The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.

Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.

But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.

Reactive vs endogenous depression

One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.

Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.

Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.

Many people working clinically in mental health accept this sub-typing. You might have read about this online.

But we think this approach is way too simple.

While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.

What we did and what we found

Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.

In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.

Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?

You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.

We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.

If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.

But after studying more than 14,000 people with depression we found the opposite.

We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.

Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.

These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.

How do genes play a role?

Genetic risk for mental disorders changes people’s sensitivity to the environment.

Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.

Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.

What does our study mean for depression?

First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.

Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.

Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.

So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.

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

Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney

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

From today, February 3, pregnant women in Australia will be eligible for a free RSV vaccine under the National Immunisation Program.

This vaccine is designed to protect young infants from severe RSV (respiratory syncytial virus). It does so by generating the production of antibodies against RSV in the mother, which then travel across the placenta to the baby.

While the RSV vaccine is a new addition to the National Immunisation Program, it’s one of three vaccines provided free for pregnant women under the program, alongside ones for influenza and whooping cough. Each offers important protection for newborn babies.

The RSV vaccine

RSV is the most common cause of lower respiratory infections (bronchiolitis and pneumonia) in infants. It’s estimated that of every 100 infants born in Australia each year, at least two will be hospitalised with RSV by six months of age.

RSV infection is most common roughly between March and August in the southern hemisphere, but infection can occur year-round, especially in tropical areas.

The vaccine works by conferring passive immunity (from the mother) as opposed to active immunity (the baby’s own immune response). By the time the baby is born, their antibodies are sufficient to protect them during the first months of life when they are most vulnerable to severe RSV disease.

The RSV vaccine registered for use in pregnant women in Australia, Abrysvo, has been used since 2023 in the Americas and Europe. Real-world experience there shows it’s working well.

For example, over the 2024 RSV season in Argentina, it was found to prevent 72.7% of lower respiratory tract infections caused by RSV and requiring hospitalisation in infants aged 0–3 months, and 68% among those aged 0–6 months. This research noted three deaths from RSV, all in infants whose mothers did not receive the RSV vaccine during pregnancy.

This was similar to protection seen in a large multinational clinical trial that compared babies born to mothers who received this RSV vaccine with babies born to mothers who received a placebo. This study found the vaccine prevented 82.4% of severe cases of RSV in infants aged under three months, and 70% under six months, and that the vaccine was safe.

In addition to the maternal vaccine, nirsevimab, a long-acting monoclonal antibody, provides effective protection against severe RSV disease. It’s delivered to the baby by an intramuscular injection, usually in the thigh.

Nirsevimab is recommended for babies born to women who did not receive an RSV vaccine during pregnancy, or who are born within two weeks of their mother having received the shot (most likely if they’re born prematurely). It may also be recommended for babies who are at higher risk of RSV due to a medical condition, even if their mother was vaccinated.

Nirsevimab is not funded under the National Immunisation Program, but is covered under various state and territory-based programs for infants of mothers who fall into the above categories.

But now we have a safe and effective RSV vaccine for pregnancy, all pregnant women should be encouraged to receive it as the first line of prevention. This will maximise the number of babies protected during their first months of life.

Flu and whooping cough

It’s also important pregnant women continue to receive flu and whooping cough vaccines in 2025. Like the RSV vaccine, these protect infants by passing antibodies from mother to baby.

There has been a large whooping cough outbreak in Australia in recent months, including a death of a two-month-old infant in Queensland in November 2024.

The whooping cough vaccine, given in combination with diphtheria and tetanus, prevents more than 90% of whooping cough cases in babies too young to receive their first whooping cough vaccine dose.

Similarly, influenza can be deadly in young babies, and maternal flu vaccination substantially reduces hospital visits associated with influenza for babies under six months. Flu can also be serious for pregnant women, so the vaccine offers important protection for the mother as well.

COVID vaccines are safe in pregnancy, but unless a woman is otherwise eligible, they’re not routinely recommended. You can discuss this with your health-care provider.

When and where can you get vaccinated?

Pregnant women can receive these vaccines during antenatal visits through their GP or in a specialised antenatal clinic.

The flu vaccine is recommended at any time during pregnancy, the whooping cough vaccine from 20 weeks (ideally before 32 weeks), and the RSV vaccine from 28 weeks (before 36 weeks).

It’s safe to receive multiple vaccinations at the same clinic visit.

We know vaccination rates have declined in a variety of groups since the pandemic, and there’s evidence emerging that suggests this trend has occurred in pregnant women too.

A recent preprint (a study yet to be peer-reviewed) found a decrease of nearly ten percentage points in flu vaccine coverage among pregnant women in New South Wales, from 58.8% in 2020 to 49.1% in 2022. The research showed a smaller drop of 1.4 percentage points for whooping cough, from 79% in 2020 to 77.6% in 2022.

It’s important to work to improve vaccination rates during pregnancy to give babies the best protection in their first months of life.

We know pregnant women would like to receive information about new and routine maternal vaccines early in pregnancy. In particular, many pregnant women want to understand how vaccines are tested for safety, and their effectiveness, which was evident during COVID.

GPs and midwives are trusted sources of information on vaccines in pregnancy. There’s also information available online on Sharing Knowledge About Immunisation, a collaboration led by the National Centre for Immunisation Research and Surveillance.

Archana Koirala, Paediatrician and Infectious Diseases Specialist, University of Sydney; Bianca Middleton, Senior Research Fellow, Menzies School of Health Research; Margie Danchin, Professor of Paediatrics and vaccinologist, Royal Childrens Hospital, University of Melbourne and Murdoch Childrens Research Institute (MCRI); Associate Dean International, University of Melbourne, Murdoch Children’s Research Institute; Peter McIntyre, Professor in Women’s and Children’s Health, University of Otago, and Rebecca Doyle, Adjunct Research Fellow, School of Nursing, Midwifery and Social Work, The University of Queensland

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