lung Health!
Take care!
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What you need to know about xylazine
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Xylazine is a non-opioid tranquilizer designed for veterinary use in animals. The sedative is not approved for use in people, yet it’s becoming more prevalent in the illicit drug supply.
Sometimes called “tranq,” it’s often mixed with other drugs, such as fentanyl, a potent opioid responsible for a growing number of overdose deaths. Last year, the White House Office of National Drug Control Policy declared fentanyl mixed with xylazine an “emerging threat.”
Read on to learn more about xylazine: what happens when people take it, what to do if an overdose is suspected, and how harm reduction tools can prevent overdose deaths.
How are people who use drugs exposed to xylazine?
Studies show people are exposed to xylazine—knowingly or unknowingly—when it’s mixed with other drugs like heroin, cocaine, meth, and, most frequently, fentanyl. When combined with opioids or other drugs, it increases the risk of a drug overdose.
What happens if someone takes xylazine?
Taking xylazine can cause drowsiness, amnesia, slow breathing, slow heart rate, dangerously low blood pressure, wounds that can become infected, and death, especially when taken in combination with other drugs.
Why does xylazine increase the risk of overdose?
Xylazine is a central nervous system depressant, which means that it slows down the body’s heart rate and breathing. It can also enhance the effects of other depressants, such as opioids, which may lead to suffocation.
What are the signs of a xylazine-related overdose?
Xylazine-related overdoses look like opioid overdoses. A person who has overdosed may exhibit a slow pulse, slow breathing, blurry vision, disorientation, drowsiness, confusion, blue skin, and loss of consciousness.
How many people die from xylazine-related overdoses in the U.S.?
Xylazine-related overdose deaths in the U.S. rose from 102 deaths in 2018 to 3,468 deaths in 2021. Most occurred in Delaware, the District of Columbia, Maryland, Pennsylvania, Virginia, and West Virginia. Fentanyl was the most frequently co-occurring drug involved in those deaths.
What should I do if an overdose is suspected?
If you suspect that a person has overdosed on any drug, call 911 and give them naloxone—sometimes sold under the brand name Narcan—a medication that can reverse an opioid overdose. You should also stay with the person who has overdosed until first responders arrive. Most states have Good Samaritan laws, which protect people who have overdosed and those assisting them from certain criminal penalties.
While naloxone cannot reverse the effects of xylazine alone, experts recommend administering naloxone if an overdose is suspected because it’s often mixed with opioids.
You can get naloxone for free from some nonprofit organizations and government-run programs. You can also purchase over-the-counter naloxone at pharmacies, grocery and convenience stores, and other retailers.
Learn how to use naloxone in this short training video from the American Medical Association, or sign up for a free online training.
How can people prevent xylazine-related overdoses?
Harm reduction programs are community programs that prevent drug overdoses, reduce the spread of infectious diseases, and connect people to medical care. These programs provide lifesaving tools like naloxone, as well as fentanyl and xylazine test strips, which can detect the presence of these drugs in a substance and prevent overdoses. Drug test strips can also be ordered online.
However, test strips are considered “drug paraphernalia” in some states and are not legal everywhere. Learn more about state laws around drug checking equipment from the Network for Public Health Law.
Learn more about harm reduction from the CDC.
This article first appeared on Public Good News and is republished here under a Creative Commons license.
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A short history of sunscreen, from basting like a chook to preventing skin cancer
10almonds is reader-supported. We may, at no cost to you, receive a portion of sales if you purchase a product through a link in this article.
Australians have used commercial creams, lotions or gels to manage our skin’s sun exposure for nearly a century.
But why we do it, the preparations themselves, and whether they work, has changed over time.
In this short history of sunscreen in Australia, we look at how we’ve slathered, slopped and spritzed our skin for sometimes surprising reasons.
At first, suncreams helped you ‘tan with ease’
This early sunscreen claimed you could ‘tan with ease’.
Trove/NLASunscreens have been available in Australia since the 30s. Chemist Milton Blake made one of the first.
He used a kerosene heater to cook batches of “sunburn vanishing cream”, scented with French perfume.
His backyard business became H.A. Milton (Hamilton) Laboratories, which still makes sunscreens today.
Hamilton’s first cream claimed you could “
Sunbathe in Comfort and TAN with ease”. According to modern standards, it would have had an SPF (or sun protection factor) of 2.The mirage of ‘safe tanning’
A tan was considered a “modern complexion” and for most of the 20th century, you might put something on your skin to help gain one. That’s when “safe tanning” (without burning) was thought possible.
This 1967 Coppertone advertisement urged you to ‘tan, not burn’.
SenseiAlan/Flickr, CC BY-SASunburn was known to be caused by the UVB component of ultraviolet (UV) light. UVA, however, was thought not to be involved in burning; it was just thought to darken the skin pigment melanin. So, medical authorities advised that by using a sunscreen that filtered out UVB, you could “safely tan” without burning.
But that was wrong.
From the 70s, medical research suggested UVA penetrated damagingly deep into the skin, causing ageing effects such as sunspots and wrinkles. And both UVA and UVB could cause skin cancer.
Sunscreens from the 80s sought to be “broad spectrum” – they filtered both UVB and UVA.
Researchers consequently recommended sunscreens for all skin tones, including for preventing sun damage in people with dark skin.
Delaying burning … or encouraging it?
Up to the 80s, sun preparations ranged from something that claimed to delay burning, to preparations that actively encouraged it to get that desirable tan – think, baby oil or coconut oil. Sun-worshippers even raided the kitchen cabinet, slicking olive oil on their skin.
One manufacturer’s “sun lotion” might effectively filter UVB; another’s merely basted you like a roast chicken.
Since labelling laws before the 80s didn’t require manufacturers to list the ingredients, it was often hard for consumers to tell which was which.
At last, SPF arrives to guide consumers
In the 70s, two Queensland researchers, Gordon Groves and Don Robertson, developed tests for sunscreens – sometimes experimenting on students or colleagues. They printed their ranking in the newspaper, which the public could use to choose a product.
An Australian sunscreen manufacturer then asked the federal health department to regulate the industry. The company wanted standard definitions to market their products, backed up by consistent lab testing methods.
In 1986, after years of consultation with manufacturers, researchers and consumers, Australian Standard AS2604 gave a specified a testing method, based on the Queensland researchers’ work. We also had a way of expressing how well sunscreens worked – the sun protection factor or SPF.
This is the ratio of how long it takes a fair-skinned person to burn using the product compared with how long it takes to burn without it. So a cream that protects the skin sufficiently so it takes 40 minutes to burn instead of 20 minutes has an SPF of 2.
Manufacturers liked SPF because businesses that invested in clever chemistry could distinguish themselves in marketing. Consumers liked SPF because it was easy to understand – the higher the number, the better the protection.
Australians, encouraged from 1981 by the Slip! Slop! Slap! nationwide skin cancer campaign, could now “slop” on a sunscreen knowing the degree of protection it offered.
How about skin cancer?
It wasn’t until 1999 that research proved that using sunscreen prevents skin cancer. Again, we have Queensland to thank, specifically the residents of Nambour. They took part in a trial for nearly five years, carried out by a research team led by Adele Green of the Queensland Institute of Medical Research. Using sunscreen daily over that time reduced rates of squamous cell carcinoma (a common form of skin cancer) by about 60%.
Follow-up studies in 2011 and 2013 showed regular sunscreen use almost halved the rate of melanoma and slowed skin ageing. But there was no impact on rates of basal cell carcinoma, another common skin cancer.
By then, researchers had shown sunscreen stopped sunburn, and stopping sunburn would prevent at least some types of skin cancer.
What’s in sunscreen today?
An effective sunscreen uses one or more active ingredients in a cream, lotion or gel. The active ingredient either works:
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“chemically” by absorbing UV and converting it to heat. Examples include PABA (para-aminobenzoic acid) and benzyl salicylate, or
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“physically” by blocking the UV, such as zinc oxide or titanium dioxide.
Physical blockers at first had limited cosmetic appeal because they were opaque pastes. (Think cricketers with zinc smeared on their noses.)
With microfine particle technology from the 90s, sunscreen manufacturers could then use a combination of chemical absorbers and physical blockers to achieve high degrees of sun protection in a cosmetically acceptable formulation.
Where now?
Australians have embraced sunscreen, but they still don’t apply enough or reapply often enough.
Although some people are concerned sunscreen will block the skin’s ability to make vitamin D this is unlikely. That’s because even SPF50 sunscreen doesn’t filter out all UVB.
There’s also concern about the active ingredients in sunscreen getting into the environment and whether their absorption by our bodies is a problem.
Sunscreens have evolved from something that at best offered mild protection to effective, easy-to-use products that stave off the harmful effects of UV. They’ve evolved from something only people with fair skin used to a product for anyone.
Remember, slopping on sunscreen is just one part of sun protection. Don’t forget to also slip (protective clothing), slap (hat), seek (shade) and slide (sunglasses).
Laura Dawes, Research Fellow in Medico-Legal History, Australian National University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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When Carbs, Proteins, & Fats Switch Metabolic Roles
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Strange Things Happening In The Islets Of Langerhans
It is generally known and widely accepted that carbs have the biggest effect on blood sugar levels (and thus insulin response), fats less so, and protein least of all.
And yet, there was a groundbreaking study published yesterday which found:
❝Glucose is the well-known driver of insulin, but we were surprised to see such high variability, with some individuals showing a strong response to proteins, and others to fats, which had never been characterized before.
Insulin plays a major role in human health, in everything from diabetes, where it is too low*, to obesity, weight gain and even some forms of cancer, where it is too high.
These findings lay the groundwork for personalized nutrition that could transform how we treat and manage a range of conditions.❞
*saying ”too low” here is potentially misleading without clarification; yes, Type 1 Diabetics will have too little [endogenous] insulin (because the pancreas is at war with itself and thus isn’t producing useful quantities of insulin, if any). Type 2, however, is more a case of acquired insulin insensitivity, because of having too much at once too often, thus the body stops listening to it, “boy who cried wolf”-style, and the pancreas also starts to get fatigued from producing so much insulin that’s often getting ignored, and does eventually produce less and less while needing more and more insulin to get the same response, so it can be legitimately said “there’s not enough”, but that’s more of a subjective outcome than an objective cause.
Back to the study itself, though…
What they found, and how they found it
Researchers took pancreatic islets from 140 heterogenous donors (varied in age and sex; ostensibly mostly non-diabetic donors, but they acknowledge type 2 diabetes could potentially have gone undiagnosed in some donors*) and tested cell cultures from each with various carbs, proteins, and fats.
They found the expected results in most of the cases, but around 9% responded more strongly to the fats than the carbs (even more strongly than to glucose specifically), and even more surprisingly 8% responded more strongly to the proteins.
*there were also some known type 2 diabetics amongst the donors; as expected, those had a poor insulin response to glucose, but their insulin response to proteins and fats were largely unaffected.
What this means
While this is, in essence, a pilot study (the researchers called for larger and more varied studies, as well as in vivo human studies), the implications so far are important:
It appears that, for a minority of people, a lot of (generally considered very good) antidiabetic advice may not be working in the way previously understood. They’re going to (for example) put fat on their carbs to reduce the blood sugar spike, which will technically still work, but the insulin response is going to be briefly spiked anyway, because of the fats, which very insulin response is what will lower the blood sugars.
In practical terms, there’s not a lot we can do about this at home just yet—even continuous glucose monitors won’t tell us precisely, because they’re monitoring glucose, not the insulin response. We could probably measure everything and do some math and work out what our insulin response has been like based on the pace of change in blood sugar levels (which won’t decrease without insulin to allow such), but even that is at best grounds for a hypothesis for now.
Hopefully, more publicly-available tests will be developed soon, enabling us all to know our “insulin response type” per the proteome predictors discovered in this study, rather than having to just blindly bet on it being “normal”.
Ironically, this very response may have hidden itself for a while—if taking fats raised insulin response without raising blood sugar levels, then if blood sugar levels are the only thing being measured, all we’ll see is “took fats at dinner; blood sugars returned to normal more quickly than when taking carbs without fats”.
You can read the study in full here:
Proteomic predictors of individualized nutrient-specific insulin secretion in health and disease
Want to know more about blood sugar management?
You might like to catch up on:
- 10 Ways To Balance Your Blood Sugars
- Track Your Blood Sugars For Better Personalized Health
- How To Turn Back The Clock On Insulin Resistance
Take care!
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Collard Greens vs Kale – Which is Healthier?
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Our Verdict
When comparing collard greens to kale, we picked the collard greens.
Why?
Once again we have Brassica oleracea vs Brassica oleracea, (the same species that is also broccoli, cauliflower, Brussels sprouts, various kinds of cabbage, and more) and once again there are nutritional differences between the two cultivars:
In terms of macros, collard greens have more protein, equal carbs, and 2x the fiber. So that’s a win for collar greens.
In the category of vitamins, collard greens have more of vitamins B2, B3, B5, B9, E, and choline, while kale has more of vitamins A, B1, B6, C, and K. Nominally a 6:5 win for collard greens, though it’s worth noting that while most of the margins of difference are about the same, collard greens have more than 10x the choline, too.
When it comes to minerals, collard greens have more calcium, iron, magnesium, manganese, and phosphorus, while kale has more copper, potassium, selenium, and zinc. A genuinely marginal 5:4 win for collard greens this time.
All in all, a clear win for collard greens over the (otherwise rightly) established superfood kale. Collard greens just don’t get enough appreciation in comparison!
Want to learn more?
You might like to read:
What’s Your Plant Diversity Score? ← another reason it’s good to mix things up rather than just using the same ingredients out of habit!
Take care!
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People with dementia aren’t currently eligible for voluntary assisted dying. Should they be?
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Dementia is the second leading cause of death for Australians aged over 65. More than 421,000 Australians currently live with dementia and this figure is expected to almost double in the next 30 years.
There is ongoing public discussion about whether dementia should be a qualifying illness under Australian voluntary assisted dying laws. Voluntary assisted dying is now lawful in all six states, but is not available for a person living with dementia.
The Australian Capital Territory has begun debating its voluntary assisted dying bill in parliament but the government has ruled out access for dementia. Its view is that a person should retain decision-making capacity throughout the process. But the bill includes a requirement to revisit the issue in three years.
The Northern Territory is also considering reform and has invited views on access to voluntary assisted dying for dementia.
Several public figures have also entered the debate. Most recently, former Australian Chief Scientist, Ian Chubb, called for the law to be widened to allow access.
Others argue permitting voluntary assisted dying for dementia would present unacceptable risks to this vulnerable group.
Inside Creative House/Shutterstock Australian laws exclude access for dementia
Current Australian voluntary assisted dying laws exclude access for people who seek to qualify because they have dementia.
In New South Wales, the law specifically states this.
In the other states, this occurs through a combination of the eligibility criteria: a person whose dementia is so advanced that they are likely to die within the 12 month timeframe would be highly unlikely to retain the necessary decision-making capacity to request voluntary assisted dying.
This does not mean people who have dementia cannot access voluntary assisted dying if they also have a terminal illness. For example, a person who retains decision-making capacity in the early stages of Alzheimer’s disease with terminal cancer may access voluntary assisted dying.
What happens internationally?
Voluntary assisted dying laws in some other countries allow access for people living with dementia.
One mechanism, used in the Netherlands, is through advance directives or advance requests. This means a person can specify in advance the conditions under which they would want to have voluntary assisted dying when they no longer have decision-making capacity. This approach depends on the person’s family identifying when those conditions have been satisfied, generally in consultation with the person’s doctor.
Another approach to accessing voluntary assisted dying is to allow a person with dementia to choose to access it while they still have capacity. This involves regularly assessing capacity so that just before the person is predicted to lose the ability to make a decision about voluntary assisted dying, they can seek assistance to die. In Canada, this has been referred to as the “ten minutes to midnight” approach.
But these approaches have challenges
International experience reveals these approaches have limitations. For advance directives, it can be difficult to specify the conditions for activating the advance directive accurately. It also requires a family member to initiate this with the doctor. Evidence also shows doctors are reluctant to act on advance directives.
Particularly challenging are scenarios where a person with dementia who requested voluntary assisted dying in an advance directive later appears happy and content, or no longer expresses a desire to access voluntary assisted dying.
What if the person changes their mind? Jokiewalker/Shutterstock Allowing access for people with dementia who retain decision-making capacity also has practical problems. Despite regular assessments, a person may lose capacity in between them, meaning they miss the window before midnight to choose voluntary assisted dying. These capacity assessments can also be very complex.
Also, under this approach, a person is required to make such a decision at an early stage in their illness and may lose years of otherwise enjoyable life.
Some also argue that regardless of the approach taken, allowing access to voluntary assisted dying would involve unacceptable risks to a vulnerable group.
More thought is needed before changing our laws
There is public demand to allow access to voluntary assisted dying for dementia in Australia. The mandatory reviews of voluntary assisted dying legislation present an opportunity to consider such reform. These reviews generally happen after three to five years, and in some states they will occur regularly.
The scope of these reviews can vary and sometimes governments may not wish to consider changes to the legislation. But the Queensland review “must include a review of the eligibility criteria”. And the ACT bill requires the review to consider “advanced care planning”.
Both reviews would require consideration of who is able to access voluntary assisted dying, which opens the door for people living with dementia. This is particularly so for the ACT review, as advance care planning means allowing people to request voluntary assisted dying in the future when they have lost capacity.
The legislation undergoes a mandatory review. Jenny Sturm/Shutterstock This is a complex issue, and more thinking is needed about whether this public desire for voluntary assisted dying for dementia should be implemented. And, if so, how the practice could occur safely, and in a way that is acceptable to the health professionals who will be asked to provide it.
This will require a careful review of existing international models and their practical implementation as well as what would be feasible and appropriate in Australia.
Any future law reform should be evidence-based and draw on the views of people living with dementia, their family caregivers, and the health professionals who would be relied on to support these decisions.
Ben White, Professor of End-of-Life Law and Regulation, Australian Centre for Health Law Research, Queensland University of Technology; Casey Haining, Research Fellow, Australian Centre for Health Law Research, Queensland University of Technology; Lindy Willmott, Professor of Law, Australian Centre for Health Law Research, Queensland University of Technology, Queensland University of Technology, and Rachel Feeney, Postdoctoral research fellow, Queensland University of Technology
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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