
Want To Age More Slowly? These 4 Social Factors Count The Most
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.
You probably know that social connection is vital for good health, and perhaps even that loneliness and isolation literally kill.
Indeed, “a lonely lifestyle” vs “family visit frequency” made it into the list of The Lifestyle Factors That Matter >8 Times More Than Genes
In the case of social connection, it:
- Maintains the parts of our brains needed for language and processing social cues
- Brings us social support in a way that will generally be protective against depression
- Means that when all goes wrong, we more likely have material support too
In the case of loneliness and isolation, it:
- Allows important parts of our brain to atrophy
- Will tend towards promoting depression, which can lead to suicidality (and at the very least a decline of physical health, even without suicidality)
- Means that if we slip in the shower, someone will find our body a month later
We wrote about some of these things, here: How To Beat Loneliness & Isolation
Cumulative social advantages
Researchers (Dr. Laura Kubzansky et al.) looked into biomarkers of epigenetic aging and systemic inflammation (which latter thing promotes many kinds of biological aging), and how they are affected by social factors.
Four key areas stood out:
- The warmth and support you received from your parents growing up
- How connected you feel to your community and neighborhood
- Your involvement in religious or faith-based communities
- The reliability of ongoing emotional support from friends and family
They hypothesized—correctly—that these factors would be inversely associated with the pro-aging epigenetic pathways and inflammatory biomarkers for which they were testing.
However, what surprised them was that this effect was cumulative over time, and had no significant associations with short-term stress markers (like cortisol, for example).
Now, some of these things are not modifiable—we can’t do much about our childhoods (alas).
Others are much more attainable for most people, like community involvement.
Religiousness… Well, we are a health science publication and don’t cover theology here, but it’s well-established that faith generally has benefits for social and mental health. It may or may not be something that a person can choose whether to have or not (any more than we can decide whether to believe the sky is green), but if you have some faith, there’s a fair argument for leaning into that rather than away from it, and by making your religious practice communal rather than solitary, if your circumstances allow.
As for that last item, the ongoing emotional support from friends and family, sometimes it can be difficult, for example, we wrote about Family Estrangement & How To Fix It.
But even without family, friends should be an option for anyone. Even if we are physically isolated, for example: Human Connection In An All-Too-Busy World ← this covers, amongst other things, how to get the most out of the options afforded to us by technology, allowing tech to enhance, rather than detract from, our social lives.
And while we’re at it, you might also want to Make Social Media Work For Your Mental Health, Rather Than Against It ← spoiler: no, it’s not about setting app timers!
Anyway, to read the paper in full, enjoy: Cumulative social advantage is associated with slower epigenetic aging and lower systemic inflammation
Want to learn more?
Check out this excellent book that we reviewed a while back:
…and, for that matter, for those of us who are for one reason or another unpartnered and for one reason or another intend to stay that way now:
The Other Significant Others: Reimagining Life with Friendship at the Center by Rhaina Cohen
…and for anyone who wants/needs it, do also check out our main feature: Singledom & Healthy Longevity
Enjoy!
Don’t Forget…
Did you arrive here from our newsletter? Don’t forget to return to the email to continue learning!
Recommended
Learn to Age Gracefully
Join the 98k+ American women taking control of their health & aging with our 100% free (and fun!) daily emails:
-
A ketamine nasal spray will be subsidised for treatment-resistant depression. Here’s what you need to know about Spravato
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.
An antidepressant containing a form of the drug ketamine has been added to the Pharmaceutical Benefits Scheme (PBS), making it much cheaper for the estimated 30,000 Australians with treatment-resistant depression. This is when a patient has tried multiple forms of treatment for major depression – usually at least two antidepressant medications – without any improvement.
From May 1, a dose of Spravato (also known as esketamine hydrochloride) will cost $A31.60 and $7.70 for concession card holders.
However, unlike oral antidepressants, Spravato can’t be taken at home. Here’s how it works, and who it’s expected to help.
WPixz/Shutterstock What is Spravato?
The chemical ketamine is used as an anaesthetic. In this formulation it combines both the right-handed (designated “R”) and left-handed (called “S”) forms of the molecule.
This means they are mirror images of each other, similar to how your left hand is a mirror image of your right hand. The left- and right-hand forms can have different effects in the body.
Spravato contains only the left-handed version, giving the drug its generic name esketamine.
Spravato works by increasing the levels of glutamate in the brain. Glutamate is a key chemical messenger molecule that excites brain nerve cells, lifting and improving mood. It also plays a role in learning and forming memories.
How is it taken?
Spravato cannot be taken at home.
A patient can self-administer, but it must be done at a registered treatment facility, such as a hospital, under the supervision of medical staff so they can look out for blood pressure changes and monitor potential side effects.
The drug is provided as a single-use nasal spray. This application means it’s absorbed directly through the nasal lining into the brain, so it starts to work within minutes.
Spravato must also be taken alongside an oral antidepressant. This will be a new one the patient hasn’t tried before. In clinical trials, it was usually an SNRI or SSRI medication.
When a patient first starts on Spravato, they are given the spray twice a week in the first month. It is then administered once a week for the second month, and then weekly or fortnightly after that.
Once there are signs the medicine is working, treatment is continued for at least six months.
You can use the spray yourself but it must be under medical supervision in a registered facility. Scarc/Shutterstock How effective is it?
Spravato was approved for sale in Australia based on clinical trial data from more than 1,600 patients who were administered the drug for a period of four weeks. Each was given either Spravato, or a nasal placebo, and an oral antidepressant.
Patients were given a starting dose of either 28 or 56mg, which could be then increased up to 84mg by their doctor.
By the end of the four weeks, a greater percentage of patients who were given Spravato were found to have had a meaningful response to the treatment when compared with patients who received the placebo. Patients who were taking Spravato were also found to relapse at a lower rate. For those who did relapse, it took the Spravato patients longer to relapse when compared with patients who took the placebo.
It is expected Spravato will benefit a wide range of patients. The clinical trials demonstrated effectiveness for men and women, people aged 18 to 64, and those from a range of different ethnic backgrounds.
Potential side effects
As with any medicine, Spravato may cause side effects, some of which can be serious. The most common include:
- dissociation (feeling disconnected from yourself or what is around you)
- dizziness
- nausea and vomiting
- drowsiness
- headache
- change in taste
- vertigo.
Because Spravato can potentially increase blood pressure, medical staff will monitor a patient before and after it is administered.
Usually, blood pressure spikes around 40 minutes after taking the drug, so a reading is taken around this time. After taking Spravato, if their blood pressure has stayed low, or it’s dropping, the patient is given the all-clear to go home.
Due to the potential for this and other serious side effects, Spravato carries a black triangle warning. This means medical staff are encouraged to report any problem or side effect to the Therapeutic Goods Administration. A black triangle warning is generally used for new medicines or medicines that are being used in a new way.
Who will be eligible?
To be eligible for a prescription, a patient will need to have been diagnosed with treatment-resistant depression. In practice, this means they will have unsuccessfully tried at least two other antidepressant drugs first.
Australia’s Therapeutic Goods Administration approved Spravato for use in Australia in 2021, meaning it was available but not subsidised. Since then, the sponsoring company, Janssen-Cilag (an Australian subsidiary of the multinational Johnson & Johnson), applied to have it added to the PBS four times.
In December 2024, the Pharmaceutical Benefits Advisory Committee recommended a PBS listing.
The new PBS listing, capping the price of a single treatment at $31.60, is a significant price drop. In 2023, single doses of branded Spravato were reported to cost anywhere between $500 and $900.
However, patients may still have to pay hundreds of dollars for appointments at private clinics where Spravato can be administered. Public places are available but limited.
Spravato may be suitable for you if you’ve tried different antidepressants without success. If it is suitable for you, then your doctor can discuss the next steps.
If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.
Nial Wheate, Professor, School of Natural Sciences, Macquarie University and Shoohb Alassadi, Associate Lecturer and Registered Pharmacist, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Share This Post
-
Cannabis & Mental Health: Good Or Bad?
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.
When it comes to readily-available non-prescription legal “downer” drugs (that is to say, drugs that promote relaxation rather than “uppers” that promote stimulation), the most popular are of course alcohol and cannabis.
We’ve written a lot more about alcohol than we have about cannabis—partly because there’s simply much more research available. While alcohol has been legal (and thus easy to research) throughout many wealthy nations for a long time, the “War on Drugs”—which did not at all reduce the use of drugs—really curtailed research for a long time, and now there’s a lot of catching-up to do.
As a result, we know that alcohol is very bad for pretty much everything, including mental health—in which category it promotes/worsens mood disorders, including depression, and while often used to self-medicate against stress/anxiety, its numbing effects are short-lived and soon give the user extra reasons to be stressed and/or anxious. And, of course, it’s addictive, which is not fabulous.
So, is cannabis better?
Let’s address the topic of addictiveness first. Contrary to popular belief, it is indeed possible to become addicted to cannabis, though the likelihood of developing a substance abuse disorder is lower than for alcohol, and much lower than for nicotine.
See: Prevalence of Marijuana Use Disorders in the United States Between 2001–2002 and 2012–2013
If you prefer just the stats without the science, here’s the CDC’s rendering of that:
Addiction (Marijuana or Cannabis Use Disorder)
However, there is an interesting complicating factor, which is age. One is 4–7 times more likely to develop a substance abuse disorder (any substance abuse disorder), if one starts use as an adolescent, rather than later as an adult:
So, if you’re in the older age group, that’s a point in favor of reduced risk.
Does cannabis increase psychiatric disease risk?
It depends. Is it occasional use, or regular? There is a difference between using it relax and unwind once in a while, and relying on it all the time.
In the US, A 2021 report from the National Survey on Drug Use and Health showed (if we extrapolate the data to a population level):
- 52,000,000 people reported cannabis use in the previous year, of whom,
- 16,300,000 met the criteria for cannabis use disorder in the previous year
So, we may assume that around 1 in 3 cannabis users meet the criteria for cannabis use disorder.
Curious about who qualifies? The DSM-5 defines cannabis use disorder as the presence of at least 2 of the following:
- Withdrawal symptoms when not using cannabis
- Cannabis is taken in larger amounts or used over a longer period than intended
- Persistent desire to cut down with unsuccessful attempts
- Excessive time spent acquiring cannabis, using cannabis, or recovering from its effects
- Cravings for cannabis use
- Recurrent use resulting in neglect of social obligations
- Continued use despite social or interpersonal problems
- Important social, occupational, or recreational activities foregone to be able to use cannabis
- Continued use despite physical harm
- Continued use despite physical or psychological problems associated with cannabis use
- Tolerance
Source: DSM-5 Criteria for Substance Use Disorders: Recommendations and Rationale
Now, with that in mind…
Researchers examined the genetic links between cannabis use, cannabis use disorder, and psychiatric conditions, and found:
- Cannabis use disorder showed strong associations with nearly all psychiatric disorders, while
- Cannabis use (not disorder) had much weaker associations, and/but showed significant links with openness and conscientiousness.
So, that’s quite a difference. But since this is a matter of genetic links (i.e. people with these genetic marks tend to have these matching traits), it’s not always immediately clear which way the causality goes, if any:
- Does the genetic marker promote cannabis use / cannabis use disorder / linked psychiatric condition(s)?
- Does the the cannabis use / cannabis use disorder cause the psychiatric condition?
- Does the psychiatric condition promote the cannabis use / cannabis use disorder?
Using a statistical technique called Mendelian randomization, some of the causality can be determined (depending on the data available, of course). Using this method, it can be known that:
- Cannabis use disorder has bidirectional causal links with psychiatric disorders, especially schizophrenia and related disorders, as well as ADHD, BPD, and PTSD.
- Major depressive disorder has the strongest reverse causal effect on cannabis use disorder. This means that people with major depressive disorder were more likely to go on to also develop cannabis use disorder.
- Cannabis use without disorder showed far fewer causal links—mostly just the non-causal links with the traits of openness and conscientiousness*.
*we might hypothesize that a person scoring highly (so to speak) on openness is more likely to try cannabis than those with lower scores on openness, and a person scoring highly (as it were) on conscientiousness is less likely to go on to develop a substance use disorder than someone with lower scores on same. However, the statistical modelling was not able to conclusively demonstrate this.
You can read the paper in full, here: The genetic relationship between cannabis use disorder, cannabis use and psychiatric disorders
Are there benefits?
The biggest benefit is “it’s a lot safer than alcohol” when one wants a way to relax and wind down, which means that it can indeed alleviate stress and anxiety—occasionally. If you’re using it all the time, however, then you may start running into the problems of feeling more stressed and anxious in its absence, of course.
Many use it for pain relief, and if that’s you, only you can judge whether the benefits outweigh the risks (and presumably you’ve concluded they do).
Many use it for sleep (indeed, it’s even sometimes prescribed for some sleep disorders), and we’ve written about that here: Sweet Dreams Are Made of THC (Or Are They?)
In the latter case, it’s worth bearing in mind that CBD alone (without THC) does seem to improve sleep (as discussed in the above-linked article), and has additional benefits too:
CBD Oil: What Does The Science Say?
Prefer a drug-free way to relax?
We recommend:
- No-Frills, Evidence-Based Mindfulness
- Meditation Games That You’ll Actually Enjoy
- Which Style Of Yoga Is Best For You?
- 7 Kinds Of Rest When Sleep Is Not Enough
- Better Sex = Longer Life (Here’s How)
Enjoy!
Share This Post
-
Top 5 Exercises For Hip Mobility
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.
Do more with less:
Let’s open things up…
Hip mobility exercises will, by default, be hip-opening exercises. The criteria used by mobility coach Liv Townsend to qualify these top 5 exercises are:
- improves both strength and range of motion
- these are the qualifying characteristics for a mobility exercise; if an exercise improves only one or the other, then it’s just a strength exercise or just a flexibility exercise
- is accessible from almost any starting point
- realistically, rather than “if you can’t do the vertical splits while balancing on one leg, start by doing the vertical splits against the wall” (yes, that’s a real piece of advice this writer saw in the wild one time)
- can be progressively loaded or deepened
- because otherwise we would get very limited benefits from it, so this characteristic is necessary too
- delivers high value by working multiple muscles
- because frankly, we have a lot of muscles, and working them all individually would take a lot longer than most of us have time to commit
With these criteria in mind, here are 5 exercises that do all those things, and do them well:
- Bulgarian split squat: ranks highest for accessibility, progression, strength, and mobility, improving hip extension in your back leg, hip flexion and internal-rotation stability in your front leg, and stretching your glutes, quads, and hip flexors through deep ranges, with balance easily assisted if needed.
- Lateral squat: delivers high value by improving mobility and strength in your glutes, quads, adductors, hamstrings, and ankles, emphasizes inner-thigh mobility and external hip rotation, and progresses with depth or load, but can be less accessible due to common form challenges.
- Single-leg Romanian deadlift: combines hamstring lengthening with strength through your full hinge range, is accessible at any flexibility level, and progresses easily with load, but ranks lower because it mainly targets a single mobility area.
- Squat: develops quad strength and stretches your quads and hip flexors on descent, is broadly accessible and scalable with depth, blocks, or bands, but offers lower overall value because it lacks hip rotation and minimal posterior-chain involvement.
- Shin box: builds strength and flexibility through internal and external hip rotation, strengthens your glutes on the lift, stretches your hip flexors and adductors at the top, and is easily progressed with load, but loses points for accessibility due to required internal rotation and starting-position demands.
For more on all of this, plus visual demonstrations, enjoy:
Click Here If The Embedded Video Doesn’t Load Automatically!
Want to learn more?
You might also like:
The Most Underrated Hip Mobility Exercise (Not Stretching)
Take care!
Share This Post
- improves both strength and range of motion
Related Posts
-
What you need to know about H5N1 bird flu
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.
On May 30, the Centers for Disease Control and Prevention reported that a Michigan dairy worker tested positive for H5N1 bird flu. It was the fourth person to test positive for H5N1 in the United States, following another recent case in Michigan, an April case in Texas, and an initial case in Colorado in 2022.
H5N1 bird flu has been spreading among bird species in the U.S. since 2021, killing millions of wild birds and poultry. In late March 2024, H5N1 bird flu was found in cows for the first time, causing an outbreak in dairy cows across several states.
U.S. public health officials and researchers are particularly concerned about this outbreak because the virus has infected cows and other mammals and has spread from a cow to a human for the first time.
This bird flu strain has shown to not only make wild mammals, including marine mammals and bears, very sick but to also cause high rates of death among species, says Jane Sykes, professor of small animal medicine at the University of California, Davis, School of Veterinary Medicine.
“And now that it has been found in cattle, [it] raises particular concern for spread to all the animal species, including people,” adds Sykes.
Even though the risk for human infection is low and there has never been human-to-human transmission of H5N1, there are several actions you can take to stay protected. Read on to learn more about H5N1 bird flu and the current outbreak.
What is H5N1?
H5N1 is a type of influenza virus that most commonly affects birds, causing them severe respiratory illness and death.
The H5N1 strain first emerged in China in the 1990s, and it has continued to spread around the world since then. In 1997, the virus spread from animals to humans in Hong Kong for the first time, infecting 18 people, six of whom died.
Since 2020, the H5N1 strain has caused “an unprecedented number of deaths in wild birds and poultry in many countries,” according to the World Health Organization.
Even though bird flu is rare in humans, an H5N1 infection can cause mild to severe illness and can be fatal in some cases. It can cause eye infection, upper respiratory symptoms, and pneumonia.
What do we know about the 2024 human cases of H5N1 in the U.S.?
The Michigan worker who tested positive for H5N1 in late May is a dairy worker who was exposed to infected livestock. They were the first to experience respiratory symptoms—including a cough without a fever—during the current outbreak. They were given an antiviral and the CDC says their symptoms are resolving.
The Michigan farm worker who tested positive earlier in May only experienced eye-related symptoms and has already recovered. And the dairy worker who tested positive for the virus in Texas in April only experienced eye redness as well, was treated with an antiviral medication for the flu, and is recovering.
Is H5N1 bird flu in the milk we consume?
The Food and Drug Administration has found traces of H5N1 bird flu virus in raw or unpasteurized milk. However, pasteurized milk is safe to drink.
Pasteurization, the process of heating milk to high temperatures to kill harmful bacteria (which the majority of commercially sold milk goes through), deactivates the virus. In 20 percent of pasteurized milk samples, the FDA found small, inactive (not live nor infectious) traces of the virus, but these fragments do not make pasteurized milk dangerous.
In a recent Infectious Diseases Society of America briefing, Dr. Maximo Brito, a professor at the University of Illinois College of Medicine, said that it’s important for people to avoid “drinking unpasteurized or raw milk [because] there are other diseases, not only influenza, that could be transmitted by drinking unpasteurized milk.”
What can I do to prevent bird flu?
While the risk of H5N1 infection in humans is low, people with exposure to infected animals (like farmworkers) are most at risk. But there are several actions you can take to stay protected.
One of the most important things, according to Sykes, is taking the usual precautions we’ve taken with COVID-19 and other respiratory viruses, including frequent handwashing, especially before eating.
“Handwashing and mask-wearing [are important], just as we learned from the pandemic,” Sykes adds. “And it’s not wearing a mask at all times, but thinking about high-risk situations, like when you’re indoors in a crowded environment, where transmission of respiratory viruses is much more likely to occur.”
There are other steps you can take to prevent H5N1, according to the CDC:
- Avoid direct contact with sick or dead animals, including wild birds and poultry.
- Don’t touch surfaces that may have been contaminated with animal poop, saliva, or mucus.
- Cook poultry and eggs to an internal temperature of 165 degrees Fahrenheit to kill any bacteria or virus, including H5N1. Generally, avoid eating undercooked food.
- Avoid consuming unpasteurized or raw milk or products like cheeses made with raw milk.
- Avoid eating uncooked or undercooked food.
- Poultry and livestock farmers and workers and bird flock owners should wear masks and other personal protective equipment “when in direct or close physical contact with sick birds, livestock, or other animals; carcasses; feces; litter; raw milk; or surfaces and water that might be contaminated with animal excretions from potentially or confirmed infected birds, livestock, or other animals.” (The CDC has more recommendations for this population here.)
Is there a vaccine for H5N1?
The CDC said there are two candidate H5N1 vaccines ready to be made and distributed in case the virus starts to spread from person to person, and the country is now moving forward with plans to produce millions of vaccine doses.
The FDA has approved several bird flu vaccines since 2007. The U.S. has flu vaccines in stockpile through the National Pre-Pandemic Influenza Vaccine Stockpile program, which allows for quick response as strains of the flu virus evolve.
Could this outbreak become a pandemic?
Scientists and researchers are concerned about the possibility of H5N1 spreading among people and causing a pandemic. “Right now, the risk is low, but as time goes on, the potential for mutation to cause widespread human infection increases,” says Sykes.
“I think this virus jumping into cows has shown the urgency to keep tracking [H5N1] a lot more closely now,” Peter Halfmann, research associate professor at the University of Wisconsin-Madison’s Influenza Research Institute tells PGN. “We have our eyes on surveillance now. … We’re keeping a much closer eye, so it’s not going to take us by surprise.”
This article first appeared on Public Good News and is republished here under a Creative Commons license.
Don’t Forget…
Did you arrive here from our newsletter? Don’t forget to return to the email to continue learning!
Learn to Age Gracefully
Join the 98k+ American women taking control of their health & aging with our 100% free (and fun!) daily emails:
-
The Energy Plan – by James Collins
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.
There’s a lot of conflicting advice out there about how we should maintain our energy levels, for example:
- Eat fewer carbs!
- Eat more carbs!
- Eat slow-release carbs!
- Eat quick-release carbs!
- Practise intermittent fasting!
- Graze constantly throughout the day!
- Forget carbs and focus on fats!
- Actually it’s all about B-vitamins!
…and so on.
What Collins does differently is something much less-often seen:
Here, we’re advised on how to tailor our meals to our actual lifestyle, taking into account the day we actually have each day. For example:
- What will our energy needs be for the day?
- Will our needs be intense, or long, or both, or neither?
- What kind of recovery have we had, or do we need, from previous activities?
- Do we need to replace lost muscle glycogen, or are we looking to trim the fat?
- Are we doing a power-up or just maintenance today?
Rather than bidding us have a five-way spreadsheet and do advanced mathematics for every meal, though, Collins has done the hard work for us. The book explains the various principles in a casual format with a light conversational tone, and gives us general rules to follow.
These rules cover what to do for different times of day… and also, at different points in our life (the metabolic needs of a 13-year-old, 33-year-old, and 83-year-old, are very different!). That latter’s particularly handy, as a lot of books assume an age bracket for the reader, and this one doesn’t.
In short: a great book for anyone who wants to keep their energy levels up (throughout life’s ups and downs in activity) without piling on the pounds or starving oneself.
Click here to check out The Energy Plan on Amazon and fuel your days better!
Don’t Forget…
Did you arrive here from our newsletter? Don’t forget to return to the email to continue learning!
Learn to Age Gracefully
Join the 98k+ American women taking control of their health & aging with our 100% free (and fun!) daily emails:
-
How Acetaminophen (Paracetamol) Suppresses Endocannabinoids
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.
…contrary to all expectations (and how this can lead to more effective acetaminophen-like pain relief, without the toxicity!
It’s well known that acetaminophen (international name: paracetamol, most well-known brand name in the US: Tylenol) is a mild painkiller and anti-fever agent; what’s not well understood is how it actually works.
Recently, a team of researchers (Dr. Michaela Dvorakova et al.) looked into this, and found something that was quite surprising, to understate it considerably.
That sounds like a clickbait headline (“and what they discovered will shock you!”) but well, we don’t do clickbait and our own headline covers it: acetaminophen suppresses endocannabinoids, when generally for painkilling purposes we want more endocannabinoids, not less.
Before we get into that, let’s take a moment to note some of the bad parts of acetaminophen’s safety profile, which is to say: it’s really not very safe.
Rather than repeat ourselves though, we’ll link to where we did a whole main feature about that, here: Before You Reach For That Tylenol…
Now, about acetaminophen and endocannabinoids
In the lead researcher’s words:
❝There are hypotheses, but we still don’t know precisely how it works. Up until now we thought that elevated endocannabinoids in our body meant less pain, but our study shows that in the case of 2-AG, it might be the opposite. Actually, reduced levels of 2-AG leads to decreased pain.❞
~ Dr. Michaela Dvorakova
You may be wondering: what’s 2-AG?
And the answer is that it’s 2-arachidonoyl glycerol, which is a cannabinoid naturally made by the human body (thus, endogenous cannabinoid, or usually written: endocannabinoid).
What the researchers found is that acetaminophen inhibits an enzyme that makes that endocannabinoid, namely, diacylglycerol lipase α (DAGLα) ← as in, this is the name of the enzyme that makes it.
Thus, inhibiting the enzyme means inhibiting endocannabinoid production. So, what gives, and why does this work as a painkiller, when it looks like it’s doing the opposite?
The researchers propose… Well, we’ll quote them:
❝This gives rise to the counterintuitive hypothesis that decreasing endocannabinoid production by DAGLα inhibition may be antinociceptive in certain settings.
Supporting this hypothesis, we find that diacylglycerol lipase (DAGL) inhibition by RHC80267 is antinociceptive in wild-type but not CB1 knockout mice in the hot-plate test.
We propose (1) that activation of DAGLα may exacerbate some forms of nociception and (2) a mechanism for the antinociceptive actions of acetaminophen, whereby acetaminophen inhibits a DAGLα/CB1-based circuit that plays a permissive role in at least one form of nociception.❞
Translating from sciencese: by stopping the endocannabinoid production, the body is triggered to engage a different, more effective method of killing pain.
You can read the paper in full here: Acetaminophen inhibits diacylglycerol lipase synthesis of 2-arachidonoyl glycerol: Implications for nociception
As for what the implications are? Per the researchers, it means that if we understand that inhibiting the enzyme DAGLα triggers a painkilling response, then new drugs can be designed to target DAGLα without the toxicity of acetaminophen.
So, keep an eye out for that, and you heard it hear first!
Want to learn more?
We’ve written quite a bit about pain management, including:
- How To Stop Pain Spreading
- How To Dial Down Your Pain
- Managing Chronic Pain (Realistically!)
- Get The Right Help For Your Pain
- The 7 Approaches To Pain Management
- Science-Based Alternative Pain Relief (When Painkillers Aren’t Helping, These Things Might)
Take care!
Don’t Forget…
Did you arrive here from our newsletter? Don’t forget to return to the email to continue learning!
Learn to Age Gracefully
Join the 98k+ American women taking control of their health & aging with our 100% free (and fun!) daily emails:









