I found out I had a copy of the Chris Hemsworth dementia gene 20 years ago. ... trends now

I found out I had a copy of the Chris Hemsworth dementia gene 20 years ago. ... trends now
I found out I had a copy of the Chris Hemsworth dementia gene 20 years ago. ... trends now

I found out I had a copy of the Chris Hemsworth dementia gene 20 years ago. ... trends now

It is more than 20 years since I discovered in my 50s that I have a copy of the gene, ApoE4, that has been linked to a raised risk of Alzheimer's.

It's the same gene that the actor Chris Hemsworth carries, although he has two copies, one from each of his parents – he learned this in 2022 after having tests for a documentary series he was making about longevity.

Now comes news of a major study that has found that almost everyone who has two copies of this gene goes on to develop early signs of Alzheimer's. Researchers at the Sant Pau Research Institute in Barcelona looked at data from 10,000 people and 3,000 brain donors and found that the majority of those with two copies showed signs of Alzheimer's by the time they reached the age of 55. The researchers estimate that around 2 per cent of people have this gene profile.

Australian actor Chris Hemsworth, 40, learned that he had two copies of the ApoE4 gene. Most people with this gene profile develop signs of Alzheimer's by the age of 55

Australian actor Chris Hemsworth, 40, learned that he had two copies of the ApoE4 gene. Most people with this gene profile develop signs of Alzheimer's by the age of 55

My ApoE4 gene was identified when I was writing about the gene tests that were then just becoming publicly available and decided to take one. It was an alarming discovery, since not only do I have no family history of Alzheimer's, but back then there was nothing to be done about it. For a while, common moments such as forgetting why I was peering into a cupboard felt like a sinister warning.

But I quickly persuaded myself that any brain malfunction wouldn't begin for years. Anyway, a cure might come along at any time and as a health journalist I could keep up with the latest research.

Yet for years there was little to be hopeful about – the few drugs that were available didn't make a difference to the disease progression.

Small bits of cutting-edge research I came across here and there convinced me to try various lifestyle approaches (more on the specifics later), but the expectation has long been that once you're heading into the medical territory that is Alzheimer's, you need heavyweight pharmaceuticals.

But the cheering, and very surprising, news is that nutritional and lifestyle advice, with some additions and tweaks, is the very latest thing in Alzheimer's prevention, with several UK charities and academic centres – including Imperial College London, Exeter University and Alzheimer's Research UK – now actively investigating this.

What's driving this dramatic U-turn is the failure of the drug industry to come up with effective and safe products. Even the newer 'wonder' drugs such as donanemab and lecanemab, which can delay the worsening of the disease by around a third in patients, can have serious side-effects – around a quarter of those who take them suffer bleeding or swelling in the brain, and some patients have experienced brain shrinkage.

These drugs work by clearing the brain of amyloid plaques, the sticky protein deposits thought to cause symptoms by disrupting communication between brain cells.

The problems with the latest drugs are detailed in a new book by leading neurologist Professor Karl Herrup. In 'How not to study a disease: The story of Alzheimer's' he writes: 'In our rush to find a cure we have gone down a blind alley. For decades we have focused more on salesmanship than scholarship. The amyloid cascade hypothesis has become a steamroller, intent on crushing any alternative models.'

One problem is that having the plaque doesn't necessarily mean you will have Alzheimer's and not having it doesn't mean you won't.

As Professor Herrup points out, 'we need to rebalance this [amyloid] hypothesis about the cause of Alzheimer's' to include 'other worthy ideas about its nature, such as those indicated by the links with diabetes and blood vessel damage and the insights gained from approaches involving diet, nutrition, and lifestyle'.

What's so radical about the nutritional and lifestyle approach is that it doesn't target a single cause but aims to improve the health of many of the body's systems – such as metabolism (how energy is used), the immune system and the vast colony of bacteria and other microbes (the microbiome) in your gut, that have a two-way connection with the brain. Keeping them all healthy can do the same for the brain.

And it means we can all take steps to protect ourselves, which is what I've tried to do.

I spoke to Tommy Wood, an assistant professor of neuroscience and paediatrics at the University of Washington, who is a principle investigator for the research charity, the Food for the Brain Foundation, which is looking at dementia amongst other brain disorders.

He told me: 'I

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