The bestselling author of Dogs That Know When Their Owners Are Coming Home offers an intriguing new assessment of modern day science that will radically. In Science Set Free (originally published to acclaim in the UK as The Science Delusion), Dr. Rupert Sheldrake, one of the world's most innovative scientists. Set Free1 (called The Science Delusion in the UK). Entirely new vistas open up when a widely accepted assumption is taken as the beginning of an inquiry.
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Science Set Free by Rupert Sheldrake - Excerpt - Free download as PDF File . pdf), Text File .txt) or read online for free. The bestselling author of Dogs That. Science Set Free: 10 Paths to New Discovery [Rupert Sheldrake] on site. com. *FREE* shipping on qualifying offers. The bestselling author of Dogs That. My website bernasungueta.tk has links to many articles, and 10 books, including Science Set Free, called The Science Delusion in the UK. .. newly posted blog called “The Wikipedia battle for Rupert Sheldrake's biography”.
Since these genes are so similar in fruit flies and in us, they cannot explain the differences between flies and humans. It was shocking to find that the diversity of body plans across so many different animal groups was not reflected in diversity at the level of the genes.
More Bad Science: 'Science Set Free' by Rupert Sheldrake
Gerhart, John; Kirschner, Marc Cells, Embryos and Evolution. Blackwell Science Evo-devo biologists and I myself use the term morphogenetic field to describe modular developmental systems, but our interpretations of how these fields work are very different.
This is the same kind of promissory materialism that developmental biologists have been coming up with for decades. Even in principle, it cannot give a satisfactory explanation for the development of form. Regulatory genes by definition regulate other genes, and hence regulate the formation of proteins.
That's what coding genes do: they code for the sequence of amino acids in protein molecules. They do not code for the shape of a wing, or an eye, or a leg. They just enable organisms to make particular proteins.
So even if the dark matter of the DNA contains complex regulatory sequences, all they will enable the developing organism to do is to make particular proteins in particular sequences.
The development of form itself, morphogenesis, is still unexplained. It's like trying to explain the construction of a computer by saying that the production of components, like transistors, results in complex chains of operations that cause the computer to assemble itself, and then start functioning spontaneously. By contrast, my hypothesis of morphogenetic fields sees them as active fields of information that shape developing organisms.
These fields inherit their own forms by the process of morphic resonance from past organisms. This is an act of faith. Like Sean B. Carroll, Visser is dismissive of alternative hypotheses, including my own.
Science Set Free
But Carroll's confidence in the face of so much uncertainty arises not from the scientific facts, but from a philosophical or ideological belief system. Carroll is a fellow of a militant sceptical organisation, the Committee for Skeptical Inquiry , publishers of the Skeptical Inquirer, and is deeply committed to a materialist worldview.
In one series, only quick learners were bred from in each generation, and in the other series only slow learners. As expected, the progeny of the quick learners tended to learn relatively quickly, while the progeny of the slow learners learned relatively slowly. However, even in the latter series, the performance of the later generations improved very markedly, in spite of repeated selection in favour of slow learning Fig.
Figure 29 The average number of errors in successive generations of rats selected in each generation for slowness of learning.
Data from McDougall, These experiments were done carefully, and critics were unable to dismiss the results on the ground of flaws in technique.
But they did draw attention to a weakness in the experimental design: McDougall had failed to test systematically the change in the rate of learning of rats whose parents had not been trained. One of these critics, F. Over the 18 generations of this experiment, Crew found no systematic change in the rate of learning either in the trained or in the untrained line.
Neither Crew nor McDougall was able to provide a satisfactory explanation of this discrepancy. But, as McDougall pointed out, since the purpose of the investigation was to bring to light any effect of training on subsequent generations, an experiment in which some rats received no training at all and many others received very little would not be qualified to demonstrate this effect.
Third, Crew adopted a policy of very intensive inbreeding, crossing only brothers with their sisters in each generation. He had not expected this to have adverse effects, since the rats came from an inbred stock to start with. Yet the history of my stock reads like an experiment in inbreeding.
There is a broad base of family lines and a narrow apex of two remaining lines. The reproductive rate falls and line after line becomes extinct.
The harmful effects of this severe inbreeding could well have masked any tendency for the rate of learning to improve. Over a period of 20 years, they measured the rates of learning of trained and untrained lines for 50 successive generations. In agreement with McDougall, they found that there was a marked tendency for rats of the trained line to learn more quickly in subsequent generations.
But exactly the same tendency was also found in the untrained line.
The answer is that he did. He thought this result was probably fortuitous, but added: It is just possible that the falling off in the average number of errors from to represents a real change of constitution of the whole stock, an improvement of it with respect to this particular faculty whose nature I am unable to suggest.
The similar improvement in both trained and untrained lines ruled out a Lamarckian interpretation. On the other hand, his results were confirmed. These results seemed completely inexplicable; they made no sense in terms of any current ideas, and they were never followed up.
But they make very good sense in the light of the hypothesis of formative causation. Of course they cannot in themselves prove the hypothesis; it is always possible to suggest other explanations, for example that the successive generations of rats became increasingly intelligent for an unknown reason unconnected with their training.
The initial rate of learning at both locations should be more or less the same. Then, according to the hypothesis of formative causation, the rate of learning should increase progressively at the location when large numbers are trained; and a similar increase should also be detectable in the rats at the second location, even though very few rats had been trained there. Obviously, precautions would need to be taken to avoid any possible conscious or unconscious bias on the part of the experimenters.
One way would be for experimenters at the second location to test the rate of learning of rats in several different tasks, at regular intervals, say monthly. Then at the first location, the particular task in which thousands of rats would be trained would be chosen at random from this set.
Moreover, the time at which the training began would also be selected at random; it might, for example, be four months after the regular tests began at the second location.
The experimenters at the second location would not be told either which task had been selected, or when the training had begun at the first location. If, under these conditions, a marked increase in the rate of learning in the selected task were detected at the second location after the training had begun at the first, then this result would provide strong evidence in favour of the hypothesis of formative causation. To demonstrate the same effect again and again, it would be necessary to change either the task or the species used in each experiment.Unfortunately Rupert Sheldrake is not a dog.
Mechanistic s cience in i tself gi ves no r eason t o su ppose t hat there is any point in life, or purpose in humanity, or that progress is inevitable. S cience was a r eturn t o t he inno cence o f t he first man, Adam, in the Garden of Eden before the Fall.
We just happen to exist in the one that has the right conditions for us.
Science Set Free by Rupert Sheldrake - Excerpt
New Scientist did indeed run a competition. Yet, it has important limitations that are becoming increasingly apparent. Each theory may have its own version of reality, but according to model-dependent realism, that is accepta- the ten d o g mas of moder n science 11 ble s o lo ng as t he t heories agr ee in t heir p redictions w henever they overlap, that is, whenever they can both be applied.