Posts filed under Medical news (288)

April 23, 2015

Don’t hold your breath

The story at the Herald (from the Telegraph) starts off dramatically, then walks its claims back, but not back far enough.

First off, the dramatic claim:

Asthma could be cured within five years after scientists discovered what causes the condition and how to switch it off.

Then the description of what the researchers actually did: ‘identified which cells cause the airways to narrow when triggered by irritants like pollution.’ That’s less dramatic; it’s also not true. The researchers looked at the same cells everyone else looks at. What they did was show that a molecule on the surface of these cells (“calcium-sensing receptor”) appears to be central to the triggering.

The other main selling point:

Crucially, drugs already exist which can deactivate the cells. They are known as calcilytics and are used to treat people with osteoporosis.

In fact, they aren’t used to treat people with osteoporosis. As the research paper says, they “were initially developed as anti-osteoporotic drugs and reached phase 2 clinical trials for this purpose”. That is, they didn’t work. They might work for asthma, but it’s not like finding a new use for an actually-marketed drug — especially as the drugs would have to be inhaled, something that hasn’t been studied in humans at all. If everything goes right, it might be possible to get the safety and effectiveness studies done and the drug approved in five years, but that’s pretty optimistic.

Also, the drugs are promising, but not as promising as the story says:

But when calcilytic drugs are inhaled, it deactivates the cells and stops all symptoms.

Most of the research was either in isolated cells (which don’t have symptoms) or in non-asthmatic mice. One experiment, in asthmatic mice, showed a reduction in airway resistance with the drugs, but not down to the level in non-asthmatic mice.  And airway resistance isn’t the same as symptoms. And these are mice.

A comment from Asthma UK raises another point that hasn’t appeared so far

“Five per cent of people with asthma don’t respond to current treatments so research breakthroughs could be life changing for hundreds of thousands of people. If this research proves successful we may be just a few years away from a new treatment for asthma”

Inhaled steroids for asthma are already pretty effective. While they aren’t enough for everyone, a more common problem is the hassle of using the inhaler twice a day every day when you’re healthy, to prevent relatively rare asthma attacks.  The new drugs will likely have the same problem  — it’s a treatment, not a cure — and their real potential isn’t for everyone with asthma, but for the relatively small subset where current treatments don’t work.


April 13, 2015

Puppy prostate perception

The Herald tells us “Dogs have a 98 per cent reliability rate in sniffing out prostate cancer, according to newly-published research.” Usually, what’s misleading about this sort of conclusion is the base-rate problem: if a disease is rare, 98% accuracy isn’t good enough. Prostate cancer is different.

Blood tests for prostate cancer are controversial because prostate tumours are common in older men, but only some tumours progress to cause actual illness.  By “controversial” I don’t mean the journalistic euphemism for “there are a few extremists who aren’t convinced”, but actually controversial.  Groups of genuine experts, trying to do the best for patients, can come to very different conclusions on when testing is beneficial.

The real challenge in prostate cancer screening is to distinguish the tumours you don’t want to detect from the ones you really, really do want to detect. The real question for the canine sniffer test is how well it does on this classification.

Since the story doesn’t give the researchers’s names finding the actual research takes more effort than usual. When you track the paper down it turns out that the dogs managed almost perfect discrimination between men with prostate tumours and everyone else. They detected tumours that were advanced and being treated, low-risk tumours that had been picked up by blood tests, and even minor tumours found incidentally in treatment for prostate enlargement. Detection didn’t depend on tumour size, on stage of disease, on PSA levels, or basically anything. As the researchers observed “The independence of tumor volume and aggressiveness, and the dog detection rate is surprising.”

Surprising, but also disappointing. Assuming the detection rate is real — and they do seem to have taken precautions against the obvious biases — the performance of the dogs is extremely impressive. However, the 98% accuracy in distinguishing people with and without prostate tumours unavoidably translates into a much lower accuracy in distinguishing tumours you want to detect from those you don’t want to detect.

April 9, 2015

Height and heart attack: genetic determinism is still wrong

From the Herald (originally from the Independent)

Short people are at a greater risk of heart attack – and there’s little they can do about it because the link is genetic.

This one is partly the fault of the researchers and partly the fault of the journalists.  The press release says

“We have shown that the association between shorter height and higher risk of coronary heart disease is a primary relationship and is not due to confounding factors such as nutrition or poor socioeconomic conditions.”

That’s partly true, and new and interesting, but (a) it’s being oversold (“the” association?) and (b) even if it were completely true, it wouldn’t imply the “there’s little they can do about it” added by the journalists.

Taking the second point first: knowing that something has a genetic component tells you absolutely nothing about how easy or hard it is to change. At a biological level hair colour and eye colour have similar degrees of genetic influence, but one of them is very easy to change and the other is more difficult and inconvenient.

Also, it’s certainly not true that height is entirely genetically determined. There is a genetic component: tall people have tall children. There is also an environmental component: most people are taller than their grandparents.  Here’s a graph (source) showing how the heights of Dutch people changed over sixty years: the Dutch went from some of the shortest people in Europe to some of the tallest, and this was an environmental change, not a genetic change.


The research paper doesn’t even claim that among modern Westerners the association between height and heart attack risk is all genetic, though if you only have the press release you have to read carefully to avoid getting that impression. Even within the (fairly homogeneous) groups of people being studied, the genetic variants they used explain only about 10% of the variation in height.

What’s new in this research is that some of the relationship between height and heart attack risk is genetic. Until now, it was possible that all the association was explained by environmental factors in childhood or before birth that made people shorter and also, separately, increased their heart attack risk.

For the part of the relationship explained by genetic variation there are basically three possible sorts of explanation:

  • Being short has some direct biological effect on risk,  for example, smaller people have smaller blood vessels, which might get blocked by smaller blood clots.
  • Being short subjects you to different environmental risks: for example, if shorter people had lower incomes (on average) they might have higher risk for various social and lifestyle reasons
  • The genetic variants that make you shorter also have some separate effect on heart attack risk: for example, the same variant might affect growth in infancy and also affect diabetes risk in later life.

These are all interesting, and there’s a reasonable hope of being able to separate them out with more data and experiments.

The last sentence of the research paper is a good counterpoint to the media coverage

More generally, our findings underscore the complexity underlying the inherited component of CAD.



[Disclosure: I work with one of the cohorts that is part of one of the consortia that is part of the whole Cardiogram group and I know some of the researchers — but that would be true of anyone in the field]

March 25, 2015

Translating from Scientist to English

Stories were coming out recently about new cancer research led by Bryony Telford in Parry Guilford’s lab at Otago, and I’d thought I’d use it for an example of translation from Scientist to English. It’s a good example for news because it really is pretty impressive, because it involved a New Zealand family with familial cancer, and because the abstract of the research paper is well written — it’s just not written in ordinary English. Combining the abstract with the press release and a bit of Google makes a translation possible.

This will be long. (more…)

March 19, 2015

Model organisms

The flame retardant chemicals in your phone made zebra fish “chubby”, says the caption on this photo at Zebra fish, as it explains, are a common model organism for medical research, so this could be relevant to people


On the other hand, as @LewSOS points out on Twitter, it doesn’t seem to be having the same effect on the model organisms in the photo.

What’s notable about the story is how much better it is than the press release, which starts out

Could your electronics be making you fat? According to University of Houston researchers, a common flame retardant used to keep electronics from overheating may be to blame.

The story carefully avoids repeating this unsupported claim.  Also, the press release doesn’t link to the research paper, or even say where it was published (or even that it was published). That’s irritating in the media but unforgivable in a university press release.   When you read the paper it turns out the main research finding was that looking at fat accumulation in embryonic zebrafish (which is easy because they are transparent, one of their other advantages over mice) was a good indication of weight gain later in life, and might be a useful first step in deciding which chemicals were worth testing in mice.

So, given all that, does your phone or computer actually expose you to any meaningful amount of this stuff?

The compounds in question, Tetrabromobisphoneol A (TBBPA) and tetrachlorobisphenol A (TCBPA) can leach out of the devices and often end up settling on dust particles in the air we breathe, the study found.

That’s one of the few mistakes in the story: this isn’t what the study found, it’s part of the background information. In any case, the question is how much leaches out. Is it enough to matter?

The European Union doesn’t think so

The highest inhalation exposures to TBBP-A were found in the production (loading and mixing) of plastics, with 8-hour time-weighted-averages (TWAs) up to 12,216 μg/m3 . At the other end of the range, offices containing computers showed TBBP-A air concentrations of less than 0.001 μg/m3 . TBBP-A exposures at sites where computers were shredded, or where laminates were manufactured ranged from 0.1 to 75 μg/m3 .

You might worry about the exposures from plastics production, and about long-term environmental accumulations, but it looks like TBBP-A from being around a phone isn’t going to be a big contributor to obesity. That’s also what the international comparisons would suggest — South Korea and Singapore have quite a lot more smartphone ownership than Australia, and Norway and Sweden are comparable, all with much less obesity.

March 18, 2015

Men sell not such in any town

Q: Did you see diet soda isn’t healthier than the stuff with sugar?

A: What now?

Q: In Stuff: “If you thought diet soft drink was a healthy alternative to the regular, sugar-laden stuff, it might be time to reconsider.”

A: They didn’t compare diet soft drink to ‘the regular, sugar-laden stuff’.

Q: Oh. What did they do?

A: They compared people who drank a lot of diet soft drink to people who drank little or none, and found the people who drank a lot of it gained more weight.

Q: What did the other people drink?

A: The story doesn’t say. Nor does the research paper, except that it wasn’t ‘regular, sugar-laden’ soft drink, because that wasn’t consumed much in their study.

Q: So this is just looking at correlations. Could there have been other differences, on average, between the diet soft drink drinkers and the others?

A: Sure. For a start, there was a gender difference and an ethnicity difference. And BMI differences at the start of the study.

Q: Isn’t that a problem?

A: Up to a point. They tried to adjust these specific differences away, which will work at least to some extent. It’s other potential differences, eg in diet, that might be a problem.

Q: So the headline “What diet drinks do to your waistline” is a bit over the top?

A: Yes. Especially as this is a study only in people over 65, and there weren’t big differences in waistline at the start of the study, so it really doesn’t provide much information for younger people.

Q: Still, there’s some evidence diet soft drink is less healthy than, perhaps, water?

A: Some.

Q: Has anyone even claimed diet soft drink is healthier than water?

A: Yes — what’s more, based on a randomised trial. I think it’s fair to say there’s a degree of skepticism.

Q: Are there any randomised trials of diet vs sugary soft drinks, since that’s what the story claimed to be about?

A: Not quite. There was one trial in teenagers who drank a lot of sugar-based soft drinks. The treatment group got free diet drinks and intensive nagging for a year; the control group were left in peace.

Q: Did it work?

A: A bit. After one year the treatment group  had lower weight gain, by nearly 2kg on average, but the effect wore off after the free drinks + nagging ended. After two years, the two groups were basically the same.

Q: Aren’t dietary randomised trials depressing?

A: Sure are.


March 13, 2015

Clinical trial reporting still not happening

According to a paper in the New England Journal of Medicine, about 20% of industry-funded clinical trials registered in the United States failed to report their summary results with no legally acceptable reason for delay. That’s obviously not good enough, and this sort of thing is why people don’t like drug companies.

As the paper says

On the basis of this review, we estimated that during the 5-year period, approximately 79 to 80% of industry-funded trials reported summary results or had a legally acceptable reason for delay. In contrast, only 49 to 50% of NIH-funded trials and 42 to 45% of those funded by other government or academic institutions reported results or had legally acceptable reasons for delay.

Um. Yes. <coughs nervously> <shuffles feet>

via Derek Lowe

Feel-good gene?

From Stuff

Suffering anxiety, is not a mark of character, but at least in part to do with the genetic lottery, he says.

“About 20 per cent of adult Americans have this mutation,” Professor Friedman says of those who produce more anandamide, whose name is taken from the Sanskrit word for bliss.

There’s good biological research behind this story, on how the gene works in both mice and people, but the impact is being oversold. The human data on anxiety in the paper look like


Combining this small difference with the claim that 20% of people  in the US carry the variant, it would explain about 1% of the population variation in the anxiety questionnaire score. Probably less of the variation in having/not having clinically diagnosable anxiety.

The story continues

“Those who do [have this mutation] may also be less likely to become addicted to marijuana and, possibly, other drugs – presumably because they don’t need the calming effects that marijuana provides.”

The New York Times version mentioned a study of marijuana dependence, which found people with the low-anxiety mutation were less likely to be dependent. However, for other drugs the opposite has been found:

Here, we report a naturally occurring single nucleotide polymorphism in the human FAAH gene, 385A, that is strongly associated with street drug use and problem drug/alcohol use.

People with the mutant, A, version of the gene, the low-anxiety variant, were more likely to have drug problems.  In fact, even the study that found (weak) evidence for lower rates of marijuana dependence found much stronger evidence of higher rates of sedative dependence.

Simple, binary, genetic explanations for complex human conditions are always tempting, but usually wrong.

March 12, 2015

Variation and mean

A lot of statistical reporting focuses on means, or other summaries of where a distribution lies. Often, though, variation is important. has a story about variation in costs of lab tests at California hospitals, based on a paper in BMJ OpenVox says

The charge for a lipid panel ranged from $10 to $10,169. Hospital prices for a basic metabolic panel (which doctors use to measure the body’s metabolism) were $35 at one facility — and $7,303 at another

These are basically standard lab tests, so there’s no sane reason for this sort of huge variation. You’d expect some variation with volume of tests and with location, but nothing like what is seen.

What’s not clear is how much this is really just variation in how costs are attributed. A hospital needs a blood lab, which has a lot of fixed costs. Somehow these costs have to be spread over individual tests, but there’s no unique way to do this.  It would be interesting to know if the labs with high charges for one test tend to have high charges for others, but the research paper doesn’t look at relationships between costs.

The Vox story also illustrates a point about reporting, with this graph


If you look carefully, there’s something strange about the graph. The brown box second from the right is ‘lipid panel’, and it goes up to a bit short of $600, not to $10169. Similarly, the ‘metabolic panel’, the right-most box, goes up to $1000 on the graph and $7303 in the story.

The graph is taken from the research paper. In the research paper it had a caption explaining that the ‘whiskers’ in the box plot go to the 5th and 95th percentiles (a non-standard but reasonable choice). This caption fell off on the way to, and no-one seems to have noticed.

February 25, 2015

Measuring what you care about

If cannabis is safer than thought (as the Washington Post says), that might explain why the reporting is careful to stay away from thought.



The problem with this new research is that it’s looking at the acute toxicity of drugs — how does the dose people usually take compare to the dose needed to kill you right away.  It’s hard to overstate how unimportant this is in debates over regulation of alcohol, tobacco, and cannabis.  There’s some concern about alcohol poisoning (in kids, mostly), but as far as I can remember I have literally never seen anti-tobacco campaigns mentioning acute nicotine poisoning as a risk, and even the looniest drug warriors don’t push fatal THC overdoses as the rationale for banning marijuana.

Alcohol is dangerous not primarily because of acute poisoning, but because of car crashes, violence, cancer, liver failure, and heart damage. Tobacco is dangerous not primarily because of acute poisoning, but because of lung cancer, COPD, heart disease, stroke, and other chronic diseases.

It’s hard to tell how dangerous marijuana is. It certainly causes dependence in some users, and there are reasons to think it might have psychological and neurological effects. If smoked, it probably damages the lungs. In all these cases, though, the data on frequency and severity of long-term effects are limited.  We really don’t know, and the researchers didn’t even try to estimate.

The conclusions of the researchers — that cannabis is over-regulated and over-panicked-about relative to other drugs — are reasonable, but the data provide very little support for them.  If the researchers had used the same methodology on caffeine, it would have looked much more dangerous than cannabis, and probably more dangerous than methamphetamine. That would have been a bit harder to sell, even with a pretty graph.


[story now in Herald, too]