To understand biological design, general principles must meet the facts of nature. Part 1 gave the principles, Part 2 the facts.
Only in Chapters 16 and 17 did I start on joining the two sides. Given the divide that remains between principles and application, why did I write this book? Because building up the two sides highlights the divide. A good failure clears the way forward.
The way forward begins with a method for how to study organismal design. How do we join general principles about the forces of design to the constraining biophysics and facts of nature?
No norms specify the proper method across all biological disciplines. Comparative predictions sometimes occur. Yet, in many fields, that comparative approach applies inconsistently, implicitly, or not at all.
Every comment about design should derive from a comparative hypothesis. As conditions change, we expect traits to change in a predicted way. Inferred causality arises from comparing altered conditions to changed traits, revealing the forces of design.
This book discussed many difficulties with this approach. But there is no better way.
Traditional phylogenetic methods of comparison between species and higher taxa have always had the right idea.75,173 However, those broad taxonomic scales of observed change often do not match the smaller scales over which conditions change and forces of design act.
Microbes provide the opportunity to match the scales of change to the underlying scales of force. Rapid generations, large populations, and great diversity at all scales allow wide choice in focal points for study.
Comments about design often arise as add-ons to studies done for other reasons. This book emphasized the failure of haphazard inference. Instead, the complexity of biological design demands a disciplined approach matched to the empirical problem.