Twenty years ago, I discovered I had a copy of Chris Hemsworth’s dementia gene. Here’s what I’ve done since then to keep the disease at bay – and what you should do too…

It’s been more than 20 years since I discovered, at age 50, that I have a copy of the gene, ApoE4, that has been linked to an increased risk of Alzheimer’s disease.

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

Now comes news of a major study showing that almost everyone who has two copies of this gene develops early signs of Alzheimer’s disease. 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 disease by the time they reached the age of 55. The researchers estimate that about 2 per cent of people have this gene profile.

My ApoE4 gene was identified when I wrote about the gene tests that were just then becoming publicly available and decided to take one. It was an alarming discovery because not only do I have no family history of Alzheimer’s, but there was nothing that could be done about it at the time. For a while, ordinary moments, like forgetting why I was peering into a closet, felt like a sinister warning.

But I quickly convinced myself that a brain disorder wouldn’t develop until years later. Either way, a cure was coming at any moment, and as a health journalist I could keep up with the latest research.

Yet for years there was little reason to be hopeful: the few drugs available made no difference in disease progression.

Little bits of groundbreaking research I’ve come across here and there have convinced me to try different lifestyle approaches (more on the details later), but the expectation has long been that once you get into the medical field of Alzheimer’s, your heavy pharmaceutical products.

But the encouraging and very surprising news is that diet and lifestyle advice, with some additions and adjustments, is the cutting edge of Alzheimer’s prevention, with several UK charities and academic centers – including Imperial College London, Exeter University and Alzheimer’s Research UK. – is now actively investigating this.

What is driving this dramatic turnaround is the drug industry’s inability to come up with effective and safe products. Even the newer ‘miracle drugs’ such as donanemab and lecanemab, which can slow the progression of the disease in patients by around a third, can have serious side effects – around a quarter of those who take them experience bleeding or swelling in the brain. and some patients have experienced brain shrinkage.

These drugs work by ridding the brain of amyloid plaques, the sticky protein deposits that are 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 haste to find a cure, we have hit a dead end. For decades we have focused more on sales than science. The amyloid cascade hypothesis has become a steamroller, intent on destroying any alternative model.”

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

As Professor Herrup notes, ‘we need to rebalance this (amyloid) hypothesis about the cause of Alzheimer’s disease’ and ‘incorporate other valuable ideas about its nature, such as those indicated by the links with diabetes and damage to blood vessels and the insights gained from approaches involving diet, nutrition and lifestyle’.

What is so radical about the diet and lifestyle approach is that it does not focus on 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 huge colony of bacteria and other microbes (the microbiome) in your gut, which has a two-way connection to the brain. Keeping them all healthy can do the same for the brain.

And it means that we can all take steps to protect ourselves, and that’s what I’ve tried to do.

I spoke with Tommy Wood, an assistant professor of neuroscience and pediatrics at the University of Washington who is a principal investigator for the research organization, the Food for the Brain Foundation, which works on dementia and other brain disorders.

He told me, “I first came across the idea of ​​multiple approaches to health and fitness when I was working with athletes as a performance consultant. Many of the systems that affected their cognitive and physical abilities were the same as those we focus on at the charity with many older people.”

Robert Lustig, professor emeritus and international expert on metabolism based at the University of California San Francisco, explains why both blood sugar and insulin must be kept at low levels to protect the brain.

Insulin’s job is to help the body use blood sugar (glucose) as fuel. Professor Lustig, who also advises the Food for the Brain Foundation, says high glucose levels – from a high-carb diet – lead to higher insulin levels. ‘Quite quickly, however, your system stops responding to insulin – known as insulin resistance – which is bad news because insulin provides the glucose needed for energy in the brain and muscles.’

This is the kind of information that has convinced me over the years to make changes to my diet. The standard advice of eating enough carbs and choosing the low-fat option was reversed and I started following a ketogenic diet that involved eating a lot more fat – mostly saturated – and containing very little carbs.

The fat is converted into small energy packets known as ketones, which can provide brain cells with energy.

I also started to increase my gym visits from a few times a week to three or four. Exercise improves blood circulation, which is necessary to remove waste products from the brain.

I started paying attention to my microbiome, the colony of microbes that live in the gut. This meant eating more fibrous vegetables every day and making and drinking kefir, a fermented drink that delivers probiotics to the gut.

And I started taking B vitamins.

Ten years after my gene was spotted, a randomized trial at the University of Oxford, led by Emeritus Professor David Smith, showed that B vitamins were essential for removing a toxic substance called homocysteine ​​from the blood.

Homocysteine ​​is caused by the breakdown of proteins and can damage cells. High levels are often found in the brains of Alzheimer’s patients.

In the Oxford study, which involved more than 200 people with mild cognitive impairment (MCI) – where memory and clear thinking are affected – half were given a high dose of vitamin B daily, the rest a placebo. Part of each group received a brain scan at the beginning and end of the two-year trial.

The results, published in the journal PLOS One in September 2010, were impressive: Not only did those in the vitamin group have reduced homocysteine ​​levels, but brain shrinkage – the sign of brain cell death – was half that of the placebo group.

However, instead of being welcomed, the process led to a protracted academic battle. Alzheimer’s charities, including one that contributed money, ignored it.

Another study that showed no benefit from B vitamins was published four years later, but it didn’t convince me. While participants in the Oxford trial had MCI, those in the later trials did not. That’s why I kept taking the tablets.

One senior academic who has picked up this research is Professor Peter Garrard, a specialist in neurodegenerative diseases such as Alzheimer’s, at St George’s Hospital in London.

When his mother Sheila began to lose her words and describe things in a roundabout way at the age of 78, he gave her a daily dose of powerful B vitamins.

‘It was very encouraging that, despite having a brain scan that showed significant cell damage, she did not get worse and then gradually started doing much better,’ says Professor Garrard. Sheila died at the age of 89. ‘We will never know how long she would have lived without the vitamins, but it must have made a difference in keeping her very fit and active.’

Professor Garrard told me that he was impressed by the research into vitamin B at Oxford and that he considered the claims that the vitamins had no benefit to be incorrect. “I monitor my patients’ homocysteine ​​levels and give them B vitamins if they are above healthy levels,” he says.

The evidence in favor of B vitamins continued to mount, including a 2020 review published by Professor Jin-Tai Yu of Fudan University in Shanghai, China’s leading expert on Alzheimer’s prevention. This published in the Journal of Neurology, Neurosurgery and Psychiatry analyzed the results of 153 randomized trials and concluded that: ‘Homocysteine-lowering treatment appears to be the most promising intervention for the prevention of Alzheimer’s disease. ‘ (The homocysteine-lowering treatment examined involved the use of folic acid (B9), vitamin B12 and vitamin B6).

As for me, I’m optimistic about the latest research on the ApoE4 gene: I’m feeling fit and well right now, thanks to a program that seems like a sensible way to prevent physical decline in general, and neurological decline in particular.