Scientists with USA addresses were underrepresented on papers about the relationships between athletic performance and innate variation

The scientometric data presented here demonstrate that compared to scientists with addresses elsewhere, scientists with USA addresses were disproportionately underrepresented as first authors, corresponding authors, and other authors listed on scientific papers about the relationships between athletic performance and innate variation in DR, ACE, ACTN3, or MSTN. These patterns of authorship were different from those of authors with addresses in other countries that were most frequently listed on papers on these topics (e.g. Germany, Italy, Japan, Norway, Spain, and the United Kingdom). Generally, authors with addresses in these countries (a) were either equally likely to be found or disproportionately more often found on papers that examined the relationship between the four innate factors and athletic performance compared to papers about the innate factors independent of athletic performance and (b) had a significantly greater proportional representation than did authors with USA addresses on papers about the relationship of the innate factors and athletic performance. However, there were several exceptions to this pattern.

First, authors with addresses in Norway were never listed on papers about the relationship between MSTN and athletic performance (Table 4). Consequently, they were disproportionately found listed on papers about MSTN independent of athletic performance (Table 4). However, the sample size of authors with addresses in Norway was small (n = 10). Second, authors with addresses in the United Kingdom were equally likely as those with addresses in the USA to be found on papers about the relationship between DR and athletic performance (Table 6). However, probably because of small sample sizes, the difference was not statistically significant (Table 6). Third, authors that listed addresses in Germany were never found on papers about MSTN independent of athletic performance (Table 3). As a consequence, authors with addresses in Germany were less likely than authors with USA addresses to be found on papers about the relationship between MSTN and athletic performance (Table 5). This was the only instance of authors with USA addresses having a significantly greater proportional representation on papers about the relationship between an innate factor and athletic performance. Last, authors with Japanese addresses were about twice as likely to be found on papers about the innate factors independent of athletic performance than on papers about the relationship between the innate factors and athletic performance (Table 4). Nevertheless, authors with Japanese addresses were more likely than those with USA addresses to be found on the pooled sample of papers that examined the relationship between the innate factors and athletic performance (Table 6). Taken together, these patterns suggest that authors based in these countries were more likely than authors with USA addresses to publish papers that examined questions about the roles of these innate factors in athletic performance.

Why are USA based scientists underrepresented as authors of papers on the relationships between athletic performance and DR, ACE, ACTN3, or MSTN?

Why didn’t scientists from USA based laboratories publish a comparable proportion of papers on the relationships between athletic performance and DR, ACE, ACTN3, or MSTN? We consider several possible explanations for this pattern.

First, perhaps the disproportionately small representation of papers from USA based authors about the relationships between athletic performance and DR, ACE, ACTN3, or MSTN because there are relatively few sports scientists in the USA? This is not a viable explanation. There are tens of thousands of American scientists interested in sports sciences and sports medicine; 90% of the 45,000 members of the American College of Sports Medicine reside in the USA (http://www.acsm.org).

Second, perhaps scientists working at USA based laboratories were simply not interested in sports so were not motivated to scientifically pursue questions about the relationships between athletic performance and innate variation in DR, ACE, ACTN3, or MSTN? This explanation is unlikely because, in general, sports interest is high in the USA. For example, Americans (a) participate in sports in large numbers (http://www.census.gov/hhes/school/data/cps/2010/tables.html; http://www.ayso.org/AboutAYSO/history.aspx; http://www.littleleague.org/learn/about/historyandmission/aroundtheworld.htm; http://www.ncaapublications.com/p-4334-1981-82-2012-13-ncaa-sports-sponsorship-and-participation-rates-report.aspx; Deaner et al. 2012), (b) are avid avid sports fans (pewresearch.org; http://www.census.gov/compendia/statab/cats/arts_recreation_travel/recreation_and_leisure_activities; http://nielsen.com/us/en/newswire/2011/ and (c) spend large sums of money on sporting equipment and activities (http://www.census.gov/compendia/statab/cats/arts_recreation_travel/recreation_and_leisure_activities.).). Collectively, these data demonstrate that the citizens of the USA devote considerable time, energy, and resources on sports activities. Even if USA scientists are less interested in sports than other Americans, we do not think that the lack of published research originating from USA based laboratories on the relationships between athletic performance and DR, ACE, ACTN3, or MSTN is primarily due to a lack of interest in sport sciences by USA scientists.

Third, a lack of government funding could be a proximate explanation for the lack of USA based published research examining the relationships between athletic performance and innate variation in DR, ACE, ACTN3, or MSTN. This is a viable, and important, explanation; neither NIH nor NSF reported funding research on these topics during the study period and NIH did not solicit any proposals to study these topics. Neither NIH nor NSF explicitly restricts funding from projects that propose to examine the relationships between athletic performance and innate variation. However, the project titles and abstracts of grant proposal not funded by NIH or NSF needed to test the hypothesis that cryptic funding restrictions (i.e., external censorship) are partly responsible for the disproportionately small number of papers originating from USA based laboratories are not easily available.

A lack of funding would negatively influence the pursuit of research on the relationship between athletic performance and innate factors for at least two reasons. First, contemporary scientific research is relatively expensive inhibiting scientists interested in these topics from pursuing them without financial support. Second, hiring, tenure, and promotion decisions at many academic institutions with a research mission in the USA are influenced, at least in part, by the ability of scientists to obtain funding from NIH or NSF and publish their results in peer-reviewed scientific journals thereby further inhibiting them from pursuing this kind of research.

It is not obvious why NIH and NSF did not fund research about the relationships between athletic performance and DR, ACE, ACTN3, or MSTN during the sample period. One possible explanation is that no researchers submitted grant proposals requesting funding to examine these topics. This hypothesis cannot be evaluated, but NIH did not solicit any proposals on these topics. Descriptions of the types of research funded by these agencies does not automatically preclude them from providing funding. The NIH, an agency of the US Department of Health and Human Services, is primarily responsible for biomedical and health-related research, with the goal of acquiring new knowledge to help prevent, detect, diagnose, and treat disease and disability (http://www.nih.gov). Although examining the biomedical correlates of DR, ACE, ACTN3, or MSTN in healthy individuals, including athletes, would appear to help meet NIH’s goals, the lack of funding for these studies may simply reflect NIH funding priorities. However, NIH did fund projects designed to examine the biomedical, but not athletic performance, correlates of DR, ACE, ACTN3, or MSTN during the sample period. Officially, NIH bases its funding decisions primarily on the scientific quality of proposals rather than targeting specific diseases but political pressure from disease advocacy organizations can have a large influence on NIH funding priorities (Best 2012). Therefore, the lack of NIH funding for studies specifically designed to focus on athletic performance is not surprising.

The NSF was created to “…to promote the progress of science; to advance the national health, prosperity, and welfare; to secure the national defense…” and funds basic biological research including that of physiological processes, development, and genetics (http://www.nsf.gov). Since 2000, NSF has funded projects designed to examine some of the correlates of MSTN in nonhumans, but not DR, ACE, or ACTN3 (http://www.nsf.gov/awardsearch). MSTN is of special interest to scientists because elucidating its biology may help provide therapies or cures for muscular dystrophy (Lee and McPherron 1999; Lee and McPherron 2001). This may help explain why 18 of the 89 (20%) of the authors on papers about the relationship between athletic performance and MSTN had USA addresses (Table 2).

Pervasive “blank slate” thinking affects the publication patterns of USA based scientists

Finally, we argue that a pervasive environmentalist paradigm within the USA best described as “blank slate thinking” (Pinker 2002) may be ultimately responsible for the disproportionately small proportion of published research about the relationship between athletic performance and DR, ACE, ACTN3, or MSTN by USA based scientists. Blank slate thinking refers to the idea that the differences in performance among individuals are best explained by environmental differences among them during development (i.e., nurture) rather than by differences in their genetic endowments (i.e., nature) (Pinker 2002; Ridley 2003).

The influence of blank slate thinking on the practice of American science has varied since 1900 (Segerstråle 2000; Alcock 2001). Early in the 20th Century many American scientists embraced the idea that genetic variation was largely responsible for individual and population variations in behavior (Segerstråle 2000). Indeed, many universities and states had departments or boards of eugenics (Kelves 1985). However, after World War II the intellectual focus shifted from biological to environmental explanations for human variation, including variations in social behavior (Segerstråle 2000). This shift occurred, at least partly, in response to the (a) atrocities of World War II resulting from Nazi philosophies of Aryan superiority and (b) 1952 UNESCO statement, “The Race Concept: Results of an Inquiry,” (http://unesdoc.unesco.org) that effectively banned biological research on human behavior (Segerstråle 2000; Selcer 2012). After the UNESCO statement, the “politically correct” view was that differences among individuals or groups were caused by differences in their social and cultural environments and had no biological bases. This perspective influenced the research programs of many scientists in the USA (Segerstråle 2000). Blank slate thinking retains a hold on many American academics and scientists (Segerstråle 2000) despite many of the recent theoretical and empirical advances in our understanding of how individual genetic variation and the environment synergistically influence human variation in the performance of a variety of different tasks (Pinker 2002; Ridley 2003; Plomin et al. 2008).

A growing body of scientific research directly challenges blank slate by revealing the important relationships between human genotypes and susceptibility to disease (e.g., Frank 2004; Tate and Goldstein 2004; Tishkoff and Kidd 2004). Indeed, physicians are coming to the realization that genotype is an important variable in considering disease diagnoses and treatment. Accordingly, NIH funds research on the relationship between genotype and disease susceptibility. The observation that NIH has funded several long several long-term studies of some physiological correlates of exercise (e.g., DREW (Morss et al. 2004), HERITAGE (Bouchard et al. 1995), INFLAME (Thompson et al. 2008), STRRIDE (Kraus et al. 2001)) that include both African-Americans and Americans of Caucasian descent as subjects is especially relevant to this study because it indicates that NIH is not adverse to funding projects that examine innate individual and population differences in physiology. This is interesting because the outcomes from studies that demonstrate individual, sex, and “racial” differences in physiology would appear to imply that these differences could result in innate differences in performance. Similarly, NSF has funded basic research on the relationship between genotypes and physiological phenotypes.

Nevertheless, the idea that innate differences among individuals play only a small role in producing differences in performance remains influential (e.g., Ericsson et al. 1993; Howe et al. 1998) despite the nearly global rejection by biologists of the idea that the phenotypic expression of morphological, physiological, and behavioral traits is determined by either genes or environment alone (Pinker 2002; Ridley 2003). Proponents of blank slate thinking provide a vivid example of how followers of the environmentalist paradigm explicitly reject modern theories and evidence about how traits are expressed. Sowell (1995) referred to the retention of incorrect theories in the face of contradictory data as the “irrelevance of evidence”.

In the end, athletic performance is a phenotype, and like all phenotypes results from the complex interactions between an individual’s genotype and its environment (Pinker 2002; Ridley 2003; Plomin et al. 2008). The lack of published scientific research originating from USA based scientists on the influence of innate variation on athletic performance is especially surprising because the hypothesis that athletic performance is not influenced by the innate differences among individuals in physical characteristics makes little biological sense.

Our findings beg the question; why don’t USA based scientists who conduct research on the relationships between genotypes and phenotypes and therefore, in general, appear to accept the idea that phenotypes result from the interaction between genes and environment, also publish scientific papers about the influences of innate variation on athletic performance? We argue that a history of slavery and its consequent explicit and implicit racism has made American scientists and USA governmental agencies like NIH and NSF reluctant about pursuing theories that posit innate variation as explanations for differences in athletic performance (Entine 2000, 2010; Smith and Hattery 2006; Smith 2007; Zirin 2008). For example, the legacy of the medical malfeasance of withholding treatment to syphilis-infected African-American men during the Tuskegee syphilis study has cast a long shadow on biomedical research in the USA (Reverby 2009).

A complete discussion of the discomfort Americans feel when confronting questions about how differences in athletic performance may be related to innate variation, especially the genetic variation among individuals of different geographic origin, is beyond the scope of this paper but is thoroughly covered by Entine (2000, 2010), Hoberman (1992, 1997) and Zirin (2008).