This is an important article with well chosen examples. But I think the headline points to the wrong "cause" of failure. Scientists, the directors of science research funding projects, and the general public can better understand what we know and what we don't know about causation from correlation if science teachers and journalists do a better job. For a long time, members of the journalistic community and members of the general public have been overinterpreting tentative scientific findings,<p><a href="http://norvig.com/experiment-design.html" rel="nofollow">http://norvig.com/experiment-design.html</a><p>and if we learn the lessons of how to interpret research findings more cautiously, we can all do our part to guide further research better.<p>As the author of the submitted article points out, "This doesn't mean that nothing can be known or that every causal story is equally problematic. Some explanations clearly work better than others, which is why, thanks largely to improvements in public health, the average lifespan in the developed world continues to increase. (According to the Centers for Disease Control and Prevention, things like clean water and improved sanitation—and not necessarily advances in medical technology—accounted for at least 25 of the more than 30 years added to the lifespan of Americans during the 20th century.) Although our reliance on statistical correlations has strict constraints—which limit modern research—those correlations have still managed to identify many essential risk factors, such as smoking and bad diets."<p>So with caution about assuming causation where the data cannot reliably show causation,<p><a href="http://escholarship.org/uc/item/6hb3k0nz" rel="nofollow">http://escholarship.org/uc/item/6hb3k0nz</a><p>the huge task of biomedical research can still go forward, eventually yielding other findings that can improve health or longevity compared to today's baseline.<p>AFTER EDIT: The question posed in the first reply below is interesting. One reason that biomarker interventions are tried more often than "hard endpoint" interventions is simply that they are faster and easier. To really check carefully for hard endpoints--reduced mortality and morbidity, for a medical treatment--takes time in a clinical trial. Sometimes an effective on a biomarker, for example serum cholesterol, can be observed right away, but if the subjects in a study are at an age at which few subjects die from any cause, it can be a long while before a study reveals which treatments actually increase rather than decrease the risk of death.<p>The case of the drug rimonabant,<p><a href="http://en.wikipedia.org/wiki/Rimonabant" rel="nofollow">http://en.wikipedia.org/wiki/Rimonabant</a><p>which had reasonably strong support from animal experiments as an antiobesity drug, is instructive. Studies of human subjects after the drug was approved in Europe revealed a huge increase in suicidal risk among patients taking rimonabant,<p><a href="http://www.pharmacist.com/AM/Template.cfm?Section=Pharmacy_News&template=/CM/ContentDisplay.cfm&ContentID=24206" rel="nofollow">http://www.pharmacist.com/AM/Template.cfm?Section=Pharmacy_N...</a><p>and eventually approval of the drug in Europe was withdrawn, and the drug was withdrawn from the market by its manufacturer, before rimonabant was ever approved in the United States.