The Appendix

Darwin, Charles.  The Descent of Man, and Selection in Relation to Sex.  Volume 1.  John Murray, London.  1871.  Darwin's 1871 book on human descent and sexual selection, in its first volume.  The article quotes it for Darwin's own case that the appendix is a shrunken rudiment, a case he built from comparative anatomy.

1. 1a.

   Pages 27–28:  “Not only is it useless, but it is sometimes the cause of death, of which fact I have lately heard two instances: this is due to small hard bodies, such as seeds, entering the passage and causing inflammation.” ↩ ↩

2. 1b.

   Page 27:  “It appears as if, in consequence of changed diet or habits, the cæcum had become much shortened in various animals, the vermiform appendage being left as a rudiment of the shortened part.” ↩ ↩

3. 1c.

   Page 27:  “With respect to the alimentary canal I have met with an account of only a single rudiment, namely the vermiform appendage of the cæcum.” ↩

4. 1d.

   Page 27:  Darwin is describing the caecum, and the spelling "kaola" is his.  “is extremely long in many of the lower vegetable-feeding mammals. In the marsupial kaola it is actually more than thrice as long as the whole body.” ↩

5. 1e.

   Page 27:  “That this appendage is a rudiment, we may infer from its small size, and from the evidence which Prof. Canestrini has collected of its variability in man. It is occasionally quite absent, or again is largely developed.” ↩

Smith, Heather F. et al.  “Morphological evolution of the mammalian cecum and cecal appendix.”  Comptes Rendus Palevol 16(1):39–57.  2017.  A comparative study of the cecal appendix, a narrow blind pouch at the end of the cecum, across 533 mammal species, using statistics that take evolutionary family trees into account.  It found that the appendix appeared at least 29 times and possibly 41 times, was lost at most 12 times, and that its presence goes with more lymphoid tissue in the cecum.  The article uses it for the repeated appearance of the appendix and for the authors' rejection of the vestigial idea.

1. 2a.

   Page 55:  “the cecal appendix has evolved a minimum of 29 times, possibly as many as 41 times, throughout mammalian evolution, while it has only been lost a maximum of 12 times. This statistically strong evidence that the appearance of the appendix is significantly more probable than its loss suggests a selective value for this structure. Thus, we can confidently reject the hypothesis that the appendix is a vestigial structure with little adaptive value or function among mammals.” ↩ ↩ ↩

2. 2b.

   Page 39, section Abstract:  “A correlation between appendix presence and concentration of cecal lymphoid tissue supports the hypothesis of an adaptive immune function for this complex.” ↩

3. 2c.

   Page 55:  “This raises the question of whether the cecum evolved as an expansion of the appendix, or vice versa, and provides additional support for considering the two structures together, as the cecoappendicular complex.” ↩

Gray's Anatomy.  Churchill Livingstone, Edinburgh.  36th edition.  Edited by Peter L. Williams and Roger Warwick.  1980.  An anatomy textbook, its 36th edition, edited by Peter L. Williams and Roger Warwick.  The article uses it to show that the textbook view of the appendix had changed by 1980, when it called the organ specialized rather than vestigial.

1. 3a.

   Page 1353:  “In view of its rich blood supply and histological differentiation, the vermiform appendix is probably more correctly regarded as a specialized than as a degenerate, vestigial structure. The configuration of the caecum and appendix in man and the anthropoid apes is probably less primitive than in the monkeys.” ↩ ↩ ↩

2. 3b.

   Page 1353:  “The lumen of the appendix may be partially or completely obliterated after mid-adult life.” ↩

Gorgollón, P.  “The normal human appendix: a light and electron microscopic study.”  Journal of Anatomy 126(1):87–101.  1978.  A 1978 study of the appendix under light and electron microscopes, using appendices removed in operations from children aged 3 to 12.  Most of those appendices were diseased in places, so the author examined only the normal areas and found three zones of lymphoid tissue (immune tissue packed with lymphocytes, a kind of white blood cell).  The author limits the finding to children, and the article uses it as the basis for its claim that this lymphoid tissue is a real feature of the organ, not a detail.

1. 4a.

   Page 100:  “The general conclusion is that the human appendix, at least in children, has the characteristics of a well-developed lymphoid organ, suggesting that it has important immunological functions.” ↩ ↩ ↩

Bollinger, R. Randal et al.  “Biofilms in the large bowel suggest an apparent function of the human vermiform appendix.”  Journal of Theoretical Biology 249(4):826–831.  2007.  A 2007 proposal, not a trial, by surgeons and immunologists at Duke University Medical Center.  They examined one deceased organ donor's colon under a microscope and found that biofilms, clusters of microbes stuck to a surface, were most prominent in the appendix; they say proof of its function may be hard to get.  The article uses it as the modern case that the appendix is a safe house for gut bacteria, and it notes that the case rests on that one donor.

1. 5a.

   Page 826:  “we propose that the human appendix is well suited as a ''safe house'' for commensal bacteria, providing support for bacterial growth and potentially facilitating re-inoculation of the colon in the event that the contents of the intestinal tract are purged following exposure to a pathogen.” ↩ ↩

2. 5b.

   Page 826:  “a 5–10 cm long and 0.5–1 cm wide pouch that extends from the cecum of the large bowel.” ↩

3. 5c.

   Page 826:  “Appendix-like structures are relatively rare in phylogeny, being found in humans, rabbits, and two species of marsupials (opossums and wombats), but not in other marsupials or in a vast host of other animal species.” ↩

4. 5d.

   Page 829:  “we examined samples taken from a fresh, normal, intact, unprepped (containing fecal material) human colon of a deceased organ donor. Blinded evaluation of the samples revealed that biofilms were most prominent in the appendix, both in terms of bacterial density and biofilm continuity along the epithelial surface (Fig. 1).” ↩ ↩

5. 5e.

   Page 829:  “Regular shedding and regeneration of biofilms within the appendix would be expected to re-inoculate the large bowel with commensal organisms in the event that the large bowel became infected by a pathogen and was flushed out as a defensive response to that infection (Fig. 2).” ↩

6. 5f.

   Page 830:  “absolute proof of such a function may be difficult to obtain since the unique nature of the human appendix may preclude the use of animals to study the issue.” ↩

7. 5g.

   Page 830:  “Certainly, this idea is consistent with the well-known observation that appendectomy is without currently discernable long-term side effects in societies with modern medical and sanitation practices.” ↩ ↩ ↩

8. 5h.

   Page 830:  “In as much as 6% of the population in industrialized countries, the appendix becomes inflamed and must be surgically removed to avoid a potentially life-threatening infection.” ↩

9. 5i.

   Page 830:  “The typical diet in countries with widespread appendicitis is substantially different than in non-industrialized countries where appendicitis is rare, and thus diet may account at least in part for the incidence of appendicitis.” ↩

Naga, Yassin S. E. et al.  “A Systematic Review and Meta-Analysis: A Prior Appendectomy Does Not Increase the Risk of Severe Clostridioides difficile Infection or Recurrence.”  Digestive Diseases and Sciences 68(9):3714–3720.  2023.  A systematic review and meta-analysis, which searched several databases up to May 2022 and pooled eight earlier studies to compare patients with and without a prior appendectomy.  The pooled results found no significant difference in severe infection or in recurrence, but higher odds of colectomy caused by C. difficile infection (odds ratio 2.16) after appendectomy.  The article uses it as the pooled answer to the question, and it shows that the recurrence effect seen in single studies does not survive pooling.

1. 6a.

   Section Abstract:  “Eight studies with 666 patients with a prior appendectomy and 3580 patients without an appendectomy were included.” ↩

2. 6b.

   Section Abstract:  “The odds ratio of recurrence in patients who underwent prior appendectomy was 1.29 (95% CI 0.82-2.02, p = 0.28). The odds ratio of colectomy due to Clostridioides difficile infection in patients who underwent prior appendectomy was 2.16 (95% CI 1.27-3.67, p = 0.004).” ↩ ↩ ↩

3. 6c.

   Section Abstract:  “Patients with appendectomy are not at increased risk for developing severe Clostridioides difficile infection or recurrence.” ↩

Frisch, Morten et al.  “Appendicitis, mesenteric lymphadenitis, and subsequent risk of ulcerative colitis: cohort studies in Sweden and Denmark.”  BMJ 338:b716.  2009.  Two national cohort studies, Swedish and Danish, that followed people after appendix removal for 11.1 million person-years and compared their rate of ulcerative colitis with the population rate, split by the reason for surgery.  Removal of an uninflamed appendix made no difference;  removal for appendicitis or swollen lymph nodes before age 20 went with about half the expected rate.  It separates the effect of the inflammation from the effect of losing the organ.  Mirror:  PMC

1. 7a.

   Section Abstract, Results:  “Appendicectomy without underlying inflammation was not associated with reduced risk (standardised incidence ratio 1.04, 95% confidence interval 0.95 to 1.15). Before the age of 20, however, appendicectomy for appendicitis (0.45, 0.39 to 0.53) or mesenteric lymphadenitis (0.65, 0.46 to 0.90) was associated with significant risk reduction.” ↩ ↩ ↩

2. 7b.

   Section Abstract, Conclusions:  “Appendicectomy itself does not protect against ulcerative colitis.” ↩

ACCURE Study Group.  “Appendicectomy plus standard medical therapy versus standard medical therapy alone for maintenance of remission in ulcerative colitis (ACCURE): a pragmatic, open-label, international, randomised trial.”  The Lancet Gastroenterology & Hepatology 10(6):550–561.  2025.  A randomised trial in 22 hospitals in the Netherlands, Ireland and the United Kingdom.  Adults whose ulcerative colitis was in remission after a relapse in the past year were assigned by computer to appendix removal plus their usual medicine or to usual medicine alone, and 197 were analysed.  Relapse within a year fell from 56 to 36 percent with removal.  Patients and doctors knew the assignment, and the trial did not study the mechanism.  Mirror:  PMC

1. 8a.

   Section Summary, Findings:  “The 1-year relapse rate was significantly lower in the appendicectomy group than in the control group (36 [36%] of 99 patients vs 55 [56%] of 98 patients; relative risk 0·65 [95% CI 0·47–0·89]; p=0·005; adjusted p=0·002).” ↩ ↩ ↩

2. 8b.

   Section Discussion:  “this trial primarily focused on clinical outcomes, and did not evaluate the appendix's immunomodulatory mechanism, so no further causal conclusions can be drawn.” ↩

Chin, Hok Leong et al.  “Appendectomy and risk of Parkinson's disease: a systematic review and meta-analysis.”  Frontiers in Neurology 16:1619236.  2025.  A meta-analysis that searched PubMed and Embase to September 2024 and pooled nine studies, seven of them cohorts, from Canada, Denmark, Sweden, the United States, Korea and the United Kingdom.  The pooled relative risk of Parkinson's disease after appendix removal was 1.01, with the single studies disagreeing strongly in both directions.  It supersedes the two-study picture that the Swedish and Ontario registries gave.

1. 9a.

   Page 2, section 3.2:  “Pooled results from the 9 included studies demonstrated no statistically significant association between appendectomy and risk of PD (Pooled RR: 1.01, 95%CI: 0.90–1.12, p = 0.89) (Figure 2). Significant heterogeneity was observed (I2 = 88%, p < 0.01).” ↩ ↩

2. 9b.

   Page 4, table 2:  “HR 1.14 (1.03–1.27)”.  Svensson and colleagues, Danish National Patient Registry.  Page 5, table 2:  “HR 1.120 (1.016–1.234)”.  Wang and colleagues, UK Biobank. ↩

Smith, Heather F. et al.  “Multiple independent appearances of the cecal appendix in mammalian evolution and an investigation of related ecological and anatomical factors.”  Comptes Rendus Palevol 12(6):339–354.  2013.  A study of 361 mammal species, in which the appendix was mapped onto a family tree of mammals alongside diet, fermentation and social traits.  It found no correlation between the appendix and changes in those traits, and it reports that the appendix evolved at least 32 times and was lost fewer than seven times, which the authors read as a sign that it is adaptive.  The article uses it as the main test of Darwin's account of the appendix.

1. 10a.

   Page 339:  “The appendix has evolved minimally 32 times, but was lost fewer than seven times, indicating that it either has a positive fitness value or is closely associated with another character that does.” ↩

2. 10b.

   Page 340:  “Darwin posited that in extant hominoids (great apes), who are for the most part frugivorous, the shift from a predominantly folivorous ancestor to a descendent with diet requiring less fermentation led to a reduction in cecal size, which was in turn associated with the appearance of the appendix.” ↩

3. 10c.

   Page 343:  “Of the 361 mammalian species sampled here, 50 were found to possess a cecal appendix.” ↩

4. 10d.

   Pages 343–344:  “Thus, among mammals, only Trichechus manatus and some catarrhine primates (especially hominoids) exhibit the predicted combination of an appendix accompanying a small cecum.” ↩ ↩

5. 10e.

   Page 351:  “Character optimization of cecum size and appendix presence refutes Darwin's hypothesis for evolution of the hominoid appendix (Darwin, 1871) as an explanation for the evolution of the appendix across all mammalian clades.” ↩

6. 10f.

   Page 351:  “his interpretation of the appendix as being associated with a reduction in cecal size is ultimately correct for this clade; however, this association does not necessarily reflect a causal link.” ↩ ↩

7. 10g.

   Page 351:  “had Darwin had access to more data regarding the occurrence of the cecal appendix in mammals, he would not have considered the evolutionary scenario for the appendix described in his seminal work.” ↩ ↩

8. 10h.

   Page 352:  “the presence or absence of an appendix may have more to do with intrinsic propensity to evolve an appendix than any other factor, including diet or social status.” ↩ ↩

Addiss, David G. et al.  “The epidemiology of appendicitis and appendectomy in the United States.”  American Journal of Epidemiology 132(5):910–925.  1990.  A study of appendicitis and appendectomy in the United States, using National Hospital Discharge Survey data for 1979 to 1984.  It estimated about 250,000 cases a year and gave a life-table estimate of the lifetime risk of appendicitis and of appendectomy.  The article uses it for the yearly case count, the lifetime risks, and the estimate of incidental removals.

1. 11a.

   Section Abstract:  “Approximately 250,000 cases of appendicitis occurred annually in the United States during this period, accounting for an estimated 1 million hospital days per year.” ↩

2. 11b.

   Section Abstract:  “A life table model suggests that the lifetime risk of appendicitis is 8.6% for males and 6.7% for females; the lifetime risk of appendectomy is 12.0% for males and 23.1% for females.” ↩ ↩

3. 11c.

   Section Abstract:  “an estimated 36 incidental procedures are performed to prevent one case of appendicitis.” ↩

Blomqvist, Paul G. et al.  “Mortality after appendectomy in Sweden, 1987–1996.”  Annals of Surgery 233(4):455–460.  2001.  A register study of all 117,424 appendectomies performed in Sweden from 1987 to 1996, counting deaths within 30 days of the operation.  It found 2.44 deaths per 1,000 operations, about seven times the death rate expected in the general population, and the highest rate in older patients.  The article uses it for how often the operation itself proved fatal.

1. 12a.

   Page 455:  “The CFR was 2.44 per 1,000 appendectomies.” ↩ ↩

2. 12b.

   Page 455:  “0.8 per 1,000 appendectomies after nonperforated appendicitis, 5.1 after perforated appendicitis.” ↩

Walker, A. R. P., and I. Segal.  “What causes appendicitis?”  Journal of Clinical Gastroenterology 12(2):127–129.  1990.  A paper that weighs the two main explanations for appendicitis, low fibre intake and improved hygiene, and concludes that the causes are still uncertain.  It records that the disease rose for a century, peaked about 1950, and has since fallen to about half its previous incidence.  The article uses it for the history of the disease's rise and fall.

1. 13a.

   Section Abstract:  “Appendicitis was rare in the past and still is in traditional Third World populations. It began to increase a century ago, peaked about 1950, and has now fallen to about half its previous incidence.” ↩ ↩

Gray, Henry.  Anatomy of the Human Body.  Lea & Febiger, Philadelphia.  20th edition.  Edited by Warren H. Lewis.  1918.  A textbook of human anatomy, first published in English in 1858, here in a 1918 revision by Warren H. Lewis, professor of physiological anatomy at Johns Hopkins University.  The article uses it for the textbook description of the appendix's shape, size and wall.

1. 14a.

   Page 1178:  “The Vermiform Process or Appendix (processus vermiformis) (Fig. 1073) is a long, narrow, worm-shaped tube, which starts from what was originally the apex of the cecum, and may pass in one of several directions: upward behind the cecum; to the left behind the ileum and mesentery; or downward into the lesser pelvis. It varies from 2 to 20 cm. in length, its average being about 8.3 cm.” ↩

2. 14b.

   Page 1179:  “The submucous coat is well marked, and contains a large number of masses of lymphoid tissue which cause the mucous membrane to bulge into the lumen and so render the latter of small size and irregular shape.” ↩

Wiedersheim, Robert.  The Structure of Man: An Index to His Past History.  Macmillan, London.  Translated by H. Bernard and M. Bernard.  1895.  A German professor's comparison of human anatomy with that of lower animals, in this 1895 English translation.  Its preface says the book supplements the works of Darwin and Huxley and sets out the human features that link man with lower forms.  The article uses it for the appendix counts Wiedersheim reported and for his list of vestigial organs.

1. 15a.

   Page 169:  “out of 100 vermiform processes 32 were found partially or wholly closed.” ↩

2. 15b.

   Page 170:  “It follows from the foregoing table that in more than 50 per cent of people over sixty years of age there is degeneration of the vermiform process.” ↩

3. 15c.

   Section Conspectus, section B, page 200:  “Retrogressively modified, the Organs having become wholly or in part functionless, some appearing in the Embryo alone, others present during Life constantly or inconstantly. For the greater part Organs which may be rightly termed Vestigial.”  Page 202:  “The appendix vermiformis.” ↩

4. 15d.

   Page 169:  This quotation is from a footnote on the same page.  “I cannot again in this connection refrain from referring to the coincidence of the existence of vestigial organs and the tendency to disease caused by them.” ↩

Scott, G. B. D.  “The primate caecum and appendix vermiformis: a comparative study.”  Journal of Anatomy 131(3):549–563.  1980.  A 1980 comparison of the caecum and appendix across the primates, using animals autopsied after death and a review of the literature.  The author examined the caeca of 39 cynomolgus monkeys, 31 rhesus monkeys, two orang-utans and a chimpanzee, and concludes that the appendix develops progressively in the higher primates, reaching its fullest form in the gorilla and man.  The article uses it against the view that the appendix is a purely degenerating organ.

1. 16a.

   Page 563:  “Although absent in prosimians and New World monkeys, there was evidence that the appendix vermiformis began to develop in certain Old World monkeys and became fully developed in the anthropoid apes, showing that, far from being a vestigial organ, it has actually developed progressively in primates.” ↩ ↩

2. 16b.

   Page 562:  “although the function of the appendix is still obscure, it should not be regarded, in the anthropoid apes and man, as a purely degenerative structure.” ↩

Coyne, Jerry A.  Why Evolution Is True.  Viking, New York.  2009.  A popular book from 2009 by Jerry A. Coyne.  The article uses it to show that Darwin's claim survived in popular books after the anatomy texts had dropped it, and it quotes the author's concession that the appendix may have some small use.

1. 17a.

   Page 61:  “In humans, who don't eat leaves and can't digest cellulose, the appendix is nearly gone.” ↩

2. 17b.

   Page 61:  “But to be fair, it may be of some small use. The appendix contains patches of tissue that may function as part of the immune system. It has also been suggested that it provides a refuge for useful gut bacteria when an infection removes them from the rest of our digestive system.” ↩

3. 17c.

   Page 62:  “When you weigh the tiny advantages of an appendix against its huge disadvantages, it's clear that on the whole it is simply a bad thing to have. But apart from whether it's good or bad, the appendix is still vestigial, for it no longer performs the function for which it evolved.” ↩

4. 17d.

   Page 61:  “Removing it doesn't produce any bad side effects or increase mortality (in fact, removal seems to reduce the incidence of colitis).” ↩

Laurin, Michel et al.  “The cecal appendix: one more immune component with a function disturbed by post-industrial culture.”  Anatomical Record 294(4):567–579.  2011.  A review of what is known about the cecal appendix, with no new measurements.  It describes the appendix as an apparent safe house that keeps normal gut bacteria and restocks the colon after diarrheal illness, and it says this job is presumably of minimal importance where food, medicine and hygiene are abundant.  The article quotes it for the contrast between diarrheal illness, a major source of selection pressure in developing countries, and appendicitis, which tracks modern hygiene.

1. 18a.

   Section Abstract:  “epidemiologic studies demonstrate that diarrheal illness is indeed a major source of selection pressure in developing countries but not in developed countries, whereas appendicitis shows the opposite trend, being associated with modern hygiene and medicine.” ↩

Sanders, Nathan L. et al.  “Appendectomy and Clostridium difficile colitis: Relationships revealed by clinical observations and immunology.”  World Journal of Gastroenterology 19(34):5607–5614.  2013.  A review with no new experiment, written by a team in the surgery department at Duke University Medical Center.  It sets out the safe-house idea and the clinical evidence on appendectomy and colitis caused by Clostridium difficile, a bacterium that can cause colitis after antibiotics wipe out normal gut bacteria, and it concludes that appendectomy apparently raises the risk of recurrent colitis but not of a first infection.  The group that proposed the hypothesis wrote it, so readers should weigh it as the proposers' own case, and the article uses it to show how the group argues from anatomy before testing that argument against clinical data.

1. 19a.

   Section The immune system and the appendix:  “Given the shape and location of the appendix, it would indeed be difficult to imagine how the appendix might not be protective of bacteria.” ↩

2. 19b.

   Section The appendix and recurrent C. difficile colitis:  “Im et al found a 2.5-fold increased risk of recurrent C. difficile colitis in patients without an appendix compared to those with an appendix.” ↩

3. 19c.

   Section Abstract:  “appendectomy does not apparently put patients at risk for an initial onset of C. difficile -associated colitis.” ↩

Im, Gene Y. et al.  “The appendix may protect against Clostridium difficile recurrence.”  Clinical Gastroenterology and Hepatology 9(12):1072–1077.  2011.  A study that reviewed the medical records of 254 adult inpatients with Clostridium difficile infection (CDI) at one tertiary-care teaching hospital near New York City from 2005 to 2007, 203 with an appendix and 51 without, most of them checked on CT scans.  Recurrence was 18 percent with an appendix and 45 percent without.  The authors say the finding needs a prospective study, one that follows patients forward in time, and the study ran during a local outbreak.  The article uses it as the first test of the idea, which came out positive.

1. 20a.

   Section Abstract:  “In a multivariate analysis of 11 clinical variables, the presence of an appendix was associated inversely with CDI recurrence (P < .0001; adjusted relative risk, .398).” ↩

2. 20b.

   Section Abstract:  “this finding requires validation in a prospective study.” ↩

3. 20c.

   Section Results:  “The CDI recurrence rate for patients with an appendix was 18%, compared with 45% in those without an appendix.”  “In a univariate analysis, the presence of an appendix (P < .0002; unadjusted relative risk, 0.404; 95% confidence interval [CI], 0.266–0.615)”.  Table 1 gives 203 patients with an appendix and 51 without. ↩ ↩ ↩

4. 20d.

   Section Results:  “There were no significant associations between the presence of an appendix and CDI-related outcomes”. ↩

5. 20e.

   Section Methods, Statistical Analysis:  “a recently developed method of multivariate analysis (in lieu of a multiple logistic regression) was used to adjust relative risks rather than odds ratios, thereby providing a more conservative analysis.” ↩

Merchant, Rashida et al.  “Association Between Appendectomy and Clostridium difficile Infection.”  Journal of Clinical Medicine Research 4(1):17–19.  2012.  A case-control study, in which the authors contacted patients who had been tested for Clostridium difficile and asked whether they had had an appendix removed.  Among 257 patients, the 136 who tested positive had fewer prior appendectomies than the 121 who tested negative, and the authors concluded that an intact appendix appears to promote the infection.  The article uses it as the second test, which went the other way, and the authors themselves say their design cannot show cause.

1. 21a.

   Section Results:  “Among the 136 who tested positive for C. difficile, 27 (19.9%) had prior appendectomies, while among 121 patients testing negative for C. difficile, 38 (31.4%) had prior appendectomies.” ↩

2. 21b.

   Section Conclusions:  “rather than being protective, an intact appendix appears to promote C. difficile acquisition, carriage, and disease.” ↩

3. 21c.

   Section Limitations:  “Our choice of case-control methodology makes it impossible for us to demonstrate causality.” ↩

Clanton, Jesse et al.  “Fulminant Clostridium difficile infection: An association with prior appendectomy?”  World Journal of Gastrointestinal Surgery 5(8):233–238.  2013.  A retrospective chart review of 55 colons removed between 2001 and 2011, all from patients whose Clostridium difficile infection (CDI) had become severe enough to need colectomy (surgical removal of the colon).  The authors found appendectomy in 43.6% of them, against a lifetime rate of 17.6%, and no link between appendectomy and death, and they call for larger prospective studies before drawing causal conclusions.  The article uses it as one of three studies of the worst cases that link appendectomy to harm.

1. 22a.

   Section Abstract:  “Appendectomy was observed in 24 of 55 specimens (0.436, 99%CI: 0.280-0.606). This was compared to the lifetime incidence of appendectomy of 17.6%.” ↩

Yong, F. A. et al.  “Appendectomy: a risk factor for colectomy in patients with Clostridium difficile.”  American Journal of Surgery 209(3):532–535.  2015.  A retrospective analysis of 507 patients hospitalized for Clostridium difficile infection at St. Francis Medical Center between 2007 and 2011, comparing those with an intact appendix with those who had had one removed.  The authors found that colectomy (surgical removal of the colon) was needed in 5.2% of the first group and 10.9% of the second, and they say appendectomy may be a risk factor for more severe infection, though the mechanism is unknown.  The article uses it as one of three studies of the worst cases that link appendectomy to harm.

1. 23a.

   Section Abstract:  “Of 388 patients with intact appendix, 20 (5.2%) developed fulminant infection and required colectomy, whereas of 119 patients with previous appendectomy, 13 (10.9%) required colectomy.” ↩

Shaikh, Danial H. et al.  “Patients with Clostridium difficile infection and prior appendectomy may be prone to worse outcomes.”  World Journal of Gastrointestinal Surgery 13(11):1436–1447.  2021.  A retrospective review of 1580 patients with Clostridium difficile infection (CDI) admitted to the authors' hospital between 2008 and 2018, comparing those with and without a prior appendectomy.  Death rates did not differ, but the severity of the infection did, and a prior appendectomy was also associated with more toxic megacolon and colectomy.  The article uses it for the finding that the appendectomy group had no mortality difference but more severe disease.

1. 24a.

   Section Abstract:  “Of the 1580 patients, 12.5% had a history of appendectomy. There was no statistical difference in mortality between patients with a prior appendectomy or without (13.7% vs 14%, P = 0.877). However, a history of appendectomy affected the severity of CDI [odds ratio (OR) = 1.32, 95% confidence interval: 1.01-1.75].” ↩

Andersson, R. E. et al.  “Appendectomy and protection against ulcerative colitis.”  New England Journal of Medicine 344(11):808–814.  2001.  A cohort study of 212,963 people who had an appendectomy before age 50 between 1964 and 1993, each compared with matched controls and followed until 1995 for ulcerative colitis (a long-term inflammatory disease of the colon).  The risk of ulcerative colitis was low after surgery for appendicitis or mesenteric lymphadenitis (inflamed lymph nodes in the abdomen), but not after surgery for nonspecific abdominal pain, and the link appeared only when surgery came before age 20.  The article uses it for the finding that appendectomy in youth is associated with a lower later risk of ulcerative colitis.

1. 25a.

   Section Abstract:  “Appendectomy for an inflammatory condition (appendicitis or lymphadenitis) but not for nonspecific abdominal pain is associated with a low risk of subsequent ulcerative colitis. This inverse relation is limited to patients who undergo surgery before the age of 20 years.” ↩

2. 25b.

   Section Abstract:  “for patients with perforated appendicitis, the adjusted hazard ratio was 0.58 [95 percent confidence interval, 0.38 to 0.87]; for those with nonperforated appendicitis it was 0.76 [95 percent confidence interval, 0.65 to 0.90]”.  “patients who underwent appendectomy for nonspecific abdominal pain had the same risk of ulcerative colitis as the controls (adjusted hazard ratio, 1.06; 95 percent confidence interval, 0.74 to 1.52)”. ↩

Kooij, I. A. et al.  “The immunology of the vermiform appendix: a review of the literature.”  Clinical and Experimental Immunology 186(1):1–9.  2016.  A literature review of the immune side of the vermiform (worm-shaped) appendix, covering how its tissue and gut bacteria interact in health and in disease.  It concludes that the appendix is an important immune organ and not a rudimentary one, and it links the appendix to the start of ulcerative colitis, though it says it is still uncertain whether the bacterial imbalance causes the disease or results from it.  The article uses it for the claim that the appendix may prime ulcerative colitis, and for the authors' statement that the vestigial idea should be discarded.

1. 26a.

   Page 1:  “multiple immunological aspects point towards the appendix as a priming site for ulcerative colitis.” ↩

2. 26b.

   Page 1:  “the idea of the appendix being a vestigial organ should therefore be discarded.” ↩

Killinger, Bryan A. et al.  “The vermiform appendix impacts the risk of developing Parkinson's disease.”  Science Translational Medicine 10(465):eaar5280.  2018.  A population study that used the Swedish national patient registry, covering more than 1.6 million people and over 91 million person-years, and that also examined healthy human appendix tissue.  It found that people who had had an appendectomy had a lower Parkinson's risk and a later age of onset, and that the healthy appendix already held clumped alpha-synuclein, the protein that builds up in Parkinson's disease.  The article uses it as one of two results linking the appendix to disease, and it notes that another study disputes this one.

1. 27a.

   Section Results:  “PD incidence was 1.60 per 100,000 person-years among individuals who had an appendectomy [95% confidence interval (CI), 1.46 to 1.75] compared to 1.98 for controls (95% CI, 1.87 to 2.10; Fig. 1A). This signifies that the overall risk of developing PD was significantly decreased by 19.3% in appendectomized individuals compared to the general population.” ↩

Marras, Connie et al.  “Appendectomy in mid and later life and risk of Parkinson's disease: A population-based study.”  Movement Disorders 31(8):1243–1247.  2016.  A population-based study that compared 42,999 people over age 35 who had an appendectomy with matched people who had their gallbladder removed and with matched people who had neither operation.  It found no difference in Parkinson's risk compared with gallbladder removal, a higher incidence within five years compared with no operation but no lasting difference after that, and the authors conclude that appendectomy in mid or late life is not linked to a lower risk.  The article uses it as the contrary result to the Killinger study.

1. 28a.

   Section Abstract:  “Among 42,999 individuals undergoing appendectomy, no difference in risk of PD was identified compared to cholecystectomy (hazard ratio = 1.004; 95% confidence interval: 0.740-1.364).” ↩

Smith, Heather F. et al.  “Comparative anatomy and phylogenetic distribution of the mammalian cecal appendix.”  Journal of Evolutionary Biology 22(10):1984–1999.  2009.  A comparative anatomy study of the appendix across mammal species, combined with a cladistic analysis, which groups species by shared traits to reconstruct their family tree.  It describes three apparent forms of the appendix, finds appendix-like structures in some species that lack a true one, and reports that the appendix evolved independently at least twice and has been kept for 80 million years or longer.  The article uses it because the same group, writing after its earlier statement that such structures are rare, found many more.

1. 29a.

   Section Abstract:  “Cladistic analyses indicate that the appendix has evolved independently at least twice (at least once in diprotodont marsupials and at least once in Euarchontoglires), shows a highly significant (P < 0.0001) phylogenetic signal in its distribution, and has been maintained in mammalian evolution for 80 million years or longer.” ↩

Guan, Lei et al.  “The global, regional, and national burden of appendicitis in 204 countries and territories, 1990–2019: a systematic analysis from the Global Burden of Disease Study 2019.”  BMC Gastroenterology 23:44.  2023.  An analysis of the Global Burden of Disease Study 2019, which estimated appendicitis in 204 countries and territories from 1990 to 2019.  It found an age-standardised incidence of 229.9 per 100,000 population in 2019, and that the global rates rose by about 20 percent over those years.  The article uses it for the worldwide scale of the disease.

1. 30a.

   Section Abstract:  Age-standardised incidence in 2019 was:  “229.9 (95% UI 180.9 to 291.0) per 100,000 population.” ↩

Schullinger, Rudolph N.  “Observations on mortality from acute appendicitis at a university hospital, 1916 to 1946.”  Annals of Surgery 126(4):448–467.  1947.  A review of the Presbyterian Hospital's own records of acute appendicitis in New York, covering 5,405 cases and 193 deaths from 1916 to 1946.  It sorts the cases by what the surgeon found at operation and gives the death rate for each group.  The article uses it for how often appendicitis killed in one New York hospital, and how that changed over time.

1. 31a.

   Pages 449–450:  All cases: 5,405, 193 deaths, 3.55 per cent; 0.43 per cent in 1945.  Page 451:  Simple acute appendicitis 0.49 per cent.  Page 454:  With peritoneal abscess, 896 cases, 81 deaths, 9.04 per cent. ↩

Nabi, Rayyan et al.  “Trends and Disparities in Appendicitis-Related Mortality Across U.S. Demographics and Regions: A 22-Year CDC WONDER Database Study.”  World Journal of Surgery 49(9):2399–2408.  2025.  A retrospective study of US death certificates in the CDC WONDER database, covering appendicitis deaths in people aged 25 and over from 1999 to 2020.  It found that the age-adjusted death rate fell from 0.38 to 0.32 per 100,000, with a rise among women from 2016 to 2020.  The article uses it for the count of American deaths.

1. 32a.

   Section Results:  “From 1999 to 2020, there were a total of 15,243 deaths due to appendicitis in the United States among individuals aged 25 years to over 85 years.” ↩

Proctor, Dominic W. et al.  “Trends in the mortality, incidence and disability-adjusted life-years of appendicitis in EU15+ countries.”  International Journal of Surgery 109(9):2608–2613.  2023.  An observational study of Global Burden of Disease data for 1990 to 2019 in EU15+ countries, tracking deaths, new cases and disability years from appendicitis.  The median death rate fell by about half over the period, while the median incidence rose slightly.  The article uses it as a European comparison for how often appendicitis kills.

1. 33a.

   Section Abstract:  ASMR means age-standardised mortality rate.  “The median ASMRs across EU15+ countries in 2019 were 0.08/100 000 and 0.13/100 000 for females and males, respectively.” ↩

Salminen, Paulina et al.  “Antibiotic Therapy vs Appendectomy for Treatment of Uncomplicated Acute Appendicitis: The APPAC Randomized Clinical Trial.”  JAMA 313(23):2340–2348.  2015.  A randomized trial in Finland of 530 patients aged 18 to 60 with appendicitis confirmed by a CT scan, who were given either antibiotics or standard open surgery.  It did not show antibiotics to be as good as surgery, but most of the antibiotic group avoided an operation during a year of follow-up.  The article uses it for how many patients treated with antibiotics never needed surgery.

1. 34a.

   Section Abstract:  “Of the 256 patients available for follow-up in the antibiotic group, 186 (72.7%; 95% CI, 66.8% to 78.0%) did not require surgery.” ↩

CODA Collaborative.  “A Randomized Trial Comparing Antibiotics with Appendectomy for Appendicitis.”  New England Journal of Medicine 383(20):1907–1919.  2020.  A pragmatic randomized trial, not blinded, at 25 US centers with 1,552 adults who had appendicitis, comparing a 10-day course of antibiotics with appendectomy.  Antibiotics were no worse than surgery on 30-day health status, but 29 per cent of the antibiotic group had an appendectomy by 90 days, and complications were more common in that group.  The article uses it for how often antibiotic treatment still ends in surgery.

1. 35a.

   Section Abstract:  “In the antibiotics group, 29% had undergone appendectomy by 90 days.” ↩

Segal, I. et al.  “Characteristics and occurrence of appendicitis in the black population in Johannesburg, South Africa.”  Journal of Clinical Gastroenterology 8(5):530–533.  1986.  A study of appendicitis in black patients admitted to Baragwanath Hospital in Johannesburg.  It found about two cases per 1,000 adult admissions a year, most often in people aged 10 to 19, with a strong male bias.  The article uses it for the report of a tenfold gap in appendectomies between urban black and white adolescents.

1. 36a.

   Section Abstract:  “a low frequency consistent with the tenfold differential of appendectomies reported to prevail in urban black and white adolescents.” ↩ ↩

Adamidis, D. et al.  “Fiber intake and childhood appendicitis.”  International Journal of Food Sciences and Nutrition 51(3):153–157.  2000.  A diet study of 203 children who had their appendix removed for appendicitis, compared with 1,922 controls, with diet recorded by the diet history method.  The children with appendicitis ate less fibre, 17.4 g a day against 20.4 g, and the authors think lower fibre intake is the cause in 70 per cent of cases.  The article uses it for its finding on children's fibre intake.

1. 37a.

   Section Abstract:  “Appendectomized children had statistically significant lower mean daily intake of fiber (17.4 g versus 20.4 g, P < 0.001).” ↩

Barker, D. J. P. et al.  “Acute appendicitis and bathrooms in three samples of British children.”  British Medical Journal 296(6627):956–958.  1988.  A study of appendectomies in three national samples of British children, set against the amenities in each child's home.  It found that the risk of the operation depended on the home's amenities, especially whether it had a bathroom, and that this held regardless of social class.  The article uses it for the link between appendicitis and Western hygiene.

1. 38a.

   Section Abstract:  “The risk of having the operation depended on the amenities present in the home, in particular whether or not there was a bathroom.” ↩

Ferris, Mollie et al.  “The Global Incidence of Appendicitis: A Systematic Review of Population-based Studies.”  Annals of Surgery 266(2):237–241.  2017.  A systematic review of 120 population studies from around the world that counted appendicitis or appendectomy.  It found a pooled incidence of 100 per 100,000 person-years in Northern America, that appendicitis incidence had stabilised in Western countries, and that data from newly industrialized countries was sparse.  The article uses it for where the disease is common and where it is rising.

1. 39a.

   Section Abstract:  “Data from newly industrialized countries is sparse, but suggests that appendicitis is rising rapidly.” ↩

Wieland, Carl, and Shaun Doyle.  “More musings on our 'useless' appendix.”  Creation.com.  Creation Ministries International.  May 7, 2008.  A 2008 article from a creationist ministry's website, by Carl Wieland and Shaun Doyle, that discusses a 1980 study of the primate caecum and appendix by G. B. Scott.  It argues that the appendix is not a degenerate organ, and that if it were useless, natural selection should have removed it, since most appendicitis strikes before reproductive age.  The article quotes its selection argument, the question of why natural selection did not remove the organ.

1. 40a.

   “since most appendicitis occurs before the age of reproduction, should not natural selection have long since eliminated such a 'useless' object?” ↩

2. 40b.

   “Assuming evolution to be true, as the authors do, it fits more readily with the opposite idea—that the appendix has gradually and progressively developed to the 'fully developed organ' seen in humans and gorilla.” ↩

Sadr Azodi, Omid et al.  “Genetic and environmental influences on the risk of acute appendicitis in twins.”  British Journal of Surgery 96(11):1336–1340.  2009.  A twin study that linked Swedish twins born from 1959 to 1985 to the national hospital register and compared how often identical and non-identical twins shared appendicitis.  Genes accounted for about 30 percent of the risk and the environment for the rest, with a large difference between men and women.  It shows that appendicitis risk is mostly, not wholly, environmental.

1. 41a.

   Section Abstract, Results:  “For the sexes combined, genetic effects accounted for 30 (5 to 40) per cent and non-shared environmental effects for 70 (60 to 81) per cent of the risk.” ↩

Glover, J. Warwick.  “The human vermiform appendix: a general surgeon's reflections.”  Journal of Creation 3(1):31–38.  1988.  A general surgeon's review of the appendix, published in the Journal of Creation.  It argues that Darwin's claim that the appendix is vestigial rested on wrong reasoning about homology and about Lamarckian inheritance (the idea that use and disuse are passed on to offspring), and that the organ is a highly specialised immune structure.  The article calls it the first serious creationist treatment of the appendix, and it was written by a surgeon.

1. 42a.

   Section Darwin's Argument:  “Darwin's argument about the appendix being vestigial was incorrect in his application of: homology, and Lamarckian inheritance.” ↩

2. 42b.

   Section Darwin and Homology:  Darwin erred by:  “regarding the caecum and appendix as part of the same unit organ, structurally and functionally, rather than (albeit in continuity) separate structures with different functions.” ↩

3. 42c.

   Section The Organ—Microscopic:  “it is now generally accepted that the appendix is a highly specialised, well-differentiated organ apparently developed to the maximum in its specialisation in man.” ↩

4. 42d.

   Section Immunological:  “it has also been shown that the appendix after the neonatal period is dispensable, meaning that normal G.A.L.T. functions remain after appendectomy.” ↩ ↩

Ham, Ken, and Carl Wieland.  “Your appendix … it's there for a reason.”  Creation 20(1):41–42.  Dec 1997.  A short 1997 magazine article by two creationist writers, Ken Ham and Carl Wieland, arguing that the appendix has a function, probably mainly in early childhood.  It blames appendicitis on the curse on a once-perfect creation and on a highly refined modern diet, and it repeats the old count of 180 vestigial structures.  The article uses it as a typical creationist source, and to show that it repeats the '180' count.

1. 43a.

   “Like the very important thymus gland in our chest, it is likely that the appendix plays its major role in early childhood.” ↩

2. 43b.

   “Death, disease, and degeneration from original perfection are all a part of the curse on a once-perfect creation. They do not reflect on the suitability of the original design.” ↩

3. 43c.

   “it is clear that appendicitis is only common in countries where a very highly refined modern diet is eaten.” ↩

4. 43d.

   “Thus, at one time evolutionists postulated there were 180 vestigial (functionless) structures (including the appendix) in the human body. Today this list has shrunk to virtually none.”  The 180 is Newman's Scopes-trial figure. ↩

Bergman, Jerry.  “Do any vestigial structures exist in humans?”  CEN Technical Journal 14(2):95–98.  2000.  A technical article by a creationist author arguing that humans have no truly vestigial organs.  It traces the list of human vestigial organs from 180 in 1890 to 0 in 1999 and rejects the newer definition of a vestigial organ as one that has only shrunk in size or lost some function.  The article uses it for the claim that the appendix is part of the immune system.

1. 44a.

   Page 96:  “The appendix is part of the immune system.” ↩

Menton, David.  “Vestigial Organs: Evidence for Evolution?”  The New Answers Book 3.  Answers in Genesis.  Jul 7, 2014.  A chapter in a creationist book of answers, written as a reply to the claim that vestigial organs prove evolution.  It reviews Darwin's list of "useless" organs, Robert Wiedersheim's list of 86 organs in 1893, and the "180" figure given at the Scopes trial of 1925, and argues that organs once called useless have been found to have functions.  The article uses it for the claim that the organs on Wiedersheim's list, the appendix among them, were later shown to be useful.

1. 45a.

   Chapter 24:  Of the organs on Wiedersheim's list:  “have been subsequently shown to have useful functions and indeed some have functions essential for life.” ↩

Doyle, Shaun.  Appendix: a bacterial 'safe house'.  Creation Ministries International.  Oct 16, 2007.  A short news commentary on the creationist website of Creation Ministries International, reacting to a 2007 report that the appendix may act as a "safe house" for useful gut bacteria.  It repeats the researchers' idea that the appendix's shape and position let it grow good bacteria and restore them after illness such as cholera, and it says this fits a designing Creator.  The article uses it as an early creationist reaction to that report.

1. 46a.

   “It once again shows that the evidence from biology is wonderfully consistent with the biblical Master Designer who created us in the beginning to eat.” ↩

Sarfati, Jonathan.  “Is there 'bad design?'.”  Creation 46(1):48–51.  Jan 2024.  A popular article by a creationist writer, the first of a series adapted from a creationist book on design in nature.  It argues that claims of "bad design" do not prove evolution, and it applies that argument to the appendix, which it calls a safe house for good gut bacteria.  The article quotes it for two points and disputes the second: that no more developed primate ancestor is shown for the appendix to have devolved from, and that removing the appendix raises the risk of a serious gut infection by C. difficile bacteria.

1. 47a.

   “there is no evidence that man's alleged primate ancestors had a more developed structure from which the appendix could devolve.” ↩

2. 47b.

   “even given evolutionary assumptions, it was lost less than seven times, which is further evidence that it's useful.” ↩

3. 47c.

   “A study showed that people who had their appendix removed are four times more likely to develop a C. difficile infection.”  Sarfati's own footnote cites a 2012 Scientific American blog post, not a study. ↩

Catchpoole, David.  Appendix shrieks 'Creation' (at least 18 times!).  Creation Ministries International.  Mar 25, 2013.  A news commentary by a creationist writer on a 2013 study that placed 361 living mammals on an evolutionary tree and found that the appendix arose independently at least 32 times, and perhaps 38 times.  It was later revised for the print magazine Creation 38(2):12–14, and it quotes an outside critic who counted 18 times using only the clear-cut cases.  The article uses it as the creationist reply to that study.

1. 48a.

   “Even using evolutionary assumptions, the appendix cannot be a degenerate evolutionary structure.” ↩

2. 48b.

   “'Only' 18 times? Even granting that the Darwinian mechanism could have achieved the evolution of a structure such as the intestine with an appendix in the first place, to have the same organ evolving in the same way independently one additional time stretches the bounds of credulity.” ↩

Answers in Genesis.  “Appendix.”  Answers magazine, Perspective.  Jul 1, 2013.  An unsigned Perspective piece in Answers magazine, the magazine of Answers in Genesis, reacting to the 2013 study of 361 mammals, about 50 of which have an appendix.  It says the appendix's scattered distribution follows no pattern and so shows that the evolutionary tree is wrong.  The article quotes it as the Answers in Genesis reply to that study.

1. 49a.

   “Amusingly, the distribution fails to follow any particular pattern. So the researchers are forced to conclude that the appendix evolved independently 32 to 38 times!” ↩

2. 49b.

   “it does provide further confirmation that the tree is invalid!” ↩

Thomas, Brian.  “The Appendix: A Thorn in Evolution's Side?”  Creation Science Update.  Institute for Creation Research.  Mar 6, 2013.  A short news item by Brian Thomas, Ph.D., a science writer at the Institute for Creation Research, about the 2013 study of 361 mammals.  It says the appendix's scattered distribution follows no evolutionary pattern, quotes ScienceNow's report of the study's estimate of at least 32 and perhaps 38 independent origins, and argues that the distribution fits creation.  The article quotes it as the ICR reply to that study.

1. 50a.

   “Although the tiny appendix dangles on the wrong branches for evolution, its distribution among mammals fits biblical creation just fine.” ↩

Guliuzza, Randy J.  “Major Evolutionary Blunders: Our Useful Appendix, Evidence of Design, Not Evolution.”  Acts & Facts 45(2).  Institute for Creation Research.  Jan 29, 2016.  An Acts & Facts article by Randy J. Guliuzza, national representative of the Institute for Creation Research.  It argues that the appendix is a fully functional organ and that evolutionists have misread it as useless, and it reviews what Darwin, Francisco Ayala, Ernst Mayr and Jerry Coyne said about the appendix.  The article uses it as an example of a reply that does not answer Coyne's "still vestigial" sentence.

1. 51a.

   “scientific research demonstrates the folly of both assertions by showing the appendix to be a fully functional organ.” ↩

Statham, Dominic.  “The appendix: functional, but still evidence for evolution?”  Creation 40(2):17–19.  Apr 2018.  A popular article in Creation magazine by Dominic Statham, a creationist writer.  It argues that the appendix is functional, and that Jerry Coyne's new definition of a vestigial organ would make every organ vestigial.  The article quotes it for Statham's reply to Coyne and for its "four times" figure, which the article calls wrong.

1. 52a.

   “if Coyne is right, then every organ should be considered vestigial as, in the thinking of evolutionists, every feature in every animal has evolved from something else.” ↩

2. 52b.

   “nowhere in his blog does he attempt to demonstrate that the appendix did evolve from an ancestral feature. Rather he just assumes this, considering it to be obvious.” ↩

3. 52c.

   “One study indicated that people whose appendix had been removed were four times more likely to suffer a recurrence of this illness.”  Statham's own footnote cites Kooij 2016, whose text carries no such figure. ↩

Im 2011 reports recurrence in 18 percent of 203 patients with an appendix and 45 percent of 51 without.²⁰  The odds of recurrence are 0.18/0.82 = 0.22 with an appendix and 0.45/0.55 = 0.82 without, a ratio of about 3.7.  The relative risk, which is what "times more likely" means, is 45/18 = 2.5.  The paper itself reports only relative risks. ↩

Bergman, Jerry.  Do 'Useless' Organs Prove Humans Evolved?  Institute for Creation Research.  Mar 30, 2018.  A question-and-answer piece by Jerry Bergman, Ph.D., a creationist who says he has taught college anatomy for over 30 years.  He argues that every organ once called useless, from the appendix to the tonsils, has been found to have a use, and that vestigial organs do not exist.  The article quotes it as an Institute for Creation Research answer to the vestigial argument.

1. 54a.

   “Do vestigial organs show evolution? No—vestigial organs don't even exist!” ↩

Cai, Shuntian et al.  “Appendectomy is associated with alteration of human gut bacterial and fungal communities.”  Frontiers in Microbiology 12:724980.  2021.  A cross-sectional study at one hospital in Xiamen, China, that sequenced the stool bacteria and fungi of 30 healthy people who had had their appendix removed and 30 who had not.  The first group had less diverse bacteria and more varied fungi, with the bacterial difference fading in those operated on longer ago.  It is small, and the authors list its single-centre design as a limit.

1. 55a.

   Section Abstract:  “the gut bacterial composition of samples from HwA was less diverse than that of samples from HwoA”.  “The HwA subgroup analysis indicated a trend toward restoration of the HwoA bacterial microbiome over time after appendectomy.”  HwA means healthy individuals with prior appendectomy;  HwoA, without. ↩

Hadžić, Matija et al.  “The association between history of appendectomy and gut microbiota composition: a follow-up cross-sectional study.”  Frontiers in Microbiology 16:1697138.  2025.  A cross-sectional study of stool-bacteria data and self-reported health records held by a European laboratory, comparing 2,615 adults who had had an appendectomy with 13,103 who had not.  The large groups differed, but so did their age, sex and weight;  among people screened as healthy, 111 with and 876 without an appendectomy showed no difference.  The timing and cause of each operation were unknown.

1. 56a.

   Section Abstract, Results:  “No significant differences were found in the gut microbiota between the 111 healthy adult subjects and 876 adults who had not undergone appendectomy (HwA vs. HnoA) at the time of stool sampling.” ↩