Posts filed under Medical news (292)

May 25, 2015

Genetic determinism: infidelity edition

New York Times columnist Richard Friedman is writing about hormones, genetics, and infidelity.  This paragraph is about recently-published research by Brendan Zietsch and colleagues (the NYT tries to link, but the URL is wrong)

His study, published last year in Evolution and Human Behavior, found a significant association between five different variants of the vasopressin gene and infidelity in women only and no relationship between the oxytocin genes and sexual behavior for either sex. That was impressive: Forty percent of the variation in promiscuous behavior in women could be attributed to genes.

If you didn’t read carefully you might think this was a claim that the  vasopressin gene association explained the “Forty percent” and that the percentage was lower in men. In fact, the vasopressin gene associations are rather weaker than that, and the variation attributed by the researchers to genes is 62% in men.

But it gets worse. The correlation with genetics was only seen in identical twins. That is, pairs of identical twins had fairly similar cheating behaviour , but there was no similarity at all between pairs of non-identical twins (of any gender combination) or between non-twin siblings.  If that’s not due to chance (which it could be), it’s very surprising. It doesn’t rule out a genetic explanation — but it means the genetics would have to be weird.  You’d need either a variant that had opposite effects with one versus two copies, or a lot of variants that only had effects with two copies and no effect with one, or an effect that switched on only when you had variant copies of multiple genes, or an effect driven by new mutations not inherited from parents.  The results for the vasopressin gene don’t have this kind of weird.

The story is all “yes, it’s surprising that you’d get this sort of effect in a complex social behaviour, but genetics! And voles!”. I’ll give him the voles, but if anything, the strong correlation between identical twins (only) argues against vasopressin gene variants being a major driver in humans, and the research paper is much more cautious on this point.



May 20, 2015

Actually it’s about neuroscience in videogame journalism

Q: Why does Stuff think playing ‘Call of Duty’ increases the risk of Alzheimer’s disease? I didn’t think old people played violent video games much.

A: I don’t think Stuff does think anything in particular about it. They just reprinted that from the Telegraph and trimmed out the casual sexism.

Q: Ok, why does the Telegraph think playing ‘Call of Duty’ increases the risk of Alzheimer’s disease? I didn’t think old people played violent video games much.

A: It’s not so much about the games they play now as the ones they played 60 years earlier

Q: What video games did they play 60 years ago?

A: Not current people with Alzheimer’s; gamers now who might get Alzheimer’s in a few decades.

Q: Ok, so why will that happen?

A: Because video game players use response learning strategies for navigation in video mazes

Q: Why is that bad?

A: Because other research found people who used those strategies had more activity in their caudate nucleus.

Q: Is this going to start making sense soon?

A:. Yes. Sorry. The research found that when navigating a virtual-reality maze habitual game players used strategies that had previously been correlated with less activity in a part of the brain involved in memory and spatial awareness than normal people did. They apparently used different strategies involving other parts of the brain.

Q: And why is this a problem?

A: Because that part of the brain, the hippocampus, is less active in people with Alzheimer’s, as well as some other neurological and psychological disorders

Q: While they’re playing video games?

A: No, all the time.

Q: Couldn’t it just be that the video gamers have developed a more efficient strategy and that their hippocampuses are perfectly fine. Or hippocampi, whatever?

A: Yes, that could also be the case.

Q: I mean, if you saw people twitching their thumbs rapidly playing a video game it would be fine, but if they were just doing that while sitting around at meetings you’d worry a bit.

A: Indeed.

Q: Did the research look at memory or cognition at all?

A: No.

Q: Do they even know that these brain differences happened after playing video games? Could it be that people who don’t use that part of the brain for video navigation are just better at games?

A: It could be, yes.

Q: The story quotes the percentages using the parts of their brain to four significant digits. Does that mean there were tens of thousands of people in the research?

A: No.

Q: How many?

A: 59: about 30 in each group

Q: If this was true, could it explain why dementia is increasingly common?

A: No.

Q: Why not?

A: Partly because it’s too soon, and partly because dementia isn’t increasingly common at a given age, at least in the US and Europe. If anything, it’s less common. There are more cases now because there are more old people.

Q: It sounds like more research might be needed before writing international headlines about the risk of a terrifying disease.

A: You think?

May 15, 2015

Useful science/health reporting

As I’ve commented before, most good-quality randomised trials of vitamins in humans have disappointing results. A few don’t, and it’s nice to see these reported accurately.  The Herald tells us about an  Australian trial which has found nicotinamide, a version of vitamin B3, can reduce the rate of new minor skin cancers in people who already have had a lot of them.  This isn’t especially dramatic, but for many older pale-skinned people in New Zealand, Australia, or South Africa it could reduce a recurrent medical annoyance.

The only real omission in the Herald story is the link to the research: there’s a conference abstract for a talk to be given at the American Society for Clinical Oncology conference later this month.


Update: yes, this sort of story is less impressive and has less public health significance than claiming WiFi causes brain cancer in children, but it does have the advantage of being true.

May 1, 2015

If it seems too good to be true

This one is originally from the Telegraph, but it’s one where you might expect the local editors to exercise a little caution in reposting it

A test that can predict with 100 per cent accuracy whether someone will develop cancer up to 13 years in the future has been devised by scientists.

It’s very unlikely that the accuracy could be 100%. Even it is was,  it’s very unlikely that the scientists could know it was 100% accurate by the time they first published results.

One doesn’t need to go as far as the open-access research paper to confirm one’s suspicions. The press release from Northwestern University doesn’t have anything like the 100% claim in it; there are no accuracy claims made at all.

If you do go to the research paper, just looking at the pictures helps. In this graph (figure 1), the red dots are people who ended up with a cancer diagnosis; the blue dots are those who didn’t. There’s a difference between the two groups, but nothing like the complete separation you’d see with 100% accuracy.


Reading the Discussion section, where the researchers tend to be at least somewhat honest about limitations of their research

Our study participants were all male and mostly Caucasian, thus studies of females and non-Caucasians are warranted to confirm our findings more broadly. Our sample size limited our ability to analyze specific cancer subtypes other than prostate cancer. Thus, caution should be exercised in interpreting our results as different cancer subtypes have different biological mechanisms, and our low sample size increases the possibility of our findings being due to random chance and/or our measures of association being artificially high.

Often, exaggerated claims in the media can be traced to press releases or to comments by researchers. In this case it’s hard to see the scientists being at fault; it looks as if it’s the Telegraph that has come up with the “100% accuracy” claim and the consequent fears for the future of the insurance industry.


(Thanks to Mark Hanna for pointing this one out on Twitter)



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.