Last week I analysed two studies which were based on tiny, very specific populations. One added little to our state of knowledge, the other was a scientifically interesting, unexpected finding that needs further investigation. Both resulted, naturally, in big scary headlines across the media.
I’m not blaming the reporters. They have a job to do, and ‘Don’t worry’ is a rubbish headline. The researchers (or their institutions) are responsible for putting out press releases and giving media sound-bites to big up their little studies. But it does help if the media put things in perspective.
The first culprit was e-cigarettes. A survey of teenagers in the US found that a vanishingly small proportion of kids who had never smoked tobacco and said they didn’t plan to, had nevertheless tried e-cigarettes. Small surprise to learn that those kids were more likely to try a tobacco cigarette than the kids who hadn’t tried e-cigarettes. The study also showed they were more open to taking risks in general. But on the basis of the six (yep, six) kids who tried tobacco after trying an e-cig, the researchers declared that e-cigarettes could get children hooked on nicotine. This was a pointless study which told us nothing of any use. I picked it apart for NHS Choices, here: No conclusive evidence that e-cigs tempt teens to smoke
The second study was more interesting. Post-mortem examinations of seven people who had died of Creutzfeld-Jakob disease (CJD) unexpectedly found one of the signs of Alzheimer’s disease – areas of amyloid beta protein, deposited in the brain tissue and in some cases in the brain arteries. None of these people had developed Alzheimer’s, and we don’t know if they would have done if they had not died of CJD. Amyloid protein accumulates in the brain as people age, and is responsible for the plaques that may be a cause of Alzheimer’s. But these people had not reached an age when you would expect to see these plaques.
So how did the amyloid protein get into their brains? The people in the study had all been infected with the prions that caused CJD as children, when treated with pituitary-gland derived human growth hormone from cadavers. The researchers looked at post mortem results from people who’d died of prion disease from other, non-medical sources, to see if amyloid was a common finding alongside prion disease. It was not.
What does that tell us? One possibility is that the amyloid had arrived in the same way as the prions – via injections of cadaveric-derived human growth hormone. If that turned out to be the case, could other medical procedures also transmit amyloid protein? Studies of people who have had blood transfusions suggest that route does not increase chances of Alzheimer’s disease.
The study raised a lot of questions for researchers to investigate, but gave no answers. The researchers said in their study that they were not suggesting Alzheimer’s was contagious. Cue headlines about whether you can ‘catch’ the disease from dental procedures. Another tiny study of people with very specific history, being hyped to scare the public. My analysis for NHS Choices here: Alzheimer’s ‘seeds’ found in seven CJD victims’ brains.