This week our featured book is The Why of Things: Causality in Science, Medicine, and Life, by Peter Rabins. Today, we are featuring another article by Peter Rabins on his unique three facet model approach to causality.
And, don’t forget to enter our book giveaway for a chance to win a free copy of The Why of Things.
In The Why of Things, I propose a three facet model of causality. Darwin’s concept of evolution and its elaboration over the past 150 years idea raise interesting questions about the role of models and hypotheses in illuminating scientific questions; the 3-facet model provides one way of examining these questions.
Evolution is built on the idea that variation exists in biological forms and that this variation affects outcome, in this instance likelihood of survival. Variation, in turn, is the result of the Watson-Crick Model of DNA and the knowledge (scientific evidence) that organisms of the same species have different nucleotides at the same location in DNA. Thus, DNA, the biological substrate of heredity, is variable. Further it is changeable, since different base pairs are occasionally found within the cells of a single person and since the offspring of two individuals with known base pair arrangements can have a base pair pattern that neither parent had.
Among the mechanisms of change are external agents such as cosmic rays, radiation from human generated sources (X-Rays, nuclear weapon explosions), environmental agents (toxins). “Internal” sources of change in DNA include mis-copying (“errors”) DNA during reproduction and as the embryo develops. One of the major findings of that has emerged as the technology to sequence individual genomes has developed is the frequency of such copying changes. Single nucleotides can be inserted, deleted or changed, resulting in a change in the protein that is coded for or in a change in the instruction that that piece of DNA contains. Whole sections of DNA can be deleted, duplicated, triplicated even “thousandicated.” Pieces of genetic material can even be palindromic, that is repeated but in the backward order, as in the littoral palindrome “a man, a plan, a canal, Panama.”
The constant nature of internally and externally generated change, and the ability of organisms to survive with them is a predisposing cause of evolution and organismal variation. A specific change in the sequence of DNA can cause a change in a single organism. Sometimes these are deleterious. For example, the several thousand diseases in which Mendelian genetics is operative, can be caused by a change in one gene. Furthermore, there are hundreds of changes within the gene that predispose to cancer. Thus, for an individual who develops cancer the gene mutation is directly causal or precipitating, but individuals who inherit the gene abnormality are predisposed until the cancerous changes occur.
This “tendency” of DNA to change does not necessarily lead to a deleterious event. In fact, many changes in DNA are recognized during replication or in the mature organism, and the cells in which the change occurs eliminated by a multiplicity of body mechanisms. Mechanisms also exist to “repair” or change the sequence back to the original sequence. More central to this discussion, however, is that a change in DNA might lead to an event that increases an organism’s capacity. Such changes could be either predisposing or precipitating. If such a change were predisposing, it would influence survival or reproduction in some circumstance and not others. One theory of why there is genetic variation in the likelihood of becoming obese is that in times of scarcity of food, having genes that make fat storage more efficient favor survival, even though in times of plenty they favor an earlier death.
The programmatic level of causality identifies outcomes that arise from the interactions among different elements of a system. It is here that Darwin himself was theorizing, and the level at which his theory first gained attention. If fitter organisms are more likely to live to the age of reproduction and produce more progeny, and these progeny in turn are more likely to reproduce, then the gene variant that they carry become more common in the population. What is it that is “selecting” certain organisms or increasing the likelihood that they will survive and reproduce? What is it that makes them “fit?” In part it is the environment, since the ability to survive is related to how the organism interacts with the environment in which it exists. Widespread changes within a species occur by this environment interaction, one example of programmatic causality. The term “environment” encompasses a very broad set of agents, among them weather, geography, predators, and infectious agents. It is this complex, multi-faceted web of interacting agents that makes the programmatic level of causality challenging to disentangle at a causal level. It is only in recent years that the mathematical, conceptual and computational tolls needed to assess programmatic cause have become widely available and enriched the understanding of complex causality.
The purposive level of causal analysis is the most controversial, especially in science, since the two constructs, purpose and science seem incompatible. This may be one of the challenges faced by evolutionists since the over-simplification of the term “survival of the fittest” implies to some a pre-established goal. I assume evolutionary biologists would disavow the idea that there is a purpose to evolution, but the idea that life is constructed somehow to reproduce seems to imply (although not necessarily) that this is a purpose. The negative connotation that some would attribute to the phrase “social Darwinism” derives from this idea, since those who justify eugenics, laissez faire capitalism, and the imposition of a system of government on others because they mirror evolutionary biology are utilizing a purpose mode of causal logic.
A second facet of causal analysis addresses the Models use to conceptualize and analyze the field. The Mendelian construct of a gene as a heritable unit is a categorical model; it both dichotomizes a trait as genetic or non-genetic and as present or absent. There are some universal characteristics of a given species that follow this Mendelian model (the autosomal recessive inheritance of cystic fibrosis is an example). However, it has become apparent, as briefly described above, that most traits and common diseases are dimensional. Height is the example mentioned above. Such characteristics are graded (organisms differ by degree or amount). There are multiple mechanisms by which genetic factors impart graded differences including the involvement of many genes, gene mechanisms that control the amount of a gene product that is produced, and complex biological feedback and feed forward systems that are under genetic control and effect end product production, behavior and adaptation. Many systems under genetic control do not follow the linear model of the dimensional model describes, but rather a non-linear, emergent model in which change appears to be sudden. Such systems are widespread but, in general, are just beginning to be understood.
The third facet describes the Logics analyzes causal relationships. The scientific method used by Mendel and the other researchers relies on empirical methods that utilize evidence that can be replicated and falsified, include multiple, convergent facts and concepts (paleontology, genetic epidemiology, field biology, animal behavior, and molecular biology, for example) and make predictions that can be tested. However, much of the power of Darwin’s argument 154 years ago and much of the explanatory power of evolution today rests on the narrative method. I believe it is the comprehensiveness and coherence of Darwin’s model, that is, its ability to “explain” so many factors of nature and its ability to do so in a clear and convincing way that has underlain its widespread acceptance since he proposed it. Not everyone is convinced, and many doubters use ecclesiastical (based on religious or spiritual reasoning) to dismiss it, but that is a logic that uses a different set of principles.
It seems reasonable to end this blog by asking what such a 3-facet approach adds to the very extensive discussion of evolution that dates back to its first presentation by Darwin (and Wallace). My hope is that it can clarify sources of agreement and disagreement, and clarify how discussion of differences can proceed. I have not discussed many of the controversies that remain, but suggest that appreciating that facts alone will not answer all disagreements, that different kinds of logic underlie some of the differences and that science and narrative not only can co-exist but have, in this example for 150 years, will encourage debate and clarity.