Author Archives: Dr Colin Holloway

Why you shouldn’t make a habit of doing a ‘just in case’ wee — and don’t tell your kids to either

Why you shouldn’t make a habit of doing a ‘just in case’ wee — and don’t tell your kids to either

September 20, 2021 3.51pm AEST


  1. Jennifer King Honorary Clinical Lecturer, University of Sydney

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Jennifer King is the chair of the Education Committee of the International Urogynecology Association and state chair of the NSW Continence Foundation. The positions are unpaid.


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A woman looks at a toilet sign in an airport.

We’ve all done done a quick “just in case” wee before heading out or because we’re passing the bathroom. If you’re a parent, you might have also told the kids to “do a wee now so we don’t have to find a toilet later.”

Doing a “just in case” wee isn’t a problem if it’s just occasional and if you have normal bladder function.

But doing it too often, making a lifetime habit of it, can kick off a vicious cycle. You can end up training your bladder to “think” it needs to go when it’s only slightly full. And the problem can worsen over time.

If you’re always ducking to the loo to wee at even the slightest tingling sensation, have a go at resisting that first urge — and consider seeing your GP or a pelvic floor physiotherapist about it.

Read more: Curious Kids: why is urine yellow?

Your bladder can probably hold more than you think

Most bladders are actually capable of holding quite a lot of fluid.

For those with normal bladders (that is, you haven’t been diagnosed as having an overactive or irritable bladder), every day capacity is between 400–600 mls. It should take about two hours for the water you drink to make its way to the bladder.

So if you drink a 600ml bottle of water, it would be perfectly reasonable not to actually need to go to the toilet until a couple of hours later. In reality, however, I know of people who say they drink just a small amount and head off to the bathroom shortly after.

What happens if you get into the ‘just in case’ habit?

To pass urine easily, we need the bladder muscle to contract and the muscles around the urethra and pelvic floor to relax.

This nice, coordinated pattern does not occur nearly as well if there is no real urge to void. You’ll probably be able to squeeze some urine out, but it’s not how the muscles are supposed to work.

The bladder’s response is to spasm and contract more aggressively and inappropriately.

The bladder gets used to holding a certain amount and if you are always emptying at that amount, it gets harder to hold more. The bladder “thinks” it is at capacity, when it is not. You end up with a pattern of uncoordinated emptying.

The good news is most people with a normal bladder can train themselves out of this habit. It’s about learning to recognise the signs and differentiate between a small urge and a real need.

You don’t need to run off at the first urge — have a go at resisting it and see what happens.

Of course, nobody is saying you should hold on until you feel absolutely tortured. If ignoring the first urge is causing real distress, you should talk to your GP or a pelvic floor physiotherapist.

Let your kids go to the toilet when they actually need to

Everyone remembers the kids who wet their pants at school or those who were always in trouble “because they should have gone to the toilet at recess”.

In fact, it’s better just to let kids go to the toilet when they need to, instead of berating them about not having gone at recess or “before we left”.

You can cause more damage (physical and psychological) in the long run if you give kids a hard time about toileting, load it with emotion, or train them into the habit of always going “just in case”. Don’t always prompt them to go to the toilet.

(In some situations, such as with people with dementia, it can be appropriate to prompt people to go to the toilet. But this is done after a reasonable number of hours when there should be a good amount of urine in the bladder. And it is a compromise arrangement where we try to minimise incontinence episodes and patient distress.)

A parent talks to her child.
It’s better just to let kids go to the toilet when they need to, instead of berating them about not having gone at recess or ‘before we left’. Shutterstock

Not everyone has a ‘normal’ bladder

The aim with toilet training is to learn to recognise the sensation of bladder filling and gradually develop the ability to resist bladder emptying until convenient and socially appropriate.

But for some people this is never completely or consistently achieved.

Many people – perhaps 30% of adults and large numbers of children – do not have a normal bladder. Rather, they have an overactive or irritable bladder.

This can make people want to go all the time or cause sudden urgency. They may not always make it to the toilet quickly enough. It can be impossible to prevent bladder leakage. Some people cope by limiting fluids or forever going “just in case”.

As with all bladder problems, it’s more common for women than men and tends to become more troublesome as we age.

Overactive bladders are unlikely to spontaneously improve. A good place to start would be to talk with your GP, a continence nurse or a specialist physiotherapist. These bladders need to be retrained using techniques learned from a specialist physio. Medication can sometimes help.

For most of us, though, overly frequent visits to the loo, or going “just in case” is a habit worth quitting.

Read more: Health Check: how do I tell if I’m dehydrated?

Dry Eyes Afflict Many of Us. Here’s What to Do About It.

Personal Health

From The New York Times.

Dry Eyes Afflict Many of Us. Here’s What to Do About It.

That gritty, itchy feeling in your eyes can arise from many causes, including too much screen time, and eye drops may only make it worse.

Jane E. Brody

By Jane E. BrodySept. 20, 2021, 5:00 a.m. ETLeer en español

I didn’t have to wait until my ninth decade to appreciate how annoying dry eyes can be. And I was flummoxed by the plethora of products on pharmacy shelves that promise relief for a problem that affects about one in five adults. Perhaps you, like me, are among the many who have tried various over-the-counter remedies that didn’t help or sometimes made matters worse.

Dry eye problems become increasingly prevalent with age. But since my mid-30s, I’ve been coping with a mild form of this condition and, despite intermittent visits to health professionals, have gotten only limited relief. With all the “extra” time I had to read for pleasure during the pandemic, the gritty feeling in my chronically dry eyes rendered this diversion anything but pleasant. Other common complaints linked to dry eyes include itching and undue sensitivity to sun and bright lights, all of which I suffer from.

In an online survey published in January, two thirds of respondents reported having symptoms of dry eye, and of those, more than a quarter said their symptoms were made worse by wearing a face mask. But Dr. Ira Udell, a professor of ophthalmology at the Zucker School of Medicine at Hofstra/Northwell, said that while masks may indeed cause ocular discomfort, an association between mask-wearing and dry eye per se is unlikely, given that exhaled moisture when wearing a mask fogs glasses and, if anything, the increased humidity would raise moisture levels around the eyes.

A more likely explanation of those findings is an association between dry eyes and pandemic-related stress. In two studies of veterans, researchers found strong links between dry eye syndrome, post-traumatic stress disorder and depression.

What causes dry eyes?

I’ve recently learned just how complicated it can be to keep my eyes moist and free of irritating dryness, a need made more challenging by an ever-greater reliance on screens for work and play. When people stare at computer screens for hours on end, they blink less often, resulting in tired, distressed and dry eyes.Sign up for the Well Newsletter  Get the best of Well, with the latest on health, fitness and nutrition. Get it in your inbox.

Inadequate lubrication of the ocular surface can also result in blurry vision, a symptom that has repeatedly prompted me to get my vision checked, only to find that my current prescription hasn’t changed even though words on a page are less clear.

Although dry eye problems are most common in people over 50, they’re also increasing among young adults, which experts attribute to the ubiquity of smartphones and computers. Younger people are also more likely to wear contact lenses, prolonged wearing of which may also cause dry eye.

Dry eye is a hallmark symptom of Sjögren’s syndrome and other autoimmune disorders that impair the body’s lubricating tissues. Dry eye also commonly occurs temporarily following cataract surgery; Lasik eye surgery, which reshapes the cornea to improve vision; and blepharoplasty, an operation to correct drooping eyelids.

Some people develop chronically dry eyes because their lids don’t close completely during sleep. If you suspect this may be your problem and you live alone, you might invite a visitor to check your eyes when you’re asleep, Dr. Udell suggested. A cellphone photo would be useful to show to your doctor.

How does the eye stay lubricated?

Think of the tear film that coats and lubricates the eye as a three-layer sandwich, with each layer produced by different glands. The meibomian glands in the upper and lower eyelids create an oily outer layer that stabilizes the film. If the film breaks up too quickly, blurry vision is the likely result. Next are two sets of lacrimal glands that supply the watery tears. Innermost is the mucin layer that attracts water and helps to spread the tear film over the surface of the cornea. Even if the tear supply is adequate, a mucin deficiency can impede wetting of the cornea and damage its surface.

Both the meibomian and lacrimal glands have receptors for the sex hormones, androgen and estrogen, and a decrease in hormone levels likely explains why dry eye problems increase in women at menopause and in men who are treated with anti-androgen therapy for prostate cancer. Indeed, the most common cause of dry eye is evaporation of moisture from the eyes from dysfunction of the meibomian glands that results in instability of the tear film.

Sometimes the attempted solution, like using multiple-use eye drops that contain preservatives, can actually make eye irritation worse. I ended up with chronically red eyes after using such drops, and the problem soon resolved when I switched to single-use lubricants that were preservative-free. While single-dose eye drops are only approved for a one-time use, Dr. Udell said that it’s usually safe to use them for up to two days if you want to cut down on cost and waste, as long as the tip isn’t touched and is covered after each use.

Medications that treat other conditions can interfere with adequate tear production. Common culprits include antihistamines, beta blockers, oral contraceptives, diuretics and drugs used to treat Parkinson’s disease, anxiety disorders, asthma, chronic obstructive pulmonary disease (C.O.P.D.) and abnormal heart rhythms.

Environmental conditions that can exacerbate dry eye problems include smoky or excessively dry air, which can result from indoor heating and air conditioning. Long before the pandemic, I began wearing eyeglasses when outdoors, especially on windy days and always when riding my bicycle, to protect my eyes from dryness and grit. A variety of glasses are available to block out wind, glare and airborne irritants.

If you swim, be sure to wear goggles to prevent salty or chemically treated water from irritating your eyes.

Another practical measure that Dr. Udell emphasized is applying warm compresses to the eyelids morning and night to assist meibomian gland function. I gently wash my eyelids from the nose outward with a warm washcloth every night. Repeat the washcloth cleanse if you wake up in the morning with “sleep in your eyes,” then apply artificial tears.

Use of artificial tears several times a day is essential for most cases of dry eye. Although no product precisely mimics the composition of natural tears, many are helpful if used regularly, Dr. Udell said. He suggested trying various products one at a time to find one that is most effective for you. You could start with a low-cost generic product and, if that doesn’t help, try the brand name version, he said.

However, if over-the-counter remedies and the practical measures described above fail to bring adequate relief, consult an eye specialist. There are prescription products and special glasses that create a high-humidity moisture chamber around the eyes, among other remedies, for severe cases of dry eye.

Jane Brody is the Personal Health columnist, a position she has held since 1976. She has written more than a dozen books including the best sellers “Jane Brody’s Nutrition Book” and “Jane Brody’s Good Food Book.”

Medicinal cannabis to manage chronic pain? We don’t have evidence it works


Medicinal cannabis to manage chronic pain? We don’t have evidence it works

March 23, 2021 5.52am AEDT


  1. Michael Vagg Conjoint Clinical Associate Professor, Deakin University School of Medicine and Specialist Pain Medicine Physician, Deakin University

Disclosure statement

Michael Vagg is currently the Dean of the Faculty of Pain Medicine, Australian and New Zealand College of Anaesthetists. In the last 5 years, payments from pharmaceutical companies for providing educational talks to medical practitioners or other honoraria have constituted less than 0.05% of his gross income. No advisory or marketing advice has been given to the pharmaceutical industry in that time. NPS Medicinewise has paid A/Prof Vagg for consultative services to develop educational materials regarding prescription of pain medications.


Deakin University

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As a pain specialist, I often have patients asking me whether they should try medicinal cannabis. There’s a common perception it can be an effective way to manage chronic pain.

But two expert groups have recently recommended against medicinal cannabis for people suffering persistent non-cancer pain.

The International Association for the Study of Pain published a position statement last week after its presidential taskforce summarised the evidence on the topic.

And yesterday the Faculty of Pain Medicine of the Australian and New Zealand College of Anaesthetists published guidance for health practitioners in the form of a Choosing Wisely recommendation. (Choosing Wisely is an initiative of NPS Medicinewise which aims to highlight low-value health care.)

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Many in the community would see this recommendation as controversial. So let’s take a look at some of the commonly held misconceptions about medicinal cannabis and chronic pain.

Myth #1: evidence shows cannabis products are effective for chronic pain

Evidence from randomised controlled trials is critically lacking when it comes to medicinal cannabis products for chronic pain.

While some studies have looked at tetrahydrocannabinol (THC, the main psychoactive component of cannabis) or a combination of THC and cannabidiol (CBD), there isn’t a single published randomised controlled trial of a CBD-only product for chronic pain of any type. Australian medicinal cannabis products are often CBD-only.

This means we can’t even judge whether the claims that medicinal cannabis can alleviate pain might be true. The results of THC-containing products in clinical trials don’t give a reliable picture one way or the other because they involve too few participants, have major technical flaws in design, or have been judged to have an unacceptably high risk of producing biased results.

The International Association for the Study of Pain taskforce looked at all the available research published in peer-reviewed journals on the use of medicinal cannabis for pain management, from preclinical studies to human trials.

They concluded overall the studies’ “quality, rigour, and transparency of reporting” of benefits and harms needs to be improved across the board. We would require higher quality data, for example through randomised controlled trials, to determine the safety and efficacy of using medicinal cannabis for pain.

In the polite and understated world of academic medicine, this is about as big a smackdown as it gets. The authors are essentially saying most of the studies are too poorly done, using unsuitable methods, to give any answer to the most basic question of whether medicinal cannabis helps with pain.

Read more: Medicinal cannabis users in Victoria could soon be allowed to drive with THC in their system. Is it safe?

Myth #2: cannabis products should be provided as a ‘last resort’

A doctor has the right to prescribe any drug they think may be effective for an individual patient based on nothing more than their clinical judgement. We do this relatively frequently, especially for chronic pain.

This is ethical if we have a scientific reason to believe the drug may be helpful. But for patients with chronic pain, we have little reason to believe medicinal cannabis offers any sustained benefit.

A further challenge to the ethical provision of cannabis products as a “last resort” is the fact they’re among the most expensive pharmaceutical products available to chronic pain patients, many of whom have very modest incomes. The only party likely to benefit is the manufacturer.

A senior man talks with a doctor.
Many people who experience chronic pain believe medicinal cannabis could help. Shutterstock

Myth #3: medical cannabis may help with the opioid crisis

There’s a consensus that much of the current use of opioid analgesics to manage chronic non-cancer pain in Australia may be of limited value.

Proponents of medicinal cannabis have suggested it may hold promise as a potential solution to this problem. While this idea has some appeal, the balance of the evidence points the other way.

Read more: 1 in 10 women with endometriosis report using cannabis to ease their pain

Data collected from Australia and New Zealand shows participation in best-practice multidisciplinary pain care, as provided by a specialist pain clinic, results in half of pain patients being able to reduce their opioids by at least 50%, with improved quality of life.

People wanting an alternative to opioid treatment for persistent pain will do best if they seek out treatment from a professional team of experts, rather than substituting cannabis for opioids.

It could be harmful

The International Association for the Study of Pain taskforce identified general known risks from using cannabis, such as in recreational settings. But no studies have characterised the way the body handles prescribed or over-the-counter medicinal cannabis products.

The TGA guidance document on medicinal cannabis notes basic research on how the drugs interact with both the body and other medications — known as pharmacokinetic and pharmacodynamic studies — is not available. Without this information, we can’t answer important questions about the safety of medicinal cannabis.

A collection of white round pills.
Medicinal cannabis isn’t the solution to the opioid crisis. Shutterstock

Medicinal cannabis products may have a role in the management of other conditions, such as relieving chemotherapy-induced nausea, or treating childhood epilepsy. The evidence around those conditions seems to be more convincing than the studies for persistent pain, though I’m not an expert in either field.

Despite the lack of evidence to support the use of medicinal cannabis for chronic pain, the legislation around medicinal cannabis in Australia continues to become more permissive.

It will be legal to sell low-dose CBD products over the counter from June this year, if they meet the very minimal requirements to be listed by the Therapeutic Goods Administration (TGA).

Meanwhile, Tasmania is set to become the last Australian state to allow GPs to prescribe medicinal cannabis from July.

Read more: Weed withdrawal: More than half of people using medical cannabis for pain experience withdrawal symptoms

The Faculty of Pain Medicine has a track record of advocacy for pain patients. We led the process that resulted in the first ever National Pain Strategy a decade ago, and were a founding partner of Painaustralia as an ongoing policy voice.

If medicinal cannabis was truly as potentially valuable as often claimed, we would be the loudest voice in favour of wider access. The weight of evidence points us away from this conclusion.

Why are we seeing more COVID cases in fully vaccinated people? An expert explains

Naron Sangnak/EPA/AAP

Why are we seeing more COVID cases in fully vaccinated people? An expert explains

September 8, 2021 4.57pm AEST


  1. Nathan Bartlett Associate Professor, School of Biomedical Sciences and Pharmacy, University of Newcastle

Disclosure statement

Nathan Bartlett does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.


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Many people are worried about reports of “breakthrough” COVID-19 infections overseas, from places like Israel and the United States.

A breakthrough infection is when someone tests positive for COVID after being fully vaccinated, regardless of symptoms.

The good news is most breakthrough infections usually result in mild symptoms or none at all, which shows us that vaccines are doing exactly what they’re supposed to do — protecting us from severe disease and death. Vaccines aren’t designed to protect us from getting infected at all (known as “sterilising immunity”).

People with breakthrough infections can go on to infect others. Preliminary evidence indicates immunised people can have high levels of virus in the nose, potentially as high as unvaccinated people.

However, if you’re vaccinated you’ll clear the virus more quickly, reducing the length of time you’re infectious and can pass the virus on.

Here’s why breakthrough cases are happening, and why you shouldn’t worry too much.

Waning immunity

Two studies from the United Kingdom suggest the immunity we get from COVID vaccines wanes over time, after about four to six months.

While the more-infectious Delta variant continues to circulate, waning immunity will lead to more breakthrough infections.

But the reduction isn’t large currently. Vaccine effectiveness is very high to begin with, so incremental reductions due to waning won’t have a significant effect on protection for some time

Israeli data shows some vaccinated people are becoming ill with COVID. But we need to keep in mind Israel’s vaccine rollout began in December 2020, and the majority of the population were vaccinated in early 2021. Most are now past six months since being fully vaccinated.

Given most people in Israel are vaccinated, many COVID cases in hospital are vaccinated. However, the majority (87%) of hospitalised cases are 60 or older. This highlights what’s known about adaptive immunity and vaccine protection — it declines with age.

Therefore we’d expect vulnerable groups like the elderly to be the first at risk of disease as immunity wanes, as will people whose immune systems are compromised. Managing this as we adjust to living with COVID will be an ongoing challenge for all countries.

What would be concerning is if we started seeing a big increase in fully vaccinated people getting really sick and dying — but that’s not happening.

Globally, the vast majority of people with severe COVID are unvaccinated.

Read more: COVID cases are rising in highly vaccinated Israel. But it doesn’t mean Australia should give up and ‘live with’ the virus

We’ll probably need booster doses

Waning immunity means booster doses will likely be needed to top up protection, at least for the next couple of years while the virus continues to circulate at such high levels.

Our currently approved vaccines were modelled on the original strain of the virus isolated in Wuhan, not the Delta variant, which is currently dominant across most of the world. This imperfect match between vaccine and virus means the level of protection against Delta is just a little lower.

Read more: What’s the Mu variant? And will we keep seeing more concerning variants?

Because the level of effectiveness is so high to begin with, this small reduction is negligible in the short term. But the effects of waning over time may lead to breakthrough infections appearing sooner.

mRNA vaccines in particular, like Pfizer’s and Moderna’s, can be efficiently updated to target prevalent variants, in this case Delta. So, a third immunisation based on Delta will “tweak”, as well as boost, existing immunity to an even higher starting point for longer-lasting protection.

We could see different variants become endemic in different countries. One example might be the Mu variant, currently dominant in Colombia. We might be able to match vaccines to whichever variant is circulating in specific areas.

The dose makes the poison

Your level of exposure to the virus is likely another reason for breakthrough infections.

If you’re fully vaccinated and have merely fleeting contact with a positive case, you likely won’t breathe in much virus and therefore are unlikely to develop symptomatic infection.

But if you’re in the same room as a positive case for a long period of time, you may breathe in a huge amount of virus. This makes it harder for your immune system to fight off.

This may be one reason we’re seeing some health-care workers get breakthrough infections, because they’re being exposed to high viral loads. They could be a priority for booster doses.

Might unvaccinated kids be playing a role?

It’s unclear if children are contributing to breakthrough infections.

Vaccines aren’t approved for young children yet (aged under 12), so we’re seeing increasing cases in kids relative to older people. Early studies, before the rise of Delta, indicated children didn’t significantly contribute to transmission.

More recent studies in populations with vaccinated adults, and where Delta is the dominant virus, have suggested children might contribute to transmission. This requires further investigation, but it’s possible that if you’re living with an unvaccinated child who contracts COVID, you’re likely to be exposed for many, many hours of the day, hence you’ll breathe in a large amount of virus.

The larger the viral dose, the more likely you’ll get a breakthrough infection.

Potentially slowing the number of breakthrough infections is one reason to vaccinate 12 to 15 year olds, and younger children in the future, if ongoing trials prove they’re safe and effective in this age group. Another is to protect kids themselves, and to get closer to herd immunity (if it’s achievable).

Read more: High priority: why we must vaccinate children aged 12 and over now

A silver lining

Breakthrough infections likely confer extra protection for people who’ve been fully vaccinated — almost like a booster dose.

We don’t have solid real-world data on this yet, but it isn’t surprising as it’s how our immune system works. Infection will re-expose the immune system to the virus’ spike protein and boost antibodies against the spike.

However, it’s never advisable to get COVID, because you could get very sick or die. Extra protection is just a silver lining if you do get a breakthrough infection.

As COVID becomes an endemic disease, meaning it settles into the human population, we’ll need to keep a constant eye on the interaction between vaccines and the virus.

The virus may start to burn out, but it’s also possible it might continually evolve and evade vaccines, like the flu does.

Read more: How will Delta evolve? Here’s what the theory tells us

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Dementia: how to make sense of the link with people who struggle to hear over background noise

Dementia: how to make sense of the link with people who struggle to hear over background noise

August 25, 2021 2.24am AEST


  1. Thomas Littlejohns Senior Epidemiologist, University of Oxford

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Thomas Littlejohns does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.


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Old woman looking isolated in a public place
‘I can’t hear what anyone is saying.’ Christian Langballe/Unsplash, CC BY-SA

The number of people living with dementia is projected to treble from 50 to 150 million worldwide by 2050. Although there’s currently no cure for the condition, researchers are continuing to learn about how people can reduce their risk through making lifestyle changes (such as exercising more or quitting smoking) and managing health issues (including diabetes and hypertension).

Hearing loss may also be a potential target for preventing dementia. Studies show that hearing impairment is linked to a greater risk of dementia – and that managing hearing problems early may be key to reducing risk.

Our recent paper confirmed these findings, while focusing on an area that has received less attention: people who struggle to pick out speech in noisy environments. The hearing of people in this category is often deemed “normal” in traditional tests, but we were able to show with a large cohort for the first time that they too are at greater risk of going on to develop dementia.

Speech-in-noise impairments

Previous studies looking at the link between hearing impairment and dementia have used a method of hearing assessment known as pure-tone audiometry to measure participants’ hearing. This is usually the gold standard to testing a person’s hearing, and works by measuring a person’s ability to detect sounds – specifically tones – in a quiet environment.

However, many people whose test shows that they have “normal” hearing can still have issues hearing when different assessment methods are used. This includes those who struggle to pick out speech in noisy places, which is known as speech-in-noise hearing.

Speech-in-noise hearing is akin to the kind of hearing we do in everyday life. To find out whether speech-in-noise hearing impairment was similarly linked with increased dementia risk, we looked at data from a total of 82,039 people aged 60 or over.

Participants’ speech-in-noise hearing was measured using what’s known as a digits triplet test. This involved asking participants to identify three spoken numbers presented in varying levels of background noise. Based on their performance, we then grouped participants into three categories: “normal”, “insufficient” and “poor”.

Participants were followed up over 11 years to see who developed dementia. A total of 1,285 people from the 82,039 total received a dementia diagnosis over that period. We found those with insufficient and poor speech-in-noise hearing had a 61% and 91% greater risk of developing dementia compared to those with normal speech-in-noise hearing. The dementia risk of those with poor speech-in-noise hearing was virtually identical to what previous studies found about people with hearing impairments that are picked up by pure-tone audiometry.

Liverpool Street Station in London as crowds of people rush through.
Struggling to hear an announcement in a busy place is one sign of poor speech-in-noise hearing. Keith Gentry/ Shutterstock

Finding the cause

There are several suggestions for why there is a link between hearing impairment and dementia. One possibility is that impaired hearing increases the likelihood of other risk factors for dementia, such as social isolation or depression. But we found little evidence to support this, with depressive symptoms and social isolation only explaining a small percentage (less than 7%) of the association between speech-in-noise hearing impairment and dementia.

It’s also possible that our findings (and those from other studies) might be detecting an association between dementia and hearing impairment when in fact both are caused by something else altogether. While we took a range of factors into account in our analyses – such as age, education level and socioeconomic status – we can’t rule out the possibility that other factors might be involved that we didn’t look at.

The other possibility is that dementia causes hearing impairment. This might seem an unusual explanation, as in our study dementia was diagnosed after hearing was measured. But the pathology of dementia typically develops years before a person receives a diagnosis. It often occurs before memory problems and other cognitive issues become apparent. This “pre-clinical” pathology results in other symptoms – such as weight loss – and could potentially cause issues with hearing.

We explored this possibility in two ways. The first was to see whether hearing impairment was associated with dementia diagnosed a long time after hearing was measured. This is because pre-clinical symptoms are more likely to manifest close to a diagnosis.

When looking at dementia diagnosed nine to 11 years after the hearing test, insufficient and poor speech-in-noise hearing was associated with a 54% and 85% increased risk of dementia. This is similar to the main findings of our study. You would have expected this group to have a lower correlation with hearing problems if pre-clinical dementia was causing them.

Our second approach was to only include people who described their health as “good”, “very good” or “excellent” at the time hearing was measured. This is because worse health might reflect the early pre-clinical symptoms of dementia. People with worse health are also probably more likely to have hearing problems.

Again, the number of people in this group who went on to develop dementia after being identified with a hearing impairment was similar to those of our initial findings. Had dementia been causing the impairment, you might have expected a disproportionately high number of those who went on to develop dementia to have been the ones already reporting generally poor health.

In both cases, this is tentative evidence that dementia might not be causing hearing impairment. But even so, some early pre-clinical symptoms of dementia can manifest decades before a diagnosis. Studies which diagnose dementia 15 or even 20 years later are necessary to disentangle these complex relationships further.

While our findings are preliminary, they add to the growing body of evidence that hearing impairment is a promising target for preventing dementia. In fact, it’s thought that if hearing impairment is indeed a cause of dementia, addressing it could prevent 8% of dementia cases in instances where dementia is not otherwise evident. This statistic is based on pure-tone audiometry hearing – so it could very well be higher when considering issues with speech-in-noise hearing.

Can you transmit allergies?

Don’t fool around with these nuts

After eating Brazil nuts 2-3 hours prior, a man had unprotected intercourse with his 20-year-old partner who had a documented Brazil nut allergy. The woman developed urticaria, angioedema, and dyspnea. To figure out the cause of this hypersensitivity reaction, UK researchers did a skin prick test in the woman using the boyfriend’s semen both before and after eating Brazil nuts.

Apparently, some nut protein got into the semen. 

“We believe this to be the first case of a sexually transmitted allergic reaction,” the researchers wrote in the Journal of Investigational Allergology and Clinical Immunology. Of note, Brazil nuts are the second most frequent nut allergy in the United Kingdom. Unfortunately for science, the couple broke up before the investigators could confirm the results.

“Our demonstration of an allergenic Brazil nut protein in the semen clearly proves the ability of such protein(s) to resist digestion. Additionally, to enter the semen, the protein would require circulation in the blood to the prostate or other reproductive organ.”

Notably, severe allergic reactions have been demonstrated in those with crustacean allergy following exposure from kissing. Also, penicillin exposure leading to allergic reaction could occur secondary to intercourse, per the literature.

The moral of this study? If you have food allergies, you might want to find out what your partner recently ate, before you get too close

Supporting menstrual health in Australia means more than just throwing pads at the problem

Supporting menstrual health in Australia means more than just throwing pads at the problem

August 27, 2021 1.02pm AEST


  1. Erin C. Hunter Lecturer in Global Health, University of Sydney
  2. Julie Hennegan Senior Research Fellow, Burnet Institute

Disclosure statement

Erin C. Hunter has received funding for research on menstrual health. She has conducted menstrual health research funded by the Bill & Melinda Gates Foundation, Grand Challenges Canada, and The Johns Hopkins Center for Qualitative Studies in Health and Medicine. She is currently an investigator on a National Health and Medical Research Council grant to study menstrual health in Myanmar.

Julie Hennegan has received funding for research on menstrual health. This has included from foundations (The Case for Her, Bill & Melinda Gates Foundation) and research councils (she is currently an investigator on a National Health and Medical Research Council grant developing a menstrual health intervention in Myanmar). She led the development of the definition of Menstrual Health as part of the Terminology Action Group of the Global Menstrual Collective.


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Menstruation has recently had a bit of a moment in Australia.

The Victorian and South Australian governments are now providing free pads and tampons in government schools, while New South Wales is trialling a pilot program to do the same.

Attention to menstruation is exciting and long overdue. But hurried efforts to provide free pads are not enough, particularly after decades of policy neglect.

To truly meet the needs of women, adolescent girls, and all people who menstruate, we must ask smart questions and develop evidence-based strategies for the long term.

Get your news from people who know what they’re talking about.

What is menstrual health and how do we achieve it?

This year, a collaboration of global stakeholders and experts defined menstrual health as a state of complete physical, mental and social well-being in relation to the menstrual cycle.

The authors also shed light on the breadth of menstrual health needs. These extend well beyond access to pads, and highlight a number of things we need to consider if we’re going to better support menstrual health in Australia.

1. Information about the menstrual cycle

Knowledge about menstrual biology, reproduction and self-care practices is important. Understanding the body helps prevent distress and facilitates informed decision-making. This might include choice of menstrual product or decisions to seek medical support for period-related difficulties.

Studies in high-income countries have found women and girls don’t have enough information about menstruation, and research on menstrual disorders in Australia has found deficits in menstrual health literacy.

So we must ensure adolescents have comprehensive and timely education about menstruation in schools to promote body literacy and support their menstrual health.

A teenage girl sits looking out a window.
Research has found women and girls don’t necessarily have all the information they need when it comes to menstruation. Shutterstock

2. Materials and facilities to care for the body

Beyond having enough products to manage a period, menstrual health requires supportive spaces to change products, dispose of single-use materials (for example, pads and tampons) or wash reusable products (for example, menstrual cups). Spaces need to be comfortable and private.

In high-income countries, little attention has been given to whether school and workplace facilities are adequately meeting these needs. This is especially relevant as reusable products such as menstrual underwear and cups are growing in popularity.

3. Diagnosis, care and treatments for discomforts and disorders

Pleasingly, we’ve seen menstrual health research and action focusing on disorders, with endometriosis receiving increased investment in the most recent federal budget.

But 92% of adolescents and young women in Australia report painful periods.

We need to see comprehensive policy that acknowledges the breadth of menstrual needs, and the varied levels of pain and discomfort associated with menstruation.

Read more: I have painful periods, could it be endometriosis?

4. Positive and respectful environments

Menstruation continues to be stigmatised around the world. Social pressure to hide any sign of menstruation can dissuade girls and women from talking about their experiences or seeking support and advice. This can harm well-being.

Family members, education institutions, workplaces and government policies all have a role to play in creating environments that support those who menstruate.

For example, freedom to visit the toilet during the school day or to work flexibly around period pain can shape experiences of menstruation.

What’s the impact of unmet menstrual health needs?

A survey of young people in New Zealand found 8% reported missing school due to a lack of menstrual products.

A review of multiple studies estimated 12% of young women in high-income countries have missed school or university because of period pain.

We know from research in low-, middle-, and high-income countries there are a variety of other consequences of unmet menstrual health needs for physical, mental and social well-being.

But we have more to learn about the magnitude of these issues across populations and sub-groups.

Read more: Imagine having your period and no money for pads or tampons. Would you still go to school?

Providing free menstrual products may seem like a “silver bullet”. But evidence from low- and middle-income countries has shown providing such products is not enough to improve menstrual health.

This is also likely to be the case in high-income countries like Australia where stigma and inadequate education around menstruation remain challenges.

A woman holds a menstrual cup and a tampon.
Pads and tampons are no longer the only way to manage periods. Shutterstock

What are we overlooking?

A narrow focus on providing pads and tampons also risks suppressing menstrual product choice, and overlooks opportunities to support more environmentally friendly options.

Policies in Australia focus on providing single-use products, which are not very good for the environment. A menstruating person will use thousands of disposable pads and tampons over their lifetime — a large proportion of which is plastic waste.

Technologies such as menstrual underwear, reusable pads and menstrual cups present environmentally and economically sustainable alternatives. The median cost of a menstrual cup is A$32 and it can be used for up to ten years: that’s just 25 cents per period.

Australian adolescents’ feelings about reusable products remain largely unexplored. If research shows they’re receptive to these options, funding could be directed accordingly.

For example, installing wash basins or toilet hoses inside toilet cubicles in schools could facilitate the use of menstrual cups.

Read more: It’s time to teach the whole story about ovulation and its place in the menstrual cycle

Menstruation matters

To inform effective policy responses, we need robust research exploring menstrual health needs in Australia and the extent to which these contribute to broader health and education outcomes.

And if we are to sustain the support of governments over the long term, we need evidence of what works. We must invest in developing effective responses and commit to evaluating the effects of our policies in supporting girls, women and all people who menstruate.

Depression and Osteoporosis

Depression and Osteoporosis

This is another article by Professor John Studd. See his CV in my last Blog – Dracula Depression.

Download this article as a PDF (63Kb)
Published in ‘Climateric’. 2010

“PROFOX” – The post HRT nightmare

The imaginary hybrid drug PROFOX is an anxious prediction of a therapeutic disaster for post menopausal women who need treatment for low bone density, depression , pelvic atrophy and vasomotor symptoms but are denied estrogens.

Physicians and psychiatrists have been slow to accept the clear benefits of estrogen therapy in the treatment of osteoporosis and depression. Is it an honest fear of side effects, ignorance of hormone therapy, misinterpretation of the data or simply a territorial hold on the condition which then condemns women to sub optimal therapy?

Although estrogens have been proven to prevent fractures in a mixed risk population and that the benefits on bone density and histology are dose dependant it has been relegated to a treatment to be used if others fail or if the woman has severe menopausal symptoms. This protection from estrogens effects not only the skeleton but also the intervertebral discs which make up one quarter of the length of the spinal column. This latter benefit is not produced by bisphosphanates. This failure of physicians to familiarise themselves with estrogen therapy has, in their minds, been justified by the results of the WHI study and by the regulatory bodies who have advised that estrogen should not be first choice therapy for osteoporosis. But in reality the physicians objections to estrogen therapy antedated the WHI study by many years. Specialists are a product of their training which for non gynaecologists does not include the subtleties of the use , the dose and route of various estrogens , gestogens and occasionally androgens.

Updated information and interpretation of the WHI study indicates that HRT, particularly estrogen alone, is both safe and protective in the younger postmenopausal woman below the age of 60. Such therapy is associated with fewer fractures , less colon cancer , fewer heart attacks , possibly less breast cancer and certainly fewer deaths. It should, in the minds of many workers, be first line therapy in this situation. However, Fosamax Once Weekly is an inexpensive alternative recommended by NICE as first line therapy and preferred by physicians. It produces lesser skeletal and systemic benefit than estrogens but it does not confuse the medical attendant with hormonal side effects such as bleeding, mastalgia and occasional PMS symptoms. These are problems that can be dealt with by any competent general practitioner but have not been learned by specialist bone physicians and rheumatologists who also seem to be complacent about considerable long term side effects of bisphosphanates.

A similar ‘turf war’ occurs with the commonplace depression in perimenopausal women. These women with estrogen responsive depression often have a history of postnatal depression and premenstrual depression which have all been shown to be effectively treated by transdermal estrogens in good controlled trials in the most prestigious journals . It is therefore surprising that none of these studies have been repeated by those mostly responsible for the treatment of depression in women. This neglect is either due to the unlikely belief that these studies are perfect or because psychiatrists and the pharmaceutical industry do not want to show the benefits or even the superiority of estrogens. For example there is only one placebo controlled study demonstrating that transdermal estrogens are effective in treating severe premenstrual depression by suppressing ovulation but there are now 50 similar studies showing that SSRIs are useful. Why should the industry fund studies that reveal that their high profit in patent drug is less effective than the much less profitable estrogens?

Psychiatrists almost invariably refuse to accept these data relying upon psycho therapy , SSRI’s and even ECT particularly in the private sector. Once again it is to the disadvantage of the women that psychiatrists have not chosen to become aware of this modality of treatment. It is commonplace to see women with perimenopausal depression who have been taking many mood stabilizing drugs for many years .They claim to have been last well during their last pregnancy after which they started or recommenced antidepressants for post natal depression , later pre menstrual depression and climacteric depression. It is difficult to obtain precise data but antidepressants are now used by about 30% percent of women in the UK and there is even a move to use this drug for the treatment of vasomotor symptoms. It is barely effective but it is becoming a new indication for SSRI therapy.

The nightmare for the future is that postmenopausal women with hot flushes, depression , sexual problems and low bone density, who need estrogens perhaps with testosterone, will be given a SSRI and bisphosphanate combination . PROFOX, a Frankenstein combination of PROzac and FOsamaX . As these two drugs are now available as cheap generics they are already being prescribed together. Unfortunately this warning of a single preparation is not a fanciful aberration as we already have close to the market a combination of a SERM for osteoporosis combined with oestrogens to prevent the symptoms of oestrogen deficiency. This was a joke comment at a British Menopause Society debate 10 years ago but has now become a reality. Unless the regulatory authorities consider the current safety data in the under 60s and modify their resistance to HRT the spectre of PROFOX will be upon us. It is a vision of the future which must be avoided.

Dracula Depression

Dracula Depression

This article below appeared on Dr John Studd’s web site recently. ( A look at Dr Studd’s CV would show that he is one of the worlds foremost experts on womens health and hormones’. He discusses a recent artilcle in a medical journal by a psychiatrist writing about the treatment of Depression in women, and their hormones.

Here is his Biography:


Professor John Studd, DSc,MD,FRCOG was Consultant Gynaecologist at the Chelsea & Westminster Hospital, London and also Professor of Gynaecology at Imperial College. He qualified in 1962 and has worked and trained in Birmingham. Zimbabwe and London. He was Consultant Gynaecologist in Salisbury, Rhodesia and Consultant and Senior Lecturer at the University of Nottingham and moved to London in 1974 as Consultant Obstetrician and Gynaecologist at King’s College Hospital. Six years ago he was invited to join the staff at the new Chelsea & Westminster Hospital, London.

His early research was on chronic renal disease and high blood pressure in pregnancy (MD thesis) but later started the first menopause clinic in the county in Birmingham in 1969. This hormone treatment for the menopause was so controversial at that time that the clinic was closed down for three months following protests from the BMA. However, the optimism placed in HRT has been confirmed and John Studd has continued to work on specific treatments for menopausal symptoms. He pioneered the sequential oestrogen/progestogen treatment and also the continuous combined oestrogen/progestogen non-bleeding treatment. He has championed the use of hormone implants for women with osteoporosis or with severe depressive or sexual problems after the menopause and as an almost routine route of HRT after hysterectomy.

He first described the use of oestrogen patches and oestrogen implants for the treatment of severe PMS and runs a PMS/Menopause clinic at the Chelsea & Westminster Hospital, the Lister Hospital and the Wellington Hospital.

He is also shows the efficacy of moderately high dose transdermal oestrogens for the treatment of hormone responsive depression in women, particularly post-natal depression, pre-menstrual depression, menopausal depression and post-hysterectomy depression. He has a D.Sc. for 25 years of published work on oestrogen therapy in women. He has written more than 500 scientific articles and written or edited more than 25 post-graduate books on gynaecology and realises the he needs to write one for the public. This is much more challenging.

He is Founder and Vice-President of the National Osteoporosis Society and has been a Council Member of the Royal College of Obstetricians and Gynaecologists for 12 years and a Past-President of the Section of Obstetrics and Gynaecology at the Royal Society of Medicine. In 2005-2007 Professor Studd was Chairman of the British Menopause Society.


Dr O has two items in The Obstetrician & Gynaecologist, which confirm my belief that oestrogen to psychiatrists is like garlic to Dracula. It is equally illogical. It is unbelievable that for an article on Postnatal Depression, oestrogen has a brief last paragraph footnote informing that oestrogen can act like an antidepressant by the effect upon the dopaminergic and serontonergic receptors. Indeed it does and for this and other logical reasons as well as scientific and clinical evidence that should be used in those conditions of depression in women related to changes in oestrogen levels. These will include premenstrual depression, postnatal depression and peri-menopausal depression. These have all been shown in double blind trials to be responsive, greater than placebo to transdermal oestrogens, yet the original Lancet paper showing the beneficial effect of this on postnatal depression is not featured in the text or references although the co-authors were psychiatrists, Dr Alan Gregoire and the distinguished expert on postnatal depression the late professor Chani Kumar .It is bad enough that these studies have not been repeated by those responsible for the care of depression i.e. psychiatrists but the refusal to reference and discuss such a paper is intolerable.

There is good evidence that postnatal depression, premenstrual depression and peri-menopausal depression confirm the same vulnerable women and it is a commonplace experience that depressed 45-year-old women will say that they were last well when they were last pregnant 10+ years ago. They then developed postnatal depression and were put on antidepressants. When the periods returned they developed a cyclical depression and towards the menopause the depression became less cyclical so they no longer even have 7 good days a week but every day as the depression is now continuous.

The tragedy is that these women were given antidepressants of doubtful value and certain side effects at the time of their postnatal depression. Over the years they then suffer ineffective multi-drug therapy frequently with ECT (particularly in the private sector). At this stage it is difficult for women to come off these powerful drugs, which they probably shouldn’t have had in the first place. It is true that women with postnatal depression and other types of hormone responsive depression do not have different hormone levels than those without depression. Nobody ever said that they did. It is simply a response to changes of oestrogen and no doubt progesterone in women, who, for some reason, are biochemically vulnerable to these hormonal changes.

The diagnosis of reproductive depression is not based upon blood tests but on the history relating the current depression to the history of being in good mood during pregnancy followed by postnatal depression. There is also a history of previous premenstrual depression and perhaps the history of menstrual headaches is a further clue to the cyclical and endocrinological basis for this condition.

I am very pleased that Dr. O reports that the article most read by psychiatrists last month was ‘Oestrogen relieves psychotic symptoms in women with schizophrenia’. This has of course been known for more than ten years. I am not reassured that psychiatrists have an interest in this but I would be more impressed if they actually used oestrogens for such an indication. But they do not. Similarly psychiatrists must learn how to use oestrogens for certain sorts of depression in women as an effective safe alternative to their usual armamentarium. It would surprise them to discover how frequently “bipolar depression” disappears once the cyclical mood changes of PMS are ablated by transdermal estrogens. In reality the psychiatrist’s dismissal of the evidence and refusal to study the issue further is merely a turf war resulting from their inadequate knowledge of the basic practicalities of hormone therapy.

How does COVID affect the brain? Two neuroscientists explain


How does COVID affect the brain? Two neuroscientists explain

August 11, 2021 6.14am AEST


  1. Trevor Kilpatrick Professor, Neurologist and Clinical Director, Florey Institute of Neuroscience and Mental Health
  2. Steven Petrou Professor and Director, Florey Institute of Neuroscience and Mental Health

Disclosure statement

Steven Petrou is an equity holder and paid consultant of Praxis Precision Medicine, though the company is not currently doing any work that relates to COVID-19. He receives funding from the Australian Government’s Medical Research Future Fund and Praxis Precision Medicines.

Trevor Kilpatrick does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.


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Scientists are becoming more and more concerned with the emergence of a syndrome termed “long COVID”, where a significant percentage of sufferers of COVID-19 experience long-lasting symptoms.

Studies suggest symptoms remain for approximately 524% of confirmed COVID cases, at least three to four months after infection.

The risk of long COVID is no longer thought to be directly linked with either age or the initial severity of the COVID illness. So younger people, and people with initially mild COVID, can still develop long-COVID symptoms.

Some long-COVID symptoms begin quickly and persist, whereas others appear well after the initial infection has passed.

Symptoms include extreme fatigue and ongoing breathing complications.

What particularly concerns us as neuroscientists is that many long COVID sufferers report difficulties with attention and planning — known as “brain fog”.

So how does COVID affect the brain? Here’s what we know so far.

How does the virus get to our brains?

There’s evidence connecting respiratory viruses, including influenza, with brain dysfunction. In records of the 1918 Spanish flu pandemic, reports abound of dementia, cognitive decline, and difficulties with movement and sleep.

Evidence from the SARS outbreak in 2002 and the MERS outbreak in 2012 suggest these infections caused roughly 15-20% of recovered people to experience depression, anxiety, memory difficulties and fatigue.

There’s no conclusive evidence the SARS-CoV-2 virus, which causes COVID, can penetrate the blood brain barrier, which usually protects the brain from large and dangerous blood-borne molecules entering from the bloodstream.

But there’s data suggesting it may “hitchhike” into the brain by way of nerves that connect our noses to our brains.

Researchers suspect this because in many infected adults, the genetic material of the virus was found in the part of the nose that initiates the process of smell — coinciding with the loss of smell experienced by people with COVID.

How does COVID damage the brain?

These nasal sensory cells connect to an area of the brain known as the “limbic system”, which is involved in emotion, learning and memory.

In a UK-based study released as a pre-print online in June, researchers compared brain images taken of people before and after exposure to COVID. They showed parts of the limbic system had decreased in size compared to people not infected. This could signal a future vulnerability to brain diseases and may play a role in the emergence of long-COVID symptoms.

COVID could also indirectly affect the brain. The virus can damage blood vessels and cause either bleeding or blockages resulting in the disruption of blood, oxygen, or nutrient supply to the brain, particularly to areas responsible for problem solving.

The virus also activates the immune system, and in some people, this triggers the production of toxic molecules which can reduce brain function.

Although research on this is still emerging, the effects of COVID on nerves that control gut function should also be considered. This may impact digestion and the health and composition of gut bacteria, which are known to influence the function of the brain.

The virus could also compromise the function of the pituitary gland. The pituitary gland, often known as the “master gland”, regulates hormone production. This includes cortisol, which governs our response to stress. When cortisol is deficient, this may contribute to long-term fatigue.

This was a recognised phenomenon in patients who were diagnosed with SARS, and in a disturbing parallel with COVID, people’s symptoms continued for up to one year after infection.

Given the already significant contribution of brain disorders to the global burden of disability, the potential impact of long COVID on public health is enormous.

There are major unanswered questions about long COVID which require investigating, including how the disease takes hold, what the risk factors might be and the range of outcomes, as well as the best way to treat it.

It’s crucial we begin to understand what causes the wide variation in symptoms. This could be many factors, including the viral strain, severity of the infection, the effect of pre-existing disease, age and vaccination status, or even the physical and psychological supports provided from the start of the disease.

While there are many questions about long COVID, there’s certainty about one thing: we need to continue doing everything we can to prevent escalating COVID cases, including getting vaccinated as soon as you’re eligible.