A recent study has suggested Shingrix, a relatively new vaccine given to protect older adults against shingles, may delay the onset of dementia.

This might seem like a bizarre link, but actually, research has previously shown an older version of the shingles vaccine, Zostavax, reduced the risk of dementia.

In this new study, published last week in the journal Nature Medicine, researchers from the United Kingdom found Shingrix delayed dementia onset by 17% compared with Zostavax.

So how did the researchers work this out, and how could a shingles vaccine affect dementia risk?

From Zostavax to Shingrix

Shingles is a viral infection caused by the varicella-zoster virus. It causes painful rashes, and affects older people in particular.

Previously, Zostavax was used to vaccinate against shingles. It was administered as a single shot and provided good protection for about five years.

Shingrix has been developed based on a newer vaccine technology, and is thought to offer stronger and longer-lasting protection. Given in two doses, it’s now the preferred option for shingles vaccination in Australia and elsewhere.

In November 2023, Shingrix replaced Zostavax on the National Immunisation Program, making it available for free to those at highest risk of complications from shingles. This includes all adults aged 65 and over, First Nations people aged 50 and older, and younger adults with certain medical conditions that affect their immune systems.

What the study found

Shingrix was approved by the US Food and Drugs Administration in October 2017. The researchers in the new study used the transition from Zostavax to Shingrix in the United States as an opportunity for research.

They selected 103,837 people who received Zostavax (between October 2014 and September 2017) and compared them with 103,837 people who received Shingrix (between November 2017 and October 2020).

By analysing data from electronic health records, they found people who received Shingrix had a 17% increase in “diagnosis-free time” during the follow-up period (up to six years after vaccination) compared with those who received Zostavax. This was equivalent to an average of 164 extra days without a dementia diagnosis.

The researchers also compared the shingles vaccines to other vaccines: influenza, and a combined vaccine for tetanus, diphtheria and pertussis. Shingrix and Zostavax performed around 14–27% better in lowering the risk of a dementia diagnosis, with Shingrix associated with a greater improvement.

The benefits of Shingrix in terms of dementia risk were significant for both sexes, but more pronounced for women. This is not entirely surprising, because we know women have a higher risk of developing dementia due to interplay of biological factors. These include being more sensitive to certain genetic mutations associated with dementia and hormonal differences.

Why the link?

The idea that vaccination against viral infection can lower the risk of dementia has been around for more than two decades. Associations have been observed between vaccines, such as those for diphtheria, tetanus, polio and influenza, and subsequent dementia risk.

Research has shown Zostavax vaccination can reduce the risk of developing dementia by 20% compared with people who are unvaccinated.

But it may not be that the vaccines themselves protect against dementia. Rather, it may be the resulting lack of viral infection creating this effect. Research indicates bacterial infections in the gut, as well as viral infections, are associated with a higher risk of dementia.

Notably, untreated infections with herpes simplex (herpes) virus – closely related to the varicella-zoster virus that causes shingles – can significantly increase the risk of developing dementia. Research has also shown shingles increases the risk of a later dementia diagnosis.

The mechanism is not entirely clear. But there are two potential pathways which may help us understand why infections could increase the risk of dementia.

First, certain molecules are produced when a baby is developing in the womb to help with the body’s development. These molecules have the potential to cause inflammation and accelerate ageing, so the production of these molecules is silenced around birth. However, viral infections such as shingles can reactivate the production of these molecules in adult life which could hypothetically lead to dementia.

Second, in Alzheimer’s disease, a specific protein called Amyloid-β go rogue and kill brain cells. Certain proteins produced by viruses such as COVID and bad gut bacteria have the potential to support Amyloid-β in its toxic form. In laboratory conditions, these proteins have been shown to accelerate the onset of dementia.

What does this all mean?

With an ageing population, the burden of dementia is only likely to become greater in the years to come. There’s a lot more we have to learn about the causes of the disease and what we can potentially do to prevent and treat it.

This new study has some limitations. For example, time without a diagnosis doesn’t necessarily mean time without disease. Some people may have underlying disease with delayed diagnosis.

This research indicates Shingrix could have a silent benefit, but it’s too early to suggest we can use antiviral vaccines to prevent dementia.

Overall, we need more research exploring in greater detail how infections are linked with dementia. This will help us understand the root causes of dementia and design potential therapies.

Ibrahim Javed, Enterprise and NHMRC Emerging Leadership Fellow, UniSA Clinical & Health Sciences, University of South Australia

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

“Charlie” is an eight-year-old child with autism. Her parents are worried because she often responds to requests with insults, aggression and refusal. Simple demands, such as being asked to get dressed, can trigger an intense need to control the situation, fights and meltdowns.

Charlie’s parents find themselves in a constant cycle of conflict, trying to manage her and their own reactions, often unsuccessfully. Their attempts to provide structure and consequences are met with more resistance.

What’s going on? What makes Charlie’s behaviour – that some are calling “pathological demand avoidance” – different to the defiance most children show their parents or carers from time-to-time?

What is pathological demand avoidance?

British developmental psychologist Elizabeth Newson coined the term “pathological demand avoidance” (commonly shortened to PDA) in the 1980s after studying groups of children in her practice.

A 2021 systematic review noted features of PDA include resistance to everyday requests and strong emotional and behavioural reactions.

Children with PDA might show obsessive behaviour, struggle with persistence, and seek to control situations. They may struggle with attention and impulsivity, alongside motor and coordination difficulties, language delay and a tendency to retreat into role play or fantasy worlds.

PDA is also known as “extreme demand avoidance” and is often described as a subtype of autism. Some people prefer the term persistent drive for autonomy or pervasive drive for autonomy.

What does the evidence say?

Every clinician working with children and families recognises the behavioural profile described by PDA. The challenging question is why these behaviours emerge.

PDA is not currently listed in the two diagnostic manuals used in psychiatry and psychology to diagnose mental health and developmental conditions, the current Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the World Health Organization’s International Classification of Diseases (ICD-11).

Researchers have reported concerns about the science behind PDA. There are no clear theories or explanations of why or how the profile of symptoms develop, and little inclusion of children or adults with lived experience of PDA symptoms in the studies. Environmental, family or other contextual factors that may contribute to behaviour have not been systematically studied.

A major limitation of existing PDA research and case studies is a lack of consideration of overlapping symptoms with other conditions, such as autism, attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder, anxiety disorder, selective mutism and other developmental disorders. Diagnostic labels can have positive and negative consequences and so need to be thoroughly investigated before they are used in practice.

Classifying a “new” condition requires consistency across seven clinical and research aspects: epidemiological data, long-term patient follow-up, family inheritance, laboratory findings, exclusion from other conditions, response to treatment, and distinct predictors of outcome. At this stage, these domains have not been established for PDA. It is not clear whether PDA is different from other formal diagnoses or developmental differences.

Finding the why

Debates over classification don’t relieve distress for a child or those close to them. If a child is “intentionally” engaged in antisocial behaviour, the question is then “why?”

Beneath the behaviour is almost always developmental difference, genuine distress and difficulty coping. A broad and deep understanding of developmental processes is required.

Interestingly, while girls are “under-represented” in autism research, they are equally represented in studies characterising PDA. But if a child’s behaviour is only understood through a “pathologising” or diagnostic lens, there is a risk their agency may be reduced. Underlying experiences of distress, sensory overload, social confusion and feelings of isolation may be missed.

So, what can be done to help?

There are no empirical studies to date regarding PDA treatment strategies or their effectiveness. Clinical advice and case studies suggest strategies that may help include:

• reducing demands
• giving multiple options
• minimising expectations to avoid triggering avoidance
• engaging with interests to support regulation.

Early intervention in the preschool and primary years benefits children with complex developmental differences. Clinical care that involves a range of medical and allied health clinicians and considers the whole person is needed to ensure children and families get the support they need.

It is important to recognise these children often feel as frustrated and helpless as their caregivers. Both find themselves stuck in a repetitive cycle of distress, frustration and lack of progress. A personalised approach can take into account the child’s unique social, sensory and cognitive sensitivities.

In the preschool and early primary years, children have limited ability to manage their impulses or learn techniques for managing their emotions, relationships or environments. Careful watching for potential triggers and then working on timetables and routines, sleep, environments, tasks, and relationships can help.

As children move into later primary school and adolescence, they are more likely to want to influence others and be able to have more self control. As their autonomy and ability to collaborate increases, the problematic behaviours tend to reduce.

Strategies that build self-determination are crucial. They include opportunities for developing confidence, communication and more options to choose from when facing challenges. This therapeutic work with children and families takes time and needs to be revisited at different developmental stages. Support to engage in school and community activities is also needed. Each small step brings more capacity and more effective ways for a child to understand and manage themselves and their worlds.

What about Charlie?

The current scope to explain and manage PDA is limited. Future research must include the voices and views of children and adults with PDA symptoms.

Such emotional and behavioural difficulties are distressing and difficult for children and families. They need compassion and practical help.

For a child like Charlie, this could look like a series of sessions where she and her parents meet with clinicians to explore Charlie’s perspective, experiences and triggers. The family might come to understand that, in addition to autism, Charlie has complex developmental strengths and challenges, anxiety, and some difficulties with adjustment related to stress at home and school. This means Charlie experiences a fight, flight, freeze response that looks like aggression, avoidance or shutting down.

With carefully planned supports at home and school, Charlie’s options can broaden and her distress and avoidance can soften. Outside the clinic room, Charlie and her family can be supported to join an inclusive local community sporting or creative activity. Gradually she can spend more time engaged at home, school and in the community.

Nicole Rinehart, Professor, Child and Adolescent Psychology, Director, Krongold Clinic (Research), Monash University; David Moseley, Senior Research Fellow, Deputy Director (Clinical), Monash Krongold Clinic, Monash University, and Michael Gordon, Associate Professor, Psychiatry, Monash University

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