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202 Epilogue For almost fifty years modern genetics was dominated by the so-called “central dogma,” framed by Sir Francis Crick in the 1960s. This is the idea that the flow of causal influence in heredity always moves from the genes outward to protein, organism , and environment, but not in the reverse direction, from environment, organism , or protein back to the genes.1 The central dogma represents the mid-twentieth century rejection of the possibility that environmental influences could act indirectly , through the body, on genes. But, since the sequencing of the human genome in the early 2000s, scientists have increasingly questioned the central dogma. The discovery that there were not enough coding human genes to do what we had been told for decades that they were probably doing led scientists to explore new approaches, and the field of epigenetics emerged as a force arguing the opposite. Epigenetics examines the developmental impact of cellular, structural, and environmental influences that alter gene action, but do not change the protein coding base sequences of messenger RNA. Epigeneticists have shown that features of the social and material environments related to poor nutrition, stress, and even child abuse can alter heredity from very early in development to produce attributes that are inherited across generations. And they are uncovering new and intriguing cellular mechanisms that explain how this happens and, therefore, how the presence of environmental influences may alter heredity to improve developmental outcomes. The development and evolution of adaptive structure, behavior, and cognition may even require such processes.2 These challenges to the central dogma have made some scientists once again receptive to a kind of Lamarckian inheritance, now understood in terms that are consistent with the known chemistry of heredity.3 This reversal in our view of the relationship between genes and environment has brought us back to Kammerer and Tandler’s basic question, a EPILOGUE 203 question that was nearly heretical just twenty years ago: what internal processes and environmental influences exist that adaptively (or maladaptively) alter heredity? Some have even suggested that Paul Kammerer was a forerunner of the changes now occurring, an issue about which there is debate.4 The resolution of that debate is less important here than the fact that, after being consistently and definitively rejected by the majority of mainstream science, a failed concept can return, albeit completely transformed, to reassert the very point that once condemned it: the environment’s formative role in affecting heredity to generate beneficial outcomes inherited by descendents. Both success and failure are relative to an historical moment, and the return of a widely rejected but plausible scientific concept highlights the historical complexity of the failure of Kammerer’s, Tandler’s, and Steinach’s vision in the 1920s. Their ideas and those of several others foreshadowed (but did not anticipate) the changes taking place in the study of heredity today. They were on a reasonable track. But they foreshadowed almost none of the important scientific details. These would be foreign to them. The terms and the spirit of their proposals, their scientific and their social base, were of a different time. But the recent changes help us see that in some sense, they did not fail as completely as it seemed they had from the point of view of the 1940s through the 1980s. That environmental change might be inherited was not a ridiculous idea, inconsistent with knowledge about heredity and condemned to unavoidable teleology. Especially when distinct scientific disciplines draw on one another’s concepts to address a question as complex as the relationship between nature and nurture, socially digested accounts of the technical and empirical accomplishments of opponents rarely capture the complexities of the effort. The result can contribute to a cultural memory of scientific success that embellishes the advances and undervalues serious challenges that were once issues of intense debate. The scientific debates about somatic induction in Central Europe in the 1920s are history. But their resonance with the recent changes in genetics makes it worth hearing their story. The idea of “flexible heredity” in any scientific dress raises difficult cultural and social questions. For example: if, as several investigators now suggest, epigenetic mechanisms greatly contribute to obesity and cancer, why is some research so concerned with applying and popularizing personal genome sequencing, so that each of us may know exactly what our individual coding DNA says? Why not pay more attention to the environments that organize and activate that DNA? How many group differences in health and well...

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