The first article attacked "the scientific method," concluding that what science proves might not be true after all and that experimentation is insufficient for settling beliefs about the world. The essay was widely discussed and criticized: see here, here, here, and here. I won't try to summarize the criticisms here, but they are worth reading.
The more recent essay narrows the focus to causal inferences. Basically, Lehrer argues that causes cannot be discovered using one-at-a-time inference techniques that treat the world as a mechanism reducible to its various parts. As an example of this, Lehrer uses the case of torcetrapib, a drug designed to improve cardiovascular health by increasing HDL cholesterol while decreasing LDL cholesterol. Lehrer points out that despite knowing a lot of things about how the cholesterol mechanism works, in human trials, torcetrapib turned out to cause heart attacks -- basically the opposite of what the manufacturers intended the drug to do. While torcetrapib did what it was supposed to do with respect to cholesterol, it also increased blood pressure. The total effect was to increase heart attack risk. And so, torcetrapib was not approved by the FDA.
The case is interesting, but the conclusion Lehrer draws is almost completely wrong. He writes:
The story of torcetrapib is a tale of mistaken causation. Pfizer was operating on the assumption that raising levels of HDL cholesterol and lowering LDL would lead to a predicatable outcome: Improved cardiovascular health. Less arterial plaque. Cleaner pipes. But that didn't happen.The only mistaken causation occurred before the human-subject trials. At that point, the researchers conjectured (reasonably) that the drug would reduce the risk of heart attack. They didn't realize that the drug increased blood pressure. But when they actually conducted the human experiment, they learned some causal facts: torcetrapib does not decrease the risk of heart attack, torcetrapib increases blood pressure, the effect of blood pressure on heart-attack risk is greater than the effect of cholesterol, etc.
At best what Lehrer is illustrating is the law of unintended consequences. After all, the researchers didn't want or expect any of their subjects to die as a result of taking the drug.
But maybe Lehrer's mischaracterization of the result is not especially surprising. He doesn't do a very good job even with basic statistical tools, like p-values.
Researchers have developed an impressive system for testing these correlations. For the most part, they rely on an abstract measure known as statistical significance, invented by English mathematician Ronald Fisher in the 1920s. This test defines a “significant” result as any data point that would be produced by chance less than 5 percent of the time.And he doesn't even try to describe any more complicated statistical techniques for causal inference: no mention of Bayes' theorem, no causal Bayes nets, no causal Markov axiom, no potential outcomes, and no structural equation models. He doesn't even try to describe the logic behind causal inference by experimentation -- how or why isolation and intervention let us make causal inferences.
The fact that Lehrer says nothing about developments in causal inference is really unfortunate, since Lehrer defended his first essay in part by arguing that we should ask whether science can work better than it currently does. I think such a question is admirable, but then, why didn't Lehrer bother to look around and see whether anyone is busy developing a better way of thinking about causal inference? Opportunity wasted.
