Ackermann et al. provide some interesting speculations about a possible scenario for the evolution of the brain mechanisms of vocal communication and language. But in the areas that I am familiar with, notably Neanderthal language (Johansson Reference Johansson2013), but also the history of the human language capacity in general (Johansson Reference Johansson2005; Reference Johansson2011), their treatment of the evidence is superficial and simplistic (see sect. 5.2), leading to their drawing conclusions that are insufficiently supported.
The authors' Section 5 supposedly provides “paleoanthropological perspectives” on their scenario, but contains little reference to paleoanthropological data. Instead it deals mainly with FOXP2, with fossil DNA virtually the only paleo-connection.
When mutations in the gene FOXP2 were found to be associated with specific language impairment (Lai et al. Reference Lai, Fisher, Hurst, Vargha-Khadem and Monaco2001), and it was shown that the gene had changed along the human lineage (Enard et al. Reference Enard, Przeworski, Fisher, Lai, Wiebe, Kitano, Monaco and Pääbo2002), it was heralded as a “language gene.” But intensive research has revealed a more complex story, with FOXP2 controlling synaptic plasticity in the basal ganglia (Lieberman Reference Lieberman2009) rather than language per se, and playing a role in vocalizations and vocal learning in a wide variety of species, from bats (Li et al. Reference Li, Wang, Rossiter, Jones and Zhang2007) to songbirds (Haesler et al. Reference Haesler, Wada, Nshdejan, Morrisey, Lints, Jarvis and Scharff2004). The changes in FOXP2 in the human lineage quite likely are connected with some aspects of language, but the connection is not nearly as direct as early reports claimed, and as Ackermann et al. apparently assume. While FOXP2 is clearly relevant at some level when modeling the brain mechanisms of language, Ackermann et al. go far beyond the data when they treat speech evolution as “FOXP2-driven” (sect. 5.2).
Likewise, the apparent presence of human FOXP2 in Neanderthals does not in itself prove that Neanderthals spoke (Benítez-Burraco & Longa Reference Benítez-Burraco, Longa, Scott-Phillips, Tamariz, Cartmill and Hurford2012). They most likely did speak, but that conclusion rests on a complex web of inferences from diverse sources of evidence, with FOXP2 just one minor piece of the puzzle (Dediu & Levinson Reference Dediu and Levinson2013; Johansson Reference Johansson2013; cf. Barceló-Coblijn & Benítez-Burraco Reference Barceló-Coblijn and Benítez-Burraco2013).
It is also imprudent to assume that Neanderthals and modern humans did not interbreed (target article, sect. 5.2), and quite improper to invoke Green et al. (Reference Green, Krause, Briggs, Maricic, Stenzel, Kircher, Patterson, Li, Zhai, Fritz, Hansen, Durand, Malaspinas, Jensen, Marques-Bonet, Alkan, Prüfer, Meyer, Burbano, Good, Schultz, Aximu-Petri, Butthof, Höber, Höffner, Siegemund, Weihmann, Nusbaum, Lander, Russ, Novod, Affourtit, Egholm, Verna, Rudan, Brajkovic, Kucan, Gusic, Doronichev, Golovanova, Lalueza-Fox, de la Rasilla, Fortea, Rosas, Schmitz, Johnson, Eichler, Falush, Birney, Mullikin, Slatkin, Nielsen, Kelso, Lachmann, Reich and Pääbo2010) in apparent support of this assumption. The jury is still out on the interbreeding issue (Johansson Reference Johansson2013), but evidence favoring interbreeding is accumulating (Green et al. Reference Green, Krause, Briggs, Maricic, Stenzel, Kircher, Patterson, Li, Zhai, Fritz, Hansen, Durand, Malaspinas, Jensen, Marques-Bonet, Alkan, Prüfer, Meyer, Burbano, Good, Schultz, Aximu-Petri, Butthof, Höber, Höffner, Siegemund, Weihmann, Nusbaum, Lander, Russ, Novod, Affourtit, Egholm, Verna, Rudan, Brajkovic, Kucan, Gusic, Doronichev, Golovanova, Lalueza-Fox, de la Rasilla, Fortea, Rosas, Schmitz, Johnson, Eichler, Falush, Birney, Mullikin, Slatkin, Nielsen, Kelso, Lachmann, Reich and Pääbo2010; Dediu & Levinson Reference Dediu and Levinson2013; Yotova et al. Reference Yotova, Lefebvre, Moreau, Gbeha, Hovhannesyan, Bourgeois, Bédarida, Azevedo, Amorim, Sarkisian, Avogbe, Chabi, Dicko, Kou'Santa Amouzou, Sanni, Roberts-Thomson, Boettcher, Scott and Labuda2011). Ackermann et al. do consider gene flow as an alternative scenario, but here the time frame is off; an emergence of the FOXP2 mutations 40,000 years ago (sect. 5.2) is not consistent with their presence in all modern human populations, as this postdates our most recent common ancestor (MRCA; Johansson Reference Johansson2011; Macaulay Reference Macaulay2005) and is not supported by a proper genetic model either (Diller & Cann Reference Diller, Cann, Botha and Knight2009).
In their main scenario of no interbreeding, Ackermann et al. have a different time-frame problem; the FOXP2 change is here constrained to be older than 400,000 years, but the fixation rate is not constrained in this case, nor is there any tight upper time limit (cf. Diller & Cann Reference Diller, Cann, Botha and Knight2009; Reference Diller, Cann, Tallerman and Gibson2012), so it is improper to conclude that it must have been “a relatively fast fixation” and thus “strong selection pressures” (target article, sect. 5.2).
Ackermann et al. dismiss the possible contribution of anatomical data from fossils in a single sentence (sect. 5.2, para. 2), and while they are correct that endocasts and cranial bases are not highly informative, other relevant anatomical evidence is available, as reviewed in Johansson (Reference Johansson2013) and Dediu & Levinson (Reference Dediu and Levinson2013).
Vocal displays as the selective driver of protolanguage evolution (target article, sect. 5.2; cf. Locke & Bogin Reference Locke and Bogin2006) are highly unlikely, as they would drive the evolution of something more resembling birdsong than language (Johansson et al. Reference Johansson, Zlatev and Gärdenfors2006). The distinct processing systems for music and language in modern humans likewise do not support such a scenario (Dediu & Levinson Reference Dediu and Levinson2013).
Ackermann et al. mention briefly many different popular works on language evolution (e.g., Bickerton Reference Bickerton2009; Mithen Reference Mithen2005; Falk Reference Falk2004), but they do not engage with them at any depth, just picking some aspect from each that fits into their own scenario, without integration.
In summary, Ackermann et al. accurately identify brain circuitry issues that need to be addressed in the context of language evolution, and they provide an interesting, if speculative, evolutionary scenario for these circuits. But as soon as they step outside the brain and attempt to engage with other types of evidence, or with possible selective scenarios driving language evolution, their treatment is insufficient.
Ackermann et al. provide some interesting speculations about a possible scenario for the evolution of the brain mechanisms of vocal communication and language. But in the areas that I am familiar with, notably Neanderthal language (Johansson Reference Johansson2013), but also the history of the human language capacity in general (Johansson Reference Johansson2005; Reference Johansson2011), their treatment of the evidence is superficial and simplistic (see sect. 5.2), leading to their drawing conclusions that are insufficiently supported.
The authors' Section 5 supposedly provides “paleoanthropological perspectives” on their scenario, but contains little reference to paleoanthropological data. Instead it deals mainly with FOXP2, with fossil DNA virtually the only paleo-connection.
When mutations in the gene FOXP2 were found to be associated with specific language impairment (Lai et al. Reference Lai, Fisher, Hurst, Vargha-Khadem and Monaco2001), and it was shown that the gene had changed along the human lineage (Enard et al. Reference Enard, Przeworski, Fisher, Lai, Wiebe, Kitano, Monaco and Pääbo2002), it was heralded as a “language gene.” But intensive research has revealed a more complex story, with FOXP2 controlling synaptic plasticity in the basal ganglia (Lieberman Reference Lieberman2009) rather than language per se, and playing a role in vocalizations and vocal learning in a wide variety of species, from bats (Li et al. Reference Li, Wang, Rossiter, Jones and Zhang2007) to songbirds (Haesler et al. Reference Haesler, Wada, Nshdejan, Morrisey, Lints, Jarvis and Scharff2004). The changes in FOXP2 in the human lineage quite likely are connected with some aspects of language, but the connection is not nearly as direct as early reports claimed, and as Ackermann et al. apparently assume. While FOXP2 is clearly relevant at some level when modeling the brain mechanisms of language, Ackermann et al. go far beyond the data when they treat speech evolution as “FOXP2-driven” (sect. 5.2).
Likewise, the apparent presence of human FOXP2 in Neanderthals does not in itself prove that Neanderthals spoke (Benítez-Burraco & Longa Reference Benítez-Burraco, Longa, Scott-Phillips, Tamariz, Cartmill and Hurford2012). They most likely did speak, but that conclusion rests on a complex web of inferences from diverse sources of evidence, with FOXP2 just one minor piece of the puzzle (Dediu & Levinson Reference Dediu and Levinson2013; Johansson Reference Johansson2013; cf. Barceló-Coblijn & Benítez-Burraco Reference Barceló-Coblijn and Benítez-Burraco2013).
It is also imprudent to assume that Neanderthals and modern humans did not interbreed (target article, sect. 5.2), and quite improper to invoke Green et al. (Reference Green, Krause, Briggs, Maricic, Stenzel, Kircher, Patterson, Li, Zhai, Fritz, Hansen, Durand, Malaspinas, Jensen, Marques-Bonet, Alkan, Prüfer, Meyer, Burbano, Good, Schultz, Aximu-Petri, Butthof, Höber, Höffner, Siegemund, Weihmann, Nusbaum, Lander, Russ, Novod, Affourtit, Egholm, Verna, Rudan, Brajkovic, Kucan, Gusic, Doronichev, Golovanova, Lalueza-Fox, de la Rasilla, Fortea, Rosas, Schmitz, Johnson, Eichler, Falush, Birney, Mullikin, Slatkin, Nielsen, Kelso, Lachmann, Reich and Pääbo2010) in apparent support of this assumption. The jury is still out on the interbreeding issue (Johansson Reference Johansson2013), but evidence favoring interbreeding is accumulating (Green et al. Reference Green, Krause, Briggs, Maricic, Stenzel, Kircher, Patterson, Li, Zhai, Fritz, Hansen, Durand, Malaspinas, Jensen, Marques-Bonet, Alkan, Prüfer, Meyer, Burbano, Good, Schultz, Aximu-Petri, Butthof, Höber, Höffner, Siegemund, Weihmann, Nusbaum, Lander, Russ, Novod, Affourtit, Egholm, Verna, Rudan, Brajkovic, Kucan, Gusic, Doronichev, Golovanova, Lalueza-Fox, de la Rasilla, Fortea, Rosas, Schmitz, Johnson, Eichler, Falush, Birney, Mullikin, Slatkin, Nielsen, Kelso, Lachmann, Reich and Pääbo2010; Dediu & Levinson Reference Dediu and Levinson2013; Yotova et al. Reference Yotova, Lefebvre, Moreau, Gbeha, Hovhannesyan, Bourgeois, Bédarida, Azevedo, Amorim, Sarkisian, Avogbe, Chabi, Dicko, Kou'Santa Amouzou, Sanni, Roberts-Thomson, Boettcher, Scott and Labuda2011). Ackermann et al. do consider gene flow as an alternative scenario, but here the time frame is off; an emergence of the FOXP2 mutations 40,000 years ago (sect. 5.2) is not consistent with their presence in all modern human populations, as this postdates our most recent common ancestor (MRCA; Johansson Reference Johansson2011; Macaulay Reference Macaulay2005) and is not supported by a proper genetic model either (Diller & Cann Reference Diller, Cann, Botha and Knight2009).
In their main scenario of no interbreeding, Ackermann et al. have a different time-frame problem; the FOXP2 change is here constrained to be older than 400,000 years, but the fixation rate is not constrained in this case, nor is there any tight upper time limit (cf. Diller & Cann Reference Diller, Cann, Botha and Knight2009; Reference Diller, Cann, Tallerman and Gibson2012), so it is improper to conclude that it must have been “a relatively fast fixation” and thus “strong selection pressures” (target article, sect. 5.2).
Ackermann et al. dismiss the possible contribution of anatomical data from fossils in a single sentence (sect. 5.2, para. 2), and while they are correct that endocasts and cranial bases are not highly informative, other relevant anatomical evidence is available, as reviewed in Johansson (Reference Johansson2013) and Dediu & Levinson (Reference Dediu and Levinson2013).
Vocal displays as the selective driver of protolanguage evolution (target article, sect. 5.2; cf. Locke & Bogin Reference Locke and Bogin2006) are highly unlikely, as they would drive the evolution of something more resembling birdsong than language (Johansson et al. Reference Johansson, Zlatev and Gärdenfors2006). The distinct processing systems for music and language in modern humans likewise do not support such a scenario (Dediu & Levinson Reference Dediu and Levinson2013).
Ackermann et al. mention briefly many different popular works on language evolution (e.g., Bickerton Reference Bickerton2009; Mithen Reference Mithen2005; Falk Reference Falk2004), but they do not engage with them at any depth, just picking some aspect from each that fits into their own scenario, without integration.
In summary, Ackermann et al. accurately identify brain circuitry issues that need to be addressed in the context of language evolution, and they provide an interesting, if speculative, evolutionary scenario for these circuits. But as soon as they step outside the brain and attempt to engage with other types of evidence, or with possible selective scenarios driving language evolution, their treatment is insufficient.