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.

Australians have used commercial creams, lotions or gels to manage our skin’s sun exposure for nearly a century.

But why we do it, the preparations themselves, and whether they work, has changed over time.

In this short history of sunscreen in Australia, we look at how we’ve slathered, slopped and spritzed our skin for sometimes surprising reasons.

At first, suncreams helped you ‘tan with ease’

Sunscreens have been available in Australia since the 30s. Chemist Milton Blake made one of the first.

He used a kerosene heater to cook batches of “sunburn vanishing cream”, scented with French perfume.

His backyard business became H.A. Milton (Hamilton) Laboratories, which still makes sunscreens today.

Hamilton’s first cream claimed you could “
Sunbathe in Comfort and TAN with ease”. According to modern standards, it would have had an SPF (or sun protection factor) of 2.

The mirage of ‘safe tanning’

A tan was considered a “modern complexion” and for most of the 20th century, you might put something on your skin to help gain one. That’s when “safe tanning” (without burning) was thought possible.

Sunburn was known to be caused by the UVB component of ultraviolet (UV) light. UVA, however, was thought not to be involved in burning; it was just thought to darken the skin pigment melanin. So, medical authorities advised that by using a sunscreen that filtered out UVB, you could “safely tan” without burning.

But that was wrong.

From the 70s, medical research suggested UVA penetrated damagingly deep into the skin, causing ageing effects such as sunspots and wrinkles. And both UVA and UVB could cause skin cancer.

Sunscreens from the 80s sought to be “broad spectrum” – they filtered both UVB and UVA.

Researchers consequently recommended sunscreens for all skin tones, including for preventing sun damage in people with dark skin.

Delaying burning … or encouraging it?

Up to the 80s, sun preparations ranged from something that claimed to delay burning, to preparations that actively encouraged it to get that desirable tan – think, baby oil or coconut oil. Sun-worshippers even raided the kitchen cabinet, slicking olive oil on their skin.

One manufacturer’s “sun lotion” might effectively filter UVB; another’s merely basted you like a roast chicken.

Since labelling laws before the 80s didn’t require manufacturers to list the ingredients, it was often hard for consumers to tell which was which.

At last, SPF arrives to guide consumers

In the 70s, two Queensland researchers, Gordon Groves and Don Robertson, developed tests for sunscreens – sometimes experimenting on students or colleagues. They printed their ranking in the newspaper, which the public could use to choose a product.

An Australian sunscreen manufacturer then asked the federal health department to regulate the industry. The company wanted standard definitions to market their products, backed up by consistent lab testing methods.

In 1986, after years of consultation with manufacturers, researchers and consumers, Australian Standard AS2604 gave a specified a testing method, based on the Queensland researchers’ work. We also had a way of expressing how well sunscreens worked – the sun protection factor or SPF.

This is the ratio of how long it takes a fair-skinned person to burn using the product compared with how long it takes to burn without it. So a cream that protects the skin sufficiently so it takes 40 minutes to burn instead of 20 minutes has an SPF of 2.

Manufacturers liked SPF because businesses that invested in clever chemistry could distinguish themselves in marketing. Consumers liked SPF because it was easy to understand – the higher the number, the better the protection.

Australians, encouraged from 1981 by the Slip! Slop! Slap! nationwide skin cancer campaign, could now “slop” on a sunscreen knowing the degree of protection it offered.

How about skin cancer?

It wasn’t until 1999 that research proved that using sunscreen prevents skin cancer. Again, we have Queensland to thank, specifically the residents of Nambour. They took part in a trial for nearly five years, carried out by a research team led by Adele Green of the Queensland Institute of Medical Research. Using sunscreen daily over that time reduced rates of squamous cell carcinoma (a common form of skin cancer) by about 60%.

Follow-up studies in 2011 and 2013 showed regular sunscreen use almost halved the rate of melanoma and slowed skin ageing. But there was no impact on rates of basal cell carcinoma, another common skin cancer.

By then, researchers had shown sunscreen stopped sunburn, and stopping sunburn would prevent at least some types of skin cancer.

What’s in sunscreen today?

An effective sunscreen uses one or more active ingredients in a cream, lotion or gel. The active ingredient either works:

• “chemically” by absorbing UV and converting it to heat. Examples include PABA (para-aminobenzoic acid) and benzyl salicylate, or

• “physically” by blocking the UV, such as zinc oxide or titanium dioxide.

Physical blockers at first had limited cosmetic appeal because they were opaque pastes. (Think cricketers with zinc smeared on their noses.)

With microfine particle technology from the 90s, sunscreen manufacturers could then use a combination of chemical absorbers and physical blockers to achieve high degrees of sun protection in a cosmetically acceptable formulation.

Where now?

Australians have embraced sunscreen, but they still don’t apply enough or reapply often enough.

Although some people are concerned sunscreen will block the skin’s ability to make vitamin D this is unlikely. That’s because even SPF50 sunscreen doesn’t filter out all UVB.

There’s also concern about the active ingredients in sunscreen getting into the environment and whether their absorption by our bodies is a problem.

Sunscreens have evolved from something that at best offered mild protection to effective, easy-to-use products that stave off the harmful effects of UV. They’ve evolved from something only people with fair skin used to a product for anyone.

Remember, slopping on sunscreen is just one part of sun protection. Don’t forget to also slip (protective clothing), slap (hat), seek (shade) and slide (sunglasses).

Laura Dawes, Research Fellow in Medico-Legal History, Australian National University

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