Recipes, Not Blueprints

The chapter starts from Bateson and Martin's 1999 comparison of an organism with a soufflé, in which nobody can point to the eggs. Developmental systems theory, drawing on Susan Oyama, treats genes as indispensable but as one of many developmental resources, alongside cells, nutrition, parental care and social surroundings. These resources are passed on by different routes and need not matter equally, so the job is to trace particular dependencies rather than to say that everything interacts. Marco Del Giudice is presented as sharing much of this outlook inside mainstream evolutionary biology. Even protein folding, where sequence carries a great deal of information, depends on cellular conditions, as Anfinsen's own account allowed.

Classic animal work is then reread. Belyaev's tame foxes show that selection on behaviour worked, although a 2020 historical study questioned the founders' origins and critics doubt a single domestication syndrome or a neural-crest cause. Levine's handled rats, and later studies linking maternal licking to methylation of a stress-hormone receptor gene, demonstrated epigenetic change within a lifetime, with cross-fostering helping to separate rearing from inheritance. The human extensions are weaker: methylation findings after childhood abuse have been inconsistent, and a large twin study found no robust blood signature. Statistical mediation, exposure in the womb and selective survival are each kept apart from claims of programming or transmission across generations.

Mary Jane West-Eberhard's idea that plastic responses can come first and be refined by selection later, through genetic accommodation, is described as testable but supported so far only by suggestive evidence. Hox genes and Wimsatt and Schank's notion of generative entrenchment show how history constrains development without making old mechanisms unchangeable.

On genetics, the author concedes that his 2001 thesis wrongly forecast that searches for causes of schizophrenia would fail. The 2022 Psychiatric Genomics Consortium study reported 287 associated regions pointing towards synaptic biology; in European-ancestry samples common variants account for about a quarter of the variance in liability, while the polygenic score explains far less and cannot diagnose anyone. Rare deletions and mutations in ten genes raise risk substantially, yet none is a gene for schizophrenia. Effects are shared across diagnoses, shrink in sibling comparisons and transfer poorly between ancestries.

In the Dutch famine of 1944–45, a natural experiment though not a randomised one, the cohort conceived at its peak later had about twice the risk of schizophrenia, but Chinese studies vary widely in quality and the pathways remain unresolved. The chapter ends by warning that a recipe can mislead too: an ingredient's role, its share of observed differences and how easily it can be changed are separate questions. It proposes using developmental systems as maps of dependencies to be tested.

Questions the chapter asks

• If genes do not specify the organism on their own, what else goes into building it?
• Have large genetic studies found genes for schizophrenia, and what do their results actually mean?
• Can famine before birth explain later mental illness, and how far can such evidence be trusted?

This is a summary of the chapter, written for this site; it is not an extract from the book. Coming soon from Amazon in Kindle, paperback and hardback editions.

Why Minds Break and these summaries are © 2026 Ian Pitchford, all rights reserved. The cover drawing is by Santiago Ramón y Cajal (1915), public domain.