Testosterone levels decline with age, not menopause, despite what you’ve heard
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Social media widely promotes testosterone as an essential part of menopausal hormone therapy (MHT, also known as hormone replacement therapy or HRT) to treat low mood, brain fog and loss of vitality.
As a result, some women who aren’t prescribed it as part of the MHT regimen feel they are missing out.
At menopause, when menstruation finally stops, oestrogen levels fall substantially, which can cause symptoms such as hot flushes, night sweats and vaginal dryness. Replacing this oestrogen with MHT relieves these symptoms.
But our new research, published this week in The Lancet journal eBioMedicine, shows testosterone doesn’t change like oestrogen when women reach perimenopause or menopause.
Rather, testosterone declines with age.
We’ve long suspected this – but early tests weren’t reliable
Our 2005 study of 1,400 women showed testosterone blood levels did not change at menopause but gradually declined from the age of about 20.
This followed a smaller study of 172 women in 2000 which found no change in testosterone blood levels at menopause.
But these older studies need to be interpreted with caution. Testosterone was measured with chemical tests that were not able to accurately measure testosterone at low levels in women.
Since then, we have used newer, gold-standard methods that can accurately measure small amounts of testosterone.
Using these methods in a 2019 study of 588 women, we found the average decline in testosterone between the ages of 18 to 39 years was around 25%.
Our latest study examined the blood testosterone levels of 1,104 participants aged 40 to 69 years. The participants provided extensive menstrual cycle information, so we could determine whether each woman was pre-menopausal, perimenopausal or postmenopausal.
We excluded women taking medications that might impact their natural hormone levels, or who had other identifiable factors that would impact their hormones from our hormone analysis. Having a higher body mass index (BMI) and being a cigarette smoker, for example, are each associated with higher testosterone.
What our new study found
Participants’ testosterone blood levels declined, on average, by 25% between the ages of 40 and 58–59 years.
There were no measurable differences between women who were premenopausal, perimenopausal or postmenopausal.
Postmenopausal women who had both ovaries surgically removed had lower blood testosterone levels than postmenopausal women with at least one ovary. This provides additional evidence that women’s ovaries continue to be the source of some testosterone after menopause.
Interestingly, testosterone blood levels subtly increased from the age of 58–59 years. This echoes our 2005 study which found testosterone blood levels bottomed out at around the age of 62 years, and then gradually increased.
All of these findings are changes that occur on average. Not everyone will experience the same changes we observed. Some might experience more or less change with age.
So how does testosterone change over a woman’s lifespan?
Combined with our past studies and other research, our latest study has enabled us to build a picture of testosterone across a woman’s lifespan.
Testosterone levels tend to decrease by around 50% from about age 20 through to about age 60.
Then they begin to subtly increase, with the trend for levels to increase continuing into the eight and ninth decades of life. We are yet to understand why these changes occur.
Whether low testosterone is associated with symptoms needs further exploration. However, research to date suggests women with low testosterone aren’t more likely to have lower sexual desire, poorer muscle mass or lower mood.
Nonetheless, the gradual increase in testosterone may partly explain the age-related hair thinning and bothersome facial hair growth many women in their sixties and older experienced.
What does this mean for testosterone therapy?
Researchers proposed the idea of an “testosterone deficiency syndrome” in menopausal women more than 20 years ago. This was before testosterone had been measured across women’s lifespans and before robust studies of the relationships between blood testosterone levels and specific symptoms.
Our research refutes the belief that menopause causes testosterone deficiency, and that testosterone supplementation is an essential part of MHT.
Multiple clinical trials have shown testosterone treatment can modestly improve sexual desire in postmenopausal women who have experienced a change in their sexual desire that bothers them.
However there is currently no robust or consistent evidence that testosterone therapy will improve any symptoms for women other than low sexual desire after menopause.
Therefore, the international clinical guidelines state it should only be prescribed for low sexual desire in postmenopausal women.
We are currently evaluating the effects of testosterone on women’s muscle function and bone density and will report these findings in 2026.
Susan Davis, Chair of Women’s Health, Monash University and YuanYuan Wang, Clinical Epidemiologist,School of Public Health and Preventive Medicine, Monash University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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How To Make Your Doctor’s Appointment Do More For You
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Doctor: “So, how are you today?”
Patient: “Can’t complain; how about you?”Hopefully your medical appointments don’t start quite like that, but there can be an element of being “along for the ride” when it comes to consultations. They ask questions, we answer, they prescribe something, we thank them.
In principle, the doctor should be able to handle that; ask the right questions, determine the problem, and not need too much from you. After all, they have been trained to deal with an unconscious patient, so the fact you can communicate at all is a bonus.
However, leaving it all to them isn’t really playing the field.
Before the appointment
Research your issue, as best you understand it. Some doctors will be very averse to you telling them about having done this (taking it as an affront to their expertise), but here’s the thing:
You don’t have to tell them.
You just have to understand as much as possible, so that you will be as “up to speed” as possible in the conversation, and not be quickly out of your depth.
Have an agenda, based on the above. Literally, have a little set of bullet-points to remind you what you came in to discuss, so that nothing escapes you in the moment. This should also include:
- If you have additional reasons for a particular concern (e.g. family history of a certain problem), make them known
- If you plan to request any specific tests or treatments, be able to clearly state your reasons for the specific tests or treatments
- If you plan to write off any specific tests or treatments as something to which you will not consent, have your reasons ready—in a way that makes it clear it’s something more than “don’t want it”, for example, “I’ve already decided that this treatment would make a sufficient hit to my quality of life, as to make it not worthwhile for me personally” (or whatever the reason may be for you). It needs to be something they can write on their notes instead of simply “patient refused treatment”.
Compile a record of your symptoms (as appropriate), and any previous tests/treatments (as appropriate), in chronological order. If you take all this with you, perhaps in a nice folder, you will enjoy the following advantages:
- not forgetting anything
- ability to answer questions accurately
- give the (correct) impression you take your health seriously, which means they are more likely to do so also—especially because they will now know that if they fob you off and/or mess something up, you’ll be taking a record of that to your next appointment.
Plan your outfit. No, you don’t have to dress for the red carpet, but you want to satisfy two main conditions:
- Accessibility for examination (for example, if you are going in with a knee pain, maybe don’t wear the tight jeans today; if they’re going to take blood, be either sleeveless or have sleeves that are easily moved out of the way, etc)
- General presentability (it’s a sad fact that doctors are not immune to biases, and will treat people better if they respect them more)
During the appointment
Be friendly; doctors (like most people) will respond much better to that than to grumpiness—even if you have good reason for grumpiness and even if the doctor has been trained to help grumpy patients.
Be confident: when we say “be friendly”, that doesn’t mean to necessarily be so agreeable as to not advocate for yourself. In particular:
- If they explain something and it isn’t clear to you, ask them to clarify
- If you disagree with them about a value judgement, say so. By “a value judgement” here we mean things in the realm of subjectivity. If the doctor says you are prediabetic, then you won’t get much mileage out of arguing otherwise; the numbers have the final say on that one. But if the doctor says “the side effects of the treatment you’re requesting will make it not worthwhile for you” and you have understood the side effects and you still disagree, then your opinion counts for more than theirs—it is your decision to make.
- If they dismiss a concern, ask them to put in writing that they dismissed your concern of X, despite you providing evidence that Y, and it being well-known that Z. Often, rather than doing that, they’ll just fold and actually address your concern instead.
Writer’s example in that last category: I recently made a request for a bone density scan. I expect my bone density is great, because I do all the right things, however, as both of my parents suffered from osteoporosis and assorted resultant crushed bones and the terrible consequences thereof, I a) have reasonable grounds for extra concern, and b) I believe that even if my bone density is fine now, it’s good to establish a baseline so I can know, in 5, 10, 20 years etc, whether there has been any deterioration. Now, happily the doctor I saw agreed with my assessment at first presentation and so I got the referral, but had she not been, I would have said “Could you please put in writing that I asked for a bone density scan, and you refused, on the grounds that [details about what happened with my parents], and that osteoporosis is known to have a strong genetic component is not, in your opinion, any reason to worry?”
Be honest, and/but err on the side of overstating your symptoms rather than understating. For example, if it is about a chronic condition and the doctor asks “are you able to do xyz”, take the question as meaning “are you able to do xyz on your worst days?”. You can clarify that if you like in your answer, but you need to include the information that xyz is something that your condition can and sometimes does impede you from doing.
Leave your embarrassment at the door. To the doctor (unless they are a very unprofessional one), you really are just one more patient with symptoms they have (unless your condition is very rare) seen a thousand times before. If your symptom is embarrassing, it will not faze them and you definitely should not hold back from mentioning it, for example. This goes extra in the case of discussions around sexual health, by the way, in which field the details you’d perhaps rather not share with anybody, are the details they need to adequately treat you.
After the appointment
Follow up on anything that doesn’t happen as promised (e.g. referrals, things ordered, etc), to make sure nothing got lost in a bureacratic error.
Get a second opinion if you’re not satisfied with the first one. Doctors are fallible, and as a matter of professional pride, it’s likely the second doctor will be glad to find something the first doctor missed.
See also: Make Your Negativity Work For You
Take care!
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Fisetin: The Anti-Aging Assassin
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Out With The Old…
Fisetin is a flavonoid (specifically, a flavonol), but it’s a little different than most. While it has the usual antioxidant, anti-inflammatory, and anti-cancer properties you might reasonably expect from flavonoids, it has an extra anti-aging trick up its sleeve that most don’t.
❝Fisetin is a flavonol that shares distinct antioxidant properties with a plethora of other plant polyphenols. Additionally, it exhibits a specific biological activity of considerable interest as regards the protection of functional macromolecules against stress which results in the sustenance of normal cells cytoprotection. Moreover, it shows potential as an anti-inflammatory, chemopreventive, chemotherapeutic and recently also senotherapeutic agent❞
~ Dr. Grynkiewicz & Dr. Demchuk
Let’s briefly do some due diligence on its expected properties, and then we’ll take a look at its bonus anti-aging effects.
The flavonol that does-it-ol
Because of the similar mechanisms involved, there are three things that often come together, which are:
- Antioxidant
- Anti-inflammatory
- Anticancer
This list often gets expanded to also include:
- Anti-aging
…although that is usually the last thing to get tested out of that list.
In today’s case, let’s kick it off with…
❝Fisetin (3,3′,4′,7-tetrahydroxyflavone) is a dietary flavonoid found in various fruits (strawberries, apples, mangoes, persimmons, kiwis, and grapes), vegetables (tomatoes, onions, and cucumbers), nuts, and wine that has shown strong anti-inflammatory, anti-oxidant, anti-tumorigenic, anti-invasive, anti-angiogenic, anti-diabetic, neuroprotective, and cardioprotective effects❞
Read more: Fisetin and Its Role in Chronic Diseases
Understanding its anticancer mechanisms
The way that fisetin fights cancer is basically “all the ways”, and this will be important when we get to its special abilities shortly:
❝Being a potent anticancer agent, fisetin has been used to inhibit stages in the cancer cells (proliferation, invasion),prevent cell cycle progression, inhibit cell growth, induce apoptosis, cause polymerase (PARP) cleavage, and modulate the expressions of Bcl‐2 family proteins in different cancer cell lines (HT‐29, U266, MDA‐MB‐231, BT549, and PC‐3M‐luc‐6), respectively. Further, fisetin also suppresses the activation of the PKCα/ROS/ERK1/2 and p38 MAPK signaling pathways, reduces the NF‐κB activation, and down‐regulates the level of the oncoprotein securin. Fisetin also inhibited cell division and proliferation and invasion as well as lowered the TET1 expression levels. ❞
Read more: Fisetin: An anticancer perspective
There’s also more about it than we even have room to quote, here:
Now For What’s New And Exciting: Senolysis
All that selectivity that fisetin exhibits when it comes to “this cell gets to live, and this one doesn’t” actions?
It makes a difference when it comes to aging, too. Because aging and cancer happen by quite similar mechanisms; they’re both DNA-copying errors that get copied forward, to our detriment.
- In the case of cancer, it’s a cell line that accidentally became immortal and so we end up with too many of them multiplying in one place (a tumor)
- In the case of aging, it’s the cellular equivalent of “a photocopy of a photocopy of a photocopy” gradually losing information as it goes
In both cases…
The cell must die if we want to live
Critically, and which quality differentiates it from a lot of other flavonoids, fisetin has the ability to selectively kill senescent cells.
To labor the photocopying metaphor, this means there’s an office worker whose job it is to say “this photocopy is barely legible, I’m going to toss this, and then copy directly from the clearest copy we have instead”, thus keeping the documents (your DNA) in pristine condition.
In fisetin’s case, this was first tested in mouse (in vivo) studies, and in human tissue (in vitro) studies, before moving to human clinical studies:
❝Of the 10 flavonoids tested, fisetin was the most potent senolytic.
The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit.❞
~ Dr. Matthew Yousefzadeh et al.
Read in full: Fisetin is a senotherapeutic that extends health and lifespan
There’s lots more science that’s been done to it since that first groundbreaking study though; here’s a more recent example:
Want some?
We don’t sell it, but here for your convenience is an example product on Amazon
Enjoy!
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How Much Difference Can Short Bursts Of Exercise Make, Long-Term?
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“Exercise is good for the health” is not breaking news, and you don’t need a health science publication to tell you that.
But, most people do not do as much exercise as we’d like (even if we have the energy, often daily life gets in the way!), so, it’s reasonable to make sure that the exercise we do have time and energy to do, counts for as much good as possible!
So, here’s the science of doing just that:
What matters more, duration or intensity?
That’s the question that a team of researchers (Dr. Minxue Shen et al.) set out to answer, and found that indeed it’s not just total movement that matters—how intensely you move plays a major role in disease prevention.
Dr. Shen and her team looked at device-measured data (from wrist-worn fitness trackers) from 96,408 participants (of whom, 56.3% women, average age 62), over the course of 7 years.
What they found, in few words: participants who regularly engaged in short bursts of vigorous activity enjoyed significantly reduced risks of cardiovascular disease, atrial fibrillation, type 2 diabetes, inflammatory diseases, liver disease, respiratory disease, kidney disease, and dementia.
In particular, higher levels of vigorous activity were linked to:
- 63% lower risk of dementia
- 60% lower risk of type 2 diabetes
- 46% lower risk of death
As for the “which is best” question, intensity had a stronger protective effect than total activity for most diseases, especially inflammatory conditions and brain-related conditions.
There several main mechanisms of action that the researchers considered foremost:
- Short bursts of vigorous activity reduce inflammation, helping explain stronger effects on arthritis and psoriasis.
- Short bursts of intense activity stimulates protective brain chemicals and improve oxygen use, supporting lower dementia risk.
You may be wondering how little you can get away with. Per this study, a few minutes daily, adding up to 15–20 minutes per week, was already sufficient to deliver meaningful benefits.
See also: How Useful Is “Exercise Snacking”, Really?
The researchers also noted that short bursts like climbing stairs quickly, rushing for a bus, or brisk walking between tasks count too—it doesn’t have to be an intentional exercise session!
Writer’s anecdote: I remember one time my fitness tracker congratulated me on my good workout, and encouraged me to keep going, while I was changing my bedsheets!
You can read the paper in full, here: Volume vs intensity of physical activity and risk of cardiovascular and non-cardiovascular chronic diseases
If you’d like to get started, a good place to begin is: How To Do HIIT (Without Wrecking Your Body) ← important, because the “high-intensity” part can cause problems for some people, if not undertaken attentively!
Want to learn more?
You might like this book we reviewed a while back:
I Will Make You Passionate About Exercise – by Bevan Eyles
What this isn’t: a “just do it!” motivational pep-talk.
What this is: a compassionate and thoughtful approach to help non-exercisers become regular exercisers, by looking at the real life factors of what holds people back (learning from his own early failures as a coach, by paying attention now to things he inadvertently neglected back then), both in the material/practical and in the psychological/emotional.
Enjoy!
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Older people’s risk of abuse is rising. Can an ad campaign protect them?
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Elder abuse is an emerging public health and safety issue for communities of high-income countries.
The most recent data from Australia’s National Elder Abuse Prevalence Study, which surveyed 7,000 older people living in the community, found one in six self-reported being a victim of some form of abuse. But this did not include older people living in residential aged care or those with cognitive impairment, such as dementia – so is likely an underestimate.
This week the Australian government announced a multi-million dollar advertising campaign it hopes will address this serious and abhorrent abuse.
But is investing in community awareness of elder abuse the best use of scarce resources?
Nuttapong punna/Shutterstock What is elder abuse?
The World Health Organization (WHO) defines elder abuse as
[…] a single, or repeated act, or lack of appropriate action, occurring within any relationship where there is an expectation of trust which causes harm or distress to an older person.
Australia usually defines older people as those over 65. The exact age varies between countries depending on the overall health status of a nation and its vulnerable population groups. The WHO definitions of an older adult for sub-Saharan Africa, for example, is over 50. And there are communities with poorer health status and shorter lifespans within country borders, including our First Nations people.
Elder abuse can take on many different forms including physical, sexual, psychological, emotional, or financial abuse and neglect.
Living longer and wealthier
The number of older people in our society is greater than it has ever been. Around 17% Australians are aged 65 and over. By 2071, older Australians will make up between 25% and 27% of the total population.
People are living longer, accumulating substantial wealth and are vulnerable to abuse due to cognitive, physical or functional limitations.
Longer lifespans increase the time of possible exposure to abuse. Australian men aged 65 can expect to live another 20.2 years, while women aged 65 are likely to live another 22.8 years. (Life expectancy for First Nations men and women remains significantly shorter.)
Australian men are now 143 times more likely to reach the age of 100 than they were in 1901. Women are 82 times more likely.
Older people hold a large proportion of our nation’s wealth, making them vulnerable to financial abuse. Recent research by the Australian Council of Social Service and UNSW Sydney reveals older households (with people over 65) are 25% wealthier than the average middle-aged household and almost four times as wealthy as the average under-35 household.
Finally, older people have higher levels of impairment in their thinking, reasoning and physical function. Cognitive impairment, especially dementia, increases from one in 67 Australians under 60 to almost one in two people aged over 90.
Over half of Australians aged 65 years and over have disability. A particularly vulnerable group are the 258,374 older Australians who receive government-funded home care.
Who perpetrates elder abuse?
Sadly, most of the perpetrators of elder abuse are known to their victims. They are usually a member of the family, such as a life partner, child or grandchild.
Elder abuse causes significant illness and even early death. Financial abuse (across all ages) costs the community billions of dollars. Specific data for financial elder abuse is limited but indicates massive costs to individual survivors and the community.
Despite this, the level of awareness of elder abuse is likely to be much lower than for family violence or child abuse. This is partly due to the comparatively recent concept of elder abuse, with global awareness campaigns only developed over the past two decades.
Is an advertising campaign the answer?
The federal government has allocated A$4.8 million to an advertising campaign on television, online and in health-care clinics to reach the broader community. For context, last year the government spent $131.4 million on all media campaigns, including $32.6 million on the COVID vaccination program, $2 million on Japanese encephalitis and $3.2 million on hearing health awareness.
The campaign will likely benefit a small number of people who may be victims and have the capacity to report their perpetrators to authorities. It will generate some heartbreaking anecdotes. But it is unlikely to achieve broad community or systemic change.
There is little research evidence to show media campaigns alter the behaviour of perpetrators of elder abuse. And suggesting the campaign raises awareness of the issue for older people who are survivors of abuse sounds more like blaming victims than empowering them.
We don’t know how the government will judge the success of the campaign, so taxpayers won’t know whether a reasonable return on this investment was achieved. There may also be opportunity costs associated with the initiative – that is, lost opportunities for other actions and strategies. It could be more effective and efficient to target high-risk subgroups or to allocate funding to policy, practice reform or research that has direct tangible benefits for survivors. https://www.youtube.com/embed/DeK2kaqplTI?wmode=transparent&start=0 The Australian Human Rights Commission’s campaign from last year.
But the campaign can’t hurt, right?
Actually, the dangers that could come with an advertising campaign are two-fold.
First it may well oversimplify a highly complex issue. Identifying and managing elder abuse requires an understanding of the person’s vulnerabilities, their decision-making capacity and ability to consent, the will and preferences of victim and the role of perpetrator in the older person’s life. Abuse happens in the context of family and social networks. And reporting abuse can have consequences for the victim’s quality of life and care.
Consider the complexities of a case where an older person declines to have her grandson reported to police for stealing her money and medication because of her fear of becoming socially isolated. She might even feel responsible for the behaviour having raised the grandson and not want him to have a criminal record.
Secondly, a public campaign can create the illusion government and our institutions have the matter “in hand”. This might slow the opportunity for real change.
Ideally, the campaign will strengthen the argument for better policies, reporting procedures, policing, prosecution and judgements that are aligned. But these ends will also need investment in more research to build better communities that take good care of older people.
Joseph Ibrahim, Professor, Aged Care Medical Research Australian Centre for Evidence Based Aged Care, La Trobe University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Securely Attached –
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A lot of books on attachment theory are quite difficult to read. They’re often either too clinical with too much jargon that can feel like incomprehensible psychobabble, or else too wishy-washy and it starts to sound like a horoscope for psychology enthusiasts.
This one does it better.
The author gives us a clear overview and outline of attachment theory, with minimal jargon and/but clearly defined terms, and—which is a boon for anyone struggling to remember which general attachment pattern is which—color-codes everything consistently along the way. This is one reason that we recommend getting a print copy of the book, not the e-book.
The other reason to invest in the print copy rather than the e-book is the option to use parts of it as a workbook directly—though if preferred, one can simply take the prompts and use them, without writing in the book, of course.
It’s hard to say what the greatest value of this book is because there are two very strong candidates:
- Super-clear and easy explanation of Attachment Theory, in a way that actually makes sense and will stick
- Excellent actually helpful advice on improving how we use the knowledge that we now have of our own attachment patterns and those of others
Bottom line: if you’d like to better understand Attachment Theory and apply it to your life, but have been put off by other presentations of it, this is the most user-friendly, no-BS version that this reviewer has seen.
Click here to check out Securely Attached, and upgrade your relationship(s)!
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GLP-1 Drugs Delay Alcohol’s Effects!
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GLP-1 drugs were designed as antidiabetic drugs, and took over the market as weight loss drugs.
Their usefulness to reduce cravings has been noted to also reduce non-food cravings, including for some addictive substances, and some compulsive behaviors.
See: Can a drug like Ozempic help treat addictions to alcohol, opioids or other substances?
But, there’s more to it than that…
It’s not just about drinking less
Researchers (Dr. Alexandra DiFeliceantonio et al.) have found that GLP-1 agonists such as semaglutide, tirzepatide, and liraglutide slow the rate at which alcohol enters the bloodstream, resulting in delayed (and weaker) intoxicating effects.
What they tested: in a randomized controlled trial, all participants fasted, ate a standardized snack, then consumed an alcoholic drink within 10 minutes. Breath alcohol, glucose, blood pressure, and pulse were then measured repeatedly over the next four hours.
What they found is that those on GLP-1 drugs had slower increases in breath alcohol concentration and consistently reported feeling less intoxicated than those not taking such.
How it works: the current hypothesis is that GLP-1 drugs likely reduce alcohol’s effects by slowing gastric emptying, delaying alcohol absorption, rather than directly affecting the brain. Because alcohol will then still be processed by the liver, it simply means the liver can process it little by little.
This is important, because it means that (so far as the data so far can tell us) it doesn’t run into the same problem as occurs when people take cannabis edibles, think “hmm, I don’t feel it”, and then take more, and then end up overdosing, because everything was just delayed batch-by-batch, rather than slowed down in a continuous process.
You can find the paper itself here: A preliminary study of the physiological and perceptual effects of GLP-1 receptor agonists during alcohol consumption in people with obesity
You may be thinking: “with obesity? Isn’t that protective against alcohol’s effects?”, and the answer is that in the case of adiposity (as opposed to being muscular) there’s a mixed effect that cancels itself out rather; yes, alcohol has a per-kg effect, but a kg of muscle is a lot more helpful metabolically than a kg of fat, which is in most cases more of a metabolic problem than a solution. Still, it cannot be said with certainty that the conclusions will applicable to all people of all body types; more research will be needed to make a definitive declaration about that.
GLP-1 drugs can protect the liver in one more way, too
It’s also known that GLP-1 drugs lower liver levels of an enzyme known by the snappy name of Cyp2e1, which normally breaks alcohol down into acetaldehyde, the highly toxic metabolite responsible for much of alcohol’s liver damage.
You can read more about this, here: GLP-1 receptor agonism results in reduction in hepatic ethanol metabolism
Want to learn more?
Here’s an unusually balanced overview of GLP-1 drugs when it comes to many aspects of life, rather than providing a glowing report or a terrible condemnation:
And if GLP-1 drugs aren’t your thing, then we cover some other approaches for those who wish to drink alcohol and minimize its harmful effects:
How To Make Drinking Less Harmful ← our main feature on such
Take care!
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