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.

This is the next article in our ‘Light and health’ series, where we look at how light affects our physical and mental health in sometimes surprising ways. Read other articles in the series.

It’s spring and you’ve probably noticed a change in when the Sun rises and sets. But have you also noticed a change in your mood?

We’ve known for a while that light plays a role in our wellbeing. Many of us tend to feel more positive when spring returns.

But for others, big changes in light, such as at the start of spring, can be tough. And for many, bright light at night can be a problem. Here’s what’s going on.

An ancient rhythm of light and mood

In an earlier article in our series, we learned that light shining on the back of the eye sends “timing signals” to the brain and the master clock of the circadian system. This clock coordinates our daily (circadian) rhythms.

“Clock genes” also regulate circadian rhythms. These genes control the timing of when many other genes turn on and off during the 24-hour, light-dark cycle.

But how is this all linked with our mood and mental health?

Circadian rhythms can be disrupted. This can happen if there are problems with how the body clock develops or functions, or if someone is routinely exposed to bright light at night.

When circadian disruption happens, it increases the risk of certain mental disorders. These include bipolar disorder and atypical depression (a type of depression when someone is extra sleepy and has problems with their energy and metabolism).

Light on the brain

Light may also affect circuits in the brain that control mood, as animal studies show.

There’s evidence this happens in humans. A brain-imaging study showed exposure to bright light in the daytime while inside the scanner changed the activity of a brain region involved in mood and alertness.

Another brain-imaging study found a link between daily exposure to sunlight and how the neurotransmitter (or chemical messenger) serotonin binds to receptors in the brain. We see alterations in serotonin binding in several mental disorders, including depression.

What happens when the seasons change?

Light can also affect mood and mental health as the seasons change. During autumn and winter, symptoms such as low mood and fatigue can develop. But often, once spring and summer come round, these symptoms go away. This is called “seasonality” or, when severe, “seasonal affective disorder”.

What is less well known is that for other people, the change to spring and summer (when there is more light) can also come with a change in mood and mental health. Some people experience increases in energy and the drive to be active. This is positive for some but can be seriously destabilising for others. This too is an example of seasonality.

Most people aren’t very seasonal. But for those who are, seasonality has a genetic component. Relatives of people with seasonal affective disorder are more likely to also experience seasonality.

Seasonality is also more common in conditions such as bipolar disorder. For many people with such conditions, the shift into shorter day-lengths during winter can trigger a depressive episode.

Counterintuitively, the longer day-lengths in spring and summer can also destabilise people with bipolar disorder into an “activated” state where energy and activity are in overdrive, and symptoms are harder to manage. So, seasonality can be serious.

Alexis Hutcheon, who experiences seasonality and helped write this article, told us:

[…] the season change is like preparing for battle – I never know what’s coming, and I rarely come out unscathed. I’ve experienced both hypomanic and depressive episodes triggered by the season change, but regardless of whether I’m on the ‘up’ or the ‘down’, the one constant is that I can’t sleep. To manage, I try to stick to a strict routine, tweak medication, maximise my exposure to light, and always stay tuned in to those subtle shifts in mood. It’s a time of heightened awareness and trying to stay one step ahead.

So what’s going on in the brain?

One explanation for what’s going on in the brain when mental health fluctuates with the change in seasons relates to the neurotransmitters serotonin and dopamine.

Serotonin helps regulate mood and is the target of many antidepressants. There is some evidence of seasonal changes in serotonin levels, potentially being lower in winter.

Dopamine is a neurotransmitter involved in reward, motivation and movement, and is also a target of some antidepressants. Levels of dopamine may also change with the seasons.

But the neuroscience of seasonality is a developing area and more research is needed to know what’s going on in the brain.

How about bright light at night?

We know exposure to bright light at night (for instance, if someone is up all night) can disturb someone’s circadian rhythms.

This type of circadian rhythm disturbance is associated with higher rates of symptoms including self-harm, depressive and anxiety symptoms, and lower wellbeing. It is also associated with higher rates of mental disorders, such as major depression, bipolar disorder, psychotic disorders and post-traumatic stress disorder (or PTSD).

Why is this? Bright light at night confuses and destabilises the body clock. It disrupts the rhythmic regulation of mood, cognition, appetite, metabolism and many other mental processes.

But people differ hugely in their sensitivity to light. While still a hypothesis, people who are most sensitive to light may be the most vulnerable to body clock disturbances caused by bright light at night, which then leads to a higher risk of mental health problems.

Where to from here?

Learning about light will help people better manage their mental health conditions.

By encouraging people to better align their lives to the light-dark cycle (to stabilise their body clock) we may also help prevent conditions such as depression and bipolar disorder emerging in the first place.

Healthy light behaviours – avoiding light at night and seeking light during the day – are good for everyone. But they might be especially helpful for people at risk of mental health problems. These include people with a family history of mental health problems or people who are night owls (late sleepers and late risers), who are more at risk of body clock disturbances.

Alexis Hutcheon has lived experience of a mental health condition and helped write this article.

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; Emiliana Tonini, Postdoctoral Research Fellow, 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.

In July 2023, rising US basketball star Bronny James collapsed on the court during practice and was sent to hospital. The 18-year-old athlete, son of famous LA Lakers’ veteran LeBron James, had experienced a cardiac arrest.

Many media outlets incorrectly referred to the event as a “heart attack” or used the terms interchangeably.

A cardiac arrest and a heart attack are distinct yet overlapping concepts associated with the heart.

With some background in how the heart works, we can see how they differ and how they’re related.

Understanding the heart

The heart is a muscle that contracts to work as a pump. When it contracts it pushes blood – containing oxygen and nutrients – to all the tissues of our body.

For the heart muscle to work effectively as a pump, it needs to be fed its own blood supply, delivered by the coronary arteries. If these arteries are blocked, the heart muscle doesn’t get the blood it needs.

This can cause the heart muscle to become injured or die, and results in the heart not pumping properly.

Heart attack or cardiac arrest?

Simply put, a heart attack, technically known as a myocardial infarction, describes injury to, or death of, the heart muscle.

A cardiac arrest, sometimes called a sudden cardiac arrest, is when the heart stops beating, or put another way, stops working as an effective pump.

In other words, both relate to the heart not working as it should, but for different reasons. As we’ll see later, one can lead to the other.

Why do they happen? Who’s at risk?

Heart attacks typically result from blockages in the coronary arteries. Sometimes this is called coronary artery disease, but in Australia, we tend to refer to it as ischaemic heart disease.

The underlying cause in about 75% of people is a process called atherosclerosis. This is where fatty and fibrous tissue build up in the walls of the coronary arteries, forming a plaque. The plaque can block the blood vessel or, in some instances, lead to the formation of a blood clot.

Atherosclerosis is a long-term, stealthy process, with a number of risk factors that can sneak up on anyone. High blood pressure, high cholesterol, diet, diabetes, stress, and your genes have all been implicated in this plaque-building process.

Other causes of heart attacks include spasms of the coronary arteries (causing them to constrict), chest trauma, or anything else that reduces blood flow to the heart muscle.

Regardless of the cause, blocking or reducing the flow of blood through these pipes can result in the heart muscle not receiving enough oxygen and nutrients. So cells in the heart muscle can be injured or die.

But a cardiac arrest is the result of heartbeat irregularities, making it harder for the heart to pump blood effectively around the body. These heartbeat irregularities are generally due to electrical malfunctions in the heart. There are four distinct types:

• ventricular tachycardia: a rapid and abnormal heart rhythm in which the heartbeat is more than 100 beats per minute (normal adult, resting heart rate is generally 60-90 beats per minute). This fast heart rate prevents the heart from filling with blood and thus pumping adequately
• ventricular fibrillation: instead of regular beats, the heart quivers or “fibrillates”, resembling a bag of worms, resulting in an irregular heartbeat greater than 300 beats per minute
• pulseless electrical activity: arises when the heart muscle fails to generate sufficient pumping force after electrical stimulation, resulting in no pulse
• asystole: the classic flat-line heart rhythm you see in movies, indicating no electrical activity in the heart.

Cardiac arrest can arise from numerous underlying conditions, both heart-related and not, such as drowning, trauma, asphyxia, electrical shock and drug overdose. James’ cardiac arrest was attributed to a congenital heart defect, a heart condition he was born with.

But among the many causes of a cardiac arrest, ischaemic heart disease, such as a heart attack, stands out as the most common cause, accounting for 70% of all cases.

So how can a heart attack cause a cardiac arrest? You’ll remember that during a heart attack, heart muscle can be damaged or parts of it may die. This damaged or dead tissue can disrupt the heart’s ability to conduct electrical signals, increasing the risk of developing arrhythmias, possibly causing a cardiac arrest.

So while a heart attack is a common cause of cardiac arrest, a cardiac arrest generally does not cause a heart attack.

What do they look like?

Because a cardiac arrest results in the sudden loss of effective heart pumping, the most common signs and symptoms are a sudden loss of consciousness, absence of pulse or heartbeat, stopping of breathing, and pale or blue-tinged skin.

But the common signs and symptoms of a heart attack include chest pain or discomfort, which can show up in other regions of the body such as the arms, back, neck, jaw, or stomach. Also frequent are shortness of breath, nausea, light-headedness, looking pale, and sweating.

What’s the take-home message?

While both heart attack and cardiac arrest are disorders related to the heart, they differ in their mechanisms and outcomes.

A heart attack is like a blockage in the plumbing supplying water to a house. But a cardiac arrest is like an electrical malfunction in the house’s wiring.

Despite their different nature both conditions can have severe consequences and require immediate medical attention.

Michael Todorovic, Associate Professor of Medicine, Bond University and Matthew Barton, Senior lecturer, School of Nursing and Midwifery, Griffith University

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