DR MICHAEL MOSLEY: Why won’t the NHS tell you the secret to treating diabetes?
DR MICHAEL MOSLEY: Why won’t the NHS tell you the secret to treating diabetes is losing weight? (Clue: Because 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 last week 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.
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 [File photo]
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.
Despite all this, the NHS Choices 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.
I was delighted last week 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 [File photo]
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 widespread 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 jet lag — 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’!
Covid-19 vaccines are like buses; you wait for one, then two come along, almost together, with other contenders coming close behind.
This week we 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.
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, 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.
Covid-19 vaccines are like buses; you wait for one, then two come along, almost together, with other contenders coming close behind [File photo]