It’s been more than 20 years since, when I was 50, I discovered that I have one copy of the ApoE4 gene, which has been linked to an increased risk of Alzheimer’s.
It is the same gene that actor Chris Hemsworth carries, although he has two copies, one from each of his parents; He found out in 2022 after taking tests for a documentary series he was making about longevity.
Now comes news of a major study that has found that almost all people who have two copies of this gene develop early signs of Alzheimer’s. Researchers at Barcelona’s Sant Pau Research Institute analyzed data from 10,000 people and 3,000 brain donors and found that most of those with two copies showed signs of Alzheimer’s by the time they reached age 55. Researchers estimate that about 2 percent of people have this genetic profile.
Australian actor Chris Hemsworth, 40, learned that he had two copies of the ApoE4 gene. Most people with this genetic profile develop signs of Alzheimer’s by age 55.
My ApoE4 gene was identified when I was writing about genetic testing that was barely publicly available and I decided to take one. It was an alarming discovery, since not only do I have no family history of Alzheimer’s, but at the time there was nothing to do about it. For a while, ordinary moments like forgetting why I was looking in a closet seemed like an ominous warning to me.
But I quickly became convinced that any brain malfunctions wouldn’t begin for years. Still, a cure could appear at any moment and, as a health journalist, I could keep up to date with the latest research.
However, for years there was little hope: the few drugs available made no difference to the progression of the disease.
Little cutting-edge research I found here and there convinced me to try various lifestyle approaches (more on the details later), but the expectation has long been that once you head into the medical territory that is Alzheimer’s, you need heavyweight pharmaceuticals.
But the encouraging and very surprising news is that nutritional and lifestyle advice, with some additions and tweaks, is the latest in Alzheimer’s prevention, with several UK charities and academic centers including Imperial College London, the University of Exeter and Alzheimer’s Research UK. – now actively researching this.
What is driving this dramatic U-turn is the pharmaceutical industry’s failure to create effective and safe products. Even newer “wonder” drugs, such as donanemab and lecanemab, which can delay the disease from worsening by about a third in patients, can have serious side effects: about a quarter of those who take them suffer bleeding or swelling in brain. , and some patients have experienced brain shrinkage.
These drugs work by clearing 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 rush to find a cure we have fallen into a dead end. For decades we have focused more on salesmanship than scholarship. The amyloid cascade hypothesis has become a steamroller, intended to crush any alternative model.’
One problem is that having plaque doesn’t necessarily mean you’ll get Alzheimer’s, and not having it doesn’t mean you won’t get it.
As Professor Herrup points out, “we need to rebalance this (amyloid) hypothesis about the cause of Alzheimer’s” to include “other valuable ideas about its nature, such as those indicated by the links with diabetes and blood vessel damage and the knowledge gained approaches that involve diet, nutrition and lifestyle.
What is so radical about the nutritional and lifestyle approach is that it does not target a single cause but instead 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 the gut, which have a bidirectional connection to 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 with Tommy Wood, an assistant professor of neuroscience and pediatrics at the University of Washington, who is a principal investigator for the research charity Food for the Brain Foundation, which looks at dementia among other brain disorders.
He told me: ‘The idea of multiple approaches to health and fitness first occurred to me when I was working with athletes as a performance consultant. Many of the systems that affected their cognitive and physical abilities were the same ones we focused on at the charity with much 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 levels must be kept low to protect the brain.
Health journalist Jerome Burne found out he has a copy of the ApoE4 gene when he was 50, more than 20 years ago. Since then he has taken steps to try to prevent the disease.
Chris Hemsworth is best known for playing Thor in the Avengers film franchise.
Insulin’s job is to help the body use sugar (glucose) in the blood for fuel. Professor Lustig, who also advises the Food for the Brain Foundation, says that high glucose levels (from a high carbohydrate diet) lead to higher insulin levels. “However, very soon your system stops responding to insulin, known as insulin resistance, which is bad news because insulin supplies the glucose needed for energy in the brain and muscles.”
This is the kind of information that convinced me over the years to make changes to my diet. The standard advice of eating lots of carbs and choosing the low-fat option was reversed and I started following a ketogenic diet which involves eating a lot more fat (mostly saturated) and is very low in carbs.
Fat is converted into small packets of energy, known as ketones, that can fuel brain cells.
I also started increasing gym visits from a couple of 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 involved eating more fibrous vegetables, as well as making and drinking kefir, a fermented drink that provides probiotics to the intestine, every day.
And I started taking vitamin B.
A decade after my gene was discovered, a randomized trial at the University of Oxford, led by Emeritus Professor David Smith, showed that B vitamins were essential for removing a toxic compound called homocysteine from the blood.
Homocysteine comes from the breakdown of proteins and can damage cells. Elevated 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), half of them received a daily high dose of vitamin B and the rest received a placebo. A proportion of each group had 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 striking: Not only did those in the vitamin group have reduced levels of homocysteine, but brain shrinkage (the sign of brain cell death) was half as low. than that of those in the placebo group.
However, instead of being welcomed, the trial sparked a long-running academic battle. Alzheimer’s charities, including one that contributed funding, ignored him.
Four years later another study was published that found no benefit from B vitamins, but I wasn’t convinced. While participants in the Oxford trial had mild cognitive impairment, those in subsequent trials did not. So I continued taking the pills.
One senior academic who has taken notice of this research is Professor Peter Garrard, a specialist in neurodegenerative diseases such as Alzheimer’s, at St George’s Hospital, London.
When his mother Sheila began losing words and describing things indirectly at the age of 78, he prescribed her a daily dose of high-potency B vitamins.
“It was very encouraging that, despite having had a brain scan showing significant cellular damage, he did not get any worse and slowly started to improve a lot,” Professor Garrard said. 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 that she stayed very fit and active.”
Professor Garrard told me that he had been impressed by the research on vitamin B carried out at Oxford and considered claims that vitamins had no benefit to be inaccurate. “I check all my patients’ homocysteine levels and give them vitamin B if they are above the healthy level,” he says.
Evidence on the benefits of B vitamins continued to accumulate, including in a 2020 review published by Professor Jin-Tai Yu of Fudan University in Shanghai, China’s leading Alzheimer’s prevention expert. Published in the Journal of Neurology, Neurosurgery and Psychiatry, he 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 treatment to reduce homocysteine analyzed involved the use of folic acid (B9), vitamin B12 and vitamin B6).
For my part, I am optimistic about the latest research on the ApoE4 gene: I currently feel good and fit, thanks to a program that seems a sensible way to avoid physical deterioration in general and neurological deterioration in particular.
