Lessons every man should learn from my dad’s prostate cancer diagnosis
Over the course of a week, I read a lot of scientific articles (so you don’t have to) and one of the things I always keep a keen eye out for is anything on prostate cancer.
It is the most common cancer in British men and, over the past decade, while deaths from other common cancers such as bowel and breast have fallen, deaths from prostate cancer have risen.
I have a particular interest in prostate cancer because my dad was diagnosed with it when he was in his 60s (roughly the same age that I am now).
I am acutely aware of the fact that because dad had prostate cancer, my chances of getting it are around two-and-a-half times higher than if he hadn’t.
So you might think that I am very pro screening for prostate cancer but if my dad’s experience taught me anything, it’s that this particular issue is far more complex than you might think.
Michael Mosley (pictured) had a particular interest in prostate cancer because his father was diagnosed with it when he was in his 60s
The prostate is a gland, about the size of a walnut, which surrounds the urethra — the tube which you pee through.
Unfortunately, it grows from our 50s onwards and men often experience symptoms caused by the prostate compressing the urethra, such as waking up frequently during the night and finding it hard to start urinating.
Although these can also be symptoms of prostate cancer, they are normally the result of an enlarged prostate.
One of the scary things about prostate cancer is there are rarely any symptoms until the tumour has got quite large or has spread.
And once that happens you might experience back pain, problems getting or keeping an erection, blood in the urine or unexplained weight loss.
Your chances of developing prostate cancer increase beyond the age of 50 and it is more common in men of African-Caribbean or African descent.
As I mentioned, your risk is two-and-a-half times greater if your brother or father had it, and there is research which suggests that being significantly overweight also increases your risk.
Which brings us back to screening. Lots of famous people have had prostate cancer, including Noel Edmonds and Robert De Niro. Most only discovered they had the cancer by taking a PSA test — a blood test which measures prostate specific antigen, a protein, levels of which increase if cancer is present.
A couple of years ago, the author and presenter Stephen Fry described, on Twitter, being diagnosed with prostate cancer after a routine health check found he had a high PSA level. It turned out they caught it just in time because it was, in Stephen’s words, ‘an aggressive little bugger’.
Examples such as his would seem to make the case for routine PSA tests, but it is not that straightforward.
PSA levels can rise not just due to cancer but also due to an infection or everyday inflammation.
When I was at medical school I was told that PSA stands for ‘promoting stress and anxiety’, and that routine PSA tests may do more harm than good.
That message was reinforced a few years ago, when I put myself through a battery of health tests for a film for BBC’s Horizon, to see which were worth doing. These included having my blood pressure measured, a PSA test and bowel scope screening (which may involve a tube up your bum).
Prostate cancer is the most common cancer in British men and, over the past decade, while deaths from other common cancers have fallen, deaths from prostate cancer have risen
I concluded having my blood pressure and my bowels checked were a good idea, but the benefits of the PSA were less clear.
Not only does it throw up lots of ‘false positives’ but it also warns you about the presence of cancers that may never impact your life; 70 per cent of men over the age of 80 have prostate cancer, but most will die of something else.
My father is a good example. He had a PSA test, as part of a private health check, and further investigations revealed he had prostate cancer. He had invasive surgery to get rid of it, but the impact of the surgery blighted the last years of his life.
It’s possible the treatment slowed the disease, but it is also possible it was a slow-growing tumour and he would have died never knowing he had it. In fact, he died of unrelated heart failure several years after the operation.
The good news is that tests that can discriminate rapidly growing cancers from more benign forms are becoming widely available.
These include a ‘multi- parametric magnetic resonance imaging’ (mpMRI) scan, which creates more detailed pictures of the prostate than a standard MRI scan. These are available on the NHS, and recent trials have shown they are significantly better at identifying dangerous prostate cancers than biopsies (where they have to stick needles into your prostate to see if it contains any cancerous cells).
Since biopsies and over-treatment — treating cancer which may never prove troublesome — often lead to impotence and incontinence, I will book myself an mpMRI should the need arise.
The other good news is that treatments have improved since my dad’s surgery 30 years ago.
There are now lots of other options, including cryotherapy (freezing the cancer cells) and high-intensity focused ultrasound — using ultrasound to heat the tumour to try to kill it.
If you do have symptoms, or are just concerned, talk to your GP.
Why it pays to go to work on an egg
I used to dash out the door every morning after a quick breakfast of toast or cereal. These days, I have a more filling, protein-rich breakfast, such as scrambled eggs or kippers.
That’s because I know it will keep me fuller for longer, so I won’t have cravings at 11am.
Another good reason is that a protein-rich breakfast may help build muscle.
A filling, protein-rich breakfast, such as scrambled eggs, will keep you fuller for longer and may help to build muscle
In a study, researchers in Japan gave 60 middle-aged women a food questionnaire, then tested their grip strength.
The women who ate more protein for breakfast did better on the grip strength tests.
Studies with animals have shown that even when they don’t consume more protein overall, protein consumed earlier in the day leads to bigger muscles.
A good excuse for a hearty breakfast.
Tricks to help you stop forgetting people’s names
As we get older most of us struggle with our memory, particularly when it comes to putting names to faces. But there are some remarkable individuals called ‘superagers’ whose brains seem to be impervious to the passage of time.
Scientists from Harvard Medical School have recently identified the secret of their success.
To do this they asked 40 superagers, with an average age of 67, to take part in a memory test while they were lying in a functional magnetic resonance imaging (fMRI) scanner, which measures brain activity, and got 25-year-olds to do the same. The researchers were interested in studying the visual cortex, the part of our brain that processes what we see.
If you struggle to remember names, try and create mental images to tag people with
It has distinct clumps of brain cells whose job is to just identify faces, animals or objects. As we get older the ability to identify particular things, called neural differentiation, diminishes. We struggle to make connections, to put names to faces.
But in this experiment superagers were as good as the 25-year-olds in the memory tests, at least in part because their brains maintained the same high level of neural differentiation as the youngsters. What is not known is if this is an innate ability or the result of some form of brain training.
I struggle to remember names and so I create mental images, which I tag people with. If I meet someone called ‘Ben’ I might imagine a huge clock (Big Ben), on his forehead to help me recall his name.
The team from Harvard have started a trial to see if a course of electromagnetic stimulation (which delivers a small electrical shock to areas of the brain) can improve memory in older adults.
I like to think I won’t need it, but you never know.
Why won’t the NHS tell you the secret to treating diabetes? Clue: It costs nothing
Eight years ago, I managed to beat type 2 diabetes by going on my 5:2 diet (cutting my calories two days a week) and losing weight — 9kg to be precise. Since then, I’ve become something of a broken record on the importance of shedding body fat to improve your blood sugar levels.
So I was delighted by the news from the Norfolk Diabetes Prevention Study — the largest of its kind in the world — which showed that even modest weight loss can have a big impact.
The Norfolk study recruited more than 1,000 people with pre-diabetes (meaning they had raised blood sugar levels). They were asked to lose weight, then were monitored for more than eight years. Those who managed to lose 2kg to 3kg, and keep it off, almost halved their risk of developing full-blown type 2.
This adds to extensive research carried out by British scientists showing that, as well as pre-diabetes, type 2 diabetes can be put into remission by going on a rapid weight-loss diet. And, as we’ve known for 20 years, weight-loss surgery can also reverse type 2.
In fact, a recent review by Danish researchers found more than 70 per cent of people with type 2 diabetes who had lost significant amounts of weight were still medication-free more than five years later.
A review found that more than 70 per cent of people with type 2 diabetes who had lost significant amounts of weight were still medication-free more than five years later
Despite all this, the NHS website still tells you type 2 diabetes is a ‘progressive’ disease that ‘usually gets worse over time’, with most people needing ever increasing levels of medication. What a depressing — and I would argue inaccurate — message.
So why aren’t they being a bit more encouraging? The situation with type 2 diabetes reminds me of a tussle I had with the medical establishment more than 25 years ago.
In 1993, I was looking around for a subject to make a science documentary, when I came across the work of two Australians, Dr Barry Marshall and Dr Robin Warren, who had a striking new theory about stomach ulcers.
At the time, stomach or duodenal ulcers (affecting the first part of the small intestine) were incredibly common but, like type 2, were seen as something of a mystery. Gut ulcers can be excruciatingly painful and lead to internal bleeding.
Doctors knew they were caused by excess acid and they could be managed by drugs such as ranitidine, which stopped the stomach from producing acid.
These drugs, known as proton pump inhibitors, were expensive but there was a lot of incentive to use them because if you didn’t, or if the drugs stopped working, there was a high chance you’d need some of your stomach and intestines removed.
Robin and Barry, however, were convinced they had a cheap and effective cure. Their research showed that most patients with ulcers were infected with a bacterium, which the two doctors called Helicobacter pylori.
The patients’ stomachs were producing more acid to get rid of the bacterium, but this failed because Helicobacter is resistant to acid attack. But it is vulnerable to the right antibiotics.
To prove the point, Barry deliberately infected himself with Helicobacter (he swallowed a flask of it) and soon developed gastritis — massive inflammation — which he cured with a short course of antibiotics. This was in 1984.
Nine years later, when I began filming with Robin and Barry, there was still widespread resistance to their claims, despite extensive proof they were right.
When I asked Barry how long he thought it would take to persuade his colleagues to take their claims seriously, he laconically replied, ‘Well it’s been ten years and ten per cent of doctors are treating ulcers this way. Perhaps in 100 years they will all be doing it.’
In fact, within ten years almost all doctors were doing it. Not least because Barry and Robin won the Nobel Prize for Medicine in 2004 for their work. But back in 1994, when my documentary, Ulcer Wars, detailing their work, came out, the medical reaction was either indifference or hostility.
A review in the British Medical Journal by a leading gastroenterologist described the film as ‘one-sided and tendentious’.
However, patients with duodenal ulcers who’d watched the programme soon began demanding antibiotic treatment.
Many later wrote to me and as one man put it: ‘I saw your programme a week before I was due to have surgery, and it was only because my doctor was prepared to listen that I was cured by antibiotics rather than having a chunk of my guts removed.’
Why did it take so long for doctors to adopt this approach, despite overwhelming evidence that eradicating Helicobacter could change patients’ lives?
This was a question that researchers from Harvard asked in 2019 — concluding that it was mainly because doctors get much of their information from pharmaceutical companies, and these companies had no incentive to promote a cheap alternative to their acid-reducing drugs (which, of course, you took for life).
The parallels with type 2 diabetes are clear. As the millions of those affected in the UK will know, type 2 is usually treated with medication.
While this will reduce the long-term damage caused by high blood sugar levels, it doesn’t deal with the underlying disease — and, like all medication, the drugs can have significant side-effects, particularly when you move on to injecting insulin.
So how long before there’s wide-spread acceptance that most cases of type 2 diabetes can be put into remission by a rapid weight-loss diet?
It is beginning to happen, but I wouldn’t guarantee that NHS Choices will be telling you the good news any time soon.
Like us, worms need to sleep. And the way their bodies prepare for sleep is also surprisingly similar to humans — one of the key triggers for a bit of shut-eye is the release of melatonin, also known as the ‘hormone of darkness’.
Melatonin is produced in your brain and levels rise when it gets dark (synthetic melatonin is a popular sleep aid and is used to treat jetlag — I find it very effective). Now researchers at the University of Connecticut have discovered how melatonin actually works — in worms at least.
It slows the release of neurotransmitters, substances that allow messages to travel between nerve cells. So melatonin effectively tells your brain cells to stop chatting to each other — the chemical equivalent of a giant ‘shhh’!
The way a worm’s body prepares for sleep is surprisingly similar to humans as it requires the release of melatonin
How our bodies – and vaccines – beat back Covid
Covid-19 vaccines are like buses; you wait for one, then two come along, almost together, with other contenders coming close behind.
We have learnt that the vaccine made by Moderna may be even more effective than Pfizer’s. That both are more than 90 per cent effective is fantastic news and a real poke in the eye for the sceptics who claimed we might never get a vaccine against Covid-19, let alone several.
These findings also suggest that our immune system is doing what evolution designed it to do: mount a strong response to the virus.
Our immune system has been severely tested by Covid but, as the new vaccines show, it just needs a bit of help to get back on top
There was a fear that Covid-19 might mutate into a more resistant form — or that our immune response might weaken. Yet recent research suggests that while antibody levels tend to fall over time, your immune system retains a ‘memory’ of the virus.
So if you encounter it again, your body is ready to begin churning out antibodies and T-killer cells.
Which makes me wonder why Boris Johnson, who’s had Covid, is self-isolating. He’s unlikely to be ‘bursting with antibodies’ as he claims, but he’s also very unlikely to get it again, or to be infectious, so I can’t see how he’s a threat to others.
Our immune system has been severely tested by Covid but, as the new vaccines show, it just needs a bit of help to get back on top.
