Editor's Choice

The pleasures of deep reading

BMJ 2003; 327 doi: http://dx.doi.org/10.1136/bmj.327.7407.0-f (Published 17 July 2003) Cite this as: BMJ 2003;327:0-f
  1. Richard Smith, editor

    The competitors of the BMJ include Hollywood films, Manchester United, and a walk in the park. We live in the “attention economy” and compete desperately for a few moments of your time. There are so many other things to do apart from read the BMJ. Consequently many readers spend only a few minutes on the journal, flicking from Minerva to the news and checking the obituaries (as a very old joke has it) to see they are not there. But there is much insight—and even pleasure—to be had from reading articles slowly, savouring every thought, word, and nuance. This issue has at least two examples.

    John Iredale has spent over 13 years studying mechanisms of fibrosis in cirrhosis and shares his insights into how it may eventually be possible to treat the underlying fibrotic process and reverse the disease (p 143). Hepatic stellate cells seem to mediate the final common pathway of fibrosis. They are activated in liver injury and transform into cells that produce fibrillar collagen. Much research concentrates on what activates the cells and how activation might be blocked or turned off.

    But most patients who present with cirrhosis already have extensive fibrosis. Could the fibrosis be reversed? It seems that the collagen rich matrix produced during fibrosis is dynamic, and it may be possible to encourage degradation of the matrix by blocking the tissue inhibitors of metalloproteinases, which themselves block the degradation that would otherwise be occurring. If the matrix is degraded then normal (or near normal) liver architecture can return. Another way to reverse fibrosis might be to encourage the hepatic stellate cells to move into apoptosis, cell suicide.

    Edward Shorter and Peter Tyrer use very different methods—illustrating in passing why medicine is so interesting—to consider why it might be that new drugs for mood and anxiety disorders dried up in the 1990s (p 159). They think that the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) is part of the problem. Published in 1980, it created a “firewall” between anxiety and depression, making them “as different as chalk and cheese.” This is unhelpful, Shorter and Tyrer argue, because the commonest form of affective disorder is mixed anxiety-depression, and the subdivision of anxiety into separate microdiagnoses is questionable.

    The pharmaceutical industry has heavily influenced the classification of these disorders because “every new diagnosis represents a new licensing opportunity… Each new anxiety diagnosis seems to create an opportunity for a phoney new drug indication… paroxetine for social anxiety disorder, fluvoxamine for obsessive compulsive disorder, and sertraline for post-traumatic stress disorder.” Perhaps—as the BMJ argued for female sexual disorder (2003;326: 45)—the companies find it easier to create new diseases than new drugs. The authors advise that “companies must start developing drugs for mixed anxiety and depression and forget about dividing this giant illness segment into salami slices.”

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