To ensure supply of the top 3 drugs used to treat COVID-19, it’s time to boost domestic medicine manufacturing


Nial Wheate, University of Sydney; Elise Schubert, University of Sydney, and Ingrid Gelissen, University of SydneyWe now know enough about how COVID works for health authorities to have issued clear guidance on which drugs doctors should use on hospitalised patients. The recommended drugs are dexamethasone, remdesivir, and tocilizumab.

Remdesivir, also known as Veklury, is not manufactured in Australia and the Therapeutic Goods Administration (TGA) has recently issued an alert warning of a shortage of tocilizumab in Australia. And the large dexamethasone manufacturers are based overseas. The website Pharmaoffer, which shows suppliers of active pharmaceutical ingredients, lists the countries that produce the active ingredient in dexamethasone; Australia is not one of them.

More broadly, Australia lacks medicines manufacturing capability and this puts us at significant risk should supplies from overseas continue to be interrupted.

One report released last year described the Australian market for pharmaceuticals as “possibly one of the most vulnerable in the OECD”.

It’s time for Australia to re-invest in domestic medicine manufacturing.

Drugs used to treat COVID-19

Many people diagnosed with COVID-19 experience only mild, or no symptoms at all, and can be managed and monitored at home. Rest is the main treatment, and medicines such as paracetamol and/or ibuprofen can provide symptomatic relief of any mild fevers.

People with moderate to severe COVID-19 are treated in hospital. The medicines doctors will prescribe in hospital depend on a patient’s clinical circumstances, such as whether or not they are receiving oxygen therapy.

The pharmaceutical treatment options include:

  • dexamethasone, a corticosteriod
  • remdesivir, an antiviral and
  • tocilizumab, a monoclonal antibody and immunosuppressive agent (monoclonal antibodies are lab-made proteins that mimic the immune system’s virus-fighting abilities).

Dexamethasone is already used for a wide range of conditions, such as certain forms of cancer and arthritis, and various other disorders. Now, it is used in treatment of COVID-19 to suppress inflammation and immune responses.

Remdesivir works by stopping the replication of viral RNA.

And tocilizumab is sometimes used when COVID-19 patients have signs of systemic inflammation.

Dexamethasone is already used for a wide range of conditions.
Nati Harnik/AP

Where are they made?

Australia is heavily reliant on supply agreements for medicines that come from overseas (and a manufacturing network might include a lot of countries). It’s been reported some of the large dexamethasone manufacturers are in Brazil and India.

To meet growing demand for remdesivir, its company (Gilead) has approved new deals for manufacturing in Egypt, India, and Pakistan. But while the remdesivir manufacturing network now includes more than 40 companies in North America, Europe, and Asia, the medicine is not manufactured in Australia.

Tocilizumab was developed in Japan and is now also licensed for manufacturing by the California-based company Genentech.

Need for Australian manufacturing base

There is an urgent need for Australia to increase local manufacturing of many types of medicines, not just COVID treatments, to secure current and future needs.

In general, Australia does have some medicine manufacturing sites in Australia but several have either closed or are slated for closure.

The Australian government has acknowledged the importance of boosting local production of medicines but it’s unclear what progress has been made.

In March this year, an interim report by the Productivity Commission on vulnerable supply chains again indicated medicines as an area of concern, noting that

the pharmaceutical industry is highly regulated, making entering the market or modifying existing facilities to respond to a crisis a slow and costly process.

The final report from this committee is currently with the government.

Manufacturing of medicines in Australia is regulated by the TGA. According to its website, it can take up to 12 months for an Australian manufacturer to get approval to bring a new manufacturing site online. This means it would take us a long time to act if a supply shortage pops up.

Significant backing from the federal government for local medicine manufacturing would reduce the risk of key medicine shortages in Australia, while also creating many highly skilled jobs.The Conversation

Nial Wheate, Associate Professor of the Sydney Pharmacy School, University of Sydney; Elise Schubert, Pharmacist and PhD Candidate, University of Sydney, and Ingrid Gelissen, Associate Professor in Pharmaceutical Sciences, School of Pharmacy, University of Sydney

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

What is drink spiking? How can you know if it’s happened to you, and how can it be prevented?


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Nicole Lee, Curtin University and Jarryd Bartle, RMIT UniversityRecent media reports suggest drink spiking at pubs and clubs may be on the rise.

“Drink spiking” is when someone puts alcohol or other drugs into another person’s drink without their knowledge.

It can include:

  • putting alcohol into a non-alcoholic drink
  • adding extra alcohol to an alcoholic drink
  • slipping prescription or illegal drugs into an alcoholic or non-alcholic drink.

Alcohol is actually the drug most commonly used in drink spiking.

The use of other drugs, such as benzodiazepines (like Rohypnol), GHB or ketamine is relatively rare.

These drugs are colourless and odourless so they are less easily detected. They cause drowsiness, and can cause “blackouts” and memory loss at high doses.

Perpetrators may spike victims’ drinks to commit sexual assault. But according to the data, the most common type of drink spiking is to “prank” someone or some other non-criminal motive.

So how can you know if your drink has been spiked, and as a society, how can we prevent it?




Read more:
Weekly Dose: GHB, a party drug that’s easy to overdose on but was once used in childbirth


How often does it happen?

We don’t have very good data on how often drink spiking occurs. It’s often not reported to police because victims can’t remember what has happened.

If a perpetrator sexually assaults someone after spiking their drink, there are many complex reasons why victims may not want to report to police.




Read more:
Almost 90% of sexual assault victims do not go to police — this is how we can achieve justice for survivors


One study, published in 2004, estimated there were about 3,000 to 4,000 suspected drink spiking incidents a year in Australia. It estimated less than 15% of incidents were reported to police.

It found four out of five victims were women. About half were under 24 years old and around one-third aged 25-34. Two-thirds of the suspected incidents occurred in licensed venues like pubs and clubs.

According to an Australian study from 2006, around 3% of adult sexual assault cases occurred after perpetrators intentionally drugged victims outside of their knowledge.

It’s crucial to note that sexual assault is a moral and legal violation, whether or not the victim was intoxicated and whether or not the victim became intoxicated voluntarily.

How can you know if it’s happened to you?

Some of the warning signs your drink might have been spiked include:

  • feeling lightheaded, or like you might faint
  • feeling quite sick or very tired
  • feeling drunk despite only having a very small amount of alcohol
  • passing out
  • feeling uncomfortable and confused when you wake up, with blanks in your memory about what happened the previous night.

If you think your drink has been spiked, you should ask someone you trust to get you to a safe place, or talk to venue staff or security if you’re at a licensed venue. If you feel very unwell you should seek medical attention.

If you believe your drink has been spiked or you have been sexually assaulted, seeking prompt medical attention can assist in subsequent criminal prosecution. Medical staff can perform a blood test for traces of drugs in your system.

How can drink spiking be prevented?

Most drink spiking occurs at licensed venues like pubs and clubs. Licensees and people who serve alcohol have a responsibility to provide a safe environment for patrons, and have an important role to play in preventing drink spiking.

This includes having clear procedures in place to ensure staff understand the signs of drink spiking, including with alcohol.

Preventing drink spiking is a collective responsibility, not something to be shouldered by potential victims.

Licensees can take responsible steps including:

  • removing unattended glasses
  • reporting suspicious behaviour
  • declining customer requests to add extra alcohol to a person’s drink
  • supplying water taps instead of large water jugs
  • promoting responsible consumption of alcohol, including discouraging rapid drinking
  • being aware of “red flag” drink requests, such as repeated shots, or double or triple shots, or adding vodka to beer or wine.
Bartender pouring drinks
Bartenders should be wary of ‘red flag’ drinks requests like people asking for double or triple shots.
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A few simple precautions everyone can take to reduce the risk of drink spiking include:

  • have your drink close to you, keep an eye on it and don’t leave it unattended
  • avoid sharing beverages with other people
  • purchase or pour your drinks yourself
  • if you’re offered a drink by someone you don’t know well, go to the bar with them and watch the bartender pour your drink
  • if you think your drink tastes weird, pour it out
  • keep an eye on your friends and their beverages too.

What are the consequences for drink spiking in Australia?

It’s a criminal offence to spike someone’s drink with alcohol or other drugs without their consent in all states and territories.

In some jurisdictions, there are specific drink and food spiking laws. For example, in Victoria, the punishment is up to two years imprisonment.

In other jurisdictions, such as Tasmania, drink spiking comes under broader offences such as “administering any poison or other noxious thing with intent to injure or annoy”.

Spiking someone’s drink with an intent to commit a serious criminal offence, such as sexual assault, usually comes with very severe penalties. For example, this carries a penalty of up to 14 years imprisonment in Queensland.

There are some ambiguities in the criminal law. For example, some laws aren’t clear about whether drink spiking with alcohol is an offence.

However, in all states and territories, if someone is substantially intoxicated with alcohol or other drugs it’s good evidence they aren’t able to give consent to sex. Sex with a substantially intoxicated person who’s unable to consent may constitute rape or another sexual assault offence.


Getting help

In an emergency, call triple zero (000) or the nearest police station.

For information about sexual assault, or for counselling or referral, call 1800RESPECT (1800 737 732).

If you’ve been a victim of drink spiking and want to talk to someone, the following confidential services can help:

– Beyond Blue: 1300 22 4636

– Kids Helpline (5-25 year olds): 1800 55 1800

– National Alcohol and other Drug Hotline: 1800 250 015.The Conversation

Nicole Lee, Professor at the National Drug Research Institute (Melbourne), Curtin University and Jarryd Bartle, Sessional Lecturer, RMIT University

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

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.




Read more:
I’ve heard COVID is leading to medicine shortages. What can I do if my medicine is out of stock?


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.




Read more:
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.




Read more:
Is remdesivir a miracle drug to cure coronavirus? Don’t get your hopes up yet


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.




Read more:
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:
We don’t need to change how we subsidise ‘breakthrough’ cancer treatments


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.