Australia’s Therapeutic Goods Administration (TGA) recently issued a safety alert requiring extra warnings to be included with the asthma and hay fever drug montelukast.

The warnings are for users and their families to look for signs of serious behaviour and mood-related changes, such as suicidal thoughts and depression. The new warnings need to be printed at the start of information leaflets given to both patients and health-care providers (sometimes called a “boxed” warning).

So why did the TGA issue this warning? And is there cause for concern if you or a family member uses montelukast? Here’s what you need to know.

First, what is montelukast?

Montelukast is a prescription drug also known by its brand names which include Asthakast, Lukafast, Montelair and Singulair. It’s used to manage the symptoms of mild-to-moderate asthma and seasonal hay fever in children and adults.

Asthma occurs when the airways tighten and produce extra mucus, which makes it difficult to get air into the lungs. Likewise, the runny nose characteristic of hay fever occurs due to the overproduction of mucus.

Leukotrienes are an important family of chemicals found throughout the airways and involved in both mucus production and airway constriction. Montelukast is a cysteinyl leukotriene receptor antagonist, meaning it blocks the site in the airways where the leukotrienes work.

Montelukast can’t be used to treat acute asthma (an asthma attack), as it takes time for the tablet to be broken down in the stomach and for it to be absorbed into the body. Rather, it’s taken daily to help prevent asthma symptoms or seasonal hay fever.

It can be used alongside asthma puffers that contain corticosteriods and drugs like salbutamol (Ventolin) in the event of acute attacks.

What is the link to depression and suicide?

The possibility that this drug may cause behavioural changes is not new information. Manufacturers knew this as early as 2007 and issued warnings for possible side-effects including depression, suicidality and anxiousness.

The United Kingdom’s Medicines and Healthcare products Regulatory Agency has required a warning since 2008 but mandated a more detailed warning in 2019. The United States’ Food and Drug Administration has required boxed warnings for the drug since 2020.

Montelukast is known to potentially induce a number of behaviour and mood changes, including agitation, anxiety, depression, irritability, obsessive-compulsive symptoms, and suicidal thoughts and actions.

Initially a 2009 study that analysed data from 157 clinical trials involving more than 20,000 patients concluded there were no completed suicides due to taking the drug, and only a rare risk of suicide thoughts or attempts.

The most recent study, published in November 2024, examined data from more than 100,000 children aged 3–17 with asthma or hay fever who either took montelukast or used only inhaled corticosteroids.

It found montelukast use was associated with a 32% higher incidence of behavioural changes. The behaviour change with the strongest association was sleep disturbance, but montelukast use was also linked to increases in anxiety and mood disorders.

In the past ten years, around 200 incidences of behavioural side-effects have been reported to the TGA in connection with montelukast. This includes 57 cases of depression, 60 cases of suicidal thoughts and 17 suicide attempts or incidents of intentional self-injury. There were seven cases where patients taking the drug did complete a suicide.

This is of course tragic. But these numbers need to be seen in the context of the number of people taking the drug. Over the same time period, more than 200,000 scripts for montelukast have been filled under the Pharmaceutical Benefits Scheme.

Overall, we don’t know conclusively that montelukast causes depression and suicide, just that it seems to increase the risk for some people.

And if it does change behaviour, we don’t fully understand how this happens. One hypothesis is that the drug and its breakdown products (or metabolites) affect brain chemistry.

Specifically, it might interfere with how the brain detoxifies the antioxidant glutathione or alter the regulation of other brain chemicals, such as neurotransmitters.

Why is the TGA making this change now?

The new risk warning requirement comes from a meeting of the Australian Advisory Committee on Medicines where they were asked to provide advice on ways to minimise the risk for the drug given current international recommendations.

Even though the 2024 review didn’t highlight any new risks, to align with international recommendations, and help address consumer concerns, the advisory committee recommended a boxed warning be added to drug information sheets.

If you have asthma and take montelukast (or your child does), you should not just stop taking the drug, because this could put you at risk of an attack that could be life threatening. If you’re concerned, speak to your doctor who can discuss the risks and benefits of the medication for you, and, if appropriate, prescribe a different medication.

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

Nial Wheate, Professor of Pharmaceutical Chemistry, Macquarie University

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

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

What’s CJD got to do with Alzehimer’s?

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Human growth hormone used to come from donated organs

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

What are the latest findings about Alzheimer’s disease?

The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.

Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

When was this process used in Australia?

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.

The risk is very low – and you can’t ‘catch’ it like a virus

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.

Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University

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