Posts filed under Medical news (333)

December 22, 2016

Mouthwash secrets: the embargo problem

On Tuesday, the Herald and some other media outlets, and the occasional journalist’s Twitter account published a story about mouthwash being able to prevent gonorrhea from spreading. Or, in some versions, cure it.  The research paper behind the story wasn’t linked and hadn’t been published. This time it seems to have been the newspapers’ fault: the stories appeared before the end of the news embargo.  The Herald story was pulled, then reappeared midday Wednesday with a link (yay)

Embargoes are an increasingly controversial topic in science journalism. The idea is that journalists get advance copies of a research paper and the press release, so they have time to look things up and ask for expert help or comment. There are organisations such as the NZ Science Media Centre to help with finding experts, or there’s your friendly neighbourhood university.

Sometimes, this works. Stories become more interesting and less slanted, or the journalist just decides the breakthrough wasn’t all that and the story is killed.  Without embargoes, allegedly, no-one would take the time to get it right. In medicine, too, there was the idea that doctors should be able to get the research paper by the time their patients saw the headlines.

On the other hand, embargoes feed into the idea that science stories are Breaking News that must be posted Right Now — that all published science is true (or important) for fifteen minutes. Ivan Oransky (who runs the Embargo Watch blog) argued recently at Vox that embargoes are no longer worthwhile; there’s also a rebuttal posted at Embargo Watch.

The Listerine/gonorrhea story, though, wasn’t new. Major outlets such as Teen Vogue and the BBC covered it in August(probably from a conference presentation). There are no details in the new Herald story that weren’t in the August stories.  It’s hard to see how anyone gains from the embargo here — except perhaps as a way of synchronising a wave of publicity.



November 26, 2016

Where good news and bad news show up

In the middle of last year, the Herald had a story in the Health & Wellbeing section about solanezumab, a drug candidate for Alzheimer’s disease. The lead was

The first drug that slows down Alzheimer’s disease could be available within three years after trials showed it prevented mental decline by a third.

Even at the time, that was an unrealistically hopeful summary. The actual news was that solanezumab had just failed in a clinical trial, and its manufacturers, Eli Lilly, were going to try again, in milder disease cases, rather than giving up.

That didn’t work, either.  The story is in the Herald, but now in the Business section. The (UK) Telegraph, where the Herald’s good-news story came from, hasn’t yet mentioned the bad news.

If you read the health sections of the media you’d get the impression that cures for lots of diseases are just around the corner. You shouldn’t have to read the business news to find out that’s not true.

November 4, 2016

Unpublished clinical trials

We’ve known since at least the 1980s that there’s a problem with clinical trial results not being published. Tracking the non-publication rate is time-consuming, though.  There’s a new website out that tries to automate the process, and a paper that claims it’s fairly accurate, at least for the subset of trials registered at  It picks up most medical journals and also picks up results published directly at — an alternative pathway for boring results such as dose equivalence studies for generics.

Here’s the overall summary for all trial organisers with more than 30 registered trials:


The overall results are pretty much what people have been claiming. The details might surprise you if you haven’t looked into the issue carefully. There’s a fairly pronounced difference between drug companies and academic institutions — the drug companies are better at publishing their trials.

For example, compare Merck to the Mayo Clinic
merck mayo

It’s not uniform, but the trend is pretty clear.


October 4, 2016

Depression and the pill

There’s a recent paper from Denmark finding that women, particularly young women, who used hormonal contraceptives were more likely also to be diagnosed with  depression.  The Guardian has a sensible story reporting on the paper (though given the topic it’s a pity the external experts they talked to were both men). There’s also an opinion piece, which conveys the importance of the issue but is clearly written by someone whose opinions were decided before the research came out. I was asked on Twitter what I thought.

One of the more difficult cases for science communication is where the evidence is neither negligible nor overwhelming, and that’s the situation here.  There’s nothing intrinsically unlikely about an effect on depression, and there are some ways that this study is very good, but there are also some limitations to the data that make the evidence weaker.

First, the good points. The study involved the entire Danish population over nearly 20 years, meaning that it was large enough to be fairly reliable on whether correlations are present or not, and also that it was comprehensive — it didn’t miss people out.  The data on who used hormonal contraceptives comes from the national health system and so should be accurate. The two definitions of depression — ‘prescribed anti-depressant drugs’ and ‘psychiatrist diagnosis of depression’ — will be measured reliably, and the decisions will have been taken by people who don’t have any particular view on the study question.  There’s information on timing, so we know the contraceptives were used before the depression. The associations are strong enough to care about, but not so strong as to be implausible. The analysis is well done given the data.

However, there are at least two alternative explanations for the correlation that aren’t ruled out by these data. The first is that the depression definitions require seeing a doctor and asking for (or at least accepting) treatment, and women who take hormonal contraceptives are probably more likely to see a doctor regularly.  The second explanation, which the researchers do consider, is that break-ups of relationships are a cause of depression, especially in younger people, and being in these relationships might be related to using hormonal contraceptives.  The researchers don’t believe this explanation, and they may be right, but their data don’t rule it out.

It’s not that either of these explanations is necessarily more likely than a direct effect of hormones, but if there weren’t alternative explanations the evidence would be stronger.  For example, if the researchers had been able to compare women using hormonal contraceptives just to those using non-hormonal contraceptives (eg copper IUDs and condoms), and had still seen the same correlation, the second explanation would be much less plausible and the evidence for a direct effect would be more convincing.

Also, if there were a straightforward hormonal explanation I would have expected different types of contraceptive to have stronger or weaker associations according to the dose of, say, progestins. In fact what they saw is that less commonly used contraceptives had stronger associations: weakest for the combined pills, stronger for progestin-only ‘mini-pills’ and stronger still for patch and implant methods. Again, this certainly doesn’t rule out a direct effect, but it weakens the evidence.

If a similar study were done in another country with different patterns of contraceptive use and found similar results, the evidence would become stronger. A study with fewer women but more detailed information on mental and emotional health — such as one of the birth-cohort studies — might be able to say more about what leads up to episodes of depression in young women and might be able to say something about who is at most risk. There’s still going to be uncertainty.

So. It’s hard to say for sure. There is definitely some evidence that hormonal contraceptives increase the risk of depression. If the effect is real, it’s useful to know that it seems to be largely in women under 20, largely in the first year of use, and might be worse for the ‘mini-pill’ than the traditional pill.  There’s a lot already known — good and bad — about hormonal contraceptives, but this research paper does add something.

September 2, 2016

A game changer?

There are stories on Stuff and the Herald about early studies of a potential Alzheimer’s drug. There was also a story on One News last night, but the video doesn’t seem to be up, and there’s one on Newshub.

The drug, adacanumab, reduced amyloid plaque buildup in people with early-stage disease. According to the most widely believed theory about Alzheimer’s, that could slow or even stop the progression of disease. And, as the stories say, if the treatment turns out to be successful in future trials, it will be a game changer.


We’ve never had an successful treatment that modifies the disease process in Alzheimer’s, but we’ve had a range of promising candidates that failed as soon the test went beyond biochemistry to improvements in memory or the ability to handle daily life.  Adacanumab might be different. Let’s hope so.

July 24, 2016

Disease awareness

One News tonight had a story about venous thromboembolism (VTE) and how people don’t know about it. I couldn’t find a reference for the research, but it wouldn’t surprise me if 50% of people hadn’t heard that term — and many of those who do recognise it might associate it only with long-distance flights.

I can see people wanting to raise awareness, and the story includes a really good animation of what actually happens in a VTE. On the other hand, this is how VTE risk varies with age (source)

Nature Reviews Cardiology 12, 464 (2015). doi:10.1038/nrcardio.2015.83

On top of that, about half of VTE is due to hospitalisation, as the story went on to describe. Given those risk patterns, it’s kind of weird to have the main example in the story be a 20-year-old law student who got a pulmonary embolism without any obvious risk factors.

Disease awareness can be valuable, but it’s probably more useful when it’s modelled on people who are at high, or at least average, risk of the disease.

June 12, 2016

Walking it back

First the headline (Herald, reprinting Daily Telegraph)

Finger-prick test that can show risk of diabetes

then it’s “on the horizon”

The finger-prick test, which could be available at GP surgeries or even chemists, looks for molecules in the blood that indicate diabetes is developing.

but in the present tense. Then

The specific biomarkers involved are being kept a closely guarded secret for now, but once a prototype test has been developed, trials will take place.

This ‘test’ not only hasn’t been evaluated in real patients; it doesn’t even exist yet.


Currently, doctors can test for diabetes only by taking blood glucose readings that show whether the disease is already present.

That’s only true if you squint from exactly the right angle. Since 2012, testing for HbA1c, a byproduct of elevated glucose, has been a general screening recommendation in NZ and one of the public health performance indicators. One of the reasons given for screening is

effective screening aims to reduce the incidence of diabetes through detection of people with pre-diabetes

You could argue ‘the disease is already present’ in people with pre-diabetes, but not in the sense that’s relevant to screening.

The current test isn’t all that good, and perhaps when they finish inventing it the new one will be better. But it’s not a test yet; it’s not a ‘health’ story yet; and with so little disclosed information it’s not clear that it’s even a science story yet.

June 3, 2016


From Stuff

Kiwi researchers have come up with a solution to the global obesity epidemic – a bitter plant extract that suppresses appetite.

As you’d expect, calling it “a solution” is completely over the top at the moment. They’ve done a placebo-controlled trial, but lasting less than one day, in only 20 men. The press release is more detailed and more restrained.

What made me mention this story, though, is the numbers. From Stuff

The researchers found that the Amarasate extract stimulated significant increases in hormones that regulate appetite and reduced food intake from 911 kJ (218 calories) to 944 kJ (226 calories).

That sounds incredibly unimpressive: an 8 calorie reduction. It’s wrong, or at least the press release is different and more plausible

.. both gastric and duodenal delivery of the Amarasate™ extract stimulated significant increases in the gut peptide hormones CCK, GLP-1 and PYY while significantly reducing total (lunch plus snack) ad libitum meal energy intake by 911 kJ (218 calories) and 944 kJ (226 calories), respectively.

They looked at two capsules to control where in the gut the stuff was released, and both types reduced calorie intake by a bit more than 200 calories, compared to placebo. The story was off by a factor of 25 or so.



[update: Those of you who read more carefully than either me or the journalist will have noticed that “reduced .. from 911 kJ .. to 944 kJ ” in the Stuff story is actually an increase, and even less excusable]

[Update next day: The numbers have been fixed —“reduced food intake by up to 944 kJ (226 calories).”  — but not the opening claim. ]

March 14, 2016

Dementia and rugby

Dylan Cleaver has a feature story in the Herald on the Taranaki rugby team who won the Ranfurly Shield in 1964. Five of the 22 have been diagnosed with dementia. Early on in the process he asked me to comment on how surprising that was.

The key fact here is 1964: the five developed dementia fairly young, in their 60s and early 70s. That happens even in people who have no family history and no occupational risks, as I know personally, but it’s unusual.

I couldn’t find NZ data, but I did find a Dutch study (PDF, Table 3) estimating that a man who is alive and healthy at 55 has a 1.5% risk of diagnosed dementia by 70 and 3.2% by 75. There’s broadly similar data from the Framingham study in the US.   The chance of getting 5 or more out of 22 depends on exact ages and on how many died earlier of other causes, but if these were just 22 men chosen at random the chance would be less than 1 in 10,000 — probably much less.  People who know about rugby tell me the fact they were all in the back line is also relevant, and that makes the chance much smaller.

There are still at least two explanations. The first, obviously, is that rugby — at least as played in those days — caused similar cumulative brain damage to that seen in American football players. The second, though, is that we’re hearing about the 1964 Taranaki team partly because of the dementia cases — there wouldn’t have been this story if there had only been two cases, and there might have been a story about some other team instead. That is, it could be a combination of a tragic fluke and the natural human tendency to see patterns.  Statistics is bad at disentangling these; the issue crops up over and over again in cancer surveillance.

In the light of what has been seen in the US, I’d say it’s plausible that concussions contributed to the Taranaki cases.  There have already been changes to the game to reduce repeated concussions, which should reduce the risk in the future. There is also a case for more systematic evaluation of former players, to get a more reliable estimate of the risk, though the fact there’s nothing that can currently be done about it means that players and family members need to be involved in that decision.

March 7, 2016

A good source of iron

Stuff has a story under the lead

Now that it’s autumn, flu season isn’t far off and there’s plenty you could be doing in the kitchen to give your body that extra oomph for the cold months ahead.

Sadly they don’t mean making a phone call to book a flu vaccine shot: they have a list of herbs and spices with unsupported health claims.

Take the first, cinnamon.  Stuff says “It is high in antioxidants, is an anti-inflammatory and has an effect in lowering blood sugar.”  The  National Center for Complementary and Integrative Health , who are about as sympathetic as you can get to this sort of thing “High-quality clinical evidence (i.e., studies in people) to support the use of cinnamon for any medical condition is generally lacking. An analysis of five clinical trials concluded that cinnamon does not appear to affect factors related to diabetes and heart disease.”

Or, for a total failure to do arithmetic, saffron. Stuff says “It is a good source of vitamins, magnesium and iron.” Now, it’s true that saffron is high in nutrients for its weight. A mere 100g of saffron will supply about two-thirds of your daily iron and magnesium, and substantial amounts of vitamins C and B-6. By weight, it does better than spinach. But the typical serving of saffron is a small fraction of a gram, with nutrient contents that would round to zero in any sensible display.

Following the lines of previous StatsChat food advice, I think the photo caption  just needs a bit of editing: “Herbs and spices are an easy way to add healthy elements  flavour to your diet.

(via Mark Hanna and Bart Janssen)