How citation distortions create unfounded authority: analysis of a citation network
Open Access
- 20 July 2009
- Vol. 339 (jul20 3), b2680
- https://doi.org/10.1136/bmj.b2680
Abstract
Objective To understand belief in a specific scientific claim by studying the pattern of citations among papers stating it. Design A complete citation network was constructed from all PubMed indexed English literature papers addressing the belief that β amyloid, a protein accumulated in the brain in Alzheimer’s disease, is produced by and injures skeletal muscle of patients with inclusion body myositis. Social network theory and graph theory were used to analyse this network. Main outcome measures Citation bias, amplification, and invention, and their effects on determining authority. Results The network contained 242 papers and 675 citations addressing the belief, with 220 553 citation paths supporting it. Unfounded authority was established by citation bias against papers that refuted or weakened the belief; amplification, the marked expansion of the belief system by papers presenting no data addressing it; and forms of invention such as the conversion of hypothesis into fact through citation alone. Extension of this network into text within grants funded by the National Institutes of Health and obtained through the Freedom of Information Act showed the same phenomena present and sometimes used to justify requests for funding. Conclusion Citation is both an impartial scholarly method and a powerful form of social communication. Through distortions in its social use that include bias, amplification, and invention, citation can be used to generate information cascades resulting in unfounded authority of claims. Construction and analysis of a claim specific citation network may clarify the nature of a published belief system and expose distorted methods of social citation.This publication has 104 references indexed in Scilit:
- Fourteen Newly Recognized Proteins at the Human Neuromuscular Junctions‐and Their Nonjunctional Accumulation in Inclusion‐Body MyositisaaAnnals of the New York Academy of Sciences, 1998
- IDIOPATHIC INFLAMMATORY MYOPATHIESNeurologic Clinics, 1997
- Apolipoprotein E alleles in sporadic inclusion‐body myositis and hereditary inclusion‐body myopathyAnnals of Neurology, 1996
- Amyloidosis causing a progressive myopathyMuscle & Nerve, 1995
- Current treatment of the inflammatory myopathiesCurrent Opinion in Rheumatology, 1994
- Expression of β-Amyloid Precursor Protein Gene Is Developmentally Regulated in Human Muscle Fibers in Vivo and in VitroExperimental Neurology, 1994
- Neurotrophic regulation of mouse muscle β‐amyloid protein precursor and α1‐antichymotrypsin as revealed by axotomyJournal of Neurobiology, 1994
- Clinical aspects of amyloidosis, including related proteins and central nervous system amyloidCurrent Opinion in Rheumatology, 1994
- Prion protein is abnormally accumulated in inclusion-body myositisNeuroReport, 1993
- Inclusion body myositis: an underdiagnosed condition?Annals Of The Rheumatic Diseases, 1993