There’s a headline in the Herald: Heart disease linked to non-stick cookware: study. There seems to have been some loss in translation for both the article and the headline.

The journal press release says

Exposure to perfluorooctanoic acid (PFOA), a manmade chemical used in the manufacture of some common household products, appears to be associated with cardiovascular disease and peripheral arterial disease in a study of 1,216 individuals

That is, PFOA is used to make non-stick cookware, but cooking with non-stick cookware isn’t an especially important source of it, and the article doesn’t say it is.

Unlike the Teflon in non-stick coatings, which is as inert as a very inert thing, PFOA is quite chemically interesting. There are traces of PFOA in all sorts of things, and it accumulated in the environment, which is why it’s interesting to public health researchers.  If you want to read more, Wikipedia is a bit alarmist about the health evidence but reasonably informative.

The story goes on to say

From a statistical point of view it’s strange  that the researchers just used four years of NHANES data, from two non-adjacent two-year periods.   The study keeps going year after year, and they are now measuring PFOA and related compounds on greater numbers of people.  As a service to the StatsChat readership, I just spent 15 minutes downloading and analysing the 2007-2008 data, which has PFOA measurements on 2100 people, 80 of whom reported coronary heart disease.  I didn’t do as thorough a job of ruling out other risk factors (such as cholesterol or high blood pressure), but it’s still interesting to note that there is absolutely no sign of an association between coronary heart disease and PFOA levels in the 2007-2008 data.

The Herald has a story about junk food being linked to dementia.  The story itself is fine, but the sources are interesting:

Too much fatty and sweet food can increase insulin levels causing fat, muscle and liver cells to stop responding to the hormone, Medical Daily explained.

When the brain stops responding to insulin our capacity to think and create new memories is hindered, according to the paper recently published in New Scientist magazine.

 Medical Daily is an aggregator of medical stories — it’s a good place to find interesting research with lively descriptions, but it’s not very selective.    It’s a very popular source for the mass media and for alternative-medicine blogs.   The unusual aspect of the story is the primary source, New Scientist.   New Scientist is not a research journal, it’s a popular science magazine.  It used to be the best source in the world for accessible, detailed, science journalism, and although it’s become a bit sensationalist, there’s still a lot of good material there.   It has never been a primary source, and it hasn’t suddenly started publishing new research.

In fact, the New Scientist article is well worth reading: it describes the theory that some (most?) Alzheimer’s disease is due to insulin resistance in the brain, with quotes from researchers and links to the original research.  The “Type III diabetes” theory of dementia is definitely a minority view, and the evidence for it is thought-provoking, but not definitive.  There doesn’t seem to be any reason why it couldn’t be at least partly true, but the same could have been said for the aluminium theory of dementia in its early days.

The only good thing about the diabetes theory of dementia is that while we’re not great at treating insulin resistance, we’re a lot better at it than we are at treating Alzheimer’s.

Andrew Gelman, of Columbia University, wrote an article a few months ago called “Statistics for Cigarette Sellers”

Remember How to Lie with Statistics? It turns out the  author worked for the cigarette companies… It appears he was also working on a book in the late 1960s called How to Lie with Smoking Statistics, which the publisher saw “high likelihood of proceeding into print.”

His blog has a largely overlapping post, but with a bit more material (and discussion in comments).

Since newspapers almost exclusively cover positive results in medical research, it’s easy to have an unrealistically optimistic view of progress.  Most weeks, there are multiple stories about some new compound or extract that kills cancer cells in the lab, but we don’t learn what happens later.  And no, these treatments aren’t suppressed by evil multinational drug companies, who are actually in desperate need of new things to sell us.  As a partial corrective, here are some relatively recent research findings that make it less likely we’ll soon get new treatments for important diseases.

Alzheimer’s:  trials of two antibodies against amyloid plaques, which had shown promise in mice, failed to  show benefits in patients (one was robustly null, the other was borderline and the company hasn’t quite given up hope).  Inhibiting one of the enzymes that makes amyloid has also failed.

Heart disease:  Raising ‘good’ HDL cholesterol was a big hope, but three separate approaches to treatment have so far failed to provide any convincing benefit in clinical trials, and genetic studies suggest that although HDL is associated with lower risk, it may not actually be responsible for the reduction.

 Diabetes:  drugs to reduce insulin resistance through a new target called PPAR were going to be the new revoluation.  Troglitazone and rosiglitazone (Avandia) got into use but turned out not to actually reduce complications of diabetes, several others didn’t make it past clinical trials.  An even more promising approach was to inhibit one of the transporter proteins in the kidney, and dump all the excess glucose in urine. It didn’t work either.

One piece of good news as balance: a very promising new antibiotic for tuberculosis has succeeded in a phase II trial of drug-resistant TB.  The trial looked at how fast patients became non-contagious, and the new antibiotic got more patients to that state, faster.  The next step, just about to start, is a longer trial to see if patients are actually cured — it could still fail, of course.

One of the problems in medical research, exacerbated by the new ability to measure millions of genetic variables at once, is that you can always divide people into sensible subgroups.

If your treatment doesn’t work, or your hated junk food isn’t related to cancer, overall, you can see if the relationship is there in men or in women.  Or in younger or older people.  Or in Portugese-speaking bassoonists. The more you chop up the data, the more likely you are to find some group where there’s a difference.  You can then focus on that group in your results.

To combat this tendency, my Seattle colleague Noel Weiss has been promoting the slogan “conclusions of difference require evidence of difference”.  That is, if you want to report that cupcakes cause cancer in men but not in women, you need evidence that the relationship is different in men and in women.  Finding supportive evidence in men but not finding it in women isn’t enough: that’s not evidence of a difference.  Needing evidence of a difference is especially important when you wouldn’t expect a difference.  We expect most things to have basically similar effects in men and women, and where the effects are different there’s usually an obvious reason.

All this is leading up to a story in the Herald, where a group of genetics researchers claim that a well-studied variant in a gene called monoamine oxidase increases happiness in women, but not in men.  We know this is surprising, because the researcher said so — they were expecting a decrease in happiness, and they don’t seem to have been expecting a male:female difference.  The researchers say that the difference could be because of testosterone — and of course it could be, but they don’t present any evidence at all that it is.

Anyway, as you will be expecting by now, I found the paper (the Herald gets points for giving the journal name), and it is possible to do a simple test for differences in `happiness’ effect between men and women. And there isn’t much evidence for a difference. For people who collect p-values: about 0.09 (Bayesian would get a similar conclusion after a lot more work). So, if we didn’t expect a benefit in  women and no difference in men, the data don’t give us much encouragement for believing that.

Testing for differences isn’t the ideal solution — even better would be to fit a model that allows for a smooth variation between constant effect and separate effect — but testing for differences is a good precursor to putting out a press release about differences and trying for headlines all over the world. We can’t expect newspapers to weed this sort of thing out if scientists are encouraging it via press releases.

Stuff has an example of the recurring problem of an perfectly good medical science story spoiled by not one, but two appalling headlines.

Currently, on the ‘Wellbeing’ section of the website you see

Feeling poorly? Try Vegemite

and on clicking through to the story

Vegemite may ward off superbugs

The story then goes on to say that high concentrations of niacin, a vitamin found in many foods, including, yes, Vegemite, has been found in test-tube and mouse studies to help in killing bacteria.  It then says

This blog has a tendency to look pro-drug and pro-alcohol, because we react to media stories and these topics are currently popular for exaggeration and over-interpretation.  It’s a nice change to find some serious anti-drug research that the media are reporting pretty sensibly. (Otago Daily Times, Stuff, Herald, 3News, TVNZ)

Researchers in Dunedin, and their international collaborators, used data from the Dunedin Study, which recruited about 1000 babies born in a Dunedin hospital in the 12 months starting April 1972.  These babies, now adults, have given a lot of data up to medical science. In particular, they had a range of neuropsychological tests at age 13 and then again at age 38, and they were interviewed about cannabis use.   The headline results were about IQ, but the study looked at a relatively broad range of cognitive function tests, and also at self-reported problems with memory and attention.   Participants who smoked cannabis as teens had broadly worse cognitive function, by a margin that’s large enough to be a concern.  This didn’t show up in people who started smoking cannabis as adults.  The paper is in PNAS; the abstract is free.

What’s most distinctive about this study is the before-after comparisons.  You often see (and we have pointed out) studies that claim to have found “changes” when they only had one time point, and so really only looked at “differences”.  The Dunedin Study has changes from before cannabis use to after cannabis use.   Also, since the participants are the same age and all from Dunedin, they are less heterogeneous in many ways than participants in other research studies.

The differences in IQ are within the range of the Flynn effect, so it’s still possible that this is a social effect rather than a biochemical one, or that it’s caused by pre-existing differences in people’s interest in the sort of activities that increase IQ test scores, or something.  Better data, however, will be extremely difficult to collect, and treating these results as probably true seems sensible.  Presumably the adverse effects would also be found with synthetic cannabimimetics, but these are too recent for there to be data, and they have other problems not present with cannabis, such as the risk of acute overdose.

A number of the stories quote Ross Bell, of the Drug Foundation, being sensible:

Simply banning drugs such as cannabis and then thinking that was the problem solved would not work, Mr Bell said. “What we’re lacking in New Zealand is support for widespread, high-quality, well-constructed prevention messages targeted at younger people.”

Stuff is reporting on a software system called Volpara for improving breast-cancer screening, from Wellington company Matakina (and 3News had a similar story).  The software is designed to give more reliable and objective estimates of breast density, with less variation due to different equipment or different radiologists.  This should be helpful in screening younger women, either to improve detection of tumours or to reduce false positives, and the software seems to have been quite successful commercially.

Medical progress is pretty incremental: even the best ideas and techniques tend to have relatively small impact on health, so while it’s good to see NZ medical contributions being recognised, it’s also useful to put them in context. (more…)

The Herald says

One in three New Zealanders have been harmed by their own alcohol drinking, a survey shows.

The survey, published in the New Zealand Medical Journal, found 33.8 per cent of current drinkers reported they had been adversely affected in the past year.

This is actually true: there is such a survey, it is published in the NZMJ, and it’s a real survey (the response rate isn’t all one could wish, but it’s not out of line with other major health surveys).  The story goes on to say that the harm was reported more often by men.

The interesting point is that the current issue of NZMJ has two articles about frequency of harm from drinking.  The other one says, also based on real survey data,

The prevalence of self-reported harm from others’ drinking was higher than harm from own drinking (18% vs 12% in the past year) and was higher in women and young people.

And this second survey isn’t pro-alcohol in the slightest — for example, it quotes the proportion of criminal offenders who had been drinking as if it was the proportion of crimes resulting from alcohol.  This is a huge overestimate, precisely because there is too much drinking in NZ: the people who are drunk and arrested in the major cities tend to be just as drunk about three times a week on average (based on Massey Uni. research that we’ve mentioned before).

The timing of these articles is perhaps not a coincidence, but in fact there’s pretty wide consensus about the harms from drinking: the real disagreement is about the costs of various sorts of regulation.

From Stuff, under the headline “Public transport ‘good for your health'”

Waiting for public transport may seem dull, but new research shows daydreaming at the bus stop may be good for your mental health.

Wouldn’t it be nice to think so? Unfortunately, what the research actually found is a bit different:

Also, the ‘good for your health’ in the headline is claiming to be a quote, but the quote doesn’t appear in the story.