Gobbledegook - update

Last month I wrote about a 'pregnancy increases your risk of heart attack three to four fold' story in The Sun, The Star and The Daily Telegraph. Rereading the 2006 study from which the papers took their soundbite the significance of this stood out where it hadn't before:

We found a higher incidence (6.2 versus 2.8 per 100 000 deliveries) and a lower case fatality rate (5.1% versus 7.3%), however, than a recent analysis that used data from a California database.10 Because the California estimate of incidence was based on data from 1991 to 2000, our estimate may reflect improved identification of cases or may reflect a true increase in the number of cases

(sorry for the bolderising, but this is important).
So, according to the study authors, since 2000 it's plausible that identification and reporting of heart attacks during delivery has improved, leading to a higher figure for its incidence. They go into a bit of detail:

Improved identification of cases may have resulted from the advent of the widespread use of troponins, which has likely resulted in the detection of small events that were previously undiagnosed. Increased detection would explain an increase in the incidence of acute myocardial infarction and a decrease in the case fatality rate. Another possible explanation for an increase in the incidence over time is the increased number of births to older women, who may have more cardiac risk factors. Between 2002 and 2003, the birth rate rose 6% for women aged 35 to 39 years and 5% for women aged 40 to 44 years.8 Since 1981, the birth rate for women aged 40 to 44 years has more than doubled.8 Another possible explanation for the higher incidence is better ascertainment of cases in the NIS database.

all of which have me nodding my head in agreement. Two paragraphs later (and they're not very long paragraphs either, so the two statements come pretty close together):

We do not have the incidence of acute myocardial infarction for women who were not pregnant. Petitti et al,14 however, published the incidence of myocardial infarction among reproductive-aged women in a large health maintenance organization. Using the age-specific rates of myocardial infarction per 100 000 women-years derived from that study and applying them to the age distribution of the women in the present study, we would have expected to find 250 myocardial infarctions as opposed to the 859 found. Therefore, the risk of acute myocardial infarction appears to be approximately 3 to 4 times higher in pregnancy.

(the line that had the PR person so excited)(and the newspapers). Clicking on the hyperlink that takes you to the reference section, and the full title of the Petitti et al study mentioned above gives it as Petitti DB, Sidney S, Quesenberry CP Jr, Bernstein A. Incidence of stroke and myocardial infarction in women of reproductive age. Stroke. 1997; 28: 280–283. A visit to the archives of Stroke and a look at line two of the Subjects and Methods section tells us that the study was conducted

May 1, 1991, through August 31, 1994, in northern California and July 15, 1991, through August 31, 1994, in southern California.

Right, so: detection and reporting between 1991 and 2000 may have led to an underestimation of incidence in one paragraph, but two paragraphs later, the same time period is being used to estimate a three to four fold increase in heart attack risk for pregnant women. Dye not reckon that maybe the 859 cases of heart attack in pregnant women found in this study were down to improved detection and reporting, and that the 250 cases in the general female population of 1991 may have been an underestimation? Just saying.
Science and health reporting isn't a job for jobbing reporters, it's a job for investigative journalists. And while I'm at it, it's high time health correspondents abandoned their slavish respect for medical authority and started reading the bleeding studies they trumpet so very loudly.

This one gets right up my nose

Or why journalists should read the original research paper and not just quote a scientist looking to hype up their own research. MHC-correlated odour preferences in humans and the use of oral contraceptive was published last week in the journal Proceedings of the Royal Society B. Studies, in animals and in humans, have shown that genes in the major histocompatibility complex (MHC) influence individual odours and that females often prefer odour of MHC-dissimilar males. The study in question here sought to investigate whether oral contraceptive use changes these odour preferences. The study found that women's preferences changed after they went on the pill - such that they went from preferring the odours of men who were MHC dissimlar to those of men who were MHC similar. The researchers also found that single women preferred men who were MHC similar, while women in relationships preferred those who were dissimilar. They speculate as to the reasons for this, suggesting that women in relationships might seek to improve offspring quality by seeking out other pairings. The study doesn't look into this, it's just a suggestion. The study also doesn't account for why single women might prefer MHC similar men, which is fair enough, as it's beyond its remit. Nor does it account for the possibility that the kind of woman who goes on the pill may have some behavioural, genetic, other, or combination of all three characteristics which may account for the change in preference over time; again, fair enough, that's not what it set out to do. The study certainly doesn't, in its own right, look into issues of fertility, relationship breakdown, or the possible consequences of MHC similarity for the health of future offspring; again, all these things are beyond its remit.

However, in the introduction the authors do suggest that

Mate preference for MHC-dissimilar individuals can be adaptive as it would increase offspring MHC heterozygosity, with beneficial influences on offspring viability through increased resistance to infectious disease or avoidance of inbreeding effects

referencing two previous studies, one, Potts & Wakeland, 1993, the other, Milinski, 2006.

The latter study, reviewing the literature on the possibility that choosing an MHC dissimilar mate may be adaptive, reports that findings have been equivocal:

Many of the studies that demonstrated or implied MHC-dependent mate choice found that the choosy sex prefers partners with somewhat dissimilar MHC alleles (e.g., Bonneaud et al. 2006; Egid & Brown 1989; Eklund et al. 1991; Freeman-Gallant et al. 2003; Landry et al. 2001; Ober et al. 1997; Olsson et al. 2003; Potts et al. 1991, 1994; Richardson et al. 2005; Wedekind & Füri 1997; Wedekind et al. 1995; Yamazaki et al. 1976, 1978). MHC disassortative mating may function to increase the resistance of offspring to infectious diseases by increasing their MHC heterozygosity (heterozygote advantage hypothesis; e.g., Apanius et al. 1997, Potts & Wakeland 1990) and/or it may operate to prevent kin-matings (inbreeding avoidance hypothesis; Brown & Eklund 1994, Potts et al. 1994), because this can have fitness benefits (Arkush et al. 2002, Meagher et al. 2000). Some correlative field studies supported the heterozygote advantage hypothesis (e.g., Carrington et al. 1999, Thursz et al. 1997) while others did not (e.g., Hill et al. 1991, Paterson et al. 1998). Also experimental studies beginning with Doherty & Zinkernagel (1975) provided ambiguous results as a recent meta-analysis showed (Penn 2002).

and concludes:

A heterozygote advantage per se has not been found by a number of studies and it is not necessarily expected either. Furthermore, as recent models have shown, a heterozygote advantage on its own fails to explain the high degree of polymorphism of the MHC (De Boer et al. 2004) in contrast to predictions of earlier models. Mate choice just for dissimilar MHC alleles would not necessarily improve the resistance of offspring nor would it help to maintain MHC polymorphism in the population.

There's a reason why journal articles contain references - it's so the reader may, if (s)he so wishes, check out the veracity of statements contained in that article. So, this one line in the introduction of the study under discussion, the only one, in fact, in that study to suggest that pairings of MHC similar mates may result in less than optimal offspring, is not, in fact, supported by the literature.

Which brings me to this:

Going for genetically similar men, detected from body odour, may increase a woman's risk of difficulties trying to conceive, miscarriage and of long intervals between pregnancies.

(from The Independent, UK - Why women can't sniff out Mr. Right when they're on the pill)
It's that 'detected from body odour' that's the outrage. It suggests that this study found this to be so. It didn't. While the science may support the idea that genetic similarity in partners is not good for their offspring, the science behind MHC similarity/dissimilarity does not show this to be so; as demonstrated above, the literature is equivocal, and certainly does not run to finding an association between MHC similarity and such dramatic outcomes as fertility problems and miscarriage. This is outright nonsense. Dangerous nonsense.

Which brings me to the reason I'm so very angry about this article. Of course, had the journalist done some research he would have turned up what I'd turned up. Had he read just the original research paper he would have realised that extrapolating wildly was inappropriate; had he read just the last three lines of the paper (again! journalists! read the conclusions! they're so very short, and so terribly important) he would have found his entire article written for him, And in this case, the conclusion even helpfully exaggerates the findings somewhat, so he wouldn't even have had to hype it himself:

We do not know whether the change in preferences related to pill use is sufficiently strong to influence partner choice, but it could do so if odour plays a significant role in actual human mate choice. Some studies have suggested that women consider the olfactory domain to be an important factor in their assessment of potential partners (e.g. Havlicek et al. 2008). Although we were unable to replicate the effect, Wedekind et al.'s (1995) demonstration of an association between MHC dissimilarity and the reminiscence of current or previous partners suggests that the influence of MHC-odour cues may extend beyond the laboratory. If this is the case, our results indicate that use of the contraceptive pill could lead to choice of an otherwise less preferred partner.

But look what we have here, a quote from Dr. Craig Roberts, one of the researchers on the study:

The preferences of women who began using the contraceptive Pill shifted towards men with genetically similar odours. Not only could MHC similarity in couples lead to infertility problems but it could ultimately lead to the breakdown of relationships when women stop using the Pill, as odour perception plays a significant role in maintaining attraction

Had he included this bit of speculation in the research paper submitted to Proceedings of the Royal Society B he would have found it rapidly run through with the editor's pen. His findings do not support this conclusion; the scientific literature does not support this conclusion; there is nothing to support this conclusion but his desire to hype his own research.
There are hundreds of reasons why a woman might choose a mate; there are equally hundreds of reasons why this mate may or may not choose to be chosen; these choices carry with them hundreds of implications, and we're a long way from unpicking the resultant 100sx100sx100s (that's lots and lots then) of possibilities that go into making babies and what those babies are like. It's unlikely many women will go off the pill as a result of this study, but if even one does, and finds herself with an unwanted pregnancy because the condom broke, then Jeremy Laurence and Dr. Craig Roberts should both be very very ashamed.

The Times does a reasonable job of reporting on this story, by the way.

The fat kid fumble

Clumsy children more likely to become obese as adults, study finds. Physical control and coordination in childhood and adult obesity: longitudinal birth cohort study by Walter Osika and Scott M. Montgomery was published yesterday in the BMJ. It's part of the National child development study in Great Britain, a longitudinal cohort study of children born between 3rd and 9th March 1958 and living in Great Britain. The study in question here gathered assessment data on hand control, coordination and general clumsiness, as assessed by teachers when the cohort was 7 and 11. Data were available for 7990 children at age 7 and 6875 at age 11. An association was found between teacher reports of 'clumsiness' and subsequent obesity (as measured by Body Mass Index) at age 33. It reads:

Among 7990 cohort members at age 7 years, teachers reported that poor hand control, poor coordination, and clumsiness "certainly applied" more often among those who would be obese adults.

Similar results were found for the cohort measured at age 11 years.
The authors caution:

Many other environmental or individual characteristics could explain the associations.

and go on to suggest, as an example, that individuals with poor motor control may be less likely to exercise, thus increasing the risk of obesity. They conclude that while the study adds to the body of evidence associating poorer cognitive functioning with obesity, neither this study nor any other which has found such a link, can tease out how or why this should be. They conclude:

Rather than being explained by a single factor, an accumulation throughout life of many associated cultural, personal, and economic exposures is likely to underlie the risks for obesity and some elements of associated neurological function.

265 words. And it took me all of twenty minutes, including the time taken to read the paper, to write. The Daily Mail gives it 221 words. I'll reproduce them in full:

Clumsy children are more likely to be obese in later life because they exercise less, research says.

A study that started 50 years ago found youngsters with poor hand control and co-ordination are far more prone to piling on the pounds during adulthood.

This puts them at higher risk of heart attack, stroke and diabetes.

The findings, published online by the British Medical Journal, found children who performed worse in tests assessing their cognitive and physical function were more likely to be obese by the age of 33.

Those who were obese were 57 per cent more likely to have suffered poor hand control aged seven, more than twice as likely to have suffered poor co-ordination and almost four times as likely to have been clumsy.

The study adds to evidence of a link between poorer cognitive function in childhood and obesity and Type 2 diabetes in adulthood.

Researchers said cognitive impairment in obese adults was assumed to be a consequence of obesity.

However, the study indicates obese adults and those with Type 2 diabetes may already have had lower levels of cognitive function in childhood 'consistent with a subtle developmental impairment'.

The research, whose authors are from the Karolinska Institute in Stockholm and Imperial College, London, is based on 11,042 people taking part in the ongoing National Child Development Study in Great Britain, which began in 1958.

And again, this time with nimby commentary:

Clumsy children are more likely to be obese in later life because they exercise less, research says.
fair enough

A study that started 50 years ago found youngsters with poor hand control and co-ordination are far more prone to piling on the pounds during adulthood.

This puts them at higher risk of heart attack, stroke and diabetes.

The findings, published online by the British Medical Journal, found children who performed worse in tests assessing their cognitive and physical function were more likely to be obese by the age of 33.
Why not just say association? What's wrong with it? 11 letters, 1 more than 'more likely' and without the connotations and grammatically questionable see-sawing between temporalities.

Those who were obese were 57 per cent more likely to have suffered poor hand control aged seven, more than twice as likely to have suffered poor co-ordination and almost four times as likely to have been clumsy.
This is where it gets seriously wonky. The odds ratios reported in the study were 1.57 (95% confidence interval 1.13 to 2.20; P=0.008) for poor hand control, 2.30 (1.52 to 3.46; P<0.001) for poor coordination, and 3.91 (2.61 to 5.87; P<0.001) for clumsiness (in the age 7 cohort); and 0.88 (0.81 to 0.96; P=0.003) for copying designs, 0.84 (0.78 to 0.91; P<0.001) for marking squares, and 1.14 (1.06 to 1.24; P<0.001) for picking up matches (a higher score indicates poor function in this test) for the age 11 cohort. Now, it should be clear, first, that the measures used to assess the two cohorts were different, and so can't be aggregated. We'll assume Daily Mail Reporter knew this, and chose to focus on the age 7 cohort. How can we assume this? The figures: the 57% figure came from one of two places. The first option is a misreading of 1.57 as 0.57 (perhaps (s)he blinked while reading). The second option comes from one of the study's results tables, which contains the number 5.7 as the incidence of teacher reports that the child 'certainly' had poor hand control. At the top of the table, and in the body of the text, it is explained that the figures in the table are percentages. Taking a look at the hard numbers, we see that there were 912 obese 33 year olds in the study, of whom 52 were reported to 'certainly' have poor hand control age 7. 52/912 x 100 gives us 5.7%. 5.7, not 57, and certainly not 57% more likely. Going back to option one, the odds ratio of 1.57, that's not 57% more likely in anyone's book

The study adds to evidence of a link between poorer cognitive function in childhood and obesity and Type 2 diabetes in adulthood.

Researchers said cognitive impairment in obese adults was assumed to be a consequence of obesity.
No they didn't

However, the study indicates obese adults and those with Type 2 diabetes may already have had lower levels of cognitive function in childhood 'consistent with a subtle developmental impairment'.
The study does not indicate this. This line comes from the introduction, and references two previous studies: Chandola T, Deary IJ, Blane D, Batty GD. Childhood IQ in relation to obesity and weight gain in adult life: the national child development (1958) study. Int J Obes 2006;30:1422-32 and Olsson GM, Hulting AL, Montgomery SM. Cognitive function in children and subsequent type 2 diabetes mellitus. Diabetes Care 2008;31:514-6. The line in question even has hyperlinks to the part of the reference section the studies are cited in, saving the bother of scrolling down the page to find them.

The research, whose authors are from the Karolinska Institute in Stockholm and Imperial College, London, is based on 11,042 people taking part in the ongoing National Child Development Study in Great Britain, which began in 1958.

Most of the words and phrases needed to report on medical research are right there in any given study. Often, the authors helpfully include a little three or four line 'Conclusion' after the discussion section that outlines the findings and puts them in context. Mangling figures does not add to the public's understanding of a study. It simply adds to the word count, pushing out space for the all important caveats and contextualisation needed in any science story. Including them for the sake of appearing learned and sciencey is about as convincing as donning a white coat, a pair of novelty thick rimmed glasses and mussing your hair up to look like Einstein.

Good news for fat rats

'The pill that lets dieters eat what they like'. 'A pill which may 'lock in' the benefits of dieting...has been discovered by scientists'.
Point the first: the pill in question is alpha-lipoic acid, a dietary supplement that has been around for quite a while (here it is at drugstore.com; there's even a book about it which shows up 10th on the google search page if you type 'alpha lipoic acid' into the little box and press enter)(in case you don't care to follow the link, the book is called 'Alpha Lipoic Acid Breakthrough: The Superb Antioxidant That May Slow Aging, Repair Liver Damage, and Reduce the Risk of Cancer, Heart Disease, and Diabetes' and it was published in 1998).
Point the second: the study in question was conducted on rats. The researchers divided the rats into a number of groups - some on supplemented calorie controlled diets, some on unsupplemented versions of the same; some on unrestricted supplemented diets, some on unrestricted unsupplemented diets; they also changed the conditions during the study, taking some rats off the unrestricted unsupplemented diets and putting them on the calorie controlled supplemented diets; taking others off the calorie controlled unsupplemented diets and putting them on supplemented unrestricted diet - and this is where the story comes in. The rats in the latter condition were found to live as long as those who had been on the calorie controlled unsupplemented diet from the beginning (calorie controlled diets have an association with longevity in rats*). Conclusion: the extended survival benefits of the calorie restricted condition persisted in the unrestricted supplemented condition. Final word (in the study):

whether this compound would induce similar effects on survival in other species used as model organisms to study ageing is not known

Point the third: (from The Independent)

Simply adding the supplement to the diet has no effect. It seems that alpha-lipoic acid fools the body into behaving as if it was still on whatever diet it was following before the supplement was added. We found there was an anti-obesity effect as well. Although weight does rise when you come off the restricted diet, if you take alpha-lipoic acid, even though you are eating normally again you still have a reduced weight

said Professor. Goyns.
'You', indeed. 'You', the rat?
Point the fourth: The print version of this article ends on this note, although it does point out that the research was conducted on rats. The online version, however, includes some words from Goyns' co-author, Brian Merry:

It is an unusual and interesting finding and it needs repeating in further research. That was as far as I was prepared to go, but Malcolm [Goyns] wanted to apply it to humans. I said I didn't agree with his interpretation and we had to wait for further studies.

People have been buying this stuff and taking it for years as a dietary supplement. I don't think anyone knows what its effect is. There have only been two studies in rats and mice [before our study].

Interestingly, Goyns is director of Immorgene Concepts, and has a book to flog at the moment, while his two co-authors, Brian Merry and Austin Kirk, simply work for the school of Biological Sciences at the University of Liverpool.

Point the fifth: Why was the most significant part of the article, namely Merry's response, left out of the Irish print version of this story?

Point the sixth: What, exactly, is Malcolm Goyns's game? He does have an actual academic post, at the University of Sunderland, a fact which makes his exaggeration of his own research particularly egregious.

Update: hmm, can't be quite sure Professor Goyns is actually employed by the University of Sunderland, as he doesn't show up on their staff pages, although he has collaborated on research with people who do.

*see e.g. Fontana & Klein, JAMA, 2007;297:986-994. Academic login required.