Doctors must now prescribe drugs using their chemical name, not brand names. That’s good news for patients



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Matthew Grant, Monash University

From today (February 1), when you receive a prescription in Australia, it will list the name of the medication’s active ingredient rather than the brand name. So, for example, instead of receiving a prescription for Ventolin, your script will say “salbutamol”.

This national legislation change, called active ingredient prescribing, is long overdue for Australian health care.

Using the name of the drug — instead of the brand name, of which there are often many — will simplify how we talk about and use medications.

This could have a range of benefits, including fewer medication errors by both doctors and patients.

What is an active ingredient?

The active ingredient describes the main chemical compound in the medicine that affects your body. It’s the ingredient that helps control your asthma or headache, for example.

Drugs are tested to ensure they contain exactly the same active ingredients regardless of which brand you buy.

There’s only one active ingredient name for each type of medical compound, although they may come in different strengths. Some types of medications may contain multiple active ingredients, such as Panadeine Forte, which contains both paracetamol and codeine.




Read more:
Prescribing generic drugs will reduce patient confusion and medication errors


There can be several brand names

Until now, doctors and other prescribers have used a mixture of brand and active ingredient names when prescribing medicines. An Australian study found doctors used brand names for 80.5% of prescriptions.

Different brands are available for most medications — up to 12 for some. Combined with active ingredient names, this equates to thousands of different names — too many for any patient, doctor, nurse or pharmacist to remember.

A senior man taking a tablet. There are a variety of medications on the table.
Older people are at higher risk of making medication errors, as they tend to take more medications.
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Here’s an example of the problem.

I ask John, a patient whom I’ve just met, whether he takes cholesterol medications, commonly called statins. The active ingredient names for this group of medications all end in “statin” (for example, pravastatin, simvastatin).

“Ummm, I’m not sure, is it a blue pill?” John asks.

“It could come in many colours. It might be called atorvastatin, or Lipitor,” I reply. “Perhaps rosuvastatin, or Crestor, or Zocor?”

“Ah yes, Crestor, I am taking that,” John exclaims, after deliberating for some time.

This is a common and important conversation, but could be simpler for both of us if John was familiar with the active ingredient name.

And while we did eventually come to the answer, this medication could have easily been overlooked, by both John and myself. This may have significant implications and interact with other medicines I might prescribe.




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Cause for confusion

The main problem with using brand names for medications is the potential for confusion, as we see with John.

A prescription written using a brand name doesn’t mean you can’t buy other brands. And your pharmacist may offer to substitute the brand specified for an equivalent generic drug. So, people often leave the pharmacy with a medication name or package that bears no resemblance to the prescription.

When the terms we use to describe medicines in conversation, on prescriptions and what’s written on the medication packet can all be different, patients might not understand which medications they’re taking, or why.

This often leads to doubling up (taking two brands of the same medication), or forgetting to take a certain medication because the name on the package doesn’t match what’s written on your medication list or prescription.

Confusion resulting from using brand names has been associated with serious medication errors, including overdoses. Elderly people are the most susceptible, as they’re most likely to take multiple medications.

Even when the confusion doesn’t cause harm, it can be problematic in other ways. If patients don’t understand their medicines, they may be less likely to be proactive in making decisions with their doctor or pharmacist about their health care.

Health professionals can also get confused, potentially leading to prescribing errors.

What are the benefits of active ingredient prescribing?

The main benefit of the switch is to simplify the language around medications.

Once we become accustomed to using one standardised name for each medicine, it will be easier to talk about medicines, whether with a family member, pharmacist or doctor.

The better we understand the medications we’re using, the fewer errors we make, and the more control we can take over our medication use and decisions.

A pharmacist studies a woman's prescription.
A pharmacist can let you know which brands of your medication are are available.
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This change will also serve to promote choice.

When you’re prescribed a medicine with a certain name, you’re more likely to buy that brand. In some cases there may be generic medicines that are cheaper and just as effective. Or there may be other forms of the medication that better suit your needs, such as a capsule only available in another brand.

Not too much will change

This new rule is not expected to lead to extra work for doctors, pharmacists or other health professionals who prescribe medicines, as most clinical software will make the transition automatically.

Doctors can elect to still include the brand name on the prescription, if they feel it’s important for the patient. But aside from some limited exceptions, the active ingredient name will need to be listed, and will be listed first.

Some active ingredient names may be a bit longer and more complex than certain brand names, so there might be a period of adjustment for consumers.

But in the long term, this change will streamline terminology around medicines and make things easier, and hopefully safer, for everyone.

Next time you receive your prescription, have a look at the name of the active ingredient. Remember it, and use that name when you talk to your family, doctor and pharmacist.




Read more:
Boomers have a drug problem, but not the kind you might think


The Conversation


Matthew Grant, Palliative Medicine Physician, Research Fellow, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Distress, depression and drug use: young people fear for their future after the bushfires



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Amy Lykins, University of New England

This week, the bushfire royal commission is due to hand down its findings. Already, the commission’s officials have warned the status quo is “no longer enough to defend us from the impact of global warming”.

Australia’s young people appear to know this all too well. Preliminary findings from our recent research show many young people are worried about the future. And those directly exposed to the Black Summer bushfires suffered mental health problems long after the flames went out.

Young people with direct exposure to the bushfires reported significantly higher levels of depression and anxiety, and more drug and alcohol use, than those not directly exposed.

It’s clear that along with the other catastrophic potential harm caused by climate change, the mental health of young people is at risk. We must find effective ways to help young people cope with climate change anxiety.

Concern about the future

Our yet-to-be published study was conducted between early March and early June this year. It involved 740 young people in New South Wales between the ages of 16 and 25 completing a series of standardised questionnaires about their current emotional state, and their concerns about climate change.

Our early findings were presented at the International Association of People-Environment Studies (IAPS) conference online earlier this year.

Some 57% of respondents lived in metropolitan areas and 43% in rural or regional areas. About 78.3% were female, about 20.4% male and around 1% preferred not to say.

Overall, just over 18% of the respondents had been directly exposed to the bushfires over the past year. About the same percentage had been directly exposed to drought in that period, and more than 83% were directly exposed to bushfire smoke.

Our preliminary results showed respondents with direct exposure to the Black Summer bushfires reported significantly higher levels of depression, anxiety, stress, adjustment disorder symptoms, and drug and alcohol use than those not directly exposed to these bushfires.

A banner reads: Sorry kids, we burned your inheritance
Many of the respondents were clearly concerned about the future.
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Many young people were clearly concerned about the future. One 16 year old female respondent from a rural/regional area told us:

From day to day, if it crosses my mind I do get a bit distressed […] knowing that not enough is being done to stop or slow down the effects of climate change is what makes me very distressed as our future and future generations are going to have to deal with this problem.

Another 24 year old female respondent from a rural/regional area said:

It makes me feel incredibly sad. Sad when I think about the animals it will effect [sic]. Sad when I think about the world my son is growing up in. Sad to think that so many people out there do not believe it is real and don’t care how their actions effect [sic] the planet, and all of us. Sad that the people in the position to do something about it, won’t.

Young people directly exposed to drought also showed higher levels of anxiety and stress than non-exposed youth.

‘I feel like climate change is here now’

Those with direct exposure to bushfires were more likely than non-exposed young people to believe climate change was:

  • going to affect them or people they knew
  • likely to affect areas near where they lived
  • likely to affect them in the nearer future.

Both groups were equally likely — and highly likely — to believe that the environment is fragile and easily damaged by human activity, and that serious damage from human activity is already occurring and could soon have catastrophic consequences for both nature and humans.

One 23 year old female respondent from a metropolitan area told us:

I feel like climate change is here now and is just getting worse and worse as time goes on.

One 19 year old male respondent from a metropolitan area said:

I feel scared because of what will happen to my future kids, that they may not have a good future because I feel that this planet won’t last any longer because of our wasteful activities.

When asked how climate change makes them feel, answers varied. Some were not at all concerned (with a minority questioning whether it was even happening). Others reported feeling scared, worried, anxious, sad, angry, nervous, concerned for themselves and/or future generations, depressed, terrified, confused, and helpless.

One 16 year old female respondent in a metropolitan area told us:

I feel quite angry because the people who should be doing something about it aren’t because it won’t affect them in the future but it will affect me.

Though they were slightly more upbeat about their own futures and the future of humanity, a significant proportion expressed qualified or no hope, with consistent criticisms about humanity’s selfishness and lack of willpower to make needed behavioural changes.

One 21 year old female respondent from a metropolitan area said she felt:

a bit dissappointed [sic], people have the chance to help and take action, but they just don’t care. I feel sad as the planet will eventually react to the damage we have done, and by then, it will be too late.

A young woman in a mask looks down.
Many participants listed COVID-19 as an extra stressor in their life.
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Extra stressors

Many participants listed COVID-19 as an extra stressor in their life. One 18 year old female said:

Slightly unrelated but after seeing all of the impacts on a lot of people during the COVID-19 pandemic, all of my hope for humanity is gone.

A 25 year old woman told us:

Due to the fact of this COVID stuff, we are not going to be able to do a lot of activitys (sic) that we did before this virus shit happen (sic).

A 16 year old male said:

At present with how people have reacted over the COVID-19 virus there is no hope for humanity. Everyone has become selfish and entitled.

Irrespective of bushfire exposure, respondents reported experiencing moderate levels of depression, moderate to severe anxiety and mild stress. They also reported drug and alcohol use at levels that, according to the UNCOPE substance use screening tool, suggested cause for concern.

What does this mean?

We are still analysing the data we collected, but our preliminary results strongly suggest climate change is linked to how hopeful young people feel about the future.

We are already locked into a significant degree of warming — the only questions are just how bad will it get and how quickly.

Young people need better access to mental health services and support. It’s clear we must find effective ways to help young people build psychological resilience to bushfires, and other challenges climate change will bring.

University of New England researchers Suzanne Cosh, Melissa Parsons, Belinda Craig
and Clara Murray contributed to this research. Don Hine from the University of Canterbury in New Zealand was also a contributor.


If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.The Conversation

Amy Lykins, Associate Professor, University of New England

This article is republished from The Conversation under a Creative Commons license. Read the original article.

COVID changed the way we use drugs and alcohol — now it’s time to properly invest in treatment



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Nicole Lee, Curtin University

During crises and disasters, alcohol and other drug use often changes. But the changes are not straightforward and impacts may be different for different groups of people.

There doesn’t seem to have been significant overall increases or decreases in alcohol or other drug use during the COVID-19 pandemic, but some groups are at increased risk. And access to treatment is more limited for those who need it.

It’s a complex picture

There’s a bit of data around, but the picture is still not quite clear.
As researchers from the Centre for Alcohol Policy Research at La Trobe University have argued in an editorial published today, we need more research to understand the influence of the pandemic on use.

There were some early indicators of increases in Australians’ alcohol consumption as the pandemic hit, possibly related to increased stress. But that effect seemed to reduce as we settled into the new normal.

At the beginning of COVID-19 restrictions in March, Commonwealth Bank reported spending had increased on alcohol, but this was then reversed in April.

And in April, a study by the Foundation for Alcohol Research and Education found that most people who had stockpiled alcohol reported drinking more. Also around the same time, Australian Bureau of Statistics data showed more people had increased their drinking (14.4%) than had decreased it (9.5%).

By May, the Australian National University found more people had decreased their drinking (27%) than had increased it (20%). The Global Drug Survey between May and June found similar results among the mostly young people who responded.

However, alcohol use seemed to increase among some groups, possibly those who are more vulnerable to harms.




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Worried about your drinking during lockdown? These 8 signs might indicate a problem


In both the ABS and ANU studies, more women had increased their drinking than decreased it, which seemed to be related to higher stress linked to increased responsibilities at home.

In a survey of people who use illicit drugs, more people increased (41%) than decreased (33%) drinking. And among people who inject drugs around 11% reported increased drinking.

There have also been indicators that family violence has increased during this time. Alcohol and other drug use is a risk factor for family violence.

We need more data about heavy drug use

Since the onset of the pandemic, two studies found cannabis use had increased but other drug use had decreased or was stable. The respondents were mostly young, used for recreational purposes and were not dependent nor did they have serious problems.

Reductions in use of drugs like MDMA and cocaine, which are associated with festivals and parties, are not surprising since these large events have been restricted for months.

Two studies suggested cannabis use was on the rise, but we still need more and better data on how the pandemic has impacted heavy users.
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Most of the research hasn’t involved people who are heavy or dependent users, so we don’t know much about changes in use in these groups.

One study of people who inject drugs (who tend to use more regularly) reported some changes to availability and purity of some drugs, and small changes in use, but again some people increased and some decreased their use.

With physical distancing and lockdowns, it’s likely more people used alone or with fewer people. This means if anything goes wrong, help is further away.

Telehealth for drug treatment?

A survey of treatment services found that among services that reported changes in demand, most had an increase. Most services also reported that mental health problems, family violence and financial stress had all increased among people who use their services. These factors can make treatment more complex.

There is some evidence fewer people accessed medication treatment for opioids during the restrictions, like methadone.

COVID-19 restrictions have changed the way many services offer treatment. Most residential rehabilitation services have reduced the number of places available so they can ensure physical distancing.

Many treatment services are reporting increased demand.
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Before COVID-19 there were already long waiting lists for residential rehabilitation, so with more than 70% of services reporting reduced capacity, people may have found it harder to access residential treatment.

Non-residential services (like counselling or day programs) haven’t significantly reduced the number of people they see, and most have partially or fully moved to telehealth.

As a result, around 35% of services said fewer people missed appointments. This might be due to the easier access telehealth provides, including the reduced travel time.

However, around 25% of services said more people missed appointments. Anecdotal interviews suggest some of this might be due to difficulty transitioning to online appointments. One person said: “I know they are on Zoom but I don’t know how to use it”.

These adaptations are more complex than they appear. The time and effort required for services to make significant changes takes time away from providing treatment.

The move to telehealth is a significant one, requiring additional hardware and software, training of staff, and help for people who use the service to work out how to use the technology. Things like ensuring confidentiality can be more difficult when someone is receiving counselling at home with family around, for example.

Piecemeal funding for treatment services

The alcohol and other drug sector was already significantly under-resourced and struggling to meet existing demand before COVID-19.

In April, federal health minister Greg Hunt announced A$6 million in funding for alcohol and other drug services. Just over half of this was allocated to three organisations to increase online access to support services. The rest went to information and awareness campaigns. But no funds were set aside for existing treatment services to make COVID-19 related changes to their services.

Various state governments have allocated some funding to support alcohol and other drug services to adjust to COVID-19:

  • Tasmania released a total of A$450,000 to help services transition to telehealth

  • Western Australia allocated a total of A$350,000 for specialist alcohol and other drug services to maintain services amid the pandemic

  • Victoria and South Australia announced additional support to help people access medication treatment.

Further funding is needed to ensure services can continue to provide COVID-safe services.

It’s important for people who use alcohol and other drugs, and for the public, that alcohol and other drug treatment is well-supported to continue to operate during these changes. We know treatment is cost-effective, reduces crime and increases participation in the community. For every dollar invested in drug treatment, $7 is saved to the community.

Getting help

If you’re worried about your own or someone else’s alcohol or other drug use, you can get help by phoning the National Alcohol and Other Drug Hotline on 1800 250 015.

You can also access support online through CounsellingOnline, Hello Sunday Morning and SMART Recovery.

You may also be eligible to access one of the new telehealth services. Talk to your GP to find out more.The Conversation

Nicole Lee, Professor at the National Drug Research Institute (Melbourne), Curtin University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Why are there so many drugs to kill bacteria, but so few to tackle viruses?



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Christine Carson, University of Western Australia and Rachel Roper, East Carolina University

As the end of the second world war neared, mass production of the newly developed antibiotic penicillin enabled life-saving treatment of bacterial infections in wounded soldiers. Since then, penicillin and many other antibiotics have successfully treated a wide variety of bacterial infections.

But antibiotics don’t work against viruses; antivirals do. Since the outbreak of the coronavirus pandemic, researchers and drug companies have struggled to find an antiviral that can treat SARS-CoV-2, the virus that causes COVID-19.




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Why are there so few antivirals? The answer boils down to biology, and specifically the fact viruses use our own cells to multiply. This makes it hard to kill viruses without killing our own cells in the process.

Exploit our differences with bacteria

The differences between bacterial and human cells are what make antibiotics possible.

Bacteria are self-contained life forms that can live independently without a host organism. They are similar to our cells, but also have many features not found in humans.

For example, penicillin is effective because it interferes with the construction of the bacterial cell wall. Cell walls are made of a polymer called peptidoglycan. Human cells don’t have a cell wall or any peptidoglycan. So antibiotics that prevent bacteria from making peptidoglycan can inhibit bacteria without harming the human taking the medicine. This principle is known as selective toxicity.

Viruses use our own cells to replicate

Unlike bacteria, viruses cannot replicate independently outside a host cell. There is a debate over whether they are really living organisms at all.

To replicate, viruses enter a host cell and hijack its machinery. Once inside, some viruses lie dormant, some replicate slowly and leak from cells over a prolonged period, and others make so many copies that the host cell bursts and dies. The newly replicated virus particles then disperse and infect new host cells.

An antiviral treatment that intervenes in the viral “life” cycle during these events could be successful. The problem is that if it targets a replication process that is also important to the host cell, it is likely to be toxic to the human host as well.

Killing viruses is easy. Keeping host cells alive while you do it is the hard part.




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In the fight against coronavirus, antivirals are as important as a vaccine. Here’s where the science is up to


Successful antivirals target and disrupt a process or structure unique to the virus, thereby preventing viral replication while minimising harm to the patient. The more dependent the virus is on the host cell, the fewer targets there are to hit with an antiviral. Unfortunately, most viruses offer few points of unique difference that can be targeted.

Another complication is that different viruses vary from each other much more than different bacteria do. Bacteria all have double-stranded DNA genomes and replicate independently by growing larger and then splitting into two, similar to human cells.

But there is extreme diversity between different viruses. Some have DNA genomes while others have RNA genomes, and some are single-stranded while others are double-stranded. This makes it practically impossible to create a broad spectrum antiviral drug that will work across different virus types.

Antiviral success stories

Nevertheless, points of difference between humans and viruses do exist, and their exploitation has led to some success. One example is influenza A, which is one form of the flu.

Influenza A tricks human cells so it can enter them. Once inside our cells, the virus needs to “undress”, removing its outer coat to release its RNA into the cell.

A viral protein called matrix-2 protein is key to this process, facilitating a series of events that releases the viral RNA from the virus particle. Once the viral RNA is released inside the host cell, it is transported to the cell nucleus to start viral replication.

But if a drug jams the matrix-2 protein, the viral RNA can’t exit the virus particle to get to the cell nucleus, where it needs to be to replicate. So, the infection stalls. Amantadine and rimantadine were early antiviral successes targeting the matrix-2 protein.

Zanamivir (Relenza) and oseltamivir (Tamiflu) are newer drugs that have also had success in treating patients infected with influenza A or B. They work by blocking a key viral enzyme, obstructing virus release from the cell, slowing the spread of infection within the body, and minimising the damage the infection causes.

We need to find what makes SARS-CoV-2 unique

A COVID-19 vaccine may be difficult to create. So testing antivirals to find one that can effectively treat COVID-19 remains an important goal.

Much depends on knowing the intricacies of the SARS-CoV-2 virus and its interactions with human cells. If researchers can identify unique elements in how it survives and replicates, we can exploit these points of weakness and make an effective antiviral treatment.




Read more:
Where are we at with developing a vaccine for coronavirus?


This article is supported by the Judith Neilson Institute for Journalism and Ideas.The Conversation

Christine Carson, Senior Research Fellow, School of Biomedical Sciences, University of Western Australia and Rachel Roper, Associate Professor of Microbiology and Immunology, East Carolina University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

What if the vaccine or drugs don’t save us? Plan B for coronavirus means research on alternatives is urgently needed



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Tammy Hoffmann, Bond University and Paul Glasziou, Bond University

The curve of the COVID-19 epidemic has been flattened in many countries around the world, and it hasn’t been new antivirals or a vaccine that has done it. We are being saved by non-drug interventions such as quarantine, social distancing, handwashing, and – for health-care workers – masks and other protective equipment.

We are all hoping for a vaccine in 2021. But what do we do in the meantime? And more importantly, what if no vaccine emerges?

The world has bet most of its research funding on finding a vaccine and effective drugs. That effort is vital, but it must be accompanied by research on how to target and improve the non-drug interventions that are the only things that work so far.

Debates still rage over basic questions such as whether the public should use face masks; whether we should stand 1, 2 or 4 metres apart; and whether we should wash our hands with soap or sanitiser. We need the answers now.




Read more:
Drugs don’t cure everything – doctors can be helped to prescribe other options


What about non-drug intervention research?

Across all health research, non-drug interventions are the subject of about 40% of clinical trials. Yet they receive far less attention than drug development and testing.

In the COVID-19 pandemic, millions of dollars have already been given to research groups around the world to develop vaccines and trial potential drug cures. Hundreds of clinical trials on drugs and vaccines are under way, but we could find only a handful of trials of non-drug interventions, and no trials on how to improve the adherence to them.

While holding our breath for the vaccine …

We all hope the massive global effort to develop a vaccine or drug treatment for COVID-19 is successful. But many experts, including Ian Frazer, who developed Australia’s HPV vaccine, think it will not be easy or quick.

If an effective vaccine or drug doesn’t materialise, we will need a Plan B that uses only non-drug interventions. That’s why we need high-quality research to find out which ones work and how to do them as effectively as possible.

Aren’t non-drug interventions straightforward?

You might think hand washing, masks and social distancing are simple things and don’t need research. In fact, non-drug interventions are often very complex.

It takes research to understand not only the “active components” of the intervention (washing your hands, for example), but also how much is needed, how to help people start and keep doing it, and how to communicate these messages to people. Developing and implementing an effective non-drug intervention is very different from developing a vaccine or a drug, but it can be just as complex.

To take one example, there has been a #Masks4All campaign to encourage everyone to wear face masks. But what type of mask, and what should it be made of? Who should wear masks – people who are ill, people who are caring for people who are ill, or everyone? And when and where? There is little agreement on these detailed questions.

Washing your hands also sounds simple. But how often? Twice a day, 10 times a day, or at specific trigger times? What’s the best way to teach people to wash their hands correctly? If people don’t have perfect technique, is hand sanitiser be better than soap and water? Is wearing masks and doing hand hygiene more effective than doing just either of them?

These are just are some of the things that we don’t know about non-drug interventions.

Existing research is lacking

We recently reviewed all the randomised controlled trials for physical interventions to interrupt the spread of respiratory viruses, including interventions such as masks, hand hygiene, eye protection, social distancing, quarantining, and any combination of these. We found a messy and varied bunch of trials, many of low quality or small sample size, and for some types of interventions, no randomised trials.

Other non-drug options to research include the built environment, such as heating, ventilation, air conditioning circulation, and surfaces (for example, the SARS-CoV-2 virus “dies” much more rapidly on copper than other hard surfaces).

Are some of the things we are doing now ineffective? Probably. The problem is we don’t know which ones. We need to know this urgently so we’re not wasting time, effort, and resources on things that don’t work.

At a time when we need to achieve rapid behaviour change on a massive scale, inconsistent and conflicting messages only creates confusion and makes achieving behaviour change much harder.

What about the next pandemic?

If a successful COVID-19 vaccine is developed, we’re out of the woods for now. But what happens when the next pandemic or epidemic arrives? Vaccines are virus-specific, so next time a new virus threatens us, we will again be in the same situation. However, what we learn now about non-drug interventions can be used to protect us against other viruses, while we wait again for another new vaccine or drug.

We have had opportunities to study non-drug interventions for respiratory viruses in the recent past, particularly during the Severe Acute Respiratory Syndrome (SARS) epidemic in 2003 and the H1N1 influenza pandemic in 2009. However, the chances for rigorous studies were largely wasted and we now find ourselves desperately scrambling for answers.




Read more:
Size does matter: why large-scale research is a must for public health


What about research for Plan B?

To prepare for the future and Plan B, the case where a vaccine doesn’t arrive, we need to conduct randomised trials into non-drug interventions to prevent the spread of respiratory viruses. The current pandemic is presenting us with a rare opportunity to rapidly conduct trials to answer many of the unknowns about this set of non-drug interventions.

Concentrating all our funding, efforts, and resources into vaccine and drug research may turn out to be a devastating and costly mistake in both healthcare and economic terms. The results will be felt not only in this pandemic, but also in future ones.The Conversation

Tammy Hoffmann, Professor of Clinical Epidemiology, Bond University and Paul Glasziou, Professor of Medicine, Bond University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Do new cancer drugs work? Too often we don’t really know (and neither does your doctor)



The effectiveness of a drug may be evaluated based on its potential to shrink tumours – but this doesn’t necessarily equate to improved survival rates.
From shutterstock.com

Barbara Mintzes, University of Sydney and Agnes Vitry, University of South Australia

It’s hard to find anyone who hasn’t been touched by cancer. People who haven’t had cancer themselves will likely have a close friend or family member who has been diagnosed with the disease.

If the cancer has already spread, the diagnosis may feel like a death sentence. News that a new drug is available can be a big relief.

But imagine a cancer patient asks their doctor: “Can this drug help me stay alive longer?” And in all honesty the doctor answers: “I don’t know. There’s one study that says the drug works, but it didn’t show whether patients lived longer, or even if they felt any better.”

This might sound like an unlikely scenario, but it’s precisely what a team of UK researchers found to be the case when it comes to many new cancer drugs.




Read more:
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A look at the research

A study published last week in the British Medical Journal reviewed 39 clinical trials supporting approval of all new cancer drugs in Europe from 2014 to 2016.

The researchers found more than half of these trials had serious flaws likely to exaggerate treatment benefits. Only one-quarter measured survival as a key outcome, and fewer than half reported on patients’ quality of life.

Of 32 new cancer drugs examined in the study, only nine had at least one study without seriously flawed methods.

The researchers evaluated methods in two ways. First, they used a standard “risk of bias” scale that measures shortcomings shown to lead to biased results, such as if doctors knew which drug patients were taking, or if too many people dropped out of the trial early.

Second, they looked at whether the European Medicines Agency (EMA) had identified serious flaws, such as a study being stopped early, or if the drug was compared to substandard treatment. The EMA identified serious flaws in trials for ten of the 32 drugs. These flaws were rarely mentioned in the trials’ published reports.

From clinical trials to treatment – faster isn’t always better

Before a medicine is approved for marketing, the manufacturer must carry out studies to show it’s effective. Regulators such as the EMA, the US Food and Drug Administration (FDA) or Australia’s Therapeutic Goods Administration (TGA) then judge whether to allow it to be marketed to doctors.

National regulators mainly examine the same clinical trials, so the findings from this research are relevant internationally, including in Australia.




Read more:
Spot the snake oil: telling good cancer research from bad


There’s strong public pressure on regulators to approve new cancer drugs more quickly, based on less evidence, especially for poorly treated cancers. The aim is to get treatments to patients more quickly by allowing medicines to be marketed at an earlier stage. The downside of faster approval, however, is more uncertainty about treatment effects.

One of the arguments for earlier approvals is the required studies can be carried out later on, and sick patients can be given an increased chance of survival before it’s too late. However, a US study concluded that post-approval studies found a survival advantage for only 19 of 93 new cancer drugs approved from 1992 to 2017.

If the evidence for a new cancer drug is flawed, this leaves patients vulnerable to false hope.
From shutterstock.com

So how is effectiveness measured currently?

Approval of new cancer drugs is often based on short-term health outcomes, referred to as “surrogate outcomes”, such as shrinking or slower growth of tumours. The hope is these surrogate outcomes predict longer-term benefits. For many cancers, however, they have been found to do a poor job of predicting improved survival.

A study of cancer trials for more than 100 medicines found on average, clinical trials that measure whether patients stay alive for longer take an extra year to complete, compared to trials based on the most commonly used surrogate outcome, called “progression free survival”. This measure describes the amount of time a person lives with a cancer without tumours getting larger or spreading further. It’s often poorly correlated with overall survival.

A year may seem like a long wait for someone with a grim diagnosis. But there are policies to help patients access experimental treatments, such as participating in clinical trials or compassionate access programmes. If that year means certainty about survival benefits, it’s worth waiting for.

Approving drugs without enough evidence can cause harm

In an editorial accompanying this study, we argue that exaggeration and uncertainty about treatment benefits cause direct harm to patients, if they risk severe or life-threatening harm without likely benefit, or if they forgo more effective and safer treatments.

For example, the drug panobinostat, which is used for multiple myeloma patients who have not responded to other treatments, has not been shown to help patients live longer, and can lead to serious infections and bleeding.

Inaccurate information can also encourage false hope and create a distraction from needed palliative care.

And importantly, the ideal of shared informed decision-making based on patients’ values and preferences falls apart if neither the doctor nor the patient has accurate evidence to inform decisions.




Read more:
If we don’t talk about value, cancer drugs will become terminal for health systems


In countries with public health insurance, such as Australia’s Pharmaceutical Benefits Scheme (PBS), patients’ access to new cancer drugs depends not just on market approval but also on payment decisions. The PBS often refuses the pay for new cancer drugs because of uncertain clinical evidence. In the cases of the drugs in this research, some are available on the PBS, while others are not.

New cancer drugs are often very expensive. On average in the US, a course of treatment with a new cancer drug costs more than US$100,000 (A$148,000).

Cancer patients need treatments that help them to live longer, or at the very least to have a better quality of life during the time that they have left. In this light, we need stronger evidence standards, to be sure there are real health benefits when new cancer drugs are approved for use.

The article has been updated to reflect Agnes Vitry’s current role at the University of South Australia.The Conversation

Barbara Mintzes, Senior Lecturer, Faculty of Pharmacy, University of Sydney and Agnes Vitry, Senior lecturer, University of South Australia

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Antibiotic resistance is not new – it existed long before people used drugs to kill bacteria



Antibiotic resistance can spread between microbes within hours.
Lightspring/Shutterstock.com

Ivan Erill, University of Maryland, Baltimore County

Imagine a world where your odds of surviving minor surgery were one to three. A world in which a visit to the dentist could spell disaster. This is the world into which your great-grandmother was born. And if humanity loses the fight against antibiotic resistance, this is a world your grandchildren may well end up revisiting.

Antibiotics changed the world in more ways than one. They made surgery routine and childbirth safer. Intensive farming was born. For decades, antibiotics have effectively killed or stopped the growth of disease-causing bacteria. Yet it was always clear that this would be a rough fight. Bacteria breed fast, and that means that they adapt rapidly. The emergence of antibiotic resistance was predicted by none other than Sir Alexander Fleming, the discoverer of penicillin, less than a year after the first batch of penicillin was mass produced.

Yet, contrary to popular belief, antibiotic resistance did not evolve recently, or in response to our use and misuse of antibiotics in humans and animals. Antibiotic resistance first evolved millions of years ago, and in the most mundane of places.

I am a bioinformatician, and my lab studies the evolution of bacterial genomes. With antibiotic resistance becoming a major threat, I’m trying to figure out how resistance to antibiotics emerges and spreads among bacterial populations.

A billion-years-old arms race

Most antibiotics are naturally produced by bacteria living in soil. They produce these deadly chemical compounds to fend off competing species. Yet, in the long game that is evolution, competing species are unlikely to sit idly by. Any mutant capable of tolerating a minimal quantity of the antibiotic will have a survival advantage and will be selected for – over generations this will produce organisms that are highly resistant.

So it’s a foregone conclusion that antibiotic resistance, for any antibiotic researchers might ever discover, is likely already out there. Yet people keep talking about the evolution of antibiotic resistance as a recent phenomenon. Why?

Resistance can and does evolve when bacteria are persistently exposed to a new antibiotic they have never encountered. Let’s call this the old-fashioned evolutionary road. Second, when bacteria are exposed to a novel antibiotic and are in contact with bacteria already resistant to this antibiotic, it is just a matter of time before they get cozy and trade genes. And, importantly, once genes have been packaged for trading, they become easier and easier to share. Bacteria then meet other bacteria, which meet more bacteria, until one of them eventually meets you.

Bacteria can evolve resistance to high levels of antibiotics in just days.

The rise and fall of sulfa drugs

For all their might, antibiotics are not the only substances capable of effectively killing bacteria (without killing us). A decade before the mass production of penicillin, sulfonamide drugs became the first commercial antibacterial agent. Sulfa drugs act by blocking an enzyme – called DHPS – that is essential for bacteria to grow and multiply.

Sulfa drugs are not antibiotics. No known organism produces them. They are chemotherapeutic agents synthesized by humans. No natural producer means no billion-year-old arms race and no pool of ancient resistance genes. We would expect bacteria to evolve resistance to sulfa drugs via the good old-fashioned way. And they did.

Just a few years after their commercial introduction, the first cases of resistance to sulfa drugs were reported. Mutations to the bacterial DHPS enzyme made sulfa drugs ineffective. Then penicillin and the antibiotic era came about. Sulfa drugs were relegated to a secondary role in medicine, but they gained popularity as cheap antimicrobials in animal husbandry. By the 1980s resistance to sulfa drugs was rampant and worldwide. What had happened?

At odds with resistance

To answer this question our research team took sequences of sulfa drug resistance genes from disease-causing bacteria and compared them to millions of “normal” versions of the DHPS enzyme in nonpathogenic bacteria.

The team identified two large groups of bacteria that had DHPS enzymes resistant to sulfa drugs. By studying their DNA sequences, we were able to show that these resistant DHPS enzymes had been present in these two groups of bacteria for at least 500 million years. Yet sulfa drugs were first synthesized in the 1910s. How could resistance be around 500 million years ago? And how did these resistance genes find their way into the disease-causing bacteria plaguing hospitals worldwide?

The clues left in gene sequences are too fuzzy to conclusively answer the latter, but we can certainly speculate. The bacteria we identified as harboring these ancient sulfa drug resistance genes are all soil and freshwater bacteria that thrive under the well-irrigated subsoil of farms. And farmers have been adding huge amounts of sulfa drugs to animal feed for the past 50 years.

The sublethal concentrations of sulfa drugs in the soil are the perfect setting for resistance genes to be transferred from these ancient resistant bacterial populations to other bacteria. All it takes is for one lucky bacterium to meet one of these ancient resistant ones in the subsoil. They trade some genes, one bacterium to the next, and resistance spreads until a newly minted resistant bacterium eventually makes it to the groundwater supply you drink from. You do the math.

Nothing new under the sun

As for why sulfa drug resistance genes would be around 500 million years ago, there are two plausible explanations. On the one hand, it could be that 500 million years ago there was a bacterium that synthesized sulfa drugs, which would explain the evolution of resistance. However, the lack of remnants from such a biosynthetic pathway makes this unlikely.

On the other hand, resistant bacteria may have been around just by chance. The argument here is that there are so many bacteria, and such diversity, that chances are that some of them are going to be resistant to anything scientists come up with. This is a sobering thought.

Then again, this is already the baseline for antibiotics. Like climate change, antibiotic resistance is one of those problems that always seem to be a couple decades away. And it may well be. A turning point for me in the climate change debate was a decade-old opinion piece in New Scientist. It stated that we should make every possible effort to prevent climate change, especially in the unlikely case that it was not caused by man, because that would mean that all we can do is palliate a natural phenomenon.

Our research points in the same direction. If resistance is already out there, drug development can offer only temporary relief. The challenge then is not to quell resistance, but to avoid its spread. It is a big challenge, but not an insurmountable one. Not feeding wonder drugs to pigs would do nicely, for starters.The Conversation

Ivan Erill, Associate Professor of Biological Sciences, University of Maryland, Baltimore County

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Legal highs: arguments for and against legalising cannabis in Australia



File 20180417 32339 16n0gjo.jpg?ixlib=rb 1.1
Many of the harms associated with cannabis use are to do with its illegality.
from http://www.shutterstock.com

Nicole Lee, Curtin University and Jarryd Bartle, RMIT University

Greens leader Richard Di Natale wants Australia to legalise cannabis for personal use, regulated by a federal agency. This proposal is for legalisation of recreational use for relaxation and pleasure, not to treat a medical condition (which is already legal in Australia for some conditions).

According to the proposal, the government agency would licence, monitor and regulate production and sale, and regularly review the regulations. The agency would be the sole wholesaler, buying from producers and selling to retailers it licences.

The proposed policy includes some safeguards that reflect lessons we’ve learned from alcohol and tobacco. These include a ban on advertising, age restrictions, requiring plain packaging, and strict licensing controls. Under the proposal, tax revenues would be used to improve funding to the prevention and treatment sector, which is underfunded compared to law enforcement.




Read more:
Greens want cannabis to be made legal


Cannabis legislation around the world

In Australia, cannabis possession and use is currently illegal. But in several states and territories (South Australia, ACT and Northern Territory) a small amount for personal use is decriminalised. That means it’s illegal, but not a criminal offence. In all others it’s subject to discretionary or mandatory diversion usually by police (referred to as “depenalisation”).

Several jurisdictions around the world have now legalised cannabis, including Uruguay, Catalonia and nine states in the United States. Canada is well underway to legalising cannabis, with legislation expected some time this year, and the New Zealand prime minister has flagged a referendum on the issue.

In a recent opinion poll, around 30% of Australians thought cannabis should be legal. Teenagers 14-17 years old were least likely to support legalistaion (21% of that age group) and 18-24 year olds were most likely to support it (36% of that age group).




Read more:
Australia’s recreational drug policies aren’t working, so what are the options for reform?


In the latest National Drug Strategy Household Survey, around a quarter of respondents supported cannabis legalisation and around 15% approved of regular use by adults for non-medical purposes.

What are the concerns about legalisation?

Opponents of legalisation are concerned it will increase use, increase crime, increase risk of car accidents, and reduce public health – including mental health. Many are concerned cannabis is a “gateway” drug.

The “gateway drug” hypothesis was discounted decades ago. Although cannabis usually comes before other illegal drug use, the majority of people who use cannabis do not go on to use other drugs. In addition, alcohol and tobacco usually precede cannabis use, which if the theory were correct would make those drugs the “gateway”.




Read more:
Could a regulated cannabis market help curb Australia’s drinking problem?


There is also no evidence legalisation increases use. But, studies have shown a number of health risks, including:

  • around 10% of adults and one in six teens who use regularly will become dependent

  • regular cannabis use doubles the risk of psychotic symptoms and schizophrenia

  • teen cannabis use is associated with poorer school outcomes but causation has not been established

  • driving under the influence of cannabis doubles the risk of a car crash

  • smoking while pregnant affects a baby’s birth weight.

What are the arguments for legalisation?

Reducing harms

Australia’s official drug strategy is based on a platform of harm minimisation, including supply reduction, demand reduction (prevention and treatment) and harm reduction. Arguably, policies should therefore have a net reduction in harm.

But some of the major harms from using illicit drugs are precisely because they are illegal. A significant harm is having a criminal record for possessing drugs that are for personal use. This can negatively impact a person’s future, including careers and travel. Decriminalisation of cannabis would also reduce these harms without requiring full legalisation.

Reducing crime and social costs

A large proportion of the work of the justice system (police, courts and prisons) is spent on drug-related offences. Yet, as Mick Palmer, former AFP Commissioner, notes “drug law enforcement has had little impact on the Australian drug market”.

Decriminalisation may reduce the burden on the justice system, but probably not as much as full legalisation because police and court resources would still be used for cautioning, issuing fines, or diversion to education or treatment. Decriminalisation and legalistaion both potentially reduce the involvement of the justice system and also of the black market growing and selling of cannabis.




Read more:
Assessing the costs and benefits of legalising cannabis


Raising tax revenue

Economic analysis of the impact of cannabis legalisation calculate the net social benefit of legalisation at A$727.5 million per year. This is significantly higher than the status quo at around A$295 million (for example from fines generating revenue, as well as perceived benefits of criminalisation deterring use). The Parliamentary Budget Office estimates tax revenue from cannabis legalisation at around A$259 million.

Civil liberties

Many see cannabis prohibition as an infringement on civil rights, citing the limited harms associated with cannabis use. This includes the relatively low rate of dependence and very low likelihood of overdosing on cannabis, as well as the low risk of harms to people using or others.

Many activities that are legal are potentially harmful: driving a car, drinking alcohol, bungee jumping. Rather than making them illegal, there are guidelines, laws and education to make them safer that creates a balance between civil liberties and safety.

What has happened in places where cannabis is legal?

Legalisation of cannabis is relatively recent in most jurisdictions so the long-term benefits or problems of legalisation are not yet known.

But one study found little effect of legalisation on drug use or other outcomes, providing support for neither opponents nor advocates of legalisation. Other studies have shown no increase in use, even among teens.

The ConversationThe research to date suggests there is no significant increase (or decrease) in use or other outcomes where cannabis legalisation has occurred. It’s possible the harm may shift, for example from legal harms to other types of harms. We don’t have data to support or dispel that possibility.

Nicole Lee, Professor at the National Drug Research Institute, Curtin University and Jarryd Bartle, Sessional Lecturer in Criminal Law, RMIT University

This article was originally published on The Conversation. Read the original article.

Four of the most life-threatening skin conditions and what you should know about them



File 20180312 30965 xaeir3.jpg?ixlib=rb 1.1
Some serious skin conditions are more likely to affect those with weaker immune systems.
from http://www.shutterstock.com

William Cranwell, Melbourne Health

This article is part of our series about skin: why we have it, what it does, and what can go wrong. Read other articles in the series here.


Dermatological emergencies are uncommon, but can cause devastating complications and death if not recognised and treated early. Some skin conditions require treatment in an intensive care unit. Here are some of the most serious skin conditions and what you should know about recognising them.

1. Necrotising fasciitis

Necrotising fasciitis is a severe infection of the skin, the tissue below the skin, and the fascia (fibrous tissue that separates muscles and organs), resulting in tissue death, or necrosis. The infection is rapid, fast-spreading and fatal if not detected and treated early. If not treated with antibiotics and surgery early, toxic shock and organ failure are common.

Necrotising fasciitis may occur in anyone. Previously healthy young people are often affected.

The cause may be one or more bacteria entering the body via an external injury or punctured internal organ. Group A streptococci bacteria, which are the organisms implicated in “strep throat”, are among the most common causes.




Read more:
Explainer: what causes necrotising fasciitis, the flesh-eating bug?


Early necrotising fasciitis is easily missed, as similar symptoms are commonly seen in less severe infection. The initial area is painful, red and swollen. This progresses to a dark, blistered, malodorous and blackened area, which is a sign of tissue death. Other symptoms include fever, intense pain, low blood pressure and shock.

The most important risk factors for necrotising fasciitis include diabetes, peripheral vascular disease, trauma, alcohol and intravenous drug use, and use of non-steroidal anti-inflammatory drugs.

Treatment of necrotising fasciitis is immediate hospitalisation, surgical removal of all dead tissue, and intravenous antibiotics. Patients often require intensive care. Management of shock and other complications reduces the risk of death. Use of a hyperbaric chamber (to increase oxygen delivery to the tissue) and immune therapy may also be required.

Around a quarter of people diagnosed with necrotising fasciitis will die, and sepsis occurs in up to 70% of cases.

Most have heard of necrotising fasciitis as the ‘flesh-eating bug’.
DermNet New Zealand

2. Scalded skin syndrome

Staphylococcal scalded skin syndrome is an uncommon major skin infection. It typically affects newborn babies, young children and adults with reduced immune systems or kidney failure. This syndrome is caused by toxins produced by the bacterium Staphylococcus aureus, which is common in throat, ear and eye infections.

Around 15-40% of adults carry Staphylococcus aureus on the skin surface and have no problems. But these adults may inadvertently introduce the bacteria into nurseries or daycare centres. Because young children have weak immunity to specific toxins, they’re at increased risk of scalded skin syndrome.

Scalded skin syndrome is characterised by a red, blistering rash resembling burns. Early symptoms include fever, skin redness and skin tenderness. Other symptoms may include sore throat or conjunctivitis.

Within 24-48 hours, fluid-filled blisters form on the entire body. The blisters may rupture, leaving areas resembling burns. Large areas of the skin peel off and fall away with only minor touch.




Read more:
Common skin rashes and what to do about them


Scalded skin syndrome requires hospitalisation for intravenous antibiotics and treatment of the wounds. Ruptured blisters require wound dressings, and the skin surface requires intense care to avoid further damage.

Other treatment includes intravenous fluid and electrolyte maintenance to prevent shock and other complications, paracetamol for pain and fever, and avoidance of severe sepsis. Sepsis is when chemicals released into the bloodstream to fight an infection trigger inflammatory responses throughout the body, which can be life-threatening.

Complications of scalded skin syndrome include severe infection, pneumonia, cellulitis (a bacterial skin infection) and dehydration. Most children treated appropriately recover well and healing is complete within a week.

Staphylococcal scalded skin syndrome is more likely to occur in people with weaker immune systems – such as children.
DermNet New Zealand

3. DRESS syndrome

Standing for “drug reaction with eosinophilia and systemic symptoms,” DRESS syndrome is a severe reaction that affects the skin and internal organs. The patient may have an extensive rash, fever, enlarged lymph nodes and damage to the liver, kidneys, lungs, heart, blood components or pancreas. Symptoms usually start two to eight weeks after the responsible drug has been taken.

The death rate is estimated between 10 and 20%, most often due to liver failure.

The most common drugs responsible include anticonvulsants, antidepressants, non-steroidal anti-inflammatory drugs, antibiotics and sulfa drugs (a type of synthetic antibiotic). The severe reaction is thought to occur due to a pre-existing genetic change in the immune system, a triggering illness (most often a viral infection) and defective breakdown of the drug by the body.

Early diagnosis is essential. The responsible drug must be stopped immediately and patients may require intensive care or burn unit management. More intensive treatment is needed if organs are involved.

DRESS syndrome appears a few weeks after taking a drug the patient is allergic to.
DermNet New Zealand

4. Life-threatening drug reactions

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are variants of a life-threatening reaction that affects the skin and mucous membranes (mouth, eyes, genitals, respiratory or gastrointestinal tracts).

These are unpredictable reactions that leave sufferers critically unwell, with widespread death of the outer skin layer (epidermis), which peels off. The rash generally begins on the trunk and extends to the limbs and face, and there is intense skin pain. Before the rash appears, symptoms include fever, sore throat, runny nose, conjunctivitis and general aches.

It’s almost always caused by medications. The most common medications causing this reaction are anticonvulsants, antibiotics, allopurinol (gout medication), non-steroidal anti-inflammatory drugs and an HIV drug. The reaction usually occurs in the first eight weeks after taking the drug. It’s more likely to happen if the patient has cancer, HIV or specific genes that may play a role.

This reaction can be fatal by causing dehydration and malnutrition, severe infection, respiratory failure, gastrointestinal complications and multi-organ failure.

The responsible drug has to be stopped, and treatment (in a burns unit and intensive care unit) includes wound care, fluid management, pain management and prevention of infection. Long-term complications, including scarring, eye, oral, genital, lung disease and mental health disorders, are common. Around a quarter of people with this reaction will die.


The Conversation


Read more:
The skin is a very important (and our largest) organ: what does it do?


This reaction to medications is totally unpredictable.
DermNet NZ

William Cranwell, Dermatology Clinical Research Fellow, Melbourne Health

This article was originally published on The Conversation. Read the original article.