Posts filed under Medical news (247)

August 20, 2014

Good neighbours make good fences

Two examples of neighbourly correlations, at least one of which is not causation

1. A (good) Herald story today, about research in Michigan that found people who got on well with their neighbours were less likely to have heart attacks

2. An old Ministry of Justice report showing people who told their neighbours whenever they went away were much less likely to get burgled.

The burglary story is the one we know is mostly not causal.  People who tell their neighbours whenever they go on holiday were about half as likely to have experienced a burglary, but only about one burglary in seven happened while the residents were on holiday. There must be something else about types of neighbourhoods or relationships with neighbours that explains most of the correlation.

I’m pretty confident the heart-disease story works the same way.  The researchers had some possible explanations

The mechanism behind the association was not known, but the team said neighbourly cohesion could encourage physical activities such as walking, which counter artery clogging and disease.

That could be true, but is it really more likely that talking to your neighbours makes you walk around the neighbourhood or work in the garden, or that walking around the neighbourhood and working in the garden leads to talking to your neighbours? On top of that, the correlation with neighbourly cohesion was rather stronger then the correlation previously observed with walking.

August 19, 2014

Fortune cookie endings

Or, often in NZ papers, “… in the UK”.

There’s a Herald story with the lead

More than 12,000 new cases of cancer every year can be attributed to the patient being overweight or obese, the biggest ever study of the links between body mass index and cancer has revealed.

Since there about about 20,000 new cases of cancer a year in NZ, that would be quite a lot.  The story never actually comes out and says the 12,000 is for the UK, but it is, and if you read the whole thing it becomes fairly clear.  It still seems the sort of context that a reader might find helpful.

August 18, 2014

Health/nutrition claims: baby and bathwater

Australia and New Zealand are introducing new food labelling legislation that will reduce the scope for bogus health and nutrition claims (the only bogus claims allowed will be the ones that slipped into the official code).  This is a Good Thing, as I have said in the past.

The legislation also says you can’t make health claims about booze. This is probably a Good Thing, although I don’t see why calorie/carbohydrate claims shouldn’t be allowed.  However, there’s a serious bug in the standards: one of the claims that’s specifically disallowed for alcoholic beverages is “gluten-free.”

It’s true that “gluten-free” has become a trendy bogus nutrition claim, but it’s also vital health information for some people, particularly those with coeliac disease. In that context, “gluten-free” is more like an allergen warning (“May contain nuts”) than a nutrition warning.  In fact, if you look at the section on “Mandatory Warning and Advisory Statements and Declarations”, Clause 4 includes

Cereals containing gluten and their products, namely, wheat, rye, barley, oats and spelt and their hybridised strains other than where these substances are present in beer and spirits standardised in Standards 2.7.2 and 2.7.5 respectively

along with peanuts, soybeans, eggs, milk, etc.  That is, declaring the presence of gluten is mandatory except in beer, where it is the only one of the Clause 4 mandatory warnings that becomes forbidden.  Banning gluten-free labelling on beer is deliberate and planned, it didn’t just fall between the cracks.

Since this is a trans-Tasman law, it’s going to be a pain to revise.  There seems to be one possible loophole. In the Nutrition/Health claims standards, there is provision for endorsements by independent endorsing bodies. These are exempted from most of the health/nutrition regulations: as the Explanatory Text says:

Endorsements are exempt from the other requirements of the Standard (except clause 7), to allow for endorsement programs which use the criteria set by the endorsing body.

It appears (though I may have missed something, and I’m not a lawyer) that Coeliac New Zealand could still endorse gluten-free beers, even though the brewers couldn’t make the same claims themselves.

[Further update: MPI contacted Keruru Brewery and say they are now working on a solution for gluten-free beer.]

[update: I heard about this on Twitter, but the blog post that kicked off Twitter is here]

August 15, 2014

Cancer statistics done right

I’ve mentioned a number of times that statistics on cancer survival are often unreliable for the conclusion people want to draw, and that you need to look at cancer mortality.  Today’s story in Stuff is about Otago research that does it right:

The report found for 11-year timeframe, cancer-specific death rates decreased in both countries and cancer mortality fell in both countries. But there was no change in the difference between the death rates New Zealand and Australia, which remained remained 10 per cent higher in New Zealand.

That is, they didn’t look at survival after diagnosis, they looked at the rate of deaths. They also looked at the rate of cancer diagnoses

“The higher mortality from all cancers combined cannot be attributed to higher incidence rates, and this suggests that overall patient survival is lower in New Zealand,” Skegg said.

That’s not quite as solid a conclusion — it’s conceivable that New Zealand really has higher incidence, but Australia compensates by over-diagnosing tumours that wouldn’t ever cause a problem — but it would be a stretch to have that happen over all types of cancer combined, as they observed.

 

August 14, 2014

Breast cancer risk and exercise

Stuff has a story from the LA Times about exercise and breast cancer risk.  There’s a new research paper based on a large French population study, where women who ended up having a breast cancer diagnosis were less likely to have exercised regularly for the past five year period.  This is just observational correlation, and although it’s a big study, with 2000 breast cancer cases in over 50000 women, the evidence is not all that strong (the uncertainty range around the 10% risk reduction given in the paper goes from an 18% reduction down to a 1% reduction).  Given that,  I’m a bit unhappy with the strength of the language in the story:

For women past childbearing age, a new study finds that a modest amount of exercise — four hours a week of walking or more intensive physical activity such as cycling for just two hours a week — drives down breast cancer risk by roughly 10 per cent.

There’s a more dramatically wrong numerical issue towards the end of the story, though:

The medications tamoxifen and raloxifene can also drive down the risk of breast cancer in those at higher than average risk. They come with side effects such as an increased risk of deep-vein thrombosis or pulmonary embolism, and their powers of risk reduction are actually pretty modest: If 1000 women took either tamoxifen or raloxifene for five years, eight breast cancers would be prevented.

By comparison, regular physical activity is powerful.

Using relative risk reduction for the (potential) benefits of exercise and absolute risk reduction for the benefits of the drugs is misleading. Using the breast cancer risk assessment tool from the National Cancer Institute, the five-year breast cancer risk for a typical 60 year old is perhaps 2%. That agrees with the study’s 2000 cases in 52000 women followed for at least nine years.  If 1000 women with that level of risk took up regular exercise for five years, and if the benefits were real,  two breast cancers would be prevented.

Exercise is much less powerful than the drugs, but it’s cheap, doesn’t require a doctor’s prescription, and the side-effects on other diseases are beneficial, not harmful.

August 13, 2014

Most things don’t work

A nice story in the Herald about a randomised trial of hand sanitiser dispensers in schools.

The study, published today in the journal PLoS Medicine, found absence rates at schools that installed dispensers in classrooms as part of the survey were similar at those “control” schools which did not.

There’s even a good description of the right way to do sample size calculations for a clinical trial

Beforehand, the authors believed a 20 per cent reduction in absences due to illness would be important enough to merit schools considering making hand sanitiser available, so designed the study to detect such a difference.

“Some previous studies suggested that there could be a bigger effect than that, but we wanted to be sure of detecting an effect of that size if it was there,” Dr Priest told the Herald.

That is, the study not only failed to find a benefit, it ruled out any worthwhile benefit. Either Kiwi kids are already washing their hands enough, or they didn’t use the supplied sanitiser.

My only quibble is that the story didn’t link to the open-access research paper.

 

August 7, 2014

Vitamin D context

There’s a story in the Herald about Alzheimer’s Disease risk being much higher in people with low vitamin D levels in their blood. This is observational data, where vitamin D was measured and the researchers then waited to see who would get dementia. That’s all in the story, and the problems aren’t the Herald’s fault.

The lead author of the research paper is quoted as saying

“Clinical trials are now needed to establish whether eating foods such as oily fish or taking vitamin D supplements can delay or even prevent the onset of Alzheimer’s disease and dementia.”

That’s true, as far as it goes, but you might have expected the person writing the press release to mention the existing randomised trial evidence.

The Women’s Health Initiative, one of the largest and probably the most expensive randomised trial ever, included randomisation to calcium and vitamin D or placebo. The goal was to look at prevention of fractures, with prevention of colon cancer as a secondary question, but they have data on dementia and they have published it

During a mean follow-up of 7.8 years, 39 participants in the treatment group and 37 in the placebo group developed incident dementia (hazard ratio (HR) = 1.11, 95% confidence interval (CI) = 0.71-1.74, P = .64). Likewise, 98 treatment participants and 108 placebo participants developed incident [mild cognitive impairment] (HR = 0.95, 95% CI = 0.72-1.25, P = .72). There were no significant differences in incident dementia or [mild cognitive impairment] or in global or domain-specific cognitive function between groups.

That’s based on roughly 2000 women in each treatment group.

The Women’s Health Initiative data doesn’t nail down all the possibilities. It could be that a higher dose is needed. It could be that the women were too healthy (although half of them had low vitamin D levels by usual criteria). The research paper mentions the Women’s Health Initiative and these possible explanations, so the authors were definitely aware of them.

If you’re going to tell people about a potential way to prevent dementia, it would be helpful to at least mention that one form of it has been tried and didn’t work.

New breast cancer gene

The Herald has a pretty good story about a gene, PALB2, where there are mutations that cause a substantially raised risk of breast cancer.  It’s not as novel as the story implies (the first sentence of the abstract is “Germline loss-of-function mutations in PALB2 are known to confer a predisposition to breast cancer.”), but the quantified increase in risk is new and potentially a useful thing to know.

Genetic testing for BRCA mutations is funded in NZ for people with a sufficiently strong family history, but the policy is to test one of the affected relatives first. This new gene demonstrates why.

If you had a high-risk family history of breast cancer, and tested negative for BRCA1 and BRCA2 mutations, you might assume you had missed out on the bad gene. It’s possible, though, that your family’s risk was due to some other mutation — in PALB2, or in another undiscovered gene — and in that case the negative test didn’t actually tell you anything. By testing a family member  first, you can be sure you are looking in the right place for your risks, rather than just in the place that’s easiest to test.

July 11, 2014

Another prostate cancer study

Today’s prostate cancer risk factor, per the Herald, is vasectomy. The press release is here; the paper isn’t open-access.

This is a much more reliable study than the one earlier in the week about cycling, and there’s reasonable case that this one is worth a press release.

In 1986, the researchers recruited about 50000 men (health professionals: mostly dentists and vets), then followed them up to see how their health changed over time.  This research involves the 43000 who hadn’t had any sort of cancer at the start of the study. As the Herald says, about a quarter of the men had a vasectomy, and there have been 6000 prostate cancer diagnoses. So there’s a reasonable sample size, and there is a good chance you would have heard about this result if no difference had been found (though probably not via the Daily Mail)

The relative increase in risk is estimated as about 10% overall and about 20% for ‘high-grade’ tumours, which is much more plausible than the five-fold increase claimed for cycling.  The researchers had information about the number of prostate cancer tests the men had had, so they can say this isn’t explained by a difference in screening — the cycling study only had total number of doctor visits in the past year. Also, the 20% difference is seen in prostate cancer deaths, not just in diagnoses, though if you only consider deaths the evidence is borderline.  Despite all this, the researchers quite rightly don’t claim the result is conclusive.

There are two things the story doesn’t say. First, if you Google the name of the lead researcher and ‘prostate cancer’, one of the top hits is another paper on prostate cancer (and coffee, protective). That is, the Health Professionals Followup Study, like its sister cohort, the Nurses Health Study, is in the business of looking for correlations between a long list of interesting exposures and potential effects. Some of what it finds will be noise, even if it appears to pass sanity checks and statistical filters. They aren’t doing anything wrong, that’s just what life is like.

Second, there were 167 lethal prostate cancers in men with vasectomies. If the excess risk of 20% is really due to vasectomy, rather than something else, that would mean about 27 cancers caused by 12000 vasectomies. Combining lethal and advanced cases, the same approach gives an estimated 38 cases from 12000 vasectomies. So, if this is causation, the risk is 2 or 3 serious prostate cancers for every 1000 vasectomies. That’s not trivial, but I think it sounds smaller than “20% raised risk”.

July 9, 2014

Would I have heard if the results were different?

The story about cycling and prostate cancer in the Herald (or the Daily Mail) is a good opportunity to look at some of the rules of thumb for deciding which stories to read or believe:

Firstly, would you have heard if the results were the other way around? Almost certainly not: prostate cancer wasn’t the main point of this study, and there wasn’t a previously-suspected relationship.

Second, for cancer specifically, is this mortality or diagnosis data? That is, are we seeing an increase in detection or in cancer? This is diagnosis data; so it could be just an increase in detection. The researchers were confident it wasn’t, but we must remember the immortal words of Mandy Rice-Davies

Thirdly, what sort of study is it? Obviously it can’t be experimental, but a good study design would be to ask people about cycling (or even better, measure cycling) and then see whether it’s the bike fanatics who develop cancer. This study was a self-selected survey of cyclists, getting self-reported data about past cycling and past diagnosis of prostate cancer. It’s a fairly extreme sample, too: half of them cycle more than 5.75 hours per week.

Fourth, how strong is the evidence of association, and what sort of sample size are we looking at? The association is just barely statistically significant (p=0.046 in one model, p=0.025 in a second), and there are only 36 prostate cancer cases in the sample.  It’s pretty borderline.  The estimated relative risk is huge, because it has to be given the sample size, but the uncertainty range is also huge. The confidence interval on the relative risk of 5 reported by the Herald goes from 1.5 to 18.

Fifth, what does previous research say? This is in the story

‘To the best of our knowledge, this is the first study to demonstrate an association between prostate cancer and cycling, so there are no studies hypothesizing a pathophysiological mechanism for such a link.’

Sixth, what do other experts think? We don’t know. The closest thing to an independent comment is this in the press release

“Physicians should discuss the potential risks and health benefits of cycling with their patients, and how it may impact their overall health,” says Ajay Nehra, MD, Editor-in-Chief of Journal of Men’s Health and Chair, Department of Urology, Director, Men’s Health, Rush University Medical Center, Chicago, IL.

He could have said that without reading the paper.

In summary, there’s borderline evidence from a weak study design for a sensational finding that isn’t supported by any prior evidence. This is fine as research, but it shouldn’t be in the headlines.

You can read the research paper here for the next month, and the journal press release here.