Posts filed under Medical news (341)

A California head-lice treatment business has had huge success in publicising its business with the claim that selfies are causing a  rise in nits among teenagers. The Herald mentions this in Sideswipe, the right place for this sort of story, but other international sites have been less discriminating.

There are no actual numbers involved, and nothing like representative data even if you’re in the South Bay area of central California. More importantly, though, there is no comparison group. The owner of the business, Mary MacQuillan, says “Every teen I’ve treated, I ask about selfies, and they admit that they are taking them every day.”  That’s probably only a slight exaggeration at most, but every teen she hasn’t treated has also probably been taking photos that way. It’s something teenagers do.  Common exposures are common.

So, why were news organisations around the world publicising this? The fact that it’s about teenagers and the internet goes a long way to explaining it.  It doesn’t need evidence because teenage use of technology is automatically scary and newsworthy: as Ms MacQuillan says ” I think parents need to be aware, and teenagers need to be aware too. Selfies are fun, but the consequences are real.”

You get the same thing happening with ‘chemicals’, as the dihydrogen monoxide parody website loves to point out

A recent stunning revelation is that in every single instance of violence in our country’s schools, …, dihydrogen monoxide was involved.

I linked earlier to Jeff Leek’s post on fivethirtyeight.com, because I thought it talked sensibly about assessing health news stories, and how to find and read the actual research sources.

While on the bus, I had a Twitter conversation with Hilda Bastian, who had read the piece (not through StatsChat) and was Not Happy. On rereading, I think her points were good ones, so I’m going to try to explain what I like and don’t like about the piece. In the end, I think she and I had opposite initial reactions to the piece from on the same starting point, the importance of separating what you believe in advance from what the data tell you. (more…)

The Herald said, on Friday “Fewer workers stoned on the job”

Information from the New Zealand Drug Detection Agency showed 81,410 on-site drug-screening tests were carried out last year, 16 per cent up from the previous year.

But only 5.5 per cent of tests showed the presence of drugs, down from 6.4 per cent in 2013

As usual, there’s no mention of the fact that NZDDA is just one of the private companies offering drug testing services. It took me a long time to realise this, until I was tipped off by a news story advertising one of their competitors.

Presumably NZDDA don’t think their customers choose them at random, and with no real reason for wanting testing. If customers were behaving even a little rationally you’d expect an expansion of drug testing to pull in lower-risk employees. If we look at the actual number of positive tests, using the quoted figures, it was about 4480 last year and about 4490 in the previous year. Given no change in the number of positive tests and a 1 percentage point change in the proportion of positive tests, from a single company, there’s not a lot of numerical evidence for an increase in number of workers with detectable cannabis in their systems.

More importantly, there’s no evidence whatsoever for the ‘stoned on the job’ headline: absolutely no information is given about this. One of the big problems with cannabis testing is that there is no useful biochemical assay for being stoned. Detectable levels persist long after impairment is over, and even when you’re actually stoned there is not a good relationship between drug concentration and impairment.  This is a real problem for Washington and Colorado, which have legalised cannabis and need to set driving laws. In contrast to alcohol, if you actually care about safe driving and cannabis, it’s really hard to get a useful and objective test.

The story ends with two examples of disasters. In one, cannabis was definitely ruled out as a contributing factor; in the other, the conclusion was only that “it could not be excluded”. The NZDDA  press release is at Scoop, and despite how the story reads, there is surprisingly little text in common.

Not, not that one, the story about eating meat.

Stuff has the more egregious version “Eating meat ‘as bad as smoking‘”, the Herald has the rather better “Protein packed diet nearly as bad as smoking – expert”.

First, the good bits. Both stories are better than the UK versions: the Herald talks to Australian experts and brings in a related study; the Fairfax story at least mentions an outside scientific opinion and gives a link (though it’s to the university press release, which doesn’t link further to the research paper).

The researchers compared people who ate high-protein diet (just under 20% of the people) to those who ate a low-protein diet (just over 5%), and found a 70% higher rate of death in the high-protein group, in people aged 55-64.  The study was observational, but it was in a representative sample of the US and was backed up by experiments in mice. That’s not completely reliable,  but it is a big step.

The 70%-higher-rate of death for  high-protein vs low-protein diets compares to slightly over 100% higher rate for current smokers vs non-smokers in previous research using data from the same survey. You could get away with calling that ‘nearly as bad’, especially as other surveys have tended to give smaller differences. So, the Herald’s headline is defensible. Stuff’s headline drops the ‘nearly’, the ‘packed’ and refers to ‘meat’ rather than ‘protein’. It would be easy for a casual reader to get the false impression that the research had found eating meat was as bad as smoking.

There are two really big holes in the coverage, though.  The Herald alludes to one of them but doesn’t follow up 

People on high-protein diets are likely to lose years of life along with the weight they shed, according to two studies.

All the statistical analyses in the paper attempted to control for weight, ie, they were trying to compare people on high and low protein diets with the same weight. That’s not the relevant question for many people on these diets — the attraction of the diet is that it’s easier to lose weight.  The relevant question for them is a comparison between a high-protein diet with lower weight or a low-protein diet with higher weight.  That question could have been addressed with the data, but it wasn’t.

A rather less subtle omission is that neither story, nor the press release, mentions a key point of the paper: that the association reverses in people over 65.

From a randomised trial of four different sets of information about vaccine benefits (via Brendan Nyhan)

Parents were randomly assigned to receive 1 of 4 interventions: (1) information explaining the lack of evidence that MMR causes autism from the Centers for Disease Control and Prevention; (2) textual information about the dangers of the diseases prevented by MMR from the Vaccine Information Statement; (3) images of children who have diseases prevented by the MMR vaccine; (4) a dramatic narrative about an infant who almost died of measles from a Centers for Disease Control and Prevention fact sheet; or to a control group.

In particular, intervention 4 is a popular and sensible idea, and it has occurred to people from Benjamin Franklin to Kiwi parents and the Herald. However:

RESULTS: None of the interventions increased parental intent to vaccinate a future child. Refuting claims of an MMR/autism link successfully reduced misperceptions that vaccines cause autism but nonetheless decreased intent to vaccinate among parents who had the least favorable vaccine attitudes. In addition, images of sick children increased expressed belief in a vaccine/autism link and a dramatic narrative about an infant in danger increased self-reported belief in serious vaccine side effects.

This research is depressing from the point of view of science communication. The problem is that the message goes in two apparently opposite ways.  One conclusion is that increasing trust in science and medicine is the only solution, which would require more public contact and communication, and openness about uncertainty.  The other conclusion is that a public health advertising campaign is a treatment, and like any other treatment it should be evaluated for safety and effectiveness before it’s applied to the population, an approach that seems to imply a reduction in open and unfiltered communication.

I don’t think the contradiction is unavoidable; I think more communication about research process — who are we and what do we actually do — will help, but also that advertising, whether government-funded or pushed by PR departments, is actually dangerous.  If we overstate claims about the biochemical effects of compounds in chocolate, or the number of deaths prevented by lowering the blood alcohol limit, why should we be trusted on important issues?

James Russell sent me a link to this story from a Canadian paper (originally from the Daily Telegraph).  The Herald has it too, with a very slightly less naff picture.  The research (open access) is good; the story is reasonably informative, but seriously credulous

Blood samples from over 17,000 generally healthy people were screened for 100 biomarkers, and those people monitored over five years.

In that time, 684 died from illnesses including cancer and cardiovascular disease. They all had similar levels of four biomarkers: albumin; alpha-1-acid glycoprotein; citrate, and a similar size of very-low-density lipoprotein particles.

Compare the last sentence to this graph from the research paper. The vertical axis is a combined score on the four biomarkers. The red dots are the people who died. As you can see, they didn’t all have similar values.

The research is impressive not because the prediction is very accurate, but because its less appalling inaccurate than usual.  Using standard risk factors (age, sex, cholesterol, smoking, diabetes, cancer) if you picked a random person who died and one who didn’t die from their cohort there’s an 80% chance the one with the worse risk factors was the one who died.  Adding the ‘death test’ measurements increases the probability to 83%.  Asking an experienced nurse to guess would probably be more accurate (and cheaper), but is hard to automate.

Despite the impression from the headline and lead, if you’re asked to predict whether someone will live another year, based on this sort of information, the safe bet is “yes”. Even among the 1% of people with the very worst values of the ‘death test’ biomarkers, 80% lived for more than a year and half were still alive at the end of the five year study.

Interestingly, the two republished versions lack the last paragraphs of the original Telegraph story, which talk about whether the test is useful

“If the findings are replicated then this test is surely something we will see becoming widespread,” added Prof Perola.

“But at moment there is ethical question. Would someone want to know their risk of dying if there is nothing we can do about it?”

Dr Kettunen added: “Next we aim to study whether some kind of connecting factor between these biomarkers can be identified.

Some of you may be enough older than me to remember yoghurt as the miracle food of the 1970s. It seems to be back. From the Independent, this time, a Herald headline “Low fat yoghurt could combat type 2 diabetes”.

The research paper is open-access, at least for now, so I looked at it.  The first thing to note is that the research did not anywhere distinguish low-fat yoghurt from full-fat. All yoghurt was grouped together in all the analyses.

While the study could not prove a conclusive causal link between eating dairy and lower diabetes risk, the association was strong.

Not all that strong. Comparing high to low yoghurt consumption they only saw a 28% lower risk; the difference in risk was less when they included other “low-fat” fermented dairy products, and the evidence wasn’t all that overwhelming even before you take into account that they looked at 9 different subsets of dairy foods.

Two headlines a month apart on the BBC news website, one of the world’s most respected sources for serious news

The older one, “Schizophrenia: talking therapy offers ‘little benefit’” is based on a summary of 50 randomised trials.

The newer one, “Schizophrenia: Talking therapies `effective as drugs‘”, is based on a report from a pilot study of 74 people that compared cognitive behavioural therapy to no treatment, not to drugs.  It doesn’t mention the earlier story.

Ezra Klein, who’s one of the United States’ top political and economic journalists, has just left the Washington Post to start a new web-based publication.  He writes

New information is not always — and perhaps not even usually — the most important information for understanding a topic. The overriding focus on the new made sense when the dominant technology was newsprint: limited space forces hard choices. You can’t print a newspaper telling readers everything they need to know about the world, day after day. But you can print a newspaper telling them what they need to know about what happened on Monday. The constraint of newness was crucial.

The web has no such limits. There’s space to tell people both what happened today and what happened that led to today.

For health and science stories there should be room for less newness and more context even on paper, since only a tiny minority of the most interesting stories are covered. But even if you can’t explain why today’s headline is different, you can at least notice that it’s the opposite of what you said a month ago.

[update: I lost the credit to Dean Rutland and Ben Goldacre for the picture in editing. My apologies to them.]

The Herald gets a bit excitable about a JAMA Internal Medicine paper saying it’s not healthy to eat lots and lots of sugar. The story says

One sugar-sweetened beverage a day is enough to increase the risk of dying from cardiovascular disease (CVD) affecting the heart and arteries.

With the statistical analysis done in the paper that’s really an assumption, not a conclusion — the analysis assumes an exponentially-increasing risk for additional sugar consumption, so if lots of sugar is bad, a little bit will automatically be thought to be bad.

The Herald’s lead was

Consuming too many sugary sweets, desserts and drinks can triple your chances of dying from heart disease.

That’s pretty much what the research paper says, but as always “compared to what?”  Here’s the graph from the paper showing the estimated risk (solid line), the uncertainty, and the actual distribution of people’s sugar consumption

There’s a lot of uncertainty around the risk line, even assuming that the model is correct. More importantly, most people, even in the US, aren’t anywhere near the levels of sugar consumption that get you a tripling of risk.

There’s more detailed commentary at the UK “Behind the Headlines”. Eating lots of additional sugar isn’t good for you. But you knew that already.

It’s not that I deliberately set out to write about the Daily Mail stories in the Herald. I decide to write a post before I get to the source line at the end. It’s just that the really bad stories tend to be imports.

Today’s story starts

Your friend swears by the Atkins diet, your colleague loves Paleo and your neighbour is raving about gluten-free.

So which diet works? Perhaps all of them, according to new research which claims dieting is all in your genes.

In a recent study, scientists claim to have identified a collection of genes that allow humans to adapt to different diets.

Actually

Here we show that Caenorhabditis elegans lifespan is regulated by their adaptive capacity to different diets, which is controlled by alh-6, a conserved proline metabolism gene. alh-6 mutants age prematurely when fed an Escherichia coli OP50 but not HT115 diet.

That is, the research is in mutant nematodes. Not humans. Not mice. Not even fruit flies. The mutations completely disabled the gene. In humans that is extremely rare (though cases have been described). Even in mutant nematodes the dietary difference had nothing to do with weight loss, which is the most common reason for people to diet. And it wasn’t that different diets were better depending on the genetic variant, it was that the difference between a bad diet and a good diet was larger in nematodes with a broken version of this gene.  And the bad diet was composed of E. coli bacteria, which don’t feature highly in Atkins, Paleo, or gluten-free. And.. just no.

It is interesting to see how the claims developed through the chain of citation. The abstract of the paper says

Collectively, our data reveal a homeostatic mechanism that animals employ to cope with potential dietary insults and uncover an example of lifespan regulation by dietary adaptation.

and the paper makes no claims about genetic sequencing or human diets.

The University of Southern California press release says

Your best friend swears by the Paleo Diet. Your boss loves Atkins. Your sister is gluten-free, and your roommate is an acolyte of Michael Pollan. So who’s right? Maybe they all are.

In new research published this month in Cell Metabolism, USC scientists Sean Curran and Shanshan Pang identify a collection of genes that allow an organism to adapt to different diets and show that without them, even minor tweaks to diet can cause premature aging and death.

Finding a genetic basis for an organism’s dietary needs suggests that different individuals may be genetically predisposed to thrive on different diets – and that now, in the age of commercial gene sequencing, people might be able to identify which diet would work best for them through a simple blood test.

introducing the trendy diets and the idea of gene sequencing to guide diets. This was also reprinted in shortened form at Science Daily.

The Daily Mail then reorganised the first paragraph, dropped Michael Pollan (whether because he’s less famous in the UK or because he’s more of a Guardian type) and introduced the assertion that the research found something about humans (rather than that it could be extrapolated to humans).   And the Herald reprinted it.

If you want to know whether a particular reasonably sane diet will work for you, the best way is to try it. That was true in the past, it’s true now, and it’s going to be true for a long time, even with advances in genetics.