From an ASM Forum bit by Casadevall and Fang:

An example of a rejected descriptive manuscript would be a survey of changes in gene expression or cytokine production under a given condition. These manuscripts usually fare poorly in the review process and are assigned low priority on the grounds that they are merely descriptive; some journals categorically reject such manuscripts (B. Bassler, S. Bell, A. Cowman, B. Goldman, D. Holden, V. Miller, T. Pugsley, and B. Simons, Mol. Microbiol. 52: 311–312, 2004). Although survey studies may have some value, their value is greatly enhanced when the data lead to a hypothesis-driven experiment. For example, consider a cytokine expression study in which an increase in a specific inflammatory mediator is inferred to be important because its expression changes during infection. Such an inference cannot be made on correlation alone, since correlation does not necessarily imply a causal relationship. The study might be labeled “descriptive” and assigned low priority. On the other hand, imagine the same study in which the investigators use the initial data to perform a specific experiment to establish that blocking the cytokine has a certain effect while increasing expression of the cytokine has the opposite effect. By manipulating the system, the investigators transform their study from merely descriptive to hypothesis driven. Hence, the problem is not that the study is descriptive per se but rather that there is a preference for studies that provide novel mechanistic insights.

But how do you choose to block the cytokine? Pharmacologically? With gene manipulations? Which cells are generating those cytokines and how do you know that? Huh? Are there other players that regulate the cytokine expression? Wait, have you done the structure of the cytokine interacting with its target?

The point is that there is always some other experiment that really, truly explains the “mechanism”. Always.

Suppose some species of laboratory animal (or humans!) are differentially affected by the infection and we happen to know something about differences in that “mediator” between species. Is this getting at “mechanism” or merely descriptive? How about if we modify the relevant infectious microbe? Are we testing other mechanisms of action…or just further describing the phenomenon?

This is why people who natter on with great confidence that they are the arbiters of what is “merely descriptive” and what is “mechanistic” are full of stuff and nonsense. And why they are the very idiots who compliment the Emperor on his fine new Nature publication clothes.

They need to be sent to remedial philosophy of science coursework.

The authors end with:

Descriptive observations play a vital role in scientific progress, particularly during the initial explorations made possible by technological breakthroughs. At its best, descriptive research can illuminate novel phenomena or give rise to novel hypotheses that can in turn be examined by hypothesis-driven research. However, descriptive research by itself is seldom conclusive. Thus, descriptive and hypothesis-driven research should be seen as complementary and iterative (D. B. Kell and S. G. Oliver, Bioessays 26:99–105, 2004). Observation, description, and the formulation and testing of novel hypotheses are all essential to scientific progress. The value of combining these elements is almost indescribable.

They almost get it. I completely agree with the “complementary and iterative” part as this is the very essence of the “on the shoulders of giants” part of scientific advance. However, what they are implying here is that the combining of elements has to be in the same paper, certainly for the journal Infection and Immunity. This is where they go badly wrong.


January 15, 2013

Of all superpowers to have, I’d pick “kill at a thought”. No question.