The big liars
The divorce between the BMA and real science is now complete. The decline of modern medicine, as so cogently reported in James Le Fanus remarkable book, has brought it to an impasse in which it is reduced to admonitory quackery. The BMA has come out with a report on Smoking and reproductive life, designed to hit the headlines, which it did most successfully. It is a long document, available on the web, and is nothing less than a celebratory festival of junk science.
Here are just a few quotations from it. Remember the normal scientific standards for significance of relative risks and watch out for the weasel words (our emphasis).
A growing body of evidence suggests that smoking may cause male sexual impotence. Certain studies suggest that smokers are at least 50 per cent more likely to suffer from erectile dysfunction. It is estimated that in the UK, 120,000 men aged 3050 years are impotent because of smoking. The effect is seen in men of all ages. One study of almost 4,500 men aged 3149 years found that in smokers, the risk of impotence was 1.5 times that in non-smokers.
Key messages: Smoking and male sexual impotence
Smoking may cause male sexual impotence.
Smoking may amplify the effects of other causes of sexual impotence.
Stopping smoking appears to reduce the risk of impotence and can improve sexual potency.
There is limited evidence to suggest that passive smoking may increase the risk of impotence.
Key messages: Smoking and menstruation
There is limited evidence that women who smoke may be more likely to have painful periods or irregular periods.
There is limited evidence to suggest that smoking is associated with missed periods in women who have previously menstruated.
Stopping smoking appears to reduce any increased risk of menstrual problems.
The graph for the next bit shows that smokers on the pill have a relative risk of 90. Oh yeah? Could they possibly have dropped a percentage sign?
Key messages: Smoking and oral contraceptives
Smoking greatly increases the risk of heart disease among women who use the combined oral contraceptive pill. (See here)
Smoking may increase the risk of stroke among women who use the combined oral contraceptive pill.
There is evidence to suggest that smoking may increase the risk of failure of the combined oral contraceptive pill.
They did not, of course, miss out the old sperm count scam. It has been debunked frequently, but still comes up with monotonous regularity (Search Junkscience.com) The tenuous claim of a reduction in sperm counts has been ascribed by epidemiologists, among other things, to GM foods, endocrine disrupters, insecticides, dioxins, pollution, canned foods, dental sealants, certain types of food, finger length, benzene, toiletries, disposable diapers, tight jeans, low folic acid levels and of course:
Key messages: Smoking and fertility
Men who smoke have a lower sperm count and a higher proportion of malformed sperm.
Women who smoke take longer to conceive.
Women who smoke are twice as likely to be infertile as non-smokers.
Men and women who smoke have a poorer response to fertility treatment.
Women who have stopped smoking take no longer to become pregnant than women who have never smoked.
Stopping smoking improves sperm count and quality.
Key messages: Smoking during pregnancy
Women who smoke are at increased risk of ectopic pregnancy.
Women who smoke during pregnancy may be at increased risk of having a miscarriage.
Women who smoke are three times more likely to have a low birth-weight baby.
Women who smoke during pregnancy are more likely to suffer a stillbirth.
Babies born to women who smoke during pregnancy are more likely to die during the first four weeks of life.
A recent review of the evidence concluded that on average, infants born to women exposed to second-hand smoke during pregnancy are 4050g lighter than those born to women who are not exposed.
Note: that is about one percent. Such precision!
Pregnant women exposed to other peoples tobacco smoke are about 20 per cent more likely to have a low birth-weight baby.
There is some evidence to suggest that women who are exposed to second-hand smoke during their pregnancy are at increased risk of giving birth prematurely.
One study found that mothers exposed daily to second-hand smoke had a 23 per cent increased risk of giving birth prematurely.
There is limited evidence to suggest that parental smoking may be linked to an increased risk of childhood cancer. Smoking by the father has been associated with an increased risk of lymphoma and brain tumours, while maternal smoking has been linked to slightly increased risk for all childhood cancer (relative risk 1.11) and leukaemia (relative risk 1.14). While certain studies have reported that children exposed to second-hand smoke during childhood have an increased risk of cancer during adulthood, a recent evaluation judged the evidence to be inconclusive.
What they choose to ignore is that tobacco, like alcohol, is a great stress reliever. Stress is a known cause of disease in people and animals. So:
Smoking rates across the country both regional and local reflect socioeconomic trends. The greater the level of socioeconomic deprivation, the higher the rate of smoking. Within England, smoking rates are lowest in the South at around 24 per cent, but highest in London151 and the North, at around 29 per cent. In Scotland, smoking rates have been found to vary between postcode areas from 15 per cent to 71 per cent. Rates of smoking among the most disadvantaged are extremely high. A lone mother with a poor level of education, living in council accommodation and receiving income support has an 80 per cent risk of being a smoker.
But of all the trashy science in this tawdry document, it is the appendix that is truly
Appendix A: Assessment of causality
Assessment of the relationship between and exposure and a particular outcome is made on the balance of all the available evidence. Sir Austin Bradford-Hill proposed several considerations to be taken into account, which have been widely used and adapted. Some key considerations follow.
Strength of the association
Strong associations are more likely to be causal than weak ones. Weak associations are more likely to be explained by undetected biases. However, this does not rule out the possibility of a weak association being causal.
Consistency of the association
An association is more likely to be causal when a number of similar results emerge from different studies done in different populations. Lack of consistency, however, does not rule out a causal association.
For an exposure to cause an outcome, it must precede the effect.
Is there a biologically plausible mechanism by which the exposure could cause the outcome? The existence of a plausible mechanism may strengthen the evidence for causality; however, lack of such a mechanism may simply reflect limitations in the current state of knowledge.
The observation that an increasing dose of an exposure increases the risk of an outcome strengthens the evidence for causality. Again, however, absence of a dose-response, does not rule out a causal association.
Coherence implies that the association does not conflict with current knowledge about the outcome.
Experimental studies in which changing the level of an exposure is found to change the risk of an outcome provide strong evidence for causality. Such studies may not, however, always be possible, for practical or ethical reasons.
Any woman who takes any drug while pregnant is guilty of inflicting it on another innocent individual, unforgivable, but that does not justify this arrogant, mendacious, tract of unscientific rubbish. The emphasised words are all additions to the great man's rules that actually completely reverse their meaning. The defilement of Hill's precepts, mainly by use of the logical fallacy argumentum ad ignorantiam, is an unprecedented disgrace, which in a just world would result in the authors being drummed out of their profession.
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