Heuristic Reevaluation of the Bacterial Hypothesis of Peptic Ulcer Disease in the 1950s Dunja ˇ Seˇ selja Christian Straßer Abstract Throughout the first half of the twentieth century the research on pep- tic ulcer disease (PUD) focused on two rivaling hypothesis: the “acidity” and the “bacterial” one. The latter was dismissed during the 1950s only to be revived with Warren’s and Marshall’s discovery of Helicobacter pylori in the 1980s. In this paper we investigate why the bacterial hypothe- sis was abandoned in the 1950s, and whether there were good epistemic reasons for its dismissal. Of special interest for our research question is Palmer’s 1954 large-scale study, which challenged the bacterial hypothesis with serious counter-evidence, and which by many scholars is considered as the shifting point in the research on PUD. However, we show that: 1. The perceived refutatory impact of Palmer’s study was dispropor- tionate to its methodological rigor. This undermines its perceived status as a crucial experiment against the bacterial hypothesis. 2. In view of this and other considerations we argue that the bacterial hypothesis was worthy of pursuit in the 1950s. Keywords: PUD; peptic ulcer disease; bacterial hypothesis; crucial exper- iment; pursuit worthiness; heuristic appraisal 1 Introduction Many historical accounts of the research on peptic ulcer disease (in short, PUD) roughly distinguish three phases separated by two landmark studies. In the first phase (from the second half of the 19th century to 1954) two main hypotheses were investigated in parallel: on the one hand, the acidity hypothesis according to which the cause of PUD was gastric acid, and on the other hand, the bacterial hypothesis according to which the cause of PUD were bacteria. Neither hypothesis gained a decisive break-through in terms of theory confirmation, nor suffered from severe refutations. The situation changed in 1954 with the publication of a large-scale study by Palmer which challenged the bacterial hypothesis with serious refutatory counter-evidence. According to Kidd and Modlin (1998, p. 10), Palmer’s study “may be credited with the envious distinction of setting back gastric bacterial research by a further 30 years”. Similarly, Fukuda et al. (2002) suggest that Palmer’s study “established the dogma that bacteria could not live in the human stomach, and as a result, 1