Posts filed under Medical news (341)

Stuff.co.nz (from Reuters) has a reasonably good article about a new research report in the journal JAMA on marijuana, tobacco, and lung function.  It’s also worth pointing out that, as usual, there is more information on line that the newspapers don’t tell you about: the abstract, and a video interview (ie, press release) with the main author.

The research report is from the CARDIA study, which is following up 5000 young adults in four US cities, primarily to look at cardiovascular disease risks.   This paper uses data on tobacco smoking, marijuana smoking, and lung function, and finds a decrease in lung function in people who took up tobacco smoking, but not in most of those who smoked pot.  The study is particularly interesting because the participants were recruited before they started smoking.

The researchers found that lung function of marijuana smokers doesn’t start going down until the cumulative exposure gets up to around 10 joint-years (ie, 1 joint/day for ten years, two/day  for five years, and so on), which is a pretty high level, reached by only a few of the CARDIA participants.  This is contrasted with tobacco, where negative effects start showing up at exposure levels that are quite common.  In fact, and this is whats getting the press, the average lung function is very slightly higher in pot smokers than non-smokers, though not by enough that you would notice without sensitive machinery and thousands of measurements.

Most of this is just that doses of marijuana are much, much lower.  In fact, the negative associations at 10 joint-years cumulative exposure to marijuana are pretty similar to those at 10 pack-years cumulative exposure to tobacco.  That is, the data are consistent with a single joint doing as much short-term lung damage  as a whole pack of cigarettes, and certainly indicate that a joint does more damage than a single cigarette.

The mysterious part is the slightly higher lung function among moderate-level pot smokers. The authors give a number of speculations.  My speculation would be that asthmatics, and other with sensitive airways, are slightly less likely to take up smoking pot.  I think this would actually be testable in the CARDIA data.  In any case, this is careful analysis of pretty high-quality data, done by people with no particular axe to grind, which makes a nice change.

Hugo Chavez, the President of Venezuela, has publicly speculated that some secret US weapon might be responsible for several Latin American heads of government getting cancer recently, which he said was “difficult to explain using the law of probabilities.” This is a perfect example of a phenomenon that is all too familiar to public-health workers: the cancer cluster. According to the American Cancer Society, more than 1000 cancer clusters are reported to state public-health departments in the US each year. How many of them turn out to be real? Approximately none.

There are two statistical phenomena here. Firstly, although individual cancer subtypes may be rare, cancer as whole is more common than most people realize. Secondly, we are very good at seeing patterns, even patterns that aren’t there.

The picture, from David Spiegelhalter, shows four 9×9 squares. Three are coloured entirely at random; one has a pattern. Before going on, decide which one you think is non-random.

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The NZ Herald online has had two stories in two days on a survey by Southern Cross Health Society.  The survey reported cancer as the number one health fear of Kiwis.  That would be the minority of Kiwis with private health insurance. Or, though the actual survey population isn’t stated anywhere, probably the smaller minority of Kiwis who are members of Southern Cross.

I don’t know whether the cancer fear finding generalises to the whole population, and neither do they, but I’m certain the screening results they report do not.  They say more than 80% of men aged 55-64, and 93% of men over 65 had a prostate cancer screening test within the past year.  Figures based on a national survey published in 2010 by the University of Otago, show that about 44% of men 60+ and 17% of men 40-60 had a PSA test in the the previous year (which includes diagnostic and post-treatment as well as screening tests).  Only 64% of men over 60 had ever had a PSA test of any sort and only 32% had ever had a screening PSA test as part of primary care.   It’s hardly surprising that people with private health insurance get more screening, though it’s still not completely clear to anyone except perhaps Paul Holmes whether the extra PSA screening is doing them any good.

The statistical message is simple: surveys only measure what they measure, not what you would like them to have measured. Get over it.

From Sonia Pollak’s winning Stat of the Week

Now, if we look at the number of people who lodged a claim on Christmas day: this was 3040.
In the 07/08 financial year there was 1.8 million claims, an average of around 5000 a day.

Telling people to look out over the Christmas period and take care is good, but from this, it would appear that actually, Christmas day has less, if not accidents, claims than the average day.

Another famous example in journalism is by Eric Meyer, (via Robert Niles)

My personal favorite was a habit we use to have years ago, when I was working in Milwaukee. Whenever it snowed heavily, we’d call the sheriff’s office, which was responsible for patrolling the freeways, and ask how many fender-benders had been reported that day. Inevitably, we’d have a lede that said something like, “A fierce winter storm dumped 8 inches of snow on Milwaukee, snarled rush-hour traffic and caused 28 fender-benders on county freeways” — until one day I dared to ask the sheriff’s department how many fender-benders were reported on clear, sunny days. The answer — 48 — made me wonder whether in the future we’d run stories saying, “A fierce winter snowstorm prevented 20 fender-benders on county freeways today.” There may or may not have been more accidents per mile traveled in the snow, but clearly there were fewer accidents when it snowed than when it did not. (more…)

The Early Breast Cancer Trialists Collaborative Group has published a combined analysis of over 400 trials of breast cancer treatments, in 400,000 women.  They were trying to ‘personalise’ treatment

Moderate differences in efficacy between adjuvant chemotherapy regimens for breast cancer are plausible, and could affect treatment choices. We sought any such differences.

And what did they find?

 In all meta-analyses involving taxane-based or anthracycline-based regimens, proportional risk reductions were little affected by age, nodal status, tumour diameter or differentiation (moderate or poor; few were well differentiated), oestrogen receptor status, or tamoxifen use.

That is, based on all the characteristics they had available, there really wasn’t any way to predict which treatment would work best for which subset of the women.

Now, we know that some more-recent treatments do only work on a subset of tumours. In breast cancer there is Herceptin, which targets one particular tumour growth mechanism and only works on tumours that grow that way, and there are similar specific inhibitors for some other cancer subtypes.  It’s still striking how difficult it is to detect  any useful variation between people in treatment effectiveness, a finding that’s also be true in other areas of medicine.  So-called ‘personalized medicine’ may one day be possible, but it’s a long way off and current technologies don’t give us any way to get there.

The Age (yes, I’m just back from the West Island) has an article on the annual cancer statistics report from the Victorian Cancer Council.  Survival from diagnosis is up for many cancers, and that’s the headline, but in only some of these diseases is there a reduction in the death rate.

The problem is that survival from diagnosis measures the interval between two time points: diagnosis, and death.  You can increase your survival time by dying later, which is a Good Thing, or by being diagnosed earlier and dying at the same time, which many people would consider bad.

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Today (or, given time zones, yesterday) the best-selling drug of all time goes off patent in the USA.

Atorvastatin (Lipitor) became such a gigantic commercial success for two main reasons: it actually works slightly better than the earlier cholesterol-lowering drugs, and Pfizer funded several large clinical trials proving that it worked better.  Despite the (often justified) cynicism about drug marketing and approval, the regulatory process does mean that effective treatments are more profitable than ineffective ones — in sharp contrast to supplements and herbals, where effective treatments don’t have any real marketing advantage.

The patent expired earlier in New Zealand: in June 2010, Pharmac found a generic supplier and reduced the price for a month’s supply from $18 (for the lowest dose) to $1.77.   In the US, Lipitor costs more than US$3 per pill, so there’s even more room for price decreases.

Q: Did you see the BBC news article about dietary fibre and bowel cancer?

A: No, but I’ll go look. [reading noises]

Q: Well?

A: They definitely  get points for linking to the article in the British Medical Journal (and it’s even an open access article that anyone can read).

Q: Haven’t we beaten that issue into the ground yet?

A: Apparently not. (more…)

As you may remember, there was a flurry of headlines recently in the Kiwi media about the new anti-clotting drug dabigatran(Pradaxa) — it’s not often than Pharmac is accused of pushing too hard for an expensive new substitute instead of  an old, cheap drug.  Now, in Australia, the reverse is happening: the Goverment has refused to list dabigatran for subsidy (going against its own experts), and the media is reporting this decision as a danger to Australian patients (with help from the manufacturer’s lobbyists).

Warfarin (yes, rat poison) is a very safe and effective anti-clotting drug if it’s given at exactly the right dose. Unfortunately, the right dose varies between people, and changes depending on almost anything else (food, medications, herbals, alcohol) you might consume.  Keeping the dose right requires frequent blood tests, which are inconvenient and expensive, and even then the dosing is often imperfect unless you and your physician are truly obsessive.  But there hasn’t been anything else that came close to the safety and efficacy of warfarin.

Now there is a rush of new medications coming out that selectively disrupt a very late stage in clot formation: as well as dabigatran there are apixaban, rivaroxaban, and betrixaban.  These don’t have the variable dosage of warfarin, so it should be possible to just prescribe them and stop worrying: a big improvement in convenience and saving in cost.  On the other hand, these drugs are new (and so less well understood), and unlike warfarin there is no antidote and no convenient lab test for overdose.  And they are quite  expensive, even with Pharmac’s well-known haggling powers.

In this case I think the evil multinational drug company is right and the Australian Health Minister is wrong: these new drugs really are safer and more effective — they were better than warfarin in a large randomized trial, where warfarin dosing is likely to be better than in free-range patients — and the reduced need for blood tests will pay for quite a bit of the increased cost.  Still, it’s hard to avoid the suspicion that the main urgency in this debate is to get dabigatran into widespread use before its competitors make it on to the market…

What’s the best strategy if you want to have a perfect record betting on the rugby?  Just bet once: that gives you a 50:50 chance.

After national statistics on colorectal cancer were released in Britain, the charity Beating Bowel Cancer pointed out that there was a three-fold variation across local government areas in the death rate.  They claimed that over 5,000 lives per year could be saved, presumably by adopting whatever practices were responsible for the lowest rates. Unfortunately, as UK blogger ‘plumbum’ noticed, the only distinctive factor about the lowest rates is shared by most of the highest rates: a small population, leading to large random variation.

 His article was picked up by a number of other blogs interested in medicine and statistics, and Cambridge University professor David Speigelhalter suggested a funnel plot as a way of displaying the information.

A funnel plot has rates on the vertical axis and population size (or some other measure of information) on the horizontal axis, with the ‘funnel’ lines showing what level of variation would be expected just by chance.

The funnel plot (click to embiggen) makes clear what the tables and press releases do not: almost all districts fall inside the funnel, and vary only as much as would be expected by chance. There is just one clear exception: Glasgow City has a substantially higher rate, not explainable by chance.

Distinguishing random variation from real differences is critical if you want to understand cancer and alleviate the suffering it causes to victims and their families.  Looking at the districts with the lowest death rates isn’t going to help, because there is nothing very special about them, but understanding what is different about Glasgow could be valuable both to the Glaswegians and to everyone else in Britain and even in the rest of the world.