Benchmarking Evolution

Behe, Michael J.  The Edge of Evolution: The Search for the Limits of Darwinism.  Free Press.  2007.  Behe is a biochemist at Lehigh University and a senior fellow of the Discovery Institute.  The wording was read from the publisher's e-book.  Page numbers were pinned on the archive.org scan of the 2007 hardback, item isbn_9780743296205, read by search-inside because the item cannot be borrowed.  Printed page equals scan leaf minus 14.  That offset was anchored on the scan's own page map at leaf 65, page 51, and leaf 152, page 138, and agrees with the pages Luskin 2019 and Durrett and Schmidt 2009 cite.  The scan's text destroys exponents, so exponents are from the e-book.

1. 1a.

   Page 60:  “Species in which there are fewer living organisms than malaria (again, other things being equal) will take proportionately longer to develop a cluster of mutations of the complexity of malaria’s resistance to chloroquine.”  Pinned on leaf 74 of the archive.org scan. ↩ ↩

2. 1b.

   Page 138:  “The best current estimate is that a person infected with HIV is burdened with a total of one to ten billion (10⁹ to 10¹⁰) virus particles.”  “Since there are approximately fifty million people worldwide infected with the virus, the math points to a total of about 10²⁰ copies of the virus having been produced in the past several decades, when HIV became widespread in human populations—roughly the same as the number of malarial cells produced each year.”  An endnote marker after the first sentence is left out.  Pinned on leaf 152 of the archive.org scan.  Exponents are from the e-book. ↩

3. 1c.

   Page 61:  “There are about five thousand species of modern mammals.  If each species had an average of a million members, and if a new generation appeared each year, and if this went on for two hundred million years, the likelihood of a single CCC appearing in the whole bunch over that entire time would be only about one in a hundred.”  Two endnote markers are left out.  5,000 × 10⁶ × 2 × 10⁸ = 10¹⁸. ↩ ↩ ↩

4. 1d.

   Page 62:  “So a CCC isn’t just the odds of a particular protein getting the right mutations; it’s the probability of an effective cluster of mutations arising in an entire organism.” ↩

5. 1e.

   Page 60:  “a generous estimate is that perhaps a trillion creatures have preceded us in the past ten million years.”  “The ratio of humanoid creatures in the past ten million years to the number of parasites needed for chloroquine resistance is one to a hundred million.”  An endnote marker after the first sentence is left out.  Pinned on leaf 74 of the archive.org scan. ↩

Lynch, Michael, and John S. Conery.  “The origins of genome complexity.”  Science 302(5649):1401–1404.  Nov 21, 2003.  Lynch is a population geneticist, then at Indiana University.  Read from the second author's copy of the publisher PDF.  The text layer flattens exponents, which were restored from the sense of the text.  Mirror:  Pages.uoregon.edu

1. 2a.

   Section Abstract, page 1401:  “According to this model, much of the restructuring of eukaryotic genomes was initiated by nonadaptive processes, and this in turn provided novel substrates for the secondary evolution of phenotypic complexity by natural selection.  The enormous long-term effective population sizes of prokaryotes may impose a substantial barrier to the evolution of complex genomes and morphologies.” ↩ ↩

2. 2b.

   Page 1401:  “For example, a large population can behave genetically like a small one if a minor fraction of individuals contribute to the reproductive pool or if beneficial chromosomal segments periodically sweep through the population.” ↩

3. 2c.

   Page 1402:  “Second, the majority of unicellular species in Fig. 1 are pathogens, and their genetic effective sizes may be highly influenced by that of their larger host, as in the case of the human malarial parasite Plasmodium falciparum.” ↩

4. 2d.

   Page 1401:  “This implies that Ne is generally greater than 10⁸ for prokaryotes and often in the range of 10⁷ to 10⁸ for unicellular eukaryotes.”  Page 1402:  “implying that Ne is on the order of 10⁴ to 10⁵.”  The second quotation is about vertebrates.  The paper prints Ne with a subscript e. ↩

Times each possible single-letter change arose equals births times the rate for one named change, which is the rate per letter divided by three.  HIV:  2 × 10⁻⁵ ÷ 3 = 6.7 × 10⁻⁶ per round of infection;³⁵  times 6 × 10²⁰ infected cells is 4 × 10¹⁵, and times 6 × 10²² particles is 4 × 10¹⁷.  The published HIV article prints 3.7 × 10¹⁷.  Malaria parasite, from the parasite article:  2.45 × 10⁻¹⁰ ÷ 3 = 8.2 × 10⁻¹¹, or one in 1.2 × 10¹⁰ parasites;¹⁸  times 1.5 to 7.5 × 10²¹ births is 1.2 to 6.2 × 10¹¹.  One named pair in the same parasite in the same generation:  (8.2 × 10⁻¹¹)² = 6.7 × 10⁻²¹, or one in 1.5 × 10²⁰.  Lenski's experiment, from its article:  2.5 × 10⁹ mutations per flask ÷ 1.39 × 10⁷ possible changes = 181 per flask, and twelve flasks give about 2,200.  Phage lambda, from its article:  7.7 × 10⁻⁸ ÷ 3 = 2.6 × 10⁻⁸ per named change,²⁶ which over 1.9 × 10¹⁰ to 1.2 × 10¹³ births is 490 to 310,000.  Dividing by three treats the three possible changes at a letter as equally likely, which is wrong by up to a factor of two. ↩ ↩ ↩ ↩ ↩

Every figure is from the parasite article on this site, except the effective size.  Census:  about 10¹⁷ alive and fewer than 10²⁰ born a year.⁷  Years:  75, from the early 1950s to 2025.²²  Generations:  365.25 ÷ 2 = 182.6 a year, and 75 × 182.6 = 13,700.  Births:  75 × 2 × 10¹⁹ = 1.5 × 10²¹ and 75 × 10²⁰ = 7.5 × 10²¹.  Mutations per birth:  2.45 × 10⁻¹⁰ × 2.33 × 10⁷ = 0.0057.^{18 18}  Mutations:  1.5 × 10²¹ × 0.0057 = 8.6 × 10¹⁸ and 7.5 × 10²¹ × 0.0057 = 4.3 × 10¹⁹.  Output:  18 amino-acid changes in the most changed form of each gene, and a round upper limit of 100 when alternative forms are counted.  18 ÷ 7.5 × 10²¹ = 2.4 × 10⁻²¹ and 100 ÷ 1.5 × 10²¹ = 6.7 × 10⁻²⁰.  The gain is chloroquine transport by PfCRT.  The loss is the deletion of pfhrp2.  Effective size is added by this article.¹⁰ ↩ ↩ ↩ ↩

Mauger, Bethany.  “'Evolution under a microscope' going strong at MSU.”  MSUToday.  Nov 11, 2025.  A university press release.  Used only for the count of generations.

1. 5a.

   Paragraph on the move to Texas:  “His group continued the experiment there to 82,000 generations.” ↩ ↩

Turner, Caroline B. et al.  “Evolution of a cross-feeding interaction following a key innovation in a long-term evolution experiment with Escherichia coli.”  Microbiology 169:001390.  2023.  Open access.  Read from the publisher PDF in the library.  Mirror:  PMC

1. 6a.

   Section Discussion:  The first sentence of the Discussion says that the ability to grow on citrate in air has so far evolved in only one of the twelve populations, even after 75,000 generations.  It is paraphrased here because three reference numbers break up the printed sentence. ↩

White, Nicholas J.  “Antimalarial drug resistance.”  Journal of Clinical Investigation 113(8):1084–1092.  Apr 2004.  A review by the Mahidol and Oxford malaria clinician.  Free to read at the journal.  Read from the publisher PDF;  page numbers are the printed folios.  The PDF text flattens exponents, which were restored from context.

1. 7a.

   Page 1091:  “This is particularly powerful in malaria, because there are only about 10¹⁷ malaria parasites in the entire world.”  “As there is a cumulative total of less than 10²⁰ malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years”.  Page 1087:  “these ill people would contain between 5 × 10¹⁶ and 5 × 10¹⁷ malaria parasites (8).”  “we have estimated that there must be less than 3 × 10¹⁶ malaria parasites in the world's asymptomatic carriers (Figure 5) (8).”  Reference 8 is White and Pongtavornpinyo 2003, Proceedings of the Royal Society B 270:545–554, which was not obtained. ↩ ↩

2. 7b.

   Page 1085:  “Resistance to chloroquine in P. falciparum has arisen spontaneously less than ten times in the past fifty years (14).  This suggests that the per-parasite probability of developing resistance de novo is on the order of 1 in 10²⁰ parasite multiplications.”  Reference 14 is Su, Kirkman, Fujioka and Wellems 1997, Cell 91:593–603. ↩ ↩

3. 7c.

   Page 1085:  “The single point mutations in the gene encoding cytochrome b (cytB), which confer atovaquone resistance, or in the gene encoding dihydrofolate reductase (dhfr), which confer pyrimethamine resistance, have a per-parasite probability of arising de novo of approximately 1 in 10¹² parasite multiplications (5).”  The sentence after the next says that much higher mutation rates than 1 in 10¹² are recorded in the laboratory, citing Rathod, McErlean and Lee 1997.  It is paraphrased here because the published sentence contains a misprint. ↩ ↩

Meyer, Justin R. et al.  “Repeatability and Contingency in the Evolution of a Key Innovation in Phage Lambda.”  Science 335(6067):428–432.  Jan 27, 2012.  Read as the PubMed Central author manuscript (NIHMS362453), both the HTML and the 14-page PDF, which carry identical text.  Every page below is an author-manuscript page read from the "Meyer et al. Page N" running head, not a Science page:  the published pagination could not be obtained, since the Science PDF is paywalled and Unpaywall and Semantic Scholar list only the PubMed Central copy.  Exponents are restored from the sense of the text, because the PDF and HTML both flatten superscripts.  Mirror:  PMC

1. 8a.

   Page 2:  “The mutants arose and fixed within 8 days, generating highly resistant populations (fig. S1), although the phage did not go extinct but instead persisted at densities of about 10⁶ to 10⁷ phage per ml, or about one phage per 10² to 10³ host cells (fig. S2).”  Superscripts restored;  both the PDF and the HTML print "106 to 107" and "102 to 103". ↩ ↩

2. 8b.

   Page 4:  “The correspondence between the use of the OmpF receptor and the presence of these four mutations, coupled with the observation that phage having only three of the four cannot use OmpF, provides evidence that all four are required for λ to infect through OmpF.” ↩ ↩

3. 8c.

   Page 4:  “As before, only some phage populations (24/96) evolved the ability to use a second receptor. This ability emerged about the same time (median 12 days; range 9–17 days; fig. S4), and all isolates with altered receptor function infected hosts through the OmpF protein.” ↩ ↩

Effective sizes are from Lynch's 2023 dataset and Charlesworth's 2009 table.^{46 10}  The two agree within a factor of about two for animals and differ sevenfold for Escherichia coli, 1.7 × 10⁸ against 2.5 × 10⁷.  The ratio of the medians for bacteria and vertebrates is 8.88 × 10⁷ ÷ 9.32 × 10⁴ = 950.  An effective size is a quotient of diversity by mutation rate, so its second digit depends on which mutation rate is used. ↩ ↩

Charlesworth, Brian.  “Effective population size and patterns of molecular evolution and variation.”  Nature Reviews Genetics 10(3):195–205.  Mar 2009.  Read from the advance online copy in the library, whose pages are numbered 1 to 11.  Printed page equals that number plus 194, which is an inference from the page count and the identical layout.

1. 10a.

   Table 1, page 199:  The table is headed "Effective population size (Ne) estimates from DNA sequence diversities".  Its rows include humans 10,400, Drosophila melanogaster 1,150,000, Escherichia coli 25,000,000 and Plasmodium falciparum 210,000–300,000.  The parasite's figure is from 204 nuclear genes. ↩ ↩ ↩ ↩ ↩

user813801.  “How many organisms have ever lived on Earth?”  Biology Stack Exchange.  Jul 10, 2014.  An answer by an anonymous user of a question-and-answer site.  Read through a browser session and saved in the library.  The published HIV article cites this answer for its count of bacteria.  The answer also gives the figure for mammals quoted here.

1. 11a.

   Section Estimate of number of mammals that ever existed:  “1.4410^17 new mice per year 200 million years = 2.88 * 10^25 total mice.”  “so the total number is probably about around 4-10 orders of magnitude less than this.  So it is probably something like 10^20 total mammals ever existed”.  The first figure is an upper limit that covers all land with mice. ↩ ↩

First route, from the parasite article:  bats are two-thirds of individuals and less than a tenth of 20 million tonnes.⁵⁴  A tenth of 20 million tonnes is 2 × 10⁹ kg.  At an assumed 10 g per bat that is at most 2 × 10¹¹ bats, and 2 × 10¹¹ ÷ (2/3) = 3 × 10¹¹ mammals.  Second route:  animals under 1 kg are more than 95% of individuals and a fifth of the weight.⁵⁴  A fifth of 20 million tonnes is 4 × 10⁹ kg.  At an assumed mean of 20 g that is 2 × 10¹¹ animals, and 2 × 10¹¹ ÷ 0.95 = 2.1 × 10¹¹ mammals.  Both routes then assume one generation a year for 2 × 10⁸ years:  3 × 10¹¹ × 2 × 10⁸ = 6 × 10¹⁹ and 2.1 × 10¹¹ × 2 × 10⁸ = 4 × 10¹⁹.  The body weights, the generation time and the constant abundance are assumptions.  The census paper prints no total count of individuals in its main text.  Sea mammals are large and few.  Livestock are recent.  The estimate in the notes behind this series is 5,000 × 5 × 10⁸ = 2.5 × 10¹² alive, times 2 × 10⁸ years ÷ 5 years = 4 × 10⁷ generations, which is 10²⁰. ↩ ↩ ↩ ↩

Mammals.  Births:  6 × 10¹⁹.¹²  New substitutions per birth:  for a mouse, 2 copies × 2.717 × 10⁹ letters × 5.35 × 10⁻⁹ = 29;⁴⁶  for a human, 63.¹⁹  Total:  6 × 10¹⁹ × 29 = 1.7 × 10²¹ and 6 × 10¹⁹ × 63 = 3.8 × 10²¹.  One named change per birth:  mouse 5.35 × 10⁻⁹ ÷ 3 × 2 copies = 3.6 × 10⁻⁹;  human 1.2 × 10⁻⁸ ÷ 3 × 2 = 8 × 10⁻⁹.  Times each arose:  3.6 × 10⁻⁹ × 6 × 10¹⁹ = 2.2 × 10¹¹ and 8 × 10⁻⁹ × 6 × 10¹⁹ = 4.8 × 10¹¹.  One named pair in the same animal in the same generation:  (3.6 × 10⁻⁹)² = 1.3 × 10⁻¹⁷ and (8 × 10⁻⁹)² = 6.4 × 10⁻¹⁷.  Times each arose:  780 and 3,800.  Malaria parasite:  6.7 × 10⁻²¹ × 1.5 to 7.5 × 10²¹ = 10 to 50.³  HIV:  (6.7 × 10⁻⁶)² = 4.4 × 10⁻¹¹, times 6 × 10²⁰ to 6 × 10²² is 3 × 10¹⁰ to 3 × 10¹².  A named triple in HIV:  (6.7 × 10⁻⁶)³ = 3 × 10⁻¹⁶, times 6 × 10²⁰ is 1.8 × 10⁵.  Pairs built in two steps, with the first change waiting in the population, arise more often than pairs arising together.  How much more often depends on whether the first change is harmful.  Treating all mammals as one genome is a simplification. ↩ ↩ ↩ ↩

One lineage:  an assumed census of 10⁶ to 10⁹ for an assumed 10⁸ generations, which is 200 million years at two years each, gives 10¹⁴ to 10¹⁷ births.  Mutations:  10¹⁴ × 29 = 3 × 10¹⁵ and 10¹⁷ × 63 = 6 × 10¹⁸.  Times each single-letter change arose:  3.6 × 10⁻⁹ × 10¹⁴ = 3.6 × 10⁵ and 8 × 10⁻⁹ × 10¹⁷ = 8 × 10⁸.  Times each named pair arose together:  1.3 × 10⁻¹⁷ × 10¹⁴ = 0.0013 and 6.4 × 10⁻¹⁷ × 10¹⁷ = 6.4.¹³  Births needed for one named pair:  1 ÷ 6.4 × 10⁻¹⁷ = 1.6 × 10¹⁶ and 1 ÷ 1.3 × 10⁻¹⁷ = 7.7 × 10¹⁶.  On Behe's count of 10¹⁸ mammals:  10¹⁸ × 1.3 × 10⁻¹⁷ = 13 and 10¹⁸ × 6.4 × 10⁻¹⁷ = 64.  On his count of 10¹² ancestors in the human line:  10¹² × 6.4 × 10⁻¹⁷ = 6 × 10⁻⁵. ↩ ↩ ↩ ↩

Durrett, Rick, and Deena Schmidt.  “Waiting for two mutations:  with applications to regulatory sequence evolution and the limits of Darwinian evolution.”  Genetics 180:1501–1509.  Nov 2008.  Two mathematicians at Cornell.  Read from the publisher PDF in the library.

1. 15a.

   Section Abstract, page 1501:  “Consistent with recent experimental observations for Drosophila, we find that a few million years is sufficient, but for humans with a much smaller effective population size, this type of change would take >100 million years.”  Page 1507:  “Multiplying by 25 years per generation gives 216 million years.”  The change meant is a pair of mutations, the first of which inactivates a binding site and the second of which creates a new one.  The same page gives 162 million years from simulation.  The PDF text prints the greater-than sign as a full stop. ↩ ↩

Rambaut, Andrew et al.  “The causes and consequences of HIV evolution.”  Nature Reviews Genetics 5:52–61.  Jan 2004.  A review.  Read from a course copy of the publisher PDF.  Page numbers are from the running feet.  Reference numbers inside the quotations are left out.  Mirror:  Pages.stat.wisc.edu

1. 16a.

   Page 56:  “Strikingly, intra-host and inter-host evolution seem to be very different processes, with positive selection dominating in the former but not the latter.” ↩

2. 16b.

   Page 56:  “First, the virus experiences a high rate of mutation, with reverse transcriptase making ~0.2 errors per genome during each replication cycle”.  “it has a viral generation time of ~2.5 days and produces ~10¹⁰–10¹² new”.  Page 52:  “an estimated 42 million people carrying the virus at present”.  The second quotation ends before the word virions, which the journal prints in small capitals as a glossary term.  Exponents restored;  the text layer prints 1010–1012. ↩ ↩

3. 16c.

   Page 57:  “the recombination rate of HIV is one of the highest of all organisms, with an estimated three recombination events occurring per genome per replication cycle”. ↩

4. 16d.

   Page 56:  “Most fixed env amino-acid changes in these patients confer a selective advantage, with an average of one adaptive fixation event every ~2.5 months.  Under these criteria, HIV shows stronger positive selection than any other organism studied so far.” ↩

Lenski, Richard E. et al.  “Long-term experimental evolution in Escherichia coli.  I.  Adaptation and divergence during 2,000 generations.”  The American Naturalist 138:1315–1341.  1991.  The founding paper of the experiment.  The library copy is a scan without a text layer.  The quotation was verified by the author of the experiment's article on this site from a fresh reading of pages 1315 to 1320.

1. 17a.

   Pages 1317–1318, section Culture Conditions:  “Cultures were propagated daily by transferring 0.1 mL of each culture into 9.9 mL of fresh medium.”  The same section gives a density at rest of about 5 × 10⁷ cells per mL in 10 mL, and about 6.64 generations a day. ↩ ↩

Hamilton, William L. et al.  “Extreme mutation bias and high AT content in Plasmodium falciparum.”  Nucleic Acids Research 45(4):1889–1901.  2017.  Open access, CC BY.  Read from the Europe PMC full text, which has no page numbers.  ELC in the quotations means one erythrocytic life cycle of 48 hours, and BPS means base-pair substitution.  Mirror:  PMC

1. 18a.

   Section Materials and Methods:  “we divided μ1 by the total genome size of P. falciparum (G), 2.33 × 10⁷ bp”.  The source prints μ with a subscript 1. ↩ ↩

2. 18b.

   Section Materials and Methods:  “the mean overall BPS rate per ELC per bp for all clone trees (2.45 × 10⁻¹⁰ BPS/ELC/bp)”.  Table 1:  Per-isolate means in units of 10⁻¹⁰:  3D7 2.10, HB3 2.95, Dd2 3.20, KH1-01 2.27, KH2-01 1.64.  A sixth isolate, W2, had too few clones for a rate.  In all, 279 clones were sequenced and 85 substitutions found. ↩ ↩ ↩

Kong, Augustine et al.  “Rate of de novo mutations and the importance of father's age to disease risk.”  Nature 488(7412):471–475.  Aug 23, 2012.  Read from the author manuscript, which has no journal page numbers.  The senior author is Kari Stefansson.  Mirror:  PMC

1. 19a.

   Section Abstract:  “Here we show that in our samples, with an average father’s age of 29.7, the average de novo mutation rate is 1.20×10⁻⁸ per nucleotide per generation.”  Section Results:  “a total of 4,933 de novo mutations, or an average of 63.2 per trio, were called.”  A trio is two parents and a child, so 63.2 is the count per child. ↩ ↩ ↩ ↩

Wielgoss, Sébastien et al.  “Mutation rate inferred from synonymous substitutions in a long-term evolution experiment with Escherichia coli.”  G3 1:183–186.  2011.  Open access.  Read from the publisher PDF in the library.  Mirror:  PMC

1. 20a.

   Section Abstract, page 183:  “The resulting molecular estimate was 8.9 × 10⁻¹¹ per base-pair per generation”.  Exponent restored;  the text layer prints "8.9 · 10211".  The ancestor's genome is 4,629,812 base pairs, which gives 4.1 × 10⁻⁴ mutations per genome per generation. ↩ ↩

Every figure is from the published HIV article on this site unless marked.  Carriers:  42 million.¹⁶  Particles:  10¹¹ made per person per day, and at most 10⁹ cells infected.³⁴  Alive at once:  4.2 × 10⁷ × 10¹¹ = 4 × 10¹⁸.  Generations:  100 years at 2.6 days, about 14,000;  the 2.6 days is from Perelson and colleagues 1996, which was not re-read, and Rambaut gives about 2.5.  Births are counted over 40 years, 14,600 days:  14,600 × 10¹¹ × 4.2 × 10⁷ = 6.1 × 10²² particles.  Mutations per round of infection:  2 × 10⁻⁵ × 9,181 letters = 0.18.³⁵  Mutations:  6.1 × 10²² × 0.18 = 1.1 × 10²².  The figures by infected cells are this article's:  14,600 × 10⁹ × 4.2 × 10⁷ = 6.1 × 10²⁰ cells, and × 0.18 = 1.1 × 10²⁰ mutations.  Both counts assume 42 million carriers for all 40 years, which is too many for the early years.  Effective size:  the HIV article reports 450 to 10⁵ per patient from a table in Althaus and colleagues 2005, which was not re-read.  Output:  the HIV article counts about 5,160 changes fixed in the groups of HIV since it entered humans and takes 5,000 as an upper bound on constructive ones.  5,000 ÷ 6 × 10²² = 8 × 10⁻²⁰ per particle, and 5,000 ÷ 6 × 10²⁰ = 8 × 10⁻¹⁸ per infected cell. ↩ ↩ ↩

Payne, D.  “Spread of chloroquine resistance in Plasmodium falciparum.”  Parasitology Today 3(8):241–246.  Aug 1987.  Read in abstract only, from the Europe PMC record.  The full text is behind a paywall and was not obtained.

1. 22a.

   Section Abstract:  “The drug was introduced in 1934, but was not in large-scale use until the early 1950s.  Anecdotal reports suggest that resistance emerged as early as 1957 both in Colombia and along the then Cambodia-Thailand border area.  But by 1960, resistance in these areas was confirmed - and may represent two separate events.” ↩ ↩

Every figure is from the experiment's article on this site.  Each flask holds 10 mL at about 5 × 10⁷ cells per mL, and 1% is moved to fresh medium daily.¹⁷  Births per flask per day:  5 × 10⁸ − 5 × 10⁶ = 4.95 × 10⁸.  Days:  82,000 generations ÷ 6.64 = 12,342.⁵  Births:  6.1 × 10¹² per flask and 7.3 × 10¹³ for twelve.  Mutations:  6.1 × 10¹² × 4.1 × 10⁻⁴ = 2.5 × 10⁹ per flask and 3.0 × 10¹⁰ for twelve.²⁰  That uses the ancestor's rate.  Six of the twelve populations later raised their mutation rate about a hundredfold, so the true total is higher.  Births are an upper estimate, because evolved cells are larger and reach lower densities.  Effective size:  about 10⁷.⁴⁹  Losses:  all twelve populations lost the ability to use ribose within 2,000 generations.⁴¹  The citrate gain counts zero nucleotides because the promoter and the gene it was joined to both existed already.  The experiment's article reports, from Van Hofwegen and colleagues 2016, that citrate use arose in as little as 19 days when cultures were left to starve between weekly transfers. ↩ ↩ ↩

Every figure is from the lambda article on this site, except the total of mutations.  Phage stood at 10⁶ to 10⁷ per mL in 10 mL flasks.⁸  A later paper by the same laboratory used 6.3 × 10⁹ per flask.²⁵  With a 1% daily transfer the births per day are about one flask-full.  Per successful flask, twelve days to the median success:  10⁷ × 12 = 1.2 × 10⁸ and 6.3 × 10⁹ × 12 = 7.6 × 10¹⁰.  For all 96 flasks over 20 days:  10⁷ × 20 × 96 = 1.9 × 10¹⁰ and 6.3 × 10⁹ × 20 × 96 = 1.2 × 10¹³.  Mutations per genome per copy:  0.0038.²⁶  Mutations for all 96 flasks are this article's product:  7.2 × 10⁷ and 4.6 × 10¹⁰.  Origins:  24 of 96 flasks,⁸ and 1 of 6 in an earlier run, so 25 of 102.  Nucleotides:  four, all required.⁸  Per birth, successful flasks only:  4 ÷ 7.6 × 10¹⁰ = 5 × 10⁻¹¹ and 4 ÷ 1.2 × 10⁸ = 3 × 10⁻⁸.  Counting the flasks that failed lowers both about fourfold.  No effective size or count of generations was published. ↩ ↩ ↩

Gupta, Animesh et al.  “Host-parasite coevolution promotes innovation through deformations in fitness landscapes.”  eLife 11:e76162.  2022.  CC BY 4.0.  Read as the eLife PDF from PubMed Central;  locators are that PDF's own "N of 22" footer pages.  Mirror:  PMC

1. 25a.

   Page 5:  “(960 generations; ~6.3×10⁹ λ particles, Figure 4—figure supplement 1; Meyer et al., 2012) and λ’s intrinsic mutation rate (7.7×10^-8 base^-1 replication^-1) (Drake, 1991).”  Page 15:  “we decided to run the simulation for a somewhat arbitrary amount of time, 960 generations which corresponds to two doublings per hour for the 20-day experiment we are trying to replicate”.  Superscripts restored from the journal XML;  the PDF text layer prints them inline.  These are the authors' simulation inputs, not a per-flask census. ↩ ↩

Drake, John W. et al.  “Rates of spontaneous mutation.”  Genetics 148(4):1667–1686.  1998.  sources/papers/drake-1998_rates-of-spontaneous-mutation.pdf, publisher PDF with printed folios.  Gupta et al. 2022 use the same lambda rate, citing Drake 1991, which this paper updates.  Mirror:  PMC

1. 26a.

   Page 1670, table 4:  The row for bacteriophage lambda gives genome size 4.9 × 10⁴ bases, mutations per base pair per replication 7.7 × 10^-8, and mutations per genome per replication 0.0038.  The row for Escherichia coli in the same table gives 5.4 × 10^-10 per base pair per replication, which is where the ratio of about 140 comes from.  Not quoted verbatim, because the PDF text layer renders the times sign as a digit and drops the superscript minus;  the values are read against the table's own column headings.  The table's footnote reads "Values are from Drake (1991), excluding the two well defined outliers and updated slightly as described in the text." ↩ ↩ ↩

Every figure is from the stickleback article on this site.  About 3,000 sea-run fish were put into each of two Alaskan lakes, Cheney in 2009 and Scout in 2011, and sampled to 2017.²⁸  Fish-generations at one year each:  3,000 × 8 + 3,000 × 6 = 42,000.  This is a floor, because the populations grew.  Mutations per fish:  5.11 × 10⁻⁹ × 2 × 463 million letters = 4.73.²⁹  Mutations:  42,000 × 4.73 = 2 × 10⁵.  The samples were pools of 100 fish, which could not have detected a new variant, so the absence of new adaptive variants is not a measured zero.  The older changes are the Pitx1 deletions, scored as a loss, and changes at Eda, Bmp6 and Fads2, scored as modifications. ↩ ↩

Roberts Kingman, Garrett A. et al.  “Predicting Future from Past:  The Genomic Basis of Recurrent and Rapid Stickleback Evolution.”  Science Advances 7(25).  Jun 18, 2021.  Read from the PMC copy, which has no page numbers, so claims give section headings.  CC BY-NC.  The supplement was not read.  Article number eabg5285.  Mirror:  PMC

1. 28a.

   Section Rapid contemporary evolution and TempoPeak identification:  “This marked congruity strongly suggests that the ancient SGV represented by Pacific EcoPeaks is the primary genomic feature enabling extremely fast evolution of freshwater phenotypes in stickleback from the northeast Pacific basin.” ↩ ↩

2. 28b.

   Section Rapid contemporary evolution and TempoPeak identification:  “Bell et al. (47) introduced ~3000 anadromous RS fish into each of two other Cook Inlet lakes without outlets that had been similarly treated to exterminate fish: Cheney Lake (CH) in 2009 and Scout Lake (SC) in 2011. Low–armor-plated (~5 to 7 plates per side) stickleback began to appear in the second and third generation after founding in CH and SC respectively, and, by 2017, they had increased to 20 to 30% (Fig. 2B).” ↩ ↩

Zhang, Chaowei et al.  “Rate of De Novo Mutations in the Three-Spined Stickleback.”  Heredity 134(7):387–395.  2025.  Read from the PMC copy.  CC BY.  Mirror:  PMC

1. 29a.

   Section Results:  “After applying a series of filters, 115 unique de novo mutations (DNMs) were detected”.  “The overall average per-generation point DNM rate was estimated to be µ = 5.11 × 10^−9/bp/gen (95% confidence interval: 4.08–6.14 × 10^−9/bp/gen, with zero-inflated method being 5.07 × 10^−9/bp/gen)”.  “Assuming a generation time of 3 years for the marine three-spined sticklebacks, the yearly mutation rate would be, on average, 1.70 × 10^−9/bp/year.” ↩ ↩

Every figure is from the article on malaria resistance alleles on this site, except the total of mutations.  The exposed population is assumed, at 10⁶, 10⁷ or 10⁸, because no census of malarial regions in past millennia exists.  Generations:  7,500 to 10,000 years at 25 years each.⁵⁶  Births:  10⁶ × 300 = 3 × 10⁸ and 10⁸ × 400 = 4 × 10¹⁰.  Mutations are this article's product with 63.2 per child:¹⁹  1.9 × 10¹⁰ and 2.5 × 10¹².  Effective size:  10,400 in Charlesworth's table and 22,118 in Lynch's dataset.^{10 46}  Gains:  sickle haemoglobin, haemoglobin E and the glycophorin rearrangement called DUP4, the last two each scored as gain with loss.  Losses:  G6PD deficiency, Duffy negativity, the thalassaemias and Southeast Asian ovalocytosis.  Modification:  haemoglobin C.  Nucleotides:  one each for haemoglobins S, E and C, and none for DUP4, which was made by rearrangement.  For scale only:  3 ÷ 4 × 10¹⁰ = 8 × 10⁻¹¹ and 3 ÷ 3 × 10⁸ = 10⁻⁸ per birth.  Those figures are not in the table because the births are assumed. ↩ ↩

Every figure is from the influenza article on this site.  Target cells in one adult upper respiratory tract:  4 × 10⁸.  Particles released per infected cell:  about 15,000, a cell-culture figure at high multiplicity.  Genomes per infection:  6 × 10¹⁰ to 6 × 10¹², on an assumption that between 1% and 100% of the cell pool is infected;  that assumption is the ledger's largest uncertainty and it is the article's own.  Cases a year:  about 1 billion.  Genomes a year:  6 × 10¹⁹ to 6 × 10²¹.  The century total corrects for a world holding 1.8 billion people in 1918 and 8.2 billion now, giving 3 × 10²¹ to 3 × 10²³.  Mutations per replicated genome:  2 to 3, measured by a twelve-class fluctuation test, so 7 × 10²¹ to 1 × 10²⁴ in total.  Genome 13,500 bases.  Output:  nine new glycosylation sites at one to three nucleotides each, about seven positions behind the major antigenic jumps, four carrying the drug resistances, and ten separating the 1918 polymerases from avian ones, which is about thirty distinct positions;  counting every adaptive substitution that fixed instead gives 100 to 300.  The gain is the glycosylation sites.  The census figure overstates the effective search badly:  the transmission bottleneck is one or two genomes, and about 10¹¹ lineages ever crossed from one person to another. ↩ ↩

Every figure is from the SARS-CoV-2 article on this site.  Infections plus reinfections to 14 November 2021:  3.80 × 10⁹, itself a lower bound.  Virions produced per infection:  10¹² to 3 × 10¹³, the arithmetic mean rather than the median.  Births:  3.8 × 10²¹ to 1.1 × 10²³.  Genome 29,903 bases, so 89,709 possible single substitutions.  Mutation rate 1.3 × 10⁻⁶ per base per replication cycle, giving 0.0389 mutations per genome copied and 1.5 × 10²⁰ to 4.4 × 10²¹ in total.  Output:  12 to under 100 nucleotides.  Nothing in the record scores as a gain.  Transmission bottleneck 1 to 8 virions. ↩ ↩

Every figure is from the tuberculosis article on this site.  Bacilli in one adult with cavitary disease:  10⁷ to 10⁹, taken as 10⁸;  that figure is the article's own, anchored on sputum counts rather than measured directly.  Cases:  10.7 million in 2024.  Drug era:  about 80 years, from streptomycin in 1944.  Births:  3 × 10¹⁸ to 3 × 10²⁰.  Genome 4,411,529 base pairs.  Mutation rate 2.01 × 10⁻¹⁰ to 2.01 × 10⁻⁹ per base pair per generation, the range being how slowly the bacillus divides inside the body, so 0.0009 to 0.009 mutations per bacillus born and 3 × 10¹⁵ to 3 × 10¹⁷ in the drug era, by two routes that agree.  Each of the 1.32 × 10⁷ possible single changes arose about 7.6 × 10⁸ times.  A named pair in one cell in one generation is one in 2.2 × 10²⁰, so about 0.05 such events in the whole drug era.  Output:  1 to about 30 nucleotides.  Nothing scores as a gain.  Generation time in the body is somewhere between 1 and 10 days and is not known, so no generation count is printed. ↩ ↩

Coffin, John, and Ronald Swanstrom.  “HIV pathogenesis:  dynamics and genetics of viral populations and infected cells.”  Cold Spring Harbor Perspectives in Medicine 3(1):a012526.  Jan 2013.  A review by two HIV researchers.  Read from the PubMed Central page, which has no page numbers.

1. 34a.

   Section Factors of HIV-1 Evolution, Drift:  “In the case of viral populations, it is important to bear in mind that the population size is determined by the number of cells infected at each round of replication, not by the number of virions produced by them.  In the case of HIV-1 infection, perhaps 10¹¹ virions are produced daily; the number of cells infected in the same time span is still a matter of some debate, but is unlikely to exceed 10⁹.” ↩ ↩

Zanini, Fabio et al.  “In vivo mutation rates and the landscape of fitness costs of HIV-1.”  Virus Evolution 3(1).  2017.  Article number vex003.  Open access, CC BY.  Read from the Europe PMC full text, which has no page numbers.  Mirror:  PMC

1. 35a.

   Section Abstract:  “At approximately neutral sites, mutations accumulate with a rate of 1.2 × 10⁻⁵ per site per day, in agreement with the rate measured in cell cultures.”  Section 1. Introduction:  “a total rate of about 2 × 10⁻⁵ mutations per site per replication cycle is reported.”  The second figure is the authors' report of earlier work in cell culture.  A replication cycle is one round of infection of a cell. ↩ ↩ ↩

Each figure is from the article linked in the row.  Lactase:  Tishkoff and colleagues name four variants,⁵⁷ and the lactase article adds a fifth and scores it as a candidate gain.  Each is one letter.  That article computes that the European letter arises about three times in a million people over 240 generations.  Beta-lactamase:  five changes, four in the protein and one in the control region, raise resistance to cefotaxime about 46,000-fold.³⁷  NylB:  two single-letter changes separate the active enzyme from its nearly inactive twin.³⁸  Which of the two forms is older has not been shown. ↩ ↩ ↩ ↩

Weinreich, Daniel M. et al.  “Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins.”  Science 312(5770):111–114.  Apr 7, 2006.  Paywalled at the publisher and reported closed by Unpaywall, OpenAlex, Europe PMC and Semantic Scholar's public API. The full text was obtained from a Wayback capture of a university course mirror of the publisher PDF, with printed folios 111 to 114 in the running feet. The library previously held the abstract only. The PDF interleaves with an unrelated economics Report, so each page was extracted separately, and Table 1 was read off a 110 dpi page image because pdftotext destroys its exponents.  Mirror:  Archive.org

1. 37a.

   Page 112:  “Applying this population genetic reasoning (12) to the data in Table 1 reveals that 102 of the 120 mutational trajectories from TEM wt to TEM* are selectively inaccessible.”  “Rather, four mutations have negligible or even negative effects on drug resistance in some combinations.” ↩ ↩

2. 37b.

   Page 111:  “These consist of four missense mutations [A42G, E104K, M182T, and G238S; numbering as in (8)] at clinically important residues (3, 9) and one 5′ noncoding mutation [g4205a; numbering as in (4)], and we denote this high-resistance quintuple mutant TEM*.”  The paper's square brackets are reproduced. The fifth change is not in the protein; it raises expression about 2.5-fold. ↩ ↩

Kato, Ko et al.  “Amino acid alterations essential for increasing the catalytic activity of the nylon-oligomer-degradation enzyme of Flavobacterium sp.”  European Journal of Biochemistry 200(1):165–169.  1991.  Free to read at the publisher.  EII is NylB and EII' is NylB'.  Copyright.

1. 38a.

   Page 168:  “An alteration, Gly181 → Asp, is made by a single nucleotide substitution (G to A) at the second base in the codon, and His266 → Asn by a substitution (C to A) at the first base in the codon.  While the nylB and nylB' genes have diverged from their common antecedent in the evolutionary process, the 140 base substitutions should have been accumulated in the 1176-bp of the coding regions [5].”  The scan's text layer prints the arrows as "-+". ↩ ↩

Blount, Zachary D. et al.  “Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli.”  Proceedings of the National Academy of Sciences 105:7899–7906.  2008.  Read from the publisher PDF in the library.  PDF page 2 carries the printed page number 7900.

1. 39a.

   Page 7900:  “This ratio implies, to a first approximation, that each population tried every typical one-step mutation many times.” ↩

Behe, Michael J.  “Experimental Evolution, Loss-of-Function Mutations, and "The First Rule of Adaptive Evolution".”  The Quarterly Review of Biology 85(4):419–445.  Dec 2010.  Behe is a professor of biological sciences at Lehigh University and a senior fellow of the Discovery Institute.  Read from the library PDF, a Wayback Machine copy of the author's own posting.  Every page prints its number in the running head.  The paper is set in two columns, so each page was extracted in reading order before any quotation was checked.  Copyright.  Mirror:  Archive.org

1. 40a.

   Page 439:  “the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100–1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.” ↩

Cooper, Vaughn S. et al.  “Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of Escherichia coli B.”  Journal of Bacteriology 183(9):2834–2841.  2001.  Read from the publisher PDF in the library.

1. 41a.

   Page 2834:  “Twelve populations of Escherichia coli B all lost D-ribose catabolic function during 2,000 generations of evolution in glucose minimal medium.”  The abstract adds that the mutants were all about 1 to 2% more fit than the ancestor. ↩ ↩

Couce, Alejandro et al.  “Changing fitness effects of mutations through long-term bacterial evolution.”  Science 383.  2024.  Article number eadd1417.  Eight authors, among them Richard Lenski and Olivier Tenaillon.  Read as the author manuscript in the library.  Copyright.

1. 42a.

   Page 12:  “To that end, we assumed that nonsense, frameshift, deletions, and insertions cause losses of function. We find that these presumptive inactivating mutations contribute most (>50%) of the early adaptive mutations in the LTEE, and they continue to be a sizable fraction over the long run (~25%, Fig. S18B).”  Page 12 of the author manuscript.  The classes are presumed from the type of mutation and were not assayed. ↩

Gabryszewski, Stanislaw J. et al.  “Combinatorial Genetic Modeling of pfcrt-Mediated Drug Resistance Evolution in Plasmodium falciparum.”  Molecular Biology and Evolution 33(6):1554–1570.  2016.  Open access, CC BY-NC.  Read from the Europe PMC full text, which has no page numbers, so places are given by section.  CQR is chloroquine resistance and md-CQ is the drug's main breakdown product.  Mirror:  PMC

1. 43a.

   Section Discussion, paragraph 2:  “As the fixation of pfcrt alleles bearing one to three mutations has not been documented in the field, we hypothesize that pfcrt-mediated CQR arose through mutational bursts with brief periods of intervening growth, whereby one or more mutations were acquired and expanded during a short time window prior to the acquisition of additional mutations.  Based on our combined IC50 and growth data, the most likely scenario would be the near-simultaneous emergence of three to four mutations.”  The source prints IC50 with a subscript. ↩

Ohta, Tomoko.  “The nearly neutral theory of molecular evolution.”  Annual Review of Ecology and Systematics 23:263–286.  1992.  Read from the publisher PDF in the library.  Page numbers are from the running heads.

1. 44a.

   Page 266:  “Thus, a codon bias in mammals appears to be largely determined by mutation pressure, but the bias in lower organisms with intermediate GC content such as in E. coli is influenced by selection because of the efficient selection in very large populations (102).” ↩

Lynch, Michael.  “The origins of eukaryotic gene structure.”  Molecular Biology and Evolution 23(2):450–468.  Feb 2006.  Free to read at the journal.  Read from the publisher's web page through a browser session and saved in the library.  The web page has no page numbers.  Lynch writes N with a subscript l for the long-term effective size.

1. 45a.

   Section Introduction:  “Second, I will summarize several sets of empirical data that show that the efficiency of natural selection declines dramatically between prokaryotes, unicellular eukaryotes, and multicellular eukaryotes.” ↩

2. 45b.

   Section The Three Genomic Perils of Increased Organism Size:  “Despite these uncertainties, it is clear that the disparity in N l across all domains of life is nearly 20 orders of magnitude less than the disparity in absolute numbers, a pattern that is consistent with a significant stochastic role of genetic draft in large populations.” ↩

3. 45c.

   Section The Three Genomic Perils of Increased Organism Size:  “Across a phylogenetically diverse set of a species, there is a strong correlation between the mutation rate per generation and genome size”.  “the extremes being 5.0 × 10⁻¹⁰ and 5.4 × 10⁻⁸ /bp/generation for prokaryotes and vertebrates, respectively.”  The words "set of a species" are the source's.  A figure reference between the two quotations is left out. ↩

4. 45d.

   Section The Three Genomic Perils of Increased Organism Size:  “small population size, tight linkage, and high background mutational activity—are jointly exacerbated as organisms increase in size, producing a synergism that causes substantial reductions in the efficiency of natural selection.” ↩

Lynch, Michael et al.  “The divergence of mutation rates and spectra across the Tree of Life.”  EMBO Reports 24(10):e57561.  2023.  Open access.  The figures used are from its Dataset EV1, a spreadsheet saved in the library.  Mirror:  PMC

1. 46a.

   Tables Dataset EV1, sheet Mutation Rates:  144 species have both a measured mutation rate and a measured diversity.  Effective size runs from 10,856 in the vervet monkey to 2.69 × 10⁹ in Pseudomonas fluorescens.  Medians by group are 8.88 × 10⁷ for 30 bacteria and 9.32 × 10⁴ for 68 vertebrates.  The row for Homo sapiens gives 22,118.  The row for Mus musculus gives a mutation rate of 5.35 × 10⁻⁹ per site per generation, a genome of 2,717 million bases and an effective size of 163,119.  The medians were computed for the Population Genetics article on this site. ↩ ↩ ↩ ↩

Lynch, Michael, and Adam Abegg.  “The rate of establishment of complex adaptations.”  Molecular Biology and Evolution 27(6):1404–1414.  Jun 2010.  Read from the publisher's web page in the library, which has no page numbers.

1. 47a.

   Section Abstract:  “In general, even in the face of deleterious intermediate steps, the time to establishment is minimized in populations with very large size.” ↩

Sanford, John et al.  “Mendel's Accountant:  a biologically realistic forward-time population genetics program.”  Scalable Computing:  Practice and Experience 8(2):147–165.  2007.  Sanford is a plant geneticist and the author of Genetic Entropy.  Read from the journal's PDF.  Page numbers are from the running heads.

1. 48a.

   Page 152:  “For organisms with smaller genomes such as yeast, which has a value for G on the order of 10⁷, the minimum absolute effect is larger.  This is consistent with the expectation that each nucleotide in a smaller genome on average plays a greater relative role in the organism’s fitness.”  G is the size of the genome in nucleotides.  Exponent restored. ↩

Good, Benjamin H. et al.  “The dynamics of molecular evolution over 60,000 generations.”  Nature 551:45–50.  2017.  Read from the author manuscript in the library.  Pages given are manuscript pages from the running head and not journal pages.

1. 49a.

   Page 4:  “When beneficial mutations are common, mutations that would otherwise drive selective sweeps can be outcompeted by other lineages carrying superior beneficial mutations”.  A reference number follows. ↩

2. 49b.

   Page 3:  “With an effective population size of Ne~10⁷, new mutations would require Δt ~ 0.1Ne ~ 10⁶ generations to reach the 10% detection threshold by genetic drift alone”.  Exponents restored;  the text layer prints 107 and 106.  A reference number follows the sentence. ↩ ↩

Desai, Michael M. et al.  “The speed of evolution and maintenance of variation in asexual populations.”  Current Biology 17(5):385–394.  2007.  Read from the author manuscript in the library.  The page given is a manuscript page and not a journal page.

1. 50a.

   Section Abstract, page 1:  “Our analysis predicts that the variation in fitness that a continuously evolving population maintains increases as the logarithm of the population size and logarithm of the mutation rate, yielding a similar logarithmic increase in the speed of evolution.” ↩

Karasov, Talia et al.  “Evidence that adaptation in Drosophila is not limited by mutation at single sites.”  PLoS Genetics 6(6):e1000924.  Jun 2010.  Open access, CC BY.  Read from the Europe PMC full text, which has no page numbers.

1. 51a.

   Section Abstract:  “This discrepancy arises because estimates of the effective population size are generally derived from levels of standing variation and thus reveal long-term population dynamics dominated by sharp—even if infrequent—bottlenecks.  The short-term effective population sizes relevant for strong adaptation, on the other hand, might be much closer to census population sizes.” ↩

Galtier, Nicolas.  “Adaptive protein evolution in animals and the effective population size hypothesis.”  PLoS Genetics 12(1):e1005774.  Jan 11, 2016.  Open access, CC BY.  Read from the publisher PDF in the library.

1. 52a.

   Section Abstract, page 1:  “The proportion of adaptive amino-acid substitution is found to be positively correlated to species effective population size.  This relationship, however, appears to be primarily driven by a decreased rate of nearly-neutral amino-acid substitution because of more efficient purifying selection in large populations.  Our results reveal that adaptive processes dominate the evolution of proteins in most animal species, but do not corroborate the hypothesis that adaptive substitutions accumulate at a faster rate in large populations.” ↩

Kuhn, Joseph A.  “Dissecting Darwinism.”  Baylor University Medical Center Proceedings 25(1):41–47.  Jan 2012.  Kuhn is a surgeon.  Read from the PubMed Central page, which has no page numbers.

1. 53a.

   Section Transitional species data:  “Evolutionary biology can be modeled over a relatively short time (30 years), while observing DNA mutations over 10²⁰ generations (40).  This is analogous to observing mutations in man or any mammal over 200 million years.”  “No gain-in-function mutations were observed in any of the long-term bacterial evolution studies.”  Kuhn's 10²⁰ is a count of organisms and not of generations.  His source for the second sentence is Behe 2010. ↩ ↩

Greenspoon, Lior et al.  “The global biomass of wild mammals.”  Proceedings of the National Academy of Sciences 120(10):e2204892120.  2023.  Open access.  Read from the Europe PMC full text, which has no page numbers.  The paper does not print a total count of individuals in its main text.  Mirror:  PMC

1. 54a.

   Section Abstract:  “We present a detailed assessment, arriving at a total wet biomass of ≈20 million tonnes (Mt) for all terrestrial wild mammals (95% CI 13-38 Mt), i.e., ≈3 kg per person on earth.”  Section Results:  “Bats (Chiroptera), for example, comprise one-fifth of species and two-thirds in terms of individual mammals, but only contribute less than one-tenth of the total biomass of wild land mammals”. ↩ ↩

2. 54b.

   Section Results:  “species with a body mass below 1 kg, while comprising >95% of all individuals, contribute only one-fifth to the total biomass”. ↩ ↩

Bar-On, Yinon M. et al.  “The biomass distribution on Earth.”  Proceedings of the National Academy of Sciences 115(25):6506–6511.  2018.  Open access.  Read from the Europe PMC full text in the library, which has no page numbers.  Mirror:  PMC

1. 55a.

   Section The Impact of Humanity on the Biosphere:  “The biomass of wild land mammals before this period of extinction was estimated by Barnosky (30) at ≈0.02 Gt C.  The present-day biomass of wild land mammals is approximately sevenfold lower, at ≈0.003 Gt C”.  Gt C is billions of tonnes of carbon.  The period meant is the loss of large land mammals between about 50,000 and 3,000 years ago on the standard timeline. ↩

Hedrick, Philip W.  “Population genetics of malaria resistance in humans.”  Heredity 107:283–304.  2011.  A review by a population geneticist at Arizona State University.  Library PDF.  PDF page N = printed page 282 + N, and every page prints its folio in the running head, which is how each locator below was fixed.  Two-column;  extracted a page at a time with pdftotext without -layout.  Where a number comes from a study Hedrick reviews rather than from his own work, the primary is named in the quotation.

1. 56a.

   Page 286:  “It appears that many of the genetic variants that provide resistance to severe malaria that have been dated are recent, not ancient, polymorphisms and that they have arisen in the last 5000–10 000 years or less (see Table 2).”  The sentence begins at the foot of p. 285;  the quoted words are on p. 286. ↩ ↩

Tishkoff, Sarah A. et al.  “Convergent adaptation of human lactase persistence in Africa and Europe.”  Nature Genetics 39(1):31–40.  Jan 2007.  University of Maryland.  Read from the PubMed Central author manuscript in the library;  locators are sections and Table 1.  Mirror:  PMC

1. 57a.

   Section Discussion, Convergent evolution of LP-associated variants:  “These data suggest that at least two, and probably four or more, distinct causal variants associated with lactase persistence (T-13910 in Europeans and C-14010, G-13907 and G-13915 in Africans) have evolved independently in European and African populations owing to convergent evolution in response to a strong selective force, adult milk consumption.” ↩ ↩

Wootton, John C. et al.  “Genetic diversity and chloroquine selective sweeps in Plasmodium falciparum.”  Nature 418:320–323.  Jul 18, 2002.  Read in abstract only, from the Europe PMC record.  The full text is behind a paywall and was not obtained.

1. 58a.

   Section Abstract:  “This disequilibrium and its decay rate in the pfcrt-flanking region are consistent with strong directional selective sweeps occurring over only approximately 20-80 sexual generations, especially a single resistant pfcrt haplotype spreading to very high frequencies throughout most of Asia and Africa.” ↩

Volkman, Sarah K. et al.  “A genome-wide map of diversity in Plasmodium falciparum.”  Nature Genetics 39(1):113–119.  Jan 2007.  Read in abstract only, from the Europe PMC record.  The abstract does not name the chromosome.  Lozovsky and colleagues, who cite this paper, place the region on chromosome 13.

1. 59a.

   Section Abstract:  “We identified multiple regions with signatures of selective sweeps in drug-resistant parasites, including a previously unidentified 160-kb region with extremely low polymorphism in pyrimethamine-resistant parasites.” ↩

Holmes, Bob.  “Bacteria make major evolutionary shift in the lab.”  New Scientist.  Jun 9, 2008.  A news report on Blount, Borland and Lenski 2008.  Read through a browser session and saved in the library.

1. 60a.

   Paragraph last:  ““The thing I like most is it says you can get these complex traits evolving by a combination of unlikely events,” he says.  “That’s just what creationists say can’t happen.””  The speaker is Jerry Coyne of the University of Chicago. ↩

Burmeister, Alita R. et al.  “Host coevolution alters the adaptive landscape of a virus.”  Proceedings of the Royal Society B 283:20161528.  2016.  CC BY 4.0.  Read as the publisher PDF from PubMed Central, nine pages numbered from 1, with the full text cross-checked against the Europe PMC XML.  Mirror:  PMC

1. 61a.

   Page 1:  “All six intermediates showed large increases in their adsorption rates on the ancestral host.”  Page 7:  “These data demonstrate that all six of the independently evolved phage genotypes had selective advantages, even before their descendants had gained the ability to use the OmpF receptor.”  “Four of the six evolved intermediate phage genotypes (A12, A7, D9 and G9) were significantly more fit than their common ancestor on the ancestral host cells”.  The first quotation is from the abstract on p. 1. ↩

Behe, Michael J.  “Can't Anybody Here Make Distinctions?”  Evolution News (now Science and Culture Today).  Apr 12, 2019.  Retrieved Sep 27, 2026.  The fourth of Behe's replies to Richard Lenski's blog series on Darwin Devolves, and his only direct answer to the lambda experiment.  Fetched by curl of the evolutionnews.org address, which redirects to scienceandculture.com;  date read from the page's datePublished metadata.  Saved as sources/web/behe-2019b_cant-anybody-here-make-distinctions.html.  Locators are the post's own section headings.

1. 62a.

   Section Solid and Interesting:  “What’s more, as Lenski’s lab later showed, the mutational pathway simply increased the initial strength of binding to the original protein until it also bound the structurally similar one.”  “the fact that some properties can develop gradually does not mean that all can (such as the book’s major example of chloroquine resistance). Thus the new lambda function is neither irreducibly complex nor beyond the edge of evolution.” ↩

Lozovsky, Elena R. et al.  “Stepwise acquisition of pyrimethamine resistance in the malaria parasite.”  Proceedings of the National Academy of Sciences 106(29):12025–12030.  Jul 21, 2009.  Read from the publisher PDF as archived by the Wayback Machine;  page numbers are the printed folios.  The paper codes each form as four digits for positions 51, 59, 108 and 164, so 0010 is S108N alone.  Mirrors:  PMC | Archive.org

1. 63a.

   Page 12025:  “The coding sequence for dihydrofolate reductase (DHFR) from the malaria parasite Plasmodium falciparum was mutagenized, and tests were carried out in Escherichia coli under conditions in which the endogenous bacterial enzyme was selectively inhibited.”  “The most frequent pathway (S108N and then C59R, N51I, and I164L) accounts for more than half of the simulated realizations.” ↩

Batten, Don.  “The adaptation of bacteria to feeding on nylon waste.”  Journal of Creation 17(3):3–5.  2003.  Batten is a plant physiologist with Creation Ministries International.  Read from the copy of the web page in the library.  The web page has no page numbers.

1. 64a.

   Section Stasis in bacteria:  “Note that the number of bacterial generations possible in over 130 years is huge—equivalent to tens of millions of years of human generations, encompassing the origin of the putative common ancestor of ape and man, according to the evolutionary story, indeed perhaps even all primates.”  The bacterium meant is Pseudomonas aeruginosa, named in 1872. ↩

uz-Zaman, Md Hassan et al.  “Promoter recruitment drives the emergence of proto-genes in a long-term evolution experiment with Escherichia coli.”  PLoS Biology 22:e3002418.  2024.  Open access, CC BY.  Read from the publisher PDF in the library.  Mirror:  PMC

1. 65a.

   Page 15:  “Future experimental studies will be required to establish whether the novel transcripts and peptides we detected affect E. coli fitness or are byproducts of mutations that are beneficial because of their effects on nearby, existing genes.” ↩